News Article | November 10, 2016
NEW ORLEANS, LA--(Marketwired - November 10, 2016) - Louisiana State University Health Sciences Center New Orleans (LSU Health New Orleans) and OmniSeq (OmniSeq®), a subsidiary of the Roswell Park Cancer Institute (RPCI), are now partnering to provide oncologists with comprehensive next generation sequencing of solid tumors for clinical decision support. "LSU Health New Orleans has an 85-year history as a premier healthcare institution in Louisiana with six professional schools and eight Centers of Excellence. We look forward to adding OmniSeq's cutting edge technology to the LSU Health New Orleans toolkit," said Carl Morrison, President and Chief Scientific Officer of OmniSeq. "Comprehensive genomic profiling should be the first step for all advanced stage solid tumors whenever targeted therapy is a treatment consideration," said Morrison. LSU Health New Orleans will utilize OmniSeq Comprehensive(SM), a pan-cancer tumor profiling diagnostic panel, to screen patients at their facilities. The 144-gene panel is New York State (NYS) CLEP-approved, the gold standard in clinical laboratory testing. Oncologists and patients at LSU Health New Orleans will receive personalized reports on the patients' individual genetic variants including: FDA-approved therapeutics, clinical trials for which the patient may qualify, and potential hereditary variants. OmniSeq Comprehensive utilizes the least amount of tissue of any commercially available comprehensive tumor profiling assay. To date, OmniSeq Comprehensive identified actionable variants -- including FDA-approved therapeutics and precision medicine trials -- for over 83% of patients tested. Through this partnership, LSUHSC will receive access to molecular tumor boards to support clinical decision making as well as collaborate with OmniSeq's customers to strategize on increasing enrollment of minority and underserved populations in the Gulf South community. Additionally, LSUHSC patients will have access to the OmniSeq CARES(SM) financial assistance program to help alleviate any patient out-of-pocket cost. "LSU Health New Orleans is excited to partner with OmniSeq as they provide a multifaceted approach to personalized medicine," said Dr. Augusto Ochoa, Director of LSU Health New Orleans Stanley S. Scott Cancer Center and principal investigator of a Minority Underserved National Cancer Institute Community Research Oncology Program (NCORP), funded by a grant to LSU Health New Orleans. "OmniSeq's cutting edge technology and clinical insights will improve access to precision medicine in our underserved community, offer our physicians' guidance in the development of actionable treatment plans, and help to continue to improve the standard of care for patients at LSU Health New Orleans. It will also allow NCORP investigators to design genomics-based clinical trials tailored to Louisiana and Mississippi patients." About OmniSeq OmniSeq, LLC, a CLIA licensed molecular laboratory was created from the Center for Personalized Medicine at Roswell Park Cancer Institute, an NCI-designated comprehensive cancer center in Buffalo, New York. OmniSeq is committed to improving access to the most informative molecular tumor profiling insights to help guide comprehensive cancer care. OmniSeq addresses the complete customer experience through their OmniSeq CARES(SM) Service Program which focuses on both the physician and patient by facilitating everything from sample retrieval and clinical report consultation, to insurance navigation, financial assistance and clinical trial site contacts. Headquartered in Buffalo, NY, OmniSeq offers services throughout the U.S. For more information, call 1-800-781-1259 or visit www.omniseq.com, twitter.com/OmniSeq, linkedin.com/company/omniseq-precision-medicine-technology, or facebook.com/OmniSeqComprehensive. About LSU Health New Orleans: LSU Health Sciences Center New Orleans educates Louisiana's health care professionals. The state's health university leader, LSU Health New Orleans includes a School of Medicine, the state's only School of Dentistry, Louisiana's only public School of Public Health, and Schools of Allied Health Professions, Nursing, and Graduate Studies. LSU Health New Orleans faculty takes care of patients in public and private hospitals and clinics throughout the region. In the vanguard of biosciences research in a number of areas in a worldwide arena, the LSU Health New Orleans research enterprise generates jobs and enormous economic impact. LSU Health New Orleans faculty have made lifesaving discoveries and continue to work to prevent, advance treatment, or cure disease. To learn more, visit www.lsuhsc.edu, twitter.com/LSUHealthNO or facebook.com/LSUHSC. About the GS-MU-NCORP: The Gulf South Minority Underserved National Cancer Institute Community Oncology Research Program (NCORP), led by Dr. Augusto Ochoa, is a consortium of community hospitals and/or oncology practices and integrated healthcare systems with a patient population of at least 30% racial/ethnic minorities or rural residents. It accrues participants to cancer prevention, control, screening and post-treatment surveillance clinical trials conducted by NCORP and to NCI's National Clinical Trials Network (NCTN) treatment, imaging and quality of life trials.
PubMed | University of Alberta, Tuskegee University, New York Medical College and LSUHSC.
Type: | Journal: American journal of physiology. Heart and circulatory physiology | Year: 2017
30% of the world population is diagnosed with metabolic syndrome. High fat/high sucrose diet (HF/HS, Western diet) correlates with metabolic syndrome prevalence. We characterized effects of the HF/HS diet on vascular (arterial stiffness, vasoreactivity, coronary collateral development) and cardiac (echocardiography) function, oxidative stress and inflammation in a rat model of metabolic syndrome (JCR). Furthermore, we determined whether male vs. female animals were affected differentially by the Western diet. Cardiovascular function in JCR male rats was impaired vs. normal rats (SD). HF/HS diet compromised cardiovascular (dys)function in JCR but not in SD male rats. In contrast, cardiovascular function was minimally impaired in JCR females on normal chow. However, cardiovascular function in JCR females on the HF/HS diet deteriorated to levels comparable to JCR males on the HF/HS diet. Similarly, oxidative stress was markedly increased in male but not female JCR rats on normal chow, but was equally exacerbated by the HF/HS diet in male and female JCR rats. These results indicate that the Western diet enhances oxidative stress and cardiovascular dysfunction in metabolic syndrome and eliminates the protective effect of female sex on cardiovascular function, implying that both males and females with metabolic syndrome are at equal risk for cardiovascular disease.
Amin A.,Tulane University |
Choi S.-K.,Tulane University |
Galan M.,Tulane University |
Kassan M.,Tulane University |
And 6 more authors.
Journal of Pathology | Year: 2012
Endoplasmic reticulum (ER) stress and inflammation are important mechanisms that underlie many of the serious consequences of type II diabetes. However, the role of ER stress and inflammation in impaired ischaemia-induced neovascularization in type II diabetes is unknown. We studied ischaemia-induced neovascularization in the hind-limb of 4-week-old db - /db- mice and their controls treated with or without the ER stress inhibitor (tauroursodeoxycholic acid, TUDCA, 150 mg/kg per day) and interleukin-1 receptor antagonist (anakinra, 0.5 μg/mouse per day) for 4 weeks. Blood pressure was similar in all groups of mice. Blood glucose, insulin levels, and body weight were reduced in db - /db- mice treated with TUDCA. Increased cholesterol and reduced adiponectin in db - /db- mice were restored by TUDCA and anakinra treatment. ER stress and inflammation in the ischaemic hind-limb in db - /db- mice were attenuated by TUDCA and anakinra treatment. Ischaemia-induced neovascularization and blood flow recovery were significantly reduced in db - /db- mice compared to control. Interestingly, neovascularization and blood flow recovery were restored in db - /db- mice treated with TUDCA or anakinra compared to non-treated db - /db- mice. TUDCA and anakinra enhanced eNOS-cGMP, VEGFR2, and reduced ERK1/2 MAP-kinase signalling, while endothelial progenitor cell number was similar in all groups of mice. Our findings demonstrate that the inhibition of ER stress and inflammation prevents impaired ischaemia-induced neovascularization in type II diabetic mice. Thus, ER stress and inflammation could be potential targets for a novel therapeutic approach to prevent impaired ischaemia-induced vascular pathology in type II diabetes. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Lentz J.J.,Louisiana State University Health Sciences Center |
Jodelka F.M.,Rosalind Franklin University of Medicine and Science |
Hinrich A.J.,Rosalind Franklin University of Medicine and Science |
Mccaffrey K.E.,Rosalind Franklin University of Medicine and Science |
And 6 more authors.
Nature Medicine | Year: 2013
Hearing impairment is the most common sensory disorder, with congenital hearing impairment present in approximately 1 in 1,000 newborns1. Hereditary deafness is often mediated by the improper development or degeneration of cochlear hair cells2. Until now, it was not known whether such congenital failures could be mitigated by therapeutic intervention3,4,5. Here we show that hearing and vestibular function can be rescued in a mouse model of human hereditary deafness. An antisense oligonucleotide (ASO) was used to correct defective pre-mRNA splicing of transcripts from the USH1C gene with the c.216G>A mutation, which causes human Usher syndrome, the leading genetic cause of combined deafness and blindness6,7. Treatment of neonatal mice with a single systemic dose of ASO partially corrects Ush1c c.216G>A splicing, increases protein expression, improves stereocilia organization in the cochlea, and rescues cochlear hair cells, vestibular function and low-frequency hearing in mice. These effects were sustained for several months, providing evidence that congenital deafness can be effectively overcome by treatment early in development to correct gene expression and demonstrating the therapeutic potential of ASOs in the treatment of deafness. Copyright © 2013 Nature America, Inc.
Alexander J.S.,LSUHSC |
Harris M.K.,LSUHSC |
Wells S.R.,LSUHSC |
Mills G.,LSUHSC |
And 6 more authors.
Multiple Sclerosis | Year: 2010
Background: Interferon-β1b (IFN-β1b), an effective treatment for multiple sclerosis (MS), lessens disease severity in MS patients. However, the mechanisms of its immunoregulatory and anti-inflammatory effects in MS remain only partially understood. Matrix metalloproteinases (MMP) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) are involved in blood brain barrier disruption and formation of MS lesions. Th1/Th17 cytokines e.g. interleukins IL-12p40, IL-17, and IL-23, are associated with MS disease activity and are significant players in pathogenesis of MS. Objective: During a 1-year prospective study, we serially measured serum MMP-8, MMP-9, TIMP-1, IL-12p40, IL-17, and IL-23 in 24 patients with relapsing-remitting MS. We compared the results to clinical course and to brain magnetic resonance imaging. IFN-β1b decreased serum MMP-8 and MMP-9 (not TIMP-1). Results: The sustained treatment with IFN-β1b attenuated the pro-inflammatory environment by significantly reducing the serum IL-12p40, IL-23, and showed a trend for decreasing IL-17. Decreased serum MMP-8, MMP-9, IL-12 and IL-23 levels were correlated with a decrease in the number of contrast-enhanced T2-weighted lesions. Conclusion: Early treatment of MS with IFN-β1b may stabilize clinical disease by attenuating levels of inflammatory cytokines and MMPs. Serial measurement of inflammatory mediators may serve as sensitive markers to gauge therapeutic responses to IFN-β1b during the first year of treatment.© 2010 The Author(s).Indications:24 in patients with relapsing remitting multiple sclerosis.Patients:24 patients, 8 males and 16 females, age range 24-30 years. Control group (healthy subjects): n=16, 6 males and 10 females, age range 24-29 years.TypeofStudy:An open study investigating whether Extavia therapy would alter serum levels of matrix metalloproteinases (MMP; MMP-8 and MMP-9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), and pro-inflammatory cytokines [interleukin (IL) 12p40 (IL-12p40), IL-17, and IL-23] in patients with relapsing remitting multiple sclerosis (RRMS).DosageDuration:250 mcg, sc, given once every other day. Duration: 12 months.Results:During the 1-year study, 6 patients experienced a total of 6 relapses and were treated with corticosteroids. The mean volume of the T2-weighted lesions was significantly decreased by Extavia therapy from 1068 mm3 to 829 mm3. The difference in plaque volume was significant. Compared to healthy controls, serum MMP-8 levels were significantly elevated in patients with RRMS. While MMP-8 was not affected at 3 months, MMP-8 at 6 and 12 months after Extavia therapy was significantly reduced compared to pre-treatment levels. TIMP-1 was not significantly different in patients with RRMS compared to healthy controls, nor was TIMP-1 levels changed at 3, 6 and 12 months of Extavia treatment in RRMS patients. Compared to healthy controls, serum levels of IL-17 were reduced at 3, 6 and 12 months after Extavia therapy. Compared to healthy controls, serum IL-12p40 were significantly elevated in patients with RRMS at baseline. While no significant changes in IL-12p40 were seen after 3 months of Extavia treatment, serum IL-12 at both 6 and 12 months after Extavia therapy showed a significant decrease compared to pre-treatment levels. Compared to healthy subjects, serum levels of IL-23 were also significantly increased in RRMS patients, which was significantly reduced by Extavia at 3, 6 and 12 months. Serum IL-23 levels were reduced to 1.98 fold normal at 3 months, and to only 43% over control levels by 12 months.AdverseEffects:No adverse events were mentioned.AuthorsConclusions:Our data here provide some of the first evidence supporting IL-12 and IL-23 as significant surrogate markers of MS disease activity which closely correlate with MRI outcomes. Larger clinical trials involving larger cohorts of treatment-naive RRMS patients will be required to validate and expand the findings of this study. Additionally, our findings highlight the roles of MMP-8 in the pathogenesis of MS and presents possible new mechanisms and targets in interferon-β1b treatment of MS.FreeText:Tests: serum levels of MMP-8, MMP-9, TIMP-1, IL-12p40, IL-23, and IL-17; Expanded Disability Status Scale score; and brain magnetic resonance imaging (MRI). Concomitant drug : corticosteroids, given intravenously (iv); gadolinium, given iv during MRI.
Manix M.,LSUHSC |
Wilden J.,LSUHSC |
Journal of NeuroInterventional Surgery | Year: 2015
A 58-year-old man had an intrathecal baclofen pump implanted. A guidewire used during removal of a previously placed lumbar drain catheter fractured, and a fragment was left within the thecal sac. Using fluoroscopic guidance, a loop snare device was used to retrieve the intrathecal foreign body successfully and without complication. The pump was placed without any difficulty, and the patient's hospital course was uneventful.
Yeh K.,LSUHSC |
Yeh K.,Louisiana State University Health Sciences Center |
Yeh M.,Louisiana State University Health Sciences Center |
Glass J.,LSUHSC |
Glass J.,Louisiana State University Health Sciences Center
Gastroenterology | Year: 2011
Background & Aims: Ferroportin (Fpn) is a multiple transmembrane protein required for iron export into the systemic circulation, in cooperation with hephaestin (Heph). Despite the importance of Fpn in iron transport, there is controversy about its topology and functional state upon interaction with Heph. Methods: The topology of Fpn was determined using monospecific antisera against its different epitopes, in sheets of cells from duodenum that were or were not permeabilized with detergent. Immunoprecipitation and blue native polyacrylamide gel electrophoresis, followed by immunoblot analysis, were used to determine the extent of interactions between Fpn and Heph. Antisera against the intracellular, C-termini of divalent metal transporter (Dmt1) and Heph served as controls. Results: Immunofluorescence analysis with antisera against amino acids 172193 of Fpn (anti-Fpn 172) detected Fpn only in permeabilized cells, whereas anti-Fpn 232 (amino acids 232249), anti-Fpn 370 (amino acids 370420), and anti-Fpn C (the C-terminus) detected Fpn in nonpermeabilized and permeabilized cells. Immunoprecipitation studies showed that Fpn and Heph coprecipitated with either anti-Fpn or anti-Heph. Blue native polyacrylamide gel electrophoresis studies revealed that a fraction of Fpn comigrates with Heph; the apparent interaction decreases after iron ingestion. Conclusions: Studies with antisera to different epitopes of Fpn indicate that the topology of Fpn is consistent with an 11-transmembrane model, with the C-terminus exposed on the cell surface. Reduced interactions between Fpn and Heph after iron ingestion indicate that this is a regulatory mechanism for limiting further iron absorption. © 2011 AGA Institute.
Javalkar V.,Louisiana State University Health Sciences Center |
Manix M.,Louisiana State University Health Sciences Center |
Wilson J.,LSUHSC |
Nanda A.,Louisiana State University Health Sciences Center
Journal of Clinical Neuroscience | Year: 2012
Open ring enhancement is considered highly specific for atypical demyelination. In this report we present a patient with a history of headache, ataxia and sensory disturbances in the lower extremities. A cranial MRI scan showed a large frontal lesion with mass effect, midline shift and with open ring enhancement. These findings are characteristics of tumefactive multiple sclerosis. Such lesions can be confused with neoplasms and abscesses. Open ring enhancement may help in differentiating atypical demyelination from a neoplasm or an abscess. © 2012 Elsevier Ltd. All rights reserved.
PubMed | Childrens Hospital New Orleans, LSUHSC and Tulane University
Type: | Journal: Fetal and pediatric pathology | Year: 2016
Chondromyxoid fibroma-like osteosarcoma (CMF-OS) is a low-grade osteosarcoma, often misdiagnosed on initial biopsy as a benign lesion, with five cases previously described. We report a 13-year-old male with an intramedullary lytic CMF-OS of the right tibial proximal metaphysis with cortical destruction and soft tissue extension. Diagnosis was based on malignant new bone formation, increased mitotic figures, lamellar bone permeation with bony destruction, and correlation with imaging studies. There were no metastasis at presentation and the tumor showed good response to standard chemotherapy with >95% necrosis.
PubMed | University of Queensland and LSUHSC
Type: Journal Article | Journal: Current pain and headache reports | Year: 2017
Management of acute pain following surgery using a multimodal approach is recommended by the American Society of Anesthesiologists whenever possible. In addition to opioids, drugs with differing mechanisms of actions target pain pathways resulting in additive and/or synergistic effects. Some of these agents include alpha 2 agonists, NMDA receptor antagonists, gabapentinoids, dexamethasone, NSAIDs, acetaminophen, and duloxetine.Alpha 2 agonists have been shown to have opioid-sparing effects, but can cause hypotension and bradycardia and must be taken into consideration when administered. Acetaminophen is commonly used in a multimodal approach, with recent evidence lacking for the use of IV over oral formulations in patients able to take medications by mouth. Studies involving gabapentinoids have been mixed with some showing benefit; however, future large randomized controlled trials are needed. Ketamine is known to have powerful analgesic effects and, when combined with magnesium and other agents, may have a synergistic effect. Dexamethasone reduces postoperative nausea and vomiting and has been demonstrated to be an effective adjunct in multimodal analgesia. The serotonin-norepinephrine reuptake inhibitor, duloxetine, is a novel agent, but studies are limited and further evidence is needed. Overall, a multimodal analgesic approach should be used when treating postoperative pain, as it can potentially reduce side effects and provide the benefit of treating pain through different cellular pathways.