关键词： 防范策略   致病因素   妊娠   慢性病门诊  

摘要： 在医院的慢性病门诊中,糖尿病患者常常提出各种疑问:糖尿病是否会影响妊娠?子女是否会遗传?为什么确诊后有人变瘦,有人却变胖?糖尿病前期能否逆转?这些问题反映了大众对糖尿病的常见误区和关注点。本文将深入探讨糖尿病的诱发原因、高危因素、确诊条件及发病前期的干预策略,帮助大家正确认识糖尿病,掌握科学的防范方法。

关键词： 2型糖尿病   糖尿病肾病   炎症指数   诊断模型  

摘要： 目的探讨炎症指数在2型糖尿病(type 2 diabetes mellitus,T2DM)与糖尿病肾病(diabetic kidney disease,DKD)中的变化特征,并构建诊断预测模型。方法选择310例T2DM患者作为研究对象,其中,101例糖尿病肾病患者为DKD组,其余209例患者为非DKD组。收集患者一般资料,采集患者血液标本,行血常规与生化检查,计算各组炎症指数。对两组患者数据进行差异性分析,使用单因素与多因素Logistics回归筛选变量并构建诊断模型,绘制列线图。使用ROC曲线与校准曲线评价模型,利用Bootstrap法进行内部验证。结果DKD组患者中性粒细胞、单核细胞数量、NLR、PLR、SII水平及高脂血症、高尿酸血症、高血压比例明显高于非DKD组(P<0.05),LMR水平、淋巴细胞数量低于非DKD组(P<0.05)。Logistics回归分析结果显示,PLR、SII水平及高脂血症是DKD的独立危险因素,而LMR水平是DKD的独立保护因素。ROC曲线与校准曲线显示,曲线下面积为0.837,截断值、特异度、敏感度分别为0.405、0.847、0.743,模型拟合度检验P=0.441(P>0.05),Brier评分为0.151分,模型区分度与拟合度良好。Bootstrap内部验证结果显示,经500次抽样,模型预测结果与实际较为符合,重复性良好。结论基于炎症指数建立的DKD诊断模型,对T2DM人群中可能进展为DKD者具有一定预警价值。

关键词： 老龄化   2型糖尿病   男性   糖尿病足   发病率  

摘要： 随着人口老龄化加剧和生活方式的显著变化,糖尿病的发病率逐年上升。全球最新研究显示,约4%~10%的糖尿病患者可能会患糖尿病足,其发病率至少为15%。也就是说,在糖尿病患者中,每六个人中就可能有一人患上糖尿病足,男性及2型糖尿病患者更容易受到影响。在中国,糖尿病足的发病率约为2%~3%,但其治疗难度较大,费用高昂。

关键词： 肾脏   调节师   生活质量   血管   眼睛   平衡点  

摘要： 糖尿病听上去像是个棘手的病,很多人一听到自己血糖高了,觉得以后啥都不能吃了,生活质量要大打折扣。其实,糖尿病远比想象中复杂,它像一个隐藏的“调节师”,影响着全身多个系统,不仅让血糖起伏,还和心脏、血管、眼睛、肾脏、神经等多个器官紧密相连。糖尿病不仅仅是个疾病,更像是一个提醒,它让人重新审视自己的生活习惯,调整饮食、管理作息、增加运动,甚至让一些原本不注重健康的人,反而开始活得更规律、更讲究。与糖尿病和谐共处,不是简单地“控糖”,而是要找到新的平衡点,让自己活得更轻松。

关键词： 血糖失控   胰岛素治疗   胰岛β细胞   外源性胰岛素  

摘要： 目前,糖尿病这个“甜蜜杀手”正在悄悄侵袭越来越多人的健康,糖尿病的核心问题是血糖失控,而胰岛素是人体调节血糖的关键激素。健康人胰腺的胰岛β细胞会分泌胰岛素,帮助葡萄糖进入细胞转化为能量,并抑制肝脏释放储存的糖分。当胰岛β细胞受损(如1型糖尿病)或胰岛素作用受阻(如2型糖尿病晚期),外源性胰岛素就成为控制血糖的“救星”。

关键词： 冷水游泳   炎症反应   转录组   NOD样受体信号通路   差异表达基因   工程化组织构建  

摘要： 背景:冷环境中运动,机体炎症反应受冷应激及运动应激双因素作用,其作用机制仍有待探究。目的:基于转录组测序技术探究冷水游泳对大鼠机体炎症反应的影响及机制。方法:40只雄性SD大鼠随机分为室温对照组、室温游泳组、冷水对照组、冷水游泳组,每组10只。室温对照组无干预,自由进食;室温游泳组游泳30 min/次,6次/周,共5周,水温(28±2)℃,水深35 cm;冷水对照组将大鼠放在水深3 cm的水箱中,水温(18±2)℃,自由活动;冷水游泳组游泳30 min/次,6次/周,共5周,水温(18±2)℃,水深35 cm。ELISA法检测各组大鼠血清白细胞介素6、肿瘤坏死因子α和高敏C-反应蛋白表达水平;基于转录组测序结果筛选差异表达基因绘制韦恩图和热图,并进行基因本体论和京都基因与基因组百科全书富集分析,蛋白互作网络筛选核心基因;RT-qPCR检测大鼠脾脏组织IRF7,OAS2,OASL mRNA表达情况。结果与结论:①ELISA检测结果显示,与室温对照组相比,室温游泳组和冷水游泳组各炎症指标水平显著升高(P<0.05),冷水对照组无显著差异;与室温游泳组相比,冷水游泳组各炎症指标表达无显著差异;与冷水对照组相比,冷水游泳组白细胞介素6和肿瘤坏死因子α表达呈上升趋势,高敏C-反应蛋白表达水平显著上升(P<0.05);②转录组分析结果显示,韦恩图显示受温度及运动干预双因素影响的差异表达基因共有39个;聚类热图分析结果表明,室温游泳组和冷水游泳组基因表达趋势整体相似,冷水对照组呈相反趋势;基因本体论和京都基因与基因组百科全书富集分析结果表明,差异表达基因富集于免疫系统、运动、核酸结合转录因子活性、NOD样受体信号通路等途径,NOD样受体信号通路富集基因数相对较多,且q value值较小,可能为关键通路;蛋白互作网络筛选出IRF7,OAS2,OASL,IFIT2,IFIT3等核心基因;③RT-qPCR验证结果显示,与室温对照组相比,室温游泳组和冷水游泳组大鼠IRF7,OAS2,OASL mRNA表达水平显著升高(P<0.01),冷水对照组无显著差异;与冷水对照组相比,冷水游泳组各基因表达水平显著升高(P<0.01);④提示冷水游泳能够促进炎症反应,其机制可能通过NOD样受体信号通路调节。

关键词： 2型糖尿病   恶性肿瘤   糖化血红蛋白波动  

摘要： 目的探讨糖化血红蛋白波动对2型糖尿病(type 2 diabetes mellitus,T2DM)患者恶性肿瘤发病的影响,为糖尿病防治提供参考。方法采用回顾性队列研究的方法将上海市恶性肿瘤登记信息与闵行区糖尿病患者管理信息进行整合,采用平均实际变异性(Average Real Variability,ARV)对不少于3次且年随访结果不超过1次的糖化血红蛋白记录进行Cox回归模型和限制立方样条函数(Restricted Cubic Splines,RCS)统计分析。ARV采用四分位数分类进行分组,分别用Q1、Q2、Q3、Q4表示。Cox回归采用未经调整的模型Ⅰ和调整性别、年龄分组等模型Ⅱ进行。结果共纳入2762名研究对象,男性45.84%,女性54.16%,平均年龄(63.58±10.11)岁,平均随访时间(9.96±3.66)年,恶性肿瘤发病率345.45/10万人年。不同ARV分组恶性肿瘤发病差异有统计学意义(P=0.01)。经模型Ⅰ和模型Ⅱ的COX回归分析显示,与Q1相比,Q4组风险显著增加,HR分别为2.72(1.56~4.74)和2.68(1.53~4.68)。限制立方样条图结果显示除≥65岁组外,均随着ARV系数的增加肿瘤的发病风险逐渐升高。结论糖化血红蛋白的波动对2型糖尿病患者恶性肿瘤的发病有促进作用,对此需加强糖化血红蛋白监测并减少因糖化血红蛋白波动带来的健康危害。

关键词： AQP4 localization   brain edema   calcium signaling   calmodulin   status epilepticus   SUR1-TRPM4  

摘要： Status epilepticus (SE) is a severe condition that results in uncontrollable cerebral edema and cognitive dysfunction. Recent studies suggest that the localization of aquaporin-4 (AQP4) in astrocytic endfeet plays a crucial role in regulating blood-brain water transport and cell volume control, particularly along perivascular pathways. However, the signaling mechanisms underlying AQP4 localization remain poorly understood. In this study, we utilized the genetically encoded fluorescent calcium (Ca2+) indicator GCaMp6f to investigate Ca2+ signals in astrocytic somata, processes, and endfeet during SE induction and observed enhanced Ca2+ signals in both the somata and perivascular endfeet of astrocytes. We employed genetic knockout of TRPM4 (Trpm4-/-) and glibenclamide treatment to explore the role of sulfonylurea receptor 1 transient receptor potential melastatin-4 (SUR1-TRPM4) channel in these Ca2+ responses. Both approaches significantly suppressed the Ca2+ signals in the astrocytic endfeet and reduced perivascular expression of the Ca2+-related signaling pathway sensor calmodulin (CaM). Furthermore, we found that AQP4 localization was no longer confined to the domains of astrocytic endfeet following SE. Inhibition of SUR1-TRPM4 through pharmacological blockade or gene deletion restored the subcellular localization of AQP4, reduced cerebral edema, and improved cognitive outcomes post-SE. Our findings suggest that SUR1-TRPM4 plays a pivotal role in regulating astrocytic Ca2+ signals and mediating the aberrant expression and subcellular localization of astrocytic AQP4 along perivascular pathways. Together, these findings demonstrate a novel molecular mechanism underscoring SUR1-TRPM4 therapy in the treatment of SE characterized by dysregulated Ca2+ signaling in astrocytic endfeet.

关键词： astrocyte   calmodulin   STIM1-Orai complex   store-operated calcium entry   trifluoperazine  

摘要： Trifluoperazine (TFP), a known inhibitor of Ca2+-bound calmodulin (Ca2+/CaM), has been reported to elevate cytosolic Ca2+ levels by disinhibiting inositol 1,4,5-triphosphate receptor 2 (IP3R2), thereby suppressing glioblastoma invasion and inducing apoptosis. Interestingly, TFP induces a sustained Ca2+ plateau, sensitive to extracellular Ca2+, suggesting involvement of Ca2+ entry such as store-operated calcium entry (SOCE). However, the underlying molecular mechanism remains elusive. Here, we report that TFP induces sustained Ca2+ signals by blocking the Ca2+/CaM-dependent desensitization of SOCE channels in cortical astrocyte cultures. TFP induces a prolonged Ca2+ response, with distinct kinetics compared to other Ca2+ modulators such as TFLLR-NH2 (a G alpha q-coupled GPCR agonist) and thapsigargin (a sacro/endoplasmic reticulum Ca2+-ATPase inhibitor). Under extracellular Ca2+-free conditions, Ca2+ levels increase without reaching a plateau, suggesting that the sustained Ca2+ signal relies on Ca2+ influx. Pharmacological analysis shows that sustained Ca2+ signals by TFP are CaM-dependent. Gene silencing targeting STIM1 and Orai1-3 confirmed their essential roles in the sustained response. We find that TFP effectively "locks open" SOCE channels by inhibiting their desensitization, maintaining SOCE activity. This effect is also observed in ex vivo hippocampal dentate gyrus astrocytes. Structural modeling supports a mechanism in which TFP disrupts the interaction between Ca2+/CaM and the SOAR domain of STIM1. Together, these findings indicate that TFP elevates cytosolic Ca2+ levels by maintaining SOCE activation, offering novel insights into the molecular actions of this drug. TFP can be a pharmacological tool for SOCE research as it locks SOCE channels open.

关键词： Seismic response  

摘要： Near-fault ground motion generally has typical velocity pulse characteristics, which can cause particularly serious harm to arch bridge. Here, to gain a deeper understanding for effects of near-fault ground motion on seismic response of arch bridge, the seismic Meta-analysis (SMa) method was firstly proposed. This method was a novel approach for performing secondary quantitative analysis based on existing study data. Afterwards, the logical process of SMa was comprehensively elaborated from SMa's analysis theme setting, study data collection and classification, analysis framework, quantitative analysis theory, selection of quantitative indexes and interpretation of analysis results. Furthermore, a comparative study was performed for effects of near-fault and non-near-fault ground motions on seismic responses of arch bridge, respectively from 3 aspects of judgment of response differences, affecting degree of response differences and effects of subdivision factors. Finally, 2 137 independent sample sets totally from 98 studies were collected for secondary analysis to verify the feasibility of SMa method and point out typical differences in effects of two types of ground motions on seismic response of arch bridge. The study showed that SMa method can perform secondary quantitative analysis from a new perspective to break away from limitations of existing conclusions and point at shortcomings of existing studies, SMa has freedoms to formulate new themes and perform supplementary analysis;within the range of seismic intensity of 0~0. difference degrees in various responses of main arch under 2 types of earthquakes increase with increase in seismic intensity, while difference degrees in responses decrease obviously after local seismic intensity exceeds 0.8g;arch bridge's displacement response and response in transverse bridge direction are most significantly affected by adverse effects of near-fault ground motions;forward oriented ground motion is the most harmful type of