Abstract Pelvic inflammatory disease (PID) is an inflammation of the upper genital tract. PID is the leading cause of some severe sequelae in the absence of timely and accurate diagnosis and treatment. An appropriate animal model is needed to explore the underlying mechanism of PID sequelae. This study introduced an animal model of PID by vaginal injection of liquid Ureaplasma urealyticum combined with fatigue and hunger (UVF). This study was designed to test the feasibility of a rat model. A rat model was established using UVF irradiation. Levels of some inflammatory cytokines in the serum and the homogenates of the fallopian tubes were measured by ELISA, RT-PCR, and flow cytometry and compared with another rat model of Ureaplasma urealyticum liquids injected into the two uterus horns during laparotomy. Inflammatory alterations and adhesions were observed after hematoxylin and eosin (H&E) staining and detected using the Blauer scoring system. The results showed that the combined UVF and rat model caused apparent obstruction, edema, and adhesion in the fallopian tubes and connective tissues. The rat model showed upregulated CD4, CD8, and CD4/CD8 in peripheral blood mononuclear cells (PBMCs) and significantly increased levels of IL-4, IL-6, IL-10, and IL-17. UVF also enhanced the expression of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, vascular endothelial growth factor (VEGF) β, and matrix metalloproteinase (MMP)-2 (P<0.05). The UVF rat model can induce inflammatory alterations in the fallopian tubes and connective tissues, and can be used as a model of PID.

Abstract Two new labdane-type diterpenoids, 5-ethoxy-3-(2-((R)-4-hydroxy-2,5,5,8a-tetramethyl-3-oxo-3,5,6,7,8,8a-hexahydronaphthalen-1-yl)ethyl)furan-2(5H)-one (1), and 5-hydroxy-4-(2-((1R,3S,7aS)-1-hydroxy-4,4,7a-trimethyl-3-propionyloctahydroisobenzofuran-1-yl)ethyl)furan-2(5H)-one (2), were isolated from the EtOH extract of the herb of Leonurus japonicus Houtt., Lamiaceae. Their chemical structures were determined by analysis of 1D, 2D NMR, HRESIMS, and by comparison with known analogs.

Our objective was to evaluate the association of rs12255372 in theTCF7L2 gene with type 2 diabetes mellitus (T2DM) in the world population. We carried out a survey of the literature about the effect of rs12255372 on genetic susceptibility to T2DM by consulting PubMed, the Cochrane Library, and Embase from 2006 to 2012, and then performed a meta-analysis of all the studies in order to evaluate the association between rs12255372 and T2DM. A total of 33 articles including 42 studies (with 34,076 cases and 36,192 controls) were confirmed to be eligible and were included in the final meta-analysis: 6 studies conducted on Europeans, 14 on Caucasians, 17 on Asians, 2 on Africans, and 3 on Americans. Overall, the effect size was as follows: for the variant allele T (OR = 1.387, 95%CI = 1.351-1.424), for the TT genotype (OR = 1.933, 95%CI = 1.815-2.057), for the GT genotype (OR = 1.363, 95%CI = 1.315-1.413), for the dominant model (OR = 1.425, 95%CI = 1.344-1.510), and for the recessive model (OR = 1.659, 95%CI = 1.563-1.761). In summary, by pooling all available qualified data from genetic studies on rs12255372 and T2DM, we have confirmed that rs12255372 is significantly associated with susceptibility to T2DM in the global population.