Effects of Guizhi and Erxian Decoction on menopausal hot flashes: insights from the gut microbiome and metabolic profiles.

AIMS: To examine the influence of GED on the gut microbiota and metabolites using a bilateral ovariectomized (OVX) rat model. We tried to elucidate the underlying mechanisms of GED in the treatment of menopausal hot flashes. METHODS AND RESULTS: 16S rRNA sequencing, metabonomics, molecular biological analysis, and fecal microbiota transplantation (FMT) were conducted to elucidate the mechanisms by which GED regulates the gut microbiota. GED significantly reduced OVX-induced hot flashes and improved disturbances in the gut microbiota metabolites. Moreover, FMT validated that the gut microbiota can trigger hot flashes, while GED can alleviate hot flash symptoms by modulating the composition of the gut microbiota. Specifically, GED upregulated the abundance of Blautia, thereby increasing l(+)-ornithine levels for the treatment of menopausal hot flashes. Additionally, GED affected endothelial nitric oxide synthase and heat shock protein 70 (HSP70) levels in the hypothalamic preoptic area by changing the gut microbiota composition. CONCLUSIONS: Our study illuminated the underlying mechanisms by which GED attenuated the hot flashes through modulation of the gut microbiota and explored the regulatory role of the gut microbiota on HSP70 expression in the preoptic anterior hypothalamus, thereby establishing a foundation for further exploration of the role of the gut-brain axis in hot flashes.

Do In-Prison Correctional Programs Affect Postrelease Employment and Earnings?

The objective of this research is to examine the effects of general educational development (GED) attainment in prison and therapeutic community participation on postrelease employment and earnings. The participants are all males released from prisons in Idaho during 2004. The dependent variables are employment and mean quarterly earnings up to 57 months after release. Propensity score matching analysis was used to enhance the equivalence of the comparison groups, with a small percentage of overly influential observations trimmed. Logistic regression was used to examine the effects of programming on employment. GED had no effect on employment. The effect of therapeutic community approached significance. The statistical analyses on earnings used generalized linear models based on the gamma distribution due to the highly skewed distribution of this variable. These analyses found that GED had no effect on earnings and that participation in a therapeutic community had a highly significant effect on mean quarterly earnings.

XZ-1 regulates cell apoptosis of gastric epithelial dysplasia via NF-κB/p53/Ki67 signaling pathway.

We aimed to determine the effect of 'Xiaozeng No. 1' (XZ-1) on cellular apoptosis changes of gastric epithelial dysplasia (GED) and to explore the underlying mechanism. Specimens taken from the pyloric area of the stomachs from rats in each group were subjected to Hematoxylin and Eosin (H&E) staining for pathological examination, TUNEL staining for apoptosis detection, and Western blot analysis for apoptosis-related proteins. The results showed that XZ-1 decreased GED incidence and enhanced gastric epithelial apoptosis. Furthermore, XZ-1 up-regulated the proapoptotic proteins including cleaved caspases (cysteine-dependent aspartate-specific protease) (-3, -8, and -9), Fas, Bax, and Bid, and facilitated the release of cytochrome c from mitochondria to the cytoplasm. Interestingly, XZ-1 enhanced protein expression of NF-κB p65, Ki67, and p53. Moreover, inhibition of NF-κB pathway suppressed the XZ-induced p53 expression, whereas inhibition of NF-κB or p53 pathway suppressed the XZ-induced Ki67. More importantly, inhibition of NF-κB or p53 pathway attenuated the XZ-1-mediated induction of gastric epithelial apoptosis and decline of GED incidence. Collectively, our results demonstrated that XZ-1, almost equivalent effect exerted by the positive control Retin-A, dramatically decreased GED incidence and enhanced gastric epithelial apoptosis. Meanwhile, XZ-1 activated the NF-κB/p53/Ki67-apoptosis signaling pathway, which might be one of the mechanisms whereby XZ-1 reversed GED.