LRH-1/hBlF and HNFl synergistically up-regulate hepatitis B virus gene transcription and DNA replication

Enhancer Ⅱ (ENⅡ) is one of the critical crs-elements in the Hepatitis B Virus (HBV) genome for the hepatic viral gene transcription and DNA replication. The liver-specific activity of ENII is regulated by multiple liver-enriched transcription factors, including LRH-1/hBlF, HNF1, HNF3β, HNF4 and C/EBP. Knowledge on the interplay of these important factors is still limited. In this study, we demonstrate a functional synergism between the orphan nuclear receptor LRH-1/hBlF and the homeoprotein HNF1 in up-regulating the liver-specific activity of ENII. This synergism is sufficient for initiating the viral gene transcription and DNA replication in non-hepatic cells. We have defined the activation domains in hB1F and HNF1 that contribute to the synergism. We further show that hB1F and HNF1 can interact directly in vitro and have mapped the domains required for this interaction.

Loss of heterozygosity on chromosome 10q22-10q23 and 22q 11.2-22q 12.1 and p53gene in primary hepatocellular carcinoma

AIM: To analyze loss of heterozygosity (LOH) and homozygous deletion on p53 gene (exon2-3, 4 and 11), chromosome 10q22-10q23 and 22q11.2 -22q12.1 in human hepatocellular carcinoma (HCC).METHODS: PCR and PCR-based microsatellite polymorphism analysis techniques were used.RESULTS: LOH was observed at D10S579 (10q22-10q23) in 4 of 20 tumors (20%), at D22S421 (22q11.2-22q12.1) in 3 of 20(15%), at TP53.A (p53gene exon 2-3) in 4 of 20 (20%), at TP53.B (p53gene exon 4) in 6 of 20(30%), and at TP53.G (p53gene exon 11)in 0 of 20(0%). Homozygous deletion was detected at 10q22-10q23(8/20; 40%), 22q11.2-22q12.1(8/20; 40%), p53 gene exon 2-3(0/20;0%), p53gene exon 4(6/20; 30%), and p53gene exon 11(2/20; 10%).CONCLUSION: There might be unidentified tumor suppressor genes on chromosome 10q22-10q23 and 22q11.2-22q12.1 that contribute to the pathogenesis and development of HCC.

Distribution and expression of non-muscle myosin light chain kinase in rabbit livers

AIM: To study the distribution and expression of non-muscle myosin light chain kinase (nmMLCK) in rabbit livers.METHODS: Human nmMLCK N-terminal cDNA was amplified by polymerase chain reaction (PCR) and was inserted into pBKcmv to construct expression vectors. The recombinant plasmid was transformed into XL1-blue. Expression protein was induced by IPTG and then purified by SDS-PAGE and electroelution, which was used to prepare the polycolonal antibody to detect the distribution and expression of nmMLCK in rabbit livers with immunofluorescene techniques.RESULTS: The polyclonal antibody was prepared, by which nmMLCK expression was detected and distributed mainly in peripheral hepatocytes.CONCLUSION: nmMLCK can express in hepatocytes peripherally, and may play certain roles in the regulation of hepatic functions.

Power Utility Maximization in an Exponential Levy Model Without a Risk-free Asset

We consider the problem of maximizing the expected power utility fromterminal wealth in a market where logarithmic securities prices follow a Lévy process. By Girsanovstheorem, we give explicit solutions for power utility of undiscounted terminal wealth in terms ofthe Lévy-Khintchine triplet.