Faculty Recital, Sonia Vlahcevic, piano

With Gamelan Raga Kusama Justin Alexande

Faculty Recital, Sonia Vlahcevic, piano

Faculty Recital Sonia Vlahcevic, piano with special guest Greg Giannascoli, marimba Sunday, October 10, 2021, 4:00 p.m. Sonia Vlahcevic Concert Hall 922 Park Avenue Richmond, VA 2328

Piano Area Recital

Studio of Dr. Vlahcevic and Dr. Zhen

Piano Area Showcase

Piano Area Showcase November 16, 2021 5:30 p.m. Students of Dr. Sonia Vlahcevic, Dr. Yin Zheng, Dr. Magdalena Adamek Recital Hall I James W. Black Music Center 1015 Grove Avenue I Richmond, Virgini

Faculty Recital, Sonia Vlahcevic, piano

With Gamelan Raga Kusama Justin Alexande

Pathogenesis of Hepatic Encephalopathy

Severe parenchymatous diseases of the liver, both acute and chronic, are frequently associated with hepatic encephalopathy. This term is preferable to that of hepatic coma, as it encompasses the whole spectrum of changes from bizarre alterations of behavior to various degrees of disturbance of consciousness, as well as protean neurologic manifestations. In many instances it is a reversible phenomenon, occurring either spontaneously or as the result of various therapeutic agents. The puzzling feature of hepatic encephalopathy is the discrepancy between dramatic clinical features and paucity of histopathological changes in the brain. The only histological changes encountered with regularity in patients with this entity are diffusely swollen and enlarged astrocytes (Adams and Foley, 1953). With no macroscopic or microscopic changes to account for cerebral dysfunction, it is likely that hepatic encephalopathy is caused by profound, yet undefined metabolic abnormalities

Faculty Showcase

Faculty Showcas

Resistance to ursodeoxycholic acid-induced growth arrest can also result in resistance to deoxycholic acid-induced apoptosis and increased tumorgenicity

BACKGROUND: There is a large body of evidence which suggests that bile acids increase the risk of colon cancer and act as tumor promoters, however, the mechanism(s) of bile acids mediated tumorigenesis is not clear. Previously we showed that deoxycholic acid (DCA), a tumorogenic bile acid, and ursodeoxycholic acid (UDCA), a putative chemopreventive agent, exhibited distinct biological effects, yet appeared to act on some of the same signaling molecules. The present study was carried out to determine whether there is overlap in signaling pathways activated by tumorogenic bile acid DCA and chemopreventive bile acid UDCA. METHODS: To determine whether there was an overlap in activation of signaling pathways by DCA and UDCA, we mutagenized HCT116 cells and then isolated cell lines resistant to UDCA induced growth arrest. These lines were then tested for their response to DCA induced apoptosis. RESULTS: We found that a majority of the cell lines resistant to UDCA-induced growth arrest were also resistant to DCA-induced apoptosis, implying an overlap in DCA and UDCA mediated signaling. Moreover, the cell lines which were the most resistant to DCA-induced apoptosis also exhibited a greater capacity for anchorage independent growth. CONCLUSION: We conclude that UDCA and DCA have overlapping signaling activities and that disregulation of these pathways can lead to a more advanced neoplastic phenotype

Influence of Neonatal Hypothyroidism on Hepatic Gene Expression and Lipid Metabolism in Adulthood

Thyroid hormones are required for normal growth and development in mammals. Congenital-neonatal hypothyroidism (CH) has a profound impact on physiology, but its specific influence in liver is less understood. Here, we studied how CH influences the liver gene expression program in adulthood. Pregnant rats were given the antithyroid drug methimazole (MMI) from GD12 until PND30 to induce CH in male offspring. Growth defects due to CH were evident as reductions in body weight and tail length from the second week of life. Once the MMI treatment was discontinued, the feed efficiency increased in CH, and this was accompanied by significant catch-up growth. On PND80, significant reductions in body mass, tail length, and circulating IGF-I levels remained in CH rats. Conversely, the mRNA levels of known GH target genes were significantly upregulated. The serum levels of thyroid hormones, cholesterol, and triglycerides showed no significant differences. In contrast, CH rats showed significant changes in the expression of hepatic genes involved in lipid metabolism, including an increased transcription of PPARα and a reduced expression of genes involved in fatty acid and cholesterol uptake, cellular sterol efflux, triglyceride assembly, bile acid synthesis, and lipogenesis. These changes were associated with a decrease of intrahepatic lipids. Finally, CH rats responded to the onset of hypothyroidism in adulthood with a reduction of serum fatty acids and hepatic cholesteryl esters and to T3 replacement with an enhanced activation of malic enzyme. In summary, we provide in vivo evidence that neonatal hypothyroidism influences the hepatic transcriptional program and tissue sensitivity to hormone treatment in adulthood. This highlights the critical role that a euthyroid state during development plays on normal liver physiology in adulthood