从临床调查看开展糖尿病健康教育的重要性

目的:探讨对糖尿病患者进行健康教育的重要性。方法:采用自制的调查表,以问卷的方式对520名糖尿病人进行调查。结果:77．2%的病人是因体检或因其他疾病而意外被发现的,31．5%的病人会坚持定期检查血糖,28．9%的病人检查过餐后血糖, 45．9%和76．6%的病人还在用副作用很大的降糖灵和优降糖,只有29．3%的病人能够正确了解胰岛素,63．4%的病人相信或是相信过虚假的广告宣传。结论:对糖尿病人群进行糖尿病知识的健康教育是很必要的。     

Notch signaling in pancreatic endocrine cell and diabetes

Recent studies have improved our understanding of the physiological function of Notch signaling pathway and now there is compelling evidence demonstrating that Notch is a key regulator of embryonic development and tissue homeostasis. Although further extensive studies are necessary to illustrate the molecular mechanisms, new insights into the role of Notch signaling in pancreas development and diabetes have been achieved. Importantly, the ability to regulate Notch signaling intensity both positively and negatively may have therapeutic relevance for diabetes. Thus, this paper reviews the current knowledge of the roles of Notch signaling in the pancreatic endocrine cell system.     

Nifedipine inhibits advanced glycation end products (AGEs) and their receptor (RAGE) interaction-mediated proximal tubular cell injury via peroxisome proliferator-activated receptor-gamma activation

There is a growing body of evidence that advanced glycation end products (AGEs) and their receptor (RAGE) interaction evokes oxidative stress generation and subsequently elicits inflammatory and fibrogenic reactions, thereby contributing to the development and progression of diabetic nephropathy. We have previously found that nifedipine, a calcium-channel blocker (CCB), inhibits the AGE-induced mesangial cell damage in vitro. However, effects of nifedipine on proximal tubular cell injury remain unknown. We examined here whether and how nifedipine blocked the AGE-induced tubular cell damage. Nifedipine, but not amlodipine, a control CCB, inhibited the AGE-induced up-regulation of RAGE mRNA levels in tubular cells, which was prevented by the simultaneous treatment of GW9662, an inhibitor of peroxisome proliferator-activated receptor-γ (PPARγ). GW9662 treatment alone was found to increase RAGE mRNA levels in tubular cells. Further, nifedipine inhibited the AGE-induced reactive oxygen species generation, NF-κB activation and increases in intercellular adhesion molecule-1 and transforming growth factor-beta gene expression in tubular cells, all of which were blocked by GW9662. Our present study provides a unique beneficial aspect of nifedipine on diabetic nephropathy; it could work as an anti-oxidative and anti-inflammatory agent against AGEs in tubular cells by suppressing RAGE expression via PPARγ activation.     

Improved activity of streptozotocin-selected insulinoma cells following microencapsulation and transplantation into diabetic mice

We have recently shown that repeated streptozotocin (STZ) treatment induces the selection of insulinoma cells (RINmS) with both improved resistance to diabetogenic toxins and functional activity, compared to parental RINm cells. The aim of the present study was to estimate the potential of RINmS cells to maintain their engineered characteristics during in vivo hyperglycemic conditions. It was found that microencapsulation and transplantation into diabetic mice preserved a three-fold higher level of insulin content in selected RINmS cells when compared to the parental ones. Retrieval of transplanted encapsulated cells from the peritoneal cavity of diabetic mice had a significantly higher insulin content and a more intense insulin response to secretogogues in selected RINmS cells when compared to retrieved RINm cells. In conclusion, our results show that RINmS cells do not lose their improved functional characteristics after encapsulation and transplantation into diabetic mice.     

营养干预对IGT 人群糖脂代谢及胰岛素抵抗的临床研究

目的：通过营养干预的手段观察其对糖耐量减低（IGT）人群糖脂代谢厦胰岛素水平的影响。方法：通过流调,以服糖耐量试验（OGTT）筛查IGT患者,随机分为对照组和干预组,干预组通过营养师进行善食调查,营养教育,饮食评价糯导总计1．5年。对照组不进行任何指导教育。两组于试验前后检查空腹血糖（FPG）,餐后2小时血糖（2hpG）,胰岛素（Ins）水平及胰岛素抵抗指教（HOMA-IR）等。结果：饮食干预组体质指数（BMI）,FPG、Ins及HomA—IR等较对照组明显下降（P〈0．01）仅2人转为糖尿病（DM）,对照组试验前后各项指标无显著变化,有6人转为DM,两组经t检验,DM的患病率有统计学意义（P〈0．05）。结论：营养干预对改善IGT患者的糖脂代谢,胰岛素抵抗有重要作用。     

趋化因子CX3CL1与冠心病合并2型糖尿病发病的相关关系

目的:探讨趋化因子CX3CL1与冠心病合并2型糖尿病发病的相关关系。方法:采用病例-对照的研究方法,收集冠心病合并2型糖尿病患者400例,收集对照组400例,利用免疫组化检测冠心病合并2型糖尿病患者颈外动脉旋切术后斑块组织中CX3CL1表达水平,分别检测上述2组不同人群血清中的CX3CL1表达水平,同时采用直接测序方法检测CX3CL1基因rs170364位点基因型及等位基因的分布频率在对照组和冠心病合并2型糖尿病人群的分布差异。结果:冠心病合并2型糖尿病患者颈外动脉斑块组织中CX3CL1表达明显增高,冠心病合并2型糖尿病患者血清中CX3CL1的表达水平明显高于对照人群中CX3CL1的表达。CX3CL1基因rs170364单核苷酸多态位点的三种基因型分布频率(GG型,GT型和TT型)在冠心病合并2型糖尿病患者的分布频率为42.7%,40.0%和17.2%,在对照组分布频率为50.2%,39.6%和10.2%,CX3CL1基因rs170364位点T等位基因是冠心病合并2型糖尿病发病的一个独立危险因素(P0.05)。Logistic回归校正性别、年龄、体重指数、吸烟、高血压、高脂血症等冠心病合并2型糖尿病的易患因素后,CX3CL1基因rs170364 T等位基因仍是冠心病合并2型糖尿病发病的一个独立的危险因素。结论:CX3CL1在冠心病合并2型糖尿病的患者血清和颈外动脉动脉血管组织中表达明显增高,CX3CL1基因rs170364T等位基因可能是冠心病合并2型糖尿病患者发病的独立危险因素。     

血清Hcy与CysC 对早期2型糖尿病肾病的临床诊断价值分析

目的:分析血清同型半胱氨酸(Hcy)与胱抑素C(CysC)对早期2型糖尿病肾病的临床诊断价值。方法:选择2013年5月至2016年5月我院收治的早期糖尿病肾病患者60例为A组,选取同期我院收治的单纯糖尿病患者60例为B组,另选我院同期健康体检者60例为C组,检测三组的血清Hcy、CysC、血尿素氮(BUN)、血肌酐(Scr)、尿蛋白排泄率(UAER)。结果:与C组比较,A组和B组的BUN、Scr、UAER均升高(P0.05),A组的UAER高于B组(P0.05),但A组的BUN、Scr与B组比较,组间差异无统计学意义(P 0.05)。A组的病程明显高于B组(P0.05)。与C组比较,A组Hcy与CysC水平升高(P0.05),B组的Hcy水平升高(P0.05),CysC水平升高,但差异无统计学意义(P 0.05);与B组比较,A组Hcy与CysC水平升高(P0.05)。A组的Hcy、CysC、Hcy+CysC阳性率均明显高于B组和C组(P0.05),B组Hcy、CysC、Hcy+CysC阳性率均明显高于C组(P0.05);A组和B组的Hcy+CysC联合检测的阳性率高于Hcy、CysC的单独检测阳性率(P0.05)。Hcy与病程、BUN、Scr、UAER均呈正相关,相关系数r=0.650、0.488、0.596、0.761,P0.05,CysC与病程、BUN、Scr、UAER均呈正相关,相关系数r=0.681、0.502、0.601、0.825,P0.05。结论:血清Hcy与CysC可及时、准确的反应2型糖尿病患者的肾损伤情况,从而有利于早期2型糖尿病肾病的及时检出。     

他克莫司联合黄葵胶囊治疗难治性膜性肾病的临床疗效

目的:探讨他克莫司联合黄葵胶囊治疗难治性膜性肾病疗效及安全性。方法:选取2014年3月-2015年10月我院收治的60例难治性膜性肾病患者,按随机数字表法分为观察组和对照组各30例,对照组给予泼尼松治疗,观察组在此基础上增加他克莫司联合黄葵胶囊口服,两组均治疗6个月,观察两组临床疗效,检测并对比两组治疗前后尿蛋白(uPRO)、血清白蛋白(sALB)、血清肌酐(sCr)、血谷丙转氨酶(sALT)、肿瘤坏死因子α(TNF-α)、转化生长因子β1(TGF-β1)以及不良反应情况。结果:观察组的有效率高于对照组(P0.05);治疗后两组uPRO、TNF-α、TGF-β1均明显降低,sALB、sCr明显升高(P0.05),且观察组uPRO、TNF-α、TGF-β1低于对照组(P0.05);两组不良反应发生率比较差异无统计学意义(P0.05)。结论:他克莫司联合黄葵胶囊治疗难治性膜性肾病具有较好的疗效,降低肾功能损伤,不良反应低,值得临床推广。     

Near Infrared Optical Projection Tomography for Assessments of β-cell Mass Distribution in Diabetes Research

By adapting OPT to include the capability of imaging in the near infrared (NIR) spectrum, we here illustrate the possibility to image larger bodies of pancreatic tissue, such as the rat pancreas, and to increase the number of channels (cell types) that may be studied in a single specimen. We further describe the implementation of a number of computational tools that provide: 1/ accurate positioning of a specimen''s (in our case the pancreas) centre of mass (COM) at the axis of rotation (AR)²; 2/ improved algorithms for post-alignment tuning which prevents geometric distortions during the tomographic reconstruction² and 3/ a protocol for intensity equalization to increase signal to noise ratios in OPT-based BCM determinations³. In addition, we describe a sample holder that minimizes the risk for unintentional movements of the specimen during image acquisition. Together, these protocols enable assessments of BCM distribution and other features, to be performed throughout the volume of intact pancreata or other organs (e.g. in studies of islet transplantation), with a resolution down to the level of individual islets of Langerhans.