Correlation between anti-Mullerian hormone levels and antral follicle counts in polycystic ovary and metabolic syndromes.

Anti-Mullerian hormone (AMH) is expressed by the granulosa cells of the pre-antral and small antral follicles in the ovary. AMH serum levels are significantly higher in women with polycystic ovary syndrome (PCOS) due to an increased antral follicle counts (AFC) and a higher production of AMH per antral follicle. This research is a cohort study design with a sample size of 60 female patients with (n = 30) and without PCOS (n = 30) in which the relationship between AMH serum level and other hormonal markers was explored. The following measurements were taken from the patients on the fifth day of the menstrual cycle: AMH, glucose, index of insulin resistance (HOMA/IR), body mass index (BMI), testosterone and cholesterol, lipoproteins, and triglycerides. The study proposes diagnostic criteria for PCOS. A twofold increase in the AMH serum levels was observed in the PCOS group when compared to the control group. The following incremental increases were seen in AMH serum levels: testosterone (18.4%); fasting blood glucose (18%); fasting insulin (83.86%); HOMA/IR (64.23%); mean cholesterol (30%); mean triglycerides (17%); and BMI (26.75%). All differences were considered significant at p ˂ 0.005. The results from the study concluded that monitoring the level of AMH allows for the prediction of ovarian hyperstimulation syndrome (OHSS) during ovulation induction and assisted reproductive technology cycles. Monitoring of anti-Mullerian hormone levels may provide an additional marker for determining treatment strategies when presented with additional risks associated with overweight, hirsutism, type II diabetes, infertility, and cardiovascular disease.

[Effects of alpha-fetoprotein on the expression of TRAIL death receptor-2 and its role on resisting the cytotoxicity of TRAIL in hepatoma cells].

OBJECTIVE: To explore the mechanism of Alpha-fetoprotein (AFP) effects on hepatocellular carcinoma cells (HCC) resistances apoptosis induced by tumor necrosis factor-related apoptosis inducing-ligand (TRAIL). METHODS: The expressed alteration of TRAIL receptor-2 (DR5) after the human hepatoma cells line Bel 7402 (AFP-producing) and HLE cells (non-AFP producing) were treated with all trans retinoic acid (ATRA) were determined by Western blot; Interaction of AFP with RAR-beta was analyzed by co-immunoprecipitation (Co-IP); Laser confocal microscopy was used to observe co-localization of AFP and RAR-beta; Short small RNA interfering (RNAi) was applied to knock down the expression of AFP in Bel 7402 cells; The full AFP gene cDNA was inserted into pcDNA3.1 vector and constructed the expressed vector of AFP (named pcDNA3.1-afp); The growth of hepatoma cells was analyzed by MTT. RESULTS: Bel 7402 and HLE cells expressed DR5, lowed dosage of ATRA (40mumol/L) had no influence on the expression of DR5 in Bel 7402 cells, but ATRA (160mumol/L) could inhibit the expression of AFP and promote the expression of DR5 significantly; Co-IP indicated that AFP had a property for interacting with RAR-beta; The results also demonstrated AFP co-localization with RAR-beta in cytoplasm of Bel 7202 cells; The expression of DR5 was enhanced while the expression of AFP was knocked down by RNAi. pcDNA3.1-afp vector was transfected into HLE cells, the growth of HLE cells were stimulated and TRAIL cytotoxicity of HLE cells were reduced. But when the expression of AFP was knocked down the sensitivity of Bel 7402 cells to TRAIL was enhanced. CONCLUSIONS: These data provided that AFP had a capability to interact with RAR-beta and suppressed the expression of DR5. AFP could play pivotal role on hepatoma cells resistance-induced apoptosis by TRAIL.