In recent years, more and more studies have shown that autophagy is closely related to female reproductive process. Autophagy is a widespread and highly conserved degradation system in eukaryotes that can be activated under conditions such as hypoxia, starvation, lack of nutrients, or extreme pH. In terms of reproductive health, autophagy can improve reproductive dysfunction by removing damaged organelles and regulating cell growth and metabolism. Appropriate regulation of autophagy helps to improve oocyte quality, delay ovarian aging, fine-regulate endometrial growth, and ensure successful implantation of embryos. However, the abnormality of autophagy pathway may cause problems such as activation of pelvic inflammatory cytokines, reduced endometrial receptivity, abnormal follicle development, and weakened invasion ability of trophoblast cells, thus leading to the occurrence and development of reproductive disorders such as endometriosis, chronic endometritis, polycystic ovary syndrome, early-onset ovarian insufficiency, and recurrent spontaneous abortion. This article reviews the mechanism and therapeutic targets of autophagy in female reproductive diseases, providing clinical ideas and diagnosis and treatment strategies for improving female reproductive health.

Polycystic ovary syndrome (PCOS), a common reproductive, endocrine and metabolic disease among women of childbearing age, is mainly characterized by ovulation dysfunction, polycystic ovary changes and hyperandrogenism. To some extent, it impacts patients' physical and mental health. In recent years, numerous researches have indicated that the occurrence and development of PCOS are closely associated with chronic low-level inflammation in the body. Tumor necrosis factor-α (TNF-α), as an inflammatory factor, induces PCOS through different means. Accordingly, TNF-α inhibitors are also used to treat PCOS, and some patients benefit from them. However, they are off-label drugs and there are few studies. Whether TNF-α inhibitors can improve PCOS and ensure the safety of mother and child remains unclear. Therefore, this paper will review the role of TNF-α in the PCOS pathogenesis and the efficacy and safety of its inhibitors in PCOS patients, so as to offer new clues for studying the PCOS pathogenesis and new ideas for its clinical treatment.

In recent years, more and more studies have shown that autophagy is closely related to female reproductive process. Autophagy is a widespread and highly conserved degradation system in eukaryotes that can be activated under conditions such as hypoxia, starvation, lack of nutrients, or extreme pH. In terms of reproductive health, autophagy can improve reproductive dysfunction by removing damaged organelles and regulating cell growth and metabolism. Appropriate regulation of autophagy helps to improve oocyte quality, delay ovarian aging, fine-regulate endometrial growth, and ensure successful implantation of embryos. However, the abnormality of autophagy pathway may cause problems such as activation of pelvic inflammatory cytokines, reduced endometrial receptivity, abnormal follicle development, and weakened invasion ability of trophoblast cells, thus leading to the occurrence and development of reproductive disorders such as endometriosis, chronic endometritis, polycystic ovary syndrome, early-onset ovarian insufficiency, and recurrent spontaneous abortion. This article reviews the mechanism and therapeutic targets of autophagy in female reproductive diseases, providing clinical ideas and diagnosis and treatment strategies for improving female reproductive health.

Polycystic ovary syndrome (PCOS), a common reproductive, endocrine and metabolic disease among women of childbearing age, is mainly characterized by ovulation dysfunction, polycystic ovary changes and hyperandrogenism. To some extent, it impacts patients' physical and mental health. In recent years, numerous researches have indicated that the occurrence and development of PCOS are closely associated with chronic low-level inflammation in the body. Tumor necrosis factor-α (TNF-α), as an inflammatory factor, induces PCOS through different means. Accordingly, TNF-α inhibitors are also used to treat PCOS, and some patients benefit from them. However, they are off-label drugs and there are few studies. Whether TNF-α inhibitors can improve PCOS and ensure the safety of mother and child remains unclear. Therefore, this paper will review the role of TNF-α in the PCOS pathogenesis and the efficacy and safety of its inhibitors in PCOS patients, so as to offer new clues for studying the PCOS pathogenesis and new ideas for its clinical treatment.

Objective To investigate the effects of glucagon like peptide 1 (GLP-1) agonist on myocardial hypoxia reoxygenation injury and its molecular mechanism. Methods H9C2 cells were divided into control group, hypoxia reoxygenation(H/ R) group, H/ R+GLP-1 group, and H/ R+GLP-1+phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002 group. The cell proliferation activity, apoptosis rate, enzyme contents in the medium and the expressions of apoptosis-related genes were detected. After animal model of myocardial ischemia reperfusion injury (I/ R) was established and was treated with GLP-1 agonist and PI3K inhibitor, serum enzyme contents were detected. Results Hypoxia reoxygenation decreased the myocardial cell proliferation activity and phosphorylated-PI3K(p-PI3K), phosphorylated-protein kinase B (p-Akt), Bcl-2 protein expressions, increased the apoptotic cell number and creatine kinase ( CK), creatine kinase-MB ( CK-MB), lactate dehydrogenase ( LDH) contents in cell culture medium and Bax, caspase-3 protein expressions, which were ameliorated by GLP-1 ( all P < 0. 05). The myocardial cell proliferation activity and Bcl-2 protein expression of H/ R+GLP-1+LY294002 group were significantly lower than those of H/ R+GLP-1 group while the apoptotic cell number and CK, CK-MB, LDH contents in cell culture medium and Bax, Caspase-3 protein expressions were significantly higher (all P<0. 05). Serum CK, CK-MB, and LDH contents in rats of I/ R group were significantly higher than those in control group and I/ R+GLP-1 group. Serum CK, CK-MB, and LDH contents in rats of I/ R+GLP-1+LY294002 group were significantly higher than those in I/ R+GLP-1 group(all P < 0. 05). Conclusion GLP-1 agonist is able to protect the myocardial hypoxia reoxygenation injury via activating PI3K/ Akt signaling pathway.

Objective To study ocular motor function in patients with Parkinson disease.Methods Videonystagmography(VNG)was used for testing ocular saccade and smooth pursuit eye movement(SPEM)in 14 patients with idiopathic Parkinson disease and 10 age and sex-matched control subjects to compare the latency of saccades,the accuracy of saeeades and SPEMGain between two groups. Results The latency of saceades was found to be much more increased in PD group (291.23±46.25)ms than that in healthy group(244.45±23.11)ms(P＜0.05);and the accuracy of saccades was found to be decreased in PD group(87.98±6.1 6)as compared to that in healthy group (95.21±8.56)(P＜0.05).PD group was found to have more decreased SPEM gain(0.81±0.12)than that in healthy group(0.90±0.1 5)(P＜0.05). Conclusions The findings suggest that ocular motor function is abnormal in Parkinson disease patients.

Objective To observe the prognosis 90 days after attack and the correlation among various risk factors in patients with transient ischemic attack (TIA). Methods The data of 90 days follow up and related risk factors of 61 patients clinically diagnosed with TIA were analyzed.We also compared the prognosis of those patients according to the change on diffusion weighted imaging (DWI). Results The incidence of various kinds of severe vascular events in 61 patients within 90 days was 16.4% (10/61). Among the patients with abnormal change on DWI, the incidence was 50% (8/16). However the incidence was 4.7% (2/43) in the patients with normal DWI. There was a statistical difference between the two groups (P