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.
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. (www.bioaffinitytech.com) 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 | May 25, 2017
DUARTE, CA--(Marketwired - May 25, 2017) - Prolacta Bioscience®, the pioneer in human milk-based neonatal nutritional products for premature infants, announced today that it passed the halfway point in a clinical trial evaluating the effect of adding Prolact CR®, a caloric fortifier made from 100 percent human milk cream, to an exclusive human milk-based diet (EHMD)1 for very low birth weight (VLBW) premature infants. The study is evaluating the length of stay and incidence of bronchopulmonary dysplasia (BPD) and has enrolled 127 of the 210 participants weighing between 500 and 1,250g (1 lb 1 oz to 2 lbs 12 oz). The randomized controlled study is evaluating whether adding the human milk cream-based caloric fortifier can decrease the length of hospital stay and reduce BPD, a form of debilitating chronic lung disease not uncommon in VLBW babies. The milk cream caloric fortifier is added as a supplement to an EHMD, which includes the use of 100 percent human milk-based fortifier Prolact+ H2MF®, and is the recommended diet for VLBW infants. "Due to the increased energy and macronutrient requirements of VLBW infants in general, and those with BPD in particular, unfortified human milk does not meet their nutritional needs," said Amy Hair, M.D., lead investigator, Assistant Professor of Pediatrics at Baylor College of Medicine, and the Director of Neonatal Nutrition at Texas Children's Hospital. "VLBW infants require 20 to 40 percent more calories than their age-matched counterparts. These infants also are at higher risk for postnatal growth failure due to disruptions in their feeding regimens. An earlier randomized clinical trial looking at growth suggested that Prolact CR® reduced the incidence and severity of BPD in the group receiving additional nutrients provided from fat." The study, "A Randomized Trial of the Use of Human Milk Cream to Decrease Length of Stay in Extremely Premature Infants," is currently being conducted at Akron Children's Hospital at Boardman, Boardman, Ohio (Linda Cooper, M.D.); Innsbruck Medical University, Innsbruck, Austria (Ursula Kiechl-Kohlendorfer, M.D.); Michigan State University-Sparrow Hospital, Lansing, Mich. (Padmani Karna, M.D.); University of Texas Health Science Center at San Antonio, San Antonio, Texas (Cynthia Blanco, M.D.); Winnie Palmer Hospital for Women & Babies, Orlando, Fla. (Jose Perez, M.D.); Wasatch Neonatal LC, Orem, Utah (Dale Gerstmann, M.D.); St. Joseph's Women's Hospital, Tampa, Fla. (Jenelle Ferry, M.D.); St. John Medical Center, Tulsa, Okla. (Craig Anderson, D.O.); Cook Children's Medical Center, Fort Worth, Texas (David Riley, M.D.); St. Louis Children's Hospital, St. Louis, Mo. (Stephanie Attarian, M.D.); The University of Oklahoma Health Sciences Center, Oklahoma City, Okla. (Andrea Willeitner, M.D.); and Texas Tech University Health Sciences Center El Paso, El Paso, Texas (Lewis Rubin, M.D.). "This clinical trial is the result of secondary findings that were observed in an earlier trial, and underscores the need for continued study of the unique properties in human milk," said Scott Elster, CEO of Prolacta. "We look forward to seeing how Prolact CR® affects lengths of stay and BPD with the hope of uncovering new therapeutic benefits for this fragile patient population." This new clinical trial seeks to verify observations on length of stay and BPD with the use of Prolact CR® from a prior multi-center, randomized trial ("Premature Infants 750-1,250g Birth Weight Supplemented with a Novel Human Milk-Derived Cream are Discharged Sooner," published in Breastfeeding Medicine in 2016). This analysis found that infants who received Prolact CR® were discharged, on average, 12 days earlier than those who did not receive the cream supplement. In the initial trial, infants who developed BPD may have derived an even greater benefit, a finding which prompted this new study. About Prolacta Bioscience Prolacta Bioscience, Inc. is a privately-held life sciences company dedicated to Advancing the Science of Human Milk®. The company pioneered the development of human milk-based neonatal nutritional products to meet the needs of critically ill, premature infants in the neonatal intensive care unit (NICU). Prolacta leads the industry in the quality and safety of nutritional products made from donor breast milk, and operates the first and only pharmaceutical-grade manufacturing facility for the processing of human milk. 1 An EHMD is when 100% percent of the protein, fat and carbohydrates in an infant's intake are derived solely from human milk.
Zhang J.,University of Texas Health Science Center at San Antonio |
Shapiro M.S.,University of Texas Health Science Center at San Antonio
Neuron | Year: 2012
M-type K+ channels, encoded by KCNQ2-KCNQ5 genes, play key roles in regulation of neuronal excitability; however, less is known about the mechanisms controlling their transcriptional expression. Here, we discovered a mechanism regulating KCNQ2/3 transcriptional expression by neuronal activity in rodent neurons, involving activation of calcineurin and nuclear factor of activated T cell (NFAT) transcription factors, orchestrated by A kinase-anchoring protein (AKAP)79/150. The signal requires Ca2+ influx through L-type Ca2+ channels and both local and global Ca2+ elevations. We postulate increased M-channel expression to act as a negative feedback to suppress neuronal hyperexcitability, demonstrated by profoundly upregulated KCNQ2/3 transcription in hippocampi from wild-type, but not AKAP150-/-, mice after drug-induced seizures. Thus, we suggest a distinct role of AKAP79/150 and the complex it organizes in activity-dependent M-channel transcription, which may potentially serve throughout the nervous system to limit overexcitability associated with disease states such as epilepsy.
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.