Texas Medical Center

About: Texas Medical Center is a healthcare organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 2845 authors who have published 2394 publications receiving 79426 citations.

Genomic segment reassortment in rotaviruses and other reoviridae.

Abstract: Publisher Summary The name reovirus was originally proposed by Sabin in 1959 to reclassify viruses designated as echovirus 10 because of their vastly different morphological and growth properties compared to other enteric cytopathogenic human orphan (ECHO) and related viruses. The name reo (respiratory, enteric, orphan) is an apt description for members of the genus Orthoreouirus, or simply reovirus, for whom the designation was first applied. These viruses infect the respiratory and intestinal tracts of humans and other vertebrate animals but have not been definitively shown to cause significant diseases after natural infection. The second group to be included among the Reoviridae were the orbiviruses, whose name is derived from the Latin word “orbis” for their ringlike appearance. These viruses were separated from other arboviruses and reclassified as Reoviridae in the early 1970s because of their morphological and physicochemical similarities to reoviruses.

The mitochondrial pyruvate carrier mediates high fat diet-induced increases in hepatic TCA cycle capacity.

Abstract: Objective Excessive hepatic gluconeogenesis is a defining feature of type 2 diabetes (T2D). Most gluconeogenic flux is routed through mitochondria. The mitochondrial pyruvate carrier (MPC) transports pyruvate from the cytosol into the mitochondrial matrix, thereby gating pyruvate-driven gluconeogenesis. Disruption of the hepatocyte MPC attenuates hyperglycemia in mice during high fat diet (HFD)-induced obesity but exerts minimal effects on glycemia in normal chow diet (NCD)-fed conditions. The goal of this investigation was to test whether hepatocyte MPC disruption provides sustained protection from hyperglycemia during long-term HFD and the differential effects of hepatocyte MPC disruption on TCA cycle metabolism in NCD versus HFD conditions. Method We utilized long-term high fat feeding, serial measurements of postabsorptive blood glucose and metabolomic profiling and 13C-lactate/13C-pyruvate tracing to investigate the contribution of the MPC to hyperglycemia and altered hepatic TCA cycle metabolism during HFD-induced obesity. Results Hepatocyte MPC disruption resulted in long-term attenuation of hyperglycemia induced by HFD. HFD increased hepatic mitochondrial pyruvate utilization and TCA cycle capacity in an MPC-dependent manner. Furthermore, MPC disruption decreased progression of fibrosis and levels of transcript markers of inflammation. Conclusions By contributing to chronic hyperglycemia, fibrosis, and TCA cycle expansion, the hepatocyte MPC is a key mediator of the pathophysiology induced in the HFD model of T2D.

Stimulation of Cellular Proliferation by Hepatitis B Virus X Protein

Abstract: Chronic infection with the hepatitis B virus (HBV) is a known risk factor in the development of human hepatocellular carcinoma (HCC). The HBV-encoded X protein, HBx, has been investigated for properties that may explain its cancer cofactor role in transgenic mouse lines. We discuss here recent data showing that HBx is able to induce hepatocellular proliferation in vitro and in vivo. This property of HBx is predicted to sensitize hepatocytes to other HCC cofactors, including exposure to carcinogens and to other hepatitis viruses. Cellular proliferation is intimately linked to the mechanism(s) by which most tumor-associated viruses transform virus-infected cells. The HBx alteration of the cell cycle provides an additional mechanism by which chronic HBV infection may contribute to HCC.