Bacterial vaginosis frequently persists, even after treatment. The role of some strains of bacteria associated with bacterial vaginosis treatment failure remains poorly defined. The aim of our study was to define the risk of bacterial vaginosis treatment failure, including pre-treatment detection of specific vaginal bacteria. Bacterial vaginosis is present when the Nugent score is ≥7 and the modified Amsel criteria is positive. Women with bacterial vaginosis were treated with intravaginal metronidazole gel nightly for 5 nights. The 454 pyrosequencing method was used to detect bacteria in vaginal fluid. By univariate analysis, a history of bacterial vaginosis, intrauterine device use and the presence of Facklamia, Corynebacterium and Veillonella were significantly associated with bacterial vaginosis treatment failure. Lactobacillus crispatus, Lactobacillus pentosus and Megasphaera were significantly associated with curing bacterial vaginosis. After logistic regression analysis and detection of these bacteria for test-of-cure, we found that women who had a history of bacterial vaginosis had a higher incidence of bacterial vaginosis treatment failure, whereas women with L. crispatus had a lower incidence of treatment failure. Post-treatment sexual activity was not associated with the treatment effect. Our data suggested that treatment failure may be not caused by drug resistance. Rather, it has a closer relationship with the failed restoration of lactobacilli.
Background:Epidemiologic and genetic studies suggest a link between insulin resistance (IR) and endometrial cancer, and endometrial hyperplasia (EH) is a precancerous stage of endometrial cancer. Adiponectin is an adipokine which previously shown to be a risk factor for endometrial cancer. The aim of the study was to develop a rat model of IR and EH and evaluate adiponectin system in circulation and uterus.Methods:This study was a 46-week animal trial from February 2014 to January 2015. Female Sprague-Dawley rats were fed with high-fat diet (HFD) for 40 weeks to induce IR. Followed by ovariectomization, rats were orally administrated to 17β-estradiol (E2) for 4 weeks to induce EH and then sacrificed. A total of 36 rats were divided into four groups: E2, HFD, HFD + E2, and control groups. Data were analyzed with Student's t-test, one-way analysis of variance (ANOVA), and Mann-Whitney U-tests. Chi-square was used to evaluate the score of immunohistochemistry.Results:The thickness of endometrial, glandular epithelium, and myometrium in the HFD-E2 group were higher than the E2 group (F = 59.02, F = 23.51 and F = 12.53, respectively, all P < 0.001). Plasma adiponectin levels in the E2 group were lower than those in the control group, and the levels in the HFD-E2 group were lower than those in the HFD group (F = 13.15, P < 0.05). However, after normalized to visceral adipose tissue, compared to the control group, plasma adiponectin levels were decreased in rat with HFD in the absence or presence of E2, respectively (F = 6.72, P < 0.05). Adiponectin gene (F = 10.48, P < 0.05) and protein (P < 0.05) levels in uterus in the HFD-E2 group were higher than those in the HFD group.Conclusions:This study manifests that IR can effectively modulate EH, which suggests the involvement of energetic metabolism in uterine alternation. The combination effects of IR and EH modulate circulating adiponectin levels. However, adiponectin gene and protein levels in uterus are mainly response to estradiol.
Background: Patients with pelvic inflammatory disease (PID) are at an increased risk of ectopic pregnancy, infertility, and varying degrees of chronic pelvic pain. The aims of this study were to establish a rat model of PID and characterize its progression in order to assist in the study of pathophysiological mechanisms and to provide animal model for future studies of PID treatments.Methods: Fifty Sprague-Dawley rats (female, 6-weeks-old) were divided into a model group (n=28) and a control group (n=22). The rat endometrium was mechanically injured by a needle which moved back and forth 3 times on the endometrial tissue, and a mixed bacterial solution (6×10 8 CFU) of equal concentrations of Escherichia coli and Staphylococcus aureus was injected into both horns of the rat uterus. Physiological characteristics including weight, temperature, blood, and inflammatory factors were compared, and immunohistochemistry and transmission electron microscopy were used to evaluate the progress and sequela of PID. Results:The model rats experienced acute PID in the first 14 days and exhibited higher body temperatures and decreased body weight. Infection-related factors in the blood were also significantly changed compared with the normal group, with obviously increased serum levels of C-reactive protein (CRP), interferon gamma (IFN-γ), and interleukin-4 (IL-4). Congestion and edema were observed in the uteri of the model rats, followed by infiltration of numerous inflammatory cells and ultrastructural morphology changes.Histological examination of the uterus showed that adhesion initially appeared at approximately 21 days.In addition to the increased collagen fibers biomass, the expression of transforming growth factor-beta 1 (TGF-β1) was elevated, which might have contributed to pelvic tissue adhesion formation in the PID sequela.Conclusions: This study clearly described the characteristics and progression of PID in a rat model. The detailed evidence increased our understanding of the pathogenesis and progression of PID and may be useful for future studies of PID treatments.
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