The University of Texas at San Antonio is a state research university in San Antonio, Texas, United States. With over 37,000 students, it is the largest university in San Antonio and the fifth-largest in the state of Texas. Its three campuses span over 747 acres of land, with its main campus being the largest in the University of Texas System. UTSA offers a wide array of academic studies, with 133 undergraduate, 51 graduate and 24 doctoral programs. In 2012 and 2013, it was selected by Times Higher Education as one of the best universities in the world under 50 years old.UTSA is a member of the Oak Ridge Associated Universities, a consortium of the nation's major doctorate-level universities dedicated to collaboration and scientific advancement. It is an institutional member of the Hispanic Association of Colleges and Universities, recognizing its influence and role as a Hispanic-serving institution. UTSA is also a member of the American Association of State Colleges and Universities, an organization of public institutions that seek to both offer educational excellence and opportunities to historically under-served populations.Established in 1969, UTSA has evolved to become one of the largest institutions within the UT System. Through an aggressive expansion of its academic funding, the university devoted over $56 million to research in 2011. Its NCAA record-breaking football team has competed in Conference USA since 2013, previously playing a stint in the WAC and as an FCS independent.Alongside seven other emerging research institutions, The University of Texas at San Antonio is currently in competition to become Texas' third flagship university. Wikipedia.
Wang Y.,University of Texas at San Antonio
BMC genomics | Year: 2012
About 6 million Americans suffer from heart failure and 70% of heart failure cases are caused by myocardial infarction (MI). Following myocardial infarction, increased cytokines induce two major types of macrophages: classically activated macrophages which contribute to extracellular matrix destruction and alternatively activated macrophages which contribute to extracellular matrix construction. Though experimental results have shown the transitions between these two types of macrophages, little is known about the dynamic progression of macrophages activation. Therefore, the objective of this study is to analyze macrophage activation patterns post-MI. We have collected experimental data from adult C57 mice and built a framework to represent the regulatory relationships among cytokines and macrophages. A set of differential equations were established to characterize the regulatory relationships for macrophage activation in the left ventricle post-MI based on the physical chemistry laws. We further validated the mathematical model by comparing our computational results with experimental results reported in the literature. By applying Lyaponuv stability analysis, the established mathematical model demonstrated global stability in homeostasis situation and bounded response to myocardial infarction. We have established and validated a mathematical model for macrophage activation post-MI. The stability analysis provided a possible strategy to intervene the balance of classically and alternatively activated macrophages in this study. The results will lay a strong foundation to understand the mechanisms of left ventricular remodelling post-MI.
Sharp Z.D.,University of Texas at San Antonio
Cellular and Molecular Life Sciences | Year: 2011
Longstanding results with calorie and growth factor restriction plus recent results with the first interventional drug suggest that retarding the pace of aging to improve the quality of life of older people is at hand. The biological system targeted by these approaches is the target of rapamycin (TOR), which is central for cellular responses to a variety of stimuli including stressors, growth factors, and nutrients and energy states. That the life-extending response to reducing its activity is highly conserved from yeast to mammals is consistent with the evolution of aging as a strategy to preserve reproductive potential of young cells and animals. © 2010 Springer Basel AG.
Garcia A.M.,University of Texas at San Antonio
PLoS genetics | Year: 2010
Using a transgenic mouse model harboring a mutation reporter gene that can be efficiently recovered from genomic DNA, we previously demonstrated that mutations accumulate in aging mice in a tissue-specific manner. Applying a recently developed, similar reporter-based assay in Drosophila melanogaster, we now show that the mutation frequency at the lacZ locus in somatic tissue of flies is about three times as high as in mouse tissues, with a much higher fraction of large genome rearrangements. Similar to mice, somatic mutations in the fly also accumulate as a function of age, but they do so much more quickly at higher temperature, a condition which in invertebrates is associated with decreased life span. Most mutations were found to accumulate in the thorax and less in abdomen, suggesting the highly oxidative flight muscles as a possible source of genotoxic stress. These results show that somatic mutation loads in short-lived flies are much more severe than in the much longer-lived mice, with the mutation rate in flies proportional to biological rather than chronological aging.
Han H.-C.,University of Texas at San Antonio
Journal of Vascular Research | Year: 2012
Tortuous arteries and veins are commonly observed in humans and animals. While mild tortuosity is asymptomatic, severe tortuosity can lead to ischemic attack in distal organs. Clinical observations have linked tortuous arteries and veins with aging, atherosclerosis, hypertension, genetic defects and diabetes mellitus. However, the mechanisms of their formation and development are poorly understood. This review summarizes the current clinical and biomechanical studies on the initiation, development and treatment of tortuous blood vessels. We submit a new hypothesis that mechanical instability and remodeling could be mechanisms for the initiation and development of these tortuous vessels. © 2012 S. Karger AG, Basel.
Oddo S.,University of Texas at San Antonio
Frontiers in Bioscience - Scholar | Year: 2012
The buildup of Abeta and tau is believed to directly cause or contribute to the progressive cognitive deficits characteristic of Alzheimer disease. However, the molecular pathways linking Abeta and tau accumulation to learning and memory deficits remain elusive. There is growing evidence that soluble forms of Abeta and tau can obstruct learning and memory by interfering with several signaling cascades. In this review, I will present data showing that the mammalian target of rapamycin (mTOR) may play a role in Abeta and tau induced neurodegeneration.