Adipose tissue in the obese state can lead to low-grade chronic inflammation while inducing or exacerbating obesity-related metabolic diseases and impairing overall health.T cells, which are essential immune cells similar to macrophages, are widely distributed in adipose tissue and perform their immunomodulatory function; they also cross-talk with other cells in the vascular stromal fraction. Based on a large number of studies, it has been found that N6 methyl adenine (m6A) is one of the most representative of epigenetic modifications, which affects the crosstalk between T cells, as well as other immune cells, in several ways and plays an important role in the development of adipose tissue inflammation and related metabolic diseases. In this review, we first provide an overview of the widespread presence of T cells in adipose tissue and summarize the key role of T cells in adipose tissue inflammation. Next, we explored the effects of m6A modifications on T cells in adipose tissue from the perspective of adipose tissue inflammation. Finally, we discuss the impact of m6a-regulated crosstalk between T cells and immune cells on the prospects for improving adipose tissue inflammation research, providing additional new ideas for the treatment of obesity.

Sirtuins are a family of NAD+ -dependent deacetylases that regulate some important biological processes, including lipid metabolism and autophagy, through their deacetylase function. Autophagy is a new discovery in the field of lipid metabolism, which may provide a new idea for the regulation of lipid metabolism. There are many tandem parts in the regulation process of lipid metabolism and autophagy of sirtuins protein family. This paper summarized these tandem parts and proposed the possibility of sirtuins regulating lipid autophagy, as well as the interaction and synergy between sirtuins protein family. Currently, some natural drugs have been reported to affect metabolism by regulating sirtuins, some of which regulate autophagy by targeting sirtuins.

Physiologically, the intestinal barrier plays a crucial role in homeostasis and nutrient absorption and prevents pathogenic entry, harmful metabolites, and endotoxin absorption. Recent advances have highlighted the association between severely damaged intestinal barriers and diabetes, obesity, fatty liver, and cardiovascular diseases. Evidence indicates that an abated intestinal barrier leads to endotoxemia associated with systemic inflammation, insulin resistance, diabetes, and lipid accumulation, accelerating obesity and fatty liver diseases. Nonetheless, the specific mechanism of intestinal barrier damage and the effective improvement of the intestinal barrier remain to be explored. Here, we discuss the crosstalk between changes in the intestinal barrier and metabolic disease. This paper also highlights how to improve the gut barrier from the perspective of natural medicine, gut microbiota remodeling, lifestyle interventions, and bariatric surgery. Finally, potential challenges and prospects for the regulation of the gut barrier-metabolic disease axis are discussed, which may provide theoretical guidance for the treatment of metabolic diseases.

White and thermal (brown and beige) adipose tissue energy storage and oxidative regulation pathways play a central role in maintaining the energy balance throughout the body, and the dysregulation of these pathways is closely related to glucose and lipid metabolism disorders and adipose tissue dysfunction, including obesity, chronic inflammation, insulin resistance, mitochondrial dysfunction, and fibrosis. Recent epigenetic studies have identified the novel regulatory element LSD1, which controls the above parameters, and have provided new mechanistic possibilities for re-encoding the fate and function of adipocytes. In this review, we outline the current advances in adipocyte metabolism in physiology and disease and discuss possible strategies for LSD1 to alter the phenotype of adipose tissue and thus influence energy utilization to improve metabolic health.

As a circadian rhythm hormone, melatonin is widely present in the body and has rich physiological functions. Compared to its prominent circadian role, melatonin has been extensively studied in many fields as an ancient antioxidant. In addition to being considered a potent antioxi-dant, melatonin has also been found to play an important role in mitochondrial homeostasis. Mito-chondrial oxidative stress plays a crucial role in the occurrence and development of atherosclerosis. Therefore, the possible therapeutic value of melatonin as an antioxidant targeting mitochondria in atherosclerosis is worth exploring. The most widespread clinical applications of melatonin are in circadian rhythms and sleep, but the cardiovascular system may be the most promising area.

N6-甲基腺嘌吟(6mA)是存在于真核生物中的表观遗传修饰,通过对线粒体DNA、非编码基因和核糖体DNA等进行修饰,进而动态调控转录.目前研究发现,6mA通过调节线粒体DNA的转录等影响线粒体活性和功能,进而参与代谢性疾病的发生发展.本文探讨6mA调控线粒体功能的机制及其在肥胖、动脉粥样硬化、高血压和癌症等代谢性疾病中的作用,有望为代谢相关疾病的防治提供新思路.

医学生临床基本技能教学是医学教育中至关重要的一环.当前教学模式下,学生缺乏同理心,难以真正学会医患交流及人文关怀.叙事医学作为连接医学专业教育与人文精神的有效媒介应用于临床基本技能教学,可助力医学生提升共情水平,实践人文关爱,从而全面增强临床基本技能的教学实效,为医患沟通能力的提高搭建和谐桥梁,为医学模式的转变提供有效支撑.

深度融合信息技术,推动医学教育改革的进一步发展已被医学教育者所广泛接受和认可,文中就多种现代信息技术在医学生临床技能教学中的应用进行了初步的探讨,并对现代信息技术深度融合背景下的医学生临床技能培养模式及发展前景做了展望.

糖尿病心肌病是糖尿病患者的一种特殊的心脏并发症,其特征主要表现为早期阶段的左心室肥大和舒张功能障碍,直至发展为心力衰竭.因此,探索糖尿病心肌病的治疗方案具有重要的临床意义.研究表明,生酮饮食具有改善糖尿病心肌病的作用,但具体机制尚未阐明.本文总结了糖尿病引发心力衰竭的途径和机制,阐述了生酮饮食改善糖尿病心肌病的潜在机制,如改善氧化应激、炎症、线粒体功能、心肌代谢等,为糖尿病心肌病的防治提供新的思路.

目的 通过运用行为阶段模型(TTM)对不同层次本科医学生临床课程学习动机进行分析,揭示不同层次本科医学生在学习动机方面的区别并探讨学习动机对学习效果的影响.方法 随机从南华大学衡阳医学院和湖南医药学院各筛选60名学生,根据学生实际情况,制定针对学习动机分析的TTM评估量表.在接受临床课程学习半学期后,请学生完善调查量表;再搜集临床课程的期末理论及迷你临床演练评估(Mini-CEX)测试成绩进行统计学分析.结果 2所高校医学生临床课程学习动机行为阶段分布比较,差异有统计学意义(P＜0.05),且学习动机所处行为阶段对学习效果有一定影响,尤其是Mini-CEX成绩.结论 根据实际情况制定的TTM可全面细致地分析和评估医学生学习动机,值得在以后的教学工作中不断改进和推广.

维生素D (vitamin D,VitD)是一类固醇类衍生物,活性维生素D通过与维生素D受体(VDR)结合发挥多种生物学功能,除了与骨骼的生长发育相关之外,其对脂肪、肝脏及肾脏等多种组织器官的功能具有重要的调节作用.肥胖诱导的代谢性炎症与心血管疾病、糖尿病、代谢综合征等疾病密切相关,然而,维生素D与肥胖引发的代谢性炎症是否有直接的联系尚不明确.为此,该文对维生素D与代谢性炎症之间的关系作综述,以便揭示维生素D在代谢性炎症防治中的作用.

随着技术的不断发展,人工智能在医学诊疗方面的运用越来越广泛,文中阐述了目前人工智能发展的技术水平和特点,对人工智能在医学生临床技能教学中的应用进行了初步探讨,并对人工智能技术在医学教育中的发展前景作了展望.

Ghrelin, a peptide hormone produced in the gastrointestinal tract, has recently been found to be associated with the onset of myocardial fibrosis (MF). The exact mechanism, however, remains elusive. This study sought to identify the function and mechanism of ghrelin on MF after acute myocardial infarction (AMI). AMI was established in Spraque-Dawley rats by ligation of the left anterior descending (LAD). Ghrelin or saline was intraperitoneally injected two times per day for 8 weeks after ligation. The weight of heart (mg) and the weight ratio of heart to body (mg/g) as well as the fibrotic area were increased, while serum level of ghrelin was decreased after AMI. Ghrelin significantly ameliorated MF and decreased deposition of collagens in perivascular fibrosis area. In addition, ghrelin inhibited Endothelial-to-mesenchymal transition (EndMT), a crucial process for MF, in perivascular fibrosis area and TGF-β1-induced human coronary artery endothelial cells (HCAECs). Mechanistically, ghrelin persistently decreased the phosphorylation of Smad2/3 and enhanced the expression of Smad7 and p-AMPK in vivo and in vitro. After the abolition of Smad7, GHSR-1a and AMPK pathway, the effect of ghrelin on EndMT was significantly inhibited. In conclusion, these results presented a novel finding that ghrelin attenuated MF after AMI via regulation EndMT in a GHSR-1a/AMPK/Smad7- dependent manner.

诊断学是医学生必修的一门重要专业课程.如何在诊断学教学过程中选择与构建优化的教学模式与方法,提高教学效果,提升学生的学习兴趣是目前各高校诊断学教学研究的主要方向.本文根据诊断学各章节教学内容的特点,探讨将微课、虚拟仿真以及翻转课堂等信息化教学方式有机运用于诊断学的教学中,有效地促进诊断学教学改革.以期为学生提供丰富的教学资源,提供直观、逼真的学习环境,提高学生动手的机会,锻炼学生的临床思维,调动学生的学习积极性,达到提升诊断学教学质量的目的.

临床技能学是医学实践课程,传统教学方式真实性差、教学效果差的劣势亟待解决.在当今互联网技术和移动终端的高速发展下,微课程将医疗工作与课堂连接,使临床技能学课程真实生动且提高受众范围,极大提高了临床技能学教学资源的利用率.

现代教育技术是培养创新人才的重要手段.随着网络技术的不断进步与信息革命的高速发展,传统教育在先进网络信息技术的冲击下面临着新的挑战.探索适合专业学位研究生的教学模式是专业学位研究生教学研究的重点.虚拟仿真教学是高校教学改革未来发展的一个重要方向,是临床专业学位研究生培养的重要教育手段之一.

Objective To explore the relationship between angiotensin-converting enzyme ( ACE ) rs4646994 gene polymorphism and idiopathic dilated cardiomyopathy ( IDC) in patients of south China .Methods We collected 64 IDC pa-tients in south China as the IDC group and 120 healthy persons as the control group , then investigated the ACE rs4646994 genotype in the fasting peripheral venous blood collected from the two groups by RT -PCR and detected the ACE concentra-tion in the plasma by UV spectrophotometer .Results In the IDC group, the frequency of DD genotype was 28.13%, which was significantly higher than that of the control group (10.00%) and the frequency of D allele was 50.79%, which was significantly higher than that of the control group (33.75%) (all P<0.05), but there was no significant difference in ID genotype, II genotype and I allele (all P>0.05).In the IDC group and control group , the ACE concentration in pa-tients with DD genotype was significantly higher than that of patients with ID genotype and II genotype ( P<0.05 or P<0.01), but no significant difference was found in the ACE concentration among the people with the same genotypes (all P>0.05).Conclusion The insertion/deletion polymorphism of ACE gene is associated with IDC , and the DD genotype and D allele of ACE gene may probably increase south China Han population at risk of IDC .

Objective: Transforming growth factor β1 (TGF-β1) is the major cytokine for stimulating endothelial cells (ECs) to transdifferentiate to mesenchymal cells (MCs) in the process known as endothelial-to-mesenchymal transition (EndMT). Recently, TGF-β1-induced EndMT has been implicated in the pathogenesis of atherosclerosis (AS). It has been identified that apolipoprotein A1 (ApoA-I) obstructs TGF-β1-induced endothelial dysfunction, providing a protective effect for ECs and also anti-AS activity. However, the exact role of ApoA-I in TGF-β1-induced EndMT is not clear. In this study, we aimed to investigate whether ApoA-I can modulate TGF-β1-induced EndMT in human coronary artery ECs (HCAECs). Methods and Results: The HCAECs were treated with TGF-β1 with or without ApoA-I. Morphological changes in HCAECs and the expression of EndMT-related markers were evaluated. HCAECs treated with TGF-β1 were found to transform to MC morphology, with inconspicuous expression of EC markers such as vascular endothelial cadherin and CD31, and conspicuous expression of fibroblast-specific protein 1 (FSP-1) and α-smooth muscle actin. The treatment of HCAECs with ApoA-I inhibited the TGF-β1-induced EndMT, and elevated expression of EC markers was observed but reduced expression of MC markers. Moreover, ApoA-I impeded the expression level of Slug and Snail, crucial transcriptional factors of EndMT, and it inhibited the TGF-β1-induced phosphorylation of Smad2 and Smad3 which affected the EC morphology. In addition, the knockdown of ABCA1 by RNA interference eliminated the inhibition effect of ApoA-I on TGF-β1-induced EndMT. Conclusions: Our findings revealed a novel mechanism for the ApoA-I protective effect on endothelium function via the inhibition of TGF-β1-induced EndMT. This might provide new insights for developing strategies for modulating AS and vascular remodeling.

目的研究1，25-二羟维生素D3（1，25（OH）2D3）对棕榈酸（PMA）诱导THP．1巨噬细胞炎症因子表达的影响及其机制。方法用1，25（OH），D，（10nmol,／L）和／或PMA（250umol／L）处理THP-1巨噬细胞6h，采用荧光定量PCR和酶联免疫吸附法（ELISA）法检测肿瘤坏死因子α（TNFα）、白细胞介素（IL）-1β、IL-6和IL-10的表达水平：用1，25（OH），D，和／或PMA处理THP-巨噬细胞60min，采用免疫印迹（Western-blot）法检测AMPKα1和磷酸化AMPKα1（p-AMPKα1）水平。结果1，25（OH）2D3（10μmol／L））明显抑制PMA（250txmol／L）作用下THP-1巨噬细胞TNFα、IL-1β和IL-6的表达，并上调IL-10的表达；1，25（OH）2D，显著上调THP-1巨噬细胞AMPKcd的磷酸化水平。结论1，25（OH）2D3抑制PMA诱导的THP．1巨噬细胞炎症因子表达，该效应可能与其激活AMPKod有关。

信号转导和转录活化因子3(the signal transducer and activator of transcription 3,STAT3)是维持生理稳态的重要凋节因子,它的活化受到多种受体系统的调节,当配体-受体结合后可引发正反馈和负反馈作用以保证生理反应的正常进行.它能调节心脏内心肌细胞、成纤维细胞、内皮细胞、干细胞以及各种炎症细胞的增殖、分化、氧化应激和(或)新陈代谢,也作为信号蛋白和转录因子参与调控相关反应.STAT3可以影响心脏各细胞间的分泌并调节心肌细胞间通讯、心脏微环境重塑、血管再生、细胞外基质的形成,以及在病理或生理应激下的炎症反应的进行.在此,根据STAT3相关功能特点,对其在心肌细胞内信号网络中介导的细胞内与细胞间通讯以协调复杂的生物进程进行总结,并讨论以其为靶点的新的治疗理念来治疗各种形式的心脏疾病.