Resistant ovary syndrome(ROS)and premature ovarian insufficiency(POI)fall under the cat-egory of hypogonadotropic amenorrhea,sharing similar clinical features that often pose challenges in differentiation.ROS can be easily misdiagnosed as POI,which presents a significant obstacle to subsequent treatment.Therefore,it is crucial for patients with fertility requirements to have a clear understanding of the etiology,clinical features,and diagnostic criteria of ROS and POI in order to establish an early diagnosis and develop an appropriate treatment plan.This article provides a systematic and comprehensive discussion on the research progress regarding the eti-ology and pathogenesis,clinical features and diagnosis,as well as individualized management of ROS and POI.The aim is to offer reference for clinicians in achieving early clarification of diagnoses,avoiding misdiagnosis or mistreatment,while assisting patients in improving symptoms and realizing their fertility aspirations through person-alized management.

Resistant ovary syndrome(ROS)and premature ovarian insufficiency(POI)fall under the cat-egory of hypogonadotropic amenorrhea,sharing similar clinical features that often pose challenges in differentiation.ROS can be easily misdiagnosed as POI,which presents a significant obstacle to subsequent treatment.Therefore,it is crucial for patients with fertility requirements to have a clear understanding of the etiology,clinical features,and diagnostic criteria of ROS and POI in order to establish an early diagnosis and develop an appropriate treatment plan.This article provides a systematic and comprehensive discussion on the research progress regarding the eti-ology and pathogenesis,clinical features and diagnosis,as well as individualized management of ROS and POI.The aim is to offer reference for clinicians in achieving early clarification of diagnoses,avoiding misdiagnosis or mistreatment,while assisting patients in improving symptoms and realizing their fertility aspirations through person-alized management.

Chronic inflammation is critical in the onset and progression of atherosclerosis (AS). The lipopolysaccharide (LPS) level in the circulation system is elevated in AS patients and animal models, which is correlated with the severity of AS. Inspired by the underlying mechanism that LPS could drive the polarization of macrophages toward the M1 phenotype, aggravate inflammation, and ultimately contribute to the exacerbation of AS, LPS in the circulation system was supposed to be the therapeutic target for AS treatment. In the present study, polymyxin (PMB) covalently conjugated to PEGylated liposomes (PLPs) were formulated to adsorb LPS through specific interactions between PMB and LPS. In vitro, the experiments demonstrated that PLPs could adsorb LPS, reduce the polarization of macrophages to M1 phenotype and inhibit the formation of foam cells. In vivo, the study revealed that PLPs treatment reduced the serum levels of LPS and pro-inflammatory cytokines, decreased the proportion of M1-type macrophages in AS plaque, stabilized AS plaque, and downsized the plaque burdens in arteries, which eventually attenuated the progression of AS. Our study highlighted LPS in the circulation system as the therapeutic target for AS and provided an alternative strategy for AS treatment.

Objective:To observe the effect of miR-217 on angiotensin II (AngII)-induced hepatic stellate cells (HSCs) activation, and carbon tetrachloride (CCl4)-induced overexpression in mice, so as to clarify miR-217 role in liver fibrosis.Methods:HSCs were stimulated with AngⅡ and the changes condition in the expression level of miR-217 were detected. HSCs were divided into control group, AngII-treated group and AngⅡ+miR-217-treated group. The expression levels of alpha-smooth muscle actin, fibroblast-specific protein 1 and collagen Ⅰ (Collagen Ⅰ) in each group were detected. The target gene of mir-217 was screened and verified by Targetscan and Dual luciferase gene reporter assay. Real-time quantitative PCR and Western blot were used to detect the effect of miR-217 on the expression level of transforming growth factor beta type Ⅱ receptor (TGFBR2). A CCl4-induced mouse liver fibrosis model was constructed. Masson staining and Sirius red staining were used to detect the effect of miR-217 overexpression on the progression of liver fibrosis in CCl4 mice. Data of two groups were compared using t-test. Data of multiple groups were statistically analyzed with one-way ANOVA. Results:The expression level of miR-217 was downregulated by AngⅡ-stimulated HSC cells. The expression levels of α-smooth muscle actin, fibroblast-specific protein 1 and Collagen Ⅰ induced by AngⅡ was inhibited by miR-217 mimics transfection. The 3'-UTR of TGFBR2 had specifically bind miR-217. The mRNA and protein expression levels of TGFBR2 was inhibited with miR-217 mimics transfection in HSCs. The overexpression of miR-217 had inhibited the expression levels of Collagen Ⅰ and Ⅲ in CCl4 mice and alleviated the progression of liver fibrosis .Conclusion:miR-217 regulates liver fibrosis by targeting TGFBR2, inhibits AngII-induced HSC activation, and slows down the process of liver fibrosis in CCl4 mice, suggesting that miR-217 may have an inhibitory effect on liver fibrosis.