San Antonio, TX, United States

The University of Texas Health Science Center at San Antonio is an institute of health science education and research located in the South Texas Medical Center, the medical district of the U.S. city of San Antonio, Texas. It is a component of the University of Texas System.The UT Health Science Center is the largest health science university in South Texas. The Health Science Center serves San Antonio and all of the 50,000 square miles area of Central and South Texas. It extends to campuses in the Texas border communities of Laredo and the Lower Rio Grande Valley.The Health Science Center has produced more than 28,000 graduates; more than 3,000 students a year train in an environment that involves more than 100 affiliated hospitals, clinics and health care facilities in South Texas. The university offers more than 65 degrees, the large majority of them being graduate and professional degrees, in the biomedical and health science fields.The Health Science Center is home to the Cancer Therapy & Research Center at The University of Texas Health Science Center San Antonio, designated a National Cancer Institute Cancer Center. The CTRC's Institute for Drug Development is internationally recognized for conducting one of the largest oncology Phase I clinical drug trials programs in the world. Fifteen of the cancer drugs most recently approved by the U.S. Food & Drug Administration underwent development or testing at the IDD. Other noted programs include: cellular and structural biology, urology, nephrology, transplantation biology, aging and longevity studies, cardiology and research imaging. The Health Science Center publishes a periodic magazine, The Mission.In 2006, $263 million of facility upgrades were allocated for the campus by the University of Texas System Board of Regents. This included a $150 million 200,000-square-foot South Texas Research Facility . The building was dedicated in October 2011. Wikipedia.

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News Article | May 3, 2017

SAN ANTONIO, Texas, May 03, 2017 (GLOBE NEWSWIRE) -- bioAffinity Technologies announced that the European Patent Office (EPO) has issued a patent that protects the Company’s proprietary CyPath® technology for the early detection of lung cancer through 2030.  Titled “System and Method for Analyzing Samples Labeled with 5, 10, 15, 20 Tetrakis (4-Carboxyphenyl) Porphine (TCPP),” the EPO patent for bioAffinity’s platform test for early cancer detection will significantly increase bioAffinity’s intellectual property (IP) portfolio that currently consists of 43 awarded patents in 22 countries. bioAffinity’s porphyrin-based CyPath® bio-label preferentially binds to cancer cells, giving them a distinctive fluorescence that is detectable and measurable by flow cytometry.  CyPath® Lung, bioAffinity’s initial product, is designed to be a highly accurate, non-invasive, early-stage lung cancer diagnostic for use by patients at risk for lung cancer. “According to the World Health Organization, nearly 30 percent of European adults are smokers, and smoking among adolescents is on the rise,” bioAffinity President and CEO Maria Zannes said.  “Tobacco use causes 16 percent of all deaths in the adult population over 30 years of age.  We expect our CyPath® product to have a significant positive impact on early detection of lung cancer in the European Union.” bioAffinity is focused on the commercialization of accurate, non-invasive diagnostics and life-saving targeted therapeutics for multiple cancers.  CyPath® Lung is a simple and cost-effective diagnostic, which will make it particularly valuable in countries with large populations and broad economic and social demographics. bioAffinity Technologies, Inc. ( is a privately held development-stage company addressing the significant unmet need for non-invasive, early-stage cancer diagnosis and treatment.  The Company develops proprietary in-vitro diagnostic tests and targeted cancer therapeutics using breakthrough technology that preferentially targets cancer cells.  Research and optimization of its platform technology is conducted in bioAffinity Technologies’ laboratories and at the University of Texas Health Science Center at San Antonio through a collaborative research agreement. The Company’s platform technology will be developed to diagnose, monitor and treat many cancers.

News Article | April 28, 2017

Bethesda, MD (April 28, 2017) -- The American Gastroenterological Association (AGA) Research Foundation is thrilled to award 52 researchers with research funding in the 2017 award year. "The AGA Research Foundation has a proven track record of funding young investigators who subsequently achieve great success in research. We are confident that the 2017 class will be no exception," said Robert S. Sandler, MD, MPH, AGAF, chair, AGA Research Foundation. "AGA is honored to invest in this year's award recipients and looks forward to seeing how each research project contributes to advancing the field of gastroenterology." The AGA Research Award Program serves to support talented investigators who are pursuing careers in digestive disease research. A grant from the AGA Research Foundation ensures that a major proportion of the recipient's time is protected for research. The awards program is made possible thanks to generous donors and funders contributing to the AGA Research Foundation. Show your support for GI research.https:/ Below are the 2017 AGA Research Foundation award recipients. To learn about upcoming research funding opportunities, visit http://www. . Shrinivas Bishu, MD, University of Michigan, Ann Arbor David Boone, PhD, Indiana University School of Medicine, Indianapolis Sarah Glover, DO, University of Florida, Gainesville Jennifer Lai, MD, MBA, The Regents of the University of California, San Francisco Jill Smith, MD, Georgetown University, Washington, D.C. Chandler Brown, Gallaudet University, Washington, D.C. Carlos Lodeiro, Texas Tech University Health Sciences Center El Paso Paul L. Foster School of Medicine Alyssa Murillo, University of Illinois at Chicago College of Medicine Kristeen Onyirioha, University of Texas San Antonio Health Sciences Center Gabriela Portilla Skerrett, San Juan Bautista School of Medicine, Puerto Rico Ray Ramirez, Eastern Virginia Medical School, Norfolk Rani Richardson, University of Pennsylvania, Philadelphia Nefertiti Tyehemba, State University of New York Upstate Medical University, Syracuse Elsie Ureta, California State University of Los Angeles Carlos Zavala, University of Illinois at Urbana-Champaign Edward Barnes, MD, MPH, University of North Carolina School of Medicine, Chapel Hill Daniel Duncan, MD, Boston Children's Hospital, MA Amy Engevik, PhD, Vanderbilt University, Nashville Tossapol Kerdsirichairat, MD, University of Michigan Health System, Ann Arbor Anne-Marie Overstreet, PhD, Indiana University School of Medicine, Indianapolis Shusuke Toden, PhD, Baylor University Medical Center/Baylor Research Institute, Houston Amy Tsou, MD, PhD, Boston Children's Hospital, MA Lavanya Viswanathan, MD, MS, Augusta University, GA Hongtao Wang, MD, PhD, Baylor College of Medicine and Texas Children's Hospital, Houston Lauren Cole, BS, University of Arizona College of Medicine, Phoenix Cindy Law, BSc, University of Ottawa, Canada Christopher Moreau, BS, University of Texas Health Science Center at San Antonio Satish Munigala, MBBS, MPH, St. Louis University, MO Rajiv Perinbasekar, MD, University of Maryland Medical Center, Baltimore Chung Sang Tse, MD, Mayo Clinic, Rochester, MN Anika Ullah, University of California, San Diego Kathy Williams, MS, Cooper Medical School of Rowan University, Camden, NJ Quan Zhou, MS, University of Michigan, Ann Arbor This year's honorees will be recognized during several AGA Research Foundation events at Digestive Disease Week® 2017, taking place May 6-9 in Chicago, IL. The American Gastroenterological Association is the trusted voice of the GI community. Founded in 1897, the AGA has grown to more than 16,000 members from around the globe who are involved in all aspects of the science, practice and advancement of gastroenterology. The AGA Institute administers the practice, research and educational programs of the organization.http://www. . Like AGA on Facebook.http://www. facebook. com/ amergastroassn> Follow us on Twitter @AmerGastroAssn.http://www. twitter. com/ amergastroassn> Check out our videos on YouTube.http://www. The AGA Research Foundation, formerly known as the Foundation for Digestive Health and Nutrition, is the cornerstone of AGA's effort to expand digestive disease research funding. Since 1984, the AGA, through its foundations, has provided more than $47 million in research grants to more than 870 scientists. The AGA Research Foundation serves as a bridge to the future of research in gastroenterology and hepatology by providing critical funding to advance the careers of young researchers between the end of training and the establishment of credentials that earn National Institutes of Health grants. Learn more about the AGA Research Foundation or make a contribution at http://www. .

Abboud H.E.,University of Texas Health Science Center at San Antonio
Experimental Cell Research | Year: 2012

Mesangial cells originate from the metanephric mesenchyme and maintain structural integrity of the glomerular microvascular bed and mesangial matrix homeostasis. In response to metabolic, immunologic or hemodynamic injury, these cells undergo apoptosis or acquire an activated phenotype and undergo hypertrophy, proliferation with excessive production of matrix proteins, growth factors, chemokines and cytokines. These soluble factors exert autocrine and paracrine effects on the cells or on other glomerular cells, respectively. MCs are primary targets of immune-mediated glomerular diseases such as IGA nephropathy or metabolic diseases such as diabetes. MCs may also respond to injury that primarily involves podocytes and endothelial cells or to structural and genetic abnormalities of the glomerular basement membrane. Signal transduction and oxidant stress pathways are activated in MCs and likely represent integrated input from multiple mediators. Such responses are convenient targets for therapeutic intervention. Studies in cultured MCs should be supplemented with in vivo studies as well as examination of freshly isolated cells from normal and diseases glomeruli. In addition to ex vivo morphologic studies in kidney cortex, cells should be studied in their natural environment, isolated glomeruli or even tissue slices. Identification of a specific marker of MCs should help genetic manipulation as well as selective therapeutic targeting of these cells. Identification of biological responses of MCs that are not mediated by the renin-angiotensin system should help development of novel and effective therapeutic strategies to treat diseases characterized by MC pathology. © 2012.

Hinck A.P.,University of Texas Health Science Center at San Antonio
FEBS Letters | Year: 2012

TGF-βs are small secreted signaling proteins that function as vital regulators of cellular growth and differentiation. They signal through a single pair of receptors, known as TβR-I and TβR-II, and are among the most recently evolved members of the signaling superfamily to which they belong. This review provides an overview of the TGF-β, BMP, and activin receptor complexes that have been determined over the past several years. These structures underscore the shared ancestry of the TGF-βs with the BMPs and activins, but also provide insight as to how the TGF-βs diverged from the BMPs and activins to bind and assemble their receptors in a distinct manner. These distinctive modes of receptor binding engender the TGF-βs with high specificity for their receptors and allow them to fulfill their essential functions in vivo without interference from the many other proteins of the superfamily. © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Nikolova Y.S.,University of Texas Health Science Center at San Antonio
Nature neuroscience | Year: 2014

We examined epigenetic regulation in regards to behaviorally and clinically relevant human brain function. Specifically, we found that increased promoter methylation of the serotonin transporter gene predicted increased threat-related amygdala reactivity and decreased mRNA expression in postmortem amygdala tissue. These patterns were independent of functional genetic variation in the same region. Furthermore, the association with amygdala reactivity was replicated in a second cohort and was robust to both sampling methods and age.

Qin Z.,University of Texas Health Science Center at San Antonio
Atherosclerosis | Year: 2012

Since their establishment thirty years ago, THP-1 cells have become one of most widely used cell lines to investigate the function and regulation of monocytes and macrophages in the cardiovascular system. However, because this cell line was derived from the blood of a patient with acute monocytic leukemia, the extent to which THP-1 cells mimic monocytes and macrophages in the vasculature is not entirely known. This article serves as a meaningful attempt to address this question by reviewing the recent publications. The interactions between THP-1 cells and various vascular cells (such as endothelial cells, smooth muscle cells, adipocytes, and T cells) provide insight into the roles of the interconnection of monocytes-macrophages with other vascular cells during vascular inflammation, particularly atherogenesis and obesity. Transcriptome, microRNA profile, and histone modifications of THP-1 cells shed new light on the regulatory mechanism of the monocytes-macrophages in response to various inflammatory mediators, such as oxidized low density lipoprotein, lipopolysaccharide, and glucose. These studies hint that under certain defined conditions, THP-1 cells not only resemble primary monocytes-macrophages isolated from healthy donors or donors with disease, such as diabetes mellitus, but also mimic the in situ alteration of macrophages in the adipose tissue of obese subjects and in atherosclerotic lesions. A potential trajectory is to use this cell line to study the novel molecular mechanisms in monocytes and macrophages in relation to the physiology and pathophysiology of the cardiovascular system, however, the conclusion of studies employing THP-1 cells requires further verification using primary cells and/or in vivo models to be generalized to monocytes and macrophages. © 2011 Elsevier Ireland Ltd.

Bouamar H.,University of Texas Health Science Center at San Antonio
Blood | Year: 2013

The characterization of immunoglobulin heavy chain (IGH) translocations provides information on the diagnosis and guides therapeutic decisions in mature B-cell malignancies while enhancing our understanding of normal and malignant B-cell biology. However, existing methodologies for the detection of IGH translocations are labor intensive, often require viable cells, and are biased toward known IGH fusions. To overcome these limitations, we developed a capture sequencing strategy for the identification of IGH rearrangements at nucleotide level resolution and tested its capabilities as a diagnostic and discovery tool in 78 primary diffuse large B-cell lymphomas (DLBCLs). We readily identified IGH-BCL2, IGH-BCL6, IGH-MYC, and IGH-CCND1 fusions and discovered IRF8, EBF1, and TNFSF13 (APRIL) as novel IGH partners in these tumors. IRF8 and TNFSF13 expression was significantly higher in lymphomas with IGH rearrangements targeting these loci. Modeling the deregulation of IRF8 and EBF1 in vitro defined a lymphomagenic profile characterized by up-regulation of AID and/or BCL6, down-regulation of PRMD1, and resistance to apoptosis. Using a capture sequencing strategy, we discovered the B-cell relevant genes IRF8, EBF1, and TNFSF13 as novel targets for IGH deregulation. This methodology is poised to change how IGH translocations are identified in clinical settings while remaining a powerful tool to uncover the pathogenesis of B-cell malignancies.

Lodge D.J.,University of Texas Health Science Center at San Antonio
Neuropsychopharmacology | Year: 2011

The prefrontal cortex (PFC) is essential for top-down control over higher-order executive function. In this study we demonstrate that the medial prefrontal cortex (mPFC) and orbitofrontal cortex (OFC) differentially regulate VTA dopamine neuron activity, and furthermore, the pattern of activity in the PFC drastically alters the dopamine neuron response. Thus, although single-pulse activation of the mPFC either excites or inhibits equivalent numbers of dopamine neurons, activation of the OFC induces a primarily inhibitory response. Moreover, activation of the PFC with a pattern that mimics spontaneous burst firing of pyramidal neurons produces a strikingly different response. Specifically, burst-like activation of the mPFC induces a massive increase in dopamine neuron firing, whereas a similar pattern of OFC activation largely inhibits dopamine activity. Taken together, these data demonstrate that the mPFC and OFC differentially regulate dopamine neuron activity, and that the pattern of cortical activation is critical for determining dopamine system output. © 2011 American College of Neuropsychopharmacology. All rights reserved.

Dahia P.L.M.,University of Texas Health Science Center at San Antonio
Nature Reviews Cancer | Year: 2014

The neuroendocrine tumours pheochromocytomas and paragangliomas carry the highest degree of heritability in human neoplasms, enabling genetic alterations to be traced to clinical phenotypes through their transmission in families. Mutations in more than a dozen distinct susceptibility genes have implicated multiple pathways in these tumours, offering insights into kinase downstream signalling interactions and hypoxia regulation, and uncovering links between metabolism, epigenetic remodelling and cell growth. These advances extend to co-occurring tumours, including renal, thyroid and gastrointestinal malignancies. Hereditary pheochromocytomas and paragangliomas are powerful models for recognizing cancer driver events, which can be harnessed for diagnostic purposes and for guiding the future development of targeted therapies. © 2014 Macmillan Publishers Limited.

DeFronzo R.A.,University of Texas Health Science Center at San Antonio
Diabetes Care | Year: 2011

Both as monotherapy and in combination with other OHAs, timed bromocriptine (Cycloset) causes a 0.6-0.7%reduction in HbA1c and reduces plasma triglyceride and FFA concentrations in type 2 diabetic patients. In a 52-week safety study, Cycloset decreased the cardiovascular composite end point by 40%. Other advantages of Cycloset include absence of hypoglycemia since insulin secretion is not stimulated, weight neutrality, no need for dose adjustment in patients with moderate renal insufficiency, lack of edema and CHF, and good side effect profile. © 2011 by the American Diabetes Association.

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