Pasadena, CA, United States
Pasadena, CA, United States

Time filter

Source Type

PASADENA, CA, November 09, 2016 /24-7PressRelease/ -- Huntington Medical Research Institutes (HMRI), an independent, leading biomedical research institute based in Pasadena, California, has announced the appointment of Allyson Simpson as Vice President of Philanthropy and Susie Silk Berry as Director of Philanthropy. Prior to joining HMRI, Allyson Simpson was the Senior Director of Gift Planning at California Institute of Technology (Caltech) in Pasadena for six years. Simpson also served as associate director of gift planning at Cedars-Sinai Medical Center in Los Angeles. Before she transitioned into development with a focus on planned, major and leadership giving, Simpson practiced corporate and regulatory law in Los Angeles for 25 years. She is a member of the Partnership for Philanthropic Planning - Los Angeles, where she has been appointed as President-Elect in 2016-2017 and will serve as President in 2017-2018. Simpson is currently Chair of the South Central Los Angeles Ministry Project Development Committee and is a member of the Mayfield Junior School Development Committee. Susie Berry will bring more than a decade of development experience to HMRI as the new Director of Philanthropy. Her new duties will include raising funds to further support the organization's biomedical research and development of new diagnostics and therapies. Prior to joining HMRI, Berry was the Director of Development at the YMCA in Los Angeles where she established goals, objectives and strategies to achieve annual revenue targets through major gifts, annual giving and foundation grants. Berry wrote grant proposals and managed the operations of the Chairman's Round Table annual funding driving sponsorships among other responsibilities. During her time with the YMCA, she successfully created the South Pasadena San Marino 5K/10K YRUN fundraiser through securing sponsors and exceeding the revenue goal by 20% through raising awareness of the Y's work in the community. "With their specialized skill sets and experience, both Simpson and Berry's work will make a tremendous impact in supporting our audacious scientific goals. They maintain strong ties in the philanthropic community and industry trade associations, and are well-respected in our community. They are true professionals who fit so well into the vision of HMRI," says Dr. Marie Csete, HMRI's President & Chief Scientist. "Simpson and Berry are exceptional, passionate individuals who will certainly make HMRI better known and better supported in our mission of changing lives through multidisciplinary, patient-focused research. I could not be happier with these new leaders of HMRI at this critical time in the organization's history with reinvigorated research programs and new labs under construction." About Huntington Medical Research Institutes Huntington Medical Research Institutes (HMRI) is a tax-exempt 501(c)(3) nonprofit, public-benefit organization based in Pasadena, California, dedicated to studying and enhancing knowledge of diseases in order to improve health and save lives. HMRI's mission is to change lives through multidisciplinary, patient-focused research. For six decades, it has been making biomedical discoveries and developments that have set new precedents in medical knowledge across the nation and around the world. HMRI is Pasadena's only independent, dedicated biomedical research organization with more than 47,000 square feet of research facilities focused on neurosciences (Alzheimer's, traumatic brain injury, migraine), cardiovascular, cell and tissue biology, advanced imaging, and liver, GI and GU research. For more information, visit:

Tong M.J.,Huntington Medical Research Institutes | Tong M.J.,University of California at Los Angeles | Trieu J.,Huntington Medical Research Institutes
Journal of Digestive Diseases | Year: 2013

Objective: Hepatitis B virus (HBV) inactive carriers are HBV e antigen (HBeAg)-negative patients with normal alanine aminotransferase (ALT) levels and HBV DNA of ≤ 10000 copies/mL. We aimed to determine the clinical impact of ALT and HBV DNA elevations during the course of HBV infection. Methods: From January 1989 to January 2012, 146 inactive carriers were prospectively followed every 6-12 months with ALT and HBV DNA measurements and with hepatocellular carcinoma (HCC) surveillance. Results: During the follow-up of 8±6.3 years, 56 of the 146 patients maintained ALT ≤ 40U/L and HBV DNA≤10000copies/mL. However, 39 had rises of ALT > 40-80U/L and 4 had ALT > 80U/L; all except one reverted to baseline values. Also, during follow up, 69 (47.3%) inactive carriers had increases in HBV DNA of > 10000-999999 copies/mL; 38 of these patients' HBV DNA returned to baseline levels, while the remaining 31 patients maintained elevated HBV DNA values but had corresponding ALT of ≤ 40U/L. There were four liver-related outcomes: 129 (88.4%) remained "inactive carriers", 13 (8.9%) had loss of hepatitis B surface antigen (HBsAg), one (0.7%) had a spontaneous reactivation to HBeAg-negative chronic hepatitis, and two (1.4%) developed HCC. Conclusions: Although the prognosis of inactive carrier is favorable, transient ALT and HBV DNA elevations may be observed but have minimal clinical significance. Moreover, continuous HCC surveillance remains necessary since the risk of development still exists. © 2013 The Authors. Journal of Digestive Diseases © 2013 Wiley Publishing Asia Pty Ltd and Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine.

Huntington Medical Research Institutes (HMRI), an independent, leading biomedical research institute based in Pasadena, California, has announced the appointment of Allyson Simpson as Vice President of Philanthropy and  Susie Silk Berry as Director..

Csete M.,Huntington Medical Research Institutes | Doyle J.,California Institute of Technology
Interface Focus | Year: 2014

Blood glucose levels are controlled by well-known physiological feedback loops: high glucose levels promote insulin release from the pancreas, which in turn stimulates cellular glucose uptake. Low blood glucose levels promote pancreatic glucagon release, stimulating glycogen breakdown to glucose in the liver. In healthy people, this control system is remarkably good at maintaining blood glucose in a tight range despite many perturbations to the system imposed by diet and fasting, exercise, medications and other stressors. Type 1 diabetes mellitus (T1DM) results from loss of the insulin-producing cells of the pancreas, the beta cells. These cells serve as both sensor (of glucose levels) and actuator (insulin/glucagon release) in a control physiological feedback loop. Although the idea of rebuilding this feedback loop seems intuitively easy, considerable control mathematics involving multiple types of control schema were necessary to develop an artificial pancreas that still does not function as well as evolved control mechanisms. Here, we highlight some tools from control engineering used to mimic normal glucose control in an artificial pancreas, and the constraints, trade-offs and clinical consequences inherent in various types of control schemes. T1DM can be viewed as a loss of normal physiologic controls, as can many other disease states. For this reason, we introduce basic concepts of control engineering applicable to understanding pathophysiology of disease and development of physiologically based control strategies for treatment. © 2014 The Authors.

Xia N.,Central South University | Liu L.,California State University, Los Angeles | Harrington M.G.,Huntington Medical Research Institutes | Wang J.,Central South University | Zhou F.,California State University, Los Angeles
Analytical Chemistry | Year: 2010

A major constituent in the deposit of the brain in a patient with Alzheimer's disease (AD) is the aggregates/fibrils of amyloid-β (Aβ) peptides containing 39-43 amino acids. The total Aβ levels and the concentration ratio between the most abundant Aβ(1-40) peptide and the more aggregation-prone Aβ(1-42) in body fluids (e.g., cerebrospinal fluid or CSF) have been suggested as possible criteria for early diagnosis of AD. By immobilizing capture antibodies specific to the two peptides in separate fluidic channels, surface plasmon resonance (SPR) has been used to quantify Aβ(1-40) and Aβ(1-42) present in CSF samples collected from AD patients and healthy donors. With signal amplification by streptavidin conjugated to an antibody that is selective to the common N-terminus of the Aβ peptides, concentrations as low as 20 pM can be readily measured. The range of Aβ peptide concentrations measurable by this method spans 4 orders of magnitude. The ability of regenerating the sensor surface for repeated measurements not only improves the reproducibility but also enhances the sample throughput. Our data reveal that the ratio of Aβ(1-40) concentration versus Aβ(1-42) concentration in CSF samples from AD patients is almost twice as high as that from healthy persons. In contrast to the commonly used enzyme-linked immunosorbent assay (ELISA), SPR obviates the need of a more expensive and less stable enzyme conjugate and the use of carcinogenic substrate for the signal detection and allows the binding events to be monitored in real time. © 2010 American Chemical Society.

Fonteh A.N.,Huntington Medical Research Institutes | Chiang J.,Huntington Medical Research Institutes | Cipolla M.,Huntington Medical Research Institutes | Hale J.,Huntington Medical Research Institutes | And 4 more authors.
Journal of Lipid Research | Year: 2013

Our aim is to study selected cerebrospinal fluid (CSF) glycerophospholipids (GP) that are important in brain pathophysiology. We recruited cognitively healthy (CH), minimally cognitively impaired (MCI), and late onset Alzheimer's disease (LOAD) study participants and collected their CSF. After fractionation into nanometer particles (NP) and supernatant fluids (SF), we studied the lipid composition of these compartments. LC-MS/MS studies reveal that both CSF fractions from CH subjects have N-acyl phosphatidylethanolamine, 1-radyl-2-acyl- sn -glycerophosphoethanolamine (PE), 1-radyl-2-acyl- sn -glycerophosphocholine (PC), 1,2-diacyl- sn -glycerophosphoserine (PS), platelet-activating factor-like lipids, and lysophosphatidylcholine (LPC). In the NP fraction, GPs are enriched with a mixture of saturated, monounsaturated, and polyunsaturated fatty acid species, while PE and PS in the SF fractions are enriched with PUFAcontaining molecular species. PC, PE, and PS levels in CSF fractions decrease progressively in participants from CH to MCI, and then to LOAD. Whereas most PC species decrease equally in LOAD, plasmalogen species account for most of the decrease in PE. A significant increase in the LPC-to-PC ratio and PLA2 activity accompanies the GP decrease in LOAD. These studies reveal that CSF supernatant fluid and nanometer particles have different GP composition, and that PLA2 activity accounts for altered GPs in these fractions as neurodegeneration progresses. Copyright © 2013 by the American Society for Biochemistry and Molecular Biology, Inc.

McCreery D.,Huntington Medical Research Institutes | Pikov V.,Huntington Medical Research Institutes | Troyk P.R.,Illinois Institute of Technology
Journal of Neural Engineering | Year: 2010

Activated iridium microelectrodes were implanted for 450-1282 days in the sensorimotor cortex of seven adult domestic cats and then pulsed for 240 h (8 h per day for 30 days) at 50 Hz. Continuous stimulation at 2 nC/phase and with a geometric charge density of 100 μC cm -2 produced no detectable change in neuronal density in the tissue surrounding the microelectrode tips. However, pulsing with a continuous 100% duty cycle at 4 nC/phase and with a geometric charge density of 200 μC cm -2 induced loss of cortical neurons over a radius of at least 150 μm from the electrode tips. The same stimulus regimen but with a duty cycle of 50% (1 s of stimulation, and then 1 s without stimulation repeated for 8 h) produced neuronal loss within a smaller radius, approximately 60 μm from the center of the electrode tips. However, there also was significant loss of neurons surrounding the unpulsed electrodes, presumably as a result of mechanical injury due to their insertion into and long-term residence in the tissue, and this was responsible for most of the neuronal loss within 150 μm of the electrodes pulsed with the 50% duty cycle. © 2010 IOP Publishing Ltd.

Fonteh A.N.,Huntington Medical Research Institutes | Cipolla M.,Huntington Medical Research Institutes | Chiang J.,Huntington Medical Research Institutes | Arakaki X.,Huntington Medical Research Institutes | Harrington M.G.,Huntington Medical Research Institutes
PLoS ONE | Year: 2014

Background: Although saturated (SAFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fatty acids are important structural components of neuronal membranes and precursors of signaling molecules, knowledge of their metabolism in Alzheimer's disease (AD) is limited. Based on recent discovery that lipids in cerebrospinal fluid (CSF) are distributed in both brain-derived nanoparticles (NP) and supernatant fluid (SF), we hypothesized that fatty acid (FA) abundance and distribution into these compartments is altered in early AD pathology. Methodology and Findings: We assayed the FA composition and abundance in CSF fractions from cognitively healthy (CH), mild cognitive impairment (MCI), and AD study participants using gas chromatography - mass spectrometry. In the SF fraction, concentration of docosahexaenoic acid [DHA, (C22:6n-3)] was less in AD compared with CH, while alpha linolenic acid [α-LNA, (C18:3n-3)] was lower in MCI compared with CH. In the NP fraction, levels of SAFAs (C15:0, C16:0) and a MUFA (C15:1) differentiated CH from MCI, while two MUFAs (C15:1, C19:1) and four PUFAs (C20:2n-6, C20:3n-3, C22:4n-6, C22:5n-3) were higher in AD compared with CH. Levels of even-chain free SAFA and total free FA levels were higher in AD, levels of odd-chain free SAFAs, MUFAs, n-3 PUFAs, and total PUFA, were lower in AD compared with CH. Free n-6 PUFA levels were similar in all three groups. Conclusions and Significance: FA metabolism is compartmentalized differently in NP versus SF fractions of CSF, and altered FA levels reflect the importance of abnormal metabolism and oxidative pathways in AD. Depleted DHA in CSF fractions in AD is consistent with the importance of n-3 PUFAs in cognitive function, and suggests that disturbed PUFA metabolism contributes to AD pathology. This study of FA levels in CSF fractions from different cognitive stages shows potential AD biomarkers, and provides further insight into cell membrane dysfunctions, including mechanisms leading to amyloid production. © 2014 Fonteh et al.

Fonteh A.N.,Huntington Medical Research Institutes
The journal of headache and pain | Year: 2013

Migraineurs are more often afflicted by comorbid conditions than those without primary headache disorders, though the linking pathophysiological mechanism(s) is not known. We previously reported that phosphatidylcholine-specific phospholipase C (PC-PLC) activity in cerebrospinal fluid (CSF) increased during migraine compared to the same individual's well state. Here, we examined whether PC-PLC activity from a larger group of well-state migraineurs is related to the number of their migraine comorbidities. In a case-control study, migraineurs were diagnosed using International Headache Society criteria, and controls had no primary headache disorder or family history of migraine. Medication use, migraine frequency, and physician-diagnosed comorbidities were recorded for all participants. Lumbar CSF was collected between the hours of 1 and 5 pm, examined immediately for cells and total protein, and stored at -80°C. PC-PLC activity in thawed CSF was measured using a fluorometric enzyme assay. Multivariable logistic regression was used to evaluate age, gender, medication use, migraine frequency, personality scores, and comorbidities as potential predictors of PC-PLC activity in CSF. A total of 18 migraineurs-without-aura and 17 controls participated. In a multivariable analysis, only the number of comorbidities was related to PC-PLC activity in CSF, and only in migraineurs [parameter estimate (standard error) = 1.77, p = 0.009]. PC-PLC activity in CSF increases with increasing number of comorbidities in migraine-without-aura. These data support involvement of a common lipid signaling pathway in migraine and in the comorbid conditions.

Charleswell C.A.,Huntington Medical Research Institutes
Ethnicity and Disease | Year: 2014

Despite efforts focused on outreach to minority populations, the literature reveals that the problem of disparities in minority involvement in clinical research persists. Thus, the objective of this article was to present an overview of the barriers to engage minorities in human subject research and the identification of promising strategies for their recruitment and retention. I identified a need for an innovative approach, which would focus recruitment efforts primarily on clinicians and researchers who contribute their own barriers to the process of recruitment and retention. In this way, the most common outreach efforts, which specifically focus on targeted minority groups, would be replaced. The inclusion of minorities in clinical research is an important bioethical issue, particularly when considering drug pharmacokinetics and pharmacodynamics, which may vary widely among different racial and ethnic populations. In conclusion, patient barriers to participation in clinical research are well-documented and remain of great importance; however, clinician and researcher barriers, equally as important, continue to be overlooked. Focusing on clinicians and researchers is needed to help increase their awareness about the barriers to minority participation that they may present. Continued research and efforts are needed to understand how best to identify, address, and overcome these barriers.

Loading Huntington Medical Research Institutes collaborators
Loading Huntington Medical Research Institutes collaborators