[Role of glycogen synthase kinase-3ß in development of severe hepatitis liver failure caused by hepatitis B virus].

OBJECTIVE: To investigate the role of glycogen synthase kinase-3ß (GSK3ß) in the development of severe hepatitis liver failure (SHLF) caused by the hepatitis B virus. METHODS: Twelve patients with chronic hepatitis B (CHB) (CHB group), 12 patients with SHLF caused by hepatitis B virus (SHLF group), and 8 normal subjects (control group), who were admitted to Beijing You'an Hospital from January 2009 to December 2011, were included in this study. Their liver tissues were collected to do some clinical examinations. The GSK3ß activity in the liver tissue was detected with a GSK3ß activity assay kit. Western blot was used to determine the expression of p-GSK3, total GSK3, and -actin. The paraffin sections of liver tissue were prepared for immunofluorescence assay. All data were expressed as mean±standard deviation, and comparison between groups was made by least significant difference t test. P < 0.05 was considered statistically significant. RESULTS: Western blot results showed that compared with the control group, the CHB group had a higher level of p-GSK3ß and the SHLF group had a significantly lower level of p-GSK3ß (P = 0.0342). The immunofluorescence assay results showed that the SHLF group had a significantly lower level of p-GSK3ß than the control group. GSK3ß activity assay results showed that compared with the control group, the CHB group had a significantly lower GSK3ß activity and the SHLF group had a significantly higher GSK3ß activity (P = 0.0289), which were consistent with the results of Western blot and immunofluorescence assay. CONCLUSION: GSK3 is activated in the development of SHLF, so it is an important signaling molecule in the pathogenesis of SHLF. Inhibiting its activity may play a role in the prevention and treatment of SHLF.

Formation of the male-specific muscle in female Drosophila by ectopic fruitless expression.

The Drosophila fruitless (fru) gene product Fru has been postulated to be a neural sex-determination factor that directs the development of at least two male-specific characteristics, namely courtship behaviour and formation of the muscle of Lawrence (MOL). The fru gene encodes a putative transcription factor with a BTB domain and two zinc-finger motifs, and with consensus Tra-binding sequences. The binding of Tra to these sequences results in sex-specific alternative splicing of the fru mRNA, leading to production of the 'male-type' or 'female-type' Fru protein. We show here that the Fru protein is not detected in the female central nervous system (CNS), despite the similar level of expression of fru mRNA in both male and female CNS. As ectopic expression of both the 'male-type' (with the sequence for the amino-terminal extension) and 'female-type' (without the sequence for the amino-terminal extension) fru cDNA can induce formation of the MOL in females, the presence or absence of the Fru protein, and not its sex-specific structure, seems to be responsible for the sexually dimorphic actions of the fru gene.