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Galveston, TX, United States

Bowick G.C.,Institute for Human Infections and Immunity | Bowick G.C.,University of Texas Medical Branch | Airo A.M.,Public Health Agency of Canada | Bente D.A.,Institute for Human Infections and Immunity | And 2 more authors.
Virology Journal | Year: 2012

Background: Crimean Congo hemorrhagic fever (CCHF) is a tick-borne hemorrhagic zoonosis associated with high mortality. Pathogenesis studies and the development of vaccines and antivirals against CCHF have been severely hampered by the lack of suitable animal model. We recently developed and characterized a mature mouse model for CCHF using mice carrying STAT1 knockout (KO). Findings. Given the importance of interferons in controlling viral infections, we investigated the expression of interferon pathway-associated genes in KO and wild-type (WT) mice challenged with CCHF virus. We expected that the absence of the STAT1 protein would result in minimal expression of IFN-related genes. Surprisingly, the KO mice showed high levels of IFN-stimulated gene expression, beginning on day 2 post-infection, while in WT mice challenged with virus the same genes were expressed at similar levels on day 1. Conclusions: We conclude that CCHF virus induces similar type I IFN responses in STAT1 KO and WT mice, but the delayed response in the KO mice permits rapid viral dissemination and fatal illness. © 2012 Bowick et al.; licensee BioMed Central Ltd.

Panchbhavi V.K.,University of Texas Medical Branch | Panchbhavi V.K.,301 University Boulevard
Journal of Orthopaedic Trauma | Year: 2012

The reduction and stabilization of diastases between the medial cuneiform and the base of second metatarsal after a Lisfranc ligament injury is a crucial objective in the open reduction and internal fixation of these injuries. To achieve this objective, a single screw is used. The present practice is to insert the screw directed from the medial cuneiform bone into the base of the second metatarsal. This technique trick describes an easier method of insertion of the screw and one that possibly provides a better fixation. Copyright © 2012 by Lippincott Williams & Wilkins.

Cushing C.A.,University of Texas Medical Branch | Phillips L.G.,301 University Boulevard
Plastic and Reconstructive Surgery | Year: 2013

LEARNING OBJECTIVES: After studying this article, the participant should be able to: 1. Cite risk factors for pressure sore development. 2. Detail the pathophysiology of pressure sores. 3. List the types and classification of pressure sores. 4. Consider the various nonsurgical conservative wound management strategies. 5. Describe the appropriate surgical interventions for each pressure sore type. 6. Understand the causes of recurrent pressure sores and methods of avoiding recurrence. SUMMARY: Pressure sores are the result of unrelieved pressure, usually over a bony prominence. With an estimated 2.5 million pressure ulcers treated annually in the United States at a cost of $11 billion, pressure sores represent a costly and labor-intensive challenge to the health care system. A comprehensive team approach can address both prevention and treatment of these recalcitrant wounds. Consideration must be given to the patient's medical and socioeconomic condition, as these factors are significantly related to outcomes. Mechanical prophylaxis, nutritional optimization, treatment of underlying infection, and spasm control are essential in management. A variety of pressure sore patterns exist, with surgical approaches directed to maximize future coverage options. A comprehensive approach is detailed in this article to provide the reader with the range of treatment options available. Copyright © 2013 by the American Society of Plastic Surgeons.

Eberth J.M.,University of South Carolina | Qiu R.,University of South Carolina | Adams S.A.,University of South Carolina | Salloum R.G.,University of South Carolina | And 4 more authors.
Lung Cancer | Year: 2014

Objectives: Although the National Lung Screening Trial (NLST) lauds the efficacy of low-dose computed tomography (LDCT) at reducing lung cancer mortality, it has not been widely used for population-based screening. By examining the availability of U.S. LDCT screening centers, and underlying rates of lung cancer incidence, mortality, and smoking prevalence, the need for additional centers may be determined. Materials and methods: Locations of 203 LDCT screening centers from the Lung Cancer Alliance Screening Centers of Excellence database, a list of active NLST and International Early Lung and Cardiac Action Program (I-ELCAP) screening centers, and an independently conducted survey of Society of Thoracic Radiology members were geocoded and mapped. County-level rates of lung cancer incidence, mortality, and smoking prevalence were also mapped and overlaid with the locations of the 203 LDCT screening centers. Results and conclusions: Results showed the majority of LDCT screening centers were located in the counties with the highest quartiles of lung cancer incidence and mortality in the Northeast and East North Central states, but several high-risk states had no or few identified screening centers including Oklahoma, Nevada, Mississippi, and Arkansas. As guidelines are implemented and reimbursement for LDCT screening follows, equitable access to LDCT screening centers will become increasingly important, particularly in regions with high rates of lung cancer incidence and smoking prevalence. © 2014 Elsevier Ireland Ltd.

Green T.A.,Center for Addiction Research | Labate D.,University of Houston | Laezza F.,Center for Addiction Research | Laezza F.,Center for Biomedical Engineering | And 2 more authors.
Biochimica et Biophysica Acta - General Subjects | Year: 2015

Background Phosphorylation plays an essential role in regulating voltage-gated sodium (Nav) channels and excitability. Yet, a surprisingly limited number of kinases have been identified as regulators of Nav channels. We posited that glycogen synthase kinase 3 (GSK3), a critical kinase found associated with numerous brain disorders, might directly regulate neuronal Nav channels. Methods We used patch-clamp electrophysiology to record sodium currents from Nav1.2 channels stably expressed in HEK-293 cells. mRNA and protein levels were quantified with RT-PCR, Western blot, or confocal microscopy, and in vitro phosphorylation and mass spectrometry to identify phosphorylated residues. Results We found that exposure of cells to GSK3 inhibitor XIII significantly potentiates the peak current density of Nav1.2, a phenotype reproduced by silencing GSK3 with siRNA. Contrarily, overexpression of GSK3β suppressed Nav1.2-encoded currents. Neither mRNA nor total protein expression was changed upon GSK3 inhibition. Cell surface labeling of CD4-chimeric constructs expressing intracellular domains of the Nav1.2 channel indicates that cell surface expression of CD4-Nav1.2 C-tail was up-regulated upon pharmacological inhibition of GSK3, resulting in an increase of surface puncta at the plasma membrane. Finally, using in vitro phosphorylation in combination with high resolution mass spectrometry, we further demonstrate that GSK3β phosphorylates T1966 at the C-terminal tail of Nav1.2. Conclusion These findings provide evidence for a new mechanism by which GSK3 modulates Nav channel function via its C-terminal tail. General significance These findings provide fundamental knowledge in understanding signaling dysfunction common in several neuropsychiatric disorders. © 2015 Published by Elsevier B.V.

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