Polycystic ovary syndrome （PCOS）， a common reproductive endocrine disorder in women， is one of the leading causes of ovulatory infertility in women of reproductive age. Due to its heterogeneous etiology， complex symptoms， and challenging treatment， PCOS has become a focal point of research in gynecological and reproductive medicine globally. The pathogenesis of PCOS is complex and may involve regulatory mechanisms such as inflammatory responses， oxidative stress， and cellular autophagy. Crown-like structures （CLSs） refer to pro-inflammatory microenvironments formed by macrophages engulfing adipocytes. The inflammatory disorders induced by CLSs are one of the key factors contributing to the development of PCOS and its complications. Current studies have indicated that the obese status in PCOS accelerates the formation of CLSs， and the density of CLSs can predict the progression of metabolic disorders and influence the outcomes of various metabolic diseases. Traditional Chinese Medicine （TCM） offers the unique advantages of a holistic view， four diagnostic methods， and syndrome differentiation and treatment to ameliorate the symptoms and signs of PCOS through multiple levels， pathways， and targets. Although studies on the mechanisms of metabolic diseases and CLS formation have been reported in China and abroad， there is still a lack of literature on the correlation between CLSs and PCOS， as well as reviews on TCM interventions targeting CLSs for treating this disease. Therefore， this paper summarized the correlation between obese PCOS and CLSs and reviewed recent studies on TCM interventions based on CLS formation （adipose tissue-macrophage inflammatory crosstalk） in the treatment of obese PCOS， aiming to provide new research perspectives for the prevention and treatment of PCOS using TCM.

Polycystic ovary syndrome （PCOS）， a common reproductive endocrine disorder in women， is one of the leading causes of ovulatory infertility in women of reproductive age. Due to its heterogeneous etiology， complex symptoms， and challenging treatment， PCOS has become a focal point of research in gynecological and reproductive medicine globally. The pathogenesis of PCOS is complex and may involve regulatory mechanisms such as inflammatory responses， oxidative stress， and cellular autophagy. Crown-like structures （CLSs） refer to pro-inflammatory microenvironments formed by macrophages engulfing adipocytes. The inflammatory disorders induced by CLSs are one of the key factors contributing to the development of PCOS and its complications. Current studies have indicated that the obese status in PCOS accelerates the formation of CLSs， and the density of CLSs can predict the progression of metabolic disorders and influence the outcomes of various metabolic diseases. Traditional Chinese Medicine （TCM） offers the unique advantages of a holistic view， four diagnostic methods， and syndrome differentiation and treatment to ameliorate the symptoms and signs of PCOS through multiple levels， pathways， and targets. Although studies on the mechanisms of metabolic diseases and CLS formation have been reported in China and abroad， there is still a lack of literature on the correlation between CLSs and PCOS， as well as reviews on TCM interventions targeting CLSs for treating this disease. Therefore， this paper summarized the correlation between obese PCOS and CLSs and reviewed recent studies on TCM interventions based on CLS formation （adipose tissue-macrophage inflammatory crosstalk） in the treatment of obese PCOS， aiming to provide new research perspectives for the prevention and treatment of PCOS using TCM.

Receptor-interacting protein kinase 1 (RIPK1) plays an essential role in regulating the necroptosis and apoptosis in cerebral ischemia-reperfusion (I/R) injury. However, the regulation of RIPK1 kinase activity after cerebral I/R injury remains largely unknown. In this study, we found the downregulation of protein arginine methyltransferase 1 (PRMT1) was induced by cerebral I/R injury, which negatively correlated with the activation of RIPK1. Mechanistically, we proved that PRMT1 directly interacted with RIPK1 and catalyzed its asymmetric dimethylarginine, which then blocked RIPK1 homodimerization and suppressed its kinase activity. Moreover, pharmacological inhibition or genetic ablation of PRMT1 aggravated I/R injury by promoting RIPK1-mediated necroptosis and apoptosis, while PRMT1 overexpression protected against I/R injury by suppressing RIPK1 activation. Our findings revealed the molecular regulation of RIPK1 activation and demonstrated PRMT1 would be a potential therapeutic target for the treatment of ischemic stroke.

Objective:To investigate associations of serum low-density lipoprotein cholesterol (LDL-C) with hematoma enlargement, early neurological deterioration (END), and outcome in patients with acute spontaneous intracerebral hemorrhage (ICH).Methods:"A multi-center registration study for spontaneous intracerebral hemorrhage in Inner Mongolia" (registration number: ChiCTR2000029494) database was used to include patients with ICH who completed their first head CT scan within 6 hours after onset, underwent blood lipid examination, CT follow-up within 24 hours of onset, and accurately measured hematoma volume using 3D Slicer software between June 2020 and September 2022. HE was defined as hematoma volume increasing >33% or >6 ml at 24 hours, or ventricular hematoma volume increasing ≥1 ml compared to the baseline. END was defined as an increase of ≥4 in the National Institutes of Health Stroke Scale (NIHSS) score from the baseline or death within 24 hours after onset. The follow-up was conducted at 3 months after onset, and the modified Rankin Scale score >2 was defined as poor outcome. Multivariate logistic analysis was used to determine the independent correlation between LDL-C and HE, END, and outcome. Results:A total of 338 patients with ICH were enrolled, including 206 males (60.9%). LDL-C was 2.39±1.22 mmol/L. Eighty-eight patients (26.0%) developed HE, 67 (19.8%) developed END, and 162 (47.9%) had poor outcome at 3 months. Multivariate logistic analysis showed that after adjusting for confounding factors, there was a significant independent negative correlation between LDL-C and HE (odds ratio 0.312, 95% confidence interval 0.208-0.467; P<0.001) and END (odds ratio 0.408, 95% confidence interval 0.275-0.606; P<0.001), but not with the outcome at 3 months. Conclusion:Lower LDL-C is associated with HE and END in patients with ICH, but not with the outcome.