Pseudo-Meigs' syndrome secondary to breast cancer with ovarian metastasis: a case report and literature review.

Ovarian metastasis of breast cancer with pseudo-Meigs' syndrome (PMS) is extremely rare. Only four cases of PMS secondary to breast cancer with ovarian metastasis have been reported to date. In this report, we present the fifth case of PMS caused by ovarian metastasis of breast cancer. On the 2nd of July 2019, a 53-year-old woman presented to our hospital with complaints of abdominal distension, irregular vaginal bleeding, and chest distress. Color Doppler ultrasound examination revealed a mass approximately 109×89 mm in size in the right adnexal area, accompanied by multiple uterine fibroids and a large amount of pelvic and peritoneal effusions. The patient had no common symptoms and showed no signs of breast cancer. The main manifestations were a right ovarian mass, massive hydrothorax, and ascites. Lab workup and imaging revealed raised CA125 (cancer antigen 125) levels and multiple bone metastases. At first the patient was misdiagnosed with ovarian carcinoma. After the rapid disappearance of oophorectomy hydrothorax and ascites, and decreased CA125 levels, from 1,831.8u/ml to normal range. According to the pathology report, breast cancer was finally diagnosed. The patient underwent endocrine therapy (Fulvestrant) and azole treatment after oophorectomy. At the 40-month follow-up, the patient was still alive and doing well.

Hippocampal FXR plays a role in the pathogenesis of depression: A preliminary study based on lentiviral gene modulation.

As a well-known bile acid receptor, the role of Farnesoid X receptor (FXR) in the digestive system and cardiovascular system has been widely explored. However, there are very few studies involving FXR in the central nervous system. In this study, we explored the role of FXR in the pathogenesis of depression, a serious and worldwide neuropsychiatric disease. It was found that chronic unpredictable mild stress (CUMS) fully enhanced the protein and mRNA expressions of FXR in hippocampus, but not medial prefrontal cortex (mPFC). Overexpression of hippocampal FXR induced notable depressive-like behaviors and decreased expression of brain-derived neurotrophic factor (BDNF) in naïve rats, while knockdown of hippocampal FXR fully prevented the effects of CUMS on rat behaviors and hippocampal BDNF expression. Taken together, our research extends the knowledge of FXR's role in the central nervous system, and may provide a potential and novel therapeutic target for treating depression.

Nitidine chloride inhibits hepatocellular carcinoma cell growth in vivo through the suppression of the JAK1/STAT3 signaling pathway.

Signal transducer and activator of transcription 3 (STAT3) is persistently activated in cancer cells and contributes to malignant progression in various types of cancer. The Janus-activated kinase (JAK) family phosphorylates STAT3 in response to stimulation by cytokines or growth factors. The JAK1-STAT3 signaling pathway plays an important role in cell proliferation and apoptosis. Nitidine chloride (NC) is a benzophenanthridine alkaloid that has been reported as an antitumor agent due to its its inhibitory effects on topoisomerase I. Using a mouse xenograft model of hepatocellular carcinoma (HCC), this study aimed to evaluate the effects of NC on tumor growth in vivo and to elucidate the underlying mechanisms. The analysis of the effects of NC on apoptosis in HCC tumor xenografts in mice was carried out by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay; the expression of Bcl-2, Bax, cyclin-dependent kinase (CDK)4, cyclin D1, p21 and proliferating cell nuclear antigen (PCNA) was analyzed by immunohistochemistry; and the protein expression of JAK1 and STAT3 was examined by western blot analysis. Our results revealed that treatment with NC decreased the tumor volume and tumor weight, suggesting that NC inhibits HCC cell growth in vivo. In addition, NC blocked the activation of JAK1-STAT3 in the tumor tissues, which in turn resulted in the induction of cancer cell apoptosis and the inhibition of proliferation. Consequently, treatment with NC downregulated the expression of cyclin D1, CDK4 and Bcl-2 and increased the level of p21 and Bax. Our data provide a molecular basis for the antitumor activity of NC.