In our previous study, a gut microbiota-targeted dietary intervention with a high-fiber diet improved the immune status of both genetically obese (Prader-Willi Syndrome, PWS) and simple obese (SO) children. However, PWS children had higher inflammation levels than SO children throughout the trial, the gut microbiota of the two cohorts was similar. As some virulence factors (VFs) produced by the gut microbiota play a role in triggering host inflammation, this study compared the characteristics and changes of gut microbial VF genes of the two cohorts before and after the intervention using a fecal metagenomic dataset. We found that in both cohorts, the high-fiber diet reduced the abundance of VF, and particularly pathogen-specific, genes. The composition of VF genes was also modulated, especially for offensive and defensive VF genes. Furthermore, genes belonging to invasion, T3SS (type III secretion system), and adherence classes were suppressed. Co-occurrence network analysis detected VF gene clusters closely related to host inflammation in each cohort. Though these cohort-specific clusters varied in VF gene combinations and cascade reactions affecting inflammation, they mainly contained VFs belonging to iron uptake, T3SS, and invasion classes. The PWS group had a lower abundance of VF genes before the trial, which suggested that other factors could also be responsible for the increased inflammation in this cohort. This study provides insight into the modulation of VF gene structure in the gut microbiota by a high-fiber diet, with respect to reduced inflammation in obese children, and differences in VF genes between these two cohorts.Based on many studies, trichosanthin (TCS) has an antiviral effect that regulates immune response, and targets cancer cells to exert broad-spectrum anti-tumor pharmacological activities. It is speculated that TCS may be a potential natural active drug for preventing as well as treating cervical cancer. But the clearer impact along with underlying TCS mechanism on cervical cancer are still unclear. The purpose of this study is to investigate the function and potential mechanism of TCS in cervical cancer. We measured the viability of cervical cancer cell lines (HeLa & caski cells) using CCK-8 analysis, detected cell proliferation efficiency through Ki-67 staining, analyzed cell apoptosis rate via flow cytometry as well as annexin V-FITC/PI double staining, performed apoptosis-related protein expression through western blotting, evaluated cell migration along with invasion by wound as well as transwell assays, carried out MMP via JC-1 and Rh123 fluorescent probes, as well as detected intracellular ATP and ROS levels by flow cytometry, respectively, to evaluate the effects of TCS. We found that TCS inhibited viability along with proliferation, induced apoptosis, as well as inhibited HeLa & caski cell migration along with invasion in a time- and dose-dependent manner. Additionally, TCS also reduced MMP, and the production of adenosine triphosphate, as well as induced the increase of intracellular reactive oxygen species in cancer cell lines. In accordance with the present studies, TCS inhibits HeLa & caski cell proliferation along with migration but promotes their apoptosis, which may be mediated by regulating oxidative stress.Long non-coding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) participates in the development of diverse cancers. Nevertheless, the impact of DANCR on cervical cancer (CC) remains largely unknown. This study aims to explore the effects of DANCR sponging microRNA-145-3p (miR-145-3p) on CC.  https://www.selleckchem.com/products/cy-09.html  Expression of KLF5, DANCR, miR-145-3p, and zinc finger E-box binding homeobox 1 (ZEB1) in CC and adjacent normal tissues was determined. Human CC cell lines were, respectively, treated with silenced DANCR or miR145-3p mimic/inhibitor. Then, the viability, migration, invasion, and apoptosis of CC cells were measured. The cell growth in vivo was observed as well. Chromatin immunoprecipitation assay was performed to analyze the binding of KLF5 and DANCR promoter. Interaction among DANCR, miR-145-3p, and ZEB1 was assessed. KLF5, DANCR, and ZEB1 were upregulated but miR-145-3p was downregulated in CC tissues. KLF5 activated DANCR expression and the high DANCR expression was related to tumor staging, infiltrating muscle depth and lymphatic metastasis of CC patients. Reduced DANCR or elevated miR-145-3p repressed malignant behaviors of CC cells. The tumor diameter and weight were also repressed by DANCR silencing or miR-145-3p elevation. The effect of DANCR knockdown on CC cells could be reversed by miR-145-3p inhibitor. MiR-145-3p was targeted by DANCR and ZEB1 was targeted by miR-145-3p. KLF5-induced overexpression of DANCR promotes CC progression via suppressing miR-145-3p to target ZEB1. This study may provide potential targets for CC treatment.
  Examination of the literature can help answer the age-old question of the extent to which rigid contact lenses can be considered an art versus a science.
 
  This work aims to assemble rigid contact lens-related publication metrics to identify the most impactful papers, authors, institutions, countries and journals.
 
  A search was undertaken of the Scopus database to identify rigid contact lens-related articles published since this lens type was first described in 1949. The 25 most highly cited papers were determined from the total list of 1,823 papers found. Rank-order lists by count were assembled for the 'top 25' in each of four categories authors, institutions, countries and journals. A subject-specific rigid contact lens h-index (h
  -index) was derived for each author, institution, country and journal to serve as a measure of impact in the field. A short list of the top constituents in each category were ranked by h
  -index and tabulated.
 
  The most highly cited paper (467 citations) is entitled 'Risk fases revealed here belies the notion that rigid lenses fitting is more of an art than a science.Supernumerary centrioles are frequently observed in diverse types of cancer cells. In this study, we investigated the mechanism underlying the generation of supernumerary centrioles during the M phase. We generated the TP53;PCNT;CEP215 triple knockout (KO) cells and determined the configurations of the centriole during the cell cycle. The triple KO cells exhibited a precocious separation of centrioles and unscheduled centriole assembly in the M phase. Supernumerary centrioles in the triple KO cells were present throughout the cell cycle; however, among all the centrioles, only two maintained an intact composition, including CEP135, CEP192, CEP295 and CEP152. Intact centrioles were formed during the S phase and the rest of the centrioles may be generated during the M phase. M-phase-assembled centrioles lacked the ability to organize microtubules in the interphase; however, a fraction of them may acquire pericentriolar material to organize microtubules during the M phase. Taken together, our work reveals the heterogeneity of the supernumerary centrioles in the triple KO cells.