作者机构：
[欧阳雅琦; 黄源] School of Nursing, University of South China, Hengyang, 421001, China;[谢鑑辉] Nursing Department, Hunan Children's Hospital, Changsha, 410007, China;[梅海波; 易银芝; 莫莎莎; 谭谦] Department of Orthopedics, Hunan Children's Hospital, Changsha, 410007, China;[赵昕] Department of Pharmacy, Hunan Children's Hospital, Changsha, 410007, China
作者机构：
[唐瑶; Zeng S.] Institute of Pathogenic Biology, Hunan Provincial Key Laboratory for Special Pathogen Prevention and Control, Hengyang Medical College, University of South China, Hengyang, 421001, China;Hunan Province Innovative Training Base for Postgraduates, University of South China and Nanyue Biopharmaceutical Co. Ltd., Hengyang, 421001, China;[李蕊; 唐鑫] School of Nursing, University of South China, Hengyang, 421001, China;[段洁; 郭开云; 黄立军; Zhang J.; 张洁雅] Institute of Pathogenic Biology, Hunan Provincial Key Laboratory for Special Pathogen Prevention and Control, Hengyang Medical College, University of South China, Hengyang, 421001, China, Hunan Province Innovative Training Base for Postgraduates, University of South China and Nanyue Biopharmaceutical Co. Ltd., Hengyang, 421001, China
通讯机构：
[Zhang, Y.] I;Institute of Pathogenic Biology, China
关键词：
幽门螺杆菌;SGC-7901细胞;外泌体;微小RNA;差异表达;巨噬细胞极化
摘要：
目的:探讨幽门螺杆菌(
H.
pylori)诱导的人胃癌SGC-7901细胞源性外泌体中微小RNA(miRNA)的差异表达，为进一步阐明
H．
pylori的致癌机制提供新线索。
方法:超高速离心法和试剂盒提取
H.
pylori刺激组和对照组细胞释放的外泌体，采用透射电镜、纳米粒子跟踪分析和Western blot对外泌体进行鉴定；荧光染料PKH67标记的外泌体与THP-1源性巨噬细胞共孵育，共聚焦显微镜观察巨噬细胞内吞外泌体的情况；miRNA基因芯片分析两组细胞外泌体miRNA差异表达谱，采用qRT-PCR对其中4个差异表达miRNA进行验证；生物信息学软件预测、分析部分差异表达miRNA结合的靶基因及其功能和可能参与的信号通路。Cy3标记差异表达miR-382-5p，观察其能否通过外泌体传递给巨噬细胞；qRT-PCR和ELISA检测miR-382-5p mimic转染巨噬细胞表型分子CD206和细胞因子TNF-α、IL-6、IL-10的表达，流式细胞术分析表达CD206和HLA-DR的细胞比例。
结果:提取的外泌体符合外泌体形态，且高表达其表面标志蛋白CD9、CD63、TSG101；外泌体与THP-1巨噬细胞共孵育12 h后被细胞内吞；与对照组相比，
H.
pylori刺激组有上调miRNA 130个、下调miRNA 111个；部分差异表达miRNA预测的靶基因主要参与调节PI3K-AKT、NF-κB、JAK-STAT、干细胞多能性等炎症和肿瘤相关通路。miR-382-5p可通过外泌体传递给巨噬细胞，诱导巨噬细胞M2型表型分子CD206和细胞因子IL-10表达，并抑制TNF-α、IL-6表达，CD206
highHLA-DR
low细胞比例升高。
结论:H．
pylori处理SGC-7901细胞导致其外泌体miRNA表达水平发生显著改变。生物信息学预测结果显示，部分差异表达miRNA的靶基因产物在炎症和肿瘤相关信号通路调节中发挥重要作用。miR-382-5p具有诱导巨噬细胞向M2极化的潜能。
摘要：
高血压是影响全球死亡率和伤残调整生命年(dis-ability-adjusted life year,DALY)的主要因素[1].中国年龄＞18岁成年人高血压患病率已达27.9％[2].高血压患者人年均治疗费约为1 874元[3],给患者家庭经济及国家社会发展带来巨大负担,因此采取科学有效管理措施迫在眉睫.临床决策支持系统(clinical de-cision support system,CDSS)是运用专家系统设计原理和方法,模拟医学专家在诊断治疗疾病过程中的思维方式所编制计算机程序,是辅助医护人员进行临床决策的工具[4-6].CDSS是医学知识工程和人工智能研究非常活跃的分支,一直是国内外研究热点.在"互联网+"的大背景下,CDSS是未来高血压管理重要发展方向,但目前其功能局限于向临床医师提供疾病诊断、信息提醒和药物推荐的内容,而缺少患者出院后疗效评估、康复指导和健康教育等方面信息[7-9].本文对CDSS在高血压中的应用现状和问题进行综述,旨在为开发更专业化、系统化的高血压CDSS提供新思路.
作者机构：
[Qi Liu; Yan-Jin Huang; Ling Zhao; Wen Wang; Shan Liu; Guo-Ping He; Li Liao; Ying Zeng] School of Nursing, University of South China, Hengyang, Hunan, China
通讯机构：
[Ying Zeng] S;School of Nursing, University of South China, Hengyang, Hunan, China
关键词：
Aged;Cross-sectional studies;Cardiovascular diseases;Knowledge;Physical examination;Risk factors;Surveys and questionnaires
摘要：
Objectives:This study aimed to describe cardiovascular risk and cardiovascular disease (CVD) knowledge among older adults,and further explore the association between knowledge and risk.Methods:In this cross-sectional study,we enrolled 1120 older adults who received physical examination in health centers.The participants were interviewed to obtain their behavioral risk factors related to CVD and clinical characteristics.A risk prediction chart was used to predict participants' cardiovascular risk based on clinical characteristics and behavioral risk factors.Participants' CVD knowledge was collected with a pretested knowledge questionnaire.Results:Among the 1120 participants,240 (21.4%) had low cardiovascular risk,353 (31.5%) had moderate cardiovascular risk,527 (47%) had high and very high cardiovascular risk.The knowledge level about CVD among 0.8% of the 1120 participants was good while that of 56.9% was poor.Lower CVD knowledge level,older age,lower income,and lower educational level were the independent factors of higher cardiovascular risk level.Conclusions:This study highlights the need to reduce the cardiovascular risk among older adults.CVD knowledge should be considered when developing health interventions.
作者机构：
[Zhao Hong; Chen Lin Xi] Univ South China, Hengyang Med Coll, Inst Pharm & Pharmacol, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Hunan, Peoples R China.;[Zhao Hong; Qiu Ting Ting] Univ South China, Coll Nursing, Hengyang 421001, Hunan, Peoples R China.;[Liu Mei Qing] Second Peoples Hosp Yunnan Prov, Dept Pharm, Kunming 650000, Yunnan, Peoples R China.
通讯机构：
[Chen Lin Xi] U;[Liu Mei Qing] S;Univ South China, Hengyang Med Coll, Inst Pharm & Pharmacol, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Hunan, Peoples R China.;Second Peoples Hosp Yunnan Prov, Dept Pharm, Kunming 650000, Yunnan, Peoples R China.
关键词：
STORE;producing;FEEDING
摘要：
Mammalian adipose tissues can be broadly divided into white adipose tissue(WAT), beige adipose tissue, and brown adipose tissue(BAT)[1]. The function of WAT is to store superfluous energy and is characterized by unilamellar lipid droplets. WAT, as a prominent endocrine organ, regulates feeding and satiety by producing hormones. Compared with WAT, beige adipose tissue has some smaller multilocular lipid droplets and is located in WAT depots. However, BAT contains an abundance of mitochondria, uncoupling protein-1(UCP1), and multilocular lipid droplets[2]. BAT is an important non-shivering thermogenesis organ, with the capacity to oxidize metabolic substrates, including fatty acids and glucose, to produce heat. The main mechanism of heat production depends on UCP1. It transports protons into mitochondria, leading to the collapse of the proton gradient for oxidative phosphorylation; subsequently, cells generate heat instead of ATP. The thermogenic activity of brown adipocytes enables them to safeguard other tissues and themselves from lipid overaccumulation. Many studies have confirmed that promoting brown adipose thermogenic activity or the browning of white fat contributes to curbing obesity, diabetes,and other metabolic diseases[3-7]. Brown adipocytes are derived from Myf5+ progenitors with a high expression of PRDM16, BMP7, and PPARγ. These transcription regulators drive progenitors to develop into mature brown adipocytes[8]. Meanwhile, a development process is required for brown adipogenesis to suppress adipogenic inhibitors,including Wnt, necdin, and preadipocyte factor-1(Pref-1). Numerous studies have confirmed that many signaling pathways promote brown adipocyte differentiation, including rhACE2, SIRT5, RGS2,STAT3, RepSox, and SENP2(Figure 1). Tu et al.[9] reported that RepSox promoted brown preadipocyte differentiation by inhibiting TGF-β signaling. Shuai et al.[10] demonstrated that SIRT5 enhanced the expression of brown adipogenic promoters, including PPARγ and PRDM16. Klepac et al.[11] identified a crucial role for RGS2, which antagonized the inhibitory effect of Gq/Rho/ROCK signaling, in the acceleration brown adipogenesis. Cantwell et al.[12] revealed the significance of STAT3 in the early induction of primary Myf5+ brown adipogenesis through its suppression of Wnt/β-catenin signaling. Kawabe et al.[13] proved that rhACE2 increased the levels of PRDMl6 and PGC1α to boost differentiation of BAT. Recently, Liang et al.[14] demonstrated that brown adipocyte differentiation was facilitated via the SENP2-mediated deSUMOylation for necdin.
