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OBJECTIVES To explore if and how the microbiota changed in PCOS women against healthy women. METHODS Eight obese PCOS (PO group), ten non-obese PCOS (PN group) and nine healthy normal-weight women (control) (C group) were enrolled. Insulin (INS), testosterone (T), follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen (E2) and dehydroepiandrosterone (DHEA) were detected with radioimmunoassay. Anti mullerian hormone (AMH), fasting glucose and hemoglobin A1c (HbA1c) were determined by chemiluminescence immunoassay, glucose oxidase method and HPLC, respectively. Gut microbiota composition was evaluated by PCR. Alpha diversity was assessed using Chao1 and Shannon index. RESULTS PCOS women showed significantly higher T, LH, LH/FSH and lower FSH levels than control(p less then 0.05). AMH level was significantly higher in PO than PN group(p less then 0.05). PO group presented significantly higher fasting insulin level and HMOA-IR scores than other groups, lower observed SVs and alpha diversity than C group, higher beta diversity than PN group(p less then 0.05), and decreased in abundances of genera (mainly butyrate producers). Regression analysis showed decreased abundances of several genera were correlated with higher circulating testosterone and impaired glucose metabolism. CONCLUSIONS PCOS is associated with changes in the gut microbiota composition. Obesity has a driving role in the development of dysbiotic gut microbiota in PCOS.This study explored inclusion of female participants in Natural Sciences and Engineering Research Council of Canada Discovery Grant-funded human cardiovascular research at Ontario universities between 2010-2018. Ninety-six publications were examined and 4 principal investigators were interviewed. Females were excluded/underrepresented in 63% of publications with 49% male-only and 5% female-only samples. The sex-bias appears to be explained by dependence on research knowledge and methodologies that maintain and reproduce a firmly established discourse of the male norm. Novelty Female participants were underrepresented in NSERC DG-funded cardiovascular research at Ontario universities between 2010-2018.Induced pluripotent stem cell (iPSC) technology refers to the reprogramming of terminally differentiated somatic cells into pluripotent stem cells by introducing specific transcription factors that are known to regulate pluripotency, including Oct4, Sox2, Klf4, and c-Myc. In this study, we reprogrammed the primary fibroblasts isolated from the Daxxflox/flox mice, which carry the Oct4-green fluorescent protein reporter, and employed wild-type littermates as a control to induce iPSCs, then knocked out Daxx by infecting with Cre virus at the cellular level. The pluripotency and self-renewal capacity of iPSCs were determined. In addition, Daxx deletion altered the pluripotency marker (Nanog, Oct4) expression and displayed neural differentiation defects. Particularly, by performing transcriptome analysis, we observed that numerous ribosome biogenesis-related genes were altered, and quantitative polymerase chain reaction revealed that the expression of rDNA-related genes, 47S and 18S, was elevated after Daxx deletion. Finally, we illustrated that the expression of the neurodevelopment-related gene was upregulated both in iPSCs and differentiated neurospheres. Taken together, we demonstrated that Daxx knockout promotes the expression of rDNA, pluripotency, and neurodevelopment genes, which may improve the differentiation abilities of mouse iPSCs (miPSCs).The airway inflammatory response is closely associated with asthma. The purpose of this article was to study the roles of innate lymphoid cells (ILCs) in the process of airway inflammatory response in asthma. We established the asthmatic mice model with intraperitoneal injected ovalbumin medium, then with the flow cytometry analysis, we detected the ILCs and their surface proteins in the mice blood samples, besides, we analyzed the amounts of inflammatory cytokines and secreted proteins in the mice bronchoalveolar lavage fluid and blood serum. Moreover, Western blot analyzed the proteins in the mice bronchial epithelial tissues. The ILC2 amounts were obviously increased in young asthmatic mice model. And, the proteins CD25 and CCR10 were highly expressed in the sorted ILC2s. Besides, the cytokines interleukin (IL)-5, IL-13, IL-33, CCL22, and CCL27 were abundant in the bronchoalveolar lavage fluid of asthmatic mice model. And, the secretion of IL-5, IL-13, IL-33, TSLP, and CCL22 in blood serum was much more in asthmatic mice model than in the normal control mice, whereas the secretion of PGD2 was suppressed in asthmatic mice bronchoalveolar lavage fluid and blood serum. Additionally, the guanine nucleotide-binding proteins Gα12 and Gα13 were upregulated in asthmatic mice bronchial tissues, and the protein SERCA2 was downregulated; moreover, the proteins NFAT, IRF4, and its downstream signal STAT6 were all upregulated in the asthmatic mice bronchial tissues. ILC2s were involved in the response of airway inflammation through secretion of proinflammatory cytokines and chemokines to dysregulate the Ca2+ homeostasis in airway in the process of asthma. this website [Figure see text].Chicken embryonic stem cells (cESCs) isolated from the egg at the stage X hold great promise for cell therapy, tissue engineering, pharmaceutical, and biotechnological applications. They are considered to be pluripotent cells with the capacity to self-renewal and differentiate into specialized cells. However, long-term maintenance of cESCs cannot be realized now, which impedes the establishment of cESC line and limits their applications. Therefore, the separation locations, isolation methods, and culture conditions especially the supplements and action mechanisms of cytokines, including leukemia inhibitory factor, fibroblast growth factor, transforming growth factor beta, bone morphogenic protein, and activin for cESCs in vitro, have been reviewed here. These defined strategies will contribute to identify the key mechanism on the self-renewal of cESCs, facilitate to optimize system that supports the derivation and longtime maintenance of cESCs, establish the cESC line, and develop the biobank of genetic resources in chicken.