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Protein annotation via the Cluster of Orthologous Groups system indicated that most proteins were involved in general function prediction, posttranslational modification, protein turnover, and chaperoning. Further, pathway analysis revealed that most of the proteins obtained participated in metabolic pathways, focal adhesion, regulation of the actin cytoskeleton, and microbial metabolism. Some tissue repair-related signaling pathways were also discovered. The identified molecules might serve as potential therapeutic targets for future studies. Copyright © 2020 Xin Xing et al.Polycystic ovary syndrome (PCOS) is a common female endocrine system disease that affects 17.8% of women of reproductive age and leads to infertility, obesity, glucose metabolic disorders, cardiovascular disease, and body-mind problems. However, the etiology of PCOS remains unclear. Follicular growth is disrupted as a result of ovarian hyperandrogenism and distorted intraovarian paracrine signaling in women with PCOS. Microcommunication between oocytes and cumulus cells plays a critical role in folliculogenesis. Gap junction alpha 1 (GJA1) plays a crucial role in the developing follicles by forming communication channels between cumulus cells and oocytes, but this has not yet been reported in women with PCOS. Therefore, we aimed to study the role of GJA1 in the microcommunication between oocytes and cumulus cells in women with PCOS. In our study, cumulus cell-oocyte complexes (COCs) from women were isolated via ultrasound-guided vaginal puncture, and oocytes were selected from COCs and categorized based on 3 oocyte maturation stages. Then, RT-qPCR and immunofluorescence analysis were performed to detect both the gene expression and protein of GJA1 in oocytes from women with and without PCOS. There was no statistically significant difference in age and BMI (body mass index), but patients with PCOS had a higher ratio of basic LH/FSH (luteinizing hormone/follicle-stimulating hormone), androstenedione, and total ovarian volume. The qRT-PCR results showed higher gene expression of GJA1 in oocytes without PCOS at the germinal vesicle (GV) stage compared with that of oocytes from women with PCOS. Immunofluorescence analysis showed that the expression level of GJA1 in oocytes from women with PCOS was very weak compared with that of oocytes from women without PCOS. In conclusion, GJA1 may play a critical role in the development of oogenesis arrest in women with PCOS throughout the oogenesis processes, including oogenesis and oocyte maturation. Copyright © 2020 Qiwei Liu et al.Purpose To explore the effects of depression on cardiac autonomic nerve function and related metabolic pathways, the heart rate variability (HRV) and urinary differential metabolites were detected on the college students with depression. Methods 12 female freshmen with depression were filtered by the Beck Depression Inventory (BDI-II) and Self-rating Depression Scale (SDS). By wearing an HRV monitoring system, time domain indexes and frequency domain indexes were measured over 24 hours. Liquid chromatography-mass spectrometry (LC-MS) was used to detect their urinary differential metabolites. Differential metabolites were identified by principal component analysis (PCA) and orthogonal projections to latent structures discriminant analysis (OPLS-DA). The metabolic pathways related to these differential metabolites were analyzed by the MetPA database. Results Stress time was significantly increased, and recovery time was markedly decreased in the depression group compared with the control group (p less then 0.001). Standard deviation of the normal-to-normal R interval (SDNN), root mean square of the beat-to-beat differences (RMSSD), high frequency (HF), and low frequency (LF) were decreased significantly (p less then 0.001). Standard deviation of the normal-to-normal R interval (SDNN), root mean square of the beat-to-beat differences (RMSSD), high frequency (HF), and low frequency (LF) were decreased significantly (. Conclusion Some autonomic nervous system disruption, high stress, and poor fatigue recovery were confirmed in college students with depression. The metabolic mechanism involved the disruption of coenzyme Q biosynthesis, glycine-serine-threonine metabolism, tyrosine metabolism, pyrimidine metabolism, and steroid metabolism under daily stress. Copyright © 2020 Shanguang Zhao et al.The usage of doxorubicin is hampered by its life-threatening cardiotoxicity in clinical practice. Dexrazoxane is the only cardioprotective medicine approved by the FDA for preventing doxorubicin-induced cardiac toxicity. Nevertheless, the mechanism of dexrazoxane is incompletely understood. The aim of our study is to investigate the possible molecular mechanism of dexrazoxane against doxorubicin-induced cardiotoxicity. We established a doxorubicin-induced mouse and cardiomyocyte injury model. Male C57BL/6J mice were randomly distributed into a control group (Con), a doxorubicin treatment group (DOX), a doxorubicin plus dexrazoxane treatment group (DOX+DEX), and a dexrazoxane treatment group (DEX). [https://www.selleckchem.com/products/gdc6036.html Selleckchem GDC-6036] Echocardiography and histology analyses were performed to evaluate heart function and structure. DNA laddering, qRT-PCR, and Western blot were performed on DOX-treated cardiomyocytes with/without DEX treatment in vitro. Cardiomyocytes were then transfected with miR-17-5p mimics or inhibitors in order to analyze its downstream target. Our results demonstrated that dexrazoxane has a potent effect on preventing cardiac injury induced by doxorubicin in vivo and in vitro by reducing cardiomyocyte apoptosis. MicroRNA plays an important role in cardiovascular diseases. Our data revealed that dexrazoxane could upregulate the expression of miR-17-5p, which plays a cytoprotective role in response to hypoxia by regulating cell apoptosis. Furthermore, the miRNA and protein analysis revealed that miR-17-5p significantly attenuated phosphatase and tensin homolog (PTEN) expression in cardiomyocytes exposed to doxorubicin. Taken together, dexrazoxane might exert a cardioprotective effect against doxorubicin-induced cardiomyocyte apoptosis by regulating the expression of miR-17-5p/PTEN cascade. Copyright © 2020 Xiaoxue Yu et al.