The University of Texas Health Science Center at Tyler is a health institution located in Tyler, Texas. Originally named "East Texas Tuberculosis Sanitarium", it was established in 1947 as a tuberculosis treatment facility at the location of Camp Fannin. The University of Texas System assumed management of the center in 1977.The center serves as both a hospital — caring for over 140,000 patients annually — and medical research facility.A Camp Fannin Memorial stands today on the campus. Wikipedia.
Turner R.J.,University of Texas Health Science Center at Tyler
Menopause | Year: 2017
OBJECTIVE:: The aim of the study was to propose a unifying theory for the role of estrogen in postmenopausal women through examples in basic science, randomized controlled trials, observational studies, and clinical practice. METHODS:: Review and evaluation of the literature relating to estrogen. DISCUSSION:: The role of hormone therapy and ubiquitous estrogen receptors after reproductive senescence gains insight from basic science models. Observational studies and individualized patient care in clinical practice may show outcomes that are not reproduced in randomized clinical trials. The understanding gained from the timing hypothesis for atherosclerosis, the critical window theory in neurosciences, randomized controlled trials, and numerous genomic and nongenomic actions of estrogen discovered in basic science provides new explanations to clinical challenges that practitioners face. Consequences of a hypo-estrogenemic duration in womenʼs lives are poorly understood. The Study of Women Across the Nation suggests its magnitude is greater than was previously acknowledged. We propose that the healthy user bias was the result of surgical treatment (hysterectomy with oophorectomy) for many gynecological maladies followed by pharmacological and physiological doses of estrogen to optimize patient quality of life. The past decade of research has begun to demonstrate the role of estrogen in homeostasis. CONCLUSIONS:: The theory of eu-estrogenemia provides a robust framework to unify the timing hypothesis, critical window theory, randomized controlled trials, the basic science of estrogen receptors, and clinical observations of patients over the past five decades.This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0 © 2017 by The North American Menopause Society.
Griffith D.E.,University of Texas Health Science Center at Tyler |
Aksamit T.R.,Rochester College
Current Opinion in Infectious Diseases | Year: 2012
PURPOSE OF REVIEW: The prevalence of nontuberculous mycobacterial (NTM) lung disease is increasing in the USA. Clinicians are therefore encountering these patients with increasing frequency, with the attendant multiple therapeutic challenges presented by NTM lung disease including relatively frequent (compared with tuberculosis) treatment failure. RECENT FINDINGS: Critical elements for the successful treatment of Mycobacterium avium complex (MAC) lung disease include aggressive first therapeutic attempts and avoidance of the emergence of macrolide-resistant MAC strains, which are associated with worse treatment response and increased mortality. Reliably effective therapy for M. abscessus lung disease remains elusive but still usually requires parenteral agents. Lung resection surgery for selected patients is an important adjunct for both MAC and M. abscessus lung disease. Aside from surgery and parenteral antibiotics, there are very few data to support the efficacy of other drugs or interventions for patients who have failed the first-line therapy. SUMMARY: Clinicians who manage NTM lung disease will inevitably encounter patients who fail the first-line therapy. The choices for effective treatment of these patients are depressingly sparse. It is critically important to avoid creation of macrolide-resistant MAC strains and to carefully choose those NTM lung disease patients who will benefit from surgery. © 2012 Lippincott Williams & Wilkins, Inc.
Nonnenmann M.W.,University of Texas Health Science Center at Tyler
Journal of occupational and environmental hygiene | Year: 2010
Work in animal production facilities often results in exposure to organic dusts. Previous studies have documented decreases in pulmonary function and lung inflammation among workers exposed to organic dust in the poultry industry. Bacteria and fungi have been reported as components of the organic dust produced in poultry facilities. To date, little is known about the diversity and concentration of bacteria and fungi inside poultry buildings. All previous investigations have utilized culture-based methods for analysis that identify only biota cultured on selected media. The bacterial tag-encoded flexible (FLX) amplicon pyrosequencing (bTEFAP) and fungal tag-encoded flexible (FLX) amplicon pyrosequencing (fTEFAP) are modern and comprehensive approaches for determining biodiversity of microorganisms and have not previously been used to provide characterization of exposure to microorganisms in an occupational environment. This article illustrates the potential application of this novel technique in occupational exposure assessment as well as other settings. An 8-hr area sample was collected using an Institute of Medicine inhalable sampler attached to a mannequin in a poultry confinement building. The sample was analyzed using bTEFAP and fTEFAP. Of the bacteria and fungi detected, 116 and 39 genera were identified, respectively. Among bacteria, Staphylococcus cohnii was present in the highest proportion (23%). The total inhalable bacteria concentration was estimated to be 7503 cells/m3. Among the fungi identified, Sagenomella sclerotialis was present in the highest proportion (37%). Aspergillus ochraceus and Penicillium janthinellum were also present in high proportions. The total inhalable fungi concentration was estimated to be 1810 cells/m3. These estimates are lower than what has been reported by others using standard epifluorescence microscope methods. However, no study has used non-culture-based techniques, such as bTEFAP and fTEFAP, to evaluate bacteria and fungi in the inhalable fraction of a bioaerosol in a broiler production environment. Furthermore, the impact of this bTEFAP and fTEFAP technology has yet to be realized by the scientific community dedicated to evaluating occupational and environmental bioaerosol exposure.
Allen T.C.,University of Texas Health Science Center at Tyler
Archives of Pathology and Laboratory Medicine | Year: 2010
Context.-The term small airways disease encompasses a generally poorly understood group of lung diseases that may arise primarily within the small airways or secondarily from diseases primarily affecting the bronchi or lung parenchyma. Their histology may be confusing; however, because treatments and prognoses vary, correct pathologic diagnosis is important. Objective.-To present a nonexhaustive review of the pathology of primary and secondary small airways diseases, including small airways disease related to tobacco; to various other exposures, including mineral dusts; to diseases involving other areas of the lung with secondary bronchiolar involvement; and to recently described bronchiolitic disorders. Data Sources.-Current literature is reviewed. Conclusions.-Small airways diseases include a wide variety of diseases of which the pathologist must consider. Uncommon conditions such as diffuse idiopathic neuroendocrine cell hyperplasia and diffuse panbronchiolitis may show relatively specific diagnostic features histologically; however, most small airways diseases exhibit nonspecific histologic features. Conditions not considered primary pulmonary diseases, such as collagen vascular diseases, bone marrow transplantation, and inflammatory bowel disease, must also be considered in patients with small airways changes histologically. Clinical and radiologic correlation is important for obtaining the best possible diagnosis.
Benwill J.L.,University of Texas Health Science Center at Tyler |
Wallace R.J.,University of Texas Health Science Center at Tyler
Current Opinion in Infectious Diseases | Year: 2014
Purpose of review Mycobacterium abscessus is the most common rapidly growing mycobacterium that causes lung disease. This review describes recently published literature regarding M. Abscessus taxonomy, environmental niche, diagnosis, management and outcome in pulmonary disease in adults and adolescents with cystic fibrosis. Recent findings The classification of M. Abscessus subsp. abscessus, M. Abscessus subsp. massiliense and M. Abscessus subsp. bolletii is useful clinically because of the discovery of the erm(41) gene, which is responsible for macrolide resistance in M. Abscessus. Macrolide susceptibility is key for successful treatment of M. Abscessus subsp. massiliense. The poor outcome and eradication of M. Abscessus subsp. abscessus remains both a diagnostic and treatment challenge in approximately 80% of isolates that are macrolide resistant. Molecular studies, such as genotyping, may allow prediction of disease progression. Overall, there is a dearth of new literature surrounding M. Abscessus. Summary New studies differentiating M. Abscessus subsp. abscessus and M. Abscessus subsp. massiliense based on the erm(41) gene demonstrate the latter to have a better prognosis and improved treatment outcomes. M. Abscessus subsp. abscessus remains a formidable pathogen in diagnosis and treatment. Copyright © 2014 Lippincott Williams & Wilkins.
Rao L.V.,University of Texas Health Science Center at Tyler
Frontiers in bioscience (Elite edition) | Year: 2012
It is generally believed that only a small fraction of the tissue factor (TF) found on cell surfaces is active whereas the vast majority is cryptic in coagulation. It is unclear how cryptic TF differs from the coagulant active TF or potential mechanisms involved in transformation of cryptic TF to the coagulant active form. Exposure of phosphatidylserine (PS) in response to various chemical or pathophysiological stimuli has been considered as the most potent inducer of TF decryption. In addition to PS, TF self-association and association with specialized membrane domains may also play a role in TF decryption. It has been suggested recently that protein disulfide isomerase regulates TF decryption through its oxidoreductase activity by targeting Cys186-Cys209 disulfide bond in TF extracellular domain or regulating the PS equilibrium at the plasma membrane. However, this hypothesis requires further validation to become an accepted mechanism. In this article, we critically review literature on TF encryption/decryption with specific emphasis on recently published data and provide our perspective on this subject.
Howard S.T.,University of Texas Health Science Center at Tyler
Tuberculosis | Year: 2013
Mycobacterium abscessus is an emerging cause of respiratory disease and soft tissue infections. Whole genome sequencing and other molecular approaches are enhancing our understanding of outbreaks, antibiotic resistance mechanisms, and virulence properties, and of the phylogeny of the M. abscessus complex. Infection models are providing further insights into factors such as colony phenotype that impact host-pathogen interactions. This paper reviews recent developments in our understanding of genetic variation in M. abscessus and the potential relevance for disease and treatment. © 2013 Elsevier Ltd.
Griffith D.E.,University of Texas Health Science Center at Tyler
Current Opinion in Infectious Diseases | Year: 2010
Purpose of Review: There is increasing awareness that nontuberculous mycobacteria (NTM) lung diseases are becoming more prevalent. Nontuberculous mycobacterial diseases could legitimately be seen as an emerging public-health threat. Recent Findings: Nontuberculous mycobacterial lung disease associated radiographically with nodules and bronchiectasis occurs primarily in women. These patients are associated with a specific morphotype, including low BMI, tall stature, scoliosis, pectus excavatum and mitral valve prolapse. The pathophysiologic link between these findings and the development of bronchiectasis and NTM disease remains unclear. As with tuberculosis, the tumor-necrosis factor alpha (TNF-alpha) blockers also predispose to NTM infection that can be severe. The most frustrating aspect of NTM therapy remains the generally poor correlation between in-vitro antibiotic susceptibility and in-vivo response to antimicrobials. A possible insight into this phenomenon is the recent discovery of an inducible macrolide resistance (erm) gene in Mycobacterium fortuitum and Mycobacterium abscessus. This gene can produce in-vivo resistance without resulting in a 'resistant' MIC for macrolides. Summary: The NTM pose an increasing problem for clinicians and are associated with significant obstacles that thwart successful treatment of NTM disease. Continued progress in the areas of disease pathogenesis and therapy will improve the outlook for these patients. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Rao L.V.M.,University of Texas Health Science Center at Tyler |
Esmon C.T.,Oklahoma Medical Research Foundation |
Pendurthi U.R.,University of Texas Health Science Center at Tyler
Blood | Year: 2014
Endothelial cell protein C receptor (EPCR) was first identified and isolated as a cellular receptor for protein C on endothelial cells. EPCR plays a crucial role in the protein C anticoagulant pathway by promoting protein C activation. In the last decade, EPCR has received wide attention after it was discovered to play a key role in mediating activated protein C (APC)-induced cytoprotective effects, including antiapoptotic, anti-inflammatory, and barrier stabilization. APC elicits cytoprotective signaling through activation of protease activated receptor-1 (PAR1). Understanding how EPCR-APC induces cytoprotective effects through activation of PAR1, whose activation by thrombin is known to induce a proinflammatory response, has become a major research focus in the field. Recent studies also discovered additional ligands for EPCR, which include factor VIIa, Plasmodium falciparum erythrocyte membrane protein, and a specific variant of the T-cell receptor. These observations open unsuspected new roles for EPCR in hemostasis, malaria pathogenesis, innate immunity, and cancer. Future research on these new discoveries will undoubtedly expand our understanding of the role of EPCR in normal physiology and disease, as well as provide novel insights into mechanisms for EPCR multifunctionality. Comprehensive understanding of EPCR may lead to development of novel therapeutic modalities in treating hemophilia, inflammation, cerebral malaria, and cancer. © 2014 by The American Society of Hematology.
Rao L.V.M.,University of Texas Health Science Center at Tyler |
Pendurthi U.R.,University of Texas Health Science Center at Tyler
Journal of Thrombosis and Haemostasis | Year: 2012
Tissue factor (TF) is a transmembrane glycoprotein and an essential component of the factor VIIa-TF enzymatic complex that triggers activation of the coagulation cascade. Formation of TF-FVIIa complexes on cell surfaces not only trigger the coagulation cascade but also transduce cell signaling via activation of protease-activated receptors. Tissue factor is expressed constitutively on cell surfaces of a variety of extravascular cell types, including fibroblasts and pericytes in and surrounding blood vessel walls and epithelial cells, but is generally absent on cells that come into contact with blood directly. However, TF expression could be induced in some blood cells, such as monocytes and endothelial cells, following an injury or pathological stimuli. Tissue factor is essential for hemostasis, but aberrant expression of TF leads to thrombosis. Therefore, a proper regulation of TF activity is critical for the maintenance of hemostatic balance and health in general. TF-FVIIa coagulant activity at the cell surface is influenced not only by TF protein expression levels but also independently by a variety of mechanisms, including alterations in membrane phospholipid composition and cholesterol content, thiol-dependent modifications of TF allosteric disulfide bonds, and other post-translational modifications of TF. In this article, we critically review the key literature on mechanisms by which TF coagulant activity is regulated at the cell surface in the absence of changes in TF protein levels with specific emphasis on recently published data and provide the authors' perspective on the subject. © 2012 International Society on Thrombosis and Haemostasis.