社区老年人糖尿病的调查分析与护理

糖尿病严重威胁着人类的健康,已成为老年人的一种最常见的疾病。针对老年糖尿病患者的生理和心理特点,设计问卷从对糖尿病基础知识、药物治疗、饮食治疗、运动治疗和自我监测等进行社区老年患者调查,旨在了解本社区老年人糖尿病患病情况及相关因素,为进一步护理干预提供依据。     

老年人肺癌发病与吸烟关系的临床分析

我们知道吸烟是人类最重要的致癌因素之一,流行病学研究表明1/3肿瘤发生与吸烟有关,吸烟者肺癌的发生率较不吸烟者高10倍,目前,世界上约有10亿吸烟者,而中国占其中的1/3,且青少年吸烟率迅速上升,因而肺癌死亡率正以每年4.5%～10%的速度递增。     

老年人的社区护理需求调查分析

目的对我社区卫生服务机构的老年人护理需求进行调查分析。方法调查分析了我社区卫生服务机构的老年人护理需求。结果共发出问卷320份,有效问卷320份,有效率为100.0%。本组老年人年龄以60～69居多,文化程度以大专及以上居多,疾病以心脑血管疾病居多,社区护理需求以老年慢性病宣教、传染病宣教、健康教育和社区急救护理居多。结论在老年人社区护理服务中要提高服务质量、扩展服务内容、开展慢性病系统管理,通过连续性、综合性服务,对老年人慢性病的发病、康复、残疾和临终的全过程进行悉心照料和护理。     

老年人胆石症与胆囊癌的关系概述

本文总结15年来文献,结合笔者自身经验,综述了老年人胆石症与胆囊癌的关系,认为胆石症与胆囊癌的发生、发展关系密切,预防胆石症诱发胆囊癌是防治原发性胆囊癌的关键环节,对老年胆石症患者尤其要密切随访。     

老年糖尿病合并肺结核52例临床分析

目的了解糖尿病合并肺结核的临床特点,提高对老年糖尿病肺结核的认识,争取早发现、早治疗。方法对2年间52例老年糖尿病肺结核病例进行临床分析。结果治疗3个月后,血糖控制在正常范围者32例,结核病变吸收和好转者39例,痰菌阴转者25例,空洞闭合或缩小者7例,空洞无变化者3例,死亡2例。结论积极控制血糖,使血糖控制在正常水平,合理的抗结核治疗对控制老年糖尿病肺结核亦起积极作用。     

社区老年人日常生活能力及影响因素研究

为了了解苏州社区老年人生活能力状况,评价老年人健康状况,为开展老年健康保障和卫生保健服务提供科学依据,我们对苏州工业园区居住时间在半年以上的60岁及60岁以上的老年人开展了调查,现将调查结果报道如下。     

老年人急性心肌梗死的护理观察与分析

目的分析老年人急性心肌梗死的护理效果。方法随机选取40例老年人急性心肌梗死患者且实施系统性护理,然后对其进行观察与数据统计分析。结果经过有效护理后总有效率为95.00%,且护理并发症较少。结论对老年人急性心肌梗死患者实施护理至关重要。     

社区糖尿病患者健康教育重点

糖尿病可有多种并发症,通过全面系统的健康教育,使患者获得了糖尿病的相关知识,能主动配合治疗,做到合理用药、合理膳食、适宜的运动锻炼,加强自我管理,对提高患者的生活质量、减少和延缓并发症的发生、有极其重要的作用。现介绍如下。     

老年人消化性溃疡的临床分析

目的探讨老年消化性溃疡的临床特点及规律。方法回顾性分析75例老年消化性溃疡并与同期住院的中青年消化性溃疡75例进行对比。结果老年消化性溃疡中典型性节律性上腹痛14例(18.66%),青壮年组45例(60%)。老年组高位溃疡15例(20%)。老年组消化性溃疡出血19例(25.33%),高于青壮年组13例(17.33%)。结论老年人与青壮年消化性溃疡的临床表现、发生部位、及并发症等方面均有自身的特点。     

老年人破伤风62例临床分析

目的了解老年人破伤风的临床特点及转归情况。方法对62例60岁以上的老年破伤风病例的临床资料及其治疗转归等进行了统计分析,并以同期住院治疗的134例青壮年破伤风病例作为对照组。结果老年人破伤风病例在创伤后的伤口继发感染率为82.76%,而对照组为66.67%,差异有显著性(χ2=5.073,P<0.05);老年组病程中均有并发症,对照组38.81%有并发症,尤其是并发肺部感染者,老年组占85.48%,而对照组为23.13%,有非常显著性差异(χ2=12.07,P<0.01);老年组中重型病例占58.07%,对照组为31.35%,有非常显著性差异(χ2=20.612,P<0.001);气管切开率老年组为41.94%,对照组为27.61%,有非常显著性差异(χ2=14.73,P<0.001);老年组的病死率为30.65%,对照组为14.92%,有显著性差异(χ2=6.57,P<0.05)。结论老年人在创伤后伤口易继发感染,发病后易发生各种并发症,病死率较高。     

Genetic Evidence for a Causal Relationship between Hyperlipidemia and Type 2 Diabetes in Mice

Dyslipidemia is considered a risk factor for type 2 diabetes (T2D), yet studies with statins and candidate genes suggest that circulating lipids may protect against T2D development. Apoe-null (Apoe^-/-) mouse strains develop spontaneous dyslipidemia and exhibit a wide variation in susceptibility to diet-induced T2D. We thus used Apoe^-/- mice to elucidate phenotypic and genetic relationships of circulating lipids with T2D. A male F2 cohort was generated from an intercross between LP/J and BALB/cJ Apoe^-/- mice and fed 12 weeks of a Western diet. Fasting, non-fasting plasma glucose, and lipid levels were measured and genotyping was performed using miniMUGA arrays. We uncovered a major QTL near 60 Mb on chromosome 15, Nhdlq18, which affected non-HDL cholesterol and triglyceride levels under both fasting and non-fasting states. This QTL was coincident with Bglu20, a QTL that modulates fasting and non-fasting glucose levels. The plasma levels of non-HDL cholesterol and triglycerides were closely correlated with the plasma glucose levels in F2 mice. Bglu20 disappeared after adjustment for non-HDL cholesterol or triglycerides. These results demonstrate a causative role for dyslipidemia in T2D development in mice.     

Relationship between Proinflammatory and Antioxidant Proteins with the Severity of Cardiovascular Disease in Type 2 Diabetes Mellitus

Type 2 diabetes mellitus patients are at significant risk of cardiovascular disease, however, the pathophysiology of these complications is complex and incompletely known in this population. The aim of this study was to compare the serum proteome of patients with type 2 diabetes mellitus presenting or not presenting cardiovascular disease with non-diabetic subjects to find essential proteins related to these cardiovascular complications. This cross-sectional study compares the serum proteome by a combination of protein depletion with 2D-DIGE (2-dimension Difference Gel Electrophoresis) methodology. The proteins differentially expressed were identified by MALDI TOF/TOF (Matrix-assisted laser desorption/ionization and Time-Of-Flight ion detector) or LC-MS/MS (Liquid Chromatography coupled to Mass-Mass Spectrometry). Type 2 diabetes mellitus patients with cardiovascular disease showed higher expression of plasma retinol binding protein and glutathione peroxidase-3 compared to those without cardiovascular disease and non-diabetic controls. These results show that proteins related to the inflammatory and redox state appear to play an important role in the pathogenesis of the cardiovascular disease in the type 2 diabetes mellitus patients.     

Statin,Calcium Channel Blocker and Beta Blocker Therapy May Decrease the Incidence of Tuberculosis Infection in Elderly Taiwanese Patients with Type 2 Diabetes

Background: It is well known that diabetes mellitus impairs immunity and therefore is an independent risk factor for tuberculosis. However, the influence of associated metabolic factors, such as hypertension, dyslipidemia and gout has yet to be confirmed. This study aimed to investigate whether the strong association between tuberculosis and diabetes mellitus is independent from the influence of hypertension and dyslipidemia, and its treatment in elderly Taiwanese patients. Methods: A total of 27,958 patients aged more than 65 years were identified from the National Health Insurance Research Database (NIHRD) in 1997 and were followed from 1998 to 2009. The demographic characteristics between the patients with and without diabetes were analyzed using the χ2 test. A total of 13,981 patients with type 2 diabetes were included in this study. Cox proportional hazard regression models were used to determine the independent effects of diabetes on the risk of tuberculosis. Results: After adjusting for age, sex, other co-morbidities and medications, calcium channel blocker, beta blocker and statin users had a lower independent association, with risk ratios of 0.76 (95% CI, 0.58–0.98), 0.72 (95% CI, 0.58–0.91) and 0.76 (95% CI, 0.60–0.97), respectively. Conclusion: Calcium channel blocker, beta blocker and statin therapy may decrease the incidence of tuberculosis infection in elderly Taiwanese patients with type 2 diabetes.     

Gut-Microbial Metabolites,Probiotics and Their Roles in Type 2 Diabetes

Type 2 diabetes (T2D) is a worldwide prevalent metabolic disorder defined by high blood glucose levels due to insulin resistance (IR) and impaired insulin secretion. Understanding the mechanism of insulin action is of great importance to the continuing development of novel therapeutic strategies for the treatment of T2D. Disturbances of gut microbiota have been widely found in T2D patients and contribute to the development of IR. In the present article, we reviewed the pathological role of gut microbial metabolites including gaseous products, branched-chain amino acids (BCAAs) products, aromatic amino acids (AAAs) products, bile acids (BA) products, choline products and bacterial toxins in regulating insulin sensitivity in T2D. Following that, we summarized probiotics-based therapeutic strategy for the treatment of T2D with a focus on modulating gut microbiota in both animal and human studies. These results indicate that gut-microbial metabolites are involved in the pathogenesis of T2D and supplementation of probiotics could be beneficial to alleviate IR in T2D via modulation of gut microbiota.     

The Role of Beta Cell Recovery in Type 2 Diabetes Remission

Type 2 diabetes (T2D) has been considered a relentlessly worsening disease, due to the progressive deterioration of the pancreatic beta cell functional mass. Recent evidence indicates, however, that remission of T2D may occur in variable proportions of patients after specific treatments that are associated with recovery of beta cell function. Here we review the available information on the recovery of beta cells in (a) non-diabetic individuals previously exposed to metabolic stress; (b) T2D patients following low-calorie diets, pharmacological therapies or bariatric surgery; (c) human islets isolated from non-diabetic organ donors that recover from “lipo-glucotoxic” conditions; and (d) human islets isolated from T2D organ donors and exposed to specific treatments. The improvement of insulin secretion reported by these studies and the associated molecular traits unveil the possibility to promote T2D remission by directly targeting pancreatic beta cells.     

黄山市2010~2013年疑似预防接种异常反应监测分析

目的分析黄山市2010~2013年疑似预防接种异常反应(adverse events following immunization,AEFI)的发生特征,评价预防接种的安全性。方法采用描述性流行病学方法对2010~2013年黄山市AEFI监测资料进行分析。结果 2010~2013年全市共报告AEFI 116例,其中一般反应99例(85.34%),异常反应11例(9.48%),偶合症5例(4.31%),接种事故1例(0.86%)。各区县均有AEFI报告,48 h内报告率为93.10%,48 h内调查率为97.14%;男女性别比为1.27∶1,年龄≤1岁占43.10%,报告疫苗以国家免疫规划(National Immunization Programme,NIP)疫苗为主;报告的AEFI病例主要集中在5~9月份,68.97%发生在接种后1 d内;AEFI报告发生率为7.39/10万,其中一般反应为6.30/10万,异常反应为0.70/10万,一般反应以发热、红肿、硬结为主,异常反应以过敏性皮疹、卡介苗淋巴结炎为主。结论全市AEFI监测质量有待继续提高,各区县报告数据差异较大。AEFI常发生于低年龄组儿童和NIP疫苗,为监测重点;各疫苗不良反应报告发生率均在预期发生范围内,安全性良好。     

Cardiovascular Characteristics of Zucker Fatty Diabetes Mellitus Rats,an Animal Model for Obesity and Type 2 Diabetes

Zucker fatty diabetes mellitus (ZFDM) rats harboring the missense mutation (fa) in a leptin receptor gene have been recently established as a novel animal model of obesity and type 2 diabetes (T2D). Here, we explored changes in cardiovascular dynamics including blood pressure and heart rate (HR) associated with the progression of obesity and T2D, as well as pathological changes in adipose tissue and kidney. There was no significant difference in systolic blood pressure (SBP) in ZFDM-Lepr^fa/fa (Homo) compared with ZFDM-Lepr^fa/+ (Hetero) rats, while HR and plasma adrenaline in Homo were significantly lower than Hetero. The mRNA expression of monocyte chemotactic protein-1 in perirenal white adipose tissue (WAT) from Homo was significantly higher than Hetero. Interscapular brown adipose tissue (BAT) in Homo was degenerated and whitened. The plasma blood urea nitrogen in Homo was significantly higher than Hetero. In summary, we demonstrated for the first time that HR and plasma adrenaline concentration but not SBP in Homo decrease with obesity and T2D. In addition, inflammation occurs in WAT from Homo, while whitening occurs in BAT. Further, renal function is impaired in Homo. In the future, ZFDM rats will be useful for investigating metabolic changes associated with the progression of obesity and T2D.     

The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus

Vascular complications are the leading cause of morbidity and mortality among patients with type 2 diabetes mellitus (T2DM). These vascular abnormalities result in a chronic hyperglycemic state, which influences many signaling molecular pathways that initially lead to increased oxidative stress, increased inflammation, and endothelial dysfunction, leading to both microvascular and macrovascular complications. Endothelial dysfunction represents the initial stage in both types of vascular complications; it represents “mandatory damage” in the development of microvascular complications and only “introductory damage” in the development of macrovascular complications. Increasing scientific evidence has revealed an important role of the Wnt pathway in the pathophysiology of the vascular wall. It is well known that the Wnt pathway is altered in patients with T2DM. This review aims to be an update of the current literature related to the Wnt pathway molecules that are altered in patients with T2DM, which may also be the cause of damage to the vasculature. Both microvascular complications (retinopathy, nephropathy, and neuropathy) and macrovascular complications (coronary artery disease, cerebrovascular disease, and peripheral arterial disease) are analyzed. This review aims to concisely concentrate all the evidence to facilitate the view on the vascular involvement of the Wnt pathway and its components by highlighting the importance of exploring possible therapeutic strategy for patients with T2DM who develop vascular pathologies.     

Comorbidity of Novel CRHR2 Gene Variants in Type 2 Diabetes and Depression

The corticotropin-releasing hormone receptor 2 (CRHR2) gene encodes CRHR2, contributing to the hypothalamic–pituitary–adrenal stress response and to hyperglycemia and insulin resistance. CRHR2−/− mice are hypersensitive to stress, and the CRHR2 locus has been linked to type 2 diabetes and depression. While CRHR2 variants confer risk for mood disorders, MDD, and type 2 diabetes, they have not been investigated in familial T2D and MDD. In 212 Italian families with type 2 diabetes and depression, we tested 17 CRHR2 single nucleotide polymorphisms (SNPs), using two-point parametric-linkage and linkage-disequilibrium (i.e., association) analysis (models: dominant-complete-penetrance-D1, dominant-incomplete-penetrance-D2, recessive-complete-penetrance-R1, recessive-incomplete-penetrance-R2). We detected novel linkage/linkage-disequilibrium/association to/with depression (3 SNPs/D1, 2 SNPs/D2, 3 SNPs/R1, 3 SNPs/R2) and type 2 diabetes (3 SNPs/D1, 2 SNPs/D2, 2 SNPs/R1, 1 SNP/R2). All detected risk variants are novel. Two depression-risk variants within one linkage-disequilibrium block replicate each other. Two independent novel SNPs were comorbid while the most significant conferred either depression- or type 2 diabetes-risk. Although the families were primarily ascertained for type 2 diabetes, depression-risk variants showed higher significance than type 2 diabetes-risk variants, implying CRHR2 has a stronger role in depression-risk than type 2 diabetes-risk. In silico analysis predicted variants’ dysfunction. CRHR2 is for the first time linked to/in linkage-disequilibrium/association with depression-type 2 diabetes comorbidity and may underlie the shared genetic pathogenesis via pleiotropy.     

Hyperinsulinemia and Its Pivotal Role in Aging,Obesity, Type 2 Diabetes,Cardiovascular Disease and Cancer

For many years, the dogma has been that insulin resistance precedes the development of hyperinsulinemia. However, recent data suggest a reverse order and place hyperinsulinemia mechanistically upstream of insulin resistance. Genetic background, consumption of the “modern” Western diet and over-nutrition may increase insulin secretion, decrease insulin pulses and/or reduce hepatic insulin clearance, thereby causing hyperinsulinemia. Hyperinsulinemia disturbs the balance of the insulin–GH–IGF axis and shifts the insulin : GH ratio towards insulin and away from GH. This insulin–GH shift promotes energy storage and lipid synthesis and hinders lipid breakdown, resulting in obesity due to higher fat accumulation and lower energy expenditure. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, cancer and premature mortality. It has been further hypothesized that nutritionally driven insulin exposure controls the rate of mammalian aging. Interventions that normalize/reduce plasma insulin concentrations might play a key role in the prevention and treatment of age-related decline, obesity, type 2 diabetes, cardiovascular disease and cancer. Caloric restriction, increasing hepatic insulin clearance and maximizing insulin sensitivity are at present the three main strategies available for managing hyperinsulinemia. This may slow down age-related physiological decline and prevent age-related diseases. Drugs that reduce insulin (hyper) secretion, normalize pulsatile insulin secretion and/or increase hepatic insulin clearance may also have the potential to prevent or delay the progression of hyperinsulinemia-mediated diseases. Future research should focus on new strategies to minimize hyperinsulinemia at an early stage, aiming at successfully preventing and treating hyperinsulinemia-mediated diseases.