Boston, MA, United States
Boston, MA, United States

Massachusetts General Hospital is the original and largest teaching hospital of Harvard Medical School and a biomedical research facility located in the West End neighborhood of Boston, Massachusetts. It is the third oldest general hospital in the United States and the oldest and largest hospital in New England with 950 beds. Massachusetts General Hospital conducts the largest hospital-based research program in the world, with an annual research budget of more than $750 million. It is currently ranked as the #2 hospital in the United States by U.S. News & World Report. Wikipedia.


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Patent
President And Fellows Of Harvard College, The Broad Institute Inc. and Massachusetts General Hospital | Date: 2015-04-17

The present invention generally relates to microfluidic devices, including systems and methods for tagging droplets within such devices. In some aspects, microfluidic droplets are manipulated by exposing the droplets (or other discrete entities) to a variety of different conditions. By incorporating into the droplets a plurality of nucleic acid tags, and optionally ligating then nucleic acids together, the conditions that a droplet was exposed to may be encoded by the nucleic acid tags. Thus, even if droplets exposed to different conditions are mixed together, the conditions that each droplet encountered may still be determined, for example, by sequencing the nucleic acids.


Patent
Dana-Farber Cancer Institute, Beth Israel Deaconess Medical Center and Massachusetts General Hospital | Date: 2015-12-11

Provided herein are methods for treating cancer that is resistant to treatment with an anti-ErbB therapeutic agent and which is associated with an activating MET gene mutation or a MET gene amplification. The methods involve administering to a subject a combination of an anti-ErbB therapeutic and an anti-MET therapeutic. Also provided are methods for reducing ErbB mediated signaling or PI3 kinase mediated signaling in a cancer cell.


Patent
The Broad Institute Inc., Massachusetts General Hospital and NanoString Technologies | Date: 2016-10-14

The present disclosure relates to method of distinguishing between two or more species of one or more organisms in a sample, by contacting a biological sample comprising ribosomal ribonucleic acid (rRNA) with a set of antisense probes, wherein the set of probes contains at least one detectable probe that is specific for a target rRNA sequence of each species to be tested, and wherein the individual probes specific for each species comprises less than about 85% sequence identity; and, detecting hybridization between one or more of the probes and the rRNA, thereby distinguishing between two or more species in a sample.


Patent
Massachusetts General Hospital | Date: 2017-03-22

Embodiments of the invention provide knee prostheses (100) which more faithfully and closely replicate the function, anatomy and physiology of the normal human knee yielding a number of advantages. Among other things, such prostheses can provide an increased range of motion and function more normally particularly in extension, deep flexion and during normal gait. Knee prostheses according to various aspects of the invention recognize that during movement of the knee, particularly during flexion, the kinematics of the bones of the knee are a result of achieving equilibrium of the forces that cause motion of the knee. In addition, the shape of the articular surfaces acting in combination with forces imposed by various muscles, ligaments and tendons, determines the direction of the large contact forces.


Patent
Siemens AG and Massachusetts General Hospital | Date: 2017-01-18

A magnetic resonance (MR) method and system are provided for generating real-time prospective motion-corrected images using fast navigators. The real-time motion correction is achieved by using a 2D EPI navigator that is obtained using a simultaneous multi-slice blipped-CAIPI technique. The navigator parameters such as field of view, voxel size, and matrix size can be selected to facilitate fast acquisition while providing information sufficient to detect rotational motions on the order of several degrees or more and translational motions on the order of several millimeters or more. The total time interval for obtaining and reconstructing navigator data, registering the navigator image, and providing feedback to correct for detected motion, can be on the order of about 100 ms or less. This prospective motion correction can be used with a wide range of MR imaging techniques where the pulse sequences do not have significant intervals of dead time.


Lin W.M.,Massachusetts General Hospital | Fisher D.E.,Massachusetts General Hospital
Annual Review of Pathology: Mechanisms of Disease | Year: 2017

Melanoma is a complex and genomically diverse malignancy, and new genes and signaling pathways involved in pathogenesis continue to be discovered. Mechanistic insights into gene and immune regulation in melanoma have led to the development of numerous successful and innovative pharmacologic agents over recent years. Multiple targeted therapies and immunotherapies have already entered the clinic, becoming new standards of care and transforming the prognosis for many patients with malignant melanoma. In this review, we provide an overview of the current understanding of signaling and immune regulation in melanoma and implications for responses to treatment, organized in the framework of hallmark characteristics in cancer. © 2017 by Annual Reviews. All rights reserved.


Brizzi K.,Massachusetts General Hospital
Current Infectious Disease Reports | Year: 2017

Purpose of Review: Chikungunya virus (CHIKV) is a RNA arbovirus that typically causes fevers and arthralgias, but reports of neurologic findings have become increasingly common. This article reviews our current understanding of CHIKV-associated neurologic manifestations. Recent Findings: In the last 5 years, CHIKV endemicity has spread to the Americas and the number of cases of CHIKV-related disease has dramatically increased. Evidence suggests increasing neurovirulence of the virus, particularly among the critically ill. The spectrum of neurologic manifestations of the disease includes encephalitis, myelitis, and Guillain-Barre syndrome, but isolated reports of cranial neuropathies and cognitive deficits associated with recent infection also are reported. Summary: Though neurologic symptoms associated with CHIKV remain relatively uncommon, their frequency appears to be increasing. Clinicians treating patients with neurologic symptoms from CHIKV endemic areas should be aware of the growing association between CHIKV and neurologic sequelae to help guide diagnostics. Research into the optimal treatment of the disease is needed to inform treatment practices. © 2017, Springer Science+Business Media New York.


Florez J.C.,Massachusetts General Hospital | Florez J.C.,Cambridge Broad Institute | Florez J.C.,Harvard University
Diabetologia | Year: 2017

In recent years, technological and analytical advances have led to an explosion in the discovery of genetic loci associated with type 2 diabetes. However, their ability to improve prediction of disease outcomes beyond standard clinical risk factors has been limited. On the other hand, genetic effects on drug response may be stronger than those commonly seen for disease incidence. Pharmacogenetic findings may aid in identifying new drug targets, elucidate pathophysiology, unravel disease heterogeneity, help prioritise specific genes in regions of genetic association, and contribute to personalised or precision treatment. In diabetes, precedent for the successful application of pharmacogenetic concepts exists in its monogenic subtypes, such as MODY or neonatal diabetes. Whether similar insights will emerge for the much more common entity of type 2 diabetes remains to be seen. As genetic approaches advance, the progressive deployment of candidate gene, large-scale genotyping and genome-wide association studies has begun to produce suggestive results that may transform clinical practice. However, many barriers to the translation of diabetes pharmacogenetic discoveries to the clinic still remain. This perspective offers a contemporary overview of the field with a focus on sulfonylureas and metformin, identifies the major uses of pharmacogenetics, and highlights potential limitations and future directions. © 2017, Springer-Verlag Berlin Heidelberg.


Raff G.L.,Oakland University | Hoffmann U.,Massachusetts General Hospital | Udelson J.E.,Tufts University
JACC: Cardiovascular Imaging | Year: 2017

Over 8 million patients seek emergency department care for acute chest pain annually in the United States alone, and <5% have an acute coronary syndrome. In the absence of overt electrocardiographic or biomarker evidence, expensive and time-consuming diagnostic strategies are frequently required. Beginning in 2000, radionuclide myocardial perfusion, stress echocardiography, cardiac magnetic resonance imaging, and coronary computed tomographic angiography have become increasingly common in evaluating these patients. This review paper focuses on randomized clinical trials that provide the evidence base for these diagnostic strategies. Novel imaging modalities combining high-sensitivity troponin with imaging or combined anatomic-physiological evaluation using fractional flow reserve by computed tomography are also discussed. © 2017 American College of Cardiology Foundation


Kaplan L.M.,Massachusetts General Hospital
Gastrointestinal Endoscopy Clinics of North America | Year: 2017

Bariatric surgical procedures, including gastric bypass, vertical sleeve gastrectomy, and biliopancreatic diversion, are the most effective and durable treatments for obesity. In addition, These operations induce metabolic changes that provide weight-independent improvement in type 2 diabetes, fatty liver disease and other metabolic disorders. Initially thought to work by mechanical restriction of food intake or malabsorption of ingested nutrients, these procedures are now known to work through complex changes in neuroendocrine and immune signals emanating from the gut, including peptide hormones, bile acids, vagal nerve activity, and metabolites generated by the gut microbiota, all collaborating to reregulate appetite, food preference, and energy expenditure. Development of less invasive means of achieving these benefits would allow much greater dissemination of effective, gastrointestinal (GI)-targeted therapies for obesity and metabolic disorders. To reproduce the benefits of bariatric surgery, however, these endoscopic procedures and devices will need to mimic the physiological rather than the mechanical effects of these operations. © 2017 Elsevier Inc.


Chinnaiyan K.M.,Beaumont Health System | Weiner R.B.,Massachusetts General Hospital
JACC: Cardiovascular Imaging | Year: 2017

Cardiovascular imaging plays a central role in the diagnosis and treatment of cardiovascular disease. Recently, increased emphasis has been placed on quality in cardiovascular imaging, and it is becoming a central priority for various stakeholders, including patients, physicians, and payers. The changing health care landscape and associated challenges imposed on cardiac imagers, including reductions in reimbursement and growing need for pre-authorization, have also helped bring quality metrics to the forefront. Continuous quality improvement initiatives provide the framework for the team of physicians, technical staff members, administrators, and other health care professionals to deliver high-quality care. Efforts to improve quality in cardiac imaging have started to form the foundation for numerous research studies in this arena, and although few in number, randomized control trials have begun to emerge. This review highlights quality improvement studies focusing on appropriate use education, reporting, and radiation dose reduction in cardiovascular imaging. © 2017 American College of Cardiology Foundation


Fintelmann F.J.,Massachusetts General Hospital
Journal of Thoracic Imaging | Year: 2017

PURPOSE:: The aim of the study was to investigate the natural history of non–small cell lung cancers (NSCLCs) associated with cystic airspaces, including histopathology and molecular analysis. MATERIALS AND METHODS:: A total of 34,801 computed tomographic (CT) scans of 2954 patients diagnosed with NSCLC between 2010 and 2015 were evaluated for association with a cystic airspace. Characteristics on serial CT, 18F-fludeoxyglucose positron emission tomography, and pathologic analysis were recorded. RESULTS:: Cystic airspaces were associated with 1% of NSCLC cases (12 men and 18 women; median age, 66 y [range, 44 to 87 y]). Of the total number of patients, 97% had a smoking history. Twenty-four adenocarcinomas, 4 squamous cell carcinomas, and 2 poorly differentiated carcinomas were distributed throughout all lobes and were predominantly peripheral. Some cystic airspaces appeared in previously normal lungs, whereas others were preceded by subcentimeter nodules. Twenty of 30 cases demonstrated increased soft tissue due to wall thickening, increased loculations, enlargement and/or increased attenuation of a mural nodule, or replacement by a mass. 18F-fludeoxyglucose uptake was present if solid components measured >8 mm. Twenty of 30 patients demonstrated >1 cystic lesion or ground-glass nodule, lymphadenopathy, or evidence of prior lung resection. Pathologic analysis revealed that cystic airspaces correspond to a check-valve mechanism, adenocarcinoma superimposed on emphysema, cystification, and adenocarcinoma parasitizing a preexisting bulla. Fourteen of 26 tumors and 64% of adenocarcinomas tested positive for an alteration of KRAS with or without other alterations. CONCLUSIONS:: Cystic airspaces preceded by nodules can evolve into NSCLCs. Wall thickening and/or mural nodularity may develop. Location in the periphery of the upper lobes, emphysema, additional cystic lesions or ground-glass nodules, lymphadenopathy, and prior lung cancer should further increase suspicion. Cystic airspaces on CT can be due to a check-valve mechanism obstructing the small airways, lepidic growth of adenocarcinoma in an area of emphysema, cystification of tumor due to degeneration, or adenocarcinoma growing along the wall of a preexisting bulla. KRAS mutations are the predominant genetic alterations. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved


Laliberte B.,Massachusetts General Hospital
Pediatric Emergency Care | Year: 2017

ABSTRACT: Serotonin syndrome (SS) is a serious toxicity that manifests with symptoms such as tremor, hyperthermia, agitation, and altered mental status that may lead to seizures, coma, or death. Selective serotonin reuptake inhibitors may precipitate SS, particularly in combination with other drugs that possess serotonergic activity. We present a case of SS in a 14-month-old after an ingestion of the selective serotonin reuptake inhibitor vilazodone. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.


OBJECTIVES:: To determine whether early lactate reduction is associated with improved survival and good neurologic outcome in patients with out-of-hospital cardiac arrest. DESIGN:: Ad hoc data analysis of a prospective, multicenter observational study. SETTING:: Out-of-hospital cardiac arrest patients at 67 emergency hospitals in Kanto, Japan between January 2012 and March 2013. PATIENTS:: Adult patients with out-of-hospital cardiac arrest admitted to the hospital after successful resuscitation were identified. INTERVENTIONS:: Blood lactate concentrations were measured at hospital admission and 6 h after hospital admission. Early lactate clearance was defined as the percent change in lactate level 6 h after a baseline measurement. MEASUREMENTS AND MAIN RESULTS:: The 543 patients (mean age, 65 ± 16 yr; 72.6% male) had a mean lactate clearance of 42.4% ± 53.7%. Overall 30-day survival and good neurologic outcome were 47.1% and 27.4%, respectively. The survival proportion increased with increasing lactate clearance (quartile 1, 29.4%; quartile 2, 42.6%; quartile 3, 51.5%; quartile 4, 65.2%; p < 0.001). Multivariate logistic regression analysis showed that lactate clearance quartile was an independent predictor of the 30-day survival and good neurologic outcome. In the Cox proportional hazards model, the frequency of mortality during 30 days was significantly higher for patients with lactate clearance in quartile 1 (hazard ratio, 3.12; 95% CI, 2.14–4.53), quartile 2 (hazard ratio, 2.13; 95% CI, 1.46–3.11), and quartile 3 (hazard ratio, 1.49; 95% CI, 1.01–2.19) than those with lactate clearance in quartile 4. Furthermore, multivariate logistic regression analysis revealed that lactate clearance was a significant predictor of good neurologic outcome at 30 days after hospital admission. CONCLUSIONS:: Effective lactate reduction over the first 6 hours of postcardiac arrest care was associated with survival and good neurologic outcome independently of the initial lactate level. Copyright © by 2017 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.


Bruinsma B.G.,Massachusetts General Hospital
Transplantation | Year: 2017

BACKGROUND: The ongoing shortage of donor livers for transplantation and the increased use of marginal livers necessitate the development of accurate pretransplant tests of viability. Considering the importance energy status during transplantation, we aimed to correlate peritransplant energy cofactors to posttransplant outcome and subsequently model this in an ex vivo setting. METHODS: Sequential biopsies were taken from 19 donor livers postpreservation, as well as 30 min after portal venous (PVR) and hepatic arterial reperfusion (HAR) and analyzed by LC-MS for energetic cofactors (ATP/ADP/AMP, NADH/NAD, NADPH/NADP, FAD, GSSG/GSH). Energy status was correlated to posttransplant outcome. In addition, 4 discarded human DCD livers were subjected to ex vivo reperfusion, modeling reperfusion injury and were similarly analyzed for energetic cofactors. RESULTS: A rapid shift towards higher energy adenine nucleotides was observed following clinical reperfusion, with a 2.45-, 3.17- and 2.12-fold increase in ATP:ADP, ATP:AMP and energy charge (EC) after PVR, respectively. Seven of the 19 grafts developed early allograft dysfunction (EAD). Correlation with peritransplant cofactors revealed a significant difference in EC between EAD and normal functioning grafts (0.09 vs. 0.31, P<0.05). In the simulated reperfusion model, a similar trend in adenine nucleotide changes was observed. CONCLUSION: A preserved energy status appears critical in the peritransplant period. Levels of adenine nucleotides change rapidly following reperfusion and ratios of ATP/ADP/AMP following reperfusion are significantly correlated to graft function. Using these markers as a viability test in combination with ex vivo reperfusion may provide a useful predictor of outcome that incorporates donor, preservation and reperfusion factors. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.


Uchida M.,Massachusetts General Hospital
Journal of Clinical Psychopharmacology | Year: 2017

OBJECTIVE: Because of concerns about potential associations between high doses of citalopram and QTc prolongation in adults, this study examined whether such associations are operant in children. We hypothesized that therapeutic doses of nontricyclic antidepressant medications (non-TCAs) prescribed to children would be cardiovascularly safe. STUDY DESIGN: The sample consisted of 49 psychiatrically referred children and adolescents 6 to 17 years old of both sexes treated with a non-TCA (citalopram, escitalopram, fluoxetine, paroxetine, sertraline, bupropion, duloxetine, venlafaxine, mirtazapine). To standardize the doses of different antidepressants, we converted doses of individual medicines into “citalopram equivalent doses” (CEDs) based on dosing recommendation for individual antidepressants. Correlation analysis was carried out to compare the continuous and weight-based CED to variables of interest. A QTc grouping was defined as normal, borderline, or abnormal, and CED was compared across QTc groupings using linear regression. An antidepressant dosage group was defined as low or high dose, and a t test compared variables of interest across dosage groups. RESULTS: No significant associations were found between total or weight-corrected CEDs of any antidepressant examined and QTc or any other electrocardiogram or blood pressure parameters. In patients taking citalopram or escitalopram, a significant correlation was found between PR interval and total daily dose, which disappeared when weight-based doses were used or when corrected by age. CONCLUSIONS: Although limited by a relatively small sample size, these results suggest that therapeutic doses of non-TCA antidepressants when used in children do not seem to be associated with prolonged QTc interval or other adverse cardiovascular effects. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.


Dagogo-Jack I.,Massachusetts General Hospital | Shaw A.T.,Massachusetts General Hospital
Annals of Oncology | Year: 2016

In 2007, a chromosomal rearrangement resulting in a gene fusion leading to expression of a constitutively active anaplasticlymphoma kinase (ALK) fusion protein was identified as an oncogenic driver in non-small-cell lung cancer (NSCLC). ALKrearrangements are detected in 3%-7% of patients with NSCLC and are particularly enriched in younger patients withadenocarcinoma and a never or light smoking history. Fortuitously, crizotinib, a small molecule tyrosine kinase inhibitor initiallydeveloped to target cMET, was able to be repurposed for ALK-rearranged (ALK+) NSCLC. Despite dramatic anddurable initial responses to crizotinib; however, the vast majority of patients will develop resistance within a few years. Diverse molecular mechanisms underlie resistance to crizotinib. This review will describe the clinical activity of crizotinib, review identified mechanisms of crizotinib resistance, and end with a survey of emerging therapeutic strategies aimed atovercoming crizotinib resistance. © The Author 2016.


Bateman M.,Massachusetts General Hospital
Topics in Magnetic Resonance Imaging | Year: 2017

ABSTRACT: Magnetic resonance (MR) diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) offer unique insight into acute ischemic stroke pathophysiology. These techniques may offer the ability to apply pathophysiology to accurately individualize acute stroke reperfusion treatment, including extending the opportunity of reperfusion treatment to well beyond the current time-based treatment windows.This review examines the use of DWI and PWI in the major stroke trials, their current clinical utility, and potential limitations for reperfusion treatment selection. DWI and PWI continue to be investigated in ongoing randomized controlled trials, and continued research into these techniques will help achieve the goal of tissue-based decision making and individualized acute stroke treatment. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.


Raymond S.B.,Massachusetts General Hospital
Topics in Magnetic Resonance Imaging | Year: 2017

ABSTRACT: Leptomeningeal collaterals provide the primary source of perfusion to ischemic brain tissue following the onset of acute ischemic stroke and are becoming an important imaging biomarker for stroke therapy triage. Collateral circulation is predictive of infarct growth, end infarct volume, and response to endovascular therapy. The strength of the collateral circulation varies among patients and is partially dependent on genetic and modifiable risk factors. Collateral circulation may be assessed by standard angiographic techniques, including digital subtraction angiography, computed tomography and magnetic resonance (MR) angiography, as well as a growing array of advanced MR techniques including arterial spin labeling and dynamic MR angiography. Simple scoring systems are used to estimate the relative strength of the collateral circulation for a given patient, although there are some discrepancies in the predictive value of these systems. In this review, we discuss methods and techniques for determining the robustness of the collateral circulation and the role of the collateral circulation in acute ischemic stroke assessment and triage. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.


ABSTRACT: The role of interleukin-6 (IL-6) in physiological processes and disease is poorly understood. The hypothesis tested in this study was that selective alpha7 acetylcholine receptor (α7AChR) agonist, GTS-21, releases of IL-6 in association with myonuclear accretion and enhances insulin signaling in muscle cells, and improves survival of burn injured (BI) mice. The in vitro effects of GTS-21 were determined in C2C12 myoblasts and 7-day differentiated myotubes (myotubes). The in vivo effects of GTS-21 were tested in BI wild type (WT) and IL-6 knockout (IL6KO) mice. GTS-21 dose-dependently (0, 100 and 200?μM) significantly increased IL-6 levels in myoblasts and myotubes at 6 and 9?h. GTS-21-induced IL-6 release in myotubes was attenuated by methyllycaconitine (α7AChR antagonist), and by Stat-3 or Stat-5 inhibitors. GTS-21 increased MyoD and Pax7 protein expression, myonuclear accretion and insulin-induced phosphorylation of Akt, GSK-3β and Glut4 in myotubes. The glucose levels of burned IL6KO mice receiving GTS-21 decreased significantly compared to sham-burn IL6KO mice. Superimposition of BI on IL6KO mice caused 100% mortality; GTS-2 reduced mortality to 75% in the IL6KO mice. The 75% mortality in burned WT mice was reduced to 0% with GTS-21. These in vitro findings suggest that GTS-21-induced IL-6 release from muscle is mediated via α7AChRs upstream of Stat-3 and -5 pathways and is associated with myonuclear accretion, possibly via MyoD and Pax7 expression. GTS-21 in vivo improves survival in burned WT mice and IL6KO mice, suggesting a potential therapeutic application of α7AChR agonists in treatment of BI. © 2017 by the Shock Society


Franceschini M.A.,Massachusetts General Hospital
Optics InfoBase Conference Papers | Year: 2016

With the foundation of our seminal frequency-domain and diffuse optical spectroscopy work on neonates, we are developing novel devices and approaches to better quantify cerebral blood flow and oxygen metabolism in the clinical setting. I will present the first fully integrated FDNIRSDCS system. I will show results of this technology in measuring infants affected by hydrocephalus in Africa, and measuring pediatric and adult patients in intensive care settings in Boston. I will conclude by describing novel optical approaches to better quantify cerebral blood flow and to assess intracranial pressure continuously and non-invasively. © OSA 2016.


Herzberg B.,Massachusetts General Hospital | Campo M.J.,Massachusetts General Hospital | Gainor J.F.,Massachusetts General Hospital
Oncologist | Year: 2017

Historically, lung cancer was long considered a poorly immunogenic malignancy. In recent years, however, immune checkpoint inhibitors have emerged as promising therapeutic agents in non-small cell lung cancer (NSCLC). To date, the best characterized and most therapeutically relevant immune checkpoints have been cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and the programmed cell death protein-1 (PD-1) pathway. In early studies, PD-1/programmed cell death ligand-1 (PD-L1) inhibitors demonstrated promising antitumor activity and durable clinical responses in a subset of patients. Based on these encouraging results, multiple different PD-1/PD-L1 inhibitors have entered clinical development, and two agents (nivolumab and pembrolizumab) have gained regulatory approval in the United States for the treatment of NSCLC. In several large, randomized studies, PD-1/PD-L1 inhibitors have produced significant improvements in overall survival compared with single-agent docetaxel delivered in the second-line setting, effectively establishing a new standard of care in NSCLC. In the present report, we provide an overview of the rationale for checkpoint inhibitors in lung cancer, recent clinical trial data, and the need for predictive biomarkers. © AlphaMed Press 2017.


McCoy L.E.,Scripps Research Institute | McCoy L.E.,University College London | Burton D.R.,Scripps Research Institute | Burton D.R.,Massachusetts General Hospital
Immunological Reviews | Year: 2017

Beginning in 2009, studies of the humoral responses of HIV-positive individuals have led to the identification of scores, if not hundreds, of antibodies that are both broadly reactive and potently neutralizing. This development has provided renewed impetus toward an HIV vaccine and led directly to the development of novel immunogens. Advances in identification of donors with the most potent and broad anti-HIV serum neutralizing responses were crucial in this effort. Equally, development of methods for the rapid generation of human antibodies from these donors was pivotal. Primarily these methods comprise single B-cell culture coupled to high-throughput neutralization screening and flow cytometry-based sorting of single B cells using HIV envelope protein baits. In this review, the advantages and disadvantages of these methodologies are discussed in the context of the specificities targeted by individual antibodies and the need for further improvements to evaluate HIV vaccine candidates. © 2017 The Authors. Immunological Reviews published by John Wiley & Sons Ltd


Lordello L.,Massachusetts General Hospital
Applied Immunohistochemistry and Molecular Morphology | Year: 2017

PAX8, estrogen receptor-α (ERα) and progesterone receptor (PR) are markers usually expressed in neoplasms of müllerian origin. We report a subdiaphragmal mass in a 41-year-old woman corresponding to a malignant biphasic tumor with nests of epithelial-like cells forming variably sized cyst-like spaces alternating with spindle cells forming intersecting fascicles. The later were juxtaposed to coalescent densely cellular nodules of spindle cells with appreciable cytologic atypia and mitotic counts up to 30/10 high-power fields. The tumor cells were AE1/AE3, EMA, ERG, ERα, PR, and PAX8 positive whereas spindle cells showed reduced immunopositivity for these markers, especially marked in coalescent nodular areas, with notable exception of PAX8, which was diffuse and strongly positive. The possibility of an endometrioid carcinoma with spindle cells was considered by the referring pathologist, but fluorescent in situ hybridization showed rearrangement of SS18 gene in 48 of 50 tumor nuclei, rendering a diagnosis of biphasic synovial sarcoma, the first reported in the English literature to the best of our knowledge expressing PAX8, ERα, and PR. Further studies evaluating the expression of these markers in synovial sarcoma and other sarcomas are needed, as sometimes the findings may lead to misdiagnosis as other neoplasms including those of the female genital tract. Additional molecular tests may be helpful to determine the molecular mechanism of this aberrant immunoprofile, which could be directly or indirectly related to t(X:18). Copyright 2017 Wolters Kluwer Health, Inc. All rights reserved.


Bozzalla Cassione E.,Massachusetts General Hospital
Current Opinion in Rheumatology | Year: 2017

PURPOSE OF REVIEW: Remarkable insights have been gleaned recently with regard to the pathophysiology of IgG4-related disease (IgG4-RD). These findings have direct implications for the development of targeted strategies for the treatment of this condition. RECENT FINDINGS: Oligoclonal expansions of cells of both the B and T lymphocyte lineages are present in the blood of patients with IgG4-RD. Oligoclonal expansions of plasmablasts are a good biomarker for disease activity. An oligoclonally expanded population of CD4+ cytotoxic T lymphocytes is found not only in the peripheral blood but also at tissue sites of active disease. This cell elaborates cytokines that may drive the fibrosis characteristic of IgG4-RD. T follicular helper cells (Tfhc), particularly the Tfhc2 subset, appear to play a major role in driving the class switch to IgG4 that typifies this disease. The relationship between malignancy and IgG4-RD remains an area of interest. SUMMARY: Advances in understanding the pathophysiology of IgG4-RD have proceeded swiftly, leading to the identification of a number of potential targeted treatment strategies. The completion of classification criteria for IgG4-RD, an effort supported jointly by the American College of Rheumatology and the European League Against Rheumatism, will further facilitate studies on this disease. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.


Carcinosarcomas (CS) are exceedingly rare in the vulva, with only 3 cases reported in the English literature, associated with squamous cell carcinoma (2) or spiradenocarcinoma (1). We first report a vulvar CS with intestinal-type mucinous adenocarcinoma associated with anaplastic pleomorphic and spindle cell carcinoma and heterologous chondro- and osteosarcomatous elements in a 62-year-old woman, who presented with a painless, slow-growing vulvar cyst for almost 2 years, that rapidly enlarged and hardened in the last 4 months forming a mass. The tumor was widely excised, but recurred 2 months later, and she died 2 months after recurrence. A review on this entity is performed highlighting its morphologic and immunohistochemical features, and discussing issues in nomenclature and potential origins within the vulva. ©2017International Society of Gynecological Pathologists


Khera A.V.,Massachusetts General Hospital | Kathiresan S.,Massachusetts General Hospital
Nature Reviews Genetics | Year: 2017

Coronary artery disease is the leading global cause of mortality. Long recognized to be heritable, recent advances have started to unravel the genetic architecture of the disease. Common variant association studies have linked approximately 60 genetic loci to coronary risk. Large-scale gene sequencing efforts and functional studies have facilitated a better understanding of causal risk factors, elucidated underlying biology and informed the development of new therapeutics. Moving forwards, genetic testing could enable precision medicine approaches by identifying subgroups of patients at increased risk of coronary artery disease or those with a specific driving pathophysiology in whom a therapeutic or preventive approach would be most useful. © 2017 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.


News Article | May 2, 2017
Site: www.rdmag.com

Deep in the brains of two patients with Alzheimer's disease, the main memory structure, the hippocampus, displays episodic seizure-like electrical activity. These non-convulsive hippocampal seizures are the first signs of 'silent' brain electrical network dysfunction described in patients with Alzheimer's disease. The discovery, published in the journal Nature Medicine, provides a better understanding of the condition and can potentially lead to new treatments for this devastating disease affecting more than 5 million people in the U.S. "About 10 years ago, we were surprised to find 'silent seizures' in mouse models of Alzheimer's disease," said co-senior author Dr. Jeffrey L. Noebels, professor of neurology, neuroscience, and molecular & human genetics, and director of the Blue Bird Circle Developmental Neurogenetics Laboratory at Baylor College of Medicine. "When we measured the animal's brain electrical activity, we detected abnormal electrical discharges in the brain with a seizure-like pattern. The mice, however, did not present with convulsions. These 'clinically silent seizures' in the deep regions of the brain, we speculated, could lead to problems of memory." It's been reported that in a group of patients with Alzheimer's disease, those that have a history of the disease in their families, convulsive seizures are common, especially in advanced cases. However, for most patients with Alzheimer's the condition does not run in the family. In this group of patients, which are said to present with the sporadic form of the disease, convulsive seizures are typically absent. "For this reason, measuring the brain's electrical activity with an electroencephalogram or EEG test is not required for diagnosis and rarely performed," Noebels said. Even if the test was performed, previous studies in the epilepsy field had shown that seizures deep in the brain, such as the hippocampal region, cannot be detected with routine scalp EEG recordings. Detecting such brain activity requires placing electrodes deep in the brain. "My colleagues and I have been interested for years in determining whether 'silent seizures' are present in the hippocampus of patients with Alzheimer's disease," Noebels said. "We were able to answer this question when my colleague and senior co-author Dr. Andrew Cole, director of Massachusetts General Hospital Epilepsy Service and professor of neurology at Harvard Medical School, told me that he had two candidates for the procedure." Cole and Dr. Alice Lam, first-author of the study and a fellow at Massachusetts General Hospital Epilepsy Service, led the team that performed the test in the patients. They used a minimally invasive recording technique involving fine wires inserted through a small natural opening in the skull. This allowed the researchers to monitor this deep region continuously for several days. Simultaneously, the researchers recorded scalp EEG readings. In the two patients, who had been diagnosed with Alzheimer's disease and had no previous history of epilepsy or behaviorally obvious seizures, the hippocampal recordings showed clear clinically silent seizures. At the same time, the EEG recordings that had been taken simultaneously showed no abnormal brain activity, confirming that EEG tests do not register changes in deep brain activity. "What was fascinating was that this activity was present at night when the patients were sleeping, a time thought to be critical for the consolidation of recent memories, a trait that is most impaired in early Alzheimer's disease," Noebels said. "Based on our observations, we are particularly intrigued by the possibility that 'silent seizure' activity per se could contribute to or accelerate the degenerative process underlying Alzheimer's disease," Cole said. In addition, Noebels and his Baylor colleague, Dr. Alica Goldman, co-author and associate professor of neurology and neurophysiology, performed genetic analysis on the patients' samples. "We determined that these two patients did not have a gene known to cause epilepsy. So Alica and I, who have been studying epilepsy genes for a long time, sequenced the patients' samples for the three genes known to be linked to Alzheimer's disease," Noebels said. "It turned out that the patients didn't have those either; they present with the sporadic form of the disease." "It is very exciting that we were able to move from an observation in genetically engineered mouse models of Alzheimer's to a demonstration of the same phenomenon in patients with verified Alzheimer's disease," said Cole. "This is a critical step toward a better understanding of network dysfunction in the disease and opens the window to novel therapeutic approaches for this common condition." "From a physician's perspective, I think this work opened my eyes toward the need to look deeper into our patients' condition in order to improve the quality of their lives as well as that of their caregivers," Goldman said. "I think this work offers an opportunity for new investigations that could be relevant for moving forward the clinical practice of Alzheimer's disease." The need for future studies "This work with two patients proves the concept that 'silent seizures' can occur in patients with Alzheimer's disease," Noebels said. "Next, we need to determine whether this finding is common in Alzheimer's disease, present in other types of progressive degenerative neurocognitive diseases, and when in the course of the disease it occurs," Cole said.


News Article | April 19, 2017
Site: www.biosciencetechnology.com

“If only,” wrote an ancient Japanese poet, “when one heard that Old Age was coming one could bolt the door….” Science is working on it. Aging is as much about the physical processes of repair and regeneration — and their slow-motion failure — as it is the passage of time. And scientists studying stem cell and regenerative biology are making progress understanding those processes, developing treatments for the many diseases whose risks increase as we get older, while at times seeming to draw close to a broader anti-aging breakthrough. If stem cells offer potential solutions, they’re also part of the problem. Stem cells, which can differentiate into many cell types, are important parts of the body’s repair system, but lose regenerative potency as we age. In addition, their self-renewing ability allows the mutations that affect every cell to accumulate across cellular generations, and some of those mutations lead to disease. “We do think that stem cells are a key player in at least some of the manifestations of age,” said Professor of Stem Cell and Regenerative Biology David Scadden, co-director of the Harvard Stem Cell Institute. “The hypothesis is that stem cell function deteriorates with age, driving events we know occur with aging, like our limited ability to fully repair or regenerate healthy tissue following injury.” When it comes to aging, certain tissue types seem to lead the charge, according to Professor of Stem Cell and Regenerative Biology Lee Rubin, who directs the Harvard Stem Cell Institute’s Therapeutic Screening Center. Particular tissues — nerve cells appear to be one — somehow signal to others that it’s time to age. This raises the prospect, Rubin said, that aging might be reversed by treating these key tissue categories, rather than designing individual treatments for the myriad tissue types that make up the body. “The process of aging involves all tissues in your body and, while different things go wrong in each tissue, they go wrong at basically the same rate,” Rubin said. “We can think of it as a process that is somehow coordinated, or there are fundamental processes in each tissue that play out.” In addition to key tissues, certain chemical pathways — like insulin signaling —seem to be able to control aging, said Rubin, whose work has received backing from the National Institute of Neurological Disorders and Stroke, as well as private foundations. The insulin signaling pathway is a chemical chain reaction in which the hormone insulin helps the body metabolize glucose. Reducing it has been shown to greatly extend life span in flies and worms, Rubin said. Also, signaling doesn’t have to be reduced in all tissues. “If you just reduce it in neurons, the whole fly or worm lives longer,” Rubin said. “Certain key tissues in those organisms, if you selectively manipulate those tissues, have a positive effect on a number of processes in other tissues.” Because it circulates throughout the body, blood is an obvious place to look for controlling or signaling molecules that prompt or coordinate aging. A key carrier of oxygen and nutrients, blood is also rich with other compounds, some of which appear to play a role in decline linked to age. Scadden described recent work done separately by Ben Ebert, a professor of medicine working at Harvard-affiliated Brigham and Women’s Hospital, and Steve McCarroll, the Dorothy and Milton Flier Associate Professor of Biomedical Science and Genetics, that identified age-related changes in the blood that can increase the risk of diseases we don’t typically think of as blood diseases. Another tantalizing study, published in 2013, used the blood of a young mouse to rejuvenate the organs of an older one. In these “parabiotic” experiments, conducted by Professor of Stem Cell and Regenerative Biology Richard Lee and Forst Family Professor of Stem Cell and Regenerative Biology Amy Wagers, the circulatory systems of the two mice were joined, allowing the blood of the young to flow through the older one’s body. The older mouse showed improvements in muscle tone and heart function. Later, similar experiments done by Rubin also showed improvements in neuronal health and brain functioning. The young mouse’s fate depended on the age of the older mouse, Rubin said. If the latter was middle-aged, the young mouse appeared to be fine. If the older mouse was very old, however, the young mouse did worse. Rubin said the experiments suggest that blood contains both positive and negative factors that influence aging. It may be, he said, that both are always present, but that positive factors outweigh negative in the young and that negative factors increase as we age. Researchers have identified but not yet confirmed candidate blood factors for the rejuvenating effects. What seems not in doubt is the overall effect of the young blood on the old mouse. Interest is intense enough that a California company, Alkahest, has begun experiments giving Alzheimer’s patients plasma from young blood in hopes of improving cognition and brain function. Even if that approach works, Rubin said, there would be practical hurdles to the widespread administration of young people’s blood plasma to older patients. But with an active compound identified, a drug could be made available to restore at least some cognitive function in Alzheimer’s patients. In addition to the overall process of aging, researchers at the Harvard Stem Cell Institute, as well as across the University and its affiliated institutions, are investigating an array of diseases whose incidence increases — sometimes dramatically — with age. The list includes several of the country’s top causes of death — heart disease, stroke, diabetes, and cancer — as well as rarer conditions such as the lethal neurodegenerative disorder amyotrophic lateral sclerosis (ALS). Two decades ago, when stem cell research hit mainstream consciousness, many thought its greatest promise would be in stem cells’ ability to grow replacement parts: organs and tissues for damage caused by trauma or disease. The stem cell revolution is still developing, Scadden said, but so far has taken a different form than many expected. The dream of harnessing stem cells to grow replacement hearts, livers, and kidneys remains, but potentially powerful uses have emerged in modeling disease for drug discovery and in targeting treatment for personalized medicine. Researchers have taken from the sick easily accessible cells, such as skin or blood, and reprogrammed them into the affected tissue type — nerve cells in the case of ALS, which most commonly strikes between 55 and 75, according to the National Institutes of Health (NIH). These tissues are used as models to study the disease and test interventions. Work on ALS in the lab of Professor of Stem Cell and Regenerative Biology Kevin Eggan has identified a drug approved for epilepsy that might be effective against ALS. This application is now entering clinical trials, in collaboration with Harvard-affiliated Massachusetts General Hospital. In the end, stem cells might have their greatest impact as a drug-discovery tool, Scadden said. “Much of stem cell medicine is ultimately going to be ‘medicine,’” he said. “Even here, we thought stem cells would provide mostly replacement parts. I think that’s clearly changed very dramatically. Now we think of them as contributing to our ability to make disease models for drug discovery.” Also evolving is knowledge of stem cell biology. Our previous understanding was that once embryonic stem cells differentiated into stem cells for muscle, blood, skin, and other tissue, those stem cells remained flexible enough to further develop into an array of different cells within the tissue, whenever needed. Recent work on blood stem cells, however, indicates that this plasticity within a particular tissue type may be more limited than previously thought, Scadden said. Instead of armies of similarly plastic stem cells, it appears there is diversity within populations, with different stem cells having different capabilities. If that’s the case, Scadden said, problems might arise in part from the loss of some of these stem cell subpopulations, a scenario that could explain individual variation in aging. Getting old may be something like the endgame in chess, he said, when players are down to just a few pieces that dictate their ability to defend and attack. “If we’re graced and happen to have a queen and couple of bishops, we’re doing OK,” said Scadden, whose work is largely funded through the NIH. “But if we are left with pawns, we may lose resilience as we age.” Scadden’s lab is using fluorescent tags to mark stem cells in different laboratory animals and then following them to see which ones do what work. It might be possible to boost populations of particularly potent players — the queens — to fight disease. “We’re just at the beginning of this,” Scadden said. “I think that our sense of stem cells as this highly adaptable cell type may or may not be true. What we observe when we look at a population may not be the case with individuals.” The “replacement parts” scenario for stem cells hasn’t gone away. One example is in the work of Harvard Stem Cell Institute co-director and Xander University Professor Douglas Melton, who has made significant progress growing replacement insulin-producing beta cells for treatment of diabetes. Another is in Lee’s research. With support from the NIH, Lee is working to make heart muscle cells that can be used to repair damaged hearts. Trials in this area have already begun, though with cells not genetically matched to the patient. In France, researchers are placing partially differentiated embryonic stem cells on the outside of the heart as a temporary aid to healing. Another trial, planned by researchers in Seattle, would inject fully differentiated heart muscle cells into a patient after a heart attack as a kind of very localized heart transplant. Lee’s approach will take longer to develop. He wants to exploit the potential of stem cell biology to grow cells that are genetically matched to the patient. Researchers would reprogram cells taken from the patient into heart cells and, as in the Seattle experiment, inject them into damaged parts of the heart. The advantage of Lee’s approach is that because the cells would be genetically identical to the patient, he or she could avoid antirejection drugs for life. “What we’re thinking about is longer-term but more ambitious,” Lee said. “Avoiding immune suppression could change the way we think about things, because it opens the door to many decades of potential benefit.” Change has been a constant in Lee’s career, and he says there’s no reason to think that will slow. Patient populations are older and more complex, disease profiles are changing, and the tools physicians have at their disposal are more powerful and more targeted. “Many of our patients today wouldn’t be alive if not for the benefit of research advances,” he said. “Cardiology has completely changed in the last 25 years. If you think it’s not going to change even more in the next 25 years, you’re probably wrong.” When Lee envisions the full potential of stem cell science, he sees treatments and replacement organs with the power to transform how we develop and grow old. “It may not be there for you and me, but for our children or their children, ultimately, regenerative biology and stem cell biology have that kind of potential,” he said. “We imagine a world where it doesn’t matter what mutations or other things you’re born with, because we can give you a good life.” Lee’s not guessing at future longevity. He’s not even sure extending life span beyond the current record, 122, is possible. Instead, he cites surveys that suggest that most Americans target 90 as their expectation for a long, healthy life. “That’s about a decade more than we get now in America,” Lee said. “We have work to do.”


News Article | April 20, 2017
Site: www.eurekalert.org

With the help of genetically engineered mice, scientists at the Massachusetts General Hospital (MGH) are moving closer to establishing the role that increased intestinal permeability, sometimes called a "leaky gut," plays in chronic inflammatory conditions. Regulated by a protein called zonulin, elevated intestinal permeability has been associated with several chronic conditions including autoimmunity, metabolic disorders, neurodegenerative diseases and even cancer. In an article published in Annals of the New York Academy of Sciences, lead author Craig Sturgeon, a graduate student in the Mucosal Immunology and Biology Research Center (MIBRC) at MGH, and colleagues provide a direct link between increased permeability of the small intestine and chronic inflammatory disease. They describe how inducing colitis in transgenic mice with two copies of the zonulin-producing gene variant led to significantly more severe symptoms and increased mortality compared with inducing colitis in animals without the zonulin gene. "This is the first time that we have been able to mechanistically link zonulin-dependent modulation of small-intestinal permeability and the resulting enhanced antigen trafficking to the development of an inflammatory disease," says Alessio Fasano, MD, director of the MIBRC and senior author of the article. "When we exposed these two groups of mice to inflammatory stress, the zonulin transgenic mice showed a remarkable increase in colon inflammation and in mortality -- up to 70 percent -- compared to normal mice." In a related finding that Fasano calls "even more remarkable," adding a zonulin inhibitor -- AT1001, also called larazotide acetate -- to the drinking water of the transgenic mice completely protected the animals from colonic inflammation and death, reducing permeability of the small intestine to normal levels, despite continued zonulin expression. Fasano's group discovered zonulin, which controls the opening of "tight junctions" between cells lining the digestive tract, in 2000. Since then it has been the subject of numerous studies implicating intestinal permeability in chronic inflammatory disease. In 2001 while at the University of Maryland School of Medicine, Fasano developed AT1001 as a therapeutic agent for celiac disease. The zonulin-blocking agent is set to undergo Phase III clinical trials later this year, according to Innovate BioPharmaceuticals, which has licensed development of the drug from Alba Therapeutics, a company co-founded by Fasano. A professor of Pediatrics at Harvard Medical School, Fasano explains that, while some alternative health care practitioners use the term "leaky gut syndrome" to describe a variety of health problems ranging from gastrointestinal complaints to neurological symptoms, he prefers the concept of loss of intestinal barrier function. "Leaky gut syndrome has been blamed by some non-mainstream practitioners as the reason for almost everything that is wrong with a person. With the development of this mouse model to study inflammation, we'll be able to separate science from speculation," he says. Lead author Sturgeon adds, "Use of these mice will allow us to gain insight into specific mechanisms by which zonulin-dependent increased intestinal permeability can affect disease onset, clinical severity and outcomes, and even possible prevention." Jinggang Lan, PhD, of the MIBRC is also a co-author of the Annals of the New York Academy of Science paper. The study was supported by National Institutes of Health grant DK048373. Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of "America's Best Hospitals."


News Article | May 1, 2017
Site: www.futurity.org

Among suicidal patients, an intervention with brief, post-discharge phone calls significantly reduced the likelihood of a future suicide attempt. In a clinical trial involving nearly 1,400 suicidal patients in the emergency departments of eight hospitals, researchers found that the intervention lowered the relative risk of new suicide attempts by 20 percent. In results published in JAMA Psychiatry, emergency department patients who received the intervention composed of specialized screening, safety planning guidance, and periodic follow-up phone check-ins made 30 percent fewer total suicide attempts compared to people who received standard ED care. “We were happy that we were able to find these results,” says Ivan Miller of Butler Hospital and the study’s lead and corresponding author. “We would like to have had an even stronger effect, but the fact that we were able to impact attempts with this population and with a relatively limited intervention is encouraging,” says Miller, professor of psychiatry and human behavior at the Warren Alpert Medical School of Brown University. While suicide prevention efforts such as hotlines are well known, published controlled trials of specific interventions have been much rarer, Miller says. This one focuses on an especially high-risk group: emergency department patients who said they had engaged in suicidal ideation or had made an attempt within a week before their ED visit. The trial took place in three phases to create three comparison groups. In the first phase, August 2010 to December 2011, 497 patients received each ED’s usual treatment as a control group. In the second phase, September 2011 to December 2012, 377 patients received additional suicide screening. In the third phase, July 2012 to November 2013, 502 patients received the experimental intervention. Those patients received additional suicide screening from ED physicians, suicide prevention information from nurses, and a personal safety plan that they could opt to fill out to be better prepared for times when they might begin to harbor suicidal thoughts again. Over the next year they also received brief, periodic phone calls from trained providers at Butler Hospital who would discuss suicide risk factors, personal values and goals, safety and future planning, treatment engagement, and problem solving. The intervention was designed to directly involve a designated loved one whenever feasible, as well. In all three phases, patients were briefly screened for suicidality at the ED and were also followed for a year with periodic assessment phone calls. Regardless of phase, patients who demonstrated a specific suicide risk during assessments were connected with the Boys Town suicide prevention hotline. Suicide attempts were not the only measure the researchers employed to understand the potential impact of the intervention. Fortunately, there were so few deaths by suicide among patients (five total deaths) that there could be no statistically valid conclusions drawn from that data point. But the researchers also created a broader suicide composite score, which included not only attempts and deaths, but also interrupted or aborted attempts, and acts to prepare an attempt. Across the three groups, 46.3 percent of the patients reported one or more of these behaviors, but the relative risk declined significantly among people in the intervention compared to the usual care group (by 15 percent), but not among people who received screening alone. While other interventions have also been found to reduce suicide risk, some of the most effective ones have involved providing patients with many hours of psychotherapy. “This intervention was significantly less costly than most other interventions,” he says. The research team is currently engaged in a cost-effectiveness analysis. He notes that the intervention was associated with significant declines in suicide attempts, even though not every patient engaged in the full intervention (e.g. only 37.4 percent reported receiving a safety plan and nearly 40 percent did not complete a follow-up phone call). The intervention’s apparent efficacy also persisted despite the study’s ethical design, in which even people in the control phases received suicide prevention counseling that could have prevented an attempt if they presented an urgent need. The report is one of several from the Emergency Department Safety Assessment and Follow-up Evaluation (ED-SAFE) study led by Miller, Professor Edwin Boudreaux of the University of Massachusetts, and Carlos Camargo of Massachusetts General Hospital and Harvard University. In further studies, the ED-SAFE team is looking at whether more intensive safety planning while patients are in the ED could help further. Miller and his colleagues are also conducting further tests of the phone follow-ups with patients from Butler Hospital and the Providence Veterans Affairs Medical Center. Additional coauthors are from Massachusetts General Hospital; the University of Colorado; the National Institutes of Health; Cape Cod Healthcare; and Brown University. The National Institute of Mental Health funded the research.


News Article | April 21, 2017
Site: www.csmonitor.com

Neuroscientist Shruti Muralidhar (front l.) and microbiologist Abhishek Chari (front r.) hold placards and chant during a rally for science, Feb. 19, 2017, in Boston. Similar marches are scheduled for Saturday, April 20, in Washington, D.C., and 500 cities around the world. Many scientists say they feel compelled to march in the name of science. But for others, the foray into activism runs the risk of worsening the polarization the march is meant to ease. —Jenny Tam spent much of her life avoiding politics. She grew up in a small town in Arkansas, as the child of Chinese immigrants who had seen the dangers of political backlash, and she always tried to stay nonpolitical. All that changed for Dr. Tam, now an immunologist and biophysicist at Massachusetts General Hospital, as she watched the current administration dismiss facts and saw a lack of understanding of how rigorous peer-reviewed studies really are. Suddenly, she felt the need to march into the fray, helping to found the group FACTS (Fostering Advocacy and Collaboration Through Science). Tam isn’t alone among scientists who feel compelled to step out of the lab or the field to stand up for science. On Saturday, which is also Earth Day, these newly minted activists and other science supporters plan to gather in Washington, D.C., and in more than 500 other cities for a March for Science. The foray into activism and politics is a tough one for some scientists. And although the organizers have taken pains to note the march is nonpartisan, concern that the focus will become political has sparked some controversy and debate among scientists. Many supporters of the march note that science is already political, and that ignoring its importance to policy is disingenuous. The march is needed, they say, due to the increased attacks on science, threats to slash funding for research, and lack of understanding of what scientists do. But critics worry that despite all the declarations that the march is “non-partisan,” it will be viewed by many Americans as anti-Trump and anti-Republican, and that it will only increase the partisan divide and cement the impression in some people’s minds that scientists are driven by ideology rather than evidence. “I worry there will be people there carrying signs that have incendiary messages, and it’s that one percent that will become the meme for the conservative blogosphere,” says Robert Young, a coastal geologist at Western Carolina University. He cringes imagining rural America’s reaction to, say, a sign saying “Make America smart again.” Dr. Young has seen first-hand the ways politicians can try to delegitimize science when he helped author a report on sea-level rise that had data that developers didn’t want to hear and state legislators dismissed. And back in his 20s, he says, he might have joined Saturday’s march himself. But Young says he’s also become more pragmatic with experience, and he worries that a march – one that he says will certainly be viewed as partisan by much of America – will only solidify barriers. “If you want to make a difference and you want to live within the political realities we live in right now, then calling these people out and embarrassing them is not going to help us win,” Young says. Other scientists say they hear that argument and acknowledge there is a risk but suggest that there is a much greater risk to not doing anything. “It’s absurd to think of science as being apolitical,” says Alan Townsend, an environmental studies professor at the University of Colorado in Boulder. “It doesn’t mean it should be partisan, but it’s embroiled in the world of politics as well, and we have to engage.” Certain groups may use the march to attack scientists, he acknowledges, but says there’s nothing new in that narrative. “And the upside potential is more meaningful and needed.” The backing for the science march has been widespread, including behemoths like the American Association for the Advancement of Science (AAAS), the world’s largest scientific society, as well as dozens of research groups, museums, small scientific organizations, and nonprofits. A huge piece of the march is simply making both science and scientists more accessible and visible to the public. Most marches have planned education stations; in Washington, nearly two dozen “teach-ins” are being offered, on topics ranging from food solutions and creek critters to carbon innovation and the physics of superheroes. “We’ll have booths set up by a variety of organizations to talk about the science they’re doing, so that the public begins to get a more expansive view of what science is,” says Scott Franklin, a physicist at the Rochester Institute of Technology and one of the organizers of the march in Rochester, N.Y. “The more visible scientists are in the community the more normalized we get.” Some participants also say that, while the march may have been catalyzed in part by the Trump administration – with its proposed cuts for research funding, its loose use of “facts,” and the nomination of some climate-change critics to prominent roles – the antagonism toward science among some policymakers in particular, has been building for several decades, and has reached a point where scientists need to push back, whatever the risks. Climate change is just one example. Once it became associated with Al Gore around the 2000 election, some Republicans who had previously proposed climate action solidified in opposition and started denying the reality of climate change, says John Holdren, a senior adviser to former President Obama on science and technology. Partisan opposition to Mr. Obama, who supported action on climate change, just intensified the divide. Is there a risk that the march will further alienate people? Of course, says Dr. Holdren. “The very notion of marching will aggravate some people. But you know it is pretty well-established reality that nothing one does in the domain of political action pleases everybody…. My own view is that the potential benefits do outweigh the downsides.” The March for Science grew out of the momentum of the Women’s March in January and has faced similar criticisms and internal turmoil about inclusion of diverse peoples and perspectives. Public critics have also suggested that the inclusion of certain advocacy groups, which they say ignore science on issues like GMOs, could make the march problematic. Those critics note that antagonism toward science is not partisan – just as climate-change denial is associated with the right, some on the left are leading the charge to dismiss science around GMOs or vaccines. “Science is not a buffet where people can pick and choose the parts that they like and disregard the rest,” wrote Alma Laney, a plant virologist and blogger, in a blog post about why he was not marching. “Climate change denial, young earth creationism, anti-vaccine and anti-genetic engineering arguments are not equal to the science on those topics. It's incredibly sad to see a group that purports to be standing up for all science to willingly partner with groups that are antiscience or hold antiscience positions.” Still, for all the criticism and disagreements, most observers have noted just how broad the support for the science march has been, including many people and groups who disagree politically, but feel deeply that a strong commitment to high-quality science and research is necessary. Many supporters of the march see it as an opportunity to shed positive light on science. As Tam, the immunology researcher, says, the march “should be a celebration of the science our country has really excelled at.” And, rather than marching for one concrete goal – increased NIH funding, say, or a broader acceptance of climate change – many of the organizers and participants express hope that the march could help demystify the scientific process for some Americans, and also encourage more scientists to be engaged in the public sphere, whether through serving on local town councils or committees, reaching out to lawmakers, or simply talking to people in their community about what they do. Michael Eisen, a computational biologist at the University of California in Berkley who recently announced his Senate candidacy, will be speaking at the march in San Francisco because “it’s about standing up for a worldview and a way of approaching problems.” “Too often we think of it as this kind of priesthood, with scientists who work in labs and produce science. But really, I think most people are basically scientists in the way they live,” and the way they apply the scientific method in their daily lives, he says. Eisen hopes the march will help connect scientists and the public and to express that science truly is for everyone. Holdren, Obama’s science advisor, sees the march as something of an experiment. “We are trying something new compared to the historical approach of writing sober op-editorial pieces, and giving talks to rotary clubs, and folks at universities talking to each other, the national academies of science, and engineering, and medicine, holding their meetings and issuing their press releases,” he says. “The more we get people talking about society's interest in science and technology, the better. If the March advances that conversation and persuades more people to engage in that conversation in more different ways, then it will have been a success."


News Article | April 17, 2017
Site: www.prweb.com

Board-certified internist and nephrologist Mark Pettus, MD joins the faculty of The American Meditation Institute (AMI) for a 30 credit hour mind/body medicine CME conference for physicians and other health care professionals, October 24-28, 2017 at the Cranwell Resort and Spa in Lenox, Massachusetts. Entitled "The Heart and Science of Yoga,” this 9th annual, comprehensive training, accredited through the American Medical Association and Albany Medical College Office of Continuing Medical Education, is designed to help prevent and relieve physician stress and burnout. Presenter Mark Pettus, MD currently serves as Medical Director of Education, Wellness and Population Health at Berkshire Health Systems, and Associate Dean of Medical Education at the University of Massachusetts Medical Center. A featured speaker on a number of nationally broadcast television and radio programs, Dr. Pettus is also the author of “The Savvy Patient” and “It’s All in Your Head: Change Your Mind, Change Your Health, & Change Your Life.” Dr. Pettus’s two lectures on ”Epigenomics and Inflammation” are designed to help relieve symptoms of physician and patient burnout by reducing allostatic load––the physiological consequences of chronic exposure to fluctuating or heightened neural or neuroendocrine responses resulting from chronic stress. Drawing on recent studies, Pettus will focus on how these areas of study are generating unprecedented medical understanding and insight into how AMI mantra meditation, gentle yoga and diaphragmatic breathing can have a fundamental influence on how our genes may express themselves. According to Dr. Pettus, “We’ve left behind the genetic perspective in which everything is preordained; the belief that whatever the translation of your genetic coding is, will manifest over the course of your life, and ultimately, there’s very little you can do about it. To the contrary, current clinical research is now suggesting a very, very different picture, in which genetic predisposition is no longer considered destiny.” The entire “Heart and Science of Yoga” CME curriculum is dedicated to providing quality, comprehensive and evidence-based education to physicians and other health care providers on Yoga Science as mind/body medicine. In addition to Epigenomics, topics this year will include mantra meditation, diaphragmatic breathing, Yoga Psychology, the chakra system as a diagnostic tool, mind function optimization, neuroplasticity, trauma, PTSD, relieving physician burnout, resilience, Functional Medicine, Ayurveda, easy-gentle yoga and lymph system detoxification. The dedication, enthusiasm, and teaching methodology of the entire AMI faculty create a dynamic and interactive course for their students. Each faculty member is committed to the advancement and training of Yoga Science as holistic mind/body medicine. In addition to Dr. Pettus, other presenters will include program director Leonard Perlmutter, AMI founder, meditational therapist, philosopher and award-winning author; Anthony Santilli MD, board-certified in Pulmonary and Critical Care Medicine; Prashant Kaushik MD, board-certified Rheumatologist; Sara Lazar PhD, instructor in the Department of Psychiatry at Harvard Medical School, and an Associate Researcher in the Psychiatry Department at Massachusetts General Hospital; Susan Lord MD, a private practice holistic physician focusing on prevention and treatment, and former course director for the The Center for Mind-Body Medicine’s “Food As Medicine” program in Washington, DC; Jesse Ritvo MD, Assistant Medical Director, Inpatient Psychiatry, University of Vermont Health Center; Beth Netter MD MT, holistic physician and acupuncturist, Albany, NY; Jyothi Bhatt BAMS, Ayurvedic practitioner and faculty member of Kripalu School of Ayurveda and Physician’s Assistant at New York Presbyterian/Weill Cornell Medical Center; and Gustavo Grodnitzky PhD, noted author and psychologist and Chair of The American Meditation Institute's Psychological Education Department; Jenness Cortez Perlmutter, faculty member of The American Meditation Institute. According to AMI founder and conference director Leonard Perlmutter, “The more consistently the therapeutic practices of meditation and yoga are incorporated into the daily lives of physicians and patients, most symptoms of stress related burnout and chronic complex diseases can be diminished or eliminated.” 2016 conference graduate, Janine Pardo, MD, a Board Certified Internist and Primary Care Physician practicing in Weston, Massachusetts fully commented, “This retreat has been the most influential factor in transforming my life and medical practice. It comprehensively provides critical information, and should be a medical school requirement.” Use this link to see this on facebook. About the American Meditation Institute The American Meditation Institute is a 501(c)3 non-profit educational organization devoted to the teaching and practice of Yoga Science, meditation and its allied disciplines as mind/body medicine. In its holistic approach to wellness, AMI combines the healing arts of the East with the practicality of modern Western science. The American Meditation Institute offers a wide variety of classes, retreats, and teacher training programs. AMI also publishes “Transformation” a bi-monthly journal of meditation as holistic mind/body medicine. Call 518.674.8714 for a mail or email subscription.


News Article | May 1, 2017
Site: www.eurekalert.org

Deep in the brains of two patients with Alzheimer's disease, the main memory structure, the hippocampus, displays episodic seizure-like electrical activity. These non-convulsive hippocampal seizures are the first signs of 'silent' brain electrical network dysfunction described in patients with Alzheimer's disease. The discovery, published in the journal Nature Medicine, provides a better understanding of the condition and can potentially lead to new treatments for this devastating disease affecting more than 5 million people in the U.S. "About 10 years ago, we were surprised to find 'silent seizures' in mouse models of Alzheimer's disease," said co-senior author Dr. Jeffrey L. Noebels, professor of neurology, neuroscience, and molecular & human genetics, and director of the Blue Bird Circle Developmental Neurogenetics Laboratory at Baylor College of Medicine. "When we measured the animal's brain electrical activity, we detected abnormal electrical discharges in the brain with a seizure-like pattern. The mice, however, did not present with convulsions. These 'clinically silent seizures' in the deep regions of the brain, we speculated, could lead to problems of memory." It's been reported that in a group of patients with Alzheimer's disease, those that have a history of the disease in their families, convulsive seizures are common, especially in advanced cases. However, for most patients with Alzheimer's the condition does not run in the family. In this group of patients, which are said to present with the sporadic form of the disease, convulsive seizures are typically absent. "For this reason, measuring the brain's electrical activity with an electroencephalogram or EEG test is not required for diagnosis and rarely performed," Noebels said. Even if the test was performed, previous studies in the epilepsy field had shown that seizures deep in the brain, such as the hippocampal region, cannot be detected with routine scalp EEG recordings. Detecting such brain activity requires placing electrodes deep in the brain. "My colleagues and I have been interested for years in determining whether 'silent seizures' are present in the hippocampus of patients with Alzheimer's disease," Noebels said. "We were able to answer this question when my colleague and senior co-author Dr. Andrew Cole, director of Massachusetts General Hospital Epilepsy Service and professor of neurology at Harvard Medical School, told me that he had two candidates for the procedure." Cole and Dr. Alice Lam, first-author of the study and a fellow at Massachusetts General Hospital Epilepsy Service, led the team that performed the test in the patients. They used a minimally invasive recording technique involving fine wires inserted through a small natural opening in the skull. This allowed the researchers to monitor this deep region continuously for several days. Simultaneously, the researchers recorded scalp EEG readings. In the two patients, who had been diagnosed with Alzheimer's disease and had no previous history of epilepsy or behaviorally obvious seizures, the hippocampal recordings showed clear clinically silent seizures. At the same time, the EEG recordings that had been taken simultaneously showed no abnormal brain activity, confirming that EEG tests do not register changes in deep brain activity. "What was fascinating was that this activity was present at night when the patients were sleeping, a time thought to be critical for the consolidation of recent memories, a trait that is most impaired in early Alzheimer's disease," Noebels said. "Based on our observations, we are particularly intrigued by the possibility that 'silent seizure' activity per se could contribute to or accelerate the degenerative process underlying Alzheimer's disease," Cole said. In addition, Noebels and his Baylor colleague, Dr. Alica Goldman, co-author and associate professor of neurology and neurophysiology, performed genetic analysis on the patients' samples. "We determined that these two patients did not have a gene known to cause epilepsy. So Alica and I, who have been studying epilepsy genes for a long time, sequenced the patients' samples for the three genes known to be linked to Alzheimer's disease," Noebels said. "It turned out that the patients didn't have those either; they present with the sporadic form of the disease." "It is very exciting that we were able to move from an observation in genetically engineered mouse models of Alzheimer's to a demonstration of the same phenomenon in patients with verified Alzheimer's disease," said Cole. "This is a critical step toward a better understanding of network dysfunction in the disease and opens the window to novel therapeutic approaches for this common condition." "From a physician's perspective, I think this work opened my eyes toward the need to look deeper into our patients' condition in order to improve the quality of their lives as well as that of their caregivers," Goldman said. "I think this work offers an opportunity for new investigations that could be relevant for moving forward the clinical practice of Alzheimer's disease." The need for future studies "This work with two patients proves the concept that 'silent seizures' can occur in patients with Alzheimer's disease," Noebels said. "Next, we need to determine whether this finding is common in Alzheimer's disease, present in other types of progressive degenerative neurocognitive diseases, and when in the course of the disease it occurs," Cole said. Other authors that contributed to this work include Gina Deck at Massachusetts General Hospital and Harvard Medical School and Emad Eskandar at Baylor College of Medicine. Financial support for this study was provided by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health, Massachusetts General Hospital, Citizens United for Research in Epilepsy (CURE) and The Blue Bird Circle Foundation.


News Article | April 21, 2017
Site: www.csmonitor.com

Neuroscientist Shruti Muralidhar (front l.) and microbiologist Abhishek Chari (front r.) hold placards and chant during a rally for science, Feb. 19, 2017, in Boston. Similar marches are scheduled for Saturday, April 20, in Washington, D.C., and 500 cities around the world. Many scientists say they feel compelled to march in the name of science. But for others, the foray into activism runs the risk of worsening the polarization the march is meant to ease. —Jenny Tam spent much of her life avoiding politics. She grew up in a small town in Arkansas, as the child of Chinese immigrants who had seen the dangers of political backlash, and she always tried to stay nonpolitical. All that changed for Dr. Tam, now an immunologist and biophysicist at Massachusetts General Hospital, as she watched the current administration dismiss facts and saw a lack of understanding of how rigorous peer-reviewed studies really are. Suddenly, she felt the need to march into the fray, helping to found the group FACTS (Fostering Advocacy and Collaboration Through Science). Tam isn’t alone among scientists who feel compelled to step out of the lab or the field to stand up for science. On Saturday, which is also Earth Day, these newly minted activists and other science supporters plan to gather in Washington, D.C., and in more than 500 other cities for a March for Science. The foray into activism and politics is a tough one for some scientists. And although the organizers have taken pains to note the march is nonpartisan, concern that the focus will become political has sparked some controversy and debate among scientists. Many supporters of the march note that science is already political, and that ignoring its importance to policy is disingenuous. The march is needed, they say, due to the increased attacks on science, threats to slash funding for research, and lack of understanding of what scientists do. But critics worry that despite all the declarations that the march is “non-partisan,” it will be viewed by many Americans as anti-Trump and anti-Republican, and that it will only increase the partisan divide and cement the impression in some people’s minds that scientists are driven by ideology rather than evidence. “I worry there will be people there carrying signs that have incendiary messages, and it’s that one percent that will become the meme for the conservative blogosphere,” says Robert Young, a coastal geologist at Western Carolina University. He cringes imagining rural America’s reaction to, say, a sign saying “Make America smart again.” Dr. Young has seen first-hand the ways politicians can try to delegitimize science when he helped author a report on sea-level rise that had data that developers didn’t want to hear and state legislators dismissed. And back in his 20s, he says, he might have joined Saturday’s march himself. But Young says he’s also become more pragmatic with experience, and he worries that a march – one that he says will certainly be viewed as partisan by much of America – will only solidify barriers. “If you want to make a difference and you want to live within the political realities we live in right now, then calling these people out and embarrassing them is not going to help us win,” Young says. Other scientists say they hear that argument and acknowledge there is a risk but suggest that there is a much greater risk to not doing anything. “It’s absurd to think of science as being apolitical,” says Alan Townsend, an environmental studies professor at the University of Colorado in Boulder. “It doesn’t mean it should be partisan, but it’s embroiled in the world of politics as well, and we have to engage.” Certain groups may use the march to attack scientists, he acknowledges, but says there’s nothing new in that narrative. “And the upside potential is more meaningful and needed.” The backing for the science march has been widespread, including behemoths like the American Association for the Advancement of Science (AAAS), the world’s largest scientific society, as well as dozens of research groups, museums, small scientific organizations, and nonprofits. A huge piece of the march is simply making both science and scientists more accessible and visible to the public. Most marches have planned education stations; in Washington, nearly two dozen “teach-ins” are being offered, on topics ranging from food solutions and creek critters to carbon innovation and the physics of superheroes. “We’ll have booths set up by a variety of organizations to talk about the science they’re doing, so that the public begins to get a more expansive view of what science is,” says Scott Franklin, a physicist at the Rochester Institute of Technology and one of the organizers of the march in Rochester, N.Y. “The more visible scientists are in the community the more normalized we get.” Some participants also say that, while the march may have been catalyzed in part by the Trump administration – with its proposed cuts for research funding, its loose use of “facts,” and the nomination of some climate-change critics to prominent roles – the antagonism toward science among some policymakers in particular, has been building for several decades, and has reached a point where scientists need to push back, whatever the risks. Climate change is just one example. Once it became associated with Al Gore around the 2000 election, some Republicans who had previously proposed climate action solidified in opposition and started denying the reality of climate change, says John Holdren, a senior adviser to former President Obama on science and technology. Partisan opposition to Mr. Obama, who supported action on climate change, just intensified the divide. Is there a risk that the march will further alienate people? Of course, says Dr. Holdren. “The very notion of marching will aggravate some people. But you know it is pretty well-established reality that nothing one does in the domain of political action pleases everybody…. My own view is that the potential benefits do outweigh the downsides.” The March for Science grew out of the momentum of the Women’s March in January and has faced similar criticisms and internal turmoil about inclusion of diverse peoples and perspectives. Public critics have also suggested that the inclusion of certain advocacy groups, which they say ignore science on issues like GMOs, could make the march problematic. Those critics note that antagonism toward science is not partisan – just as climate-change denial is associated with the right, some on the left are leading the charge to dismiss science around GMOs or vaccines. “Science is not a buffet where people can pick and choose the parts that they like and disregard the rest,” wrote Alma Laney, a plant virologist and blogger, in a blog post about why he was not marching. “Climate change denial, young earth creationism, anti-vaccine and anti-genetic engineering arguments are not equal to the science on those topics. It's incredibly sad to see a group that purports to be standing up for all science to willingly partner with groups that are antiscience or hold antiscience positions.” Still, for all the criticism and disagreements, most observers have noted just how broad the support for the science march has been, including many people and groups who disagree politically, but feel deeply that a strong commitment to high-quality science and research is necessary. Many supporters of the march see it as an opportunity to shed positive light on science. As Tam, the immunology researcher, says, the march “should be a celebration of the science our country has really excelled at.” And, rather than marching for one concrete goal – increased NIH funding, say, or a broader acceptance of climate change – many of the organizers and participants express hope that the march could help demystify the scientific process for some Americans, and also encourage more scientists to be engaged in the public sphere, whether through serving on local town councils or committees, reaching out to lawmakers, or simply talking to people in their community about what they do. Michael Eisen, a computational biologist at the University of California in Berkley who recently announced his Senate candidacy, will be speaking at the march in San Francisco because “it’s about standing up for a worldview and a way of approaching problems.” “Too often we think of it as this kind of priesthood, with scientists who work in labs and produce science. But really, I think most people are basically scientists in the way they live,” and the way they apply the scientific method in their daily lives, he says. Eisen hopes the march will help connect scientists and the public and to express that science truly is for everyone. Holdren, Obama’s science advisor, sees the march as something of an experiment. “We are trying something new compared to the historical approach of writing sober op-editorial pieces, and giving talks to rotary clubs, and folks at universities talking to each other, the national academies of science, and engineering, and medicine, holding their meetings and issuing their press releases,” he says. “The more we get people talking about society's interest in science and technology, the better. If the March advances that conversation and persuades more people to engage in that conversation in more different ways, then it will have been a success."


News Article | April 17, 2017
Site: www.eurekalert.org

A patchwork of state laws creates a labyrinth that can make it confusing to navigate incapacitated patients' medical wishes. Without clear national standards, the problem may worsen as the nation's 75 million baby boomers continue to age, according to medical ethics research published Wednesday in the New England Journal of Medicine. "Decisions about withdrawing or withholding life-sustaining care are incredibly emotional and challenging," said Erin Sullivan DeMartino, MD, a pulmonary and critical care medicine physician at Mayo Clinic in Minnesota who led the study as part of a fellowship with the University of Chicago's MacLean Center for Clinical Medical Ethics. "But when there is ambiguity about who is responsible for decision-making, it adds much more stress to that moment." Fewer than 30 percent of Americans have "advance directives" or legal documents outlining their treatment preferences that can also grant someone power to make medical decisions on their behalf. The documents are often used when a patient is unconscious, incapacitated or unable to speak for himself and can dictate how to treat - or not treat -- anything from a minor illness to a life-threatening injury. On average, 40 percent of hospitalized adults can't make their own medical decisions. In some intensive care units, that figure skyrockets to 90 percent. "We have medical technology we didn't have 50 years ago, so we have a whole group of people who - transiently or sometimes permanently -- can't communicate with us and can't participate in their own life-and-death decisions," DeMartino said. For patients without advance directives, most states have laws dictating that medical decisions fall to someone else -- typically a spouse, parent, or child. But the legal surrogate may not always be someone who understands the patient's specific values and wishes. That presents both ethical and health care policy problems, researchers said. DeMartino and her team reviewed laws in 50 states and the District of Columbia to compile what's thought to be the first comprehensive analysis of the country's medical decision-making statutes. Their examination revealed a complex, conflicting and often confusing system that poses barriers to "safeguarding of patients' choices in their most vulnerable moments," according to the study. The inconsistencies spanned topics that are both basic and complex. For example, 30 states require "alternate decision makers" to demonstrate an ability to engage in complex medical decisions, but none explain how to assess that ability. Only thirty-five states have what researchers call a "surrogacy ladder" establishing a hierarchy for who gets to make medical decisions in the absence of a durable power of attorney for health care, but these vary widely in regards what sorts of decisions a surrogate can actually make. In addition, some states included countless details for what constitutes an appropriate decision-maker, listing everything from frequency of someone's contact with a patient to their availability to meet with clinicians in person, to their familiarity with a patient's values and religious beliefs. Other states don't mention anything aside from requiring decision makers to be an adult. (The states even had conflicting definitions of "adult.") While it's unclear whether this variation in statutes impacts clinical care, the research team said one thing is certain: disputes about medical treatment are happening on a regular basis inside hospitals and hospice programs and there's no national standard or benchmark to guide families or physicians. "One important message from this study is that, in the absence of a clearly identified spokesperson, the decision-making process for incapacitated patients may vary widely depending on where they live," said Daniel B. Kramer, MD, MPH, a cardiac electrophysiologist at the Richard A. and Susan F. Smith Center for Outcomes Research in Cardiology and Beth Israel Deaconess Medical Center in Boston, who was the study's senior author. "The next steps will be to study how this variability plays out in practice, and whether specific kinds of treatment decisions, such as withdrawing life-sustaining therapy or mental health interventions, actually turn out differently in different states due to the way these laws are written." Four of the paper's nine authors are affiliated with UChicago's MacLean Center, which pioneered the formal study of clinical medical ethics in the early 1980s. The center runs the world's largest clinical medical ethics fellowship for health care providers. "This study continues the MacLean Center's longstanding mission of examining critical issues in clinical medicine through research and training," said Mark Siegler, MD, MACP, an internist at the University of Chicago who directs the MacLean Center. "As medical ethicists - and practicing health care providers -- we wanted to provide a comprehensive resource to help guide patients, families, and other health care providers who are trying to resolve complicated ethical dilemmas." In addition to DeMartino, Kramer and Siegler, other authors of Who Decides When A Patient Can't? Statues On Alternate Decision Makers include: David M. Dudzinski, MD, JD, from Massachusetts General Hospital; Cavan K. Doyle, JD, LLM, of the MacLean Center for Clinical Medical Ethics at the University of Chicago; Beau P. Sperry, of Mayo Clinic; Sarah E. Gregory of the Beazley Institute for Health Law and Policy at Loyola University Chicago; Daniel P. Sulmasy, MD, PhD, of the Pellegrino Center for Clinical Bioethics and Kennedy Institute of Ethics at Georgetown


News Article | April 21, 2017
Site: www.chromatographytechniques.com

A collaborative study between researchers at Massachusetts General Hospital (MGH) and Boston University School of Medicine (BUSM) has found evidence implying that alcoholism may have different effects on the reward system in the brains of women than it does in men. In their paper published in Psychiatry Research Neuroimaging, the team reports that reward system structures are larger in alcoholic women than in nonalcoholic women, and their report confirmed earlier studies that found the same structures were smaller in alcoholic men than in nonalcoholic men. The study, which enrolled currently abstinent individuals with a history of long-term alcohol use disorder, also found a negative association between the length of sobriety and the size of the fluid-filled ventricles in the center of the brain, suggesting possible recovery of the overall brain from the effects of alcoholism "Until now, little has been known about the volume of the reward regions in alcoholic women, since all previous studies have been done in men," says co-author Gordon Harris, of the 3-D Imaging Service and the Center for Morphometric Analysis in the Martinos Center for Biomedical Imaging at MGH. "Our findings suggest that it might be helpful to consider gender-specific approaches to treatment for alcoholism." The brain's reward system is a group of structures - including the amygdala and the hippocampus - that reinforce beneficial experiences, are involved in memory and complex decision-making and have been implicated in the development of substance use disorders. Since there are known difference between the psychological and behavioral profiles of women and men with alcoholism - women tend toward having higher levels of anxiety, while men are more likely to exhibit anti-social characteristics - the current study was designed to investigate whether the alcoholism-associated reward system differences previously observed in men would also be seen in women. The study enrolled 60 participants with histories of long-term alcoholism - 30 women and 30 men - and an equivalent group of nonalcoholic volunteers. The alcoholic participants had been abstinent for time periods ranging from four weeks to 38 years. Participants completed detailed medical histories and neuropsychological assessments with the BUSM researchers before having MRI brain scans at the Martinos Center that were analyzed both in terms of the total brain and of the structures in the reward network. Replicating the results of earlier studies, the average sizes of reward region structures of alcoholic men were 4.1 percent smaller than those of nonalcoholic men, but the average sizes of the same structures were 4.4 percent larger in alcoholic than in nonalcoholic women. While factors such as the duration and intensity of heavy drinking appeared to reinforce these gender-specific effects, the research team notes that the current study cannot determine whether these differences preceded or resulted from the development of alcoholism. Among participants with alcoholism - both women and men - each year of sobriety was associated with a 1.8 percent decrease in the size of the ventricles, suggesting recovery from the damaging effects of alcoholism on the brain. "We're planning to take a more detailed look at the impact of factors such as the severity of drinking and the length of sobriety on specific brain structure, and hope to investigate whether the imaging differences seen in this and previous studies are associated with gender-based differences in motivational and emotional functions," says co-author Marlene Oscar-Berman, a professor of psychiatry, neurology, and anatomy & neurobiology at BUSM.


News Article | April 7, 2017
Site: www.techtimes.com

This year's World Health Day is once again bringing into focus the dire need to continue worldwide efforts to combat HIV and AIDS infections in underprivileged countries. In sub-Saharan Africa, there are currently 1.8 million children living with HIV, with 400 new reports of HIV infections every day. Another 1.5 million HIV-positive women become pregnant annually. Statistics show that only half of pediatric HIV cases have access to life-saving antiretroviral treatment. AIDS remains the leading cause of death among children and adolescents in this part of the world. In view of this, health organizations call for even more sustained endeavors to carry on the progress already made by the U.S. President's Emergency Plan for AIDS Relief (PEPFAR, launched in 2003), the Global Fund to Fight AIDS, Tuberculosis and Malaria, as well as other partnering groups. In its 15-year activity, PEPFAR has already achieved a significant decrease in HIV/AIDS-related mortality and morbidity, reducing the number of new pediatric infections worldwide by roughly 70 percent. Thanks to large investments by the U.S. government in the sum of nearly $2 billion, as well as a strong partnership with the private sector, this foreign assistance program has provided treatment for millions of people in countries that in the early 2000s had no means to suppress HIV. According to a PEPFAR news release, the program presently supplies antiretroviral therapy for approximately 11.5 million people in the most affected countries, 50 percent more than in 2014. The PEPFAR continuous support has resulted in nearly 2 million babies being born HIV-free to pregnant women living with HIV - almost double the number reported in 2013. The program also provides assistance to around 6.2 million orphans, vulnerable children, and their caregivers. "These investments are paying impressive dividends," says U.S. Special Representative for Global Health Diplomacy Deborah Birx, pointing out that "recent Public Health Impact Assessments in three African countries show that the HIV/AIDS epidemic is becoming controlled there." "Evidence suggests that we are poised to control the epidemic in 10 African countries over the next four years," Birx continues, citing 2016 data. Through U.S. funding and the help of nongovernmental organizations, PEPFAR has enabled access to life-saving care, to services that prevent HIV transmission from mother to child, and to surveillance and health information systems across Africa. The program's activity is focused on dispensing treatment, as well as building a health infrastructure that can successfully neutralize HIV strains. By investing in laboratories and highly trained specialists, PEPFAR has enabled clinicians to better diagnose and treat HIV infections, qualifying approximately 220,000 health care workers to deliver targeted care and generalized health assistance. Maintaining the program's funding is critical, states National Review, since it could soon lead to a historic public health achievement: the end of the AIDS epidemic for an entire generation of children. Global efforts are needed to persist with the noteworthy advancements in the battle against HIV/AIDS made possible by the program, which - as Washington Post columnist Michael Gerson remarked after a visit in Africa - "exists entirely because of a willing leader, a creative policy team, a smattering of activists, and a vast, bleeding need." "Investing in the well-being of our partner countries not only saves lives, but also enhances global public health and security. In our interconnected world, there is no better investment," concludes Birx. PEPFAR's actions are also supported by the United Nations, which vowed to end the AIDS epidemic by 2030 and is currently promoting a global anti-HIV campaign. Called "UN AIDS 90-90-90," the campaign aims to ensure that 90 percent of people living with HIV have access to sustained antiretroviral medication, 90 percent of treated patients are virally suppressed, and 90 percent of all people diagnosed with HIV have complete adherence to therapy. A study recently published in the Journal of the International AIDS Society details only around 60 percent of HIV patients are in active treatment. Adherence to therapy is affected by many factors, explains Specialty Pharmacy Times, and typically reduces as treatment duration increases. The research, by Massachusetts General Hospital and Harvard Medical School, provides insight on expert interventions that have the potential of reaching mass populations. The scientists advise one way of making sure patients keep to their treatment is through electronic pharmacy refill tracking systems. Their recommendation is to collect data from these systems in order to design specific interventions that encourage adherence. This method could enable health care providers to reach out to patients who miss a refill, and also determine the causes of nonadherence so that it can be curbed. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


News Article | May 1, 2017
Site: www.chromatographytechniques.com

Deep in the brains of two patients with Alzheimer's disease, the main memory structure, the hippocampus, displays episodic seizure-like electrical activity. These non-convulsive hippocampal seizures are the first signs of 'silent' brain electrical network dysfunction described in patients with Alzheimer's disease. The discovery, published in the journal Nature Medicine, provides a better understanding of the condition and can potentially lead to new treatments for this devastating disease affecting more than 5 million people in the U.S. "About 10 years ago, we were surprised to find 'silent seizures' in mouse models of Alzheimer's disease," said co-senior author Jeffrey L. Noebels, professor of neurology, neuroscience, and molecular & human genetics, and director of the Blue Bird Circle Developmental Neurogenetics Laboratory at Baylor College of Medicine. "When we measured the animal's brain electrical activity, we detected abnormal electrical discharges in the brain with a seizure-like pattern. The mice, however, did not present with convulsions. These 'clinically silent seizures' in the deep regions of the brain, we speculated, could lead to problems of memory." It's been reported that in a group of patients with Alzheimer's disease, those that have a history of the disease in their families, convulsive seizures are common, especially in advanced cases. However, for most patients with Alzheimer's the condition does not run in the family. In this group of patients, which are said to present with the sporadic form of the disease, convulsive seizures are typically absent. "For this reason, measuring the brain's electrical activity with an electroencephalogram or EEG test is not required for diagnosis and rarely performed," Noebels said. Even if the test was performed, previous studies in the epilepsy field had shown that seizures deep in the brain, such as the hippocampal region, cannot be detected with routine scalp EEG recordings. Detecting such brain activity requires placing electrodes deep in the brain. "My colleagues and I have been interested for years in determining whether 'silent seizures' are present in the hippocampus of patients with Alzheimer's disease," Noebels said. "We were able to answer this question when my colleague and senior co-author Andrew Cole, director of Massachusetts General Hospital Epilepsy Service and professor of neurology at Harvard Medical School, told me that he had two candidates for the procedure." Cole and Alice Lam, first-author of the study and a fellow at Massachusetts General Hospital Epilepsy Service, led the team that performed the test in the patients. They used a minimally invasive recording technique involving fine wires inserted through a small natural opening in the skull. This allowed the researchers to monitor this deep region continuously for several days. Simultaneously, the researchers recorded scalp EEG readings. In the two patients, who had been diagnosed with Alzheimer's disease and had no previous history of epilepsy or behaviorally obvious seizures, the hippocampal recordings showed clear clinically silent seizures. At the same time, the EEG recordings that had been taken simultaneously showed no abnormal brain activity, confirming that EEG tests do not register changes in deep brain activity. "What was fascinating was that this activity was present at night when the patients were sleeping, a time thought to be critical for the consolidation of recent memories, a trait that is most impaired in early Alzheimer's disease," Noebels said. "Based on our observations, we are particularly intrigued by the possibility that 'silent seizure' activity per se could contribute to or accelerate the degenerative process underlying Alzheimer's disease," Cole said. In addition, Noebels and his Baylor colleague, Alica Goldman, co-author and associate professor of neurology and neurophysiology, performed genetic analysis on the patients' samples. "We determined that these two patients did not have a gene known to cause epilepsy. So Alica and I, who have been studying epilepsy genes for a long time, sequenced the patients' samples for the three genes known to be linked to Alzheimer's disease," Noebels said. "It turned out that the patients didn't have those either; they present with the sporadic form of the disease." "It is very exciting that we were able to move from an observation in genetically engineered mouse models of Alzheimer's to a demonstration of the same phenomenon in patients with verified Alzheimer's disease," said Cole. "This is a critical step toward a better understanding of network dysfunction in the disease and opens the window to novel therapeutic approaches for this common condition." "From a physician's perspective, I think this work opened my eyes toward the need to look deeper into our patients' condition in order to improve the quality of their lives as well as that of their caregivers," Goldman said. "I think this work offers an opportunity for new investigations that could be relevant for moving forward the clinical practice of Alzheimer's disease." The need for future studies "This work with two patients proves the concept that 'silent seizures' can occur in patients with Alzheimer's disease," Noebels said. "Next, we need to determine whether this finding is common in Alzheimer's disease, present in other types of progressive degenerative neurocognitive diseases, and when in the course of the disease it occurs," Cole said.


News Article | March 29, 2017
Site: www.techtimes.com

Loss of memory is the painful part of Alzheimer's disease. However, new research is throwing promising hints of methods that can rekindle memories after a successful experiment on mice that was conducted by doctoral student Dheeraj Roy at Massachusetts Institute of Technology. Deep-brain stimulation (DBS) has been used as a treatment method for Alzheimer's to help patients recover cognitive functions albeit temporarily. However, deep-brain stimulation mainly helps Parkinson's patients and it has been showing limited benefits to Alzheimer's affected. The turning point in the efforts at retrieving memory in Alzheimer's has been the success of scientists in activating the cells at the hippocampi of mice where memory is stored to fire neurons in the brain with lasers. In Roy's trials with the optogenetic laser method, the hippocampus of a seven-month-old mouse with early Alzheimer's was targeted. Roy targeted memory cells of the brain called engram cells with a gene as part of optogenetics. It was Channelrhodopsin gene that created pores in the neuron membranes and filled the cells with positively charged ions to fire the neurons. The circuitry, however, in the brains of older mice was different, as they are packed with the protein plaques and needed a new approach. By drilling a hole in the seven-month-old mouse's skull and inserting fibre-optic cable, Roy stimulated the engram cells with light pulses and bolstered the synaptic connections between neurons to reignite memories to re-form. "I think what deep-brain is doing is broadly strengthening many inputs to the hippocampus," Roy said. Roy is now working to address the challenge of finding out memory neurons to target and fire without any invasive fibre-optic cable. Mice in the early stages of Alzheimer's proved that it can add new memories and retrieve "forgotten" memories with a little help. This holds promise for millions of Alzheimer's patients worldwide and is a reminder that improving memory is possible beyond the modest gains coming from existing drugs. Roy's mice trials have now been appreciated. "I thought that the results were both remarkable and exciting," said Raymond Kelleher, assistant professor of neurology at Massachusetts General Hospital. Kelleher said it stimulated interest in the neglected area of memory retrieval or recall. Meanwhile, the problem of Alzheimer's not showing any biological signal until it erupts fully is bothering neuroscientists. "Neurology researchers throughout the world are therefore on the hunt for a specific biomarker signal for Alzheimer's," said Peter Dal-Bianco, Alzheimer's expert from MedUni Vienna. Dal-Bianco said lack of biological markers to alert the onset of Alzheimer's treatment is affecting treatment and delays it until the disease manifests clinically. The disease lies suppressed in people who appear as healthy. He also said that the preventive solution is to screen people in risk groups from the mid-30s to diagnose the disease with 100 percent certainty or tell them that they face no risk. It has been found that Tau proteins play a crucial role in material transport within neurons. They are important reference points for assessing whether they are hyperphosphorylated, resulting in functional disturbances with cell death in tow. An immunotherapy for reducing harmful Tau proteins was tested under the Neurology Department in Graz and MedUni Vienna. The results have been promising and could lead to a vaccination against this Tau issue of Alzheimer's. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


News Article | April 17, 2017
Site: www.newscientist.com

It tastes foul and makes people vomit. But ayahuasca, a hallucinogenic concoction that has been drunk in South America for centuries in religious rituals, may help people with depression that is resistant to antidepressants. Tourists are increasingly trying ayahuasca during holidays to countries such as Brazil and Peru, where the psychedelic drug is legal. Now the world’s first randomised clinical trial of ayahuasca for treating depression has found that it can rapidly improve mood. The trial, which took place in Brazil, involved administering a single dose to 14 people with treatment-resistant depression, while 15 people with the same condition received a placebo drink. A week later, those given ayahuasca showed dramatic improvements, with their mood shifting from severe to mild on a standard scale of depression. “The main evidence is that the antidepressant effect of ayahuasca is superior to the placebo effect,” says Dráulio de Araújo of the Brain Institute at the Federal University of Rio Grande do Norte in Natal, who led the trial. Shamans traditionally prepare the bitter, deep-brown brew of ayahuasca using two plants native to South America. The first, Psychotria viridis, is packed with the mind-altering compound dimetheyltryptamine (DMT). The second, the ayahuasca vine (Banisteriopsis caapi), contains substances that stop DMT from being broken down before it crosses the gut and reaches the brain. To fool placebo recipients into thinking they were getting the real thing, de Araújo and his team concocted an equally foul tasting brown-coloured drink. They also carefully selected participants who had never tried ayahuasca or other psychedelic drugs before. A day before their dose, the participants filled in standard questionnaires to rate their depression. The next day, they spent 8 hours in a quiet, supervised environment, where they received either the placebo or the potion, which produces hallucinogenic effects for around 4 hours. They then repeated filling in the questionnaires one, two and seven days later. Both groups reported substantial improvements one and two days after the treatment, with placebo scores often as high as those of people who had taken the drug. In trials of new antidepressant drugs, it is common for as many as 40 per cent of participants to respond positively to placebos, says de Araújo. But a week into this trial, 64 per cent of people who had taken ayahuasca felt the severity of their depression reduce by 50 per cent or more. This was true for only 27 per cent of those who drank the placebo. “The findings suggest a rapid antidepressant benefit for ayahuasca, at least for the short term,” says David Mischoulon of Massachusetts General Hospital in Boston. “But we need studies that follow patients for longer periods to see whether these effects are sustained.” “There is clearly potential to explore further how this most ancient of plant medicines may have a salutary effect in modern treatment settings, particularly in patients who haven’t responded well to conventional treatments,” says Charles Grob at the University of California, Los Angeles. If the finding holds up in longer studies, it could provide a valuable new tool for helping people with treatment-resistant depression. An estimated 350 million people worldwide experience depression, and between a third to a half of them don’t improve when given standard antidepressants. Ayahuasca isn’t the only psychedelic drug being investigated as a potential treatment for depression. Researchers have also seen some benefits with ketamine and psilocybin, extracted from magic mushrooms, although psilocybin is yet to be tested against a placebo.


BOCA RATON, FL--(Marketwired - April 11, 2017) - The 25th Annual Spring Congress concluded on Saturday April 8th, after two consecutive days of exciting education and research. The Congress provided the latest advancements in preventive and functional medicine through educational sessions, interactive lectures, and an exhibit hall that hosted 250 exhibitors with products ranging from aesthetic devices and equipment to high-tech medical products. The event also offered 14.25 hours of continuing education and board certifications through oral and written exams. The Congress featured 38 lectures, 40 speakers, 8 learning tracks, 5 sponsored workshops, and several product presentations. This year's keynotes included renowned doctors and lecturers from across the globe, all of whom spoke about the most recently developed practices and protocols in modern integrative medicine. Dr. Alessio Fasano, a pediatric gastroenterologist who runs the Center for Celiac Research and Treatment at Massachusetts General Hospital, examined celiac disease and the impact of nutrition on the microbiome and intestinal permeability. Dr. Heather Tick discussed holistic pain health, and the ways in which to manage pain through nutrition and an anti-inflammatory diet. Dr. Robynne Chutkan, an integrative gastroenterologist previously featured on Oprah, focused on the interface between genetics and the microbiome. Further topics addressed were epigenetics, traumatic brain injuries, hormones, stem cell therapy, and aesthetics. In addition to keynote lectures and afternoon sessions, there were three specialty pre-conference workshops, designed to provide additional clinical education. The Chronic Infections symposium concentrated on inflammation, biotoxins, and the emergence and treatment of chronic infections. The Pain Management & Sleep Disorders symposium provided education surrounding functional medicine approaches to treating chronic pain and sleep disorders. A Peptides workshop discussed both the functionality and purposes of peptides and other compounds, with celebrity Maksim Chmerkovskiy from TV's "Dancing with the Stars" discussing his successful treatment with peptide therapy. A popular two-day Practice Enhancement Training workshop was launched to assist practitioners in the business and marketing of a functional medicine clinic. These conference events function as the optimal platform for healthcare practitioners to establish new professional contacts, receive comprehensive and thorough education, and network with other medical professionals from an array of disciplines and fields. CEO of Tarsus Medical Doreen Brown stated: "A4M marks its 25th year of extraordinary innovation. We are proud to be the leader in the space of redefining medicine. Our success is credited to our brilliant faculty, all of whom are true visionaries." Attendees left ready to head back to their practices armed with increased education, business insight, and an arsenal of necessary tools to advance and progress in the ever-changing field of healthcare. About the American Academy of Anti-Aging Medicine: Established in 1992, A4M is the leading nonprofit medical society dedicated to the detection, prevention, and treatment of diseases associated with aging. The organization is comprised of over 26,000 members from 120 nations across the globe, and is dedicated to educating medical and public health professionals and practitioners on the most progressive and innovative research, in addition to cutting-edge scientific technologies.


News Article | April 29, 2017
Site: www.eurekalert.org

PROVIDENCE, R.I. [Brown University] -- In a clinical trial involving nearly 1,400 suicidal patients in the emergency departments of eight hospitals, a team led by Brown University and Butler Hospital psychologist Ivan Miller found that a multifaceted intervention lowered the relative risk of new suicide attempts by 20 percent. In results published in JAMA Psychiatry, emergency department (ED) patients who received the intervention composed of specialized screening, safety planning guidance and periodic follow-up phone check-ins made 30 percent fewer total suicide attempts compared to people who received standard ED care. "We were happy that we were able to find these results," said Miller, the study's lead and corresponding author and a professor of psychiatry and human behavior at the Warren Alpert Medical School of Brown University. "We would like to have had an even stronger effect, but the fact that we were able to impact attempts with this population and with a relatively limited intervention is encouraging." While suicide prevention efforts such as hotlines are well known, published controlled trials of specific interventions have been much rarer, Miller said. This report was one of several from the Emergency Department Safety Assessment and Follow-up Evaluation (ED-SAFE) study led by Miller, Professor Edwin Boudreaux of the University of Massachusetts and Dr. Carlos Camargo of Massachusetts General Hospital and Harvard University. This study might be the largest intervention trial conducted so far in the U.S., Miller said. It focused on an especially high-risk group: emergency department patients who said they had engaged in suicidal ideation or had made an attempt within a week before their ED visit. The trial took place in three phases to create three comparison groups. In the first phase, August 2010 to December 2011, 497 patients received each ED's usual treatment as a control group. In the second phase, September 2011 to December 2012, 377 patients received additional suicide screening. In the third phase, July 2012 to November 2013, 502 patients received the experimental intervention. Those patients received additional suicide screening from ED physicians, suicide prevention information from nurses and a personal safety plan that they could opt to fill out to be better prepared for times when they might begin to harbor suicidal thoughts again. Over the next year they also received brief, periodic phone calls from trained providers at Butler Hospital who would discuss suicide risk factors, personal values and goals, safety and future planning, treatment engagement, and problem solving. The intervention was designed to directly involve a designated loved one whenever feasible, as well. In all three phases, patients were briefly screened for suicidality at the ED and were also followed for a year with periodic assessment phone calls. Regardless of phase, patients who demonstrated a specific suicide risk during assessments were connected with the Boys Town suicide prevention hotline. The number of suicide attempts and the proportion of people attempting suicide declined significantly in the intervention group compared to treatment as usual. The middle group, which received only additional screening, did not show a significant drop compared to the treatment as usual group. Suicide attempts were not the only measure the researchers employed to understand the potential impact of the intervention. Fortunately, there were so few deaths by suicide among patients (only five total) that there could be no statistically valid conclusions drawn from that data point. But the researchers also created a broader suicide composite score which included not only attempts and deaths, but also interrupted or aborted attempts, and acts to prepare an attempt. Across the three groups, 46.3 percent of the patients reported one or more of these behaviors, but the relative risk declined significantly among people in the intervention compared to the usual care group (by 15 percent), but not among people who received screening alone. While other interventions have also been found to reduce suicide risk, some of the most effective ones have involved providing patients with many hours of psychotherapy. "This intervention was significantly less costly than most other interventions," he said. The research team is currently engaged in a cost-effectiveness analysis. He noted that the intervention was associated with significant declines in suicide attempts, even though not every patient engaged in the full intervention (e.g. only 37.4 percent reported receiving a safety plan and nearly 40 percent did not complete a follow-up phone call). The intervention's apparent efficacy also persisted despite the study's ethical design, in which even people in the control phases received suicide prevention counseling that could have prevented an attempt if they presented an urgent need. In further studies, the ED-SAFE team is looking at whether more intensive safety planning while patients are in the ED could help further. Miller and his colleagues are also conducting further tests of the phone follow-ups with patients from Butler Hospital and the Providence Veterans Affairs Medical Center. In addition to Miller, Boudreak and Camargo, the paper's other authors are Drs. Sarah Arias and Richard Jones of Brown; Ashley Sullivan, Janice Espinola and Dr. Kohei Hasegawa of Massachusetts General Hospital; Dr. Michael Allen of the University of Colorado; Dr. Amy Goldstein of the National Institutes of Health; and Dr. Anne Manton of Cape Cod Healthcare. Drs. Lisa Uebelacker, Brandon Gaudiano and Lauren Weinstock of Brown University also contributed to the work. The National Institute of Mental Health (grant: U01MH088278) funded the research.


News Article | May 2, 2017
Site: www.biosciencetechnology.com

Deep in the brains of two patients with Alzheimer's disease, the main memory structure, the hippocampus, displays episodic seizure-like electrical activity. These non-convulsive hippocampal seizures are the first signs of 'silent' brain electrical network dysfunction described in patients with Alzheimer's disease. The discovery, published in the journal Nature Medicine, provides a better understanding of the condition and can potentially lead to new treatments for this devastating disease affecting more than 5 million people in the U.S. "About 10 years ago, we were surprised to find 'silent seizures' in mouse models of Alzheimer's disease," said co-senior author Dr. Jeffrey L. Noebels, professor of neurology, neuroscience, and molecular & human genetics, and director of the Blue Bird Circle Developmental Neurogenetics Laboratory at Baylor College of Medicine. "When we measured the animal's brain electrical activity, we detected abnormal electrical discharges in the brain with a seizure-like pattern. The mice, however, did not present with convulsions. These 'clinically silent seizures' in the deep regions of the brain, we speculated, could lead to problems of memory." It's been reported that in a group of patients with Alzheimer's disease, those that have a history of the disease in their families, convulsive seizures are common, especially in advanced cases. However, for most patients with Alzheimer's the condition does not run in the family. In this group of patients, which are said to present with the sporadic form of the disease, convulsive seizures are typically absent. "For this reason, measuring the brain's electrical activity with an electroencephalogram or EEG test is not required for diagnosis and rarely performed," Noebels said. Even if the test was performed, previous studies in the epilepsy field had shown that seizures deep in the brain, such as the hippocampal region, cannot be detected with routine scalp EEG recordings. Detecting such brain activity requires placing electrodes deep in the brain. "My colleagues and I have been interested for years in determining whether 'silent seizures' are present in the hippocampus of patients with Alzheimer's disease," Noebels said. "We were able to answer this question when my colleague and senior co-author Dr. Andrew Cole, director of Massachusetts General Hospital Epilepsy Service and professor of neurology at Harvard Medical School, told me that he had two candidates for the procedure." Cole and Dr. Alice Lam, first-author of the study and a fellow at Massachusetts General Hospital Epilepsy Service, led the team that performed the test in the patients. They used a minimally invasive recording technique involving fine wires inserted through a small natural opening in the skull. This allowed the researchers to monitor this deep region continuously for several days. Simultaneously, the researchers recorded scalp EEG readings. In the two patients, who had been diagnosed with Alzheimer's disease and had no previous history of epilepsy or behaviorally obvious seizures, the hippocampal recordings showed clear clinically silent seizures. At the same time, the EEG recordings that had been taken simultaneously showed no abnormal brain activity, confirming that EEG tests do not register changes in deep brain activity. "What was fascinating was that this activity was present at night when the patients were sleeping, a time thought to be critical for the consolidation of recent memories, a trait that is most impaired in early Alzheimer's disease," Noebels said. "Based on our observations, we are particularly intrigued by the possibility that 'silent seizure' activity per se could contribute to or accelerate the degenerative process underlying Alzheimer's disease," Cole said. In addition, Noebels and his Baylor colleague, Dr. Alica Goldman, co-author and associate professor of neurology and neurophysiology, performed genetic analysis on the patients' samples. "We determined that these two patients did not have a gene known to cause epilepsy. So Alica and I, who have been studying epilepsy genes for a long time, sequenced the patients' samples for the three genes known to be linked to Alzheimer's disease," Noebels said. "It turned out that the patients didn't have those either; they present with the sporadic form of the disease." "It is very exciting that we were able to move from an observation in genetically engineered mouse models of Alzheimer's to a demonstration of the same phenomenon in patients with verified Alzheimer's disease," said Cole. "This is a critical step toward a better understanding of network dysfunction in the disease and opens the window to novel therapeutic approaches for this common condition." "From a physician's perspective, I think this work opened my eyes toward the need to look deeper into our patients' condition in order to improve the quality of their lives as well as that of their caregivers," Goldman said. "I think this work offers an opportunity for new investigations that could be relevant for moving forward the clinical practice of Alzheimer's disease." The need for future studies "This work with two patients proves the concept that 'silent seizures' can occur in patients with Alzheimer's disease," Noebels said. "Next, we need to determine whether this finding is common in Alzheimer's disease, present in other types of progressive degenerative neurocognitive diseases, and when in the course of the disease it occurs," Cole said.


The Department of Biomedical Informatics at Harvard Medical School has named Bill Geary to its advisory council. Geary joins a group of distinguished individuals and thought leaders charged with advising department chair Isaac Kohane as he scales up the research and education activities at Harvard Medical School’s newest academic department. The Department of Biomedical Informatics was established in 2015 to propel a radical transformation in scientific discovery, clinical medicine and population health by harnessing the power of computation to generate new insights. The department seeks to develop the methods, tools and infrastructure required for a new generation of research investigators and health care providers to move biomedicine forward by taking full advantage of existing and emerging data resources. Geary is a general partner and cofounder of Flare Capital Partners, a healthcare technology and digital health venture capital firm. Prior to that, Geary was with North Bridge Venture Partners since inception,  a partner at Hambro International Equity Partners, and the chief financial officer of MathSoft, a science and engineering applications software start-up. Geary holds an undergraduate degree from the Carroll School of Management at Boston College and served as chair of the university’s Board of Trustees. Geary is a member of the Massachusetts General Hospital Institute of Health Professions Board of Trustees. He was previously appointed by the Massachusetts governor to the oversight council of the Center for Health Information and Analysis. Additionally, Geary represents Flare Capital Partners on the Boards of Directors as an investor in numerous healthcare technology and digital health companies. Harvard Medical School  Harvard Medical School (http://hms.harvard.edu) has more than 11,000 faculty working in 10 academic departments located at the School’s Boston campus or in hospital-based clinical departments at 15 Harvard-affiliated teaching hospitals and research institutes: Beth Israel Deaconess Medical Center, Boston Children’s Hospital, Brigham and Women’s Hospital, Cambridge Health Alliance, Dana-Farber Cancer Institute, Harvard Pilgrim Health Care Institute, Hebrew SeniorLife, Joslin Diabetes Center, Judge Baker Children’s Center, Massachusetts Eye and Ear/Schepens Eye Research Institute, Massachusetts General Hospital, McLean Hospital, Mount Auburn Hospital, Spaulding Rehabilitation Network and VA Boston Healthcare System.


News Article | April 17, 2017
Site: www.eurekalert.org

Multiple myeloma is a cancer of the plasma cells, which are white blood cells produced in bone marrow that churn out antibodies to help fight infection. When plasma cells become cancerous, they produce abnormal proteins, and the cells can build up in bone marrow, ultimately seeping into the bloodstream. The disease is typically diagnosed through a bone marrow biopsy, in which a needle is inserted near a patient's hip bone to suck out a sample of bone marrow -- a painful process for many patients. Clinicians can then isolate and analyze the plasma cells in the bone marrow sample to determine if they are cancerous. There is currently no way to easily detect plasma cells that have escaped into the bloodstream. Circulating plasma cells are not normally found in healthy people, and the ability to detect these cells in blood could enable doctors to diagnose and track the progression of multiple myeloma. Now engineers at MIT have devised a microfluidic technique to capture and count circulating plasma cells from small samples of blood. The technique, which relies on conventional blood draws, may provide patients with a less painful test for multiple myeloma. "Procedures of the traditional tissue biopsy are painful, associated with complications such as potential infections, and often available only in central hospitals which require patients to travel long distances," says former MIT postdoc Mohammad Qasaimeh. "Capturing plasma cells from blood samples can serve as a liquid biopsy, which can be performed in clinics as often as required, and serve as a diagnostic and prognostic test during and after chemotherapy treatment. Moreover, captured cells can be used for drug testing and thus serve as a tool for personalized medicine." Qasaimeh and his colleagues have published their results today in the journal Scientific Reports. His co-authors include Rohit Karnik, an associate professor in MIT's Department of Mechanical Engineering; Yichao Wu and Suman Bose, both former students; Jeffrey Karp, an associate professor in the Harvard-MIT Division of Health Sciences and Technology; and Rao Prabhala, an instructor in medicine at Dana-Farber Cancer Institute and Harvard Medical School. The group's technique builds on a microfluidic design that was previously developed by George Whitesides, a professor of chemistry at Harvard University. Whitesides and his colleagues fabricated a small microchip, the channel of which they etched with repeating, V-shaped grooves, similar to a herringbone pattern. The grooves cause any fluid flowing through the microchip to swirl about in eddies, rather passing straight through. The cells within the fluid therefore have a higher chance of making contact with the floor of the device, as first shown by Memhmet Toner at Massachusetts General Hospital. Researchers including Karnik have since reproduced this microfluidic design, coating the microchip's floor with certain molecules to attract cells of interest. In its latest work, Karnik's team used the microfluidic herringbone design to capture circulating plasma cells. They coated the channels of a microchip, about the size of a glass slide, with CD138, an antibody that is also expressed on the membranes of plasma cells. The team then flowed small, 1-milliliter samples of blood through the device. The herringbone grooves circulated the blood in the microfluidic channels, where the antibodies, acting as tiny Velcro pads, grabbed onto any passing plasma cells while letting the rest of the blood flow out of the device. Once the cells were isolated in the microchip, the researchers could count the cells, as well determine the kinds of antibodies that each cell secretes. "With the ease of a blood draw" The researchers tested the device using blood samples from healthy donors as well as patients with the disease. After counting the number of cells captured in each sample, they observed very low numbers of circulating plasma cells in healthy samples -- about two to five cells per milliliter of blood -- versus substantially higher counts in patients diagnosed with multiple myeloma, of about 45 to 184 cells per milliliter. The team also analyzed the captured plasma cells to determine the type of antibodies they produced. Plasma cells can generate one of two kinds of antibodies, known as kappa- and lambda-type. In addition to conducting bone marrow biopsies, clinicians can analyze blood samples for the ratio of these two antibodies, which can be an indicator of how the disease is progressing. Karnik and his colleagues determined the ratio of plasma cells producing kappa- and lambda-type antibodies, and compared them to conventional blood tests for the same antibodies, for both healthy subjects and patients with multiple myeloma. Encouragingly, they found both sets of results matched, validating the microfluidic device's accuracy. Surprisingly, the team noted that patients who were in remission exhibited higher counts of circulating plasma cells than healthy donors. These same patients had shown normal ratios of antibodies in conventional blood tests. Karnik says that the group's new device may reveal more subtle information about a patient's state, even in remission. "When patients go into remission, their antibody levels can look normal," Karnik says. "But we detect a level of circulating plasma cells that is above the baseline. It's hard to tell whether these cells are cancerous, but at least this technique is giving us more information. With the ease of a blood draw, this may enable us to track cancer in a much better way." Karnik adds that in the future, researchers may use the group's design to perform genetic tests on the captured cells, or to look for mutations in the cells that may further characterize the disease. "We can capture and stain these cells in the device, which opens the possibility of studying whether there are new mutations in the cells," Karnik says. "With cancers like multiple myeloma, even for patients in remission, cancer can recur. Detecting the level or mutation of plasma cells in blood might provide an early detection method for these patients." This research was supported, in part, by the National Institutes of Health and the Al Jalila Foundation.


News Article | April 25, 2017
Site: www.sciencedaily.com

An intestinal enzyme previously shown to keep bacterial toxins from passing from the gastrointestinal system into the bloodstream may be able to prevent or reduce the liver damage caused by excess alcohol consumption. In their report that will appear in the journal Digestive Diseases and Sciences and has been published online, a Massachusetts General Hospital (MGH) research team describes how oral doses of intestinal alkaline phosphatase (IAP) prevented the development of fatty liver in mouse models of both binge drinking and chronic alcohol consumption. The study also provides the first evidence of an expanded role of the liver's stellate cells in alcoholic liver disease. "Liver damage is one of the most devastating effects of excess alcohol consumption, and so blocking this process could save millions of lives lost to alcohol-related liver diseases such as cirrhosis and liver cancer," says Richard Hodin, MD, of the MGH Department of Surgery, the study's senior author. "Along with direct toxic effects on the liver itself, alcohol appears to damage the liver through its effects on the intestinal lining, allowing bacterial toxins from the gut to cross the barrier and reach the liver. Since we know that IAP works to maintain a healthy gut barrier by blocking passage of an important toxic molecule, we investigated its potential to protect the liver from alcohol-induce damage." Previous research by Hodin's group revealed that IAP helps to maintain a healthy intestinal microbial population by blocking the damaging effects of lipopolysaccharide (LPS), a molecule responsible for the toxic effects of several species of bacteria, and that the enzyme's anti-LPS effects could prevent the development of metabolic syndrome -- a constellation of symptoms including obesity, abnormal glucose and lipid metabolism, and fatty liver -- in mice fed a high-fat diet. Since LPS is known to play a role in alcohol-induced liver inflammation and its levels are known to rise with alcohol consumption, the MGH team investigated whether oral IAP supplementation could prevent alcoholic liver disease both by detoxifying the LPS released by gut bacteria and by preventing its passage from the gut into the liver's blood supply. The team conducted experiments in two mouse models of binge drinking -- either one large dose or three large doses given at 12-hour intervals -- and a model of chronic alcohol consumption -- steady alcohol consumption for 10 days. The results indicated that giving IAP either before or at the same time as an alcohol dose reduced levels of the ALT enzyme, a common sign of liver damage; reduced the accumulation of fat in the liver, the first sign of alcoholic liver disease; and reduced the production of inflammatory factors. While mice that did not receive the enzyme before or during an alcohol dose were found to have elevations in circulating LPS, decreased expression of the tight junction proteins that maintain the barrier function of the intestinal lining, and increased intestinal inflammation, IAP supplementation prevented those effects. Activation of the hepatic stellate cells, which recently have been shown to contribute to alcoholic fatty liver disease, was also prevented by pretreatment with IAP. Administering IAP after alcohol dosing had no protective effects. "Hepatic stellate cells are considered to be the central player in causing liver fibrosis -- scarring or cirrhosis -- which is the common endpoint leading to death in most liver diseases," says co-author Michael Choi, MD, of the MGH Gastrointestinal Unit. "Our results suggest that activated hepatic stellate cells are involved in even earlier stages of alcoholic liver disease and that activation can be prevented by pretreatment with IAP. Along with following up this study with human trials of IAP's protective effects, we also would like to know which gut bacterial components besides LPS are important in inducing liver inflammation, to understand more deeply the role of hepatic stellate cells in liver disease and to find ways to block their activation."


A collaborative study between researchers at Massachusetts General Hospital (MGH) and Boston University School of Medicine (BUSM) has found evidence implying that alcoholism may have different effects on the reward system in the brains of women than it does in men. In their paper published in Psychiatry Research Neuroimaging, the team reports that reward system structures are larger in alcoholic women than in nonalcoholic women, and their report confirmed earlier studies that found the same structures were smaller in alcoholic men than in nonalcoholic men. The study, which enrolled currently abstinent individuals with a history of long-term alcohol use disorder, also found a negative association between the length of sobriety and the size of the fluid-filled ventricles in the center of the brain, suggesting possible recovery of the overall brain from the effects of alcoholism "Until now, little has been known about the volume of the reward regions in alcoholic women, since all previous studies have been done in men," says co-author Gordon Harris, PhD, of the 3D Imaging Service and the Center for Morphometric Analysis in the Martinos Center for Biomedical Imaging at MGH. "Our findings suggest that it might be helpful to consider gender-specific approaches to treatment for alcoholism." The brain's reward system is a group of structures - including the amygdala and the hippocampus - that reinforce beneficial experiences, are involved in memory and complex decision-making and have been implicated in the development of substance use disorders. Since there are known difference between the psychological and behavioral profiles of women and men with alcoholism - women tend toward having higher levels of anxiety, while men are more likely to exhibit anti-social characteristics - the current study was designed to investigate whether the alcoholism-associated reward system differences previously observed in men would also be seen in women. The study enrolled 60 participants with histories of long-term alcoholism - 30 women and 30 men - and an equivalent group of nonalcoholic volunteers. The alcoholic participants had been abstinent for time periods ranging from four weeks to 38 years. Participants completed detailed medical histories and neuropsychological assessments with the BUSM researchers before having MRI brain scans at the Martinos Center that were analyzed both in terms of the total brain and of the structures in the reward network. Replicating the results of earlier studies, the average sizes of reward region structures of alcoholic men were 4.1 percent smaller than those of nonalcoholic men, but the average sizes of the same structures were 4.4 percent larger in alcoholic than in nonalcoholic women. While factors such as the duration and intensity of heavy drinking appeared to reinforce these gender-specific effects, the research team notes that the current study cannot determine whether these differences preceded or resulted from the development of alcoholism. Among participants with alcoholism - both women and men - each year of sobriety was associated with a 1.8 percent decrease in the size of the ventricles, suggesting recovery from the damaging effects of alcoholism on the brain. "We're planning to take a more detailed look at the impact of factors such as the severity of drinking and the length of sobriety on specific brain structure, and hope to investigate whether the imaging differences seen in this and previous studies are associated with gender-based differences in motivational and emotional functions," says co-author Marlene Oscar-Berman, PhD, a professor of Psychiatry, Neurology, and Anatomy & Neurobiology at BUSM. Harris is a professor of Radiology at Harvard Medical School. Kayle Sawyer of Oscar-Berman's BUSM team is lead and corresponding author of the Psychiatry Research Neuroimaging paper. Additional co-authors are Olivier Barthelemy, BUSM, and George Papadimitriou and Nikos Makris, MD, Martinos Center. Support for the study includes National Institute on Alcohol Abuse and Alcoholism grants R01-AA07112 and K05-AA00219, Department of Veterans Affairs grant I01-CX000326 , National Institute on Aging/National Institute of Mental Health grant R01-AG042512, National Center for Complementary and Integrative Health grant R21-AT008865; and National Center for Research Resources grant P41RR14075. Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of "America's Best Hospitals."


A study led by a Massachusetts General Hospital (MGH) investigator may have answered a major debate in HIV research - whether the tiny amounts of HIV that persist in patients receiving long-term antiretroviral treatment (ART) cause or are caused by the elevated levels of inflammation and immune system activation that also persist during ART. In a report published in the open-access journal PLOS Pathogens, a research team from the NIH-funded AIDS Clinical Trials Group (ACTG) describes finding that pretreatment viral levels and immune activation appear to determine the extent of HIV persistence and inflammation during ART. They also found that the low levels of HIV in the blood - below what can be detected using commercial tests - did not seem to influence persistent inflammation in people on treatment. "Our findings suggest that damage to the immune system that occurs before people are started on treatment leads to continued immune activation, even though the medicines are keeping the virus in check," says Rajesh Gandhi, MD, of the MGH Division of Infectious Diseases, lead and corresponding author of the report. "This suggests that diagnosing HIV and starting antiretroviral therapy as soon as possible may prevent the elevated immune activation that can lead to health problems, such as heart disease. The results also suggest that new strategies focused on reducing immune activation may need to be added to novel interventions designed to reduce and eventually eliminate HIV." Previous studies looking for possible relationships between viral levels - detected by sensitive research measures of HIV genetic material - and measures of immune activation while on ART had conflicting results, probably because they examined a single point in time without reference to patients' pretherapy status. The current investigation examined plasma and blood cell samples taken over time from 101 participants in ACTG studies - samples taken before ART, 1 and 4 years into treatment, and another taken between years 6 and 15. All participants reached and maintained viral levels undetectable by standard commercial measures by 1 year into treatment and maintained viral suppression for an average of 7 years, some for more than a decade. Measures of HIV genetic material revealed the greatest drop in viral levels occurred during the first four years on ART but also revealed a continuing but slower decline during subsequent years. While HIV levels were correlated with markers of immune system activation in pretreatment samples, the association between viral levels and inflammatory markers disappeared once ART was initiated. Instead it was the pretreatment levels of both factors that appeared to determine levels of viral persistence and immune activation while on ART. Senior author John Mellors, MD, chief of the Division of Infectious Diseases and a professor of Medicine at University of Pittsburgh School of Medicine, says, "It appears that different mechanisms are driving the stubborn persistence of HIV reservoirs and the harmful, chronic immune activation that are characteristic of HIV infection despite current treatments. This important finding is a first step towards identifying specific therapies for each problem." Adds Gandhi, who is an associate professor of Medicine at Harvard Medical School, "Now we need to investigate viral and human genetic factors that affect HIV persistence and immune activation in people on ART and develop strategies to reduce HIV levels and inflammation that go beyond our current antiretroviral medications. Since most HIV lives in tissues, such as lymph nodes, and not in the blood, we need to look into HIV persistence and immune activation in tissues as well." After the embargo drops, this study will be publicly accessible at: http://journals. . Additional co-authors of the PLOS Pathogens paper are Deborah McMahon, Joshua Cyktor, Bernard Macatangay, Charles Rinaldo and Sharon Riddler, University of Pittsburgh; Ronald Bosch and Christina Lalama, Harvard T.H. Chan School of Public Health; Evelyn Hogg, Social & Scientific Systems, Inc.; Catherine Godfrey, National Institute of Allergy and Infectious Diseases; Ann Collier, University of Washington; and Joseph Eron, University of North Carolina. Support for the study includes National Institutes of Health grants UM1 AI068634, UM1 AI068636 and UM1 AI106701. Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, genomic medicine, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of "America's Best Hospitals."


News Article | May 2, 2017
Site: www.prweb.com

According to Leonard Perlmutter, founder of The American Meditation Institute, the curriculum presented at AMI’s ninth annual CME conference October 24-28, 2017 at the Cranwell Resort and Spa in Lenox, Massachusetts can help physicians relieve and prevent burnout. Entitled “The Heart and Science of Yoga” this comprehensive 30 credit hour training is accredited through the Albany Medical College Office of Continuing Medical Education. In addition to a core Yoga Science curriculum including meditation, diaphragmatic breathing and gentle yoga exercises, three testimonial lectures will be presented by Tony Santilli MD, Beth Netter MD and Prashant Kaushik MD—each of whom has successfully used Yoga Science techniques to reduce and eliminate their own physicians burnout symptoms. Coverys Risk Management, reporting on Medscape’s Lifestyle Report 2017: Race and Ethnicity, Bias and Burnout reports that the overall burnout rate for physicians is now at 51 percent, an increase from 40 percent in 2013. The survey also found, “the highest percentages of burnout occurred among physicians practicing emergency medicine (59%), followed by ob/gyns (56%) and family physicians, internists, and infectious disease physicians (all at 55%).” This year’s American Meditation Institute “Heart and Science of Yoga” CME conference is dedicated to providing physicians a quality, comprehensive and evidence-based education that prevents and reverses the debilitating causes and effects of physician burnout. Lectures include mantra meditation, diaphragmatic breathing, easy-gentle yoga, Yoga psychology, meditation and neuroplasticity, PTSD, trauma, resilience, chakra system therapy, mind function optimization, epigenomics, Ayurveda, nutrition, functional medicine, and lymph system detoxification. According to previous conference attendee, board certified psychiatrist, Rebecca Aspden MD, “Since attending this retreat, my mind is open to a different way of seeing the world. I am looking forward to implementing what I learned in my own life and imparting this new knowledge and new perspective to my patients.” Each faculty member at this year’s CME conference is committed to the advancement and training of Yoga Science as holistic mind/body medicine. Presenters will include program director Leonard Perlmutter, AMI founder, meditational therapist and award-winning author; Mark Pettus MD, Director of Medical Education and Population Health at Berkshire Health Systems; Anthony Santilli MD, board-certified in Pulmonary and Critical Care Medicine; Prashant Kaushik MD, board-certified Rheumatologist; Sara Lazar PhD, instructor in the Department of Psychiatry at Harvard Medical School, and an Associate Researcher in the Psychiatry Department at Massachusetts General Hospital; Susan Lord MD, a private practice holistic physician focusing on prevention and treatment, and former course director for the The Center for Mind-Body Medicine’s “Food As Medicine” program in Washington, DC; Jesse Ritvo MD, Assistant Medical Director, Inpatient Psychiatry, University of Vermont Health Center; Beth Netter MD MT, holistic physician and acupuncturist, Albany, NY; Jyothi Bhatt BAMS, Ayurvedic practitioner and faculty member of Kripalu School of Ayurveda and Physician’s Assistant at New York Presbyterian/Weill Cornell Medical Center; Gustavo Grodnitzky PhD, noted author and psychologist and Chair of The American Meditation Institute's Psychological Education Department; and Jenness Cortez Perlmutter, faculty member of The American Meditation Institute. Noted physicians Mehmet Oz (Dr. Oz), Dean Ornish, Bernie Siegel and Larry Dossey have endorsed Mr. Perlmutter’s “The Heart and Science of Yoga” treatise, which serves as the primary curriculum for the conference. According to program director Leonard Perlmutter, “Now in its ninth year, this CME conference provides the only complete curriculum of the world’s most ancient mind/body medicine. The more physicians incorporate the therapeutic practices of Yoga Science and AMI Meditation into their daily lives, most symptoms of stress related burnout and chronic complex diseases can be diminished or eliminated.” About the American Meditation Institute The American Meditation Institute is a 501(c)3 non-profit educational organization devoted to the teaching and practice of Yoga Science, meditation and its allied disciplines as mind/body medicine. In its holistic approach to wellness, AMI combines the healing arts of the East with the practicality of modern Western science. The American Meditation Institute offers a wide variety of classes, retreats, and teacher training programs. AMI also publishes “Transformation” a bi-monthly journal of meditation as holistic mind/body medicine. Call 518.674.8714 for a mail or email subscription.


News Article | May 1, 2017
Site: www.PR.com

Santa Barbara, CA, May 01, 2017 --( “Dr. Miller has a very real and genuine empathy for those who have been given a diagnosis they cannot control and has dedicated his life to helping people prepare for death,” said Dream Foundation’s Chief Executive Officer Kisa Heyer. “Dream Foundation joins Dr. Miller in the belief that dying is not about the disease but rather making the most out of the remaining days that life offers.” As Honorary Medical Chair, Dr. Miller will provide guidance and support to the Dream Foundation team about the palliative care of Dreamers, and allow Dream Foundation to continue focusing on improving the quality of life for the patients and families Dream Foundation is honored to serve. “Death presents us all with the creative challenge of living the best life we can while we can, not just for ourselves but for each other,” says Dr. Miller. “Dream Foundation proves this point and I’m thrilled and proud to be part of it.” Dr. BJ Miller sees patients in the Symptom Management Service of the UCSF Helen Diller Family Comprehensive Cancer Center, one of the very first outpatient palliative care clinics in the US. BJ Miller, a native of Chicago, studied art history as an undergraduate at Princeton University. He worked for several years for art and disability-rights nonprofit organizations before earning a medical degree at UCSF. He completed an internal medicine residency at Cottage Hospital in Santa Barbara, where he was chief resident, and a fellowship in Hospice and Palliative Medicine at Harvard Medical School, working at the Massachusetts General Hospital and Dana-Farber Cancer Institute. In his work, he connects art, spirituality and medicine in end-of-life care. Miller is an assistant clinical professor of medicine in the Division of General Internal Medicine. Miller’s TED Talk, “What Really Matters at the End of Life,” has garnered over 5.5 million views to date and ranked among the Top 15 Most Viewed Talks of 2015. About Dream Foundation: Dream Foundation, the only national dream-granting organization for terminally-ill adults, fulfills final Dreams that provide inspiration, comfort and closure at the end of life. With the support of a nationwide network of volunteers, hospices, health care organizations and committed donors, Dream Foundation has given life to more than 25,000 final Dreams over the past two decades and has never turned down a qualified applicant. Dream Foundation does not receive any federal or state funding and relies solely on individual donations and corporate partnerships to fund its programs. The Foundation is proud to maintain Charity Navigator’s four-star rating—its highest—for sound fiscal management ensuring its donors and partners that their investment will be used wisely. For more information, please visit DreamFoundation.org. Click here to view the list of recent Press Releases from Dream Foundation


Massachusetts General Hospital (MGH) investigators have identified silent, seizure-like activity in the hippocampus - a brain structure significantly affected in Alzheimer's disease - in two patients with Alzheimer's disease and no known history of seizures. These alterations in the brain's electrical activity could not be detected by standard EEG readings taken on the scalp and primarily occurred during sleep, a time when the preceding day's memories are consolidated. The report is receiving advance online publication in Nature Medicine. "While it is not surprising to find dysfunction in brain networks in Alzheimer's disease, our novel finding that networks involved in memory function can become silently epileptic could lead to opportunities to target that dysfunction with new or existing drugs to reduce symptoms or potentially alter the course of the disease," says Andrew Cole, MD, director of the MGH Epilepsy Service and senior author of the Nature Medicine paper. "We now have to study more individuals to validate this finding and understand how prevalent it is in Alzheimer's patients, whether it occurs in other neurodegenerative disorders and how it responds to treatment." The investigators describe two patients - both women in their 60s - who had developed symptoms suggestive of Alzheimer's disease, such as confusion and repeatedly asking the same questions. Brain imaging studies and cerebrospinal fluid analysis for both patients were consistent with Alzheimer's disease. It is common for patients with Alzheimer's to experience fluctuations in their symptoms, but in both of these patients, those fluctuations were more exaggerated than typically seen. While scalp EEG recordings did not reveal seizure-like activity, the investigators suspected that there may be undetected seizures within the hippocampus - a key structure affected by Alzheimer's disease that is critical for memory consolidation and is a common source of seizures in people with epilepsy. They decided to try a more direct way of monitoring electrical activity in the hippocampus and related structures. Electrodes were placed adjacent to those structures on both sides of the brain through the foramen ovale (FO), naturally occurring openings at the base of the skull. Each patients' brain activity was monitored simultaneously with both implanted electrodes and with scalp EEG for more than 24 to 72 hours. In one patient, the FO electrodes revealed frequent bursts of electrical activity called spikes, often associated with seizures, most which were not detectible by scalp EEG. During a 12-hour period she experienced three seizures, all taking place during sleep but not producing any visible symptoms. Treatment with an anti-seizure medication eliminated the seizure-like activity, and in the following year, she experienced only one episode of confusion, which occurred after she missed several doses of her anti-seizure medication. FO electrode recording in the other patient also revealed frequent spiking during sleep, but anti-seizure treatment had to be discontinued because of adverse effects on her mood. "Our findings confirmed the presence of serious dysfunction of the neuronal networks affected by Alzheimer's disease and confirmed our hypothesis that epileptic phenomena are an important component of that disturbance," says Cole, who is a professor of Neurology at Harvard Medical School. "Additional recordings with FO electrodes in patients with Alzheimer's disease will help us develop better tools based on computerized analysis of EEG signals and possibly functional neuroimaging studies to ascertain how common silent seizures are in Alzheimer's disease without the need for the minimally invasive electrodes we used in these patients." A recent study led by Alice Lam, MD, PhD, also of the MGH Epilepsy Service and lead author of the current study demonstrated a novel tool for detecting hippocampal seizures not detectible by scalp EEGs in patients with epilepsy, Cole adds, and his team is working to refine this tool and apply it to Alzheimer's disease. Since there also is evidence that higher levels of neuronal activity can increase the production and deposition of Alzheimer's associated proteins such as tau and amyloid-beta, understanding whether seizure-like activity accelerates the progression of Alzheimer's disease will be a high priority for their team. Additional co-authors of the Nature Medicine paper are Gina Deck, MD, MGH Epilepsy Service; Emad Eskandar, MD, MGH Department of Neurosurgery; and Alicia Goldman, MD, PhD, and Jeffrey Noebels, MD, PhD, Baylor College of Medicine. Support for the study includes National Institute of Neurological Disorders and Stroke grants R25-NS065743, U01-NS090362, and R01-NS029709; and grants from Citizens United for Research in Epilepsy and the Blue Bird Circle Foundation. Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, genomic medicine, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of "America's Best Hospitals."


News Article | April 17, 2017
Site: www.eurekalert.org

Boston, MA - South Carolina saw a 22 percent reduction in post-surgical deaths in hospitals that completed a voluntary, statewide program to implement the World Health Organization Surgical Safety Checklist. The findings of the five-year project between the South Carolina Hospital Association, Ariadne Labs, and Harvard T.H. Chan School of Public Health will appear in the August 2017 print issue of the Annals of Surgery and is published online. The study is the first to demonstrate large-scale population-wide impact of the checklist. "That is a major reduction in post-surgical mortality and it demonstrates that when done right, the Surgical Safety Checklist can significantly improve patient safety at large scale," said lead author Dr. Alex B. Haynes, associate director of the Ariadne Labs Safe Surgery Program and a surgeon at Massachusetts General Hospital. Adoption of a safe surgery checklist has been demonstrated to reduce deaths in controlled research studies since 2009. But the ability to produce improved outcomes at large scale has remained questioned. In the Safe Surgery South Carolina program, all hospitals in the state were invited to participate in a voluntary, statewide effort to complete a twelve-step implementation program with Ariadne Labs that included customizing the checklist for the local setting, doing small scale testing, and observing and coaching on checklist performance. Fourteen hospitals, representing nearly 40 percent of the inpatient surgery volume in the state, completed the program. Researchers compared the 30-day post-surgery mortality outcomes between these hospitals with the mortality outcomes of the rest of the hospitals in the state. Surgical procedures in the analysis represent a wide range of specialties, from neurological, thoracic and cardiac, to soft tissue and orthopedic. The study found that the post-surgery death rate in the 14 hospitals that completed the program was 3.38 percent in 2010 (prior to implementation) and fell to 2.84 percent in 2013 after implementation. In the other 44 hospitals in the state, mortality was 3.5 percent in 2010 and 3.71 percent in 2013. This corresponded to a 22 percent difference in mortality between the groups. With these results, South Carolina offers a national model of best practices in implementing a team-based, communication checklist to drive quality improvement in the operating room. "We are honored to be a learning lab for the rest of the country," said Thornton Kirby, President and CEO of the South Carolina Hospital Association. "The study validates what we hoped and believed from the outset -- if you change the operating room culture of how you communicate and coordinate your efforts, you can produce better outcomes." Ariadne Labs' Executive Director Dr. Atul Gawande led the development of the WHO Surgical Safety Checklist in 2008 with a team of international experts. The 19-item checklist prompts surgical team discussion of the surgical plan, risks, and concerns. Following surgery, patients are at risk of complications and death from a variety of causes such as infection, hemorrhage, and organ failure. Collectively, the checklist items create a culture of operating room communication that improves overall surgical care and safety. Evidence from a 2009 pilot study with selected operating teams in eight countries around the world demonstrated a 47 percent decrease in post-surgical mortality. Further studies went on to confirm the powerful effect. But translating the checklist into population-wide mortality reduction has not been proven until now. "Safety checklists can significantly reduce death in surgery. But they won't if surgical teams treat them as just ticking a box," said Gawande. "With this work, South Carolina has demonstrated that surgery checklists can save lives at large scale -- and how hospitals can support their teams to do it." Visit the Harvard Chan School website for the latest news, press releases, and multimedia offerings. Ariadne Labs is a global leader in health systems innovation, fostering a new discipline of research and discovery for better patient care from birth to surgery to the end of life. A joint center of Brigham & Women's Hospital and the Harvard T.H. Chan School of Public Health, Ariadne Labs was founded by public health researcher and surgeon Dr. Atul Gawande. The mission is to develop simple, high-impact and scalable solutions that reduce suffering and save lives at the most critical moments in people's lives everywhere. The South Carolina Hospital Association (SCHA) is a private, not-for-profit organization made up of some 100 member hospitals and health systems. Established in 1921 to serve as the collective voice of the state's hospital community, SCHA is proud to be a part of the state's hospital industry, adding value to hospitals' efforts to care for the people of South Carolina. By helping to keep South Carolina's hospitals healthy, we are helping to keep our state healthy. Harvard T.H. Chan School of Public Health brings together dedicated experts from many disciplines to educate new generations of global health leaders and produce powerful ideas that improve the lives and health of people everywhere. As a community of leading scientists, educators, and students, we work together to take innovative ideas from the laboratory to people's lives--not only making scientific breakthroughs, but also working to change individual behaviors, public policies, and health care practices. Each year, more than 400 faculty members at Harvard Chan School teach 1,000-plus full-time students from around the world and train thousands more through online and executive education courses. Founded in 1913 as the Harvard-MIT School of Health Officers, the School is recognized as America's oldest professional training program in public health.


News Article | April 21, 2017
Site: www.biosciencetechnology.com

Harvard Medical School researchers at Massachusetts General Hospital have identified a surprising new role for macrophages, the white blood cells primarily known for removing pathogens, cellular debris and other unwanted materials from the body. In a paper published in Cell on April 20, they describe their discovery of how macrophages are also essential for the healthy functioning of the heart by helping conduct the electric signals that coordinate the heartbeat. “Our finding that a new cell type is involved in cardiac conduction may lead to better understanding of normal heart function. What really surprised me was that macrophages can depolarize—change their electric charge—when coupled to a heart muscle cell. Down the line, this work on the role of macrophages in conduction may lead to new treatments for cardiac arrhythmias,” said corresponding author Matthias Nahrendorf, HMS associate professor of radiology at Mass General. Best known for their role in the immune system, macrophages are primarily responsible for engulfing and digesting microbes, damaged cells and foreign substances. They are found in tissues throughout the body and have recently been shown to have additional functions related to the tissues where they reside. While macrophages are required for healing damaged tissues in the heart, their presence within healthy heart muscle suggests a role in normal heart function. Nahrendorf’s study was designed to investigate their potential role in transmitting and coordinating the electrical signals that stimulate heart muscle contraction. Initial experiments in mice revealed that cardiac macrophages are more abundant in the atrioventicular (AV) node—a key structure connecting the atria (upper chambers) to the ventricles (lower chambers)—which coordinates contraction timing for the upper and lower chambers. Similarly high concentrations of macrophages were found in AV nodes from human autopsy samples. Subsequent animal experiments found that macrophages connect to heart muscle cells via gap junctions—pore-like structures known to coordinate heart muscle contractions—and that the shifts in electric charge that carry the conduction signal are synchronized between macrophages and adjacent heart muscle cells called myocytes. Mice lacking a key, gap-junction protein showed an abnormal slowing of signal conduction through the AV node, and a complete depletion of tissue macrophages led to the development of AV block—a delay in conduction between the atria and ventricles that, in human patients, requires pacemaker implantation. Overall, the findings suggest that cardiac macrophages are essential participants in the cardiac conduction system and that changes in their numbers or properties may contribute to heart rhythm abnormalities. Nahrendorf and his colleagues are continuing to explore the role of macrophages in both the healthy heart and in common disorders of signal conduction. He adds that the cells’ natural propensity to surround and take up materials for disposal could be used to induce macrophages to ingest drugs carried on nanoparticles.


Nanodiamonds - synthetic industrial diamonds only a few nanometers in size - have recently attracted considerable attention because of the potential they offer for the targeted delivery of vaccines and cancer drugs and for other uses. Thus far, options for imaging nanodiamonds have been limited. Now a team of investigators based at the Athinoula A. Martinos Center for Biomedical Imaging at Massachusetts General Hospital has devised a means of tracking nanodiamonds noninvasively with magnetic resonance imaging (MRI), opening up a host of new applications. They report their findings today in the online journal Nature Communications. "With this study, we showed we could produce biomedically relevant MR images using nanodiamonds as the source of contrast in the images and that we could switch the contrast on and off at will," says David Waddington, lead author of the paper and a PhD student at the University of Sydney in Australia. Waddington is currently working with Matthew Rosen, PhD, in the Low-Field Imaging Laboratory at the Martinos Center. "With competing strategies, the nanodiamonds must be prepared externally and then injected into the body, where they can only be imaged for a few hours at most. However, as our technique is biocompatible, we can continue imaging for indefinite periods of time. This raises the possibility of tracking the delivery of nanodiamond-drug compounds for a variety of diseases and providing vital information on the efficacy of different treatment options." Waddington began this work three years ago as part of a Fulbright Scholarship awarded early in his graduate work at the University of Sydney, where he is a member of a team led by study co-author David Reilly, PhD, in the new Sydney Nanoscience Hub - the headquarters of the Australian Institute for Nanoscale Science and Technology, which launched last year. As part of the Reilly group, Waddington played a crucial role in early successes with nanodiamond imaging, including a 2015 paper in Nature Communications. He then sought to extend the potential of the approach by collaborating with Rosen at the Martinos Center and Ronald Walsworth, PhD, at Harvard University, also a co-author of the current study. Rosen's group is a world leader in the area of ultra-low-field magnetic resonance imaging, a technique that proved essential to the development of in vivo nanodiamond imaging. Previously, the use of nanodiamond imaging in living systems was limited to regions accessible using optical fluorescence techniques. However, most potential diagnostic and therapeutic applications of nanoparticles, including tracking of complex disease processes like cancer, call for the use of MRI - the gold standard for noninvasive, high-contrast, three-dimensional clinical imaging. In the present study, the researchers show that they could achieve nanodiamond-enhanced MRI by taking advantage of a phenomenon known as the Overhauser effect to boost the inherently weak magnetic resonance signal of diamond through a process called hyperpolarization, in which nuclei are aligned inside a diamond so they create a signal detectable by an MRI scanner. The conventional approach to hyperpolarization uses solid-state physics techniques at cryogenic temperatures, but the signal boost doesn't last very long and is nearly gone by the time the nanoparticle compound is injected into the body. By combining the Overhauser effect with advances in ultra-low-field MRI coming out of the Martinos Center, the researchers were able to overcome this limitation - thus paving the way for high-contrast in vivo nanodiamond imaging over indefinitely long periods of time. High-performance ultra-low-field MRI is itself a relatively new technology, first reported in Scientific Reports in 2015 by Rosen and Martinos Center colleagues. "Thanks to innovative engineering, acquisition strategies and signal processing, the technology offers heretofore unattainable speed and resolution in the ultra-low-field MRI regime," says Rosen, director of the Low-Field Imaging Laboratory, an assistant professor of Radiology at Harvard Medical School and the senior author of the current paper. "And importantly, by removing the need for massive, cryogen-cooled superconducting magnets, it opens up a number of new opportunities, including the nanodiamond imaging technique we've just described." The researchers have noted several possible applications for their new approach to nanodiamond-enhanced MRI. These include the accurate detection of lymph node tumors, which can aid in the treatment of metastatic prostate cancer, and exploring the permeability of the blood-brain barrier, which can play an important role in the management of ischemic stroke. Because it provides a measurable MR signal for periods of over a month, the technique could benefit applications such as monitoring the response to therapy. Included in treatment monitoring are applications in the burgeoning field of personalized medicine. "The delivery of highly specific drugs is strongly correlated with successful patient outcomes," says Waddington, who was honored with the Journal of Magnetic Resonance Young Scientist Award at the 2016 Experimental NMR Conference in recognition of this work. "However, the response to such drugs often varies significantly on an individual basis. The ability to image and track the delivery of these nanodiamond-drug compounds would, therefore, be greatly advantageous to the development of personalized treatments." The researchers continue to explore the potential of the technique and are now planning a detailed study of the approach in an animal model, while also investigating the behavior of different nanodiamond-drug complexes and imaging them with the new capability. Other authors of the Nature Communications paper include Mathieu Sarracanie and Najat Salameh of the Martinos Center; Huiliang Zhang, and David R. Glenn of the Walsworth team at Harvard University; and Ewa Rej, Torsten Gaebel, and Thomas Boele of the Reilly team at the ARC Centre of Excellence for Engineered Quantum Systems, University of Sydney. Support for the study includes funding from the U.S. Department of Defense/USAMRMC, the Australian Nuclear Science and Technology Organisation and the Australian-American Fulbright Commission. Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, genomic medicine, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of "America's Best Hospitals."


News Article | May 1, 2017
Site: www.eurekalert.org

AURORA, Colo. (May 1, 2017) - In perhaps the largest national suicide intervention trial ever conducted, researchers at the University of Colorado Anschutz Medical Campus and Brown University found that phone calls to suicidal patients following discharge from Emergency Departments led to a 30 percent reduction in future suicide attempts. The study was published recently in JAMA Psychiatry. The year-long trial, which involved 1,376 patients in eight locations nationwide, provided suicidal patients with interventions that included specialized screening, safety planning guidance and follow-up telephone calls. "People who are suicidal are often disconnected and socially isolated," said study co-author Dr. Michael Allen, MD, professor of psychiatry and emergency medicine at the Helen and Arthur E. Johnson Depression Center at CU Anschutz. "So any positive contact with the world can make them feel better." Allen is also medical director of Rocky Mountain Crisis Partners in Denver which has already implemented a similar program where counselors call suicidal patients following their discharge from Emergency Departments (EDs). Suicide is the 10th leading cause of death in the U.S. In 2015, there were 44,193 deaths by suicide nationally. Over one million people attempt to take their own life every year. Colorado routinely ranks among the top 10 states for suicide with about 1,000 deaths a year. Last year, it was number seven in the country. The state Legislature has set a goal of reducing suicides by 20 percent by 2024. Allen said simply handing a suicidal patient a psychiatric referral when discharged isn't enough. "We call them up to seven times to check on them after discharge," he said. "If they aren't there we leave a message and call again. For many, this telephone call is all they get." The crisis center has worked with 17 of Colorado's 88 EDs and is hoping to increase that number and eventually go statewide. "We don't need more brick and mortar buildings, we can reduce suicide risk by simply calling people on the phone," Allen said. "Telephone follow-up programs offer a great way to help bridge an ED visit to outpatient mental health care and hopefully save lives," said Betz, an associate professor of emergency medicine at CU Anschutz who has conducted extensive research on suicide. "It would be great to see such programs become more widely implemented. Suicide is a leading cause of death, especially in Colorado, and a shortage of inpatient and outpatient mental health care options make innovative approaches like telephone counseling even more attractive." The study was led by Brown University and Butler Hospital psychologist Ivan Miller. Miller, a professor of psychiatry and human behavior at the Warren Alpert Medical School of Brown University, said he was encouraged that they were able to impact suicide attempts among this population with a relatively limited intervention. While suicide prevention efforts such as hotlines are well known, published controlled trials of specific interventions are much rarer, Miller said. "We were happy that we were able to find these results," he said. This report was one of several from the Emergency Department Safety Assessment and Follow-up Evaluation (ED-SAFE) study led by Miller, Professor Edwin Boudreaux of the University of Massachusetts and Dr. Carlos Camargo of Massachusetts General Hospital and Harvard University. Dr. Betz was the principal investigator for Colorado's ED-SAFE site. The trial took place in three phases to create three comparison groups. In the first phase, 497 patients received each ED's usual treatment as a control group. In phase two universal screening was implemented and 377 patients received additional attention in the ED. In the third phase, 502 patients received the experimental intervention. Those patients received the same Phase 2 care including additional suicide screening from ED physicians, suicide prevention information from nurses and a personal safety plan they could fill out to prepare for times when they might begin harboring suicidal thoughts again. Over the next year, they also received periodic phone calls from trained providers at Butler Hospital in Providence, R.I., who would discuss suicide risk factors, personal values and goals, safety and future planning, treatment engagement, and problem solving. The number of suicide attempts and the proportion of people attempting suicide declined significantly in the intervention group compared to treatment as usual. The middle group, which received only additional screening, did not show a significant drop compared to the treatment as usual group. "This is a remarkably low cost, low tech intervention that has achieved impressive results," Dr. Allen said.


News Article | April 20, 2017
Site: www.eurekalert.org

A Massachusetts General Hospital (MGH)-led research team has identified a surprising new role for macrophages, the white blood cells primarily known for removing pathogens, cellular debris and other unwanted materials. In their paper published in Cell the investigators describe discovering that macrophages are also essential to the healthy functioning of the heart, helping conduct the electric signals that coordinate the heartbeat. "Our finding that a new cell type is involved in cardiac conduction may lead to better understanding of normal heart function. What really surprised me was that macrophages can depolarize -- change their electric charge -- when coupled to a myocyte. Down the line, this work on the role of macrophages in conduction may lead to new treatments for cardiac arrhythmias," says corresponding author Matthias Nahrendorf, MD, PhD, of the MGH Center for Systems Biology. Best known for their immune system activity of engulfing and digesting microbes, damaged cells and foreign substances, macrophages are found in tissues throughout the body and have recently been shown to have additional functions related to the tissues where they reside. While macrophages are required for healing damaged tissues in the heart, their presence within healthy heart muscle suggests a role in normal heart function. Nahrendorf's study was designed to investigate their potential role in transmitting and coordinating the electrical signals that stimulate heart muscle contraction. Initial experiments in mice revealed that cardiac macrophages are more abundant in the atrioventicular (AV) node -- a key structure connecting the atria (upper chambers) to the ventricles (lower chambers) -- which coordinates contraction timing for the upper and lower chambers. Similarly high concentrations of macrophages were found in AV nodes from human autopsy samples. Subsequent animal experiments found that macrophages connect to heart muscle cells via gap junctions -- pore-like structures known to coordinate heart muscle contractions -- and that the shifts in electric charge that carry the conduction signal are synchronized between macrophages and adjacent heart muscle cells called myocytes. Mice lacking a key gap junction protein showed an abnormal slowing of signal conduction through the AV node, and a complete depletion of tissue macrophages led to the development of AV block -- a delay in conduction between the atria and ventricles that, in human patients, requires pacemaker implantation. Overall, the findings suggest that cardiac macrophages are essential participants in the cardiac conduction system and that changes in their numbers or properties may contribute to heart rhythm abnormalities. Nahrendorf and his colleagues are continuing to explore the role of macrophages in both the healthy heart and in common disorders of signal conduction. He adds that the cells' natural propensity to surround and take up materials for disposal could be used to induce macrophages to ingest drugs carried on nanoparticles. The co-lead authors of the Cell paper are Maarten Hulsmans, PhD, of the MGH Center for Systems Biology and Sebastian Clauss, MD, and Ling Xiao, PhD, of the MGH Cardiovascular Research Center. Additional co-authors include David Milan, MD, and Patrick Ellinor, MD, PhD, of the CVRC. Support for the study includes National Institutes of Health grants NS084863, HL128264, HL114477, HL117829, HL092577, HL105780, and HL096576. The MGH has filed a patent application covering the work described in this paper. Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, genomic medicine, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of "America's Best Hospitals."


NEUCHATEL, Switzerland AND BOSTON, April 25, 2017 /PRNewswire/ -- 1Drop Diagnostics, a Switzerland- and Boston-based medical diagnostics and life sciences company, has announced that the funding of their collaboration with clinicians at the Massachusetts General Hospital (MGH) on portable...


News Article | April 25, 2017
Site: www.eurekalert.org

An intestinal enzyme previously shown to keep bacterial toxins from passing from the gastrointestinal system into the bloodstream may be able to prevent or reduce the liver damage caused by excess alcohol consumption. In their report that will appear in the journal Digestive Diseases and Sciences and has been published online, a Massachusetts General Hospital (MGH) research team describes how oral doses of intestinal alkaline phosphatase (IAP) prevented the development of fatty liver in mouse models of both binge drinking and chronic alcohol consumption. The study also provides the first evidence of an expanded role of the liver's stellate cells in alcoholic liver disease. "Liver damage is one of the most devastating effects of excess alcohol consumption, and so blocking this process could save millions of lives lost to alcohol-related liver diseases such as cirrhosis and liver cancer," says Richard Hodin, MD, of the MGH Department of Surgery, the study's senior author. "Along with direct toxic effects on the liver itself, alcohol appears to damage the liver through its effects on the intestinal lining, allowing bacterial toxins from the gut to cross the barrier and reach the liver. Since we know that IAP works to maintain a healthy gut barrier by blocking passage of an important toxic molecule, we investigated its potential to protect the liver from alcohol-induce damage." Previous research by Hodin's group revealed that IAP helps to maintain a healthy intestinal microbial population by blocking the damaging effects of lipopolysaccharide (LPS), a molecule responsible for the toxic effects of several species of bacteria, and that the enzyme's anti-LPS effects could prevent the development of metabolic syndrome - a constellation of symptoms including obesity, abnormal glucose and lipid metabolism, and fatty liver - in mice fed a high-fat diet. Since LPS is known to play a role in alcohol-induced liver inflammation and its levels are known to rise with alcohol consumption, the MGH team investigated whether oral IAP supplementation could prevent alcoholic liver disease both by detoxifying the LPS released by gut bacteria and by preventing its passage from the gut into the liver's blood supply. The team conducted experiments in two mouse models of binge drinking - either one large dose or three large doses given at 12-hour intervals - and a model of chronic alcohol consumption - steady alcohol consumption for 10 days. The results indicated that giving IAP either before or at the same time as an alcohol dose reduced levels of the ALT enzyme, a common sign of liver damage; reduced the accumulation of fat in the liver, the first sign of alcoholic liver disease; and reduced the production of inflammatory factors. While mice that did not receive the enzyme before or during an alcohol dose were found to have elevations in circulating LPS, decreased expression of the tight junction proteins that maintain the barrier function of the intestinal lining, and increased intestinal inflammation, IAP supplementation prevented those effects. Activation of the hepatic stellate cells, which recently have been shown to contribute to alcoholic fatty liver disease, was also prevented by pretreatment with IAP. Administering IAP after alcohol dosing had no protective effects. "Hepatic stellate cells are considered to be the central player in causing liver fibrosis - scarring or cirrhosis - which is the common endpoint leading to death in most liver diseases," says co-author Michael Choi, MD, of the MGH Gastrointestinal Unit. "Our results suggest that activated hepatic stellate cells are involved in even earlier stages of alcoholic liver disease and that activation can be prevented by pretreatment with IAP. Along with following up this study with human trials of IAP's protective effects, we also would like to know which gut bacterial components besides LPS are important in inducing liver inflammation, to understand more deeply the role of hepatic stellate cells in liver disease and to find ways to block their activation." The co-lead authors of the Digestive Diseases and Sciences paper are Sulaiman Hamarneh, MD, MGH Department of Surgery; and Byeong-Moo Kim, PhD, MGH Gastrointestinal Unit. The study was supported by National Institutes of Health grants T32 DK007754 and P30 DK040561 and by the Ellison Foundation. Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, genomic medicine, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of "America's Best Hospitals."


News Article | May 4, 2017
Site: www.eurekalert.org

Already extolled for their health benefits as a food compound, omega-3 fatty acids now appear to also play a critical role in preserving the integrity of the blood-brain barrier, which protects the central nervous system from blood-borne bacteria, toxins and other pathogens, according to new research from Harvard Medical School. Reporting in the May 3 issue of Neuron, a team led by Chenghua Gu, associate professor of neurobiology at Harvard Medical School, describes the first molecular explanation for how the barrier remains closed by suppressing transcytosis--a process for transporting molecules across cells in vesicles, or small bubbles. They found that the formation of these vesicles is inhibited by the lipid composition of blood vessel cells in the central nervous system, which involves a balance between omega-3 fatty acids and other lipids maintained by the lipid transport protein Mfsd2a. While the blood-brain barrier is a critical evolutionary mechanism that protects the central nervous system from harm, it also represents a major hurdle for delivering therapeutic compounds into the brain. Blocking the activity of Mfsd2a may be a strategy for getting drugs across the barrier and into the brain to treat a range of disorders such as brain cancer, stroke and Alzheimer's. "This study presents the first clear molecular mechanism for how low rates of transcytosis are achieved in central nervous system blood vessels to ensure the impermeable nature of the blood-brain barrier," Gu said. "There is still a lot we do not know about how the barrier is regulated. A better understanding of the mechanisms will allow us to begin to manipulate it, with the goal of getting therapeutics into the brain safely and effectively." The blood-brain barrier is composed of a network of endothelial cells that line blood vessels in the central nervous system. These cells are connected by tight junctions that prevent most molecules from passing between them, including many drugs that target brain diseases. In a 2014 study published in Nature, Gu and colleagues discovered that a gene and the protein it encodes, Mfsd2a, inhibits transcytosis and is critical for maintaining the blood-brain barrier. Mice that lacked Mfsd2a, which is found only in endothelial cells in the central nervous system, had higher rates of vesicle formation and leaky barriers, despite having normal tight junctions. In the current study, Gu, Benjamin Andreone, a neurology student at Harvard Medical School, and their colleagues examined how Mfsd2a maintains the blood-brain barrier. Mfsd2a is a transporter protein that moves lipids containing DHA, an omega-3 fatty acid found in fish oil and nuts, into the cell membrane. To test the importance of this function to the barrier, the team created mice with a mutated form of Mfsd2a, in which a single amino acid substitution shut down its ability to transport DHA. They injected these mice with a fluorescent dye and observed leaky blood-brain barriers and higher rates of vesicle formation and transcytosis--mirroring mice that completely lacked Mfsd2a. A comparison of the lipid composition of endothelial cells in brain capillaries against those in lung capillaries--which do not have barrier properties and do not express Mfsd2a--revealed that brain endothelial cells had around two- to five-fold higher levels of DHA-containing lipids. Additional experiments revealed that Mfsd2a suppresses transcytosis by inhibiting the formation of caveolae--a type of vesicle that forms when a small segment of the cell membrane pinches in on itself. As expected, mice with normal Cav-1, a protein required for caveolae formation, and that lacked Mfsd2a exhibited higher transcytosis and leaky barriers. Mice that lacked both Mfsd2a and Cav-1, however, had low transcytosis and impermeable blood-brain barriers. "We think that by incorporating DHA into the membrane, Mfsd2a is fundamentally changing the composition of the membrane and making it unfavorable for the formation of these specific type of caveolae," Andreone said. "Even though we observed low rates of vesicle formation and transcytosis in blood-brain barrier cells decades ago, this is the first time that a cellular mechanism can explain this phenomenon." By revealing the role of Mfsd2a and how it controls transcytosis in the central nervous system, Gu and her colleagues hope to shed light on new strategies to open the barrier and allow drugs to enter and remain in the brain. They are currently testing the efficacy of an antibody that potentially can temporarily block the function of Msfd2a, and whether caveolae-mediated transcytosis can be leveraged to shuttle therapeutics across the barrier. "Many of the drugs that could be effective against diseases of the brain have a hard time crossing the blood-brain barrier," Gu said. "Suppressing Mfsd2a may be an additional strategy that allows us to increase transcytosis, and deliver cargo such as antibodies against beta-amyloid or compounds that selectively attack tumor cells. If we can find a way across the barrier, the impact would be enormous." This work was supported by The National Institutes of Health (grants F31NS090669, NS092473), the Mahoney postdoctoral fellowship, the Howard Hughes Medical Institute, the Kaneb Fellowship, Fidelity Biosciences Research Initiative and the Harvard Blavatnik Biomedical Accelerator. Harvard Medical School has more than 11,000 faculty working in 10 academic departments located at the School's Boston campus or in hospital-based clinical departments at 15 Harvard-affiliated teaching hospitals and research institutes: Beth Israel Deaconess Medical Center, Boston Children's Hospital, Brigham and Women's Hospital, Cambridge Health Alliance, Dana-Farber Cancer Institute, Harvard Pilgrim Health Care Institute, Hebrew SeniorLife, Joslin Diabetes Center, Judge Baker Children's Center, Massachusetts Eye and Ear/Schepens Eye Research Institute, Massachusetts General Hospital, McLean Hospital, Mount Auburn Hospital, Spaulding Rehabilitation Network and VA Boston Healthcare System.


But of course, finding evidence of life is no easy task. In addition to concerns over contamination, there is also the and the hazards the comes with operating in extreme environments – which looking for life in the solar system will certainly involve. All of these concerns were raised at a new FISO conference titled "Towards In-Situ Sequencing for Life Detection", hosted by Christopher Carr of MIT. Carr is a research scientist with MIT's Department of Earth, Atmospheric and Planetary Sciences (EAPS) and a Research Fellow with the Department of Molecular Biology at Massachusetts General Hospital. For almost 20 years, he has dedicated himself to the study of life and the search for it on other planets. Hence why he is also the science principal investigator (PI) of the Search for Extra-Terrestrial Genomes (SETG) instrument. Led by Dr. Maria T. Zuber – the E. A. Griswold Professor of Geophysics at MIT and the head of EAPS – the inter-disciplinary group behind SETG includes researchers and scientists from MIT, Caltech, Brown University, arvard, and Claremont Biosolutions. With support from NASA, the SETG team has been working towards the development of a system that can test for life in-situ. Introducing the search for extra-terrestrial life, Carr described the basic approach as follows: "We could look for life as we don't know it. But I think it's important to start from life as we know it – to extract both properties of life and features of life, and consider whether we should be looking for life as we know it as well, in the context of searching for life beyond Earth." Towards this end, the SETG team seeks to leverage recent developments in in-situ biological testing to create an instrument that can be used by robotic missions. These developments include the creation of portable DNA/RNA testing devices like the MinION, as well as the Biomolecule Sequencer investigation. Performed by astronaut Kate Rubin in 2016, this was first-ever DNA sequencing to take place aboard the International Space Station. Building on these, and the upcoming Genes in Space program – which will allow ISS crews to sequence and research DNA samples on site – the SETG team is looking to create an instrument that can isolate, detect, and classify any DNA or RNA-based organisms in extra-terrestrial environments. In the process, it will allow scientists to test the hypothesis that life on Mars and other locations in the solar system (if it exists) is related to life on Earth. To break this hypothesis down, it is a widely accepted theory that the synthesis of complex organics – which includes nucleobases and ribose precursors – occurred early in the history of the solar system and took place within the Solar nebula from which the planets all formed. These organics may have then been delivered by comets and meteorites to multiple potentially-habitable zones during the Late Heavy Bombardment period. Known as lithopansermia, this theory is a slight twist on the idea that life is distributed throughout the cosmos by comets, asteroids and planetoids (aka. panspermia). In the case of Earth and Mars, evidence that life might be related is based in part on meteorite samples that are known to have come to Earth from the Red Planet. These were themselves the product of asteroids striking Mars and kicking up ejecta that was eventually captured by Earth. By investigating locations like Mars, Europa and Enceladus, scientists will also be able to engage in a more direct approach when it comes to searching for life. As Carr explained: "There's a couple main approaches. We can take an indirect approach, looking at some of the recently identified exoplanets. And the hope is that with the James Webb Space Telescope and other ground-based telescopes and space-based telescopes, that we will be in a position to begin imaging the atmospheres of exoplanets in much greater detail than characterization of those exoplanets has [allowed for] to date. And that will give us high-end, it will give the ability to look at many different potential worlds. But it's not going to allow us to go there. And we will only have indirect evidence through, for example, atmospheric spectra." Mars, Europa and Enceladus present a direct opportunity to find life since all have demonstrated conditions that are (or were) conducive to life. Whereas there is ample evidence that Mars once had liquid water on its surface, Europa and Enceladus both have subsurface oceans and have shown evidence of being geologically active. Hence, any mission to these worlds would be tasked with looking in the right locations to spot evidence of life. On Mars, Carr notes, this will come down to looking in places there there is a water-cycle, and will likely involve some a little spelunking: "I think our best bet is to access the subsurface. And this is very hard. We need to drill, or otherwise access regions below the reach of space radiation which could destroy organic materiel. And one possibility is to go to fresh impact craters. These impact craters could expose material that wasn't radiation-processed. And maybe a region where we might want to go would be somewhere where a fresh impact crater could connect to a deeper subsurface network – where we could get access to material perhaps coming out of the subsurface. I think that is probably our best bet for finding life on Mars today at the moment. And one place we could look would be within caves; for example, a lava tube or some other kind of cave system that could offer UV-radiation shielding and maybe also provide some access to deeper regions within the Martian surface." As for "ocean worlds" like Enceladus, looking for signs of life would likely involve exploring around its southern polar region where tall plumes of water have been observed and studied in the past. On Europa, it would likely involve seeking out "chaos regions", the spots where there may be interactions between the surface ice and the interior ocean. Exploring these environments naturally presents some serious engineering challenges. For starters, it would require the extensive planetary protections to ensure that contamination was prevented. These protections would also be necessary to ensure that false positives were avoided. Nothing worse than discovering a strain of DNA on another astronomical body, only to realize that it was actually a skin flake that fell into the scanner before launch! And then there are the difficulties posed by operating a robotic mission in an extreme environment. On Mars, there is always the issue of solar radiation and dust storms. But on Europa, there is the added danger posed by Jupiter's intense magnetic environment. Exploring water plumes coming from Enceladus is also very challenging for an orbiter that would most likely be speeding past the planet at the time. But given the potential for scientific breakthroughs, such a mission it is well worth the aches and pains. Not only would it allow astronomers to test theories about the evolution and distribution of life in our solar system, it could also facilitate the development of crucial space exploration technologies, and result in some serious commercial applications. Looking to the future, advances in synthetic biology are expected to lead to new treatments for diseases and the ability to 3-D print biological tissues (aka. "bioprinting"). It will also help ensure human health in space by addressing bone density loss, muscle atrophy, and diminished organ and immune-function. And then there's the ability to grow organisms specially-designed for life on other planets (can you say terraforming?) On top of all that, the ability to conduct in-situ searches for life on other Solar planets also presents scientists with the opportunity to answer a burning question, one which they've struggled with for decades. In short, is carbon-based life universal? So far, any and all attempts to answer this question have been largely theoretical and have involved the "low hanging fruit variety" – where we have looked for signs of life as we know it, using mainly indirect methods. By finding examples that come from environments other than Earth, we would be taking some crucial steps towards preparing ourselves for the kinds of "close encounters" that could be happening down the road. Explore further: The search for extraterrestrial life in the water worlds close to home


News Article | April 17, 2017
Site: www.prweb.com

More than six dozen doctors, survivors and family members join BAF on March 29 in Washington, D.C. The Brain Aneurysm Foundation will lead a delegation made up of 100 brain aneurysm survivors, family members of those affected by the disease, advocates and medical professionals from around the country for a Congressional Advocacy Day on Wednesday, March 29, 2017. The effort set forth is to raise awareness of brain aneurysm disease and to seek support for Ellie’s Law. Ellie’s Law is a bill that seeks federal funding for brain aneurysm research. It is named in honor of Ellie Helton, a 14-year-old Apex, NC teenager, who died on July 16, 2014 as a result of a brain aneurysm. The bill, HR 1648, provides $5 million each fiscal year, for five years, to the National Institute of Neurological Disorders and Stroke (NINDS) to conduct or support further comprehensive research on brain aneurysms, studying a broader patient population diversified by age, sex, and race. This legislation will allow NINDS to conduct critical research on what causes aneurysms, what causes aneurysms to rupture, determining the efficacy of intervention on smaller unruptured aneurysms, development of drugs or treatments, development of neuroprotection or regeneration for brain injury from ruptures, detecting unstable aneurysms using imaging, preventing aneurysm recurrence, finding a biomarker for aneurysm and family genetics, socioeconomic research on aneurysm treatments, costs, and systems of care. “Increased funding for brain aneurysm research is essential to find effective treatments, interventions, and ways to prevent aneurysms from developing,” said Christine Buckley, Executive Director, Brain Aneurysm Foundation. “The passage of “Ellie’s Law” represents a real, long-term investment in brain aneurysm research, with the goal of eradicating the devastation of brain aneurysm disease.” Federal funding for brain aneurysm research is disproportionately low. Despite the widespread prevalence of this disease, for which there is no cure, and the high societal cost it imposes on the nation, the federal government only spends approximately $0.83 per year on brain aneurysm research for each person afflicted with a brain aneurysm. The BAF delegation is scheduled to meet approximately 200 key legislators including Senator Edward Markey (D-MA). The Brain Aneurysm Foundation is joined in this advocacy effort by three brain aneurysm survivors. Tonya Robinson of Michigan, Kerri Messinger of New Jersey and Ann Waldo of Washington, D.C., will take part in Advocacy Day activities and speak to legislators and their staffs about their personal stories of suffering from one or more large or giant wide-necked, unruptured aneurysms. Medtronic, one of the world's largest medical technology, services and solutions companies, will also join the Brain Aneurysm Foundation by providing educational materials, including animation of brain aneurysms, as well as medical devices to help explain possible treatments for the disease. The Bee Foundation, a non-profit brain aneurysm organization based in Wayne, PA, will also participate. “This is our sixth year participating in Congressional Advocacy Day and the effort is so important to our mission in helping to reduce the healthcare disparities associated with brain aneurysm statistics,” said Buckley. “Legislators throughout the country have been very supportive of looking at funding for research, as well as for awareness and education initiatives, but they often tell us that we’re the first people to bring this disease to their attention. And to have so many people representing so much of the country on this important day is truly gratifying.” Brain aneurysms are weakened arterial walls that can rupture; causing bleeding that damages the brain. Researchers estimate six million Americans have an unruptured brain aneurysm. This disease strikes indiscriminately, but communities of color have a higher risk of rupture often causing death or cognitive disability. In general, women are at a greater risk to form a brain aneurysm than men. Brain aneurysms are a silent killer, providing little or no warning and lead to an estimated 30,000 ruptures annually and cause nearly 500,000 deaths worldwide. ABOUT THE BRAIN ANEURYSM FOUNDATION The Brain Aneurysm Foundation is the globally recognized leader in brain aneurysm awareness, education, support, advocacy and research funding. Now celebrating more than 20 years ‘of service and led by Executive Director Christine Buckley, the Brain Aneurysm Foundation was established in 1994 at Massachusetts General Hospital in Boston, Massachusetts. Its mission is to promote early detection of brain aneurysms by providing knowledge and raising awareness of the signs, symptoms and risk factors; work with the medical communities to provide support networks for patients and families; as well as to further research that will improve patient outcomes and save lives. The Foundation is unique in that it has a Medical Advisory Board of Directors, which is made up of more than three-dozen doctors—neurologists, neurosurgeons, and interventional neuroradiologists—representing the best research hospitals, facilities, and universities throughout the country. Its members provide expertise and support to the Foundation in a variety of ways. For more information about the Brain Aneurysm Foundation, visit http://www.bafound.org


News Article | May 1, 2017
Site: www.eurekalert.org

Bottom Line: A noninvasive PET imaging method that measures granzyme B, a protein released by immune cells to kill cancer cells, was able to distinguish mouse and human tumors that responded to immune checkpoint inhibitors from those that did not respond early in the course of treatment. Journal in Which the Study was Published: Cancer Research, a journal of the American Association for Cancer Research. Author: Umar Mahmood, MD, PhD, professor of radiology at Harvard Medical School and director of the Division of Precision Medicine at Athinoula A. Martinos Center for Biomedical Imaging in Massachusetts General Hospital (MGH), Boston. Background: Although immunotherapies, such as checkpoint inhibitors, have revolutionized cancer treatment, they only work in a minority of patients, which means that most patients receiving this treatment will not benefit but still have the increased risk of side effects, besides losing time that they could spend on other therapies, Mahmood explained. Response to immunotherapy often cannot be measured effectively at early time points by traditional imaging techniques that measure tumor size, such as CT and MRI scans, or those that measure tumor glucose uptake, such as FDG PET, because these techniques cannot distinguish a nonresponding tumor from a tumor that is responding to immunotherapy but appears to grow in size because it is filled with immune cells and accompanied by increased glucose uptake, Mahmood noted. Tissue biopsies can be unreliable because of tumor heterogeneity and constant changes in the levels of the biomarker proteins measured. How the Study Was Conducted: Mahmood and colleagues designed a probe that binds to granzyme B--a protein that immune cells release to kill their target--after it is released from the immune cells, so they could directly measure tumor cell killing. The researchers attached the probe to a radioactive atom and used PET scanning to noninvasively image the entire body and see where immune cells are actively releasing tumor-killing granzyme B. Results:The team tested their probe in tumor-bearing mice before and after treatment with immune checkpoint inhibitors and found that one group of mice had high PET signal, meaning high levels of granzyme B in the tumors, while the other group had low levels of PET signal in the tumors. When the two groups of mice were followed, all mice with high PET signal responded to the therapy and their tumors subsequently regressed, whereas those with low PET signal did not respond to the therapy, and their tumors continued to grow. "Because PET imaging is quantitative, we could measure the degree of effectiveness and put a number on it," Mahmood added. When they compared the data from monotherapy and combination therapy, they saw a significant increase in tumor granzyme B PET signal in the combination group. The researchers then collaborated with Keith Flaherty, MD, and Genevieve Boland, MD, PhD, from MGH, and tested their probe on nine human melanoma biopsy samples, six from patients treated with nivolumab (Opdivo) and three from those treated with pembrolizumab (Keytruda). They detected high levels of granzyme B in the samples from responders and much lower levels in the samples from nonresponders. Author Comment: "The ability to differentiate early in the course of treatment patients who are likely to benefit from immunotherapy from those who will not can greatly improve individual patient care and help accelerate the development of new therapies," Mahmood said. "In our study, we found a marker that was highly predictive of response to immunotherapy at a very early time after starting treatment, and we were able to design an imaging probe to detect this marker and accurately predict response noninvasively," said Mahmood. "These findings could have a significant impact on drug development, as different combinations could be imaged at very early time points in patients and the levels of tumor granzyme B used to compare treatments and rank effectiveness," Mahmood said. "Further, therapeutics that achieve high levels of granzyme B release can be advanced faster and those leading to low granzyme B release can be altered or eliminated." Limitations: A limitation of the study is that the probe has not yet been tested in the clinic, but the researchers are actively pursuing it, Mahmood noted. Funding & Disclosures: This study was funded by the National Institutes of Health. Mahmood is the cofounder and consultant at CytoSite BioPharma, a company that is further developing the granzyme B PET imaging probe for clinical translation. Founded in 1907, the American Association for Cancer Research (AACR) is the world's first and largest professional organization dedicated to advancing cancer research and its mission to prevent and cure cancer. AACR membership includes more than 37,000 laboratory, translational, and clinical researchers; population scientists; other health care professionals; and patient advocates residing in 108 countries. The AACR marshals the full spectrum of expertise of the cancer community to accelerate progress in the prevention, biology, diagnosis, and treatment of cancer by annually convening more than 30 conferences and educational workshops, the largest of which is the AACR Annual Meeting with more than 21,900 attendees. In addition, the AACR publishes eight prestigious, peer-reviewed scientific journals and a magazine for cancer survivors, patients, and their caregivers. The AACR funds meritorious research directly as well as in cooperation with numerous cancer organizations. As the Scientific Partner of Stand Up To Cancer, the AACR provides expert peer review, grants administration, and scientific oversight of team science and individual investigator grants in cancer research that have the potential for near-term patient benefit. The AACR actively communicates with legislators and other policymakers about the value of cancer research and related biomedical science in saving lives from cancer. For more information about the AACR, visit http://www. .


News Article | May 4, 2017
Site: www.techtimes.com

A new study has concluded that long-term gluten intake has no links to heart disease risks in people who do not suffer from celiac disease. On the contrary, it found that restricting whole grain consumption to stay low on gluten in non-celiac patients may actually increase the likelihood of heart conditions. But what really happens when you give up gluten? Here’s a quick investigation on quitting gluten, a type of protein in rye, wheat, and barley, and has been pinpointed for triggering inflammation and intestinal damage among individuals with celiac disease. Dr. Alessio Fasano, author of “Gluten Freedom” and founder of the Center for Celiac Research at Massachusetts General Hospital, do not see the gluten-free industry — currently a $1 billion industry — slowing down anytime soon. “Unlike other fad diets, there are people who actually need to consume gluten-free foods for medical reasons, so they’ll always be available,” Fasano told Prevention. Here are some things one can expect to happen after going gluten-free: Your fiber intake can dramatically drop. Over 90 percent of Americans do not meet recommended fiber requirements, which are 25 grams for women and 38 grams for men. This can further decrease with gluten-free foods, and the gut can suffer as a result. Fasano explained that fiber feeds the microbiome, so when there’s not enough of it for intestinal bacteria to feed on, one may be susceptible to developing gut inflammation, irritable bowel syndrome, and related conditions. You won’t readily lose weight. Gluten-free does not necessarily mean calorie-free, and many of these foods actually contain more calories, fat, sugar, and sodium than their gluten counterparts. If you’re keen on giving up gluten, add more vegetables, fruits, and lean meats to your diet. You may want to stay in bed more. A gluten-free fare can also eliminate other nutrients that come with those foods, including fiber, iron, zinc, folic acid, and vitamin D. A diet expert should supervise you to make sure you are not missing out on these nutrients, as deficiency could lead to weakness and fatigue, hair loss, changes in mood, and constipation. You may be at a greater risk for cancer. Many people go gluten-free to go Paleo, a popular diet that mimics the “caveman” style or the way our ancestors ate. This promotes increased meat intake, which will pump more protein into your body and boost your cancer risk. You could feel happier. There are people who don’t test positive for celiac but are afflicted with nonceliac gluten sensitivity, who get GI distress, depression, and brain fog when they consume gluten. A study saw NCGS patients experience greater depressive symptoms when on a gluten-filled diet. There are quite a number of people on gluten-free diets yet do not have a medically needed dietary restriction. In short, they may be eating gluten-free as a fad diet and with the belief that it’s lower in calories and fat, for instance. Watch out in case you’re one of them, advised nutritionist Jessica Fishman Levinson. “Personally I do not believe there is a benefit to eating gluten-free if you don't have gluten intolerance," Levinson said in a Live Science report, explaining that gluten-free food is not always healthier. But those who are truly gluten-sensitive or allergic should take extra careful steps around their diet, staying alert for cross-contamination and when eating out at restaurants and even when presented with gluten-free choices on the menu. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


News Article | May 6, 2017
Site: news.yahoo.com

A possible suspect who was involved in a gun fight with the law enforcement authorities and was injured in the process is now in the hospital. Two people were found dead at an apartment complex at 141 Dorchester Avenue in South Boston on Friday night, police said. A possible suspect was involved in a gun fight with the authorities and was injured in the process. Police arrived at the scene after reports of a man with a gun. The man allegedly began firing shots after which the police returned fire, injuring the possible suspect a number of times. According to reports, the suspect was taken to Boston’s Tufts Medical Center and was alive. Read: Gunman Killed In Mass Shooting At Apartment Complex In San Diego, Police Investigating Possible Hate Crime “It looks like you have a double homicide in this apartment here,” Boston Police Commissioner William Evans was reported saying by the Boston Globe. “We also have an officer shooting with one individual shot, non-life-threatening. We’re just trying to piece it together.” Sources told CBS that the victims were a man and woman who were found bound and had their throats slashed. The network was also told that the three people involved in the incident knew each other. Police officials, however, reportedly said that they were still attempting to determine whether the victims at the Macallen Building were shot or stabbed. A resident of the building, who lives on the second floor, told the Globe he reached home a little before 9 p.m. EDT and found around six or seven police vehicles arriving at the scene. “As I was coming out of the T across the street, they were literally just coming up in front of the building,” Peter Dziedzic told the publication. He added that he saw police presence increase as he watched from his house. Dziedzic added that parts of Dorchester Avenue, Broadway, and West 4th Street were closed to traffic. He also said he saw police dressed in tactical gear accompanied by K-9 units but no violence was seen or heard, adding that he believed the focus of law enforcement was on a higher floor. Dziedzic said: “It’s a pretty soundproof building. I don’t even hear my neighbors.” “As it was building up there were more and more police cars. … At the height of this there must have been easily 40 or 50 police vehicles,” he said. In another unrelated incident Friday night, a police officer was shot while responding to an incident at Motel 6 in Braintree, Massachusetts. The motel is located off Route 3 on Union Street. According to reports, one person was barricaded inside the motel, while the officer involved in the shooting was taken to Massachusetts General Hospital and is undergoing surgery. Braintree police Chief Paul Shastany said officers responded the motel around 9:30 p.m. to check the warrant status of an individual, NBC Boston reported. Soon after, the suspect opened fire on the officers and also hit one of the law enforcement officers in the face. The injuries sustained by the officer were not life-threatening and according to the NBC report, he was alert and talked to paramedics as he left the scene. At a press conference, Shastany announced the suspect was found dead in the motel room and that the death was being investigated.


A new research established that long-term intake of gluten has no association with heart disease risks in individuals who do not suffer from celiac disease. On the contrary, the study found that restricting consumption of whole grains to maintain a low-gluten diet in individuals without celiac disease, may increase their propensity to heart diseases. For the unfamiliar, gluten is a type of storage protein found in rye, wheat, and barley. Consumption of this protein can trigger inflammation and may also damage the intestines of people suffering from celiac disease. The autoimmune reaction triggered by the ingestion of gluten or food products containing the protein is called celiac disease. The autoimmune reaction prevents the intestine from digesting the nutrients and over time, this particular disease can lead to other complications such as heart ailments, osteoporosis, anemia, and more. Scientists from the Massachusetts General Hospital/Harvard Medical School and Columbia University Medical Center conducted the research entitled "Long-term Gluten Consumption in Adults without Celiac Disease and the Risk of Coronary Heart Disease: Prospective Cohort Study." Lead author of the study Benjamin Lebwohl revealed that gluten is very harmful for individuals with celiac disease. However, many diet books state that a low-gluten diet is beneficial for one and all. These conclusions are drawn solely on the basis of circumstantial and anecdotal evidence. The study's findings reveal that limiting gluten in one's daily diet has no health benefits — at least with regard to heart health in people who are non-celiac. On the other hand, it may have a negative effect on their health as the whole grains, which are restricted under the low-gluten diet may extend protection to the heart. To determine whether a low-gluten diet has any effect on the heart health status, the researchers observed and analyzed coronary disease and data, as well as the dietary information of 65,000 females who participated in the Nurses Health Study. The researchers also studied the data taken on the same lines from 45,000 male participants from the Health Professionals Follow-up Study. Both the studies excluded female and male participants with celiac disease at the outset. Every four years — from 1986 to 2010 — the subjects filled out questionnaires detailing their dietary habits. All the participants were divided into five categories depending on their gluten intake. "We decided to look at heart disease because it's a leading killer, and because it's generally understood that heart health can be affected by diet," Dr. Lebwohl shared. After thorough analysis of the data it was discovered that no link between heart disease risk and gluten intake existed. Researchers stated that the study's participants who consumed minimum gluten in their food had the same level of coronary heart ailments as those having high gluten consumption. Senior investigator of the study Andre Chan remarked that recommendation of a low-gluten diet to avoid coronary heart disease risks is unwarranted. In future research, the scientists intend to observe the effects of gluten consumption on more health issues such as other autoimmune disease and cancer. The findings of the study have been published in the British Medical Journal on Tuesday, May 2. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


A gene previously identified as critical for tumor growth in many human cancers also maintains intestinal stem cells and encourages the growth of cells that support them, according to results of a study led by Johns Hopkins researchers. The finding, reported in the Apr. 28 issue of Nature Communications, adds to evidence for the intimate link between stem cells and cancer, and advances prospects for regenerative medicine and cancer treatments. Study leader Linda M. S. Resar, M.D., professor of medicine, oncology and pathology at the Institute for Cellular Engineering at the Johns Hopkins University School of Medicine, has been studying genes in the high-mobility group (HMG) family for over two decades. Several years ago, while creating a genetically engineered mouse that expresses high levels of the mouse HMGA1 gene to investigate its role in leukemia, Resar and her colleagues made the chance finding that the intestines of these animals were much larger and heavier than those of "wild-type" animals (or control mice that were not genetically modified). The mouse intestines were also riddled with polyps, abnormal growths projecting from the intestinal lining that can be precursors of cancer. In fact, polyps in humans frequently progress to colon cancer, which is why they are removed during screening colonoscopies in people over 50 and others at risk for colon cancer. To better understand how HMGA1 affected the rodents' intestines, Resar and Lingling Xian, M.D., Ph.D., research associate at the Johns Hopkins University School of Medicine, and their colleagues examined the transgenic animals' intestinal cells to determine which ones were expressing this gene. Several different experiments localized the active gene and its protein to stem cells buried within the crypts, or deep grooves in the intestinal lining. After isolating these stem cells from both transgenic and wild-type mice, the researchers found that those carrying the HMGA1 transgene multiplied far more rapidly, forming identical daughter cells in a process called self-renewal, which is a defining property of all stem cells. These transgenic stem cells also readily created intestinal tissues called "organoids" in laboratory dishes. These organoids had more stem cells than those isolated from wild-type mice. Further investigation, says Resar, showed that these unusual properties arise from the ability of HMGA1 to turn on several genes involved in the Wnt pathway, a network of proteins necessary for embryonic development and stem cell activity. Stem cells do not function in isolation, explains Resar. They need a "niche" to survive and maintain an undifferentiated state. From the French word nicher, which means to build a nest, a niche is a nest-like compartment comprised of cells that secrete growth factors and other proteins that help stem cells survive. The niche also prevents stem cells from morphing into mature intestinal cells until new intestinal cells are needed. Intestinal stem cells are particularly important because a new intestinal lining is generated about every 4-5 days. Looking further into the intestinal crypts of both the transgenic and wild-type mice, the research team made what they consider a surprising finding: Not only was HMGA1 causing the stem cells themselves to self-renew or proliferate more rapidly in the transgenic animals, but it was also increasing the number of Paneth cells, a type of niche cell known to support intestinal stem cells. Additional experiments showed that the protein produced by HMGA1 activates another gene called Sox9, which is directly responsible for turning stem cells into Paneth cells. "We suspected that HMGA1 might generate new stem cells, but we were extremely surprised that it also helps support these cells by building a niche," Resar says. "We believe that our experiments provide the first example of a factor that both expands the intestinal stem cell compartment and builds a niche." Many genes that are involved in the growth and development of embryos or adult stem cells also play roles in cancer, Resar adds. After scanning the Cancer Genome Atlas, a database of genes expressed in human cancers, the research team discovered that the activity of both HMGA1 and SOX9 genes are tightly correlated in normal colon tissue, and both genes become highly overexpressed in colon cancer. "This tells us that the pathway turned on by HMGA1 in normal intestinal stem cells becomes disrupted and hyperactive in colon cancer," Resar says. Resar says the team plans to continue investigating the function of HMGA1 and SOX9 in intestinal and other cancers as well as their role in stem cells. Both avenues of investigation could eventually lead to clinical applications, she adds. For example, if scientists can find a way to turn down overexpression of these genes in cancer, we could disrupt cancer growth and prevent tumor progression. On the flip side, turning up expression of these genes or their pathways could help researchers grow new intestinal tissue to replace tissue destroyed by diseases such as inflammatory bowel disease or radiation treatment for cancer. "What we discovered is something referred to as the Goldilocks paradox," she says. "Too little of this protein disrupts normal stem cell function, but too much can promote abnormal growth and lead to cancer. For our work to help patients, we will need to find ways to get the amount just right and in the appropriate cell context." To view the video that accompanies this release please click here. Other Johns Hopkins researchers who participated in this research include Dan Georgess, Tait Huso, Leslie Cope, Amy Belton, Yu-Ting Chang, Wenyong Kuang, Qihua Gu, Xiaoyan Zhang, David L. Huso and Andrew J. Ewald. This work also included Alessio Fasano and Stefania Senger from Massachusetts General Hospital for Children. This work was supported by grants from the National Cancer Institute (grant numbers CA182679, CA164677, and CA149550) and the Maryland Stem Cell Research Fund (grant numbers 2011-MSCRFE-0102 and 2015-MSCRFE-1759).


News Article | April 20, 2017
Site: www.eurekalert.org

Macrophages, immune cells known for their PAC-MAN-like ingestion of microbial intruders and biological waste, have a previously unrecognized role in helping the mammalian heart beat in rhythm. Massachusetts General Hospital researchers discovered that macrophages aggregate around central cardiac cells that regulate electrical impulses within the mouse heart, helping the cells conduct electricity. Mice that were genetically engineered to lack macrophages have irregular heartbeats, hinting that these immune cells may also play a role in heart disease. The findings appear April 20 in the journal Cell. "This work opens up a completely new view on electrophysiology; now, we have a new cell type on the map that is involved in conduction," says senior author Matthias Nahrendorf, a systems biologist at Massachusetts General Hospital, Harvard Medical School. "Macrophages are famous for sensing their environment and changing their phenotype very drastically, so you can think about a situation where there is inflammation in the heart that may alter conduction, and we now need to look at whether these cells are causally involved in conduction abnormalities." Researchers have known for decades that macrophages are in high abundance around inflamed or diseased hearts, but Nahrendorf's investigation began when he asked what the immune cells were doing in a healthy heart. After sending a mouse model depleted of macrophages for a heart MRI and electrocardiogram, the technician reported back that something was wrong; the mouse's heart was beating too slowly. Tests in a healthy rodent revealed a high density of resident macrophages at the heart's atrioventricular node, which passes electricity from the atria to the ventricles. Nahrendorf showed the results to his colleagues, David Milan and Patrick Ellinor, both electrophysiologists at Massachusetts General Hospital, who responded by opening the doors to their labs. Together, the teams found that macrophages extend their cell membranes between cardiac cells and create pores, also called gap junctions, for the electrical current to flow through. The macrophages contribute by preparing the conducting heart cells for the next burst of electricity so conducting cells are able to keep up with a fast contraction rhythm. "When we got the first patch clamp data that showed the macrophages in contact with cardiomyoctes were rhythmically depolarizing, that was the moment I realized they weren't insulating, but actually helping to conduct," Nahrendorf says. "This work was very exciting because it was an example of how team science can help to connect fields that are traditionally separated--in this case, immunology and electrophysiology." The group will follow up by looking at whether macrophages are involved in common conduction abnormalities. There are also potential connections between macrophages and anti-inflammatory drugs, which are widely reported to help with heart disease. If macrophages do play a role in disease, the researchers say it can open up a new line of therapeutics, as these immune cells naturally consume foreign molecules in their presence and are easy to target as a result. This work was funded in part by the National Institutes of Health. The General Hospital Corporation has filed a patent application based on the research. Cell, Hulsmans, Clauss, and Xiao et al.: "Macrophages Facilitate Electrical Conduction in the Heart" http://www.cell.com/cell/fulltext/S0092-8674(17)30412-9 Cell (@CellCellPress), the flagship journal of Cell Press, is a bimonthly journal that publishes findings of unusual significance in any area of experimental biology, including but not limited to cell biology, molecular biology, neuroscience, immunology, virology and microbiology, cancer, human genetics, systems biology, signaling, and disease mechanisms and therapeutics. Visit http://www. . To receive Cell Press media alerts, contact press@cell.com.


News Article | April 24, 2017
Site: www.eurekalert.org

(Entertainment Industry Foundation) SU2C awarded $250k to each of four teams of SU2C-affiliated scientists who have not previously worked together: René Bernards, Ph.D., Netherlands Cancer Institute, and Siwen Hu-Lieskovan, M.D., Ph.D., UCLA; Matthew Levy, Ph.D., Albert Einstein CoM and Cassian Yee, M.D., MD Anderson Cancer Center; David T. Ting, M.D., Massachusetts General Hospital and Shelley Berger, Ph.D., University of Pennsylvania; and Matthew Vander Heiden, M.D., Ph.D., Massachusetts Institute of Technology, and Melissa Skala, Ph.D., Morgridge Institute for Research.


"We are pleased to have some of the industry's most innovative, experienced and passionate connected health champions to help set the agenda and create insightful, ahead-of-the-curve programming for this year's event," said Joseph C. Kvedar MD, Vice President, Connected Health, Partners HealthCare, and CHC17 Program Chair. "Attendees will get the best thinking from some of the best minds in personal connected health. We are pleased to work with such a distinguished group of advisors." The CHC17 Advisory Board members represent the complete ecosystem, from healthcare providers, pharma and life sciences companies, and payers to the leaders in the tech sector, investors and innovators: "The 2017 Connected Health Conference will deliver the best our field has to offer, showcasing forward-thinking approaches, new evidence and technologies shaping clinical care, consumer health and investment in personal connected health," added Richard Scarfo, Vice President, PCHAlliance, and Director of the Connected Health Conference. "We're taking a fresh approach, creating unique learning experiences delivered by those on the front lines; and developing a dynamic, interactive and experiential exhibition floor, designed to facilitate collaborations, networking and, especially, innovation." CHC17 focuses on one of the hottest topics facing healthcare -- and society: Healthy aging and how connected approaches support health across the decades. This year's theme, The Connected Life Journey: Shaping Health and Wellness for Every Generation, reimagines health and wellbeing throughout the life cycle, emphasizing new research, evidence and real-world examples, business models and actionable knowledge to support the adoption and implementation of personal connected health at every age and stage of life.  The Conference will take place October 25-27 at the Seaport World Trade Center in Boston. GENERAL REGISTRATION:  Registration is now open. Please visit the CHC17 website for details and easy online registration. Partners Connected Health Partners Connected Health, at Partners HealthCare, is leveraging information technology – mobile phones, tablets, wearables, sensors and remote health monitoring tools – to deliver quality patient care outside of traditional medical settings. Partners Connected Health programs are also helping providers and patients better manage chronic conditions, maintain health and wellness and improve adherence, engagement and clinical outcomes. The Connected Health team creates and deploys mobile technologies in a number of patient populations and care settings, and is conducting innovative research studies to test the effectiveness of mobile health technologies in various clinical applications, including medication adherence, care coordination, chronic disease management, prevention and wellness. Partners HealthCare, an integrated health system founded by Brigham and Women's Hospital and Massachusetts General Hospital, includes two academic medical centers, community and specialty hospitals, a managed care organization, community health centers, a physician network, home health and long-term care services, and other health care entities. It is a principal teaching affiliate of Harvard Medical School. About the Personal Connected Health Alliance The Personal Connected Health Alliance (PCHAlliance) aims to make health and wellness an effortless part of daily life. The PCHAlliance, a non-profit organization formed by HIMSS, believes that health is personal and extends beyond healthcare. The Alliance mobilizes a coalition of stakeholders to realize the full potential of personal connected health. PCHAlliance members are a vibrant ecosystem of technology and life sciences industry icons and innovative, early stage companies along with governments, academic institutions, and associations from around the world. To support its vision, PCHAlliance convenes the global personal connected health community at the annual Connected Health Conference, the premier international event for the exchange of research, evidence, ideas, innovations and opportunities in personal connected health. The Alliance publishes and promotes adoption of the Continua Design Guidelines. Continua is recognized by the International Telecommunication Union (ITU) as the international standard for safe, secure, and reliable exchange of data to and from personal health devices. PCHAlliance accelerates technical, business, policy and social strategies necessary to advance personal connected health through its flagship Academy for Healthy Longevity to promote lifelong health and wellness. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/redesigned-2017-connected-health-conference-announces-advisory-board-opens-registration-300439960.html


This year's David Martin Carter Mentor Award was presented to Dr. Richard Edelson, Chair and Professor, Department of Dermatology, Yale School of Medicine. For over four decades Dr. Richard Edelson has influenced the field of dermatology as a distinguished dermatologist, researcher, educator and esteemed mentor. He is a notable author and editor, having worked on hundreds of scholarly articles, other writings, and six books. Dr. Edelson is the past president of the Dermatology Foundation, and has held leadership positions with the National Cancer Institute and Association of Professors of Dermatology. "We were proud to honor Dr. Richard Edelson with the 2017 David Martin Carter Mentor Award," commented Dr. Steven R. Cohen, Chair of the Mentor Award Committee. "A world-renowned dermatologist and researcher, Dr. Edelson is the 25th honoree to receive this prestigious award. He has been a devoted mentor and educator, and is truly laudable in the field of dermatology." Recent recipients of the David Martin Carter Mentor Award include Dr. Jouni Uitto (2013) of Jefferson Medical College, Dr. Gerald Lazarus (2014) of Johns Hopkins School of Medicine, and Dr. Howard Baden of Harvard Medical School and Massachusetts General Hospital (2015), and Dr. Barbara A. Gilchrest of Harvard Medical School and Massachusetts General Hospital (2016). The Research Achievement Awards were instituted in 1989 to identify established scientists in investigative dermatology and cutaneous biology. This year they recognize those who have greatly advanced work related to autoimmune and inflammatory skin diseases, melanoma and non-melanoma skin cancer, vitiligo, and pigment cell disorders. "This year's Research Achievement Award winners are truly an exceptional group, all of whom have made great strides in their respective fields," said Dr. David Norris. "ASA is proud to celebrate their outstanding achievements." Research Achievement Award in Vitiligo & Pigment Cell Biology Zalfa Abdel-Malek, PhD of University of Cincinnati Cancer Institute Research Achievement Award in Melanoma & Skin Cancer Ruth Halaban, PhD of Yale School of Medicine Research Achievement Award in Psoriasis James G. Krueger, MD, PhD of The Rockefeller University Research Achievement Award in Autoimmune & Inflammatory Skin Disorders Robert E. Tigelaar, MD of Yale School of Medicine "On behalf of the Board of Directors of American Skin Association, I would like to commend all of this year's award recipients," said Howard P. Milstein, Chairman of ASA. "Their work in the field of investigative dermatology is vital to the search for a cure for melanoma, skin cancer and other skin diseases. We are pleased to support these outstanding researchers." ABOUT AMERICAN SKIN ASSOCIATION A unique collaboration of patients, families, advocates, physicians and scientists, ASA has evolved over thirty years as a leading force in efforts to defeat melanoma, skin cancer, and other skin diseases. Established to serve the now more than 100 million Americans – one third of the U.S. population – afflicted with skin disorders, the organization's mission remains to: advance research, champion skin health - particularly among children, and drive public awareness about skin disease. For more information, visit americanskin.org. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/american-skin-association-asa-honors-outstanding-researchers-during-annual-meeting-of-the-society-for-investigative-dermatology-300447174.html


News Article | May 4, 2017
Site: www.prnewswire.com

Excel's 7th Annual Users' Conference, 2017, has expanded to three days with two connected tracks – a research track and a new clinical track. It brings together leading users, healthcare visionaries, physicians, clinicians, medical researchers, data scientists and technology partners from around the world who are focused on complex physiological data analytics, clinical workflows and medical device data. The event will include more than 20 user presentations, demos, panel discussions and breakout sessions that will expose participants to a comprehensive wave of current and future projects, trends, best practices, thought leadership, innovations and visions for ongoing development and collaboration. The Users' meeting will feature presentations by healthcare industry leaders from: This year's event is designed to stimulate discussion and continued development and application of high-value technologies for clinicians and researchers, and ramp up dialogue and collaboration between clinicians, academics and researchers using Excel's technologies. "We're excited to gather again with our rapidly expanded community of customers, partners, collaborators and innovators for three days of insights, knowledge exchange, planning and innovation at the front edge of translational medicine," said John Hoffman, co-founder, president and principal engineer at Excel Medical. "Our annual conference is the best place to be and we're delighted and grateful for everyone's upcoming participation." Academic institutions and hospital enterprises participating in the 2017 conference include Emory University Healthcare System, University of Maryland School of Medicine & R. Adams Cowley Shock Trauma Center, Milwaukee VA Medical Center and Massachusetts General Hospital. The 2017 conference will also provide attendees with a preview of Excel's soon-to-be-released next-generation clinical decision support software platform. Excel Medical is an industry innovator in medical device data acquisition, storage, and clinical integration across the hospital enterprise. Its products transform clinical workflow by liberating data and making it more accessible to clinicians through untethered access and Next-Generation Medical Device Integration™ with electronic medical records (EMR). Excel's technologies have direct impact on improving patient safety and care, workflow efficiency, and decreasing institutional risk. Partnering with IBM's TJ Watson Laboratory since 2011, Excel has developed a first-of-a-kind clinical streaming analytics platform that is shaping the future of critical care medicine. Excel's products are used by more than 80% of the top medical centers and children's hospitals in the United States. The company is headquartered in Jupiter, Florida, and has customers throughout North America, Europe, Australia, and Asia. More information at: www.excel-medical.com. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/excel-medical-announces-7th-annual-users-conference-2017-300451586.html


CAMBRIDGE, Mass.--(BUSINESS WIRE)--InVivo Therapeutics Holdings Corp. (NVIV) today provided a clinical update, an update on patients in the INSPIRE study of the Neuro-Spinal Scaffold™, and reported financial results for the quarter ended March 31, 2017. Mark Perrin, InVivo’s Chief Executive Officer and Chairman, said, “In the first quarter, we continued to make significant progress at InVivo and with the INSPIRE study. By early April, we had enrolled four new patients into the INSPIRE study, with three patients enrolled within 30 days of each other. We also announced four new clinical sites for the INSPIRE study. In addition to progress with INSPIRE enrollment and sites, we achieved several regulatory milestones. Health Canada approved the company’s Investigational Testing Authorization application to commence a clinical study of the Neuro-Spinal Scaffold in patients with acute, complete (AIS A) cervical (C5-T1) spinal cord injuries (SCIs), and we announced the opening of our first site for the cervical study, Toronto Western Hospital. We also announced the Medicines Healthcare Products Regulatory Agency (MHRA) approval of the company’s Clinical Trial Authorization Application to commence the INSPIRE study in the United Kingdom. Finally, we submitted the first module of our Humanitarian Device Exemption (HDE) application to the FDA. Looking forward, we anticipate completing enrollment in the INSPIRE study in the third quarter and filing an HDE application for marketing approval of the Neuro-Spinal Scaffold in early 2018.” There are currently 14 INSPIRE patients in follow-up, and eight have reached the six-month primary endpoint. Of these eight patients, five had an AIS grade improvement (compared to baseline) and three did not have an AIS grade improvement at 6 months post-injury (a 62.5% conversion rate at 6 months). The INSPIRE AIS improvement rate remains considerably higher than rates observed in a range of SCI natural history databases. InVivo announced in January 2017 that a patient enrolled into INSPIRE in December 2016 had improved from a complete AIS A spinal cord injury to an incomplete AIS B spinal cord injury at the one-month evaluation. At a recent follow-up visit (the first since January), the patient was assessed to have reverted back to a complete AIS A spinal cord injury. Separately, in March 2017 InVivo announced that a patient enrolled in January 2017 had improved from a complete AIS A spinal cord injury to an incomplete AIS B spinal cord injury at the two-month evaluation. At the recent three-month follow-up evaluation, the patient was assessed to have reverted back to a complete AIS A spinal cord injury. There are previously published examples of patients with baseline AIS A spinal cord injury that are assessed to have an AIS grade improvement followed by a return to complete AIS A status within the first year after injury. In a 2009 article, 12.5% (2/16) of baseline AIS A spinal cord injury patients (cervical and thoracic) who experienced an AIS grade improvement were later assessed to return to complete AIS A status within the first year after injury. Of those two patients, one patient improved back to an incomplete AIS grade within the same year.* “The AIS grade improvement rate observed thus far in the INSPIRE study compares favorably to the natural history of spinal cord injury,” CEO and Chairman Mark Perrin said. “We look forward to monitoring these patients’ progress as they reach the primary endpoint at six months post-injury and as we work towards completing enrollment of INSPIRE.” For the three-month period ended March 31, 2017, the Company reported a net loss of approximately $6.4 million, or $0.20 per diluted share, compared to a net loss of $6.6 million, or $0.24 per diluted share, for the three-month period ended March 31, 2016. The results for the three-month period ended March 31, 2017 were unfavorably impacted by increases in operating expenses of $816,000 in research and development and $286,000 in general and administrative, partially offset by a non-cash gain on the derivative warrant liability of $241,000 reflecting changes in the fair market value of the derivative warrant liability. The results for the three-month period ended March 31, 2016 were unfavorably impacted by a non-cash loss on the derivative warrant liability of $1.0 million. Excluding the impact of the derivative warrant liability, adjusted net loss for the three-month period ended March 31, 2017 was $6.6 million, or $0.21 per diluted share, compared to adjusted net loss of $5.6 million, or $0.20 per diluted share, for the three-month period ended March 31, 2016. The Company ended the quarter with $26.8 million of cash, cash equivalents, and marketable securities. Adjusted net loss and adjusted net loss per share are non-GAAP financial measures that exclude the impact of the derivative warrant liability. A reconciliation of these measures to the comparable GAAP measure is included with the tables contained in this release. The Company believes a presentation of these non-GAAP measures provides useful information to investors to better understand the Company's operations, on a period-to-period comparable basis, with financial amounts both including and excluding the identified items. * Spiess et al. Conversion in ASIA Impairment Scale during the First Year after Traumatic Spinal Cord Injury. Journal of Neurotrauma 26: 2027-2036 (November 2009). The INSPIRE Study: InVivo Study of Probable Benefit of the Neuro-Spinal Scaffold™ for Safety and Neurologic Recovery in Subjects with Complete Thoracic AIS A Spinal Cord Injury, is designed to demonstrate the safety and probable benefit of the Neuro-Spinal Scaffold™ for the treatment of complete T2-T12/L1 spinal cord injury in support of a Humanitarian Device Exemption (HDE) application for approval. The FDA has recommended that InVivo include a control arm in the study as part of a Study Design Consideration. We are in discussions with the FDA on this recommendation, and we continue to believe that our current study design is sufficient to demonstrate safety and probable benefit in support of an HDE application for marketing approval. For more information, refer to https://clinicaltrials.gov/ct2/show/study/NCT02138110. Following acute spinal cord injury, surgical implantation of the biodegradable Neuro-Spinal Scaffold within the decompressed and debrided injury epicenter is intended to support appositional healing, thereby reducing post-traumatic cavity formation, sparing white matter, and allowing neural regeneration across the healed wound epicenter. The Neuro-Spinal Scaffold, an investigational device, has received a Humanitarian Use Device (HUD) designation and currently is being evaluated in The INSPIRE Study for the treatment of patients with acute, complete (AIS A), thoracic traumatic spinal cord injury and a pilot study for acute, complete (AIS A), cervical (C5-T1) traumatic spinal cord injury. For more information on the cervical study, refer to https://clinicaltrials.gov/ct2/show/study/NCT03105882. InVivo Therapeutics Holdings Corp. is a research and clinical-stage biomaterials and biotechnology company with a focus on treatment of spinal cord injuries. The company was founded in 2005 with proprietary technology co-invented by Robert Langer, Sc.D., Professor at Massachusetts Institute of Technology, and Joseph P. Vacanti, M.D., who then was at Boston Children’s Hospital and who now is affiliated with Massachusetts General Hospital. In 2011, the company earned the David S. Apple Award from the American Spinal Injury Association for its outstanding contribution to spinal cord injury medicine. In 2015, the company’s investigational Neuro-Spinal Scaffold received the 2015 Becker’s Healthcare Spine Device Award. The publicly-traded company is headquartered in Cambridge, MA. For more details, visit www.invivotherapeutics.com. Any statements contained in this press release that do not describe historical facts may constitute forward-looking statements within the meaning of the federal securities laws. These statements can be identified by words such as "believe," "anticipate," "intend," "estimate," "will," "may," "should," "expect," “designed to,” “potentially,” and similar expressions, and include statements regarding the safety and effectiveness of the Neuro-Spinal Scaffold and the progress of the clinical program. Any forward-looking statements contained herein are based on current expectations, and are subject to a number of risks and uncertainties. Factors that could cause actual future results to differ materially from current expectations include, but are not limited to, risks and uncertainties relating to the company’s ability to successfully open additional clinical sites for enrollment and to enroll additional patients; the timing of the Institutional Review Board process; the company's ability to complete The INSPIRE Study, submit an HDE application, and receive regulatory approval for the Neuro-Spinal Scaffold, the company’s ability to commercialize its products; the company’s ability to develop, market and sell products based on its technology; the expected benefits and efficacy of the company’s products and technology in connection with the treatment of spinal cord injuries; the availability of substantial additional funding for the company to continue its operations and to conduct research and development, clinical studies and future product commercialization; and other risks associated with the company’s business, research, product development, regulatory approval, marketing and distribution plans and strategies identified and described in more detail in the company’s Quarterly Report of the three months ended March 31, 2017, and its other filings with the SEC, including the company’s Form 10-Qs and current reports on Form 8-K. The company does not undertake to update these forward-looking statements.


JUNO BEACH, Fla. & CAMBRIDGE, Mass.--(BUSINESS WIRE)--Document Storage Systems, Inc. and LiveData, Inc. today announced their participation in the 2017 Annual Meeting of the Association of VA Surgeons (AVAS), May 7-9 in Houston. The companies will exhibit their VistA-integrated perioperative workflow solution. WHO: Document Storage Systems, Inc. (DSS) and LiveData, Inc. (LiveData) DETAILS: DSS and LiveData will demonstrate LiveData PeriOp Manager™, an automated perioperative workflow solution including two new modules: LiveData PeriOp Planner™ and LiveData PeriOp Manager Analytics™. DSS and LiveData have partnered to deliver and install a perioperative workflow solution for users of VistA, the Veterans Health Information Systems and Technology Architecture electronic health record system. LiveData PeriOp Manager synchronizes patient workflow from initial referral through surgery to create an optimal care environment for patients and staff alike. Coordinating patient flow, patient care, and related resources from preoperative assessment to discharge, all in real-time, PeriOp Manager streamlines OR throughput, promotes full compliance with CMS and The Joint Commission critical patient safety mandates along with VA initiatives to improve access to care. The annual meeting of the Association of Veterans Affairs Surgeons (AVAS) is attended by general, specialist, and critical care surgeons, and anesthesia providers from VA hospitals throughout the United States. Many university-based surgeons, surgery residents, and medical students from programs with VA affiliations typically attend this meeting. Additional information on the association and the meeting can be found at http://www.vasurgeons.org/2017-meeting.html NOTE TO EDITORS: To book appointments with executives or technical representatives of DSS contact Andrea Sucre, 561-284-7023 (asucre@dssinc.com) or LiveData contact Diane Poth, 781-775-1759 (dpoth@livedata.com). About Document Storage Systems DSS, Inc. is a leading software and services company that creates and delivers advanced health information technology (HIT) solutions. For 25 years, healthcare organizations have benefited from our technical and service integration expertise. DSS has extensive experience working with federal, private, and public healthcare facilities to modernize their legacy systems and to improve efficiencies for clinical and administrative users through breakthrough technology. For more information about DSS, visit http://www.dssinc.com. About LiveData LiveData, Inc. is a leading innovator in real-time operational intelligence solutions that enable caregivers to plan, visualize, and analyze the patient’s surgical journey. Leading medical institutions, including Massachusetts General Hospital, Memorial Sloan-Kettering Cancer Center, and Veterans Health Administration facilities have selected LiveData solutions to improve patient safety, team communication, and perioperative efficiency. LiveData is headquartered in Cambridge, Massachusetts. For more information, visit http://www.livedata.com. LiveData is a registered trademark of LiveData, Inc. LiveData PeriOp Manager, PeriOp Planner, and PeriOp Manager Analytics are trademarks of LiveData, Inc. All other marks are the property of their respective owners and are used for identification purposes only.


Despite successful treatment, people receiving antiretroviral drugs continue to have small amounts of human immunodeficiency virus (HIV) in their blood, as well as elevated immune system activation. However, new research published in PLOS Pathogens shows no correlation between these two measurements. Previous research has revealed links between elevated immune system activation and medical complications such as heart disease. Knowing why patients on antiretroviral drugs have elevated immune activation could help address or prevent such complications. However, the mechanism behind this elevated activation is unclear and actively debated. To gain new insight, Rajesh Gandhi of Massachusetts General Hospital, Boston, and colleagues in the AIDS Clinical Trials Group (ACTG) tested whether elevated immune activation drives or is driven by the low levels of HIV still found in patients undergoing treatment. Using blood samples from people who took part in ACTG clinical trials, they measured molecular markers of HIV, immune system activation, and inflammation in 101 people before and during treatment with antiretroviral drugs for a median of 7 years. During treatment, the participants had undetectable levels of virus in the blood on standard commercial tests but HIV could still be detected using sensitive research techniques. Before treatment, the researchers found a correlation between HIV levels, immune activation, and inflammation in the patients. However, this correlation did not persist during treatment. This result suggests that elevated immune activation during treatment does not drive and is not driven by HIV in the blood. Instead, people with higher HIV levels before treatment tended to have higher HIV levels during treatment (even though the total virus amount was significantly reduced). Similarly, patients with higher pre-treatment levels of inflammation and immune system activation tended to show signs of higher activation during treatment, even though the antiretroviral drugs successfully controlled the virus. "We need to understand why events that happen before treatment is started continue to impact activation many years afterwards, despite the fact that the medicines are holding the virus in check. We also need to diagnose and treat HIV earlier to prevent immune damage that may lead to heightened activation." Based on these findings, the authors suggest a need for strategies to reverse the effects of immune events that cause elevated activation before treatment. They call for investigation of viral and human genetic factors that may affect this activation. Finally, they suggest that "interventions aimed at curing HIV may differ from those needed to decrease activation". In your coverage please use this URL to provide access to the freely available article in PLOS Pathogens: http://journals. Citation: Gandhi RT, McMahon DK, Bosch RJ, Lalama CM, Cyktor JC, Macatangay BJ, et al. (2017) Levels of HIV-1 persistence on antiretroviral therapy are not associated with markers of inflammation or activation. PLoS Pathog 13(4): e1006285. doi:10.1371/journal.ppat.1006285 Funding: Research reported in this publication was supported by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health under Award Number UM1 AI068634, UM1 AI068636 and UM1 AI106701. Additional funding provided by NIH grants AI069481 and AI27757. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Competing Interests: The authors have declared that no competing interests exist.


News Article | April 19, 2017
Site: www.prnewswire.com

The NCCN Radiation Therapy Compendium™ provides guidance on all RT modalities recommended within the NCCN Guidelines, including Intensity Modulated Radiation Therapy (IMRT), Intra-Operative Radiation Therapy (IORT), Stereotactic Radiosurgery (SRS)/Stereotactic Body Radiotherapy (SBRT)/Stereotactic Ablative Radiotherapy (SABR), Image-guided Radiotherapy (IGRT), Low dose-rate brachytherapy (LDR)/High dose-rate brachytherapy (HDR), Radioisotope, and Particle Therapy. Transparency of NCCN Guidelines and Compendia development is central to the philosophy, policies, and procedures of NCCN. NCCN posts the policies and processes for developing and maintaining the NCCN Guidelines. These policies are available to the public on the NCCN website. Identification of newly published research, NCCN Member Institution review, external stakeholder submissions, and panel review occur on an ongoing basis with at least annual review performed for NCCN Guidelines for each disease. The NCCN Guidelines are the recognized standard for clinical policy in cancer care and are the most thorough and most frequently updated clinical practice guidelines available in any area of medicine. Other NCCN Guidelines derivative products include: For more information and to access the NCCN Radiation Therapy Compendium™, visit NCCN.org/RTCompendium. The National Comprehensive Cancer Network® (NCCN®), a not-for-profit alliance of 27 of the world's leading cancer centers devoted to patient care, research, and education, is dedicated to improving the quality, effectiveness, and efficiency of cancer care so that patients can live better lives. Through the leadership and expertise of clinical professionals at NCCN Member Institutions, NCCN develops resources that present valuable information to the numerous stakeholders in the health care delivery system. As the arbiter of high-quality cancer care, NCCN promotes the importance of continuous quality improvement and recognizes the significance of creating clinical practice guidelines appropriate for use by patients, clinicians, and other health care decision-makers. The NCCN Member Institutions are: Fred & Pamela Buffett Cancer Center, Omaha, NE; Case Comprehensive Cancer Center/University Hospitals Seidman Cancer Center and Cleveland Clinic Taussig Cancer Institute, Cleveland, OH; City of Hope Comprehensive Cancer Center, Los Angeles, CA; Dana-Farber/Brigham and Women's Cancer Center | Massachusetts General Hospital Cancer Center, Boston, MA; Duke Cancer Institute, Durham, NC; Fox Chase Cancer Center, Philadelphia, PA; Huntsman Cancer Institute at the University of Utah, Salt Lake City, UT; Fred Hutchinson Cancer Research Center/Seattle Cancer Care Alliance, Seattle, WA; The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD; Robert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, IL; Mayo Clinic Cancer Center, Phoenix/Scottsdale, AZ, Jacksonville, FL, and Rochester, MN; Memorial Sloan Kettering Cancer Center, New York, NY; Moffitt Cancer Center, Tampa, FL; The Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove Research Institute, Columbus, OH; Roswell Park Cancer Institute, Buffalo, NY; Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine, St. Louis, MO; St. Jude Children's Research Hospital/The University of Tennessee Health Science Center, Memphis, TN; Stanford Cancer Institute, Stanford, CA; University of Alabama at Birmingham Comprehensive Cancer Center, Birmingham, AL; UC San Diego Moores Cancer Center, La Jolla, CA; UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA; University of Colorado Cancer Center, Aurora, CO; University of Michigan Comprehensive Cancer Center, Ann Arbor, MI; The University of Texas MD Anderson Cancer Center, Houston, TX; University of Wisconsin Carbone Cancer Center, Madison, WI; Vanderbilt-Ingram Cancer Center, Nashville, TN; and Yale Cancer Center/Smilow Cancer Hospital, New Haven, CT. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/nine-new-disease-sites-added-to-the-nccn-radiation-therapy-compendium-300441832.html


The survey was conducted during the period of congressional debate over the American Health Care Act (AHCA), which was withdrawn the afternoon of March 24 when it became clear there were not enough votes to pass the legislation. Responding to the survey were 76 oncology professionals, including physicians, academic and community; nurses; physician assistants; pharmacists; industry professionals; payers and patient advocates. "The American Health Care Act is tabled and the ACA remains in place, but concerns about access to cancer screening, care, and research funding remain. Today, patients are in limbo, not knowing what action the federal and state governments will take," said Robert W. Carlson, MD, Chief Executive Officer of NCCN. "NCCN agrees there are ways to improve the current health care system for Americans with cancer, the clinical professionals who care for them, and payers. However, we are concerned for Americans with cancer that affordability, coverage of products and services in cancer treatment, and overall access will be impeded by allowing health insurers to set their own rates, or by providing states the ability to experiment with Medicaid coverage, without appropriate patient protections." "President Trump included three key elements in his approach to health coverage reform: repairing necessary aspects of the ACA, ensuring greater access, and lowering the total cost of care," Dr. Carlson said. "We are ready to share our Network's expertise with lawmakers to deliver a value-based health policy to ensure that all Americans with cancer have access to high-quality, effective, and efficient cancer care." Below is a link to Dr. Carlson's March 21, 2017 letter to Congress outlining NCCN's concerns about the health policy proposal and patient access to care: https://www.nccn.org/professionals/meetings/oncology_policy_program/pdf/2017_NCCN_AHCA_Letter_Walden_03-22-2017.pdf For more information about NCCN's health care policy initiatives, visit NCCN.org/policy. The National Comprehensive Cancer Network® (NCCN®), a not-for-profit alliance of 27 of the world's leading cancer centers devoted to patient care, research, and education, is dedicated to improving the quality, effectiveness, and efficiency of cancer care so that patients can live better lives. Through the leadership and expertise of clinical professionals at NCCN Member Institutions, NCCN develops resources that present valuable information to the numerous stakeholders in the health care delivery system. As the arbiter of high-quality cancer care, NCCN promotes the importance of continuous quality improvement and recognizes the significance of creating clinical practice guidelines appropriate for use by patients, clinicians, and other health care decision-makers. The NCCN Member Institutions are: Fred & Pamela Buffett Cancer Center, Omaha, NE; Case Comprehensive Cancer Center/University Hospitals Seidman Cancer Center and Cleveland Clinic Taussig Cancer Institute, Cleveland, OH; City of Hope Comprehensive Cancer Center, Los Angeles, CA; Dana-Farber/Brigham and Women's Cancer Center | Massachusetts General Hospital Cancer Center, Boston, MA; Duke Cancer Institute, Durham, NC; Fox Chase Cancer Center, Philadelphia, PA; Huntsman Cancer Institute at the University of Utah, Salt Lake City, UT; Fred Hutchinson Cancer Research Center/Seattle Cancer Care Alliance, Seattle, WA; The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD; Robert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, IL; Mayo Clinic Cancer Center, Phoenix/Scottsdale, AZ, Jacksonville, FL, and Rochester, MN; Memorial Sloan Kettering Cancer Center, New York, NY; Moffitt Cancer Center, Tampa, FL; The Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove Research Institute, Columbus, OH; Roswell Park Cancer Institute, Buffalo, NY; Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine, St. Louis, MO; St. Jude Children's Research Hospital/The University of Tennessee Health Science Center, Memphis, TN; Stanford Cancer Institute, Stanford, CA; University of Alabama at Birmingham Comprehensive Cancer Center, Birmingham, AL; UC San Diego Moores Cancer Center, La Jolla, CA; UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA; University of Colorado Cancer Center, Aurora, CO; University of Michigan Comprehensive Cancer Center, Ann Arbor, MI; The University of Texas MD Anderson Cancer Center, Houston, TX; University of Wisconsin Carbone Cancer Center, Madison, WI; Vanderbilt-Ingram Cancer Center, Nashville, TN; and Yale Cancer Center/Smilow Cancer Hospital, New Haven, CT. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/nccn-survey-reveals-oncologys-concerns-about-financial-distress-patient-access-to-care-300441795.html


News Article | May 4, 2017
Site: globenewswire.com

MENLO PARK, Calif., May 04, 2017 (GLOBE NEWSWIRE) -- GRAIL, Inc., a life sciences company whose mission is to detect cancer early when it can be cured, today announced the appointment of José Baselga, M.D., Ph.D., Brook Byers and Kaye Foster to its Board of Directors. The three new board members will join GRAIL’s existing board of directors: Bill Rastetter, Jeff Huber, Richard Klausner and Robert Nelsen. “I am very pleased to welcome José, Brook and Kaye, three extremely seasoned and accomplished executives, to our Board at this pivotal time for GRAIL,” said Jeff Huber, GRAIL’s Chief Executive Officer. “With these leaders, we are increasing the breadth of strategic leadership, industry experience and operational excellence within our Board. As we work to expand our operations and build integrated programs in science, technology and clinical development, their expertise and counsel will be invaluable. We are looking forward to working with them in our pursuit to transform the way cancer is diagnosed and treated.” José Baselga is the Physician-in-Chief and Chief Medical Officer at Memorial Sloan Kettering Cancer Center (MSK) and Professor of Medicine at Weill Cornell Medical College. Prior to MSK, Dr. Baselga was the Chief of the Division of Hematology/Oncology, Associate Director of the Massachusetts General Hospital Cancer Center and Professor of Medicine at Harvard Medical School. He also was the Chairman of Medical Oncology and Founding Director of the Vall d’Hebron Institute of Oncology in Barcelona, Spain. Dr. Baselga is a past President of the American Association of Cancer Research (AACR) and of the European Society for Medical Oncology, and a past member of the Board of Directors for the American Society of Clinical Oncology (ASCO) and AACR. He is an elected member of the National Academy of Medicine, the American Society of Clinical Investigation, the Association of American Physicians, and a Fellow of the AACR Academy. He is a past member of the Editorial Boards of Cancer Cell, Journal of Clinical Oncology, and Clinical Cancer Research and is the founding editor-in-chief for the AACR flagship journal Cancer Discovery. In addition to joining GRAIL’s Board of Directors, Dr. Baselga is also the Chairman of GRAIL’s Scientific Advisory Board. Dr. Baselga earned his M.D. from Universitat Autonoma de Barcelona and completed residencies in internal medicine at Vall d'Hebron University Hospital and SUNY - Health Sciences Center at Brooklyn. Brook Byers is a senior partner and founding member of the venture capital firm Kleiner Perkins Caufield & Byers (KPCB). Mr. Byers formed the first life sciences practice group in the venture capital profession and led KPCB to become a premier venture capital firm in the medical, healthcare, and biotechnology sectors. Brook has been a pioneer in the fields of precision medicine, molecular diagnostics and genomics, serving as a Steering Committee member for the Coalition of 21st Century Medicine, and through investment and board leadership in companies such as Foundation Medicine, Genomic Health and Veracyte. Brook currently serves on the Board of Directors of Cell Design Labs, Enjoy, Newsela, and Zephyr Health. He also serves on the Board of Overseers of the University of California San Francisco medical campus and hospitals, the Stanford Medicine Advisory Council and the Board of Directors of the New Schools Foundation. Mr. Byers holds a bachelor’s degree in Electrical Engineering from Georgia Institute of Technology and an MBA from Stanford University. He is also the recipient of an honorary Ph.D. from Georgia Institute of Technology. Kaye Foster has over 25 years of experience in the pharmaceutical industry leading large, global human resources organizations. She currently advises CEOs and leadership teams focusing on business transformations, talent management strategy and Human Resources strategy development and implementation. Most recently, she was Senior Vice President, Global Human Resources for Onyx Pharmaceuticals where she led all aspects of human resources for U.S. and global operations. Ms. Foster joined Onyx from Johnson & Johnson where she served as an Executive Committee member and Chief Human Resources Officer, leading a worldwide team of over 3,000 human resources professionals. She also held several Human Resources executive positions with Pfizer Inc., supporting its pharmaceutical businesses in Japan, Asia, Africa, Middle East and Latin America, and she led the integration of both the Warner-Lambert and Pharmacia mergers for these regions. She is a Senior Advisor with The Boston Consulting Group (BCG) and sits on the Board of Directors of Agios Pharmaceuticals as well as the Board of Trustees of Spelman College, Stanford Healthcare, ValleyCare Health System and Glide Memorial Church in San Francisco. Kaye holds a bachelor’s degree from Baruch College and an MBA from Columbia Business School. About GRAIL GRAIL is a life sciences company whose mission is to detect cancer early when it can be cured. GRAIL is using the power of high-intensity sequencing, population-scale clinical trials, and state of the art Computer Science and Data Science to enhance the scientific understanding of cancer biology and develop blood tests for early-stage cancer detection. The company’s funding was led by ARCH Venture Partners and includes Amazon, Bezos Expeditions, Bill Gates, Bristol-Myers Squibb, Celgene, GV, Illumina, Johnson & Johnson Innovation, Merck, McKesson Ventures, Sutter Hill Ventures, Tencent, Varian Medical Systems, and other financial partners. For more information, please visit www.grail.com.


News Article | May 4, 2017
Site: www.futurity.org

Researchers identified one damaged, or mutant, “high confidence” risk gene for Tourette syndrome as well as three others they believe are genes whose mutation is a probable risk for the disorder. These findings, published in Neuron, are important because the genetics of Tourette syndrome has been a mystery. The goal of the continuing study is to identify inherited factors that play a role in causing Tourette’s and other related disorders, such as obsessive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD). “This research is the first of its kind establishing Tourette disorder as a genetic disease similar to other neuropsychiatric disorders like autism, where not just one gene has been identified as the cause,” says Jay Tischfield, a professor of genetics at Rutgers University and a senior author of the study. “We are confident that this new information will lead us to the genetic and brain pathways that cause this disorder and enable the development of more effective treatments.” The Tourette International Collaborative Genetics (TIC Genetics) study is the largest and most comprehensive genomic analysis conducted. The research began a decade ago when Rutgers started collaborating with New Jersey Center for Tourette Syndrome and Associated Disorders, Inc. to establish the NJCTS Cell and DNA Repository. The study included 311 families involved with TIC Genetics in which the child had Tourette syndrome but neither parent did. Another study was done through the Tourette Association of America International Consortium for Genetics with 173 similar families and found the same results. The one damaged gene that was identified as having a high risk for Tourette syndrome, called WWC1, is involved in brain development and memory. Two of the other damaged genes considered to be probable risks for the disorder are involved in brain circuitry and the third is involved in gene expression which allows a cell to respond to its changing environment. “The fact of finding this one gene in two families would be like lightning striking the same individual twice,” says Gary Heiman, associate professor in the genetics department in the School of Arts and Sciences and a senior author on the project. “And it is the reason why it is crucial for us to continue studying families affected by this often debilitating disorder.” In conducting the study, blood samples were collected from family members to identify rare genetic mutations that are not inherited from their parents but occur spontaneously in affected individuals at birth. While many inherited diseases, such as sickle cell anemia, hemophilia, and cystic fibrosis, are caused by mutations to a single gene, this new research indicates that Tourette syndrome, like other neuropsychiatric disorders, is the result of multiple gene mutations. Rutgers researchers and their colleagues estimate that there are approximately 400 mutated genes that could pose a risk for Tourette syndrome, which affects one out of 100 people. The neuropsychiatric disorder—linked to problems in the basal ganglia, the part of the brain responsible for voluntary motor control, procedural learning, and eye movement, as well as cognitive and emotional function—is characterized by grimacing, eye blinking, and shoulder shrugging. It is often accompanied by co-occurring conditions, such as depression, obsessive-compulsive disorder, or attention deficit disorder. Faith Rice, director of NJCTS, and mother of an adult son with the disorder, says those involved in this study are grateful to have been a part of the research. “It is very empowering for families to be involved in something that will make a difference,” says Rice. “Many are calling me and telling me that for the first time, this is giving them hope.” The scientists say more samples from families, in which only one child is affected with Tourette’s and both parents are available to participate, are needed to better understand how these and other damaging mutations lead to Tourette disorder. “I want to thank all the individuals with Tourette disorder and their family members from New Jersey, around the country, in Europe and South Korea for their participation and advocacy,” says Heiman. “Progress has been slow and disappointing up until now. But I think this research will lead to the development of more specific treatments that are personalized for individuals or groups of people.” Grants from the National Institute of Mental Health and New Jersey Center for Tourette Syndrome and Associated Disorders, Inc. funded the research. Researchers from Rutgers University-New Brunswick; University of California, San Francisco; Massachusetts General Hospital; the University of Florida; Yale University; and other institutions across the world participated in the study.


News Article | April 21, 2017
Site: www.prnewswire.com

The Global Translational Regenerative Medicine market is expected to grow significantly over the forecast period. The Global Translational Regenerative Medicine market was valued at $5.8bn in 2016. Visiongain forecasts this market to increase to $14.5bn in 2021. The market is estimated to grow at a CAGR of 19.9% in the first half of the forecast period and 17.7% from 2016 to 2027. How this report will benefit you Read on to discover how you can exploit the future business opportunities emerging in this sector. In this brand new report you find 316-page report you will receive 107 tables and 66 figures - all unavailable elsewhere. The 316-page report provides clear detailed insight into the Global Translational Regenerative Medicine market. Discover the key drivers and challenges affecting the market. By ordering and reading our brand new report today you stay better informed and ready to act. • Forecasts from 2017-2027 of the leading products in the Global Translational Regenerative Medicine market: - Osteocel Plus - Trinity ELITE - TEMCELL /Prochymal - Apligraf - Dermagraft - Epifix - ReCell - Neovasculgen - Glybera (alipogene tiparvovec) - IMLYGIC (talimogene laherparepvec) • SWOT and Porter's Five Force analysis of the translational regenerative medicine market Visiongain's study is intended for anyone requiring commercial analyses for the Translational Regenerative Medicine Market and leading companies. You find data, trends and predictions. To request a report overview of this report please email Sara Peerun at sara.peerun@visiongain.com or call Tel: +44-(0)-20-7336-6100 List of Organisations Mentioned in the Report Arthritis Research UK Associazione Infermieristica per lo Studio delle Lesioni Cutanee (AISLeC) [China] Australian Regenerative Medicine Institute Australian Sports Anti-Doping Authority (ASADA) Biomedical Advanced Research and Development Authority (BARDA) British Heart Foundation [UK] California Institute of Regenerative Medicine (CIRM) Cambridge Stem Cell Biology Institute [UK] Case Western Reserve University Catalan Institution for Research and Advanced Studies Center for Biologics Evaluation and Research (CBER) [US] CHA General Hospital [Korea] Cryocenter Saint Petersburg Drugs Controller General of India (DCGI) European Group for Blood and Marrow Transplantation (EBMT) European Medicines Agency Food and Drugs Agency (FDA) [US] Haute Autorité de santé [France] Heriot-Watt University Human Fertilisation and Embryology Authority (HFEA) Institute of Biomedical Research and Innovation Hospital [Japan] International Society for Stem Cell Research (ISSCR) Karolinska Institute [Sweden] Massachusetts General Hospital (MGH) Mayo Clinic [US] Medical Research Council [UK] MiMedx Ministry of Food and Drug Safety, MFDS) [Korea] Ministry of Health, Labour and Welfare (MHLW) [Japan] Ministry of Science and Technology [China] Moorfields Eye Hospital National Tissue Engineering Center (NTEC) [China] New York Blood Center Riken Center for Developmental Biology RUSH University Medical Center [US] Russian Ministry of Healthcare and Social Development Scottish Centre for Regenerative Medicine St. Jude's Children Research Hospital State Food and Drug Administration (SFDA) [China] SUNY Upstate Medical University The Genetico Center [Russia] The StemGen Organisation Therapeutics Goods Administration (TGA) [Australia] UH San Diego Sanford Stem Cell Clinical Center UK Medicines and Healthcare Products Regulatory Agency (MHRA) Universitat Autònoma de Barcelona [Spain] University College London University of Edinburgh MRC Centre for Regenerative Medicine [UK] University of Massachusetts (UMass) Memorial Hospital University of Modena Centre for Regenerative Medicine [Italy] University of Wisconsin US National Institute of Health Wake Forest Institute Wellcome Trust World Health Organization To see a report overview please email Sara Peerun on sara.peerun@visiongain.com


News Article | April 21, 2017
Site: www.prnewswire.co.uk

The Global Translational Regenerative Medicine market is expected to grow significantly over the forecast period. The Global Translational Regenerative Medicine market was valued at $5.8bn in 2016. Visiongain forecasts this market to increase to $14.5bn in 2021. The market is estimated to grow at a CAGR of 19.9% in the first half of the forecast period and 17.7% from 2016 to 2027. How this report will benefit you Read on to discover how you can exploit the future business opportunities emerging in this sector. In this brand new report you find 316-page report you will receive 107 tables and 66 figures - all unavailable elsewhere. The 316-page report provides clear detailed insight into the Global Translational Regenerative Medicine market. Discover the key drivers and challenges affecting the market. By ordering and reading our brand new report today you stay better informed and ready to act. • Forecasts from 2017-2027 of the leading products in the Global Translational Regenerative Medicine market: - Osteocel Plus - Trinity ELITE - TEMCELL /Prochymal - Apligraf - Dermagraft - Epifix - ReCell - Neovasculgen - Glybera (alipogene tiparvovec) - IMLYGIC (talimogene laherparepvec) • SWOT and Porter's Five Force analysis of the translational regenerative medicine market Visiongain's study is intended for anyone requiring commercial analyses for the Translational Regenerative Medicine Market and leading companies. You find data, trends and predictions. To request a report overview of this report please email Sara Peerun at sara.peerun@visiongain.com or call Tel: +44-(0)-20-7336-6100 List of Organisations Mentioned in the Report Arthritis Research UK Associazione Infermieristica per lo Studio delle Lesioni Cutanee (AISLeC) [China] Australian Regenerative Medicine Institute Australian Sports Anti-Doping Authority (ASADA) Biomedical Advanced Research and Development Authority (BARDA) British Heart Foundation [UK] California Institute of Regenerative Medicine (CIRM) Cambridge Stem Cell Biology Institute [UK] Case Western Reserve University Catalan Institution for Research and Advanced Studies Center for Biologics Evaluation and Research (CBER) [US] CHA General Hospital [Korea] Cryocenter Saint Petersburg Drugs Controller General of India (DCGI) European Group for Blood and Marrow Transplantation (EBMT) European Medicines Agency Food and Drugs Agency (FDA) [US] Haute Autorité de santé [France] Heriot-Watt University Human Fertilisation and Embryology Authority (HFEA) Institute of Biomedical Research and Innovation Hospital [Japan] International Society for Stem Cell Research (ISSCR) Karolinska Institute [Sweden] Massachusetts General Hospital (MGH) Mayo Clinic [US] Medical Research Council [UK] MiMedx Ministry of Food and Drug Safety, MFDS) [Korea] Ministry of Health, Labour and Welfare (MHLW) [Japan] Ministry of Science and Technology [China] Moorfields Eye Hospital National Tissue Engineering Center (NTEC) [China] New York Blood Center Riken Center for Developmental Biology RUSH University Medical Center [US] Russian Ministry of Healthcare and Social Development Scottish Centre for Regenerative Medicine St. Jude's Children Research Hospital State Food and Drug Administration (SFDA) [China] SUNY Upstate Medical University The Genetico Center [Russia] The StemGen Organisation Therapeutics Goods Administration (TGA) [Australia] UH San Diego Sanford Stem Cell Clinical Center UK Medicines and Healthcare Products Regulatory Agency (MHRA) Universitat Autònoma de Barcelona [Spain] University College London University of Edinburgh MRC Centre for Regenerative Medicine [UK] University of Massachusetts (UMass) Memorial Hospital University of Modena Centre for Regenerative Medicine [Italy] University of Wisconsin US National Institute of Health Wake Forest Institute Wellcome Trust World Health Organization To see a report overview please email Sara Peerun on sara.peerun@visiongain.com


News Article | May 4, 2017
Site: www.prnewswire.com

Morgan Stanley, Piper Jaffray & Co. and Barclays Capital Inc. are acting as joint book-running managers for the proposed offering. William Blair & Company, L.L.C. is acting as lead manager.  Needham & Company, LLC is acting as co-manager. The offering will be made only by means of a prospectus.  When available, copies of the final prospectus related to the offering may be obtained from the offices of Morgan Stanley & Co. LLC, Attention: Prospectus Department, 180 Varick Street, 2nd Floor, New York, New York 10014; or from Piper Jaffray & Co., Attention: Prospectus Department, 800 Nicollet Mall, J12S03, Minneapolis, MN 55402, or by telephone at (800) 747-3924, or by email at prospectus@pjc.com; or from Barclays Capital Inc., c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, NY 11717, telephone: (888) 603-5847, e-mail: Barclaysprospectus@broadridge.com. A registration statement relating to these securities has been filed with, and declared effective by, the Securities and Exchange Commission (the "SEC"). Copies of the registration statement can be accessed through the SEC's website at www.sec.gov. This press release shall not constitute an offer to sell, or the solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction. Biohaven is a clinical-stage biopharmaceutical company with a portfolio of innovative, late-stage product candidates targeting neurological diseases, including rare disorders. Biohaven has licensed intellectual property from companies and institutions including Bristol-Myers Squibb Company, AstraZeneca AB, Yale University, Catalent, ALS Biopharma LLC and Massachusetts General Hospital.  Biohaven is a company organized under the laws of the British Virgin Islands and its United States operations are based in New Haven, Connecticut. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/biohaven-announces-pricing-of-initial-public-offering-of-common-shares-300451520.html

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