The underlying mechanisms in atherosclerotic vascular diseases are not entirely clear, posing a challenging hurdle to treatment. Inflammation is a root cause of atherosclerosis (AS); therefore, anti-inflammatory agents have potential for its management. Sweroside, possessing anti-inflammatory properties, emerges as a potential agent to impede AS progression. In this study, we investigated the effects of sweroside on AS mice and elucidated its molecular mechanisms. We conducted in vivo experiments using an apolipoprotein E mice model of AS to explore the effects of sweroside on vascular inflammation adhesion responses, endothelial injury and AS. In vitro experiments, mouse aorta endothelial cells were treated with palmitic acid (PA) and sweroside, and the protective effects of sweroside on endothelial injury were analysed. AS is a chronic inflammatory disease and activation of nuclear factor κB (NF-κB) signalling contributes to inflammatory reactions and AS. Mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) has been identified as an upstream target of NF-κB signalling. We detected MAP4K4/NF-κB signalling pathways using gene siRNA silencing and knockdown assays and investigated the protective effects of sweroside in PA-mediated endothelial injury and western-diet-induced AS. The findings demonstrated that sweroside attenuated vascular inflammation, adhesion responses, and leukocyte homing and alleviated endothelial injury and atherosclerosis in vivo. Sweroside attenuated endothelial inflammation, apoptosis, permeability and adhesion responses induced by PA in vitro. Sweroside alleviated endothelial injury and atherosclerosis through MAP4K4/NF-κB signalling. Hence, sweroside is a promising candidate for treating AS, acting by targeting the MAP4K4/NF-κB pathway.

Tetrahydroxy stilbene glucoside (TSG) from Polygonum multiflorum exerts neuroprotective effects after ischemic stroke. We explored whether TSG improved ischemic stroke injury via PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy. Oxygen glucose deprivation/reoxygenation (OGD/R) in vitro model and middle cerebral artery occlusion (MCAO) rat model were established. Cerebral injury was assessed by neurological score, hematoxylin and eosin staining, 2,3,5-triphenyltetrazolium chloride staining, and brain water content. Apoptosis, cell viability, and mitochondrial membrane potential were assessed by flow cytometry, cell counting kit-8, and JC-1 staining, respectively. Colocalization of LC3-labeled autophagosomes with lysosome-associated membrane glycoprotein 2-labeled lysosomes or translocase of outer mitochondrial membrane 20-labeled mitochondria was observed with fluorescence microscopy. The ubiquitination level was determined using ubiquitination assay. The interaction between molecules was validated by coimmunoprecipitation and glutathione S-transferase pull-down. We found that TSG promoted mitophagy and improved cerebral ischemia/reperfusion damage in MCAO rats. In OGD/R-subjected neurons, TSG promoted mitophagy, repressed neuronal apoptosis, upregulated Y-box binding protein-1 (YBX1), and activated PINK1/Parkin signaling. TSG upregulated ubiquitin-specific peptidase 10 (USP10) to elevate YBX1 protein. Furthermore, USP10 inhibited ubiquitination-dependent YBX1 degradation. USP10 overexpression activated PINK1/Parkin signaling and promoted mitophagy, which were reversed by YBX1 knockdown. Moreover, TSG upregulated USP10 to promote mitophagy and inhibited neuronal apoptosis. Collectively, TSG facilitated PINK1/Parkin pathway-mediated mitophagy by upregulating USP10/YBX1 axis to ameliorate ischemic stroke.

In this study, we investigate the effect of neuregulin 4 (NRG4) on podocyte damage in a mouse model of diabetic nephropathy (DN) and we elucidate the underlying molecular mechanisms. In vivo experiments were conducted using a C57BL/6 mouse model of DN to determine the effect of NRG4 on proteinuria and podocyte injury, and in vitro experiments were performed with conditionally immortalized mouse podocytes treated with high glucose and NRG4 to assess the protective effects of NRG4 on podocyte injury. Autophagy-related protein levels and related signaling pathways were evaluated both in vivo and in vitro. The involvement of the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway was detected using chloroquine or AMPK inhibitors. The results showed that the AMPK/mTOR pathway was involved in the protective roles of NRG4 against high glucose-mediated podocyte injury. Also, NRG4 significantly decreased albuminuria in DN mice. PAS staining indicated that NRG4 mitigated glomerular volume and mesangium expansion in DN mice. Consistently, western blot and RT-PCR analyses confirmed that NRG4 decreased the expression of pro-fibrotic molecules in the glomeruli of DN mice. The immunofluorescence results showed that NRG4 retained expression of podocin and nephrin, whereas transmission electron microscopy revealed that NRG4 alleviated podocyte injury. In DN mice, NRG4 decreased podocyte apoptosis and increased expression of nephrin and podocin, while decreasing the expression of desmin and HIF1α. Overall, NRG4 improved albuminuria, glomerulosclerosis, glomerulomegaly, and hypoxia in DN mice. The in vitro experiments showed that NRG4 inhibited HG-induced podocyte injury and apoptosis. Furthermore, autophagy of the glomeruli decreased in DN mice, but reactivated following NRG4 intervention. NRG4 intervention was found to partially activate autophagy via the AMPK/mTOR signaling pathway. Consequently, when the AMPK/mTOR pathway was suppressed or autophagy was inhibited, the beneficial effects of NRG4 intervention on podocyte injury were diminished. These results indicate that NRG4 intervention attenuates podocyte injury and apoptosis by promoting autophagy in the kidneys of DN mice, in part, by activating the AMPK/mTOR signaling pathway.

In this study, we investigated the effect of sweroside (SOS) on hepatic steatosis in mice and elucidated its molecular mechanisms. We conducted in vivo experiments using a C57BL/6 mice model of nonalcohol fatty liver disease (NAFLD) to explore the effect of SOS on hepatic steatosis in NAFLD mice. In in vitro experiments, primary mouse hepatocytes were treated with palmitic acid and SOS, and the protective effects of SOS on inflammation, lipogenesis, and fat deposition were analyzed. Autophagy-related protein levels and their related signaling pathways were evaluated in both in vivo and in vitro experiments. The results demonstrated that SOS decreased the high-fat-induced intrahepatic lipid content both in vivo and in vitro. The autophagy level in the liver was decreased in NAFLD mice but was reactivated following SOS intervention. SOS intervention was found to partially activate autophagy via the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway. Consequently, when the AMPK/mTOR pathway was suppressed or autophagy was inhibited, the beneficial effects of SOS intervention on hepatic steatosis were diminished. These results indicate that SOS intervention attenuates hepatic steatosis by promoting autophagy in the liver of NAFLD mice, in part by activating the AMPK/mTOR signaling pathway.

目的 探讨基于学习通平台的7E教学模式在诊断学问诊教学中的应用效果.方法 选取2018级临床医学专业本科三年级学生126名(对照组)和2019级临床医学专业本科三年级学生133名(观察组)作为研究对象.对照组采用传统教学法进行教学,观察组采用基于学习通平台的7E教学方法进行教学.教学结束后对两组学生进行问诊技能考核,比较两组学生的问诊技能考核评分及对问诊教学模式的评价情况.结果 观察组学生的问诊技能考核成绩及对问诊教学模式的满意程度均高于对照组(均P<0.05);观察组学生对激发学习兴趣、提高学习效率、增强与患者沟通的信心与能力、加深对常见症状的理解、明确常见症状的问诊内容和思路、提升人文关怀能力等方面的评价均优于对照组(均P<0.05).结论 基于学习通平台的7E教学模式能更好提升临床医学生诊断学问诊的教学效果,提高学生临床问诊的实践技能水平.

Aim To investigate the blood lipid status and dyslipdemia of 41 years old people group.Method Observe 4 219 cases of 41 years old people who come to take physical examination in hospital from 2004 to 2005.Blood lipid checking items include total cholesterol,low density lipoprotein cholesterol,high-density lipoprotein cholesterol and triglyceride.Result The blood lipid level of the group increases by age.Female's TC and LDLC are higher than male after 51,and female's HDLC is higher than male in all ages.High TC blood syndromes are more than high TG blood syndromes in each age groups.The rate of high TC of male in 41-60 age group is 29.5%,and that of female is 36.3%.41.0% for 60 age group of male and female 50.6%.The rate of high TG of male in 41-60 age group is 28.4%,and that of female is 10.9%.19.5% for 60 age group of male and female 15.5%.Conclusion The rate of dyslipdemia of above 41years old people in Huaihua city is high,it predicts that the risk of atherosclerotic cardiovascular disease increases.It is necessary to propaganda reasonable food structure arrangement and to prevent dyslipdemia.

Objective To observe the clinical effects of Wuji Baifengwan on menopausal syndrome. Methods 120 cases treated in the hospital from 2002 to 2004 were given orally Wuji Baifengwan as well as psychotherapy, following up for one year. Results After 3 months of oral administration of Wuji Baifengwan, the symptoms of sweating caused by tidal fever and animation by vexation-restlessness. Kupperman scoring descended obviously, difference being remarkable before and after the administration (P 0.01). There was no adverse reaction of gastrointestinal tract and vaginal massive hemorrhage. Conclusion Wuji Baifengwan can improve clinical symptoms of menopausal syndrome and its therapeutic effects are remarkable.

目的分析心脏继发性淋巴瘤(SLH)的临床特征、治疗效果和预后因素,提高诊治水平.方法回顾性分析65例SLH的临床表现、病理类型、治疗疗效及预后因素.结果初诊时表现为浅表淋巴结肿大的17例( 26.2%),纵隔淋巴结肿大35例( 53.8%).54例( 83.1%)临床分析为Ⅳ期,心功能Ⅲ或Ⅳ级占22例( 33.8%).弥漫大B细胞性淋巴瘤、弥漫性小淋巴细胞性淋巴瘤、T淋巴母细胞性淋巴瘤和结节硬化型霍奇金淋巴瘤共占47例( 72.3%).非霍奇金淋巴瘤(NHL)和霍奇金淋巴瘤(HL)的有效率分别为 63.2%和100%,中位生存期分别为18个月和47个月.结论浅表或纵隔淋巴结肿大为SLH最常见症状,多数患者为晚期,多因素分析表明心功能分级(P= 0.013)和治疗效果(P= 0.006)为独立的预后因素.