ObjectivesTo investigate the relationship between endogenous androgens and body fat distribution in early and late postmenopausal women.Materials and MethodsWe enrolled postmenopausal women consisting of an early group (≤5 years since menopause, n = 105) and a late group (≥10 years since menopause, n = 107). Each group was subdivided into normal weight (BMI <24 kg/m2) group, overweight and obese (BMI ≥24 kg/m2) group. Fasting total testosterone (T), dehydroepiandrosterone-sulfate (DHEA-S) and sex hormone-binding globulin (SHBG) levels were measured. Body fat distribution was evaluated by dual-energy X-ray absorptiometry (DEXA).ResultsLate postmenopausal women had a higher proportion of body fat than early postmenopausal women. The body fat of the overweight and obese women had a greater tendency to accumulate in the abdomen compared with the normal weight women both in early and late postmenopausal groups. The overweight and obese women had a higher free testosterone (FT) than the normal weight women in early postmenopausal women (P<0.05). In late postmenopausal women, the overweight and obese women had higher DHEA-S levels than normal weight women (P<0.05). No direct relationship was observed between the T levels and body fat distribution both in early and late postmenopausal groups (P>0.05).The FT in early postmenopausal women and the DHEA-S levels in late postmenopausal women correlated positively with the trunk/leg fat ratio (T/L) and the proportion of android fat whereas correlated negatively with the proportion of gynoid fat in the partial correlation and multiple linear regression analyses (all P<0.05).ConclusionsSerum T levels do not correlate directly with body fat distribution, the FT in early postmenopausal women and DHEA-S levels in late postmenopausal women correlate positively with abdominal fat accumulation.

We conclude that daidzein can improve insulin resistance induced by ovariectomy by decreasing weight gain, visceral fat accumulation, blood lipids, TNF-α, leptin and IL-6 levels.

Background: The deubiquitinating (DUB) enzyme ubiquitin-specific protease 18 (USP18), also known as UBP43, is an ubiquitin-specific protease linked to several human malignancies. However, USP18's underlying function in human cervical cancer remains unclear. In the current study, we aimed to analyse the role of USP18 and its signalling pathways in cervical cancer. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical staining were performed to analyse USP18 levels in cervical cancer and matched to adjacent normal tissues. Moreover, RNA interference (RNAi) and lentiviral-mediated vector transfections were performed to silence and overexpress USP18, respectively, in cervical cancer cells. Further, Cell Counting Kit-8 (CCK-8) and Annexin V/PI staining assays were used to assess its biological function in cell proliferation and apoptosis, respectively. A xenograft model was used to examine USP18's function in vivo. Results: The present findings demonstrated that USP18 was overexpressed in cervical cancer specimens and cell lines. Silencing USP18 in SiHa and Caski cervical cancer cell lines inhibited cell proliferation, induced apoptosis, and promoted cleaved caspase-3 expression. In contrast, USP18 overexpression showed the opposite effects in human HcerEpic cells. A Gene Set Enrichment Analysis revealed that USP18 was enriched in the PI3K/AKT signalling pathway in cervical cancer. Hence, the PI3K/AKT inhibitor LY294002 was used to determine the relationship between USP18 and AKT in cervical cancer cells. Importantly, LY294002 significantly abolished the effects of USP18 overexpression in cervical cancer cells. In vivo, USP18 silencing inhibited human cervical cancer cells' tumorigenicity. Conclusions: The current study indicates that USP18 is an oncogenic gene in cervical cancer. Our findings not only deepened the understanding of USP18's biological function in cervical cancer pathogenesis, but we also provided novel insight for cervical cancer therapy. Trial registration: Retrospectively registered.

Objective: The aim of the study was to investigate the effectiveness and safety of a new, improved herbal formula of a traditional Chinese medicine, improved Gengnianchun (I-GNC), on hot flushes, depression, anxiety, and sleep in peri- and postmenopausal women in China. Methods: A randomized, single-blind, placebo-controlled trial of peri- and postmenopausal women with Kupperman Index (KMI) scores of 15 or higher was conducted for 12 weeks. Hot flush frequencies, KMI scores, Hamilton depression scale scores, Hamilton anxiety scale scores, and Pittsburgh Sleep Quality Index scores were evaluated. Each outcome was evaluated every 4 weeks. Results: Ninety-eight participants completed the study. The I-GNC formula significantly reduced the mean (SD) frequency of hot flushes from 7 (4.554) to 1.2 (1.675) in the I-GNC group and from 6.74 (3.43) to 3.66 (2.635) in the placebo group (P < 0.01). The KMI (P < 0.01), Hamilton depression scale (P < 0.01), and Hamilton anxiety scale (P < 0.01) scores decreased in both groups after treatment, and significant differences were observed between the two groups (P < 0.01); however, no significant difference in the Pittsburgh Sleep Quality Index score was observed. I-GNC had no effect on serum follicle-stimulating hormone or E2 levels. There were no obvious adverse effects. Conclusions: The traditional Chinese medicine herbal formula I-GNC can alleviate the symptoms of menopausal syndrome and improve quality of life among peri- and postmenopausal women. I-GNC is safe and has no notable adverse effects.

Tripartite motif-containing (TriM) 14 is a protein of the TriM family. Studies have indicated that TriM14 may be used as an oncogene in tumor cells, such as osteosarcoma, non-small cell lung cancer and breast cancer through different pathways. However, the functions of TriM14 in cervical cancer cells remain unclear. Therefore, this study aimed to investigate the functions of TriM14 in cervical cancer cells and its underlying mechanism. caski cells stably expressing TriM14 and SiHa, and Hela cells stably expressing TriM14 short hairpin rna were constructed by lentivirus-mediated overexpression or knockdown systems. The effects of TriM14 on proliferation and apoptosis of cervical cancer cells were detected by cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. in addition, reverse transcription-quantitative (rT-q) Pcr and western blotting were used to investigate the expression levels of TriM14 and of signaling pathway marker protein including P21, caspase-3, cleaved caspase-3, akt and phosphorylated akt. The results of rT-qPcr and western blotting revealed that TriM14 was highly expressed in human cervical cancer tissues and cell lines compared with adjacent normal tissues and normal cervical epithelial cells. TriM14 also regulated cell proliferation and apoptosis of human SiHa, Hela and caski cervical cancer cell lines through the akt signaling pathway. additionally, TriM14 protein levels were related to the clinical and pathological features of cervical cancer. CCK-8 assay and flow cytometry demonstrated that TRIM14 expression could promote cervical cancer cell proliferation and autophagy suppression. Taken together, TriM14-induced cell proliferation and apoptosis inhibition may by evoked by the activation of the akt pathway. This study demonstrated the role of TriM14 in cervical cancer, and reveals its mechanism of action as a potential therapeutic target for cervical cancer.