Search

Yijie Chen,1,&ast; Jingjing Yu,2,&ast; Lan Shi,1 Shuyang Han,1 Jun Chen,1 Zhumei Sheng,3 Miao Deng,3 Xuejing Jin,1,3 Zhifen Zhang1,3 1The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China; 2School of Public Health, Hangzhou Normal University, Hangzhou, People’s Republic of China; 3Department of the Reproductive Endocrinology Division, Hangzhou Women’s Hospital (Hangzhou Maternity and Child Health Care Hospital), Hangzhou, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Zhifen Zhang; Xuejing Jin, The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, 548 Binwen Road, Binjiang District, Hangzhou, Zhejiang, 310053, People’s Republic of China, Email zhangzf@zju.edu.cn; jxj20210928@163.comObjective: The aim of this research was to determine whether systemic inflammatory indicators, including aggregate index of systemic inflammation (AISI), neutrophils lymphocyte to platelet ratio (NLPR), systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI), are related to bone mineral density (BMD) in perimenopausal and postmenopausal women.Methods: One hundred and eighty-one perimenopausal and 390 postmenopausal women were enrolled in this cross-sectional study. Continuous variables by analysis of variance and Kruskal Wallis test for comparing the clinical characteristics. Linear regression analysis was conducted to investigate the associations between inflammatory indicators with BMD. The comparison between the subgroups was performed using the nonparametric test and the T-test.Results: AISI, NLPR, SII, and SIRI quartile values were inversely associated with BMD in menopausal women (P = 0.021; P = 0.047; P < 0.001; P < 0.001, respectively). After adjusting for confounding factors, four inflammatory indicators remained significantly associated with BMD (all P for trend < 0.001). Analysis accord

Large clostridial toxins (LCTs) are a family of homologous proteins toxins that are directly responsible for the symptoms associated with a number of clostridial infections that cause disease in humans and in other animals. LCTs damage tissues by delivering a glucosyltransferase domain, which inactivates small GTPases, across the endosomal membrane and into the cytosol of target cells. Elucidating the mechanism of translocation for LCTs has been hampered by difficulties associated with identifying marginally hydrophobic segments that insert into the bounding membrane to form the translocation pore. Here, we directly measured the membrane-insertion partitioning propensity for segments spanning the putative pore-forming region using a translocon-mediated insertion assay and synthetic peptides. We identified membrane-inserting segments, as well as a conserved and functionally important negatively charged residue that requires protonation for efficient membrane insertion. We provide a model of the LCT pore, which provides insights into translocation for this enigmatic family of a-helical translocases.

In this paper we provide the greatest lower bound about the number of (non-infinitesimal) limit cycles surrounding a unique singular point for a planar polynomial differential system of arbitrary degree.

In this paper we provide the greatest lower bound about the number of (non-infinitesimal) limit cycles surrounding a unique singular point for a planar polynomial differential system of arbitrary degree.