Longitudinal investigation of carriage rates and genotypes of toxigenic Clostridium difficile in hepatic cirrhosis patients.

Toxigenic Clostridium difficile (C. difficile) carriers represent an important source in the transmission of C. difficile infection (CDI) during hospitalisation, but its prevalence and mode in patients with hepatic cirrhosis are not well established. We investigated longitudinal changes in carriage rates and strain types of toxigenic C. difficile from admission to discharge among hepatic cirrhosis patients. Toxigenic C. difficile was detected in 104 (19.8%) of 526 hepatic cirrhosis patients on admission, and the carriage status changed in a portion of patients during hospitalisation. Approximately 56% (58/104) of patients lost the colonisation during their hospital stay. Among the remaining 48 patients who remained positive for toxigenic C. difficile, the numbers of patients who were positive at one, two, three and four isolations were 10 (55.6%), three (16.7%), two (11.1%) and three (16.7%), respectively. Twenty-eight patients retained a particular monophyletic strain at multiple isolations. The genotype most frequently identified was the same as that frequently identified in symptomatic CDI patients. A total of 25% (26/104) of patients were diagnosed with CDI during their hospital stay. Conclusions: Colonisation with toxigenic C. difficile strains occurs frequently in cirrhosis patients and is a risk factor for CDI.

The role of the SDF-1/ CXCR7 axis on the growth and invasion ability of endometrial cancer cells.

PURPOSE: Stroma-derived factor-1 (SDF-1) and its receptor C-X-C chemokine receptor-4 (CXCR4) are involved in human endometrial carcinoma (EC) progression. CXCR7 is another important receptor of SDF-1 and has a higher affinity with SDF-1 compared with that of CXCR4. This paper aims to study the effects of the SDF-1/CXCR7 axis on the growth and invasion ability of EC cells. METHODS: CXCR7 expression was evaluated by quantitative RT-PCR, immunohistochemistry, immunocytochemistry and Western blotting in EC cell lines and 30 cases of primary EC tissue from patients. EC cell line proliferation and migration were assessed following knockdown of CXCR7 by MTT and transwell assays. RESULTS: The results showed that CXCR7 was highly expressed at both mRNA and protein levels in the EC cells and tissue. siCXCR7 effectively silenced CXCR7 in Ishikawa and AN3CA cells. Treatment with 17ß-oestradiol (17ß-E2) significantly increased the levels of CXCR7 and SDF-1 in Con, siCon and siCXCR7 treated Ishikawa. siCXCR7 persistently inhibited CXCR7 expression, even in cells treated with 17ß-E2. Moreover, in vitro functional analyses, silencing CXCR7 resulted in decreased proliferation in Ishikawa and AN3CA cells. Treatment with 17ß-E2 and SDF-1 significantly promoted the growth and migration in siCon treated Ishikawa and AN3CA. Interestingly, in response to 17ß-E2 and SDF-1 stimulation, siCXCR7 continuously inhibited the growth and invasion of Ishikawa and AN3CA cells. CONCLUSION: Our results indicate that SDF-1/CXCR7 plays a positive role in the proliferation and invasion of EC cells. CXCR7 inhibition treatment may provide a promising strategy for anti-tumour therapy for EC.

B Lymphocytes Are Predictors of Insulin Resistance in Women with Gestational Diabetes Mellitus.

Backgroud: The present study aimed to investigate the association between immune cells and gestational diabetes mellitus (GDM) and identify a reasonable predictor of insulin resistance in women with GDM. OBJECTIVE: The clinical and biochemical characteristics of 124 women with GDM and 168 healthy pregnant women were compared. METHODS: The percentage of immune cells in the blood of the subjects was analyzed by flow cytometry. Pearson's correlation analysis revealed the correlation between the percentage of B lymphocytes and insulin resistance. A cutoff point was determined for the percentage of B lymphocytes, based on insulin resistance, using receiver operating characteristic (ROC) curves. RESULTS: Compared to the healthy pregnant women, the percentages of B lymphocytes and IgA produced by B-cells were significantly different in women with GDM. The percentage of B lymphocytes was positively related to insulin resistance.The number of 14.05% of B lymphocytes was an optimal cutoff point that predicted the insulin resistance in women with GDM. CONCLUSION: The percentage of B lymphocytes was positively associated with insulin resistance, and hence, might serve as an appropriate predictor of insulin resistance in women with GDM.

Estrogen induces endometrial cancer cell proliferation and invasion by regulating the fat mass and obesity-associated gene via PI3K/AKT and MAPK signaling pathways.

Obesity is generally acknowledged as a risk factor for endometrial cancer, as accumulated adipocytes partly contribute to the increased production of estrogen which is involved in dysregulated cell growth and metastasis in early endometrial carcinogenesis. Thus we evaluated in this study expression of the fat mass and obesity-associated (FTO) gene in endometrial tumor tissues and further explored its role in ß-estradiol (E2)-induced endometrial cancer cell proliferation and invasion. IHC staining showed that FTO overexpressed in endometrial carcinoma. Additionally, E2-induced FTO via activation of the PI3K/AKT and MPAK signal pathways contributed to enhanced proliferation and invasion. Therefore, this study provides a new insight on the mechanisms of E2-induced proliferation and invasion and the link between obesity and endometrial cancer, implying the possibility of using FTO as a potential therapeutic target for the treatment of endometrial cancer.