糖尿病致盲的局部和全身因素分析

本文检查了705例(1409只眼)糖尿病患者,对眼局部致盲原因和与盲有关全身因素进行了分析。双眼盲77例,占10.9％,单眼盲139例,占19.7％。盲目眼的局部原因以DR居首位,其中玻璃体出血、牵拉性视网膜脱离及新生血管性青光眼为主要致盲眼疾。全身相关因素显示,尿蛋白、收缩压、性别及病程与盲目密切相关,血糖与盲亦相关。     

Therapeutic Effect of Berberine on 60 Patients with Non－Insulin Dependent Diabetes Mellitus and Experimental Research

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非胰岛素依赖型糖尿病患者肺功能检查的初步探讨

对２５例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者及２４例正常人进行全套肺功能检查，并作对比分析，结果表明：ＮＩＤＤＭ组比正常对照组Ｖ２５／ＨＴ减低。差异有高度显著性（Ｐ＜０．０１）；ＤＬＣＯ减低差异有显著性（Ｐ＜０．０５），并认为ＮＩＤＤＭ患者小气道功能、弥散功能减低与糖代谢紊乱，致机体抵抗力降低、免疫功能下降，并与肺胞毛细血管基底膜增厚有关。检查ＮＩＤＤＭ患者小气道功能和肺泡弥散功能，具有一定临床意义。     

葛根素联用甲钴胺治疗糖尿病周围神经病变32例

目的 观察葛根素联用甲钴胺治疗糖尿病周围神经病变(DPN)的疗效。方法 将诊断明确的64例DPN患者随机分为治疗组和对照组各32例,两组均给予糖尿病饮食和降糖治疗,治疗组给予葛根素联用甲钴胺治疗,对照组单给予葛根素治疗。10天为一疗程,共治疗两疗程,对两组疗效进行比较。结果 治疗组总有效率和神经传导速度改善均好于对照组(P<0.01),且无明显副作用。结论 葛根素联用甲钴铵治疗DPN比单用葛根素疗效好,值得临床推广应用。     

老年2型糖尿病患者骨密度及临床相关因素分析

目的 了解老年2型糖尿病患者骨密度的变化，初步探讨临床相关因素对骨密度变化的影响。方法 采用双能X线骨密度仪测定65例老年2型糖尿病患者及80例年龄、性别匹配的正常对照者腰椎及髋部骨密度，同时测定前者空腹血糖（FBG）、餐后2h血糖（PBG）、空腹C肽、餐后2hC肽、果糖胺（FA）、糖化血红蛋白（HBAle）、胆固醇（chol）、甘油三酯（TG）。结果 65例糖尿病患者各部位骨密度值均低于正常对照者，但仅腰椎降低有统计学意义（P〈0．05）；糖尿病组30例（45％）合并骨质疏松（OP）。OP与非0P组病程有显著性差异（P〈0．05）。结论 2型糖尿病会导致骨矿密度减低，并与糖尿病病程密切相关。     

行为干预对糖尿病患者健康相关行为的研究

目的观察行为干预对糖尿病(diabetesmellitus,DM)患者健康行为的影响。方法将本科收治172例DM患者作为目标人群进行健康教育,建立目标人群管理档案,进行目标人群健康行为干预,比较教育前后相关行为的改变。结果DM患者10项健康行为和10项危险健康行为有明显改观,统计学检验干预前后差异显著P<0.01。结论通过行为干预,有效的使DM患者完全遵从医嘱合理用药,完全依从健康行为,从而减少危险行为的发生。     

继发性骨质疏松防治的研究

目的总结继发性骨质疏松预防与治疗的经验及提出见解.方法用钙代谢平衡的方法研究了钙代谢的基本情况,比较了补钙与不补钙在若干种生理状态对骨密度的影响,总结继发性骨质疏松的病因及对其采取不同方法的治疗经验.结果中国人膳食含钙量属于正常范围低水平状态,与适宜摄入量(AI)比较是不足的,在一定的生理状态下应予补钙.缺钙是原发性骨质疏松与继发性骨质疏松的不利因素.氟中毒骨病、糖尿病、性腺功能减退、肿瘤、糖皮质激素过多和甲亢均有其各别的病理生理,导致继发性骨质疏松,防治方法各异.结论从胚胎至老年都应防治骨质疏松.不同情况采取方法各异,但有效.     

糖骨康胶囊治疗糖尿病骨质疏松临床研究

目的:观察糖骨康胶囊对糖尿病骨质疏松的治疗作用。方法:将216例患者,遵照随机、盲法、对照原则分为治疗组144例、对照组72例,其中治疗组给予糖骨康胶囊,对照组给予甘露消渴丸,治疗8w后观察疗效。结果:治疗组显效率为40.0%;总有效率为88.6%。对照组显效率为28.9%,总有效率为82.6%。结论:糖骨康胶囊对2型糖尿病骨质疏松有显著的防治作用。     

Activity and distribution of phosphoinositidase C in rat sciatic nerve.

The hydrolysis of phosphatidylinositol-4,5-bisphosphate (PIP2) by rat sciatic nerve cytosolic phosphoinositidase C [phosphoinositide-specific phospholipase C (PIC)] was studied at neutral pH and at ionic concentrations that approximate intracellular conditions. The principal water-soluble product formed was shown to be inositol trisphosphate by anion exchange chromatography. The maximum hydrolysis rate (2.5 nmol/min/mg protein) was achieved at less than 100 nM Ca2+. Hydrolysis was markedly increased to 15 nmol/min/mg protein by inclusion of K+ in the reaction mixture. In the presence of 200 mM K+, the optimum Ca2+ was increased to approximately 600 nM. Higher Ca2+ concentrations progressively inhibited PIP2 hydrolysis. Mg2+ also inhibited the reaction, but the presence of equimolar amounts of ATP and Mg2+ had no effect. Appreciable degradation of phosphatidylinositol-4-phosphate (PIP) also occurred in the nanomolar Ca2+ range, whereas breakdown of phosphatidylinositol (PI) required millimolar Ca2+. The presence of PIP but not PI inhibited PIP2 hydrolysis. Upon subcellular fractionation of nerve, more than 50% of recovered PIC activity was in the cytosol and about 20% was located in a myelin-enriched fraction. Using PIP2 as substrate, PIC activities in nerves from normal and streptozotocin-induced diabetic animals were not different. However, the myelin-associated enzyme from diabetic animals was more labile to freezing and thawing.