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Galveston, TX, United States

The University of Texas Medical Branch is a component of the University of Texas System located in Galveston, Texas, United States, about 50 miles southeast of Downtown Houston. It is an academic health center with 11,000 employees and a medical school that is the oldest in Texas. In November 2014 it had an endowment of $508 million. Established in 1891 as the University of Texas Medical Department, UTMB has grown from one building, 23 students and 13 faculty members to more than 70 buildings, more than 2,500 students and more than 1,000 faculty. It has four schools, three institutes for advanced study, a comprehensive medical library, three on-site hospitals , a network of clinics that provide primary and specialized medical care and numerous research facilities.UTMB's primary missions are health science education, medical research and health care services. Its Emergency Room at John Sealy Hospital is certified as a Level I Trauma Center and serves as the lead trauma facility for a nine-county region in Southeast Texas; it is one of only three Level I Trauma centers serving all ages in Southeast Texas.In fiscal year 2012, UTMB received 20 percent of its $1.5 billion budget from the State of Texas to help support its teaching mission, hospital operation and Level 1 Trauma Center; UTMB generates the rest of its budget through its research endeavors, clinical services and philanthropy. It provides a significant amount of charity care , and treats complex cases such as transplants and burns.In 2003 UTMB received funding to construct a $150 million Galveston National Biocontainment Laboratory on its campus, one of the few non-military facilities of this level. It houses several Biosafety Level 4 research laboratories, where studies on highly infectious materials can be carried out safely. It has schools of medicine, nursing, allied health professions, and a graduate school of biomedical science, as well as an institute for medical humanities. UTMB also has a major contract with the Texas Department of Corrections to provide medical care to inmates at all TDC sites in the eastern portion of Texas. UTMB also has similar contracts with local governments needing inmate medical care. Wikipedia.


Szabo C.,University of Texas Medical Branch
Antioxidants and Redox Signaling | Year: 2012

Significance: Diabetes and its complications represent a major socioeconomic problem. Recent Advances: Changes in the balance of hydrogen sulfide (H2S) play an important role in the pathogenesis of β-cell dysfunction that occurs in response to type 1 and type 2 diabetes. In addition, changes in H2S homeostasis also play a role in the pathogenesis of endothelial injury, which develop on the basis of chronically or intermittently elevated circulating glucose levels in diabetes. Critical Issues: In the first part of this review, experimental evidence is summarized implicating H2S overproduction as a causative factor in the pathogenesis of β-cell death in diabetes. In the second part of our review, experimental evidence is presented supporting the role of H2S deficiency (as a result of increased H2S consumption by hyperglycemic cells) in the pathogenesis of diabetic endothelial dysfunction, diabetic nephropathy, and cardiomyopathy. Future Directions: In the final section of the review, future research directions and potential experimental therapeutic approaches around the pharmacological modulation of H2S homeostasis in diabetes are discussed. © 2012 Mary Ann Liebert, Inc. Source


We have identified a large expansion of an ATTCT repeat within intron 9 of ATXN10 on chromosome 22q13.31 as the genetic mutation of spinocerebellar ataxia type 10 (SCA10). Our subsequent studies indicated that neither a gain nor a loss of function of ataxin 10 is likely the major pathogenic mechanism of SCA10. Here, using SCA10 cells, and transfected cells and transgenic mouse brain expressing expanded intronic AUUCU repeats as disease models, we show evidence for a key pathogenic molecular mechanism of SCA10. First, we studied the fate of the mutant repeat RNA by in situ hybridization. A Cy3-(AGAAU)(10) riboprobe detected expanded AUUCU repeats aggregated in foci in SCA10 cells. Pull-down and co-immunoprecipitation data suggested that expanded AUUCU repeats within the spliced intronic sequence strongly bind to hnRNP K. Co-localization of hnRNP K and the AUUCU repeat aggregates in the transgenic mouse brain and transfected cells confirmed this interaction. To examine the impact of this interaction on hnRNP K function, we performed RT-PCR analysis of a splicing-regulatory target of hnRNP K, and found diminished hnRNP K activity in SCA10 cells. Cells expressing expanded AUUCU repeats underwent apoptosis, which accompanied massive translocation of PKCdelta to mitochondria and activation of caspase 3. Importantly, siRNA-mediated hnRNP K deficiency also caused the same apoptotic event in otherwise normal cells, and over-expression of hnRNP K rescued cells expressing expanded AUUCU repeats from apoptosis, suggesting that the loss of function of hnRNP K plays a key role in cell death of SCA10. These results suggest that the expanded AUUCU-repeat in the intronic RNA undergoes normal transcription and splicing, but causes apoptosis via an activation cascade involving a loss of hnRNP K activities, massive translocation of PKCdelta to mitochondria, and caspase 3 activation. Source


Jacobs D.,University of Texas Medical Branch
New England Journal of Medicine | Year: 2014

An otherwise healthy 50-year-old woman presents with painless rectal bleeding; she occasionally sees small amounts of red blood on the toilet paper immediately after defecation and in the toilet water. She also has constipation and intermittent perianal itching with a sense of swelling and aching discomfort around the anal orifice. How should her case be evaluated and managed? Copyright © 2014 Massachusetts Medical Society. Source


Kayed R.,University of Texas Medical Branch
Acta neuropathologica communications | Year: 2014

BACKGROUND: Progressive supranuclear palsy (PSP) is a neurodegenerative tauopathy which is primarily defined by the deposition of tau into globose-type neurofibrillary tangles (NFT). Tau in its native form has important functions for microtubule dynamics. Tau undergoes alternative splicing in exons 2, 3, and 10 which results in six different isoforms. Products of splicing on exon 10 are the most prone to mutations. Three repeat (3R) and four repeat (4R) tau, like other disease-associated amyloids, can form oligomers which may then go on to further aggregate and form fibrils. Recent studies from our laboratory and others have provided evidence that tau oligomers, not NFTs, are the most toxic species in neurodegenerative tauopathies and seed the pathological spread of tau.RESULTS: Analysis of PSP brain sections revealed globose-type NFTs, as well as both phosphorylated and unphosphorylated tau oligomers. Analysis of PSP brains via Western blot and ELISA revealed the presence of increased levels of tau oligomers compared to age-matched control brains. Oligomers were immunoprecipitated from PSP brain and were capable of seeding the oligomerization of both 3R and 4R tau isoforms.CONCLUSIONS: This is the first time tau oligomers have been characterized in PSP. These results indicate that tau oligomers are an important component of PSP pathology, along with NFTs. The ability of PSP brain-derived tau oligomers to seed 3R and 4R tau suggests that these oligomers represent the pathological species responsible for disease propagation and the presence of oligomers in a pure neurodegenerative tauopathy implies a common neuropathological process for tau seen in diseases with other amyloid proteins. Source


Brasier A.R.,University of Texas Medical Branch
Cardiovascular Research | Year: 2010

Vascular inflammation is a common pathophysiological response to diverse cardiovascular disease processes, including atherosclerosis, myocardial infarction, congestive heart failure, and aortic aneurysms/dissection. Inflammation is an ordered process initiated by vascular injury that produces enhanced leucocyte adherence, chemotaxis, and finally activation in situ. This process is coordinated by local secretion of adhesion molecules, chemotactic factors, and cytokines whose expression is the result of vascular injury-induced signal transduction networks. A wide variety of mediators of the vascular injury response have been identified; these factors include vasoactive peptides (angiotensin II, Ang II), CD40 ligands, oxidized cholesterol, and advanced glycation end-products. Downstream, the nuclear factor-B (NF-B) transcription factor performs an important signal integration step, responding to mediators of vascular injury in a stimulus-dependent and cell type-specific manner. The ultimate consequence of NF-B signalling is the activation of inflammatory genes including adhesion molecules and chemotaxins. However, clinically, the hallmark of vascular NF-B activation is the production of interleukin-6 (IL-6), whose local role in vascular inflammation is relatively unknown. The recent elucidation for the role of the IL-6 signalling pathway in Ang II-induced vascular inflammation as one that controls monocyte activation as well as its diverse signalling mechanism will be reviewed. These new discoveries further our understanding for the important role of the NF-B-IL-6 signalling pathway in the process of vascular inflammation. © The Author 2009. For permissions please. Source

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