Ⅱ型糖尿病患者红细胞膜MDA与膜钠泵K~＋－pNPPase活性的关系

本文测定５５例ＮＩＤＤＭ患者血浆及红细胞膜ＭＤＡ水平和钠泵Ｋ＋－ｐＮＰＰａｓｅ活性。结果显示，ＮＩＤＤＭ患者血浆和红细胞膜ＭＤＡ水平明显高于正常对照组，钠泵Ｋ＋－ｐＮＰＰａｓｅ活性明显低于对照，在伴有视网膜病变者上述改变更为显著，红细胞膜ＭＤＡ升高和钠泵Ｋ＋－ｐＮＰＰａｓｅ活性降低呈明显负相关。提示红细胞膜ＭＤＡ升高可能是导致Ｋ＋－ｐＮＰＰａｓｅ活性降低的一重要因素。     

非胰岛素依赖型糖尿病患者的红细胞免疫功能

血管病变、感染为糖尿病（ＤＭ）常见的并发症。为了观察非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者的红细胞免疫功能 ,探讨其与血管病变、感染的关系 ,我们采用酵母菌花环试验 ,测定了４２例ＮＩＤＤＭ患者外周血ＲＢＣ Ｃ３ｂＲ花环率及ＲＢＣ ＩＣＲ花环率。１材料和方法１ .１材料研究对象 :按ＷＨＯ１９８５年诊断标准临床确诊为ＮＩＤＤＭ的患者４２例,年龄３１～７７岁,病程０．５～２１年,所有患者均无酮症酸中毒及心衰。对照组为２０例健康体检者 ,年龄３０～６４岁。主要试剂 :补体致敏及未致敏的冻干ＹＳ酵母菌体 ,购自第二军医…     

Graves病患者红细胞膜钠泵活性的初步研究

Ｇｒａｖｅｓ病患者红细胞膜钠泵活性的初步研究严孙杰，卓孝福，潘时中，王中心（福建医学院附属第一医院内二科，福州３５０００５）作者测定了正常人及Ｇｒａｖｅｓ病患者红细胞膜钠泵活性，并分析其活性改变的可能机制。实验对象：正常人１０７名（男７５名，女３２名...     

老年糖尿病患者红细胞膜脂质成分的改变

本文测定２８例老年ＮＩＤＤＭ患者红细胞膜脂质成分和脂质过氧化水平。结果显示：老年ＮＩＤＤＭ患者红细胞膜胆固醇，胆固醇／磷脂比值及过氧化脂质水平明显升高，膜磷脂降低；膜脂质成分改变与高血糖，高血脂及血浆脂蛋白异常存在一定关系。提示老年糖尿病患者红细胞膜成分存在异常，膜成分异常与代谢紊乱存在一定关系。     

老化红细胞变形能力与膜钙依赖中性蛋白酶活性的关系

研究表明，老化红细胞变形能力明显降低，且其降低与血红蛋白浓度增高及膜弹性降低有关，而与红细胞膜钙依赖中性蛋白酶（Ｃａｌｐａｉｎ）活性的关系尚不清楚。为此，我们检测４２例健康人老化红细胞及年轻红细胞变形能力、Ｃａｌｐａｉｎ和Ｃａ２＋－ＡＴＰ酶活性及膜收...     

NIDDM红细胞钠锂交换活性变化的探讨

ＮＩＤＤＭ红细胞钠锂交换活性变化的探讨山东省临沂市人民医院（临沂２７６００３）上海二医大附属瑞金医院内分泌科高冠起，宁光，罗邦尧，许曼音胰岛素非依赖型糖尿病（ｎｏｎ一ｉｎｓｕｌｉｎｄｅｐｅｎｄｅｎｔｄｉａｂｅｔｅｓｍｅｌｌｉｔｕｓ．ＮＩＤＤＭ）和原发...     

老化红细胞变形能力与膜钙依赖中性蛋白酶活性的关系

研究表明,老化红细胞变形能力明显降低,且其降低与血红蛋白浓度增高及膜弹性降低有关［１］。红细胞膜钙依赖中性蛋白酶（Ｃａｌｐａｉｎ）和它的内源性抑制剂（Ｃａｌｐａｓｔａｔｉｎ）形成红细胞中一个蛋白水解系统,参与红细胞中的信号传导,调节细胞形状、体积和细胞膜通透性,与高血压、细胞老化等生理、病理现象密切相关。Ｃａｌｐａｉｎ可限制性水解红细胞膜骨架蛋白和其它膜内蛋白,导致红细胞损伤［２,３］。而老化红细胞变形能力降低与Ｃａｌｐａｉｎ的关系尚不清楚,为此我们检测了４２例健康人老化及年轻红细胞变形能力、Ｃ…     

慢性丙型肝炎与Ⅱ型糖尿病关系的研究

目的：探讨慢性丙型肝炎病毒（HCV）感染与Ⅱ型糖尿病发病的关系。方法：①对227例慢性乙型肝炎（乙型肝炎后肝硬化86例）与126例慢性丙型肝炎患者（丙型肝炎后肝硬化30例）进行病例分析研究，明确其是否合并糖尿病。②用ELISA方法对160例Ⅱ型糖尿病患者及223例体检人群进行抗HCV、HBsAg检测。结果：①126例慢性丙型肝炎患者合并Ⅱ型糖尿病24例（19．05％），227例慢性乙型肝炎患者合并Ⅱ型糖尿病19例（8．37％），二者比较差异有显著性（P＜0．01），年龄及丙型肝炎为发生糖尿病的独立危险因素。②160例Ⅱ型糖尿病患者中抗HCV阳性5例（3．12％），HBsAg阳性7例（4．37％），223例体检人群抗HCV阳性0例，与糖尿病人群差异有显著性（P＜0．05），HBsAg阳性12例（5．38％），与糖尿病人群差异无显著性（P＞0．05）。结论：①慢性丙型肝炎病毒感染易合并Ⅱ型糖尿病。②Ⅱ型糖尿病患者中丙型肝炎感染率高于普通人群，提示HCV感染与糖尿病的发生有一定关系，HCV感染可能为Ⅱ型糖尿病发病因素之一。     

慢性肾功能衰竭红细胞变形能力与红细胞膜的研究

本文报道了慢性肾功能衰竭患者红细胞的变形能力、红细胞膜胆固醇与磷脂比值及膜微粘度。结果表明,红细胞可变形能力明显降低,膜胆固醇与磷脂比值及膜微粘度明显增加,提示红细胞变形能力可能与红细胞膜的流动性有关。     

Erythrocyte changes in canine diabetes mellitus: in vitro effects of hyperglycaemia and ketoacidosis

Diabetes mellitus (DM) is a common metabolic disorder in dogs, which occurs often in association with some complications, including haematological problems. Some abnormalities of erythrocyte metabolism have been described both in human patients and in dogs affected by DM. The aim of this work was to test in vitro the direct effects of hyperglycaemia and ketoacidosis on canine erythrocytes (RBCs). RBCs from healthy dogs were incubated in normoglycaemic, mild hyperglycaemic, severe hyperglycaemic and severe hyperglycaemic + ketoacidotic media. The following parameters were examined: osmotic fragility (OF), the concentrations of 2,3-diphosphoglycerate (2,3DPG), reduced glutathione (GSH) and adenosine triphosphate (ATP), the activities of glutathione peroxidase (GPX), glucose-6-phosphate dehydrogenase (G6PD) and pyruvate kinase (PK), sodium (Na⁺) and potassium (K⁺) intracellular concentrations, production of lactate. In comparison with t0, incubated cells showed higher OF (P<0.001) and lower 2,3DPG (P<0.001) and ATP (P<0.001) concentrations. In comparison with normoglycaemic conditions, hyperglycaemia induced minimal changes, such as increased OF (P<0.001) and 2,3DPG (P<0.01) concentrations. Major changes were induced by hyperglycaemic + ketoacidotic media, such as increases in mean corpuscular volume (MCV), OF, PK activity and ATP concentration; this suggested that oxidative stress had occurred. In hyperglycaemic media, lactate production was not associated with glucose concentration, but the higher consumption of glucose suggests the activation of metabolic pathways other than glycolysis. These alterations could be partly responsible for some hypoxic complications during DM.     

Erythrocyte deformability in aging

Blood viscosity and the deformability and other properties of erythrocytes were compared among 60-, 150-, 320- and 710-day-old rats. Blood viscosity was remarkably higher in the 320- and 710-day old rats than in those 60- and 150 days' old. Measurement by the capillary centrifugal method showed that the deformability of erythrocytes is sginficantly decreased with age. The increase in blood viscosity with aging could be attributed to the decrease in erythrocyte deformation. Osmotic fragility and the number of higher density erythrocytes also increase with age. The negative surface charge in erythrocytes obtained from old rats was higher than in those from younger rats.     

Altered sodium permeability,calcium binding and Na−K-ATPase activity in the red blood cell membrane in essential hypertension

Summary Red blood cells (RBC) of patients with essential hypertension differ from those of normotensive individuals by their higher passive permeability for sodium ions (the rate constant of steady-state Na/Na exchange in RBC is 1.52±0.12 vs 0.70±0.12 · 10⁻⁵ mole/min · l of cells). Calcium depletion of the RBC by EDTA results in the removal of more calcium ions from the outer part of the RBC membrane in the case of hypertensive patients (60±5 vs 41±3 μeq/l of RBC); this may be considered as evidence of alteration of calcium binding in the outer RBC membrane in essential hypertension. By varying the total concentration of intracellular calcium (Ca_t) in reconstituted RBC (resealed cells, RRBC from 0–500 μmole/l [various concentrations of free calcium (Ca²⁺ _f), up to 41 μmole/l, being maintained by a Ca²⁺-ATP buffer] a lower level of Na-K-ATPase activity in hypertensive patients is observed: when [Ca²⁺]_f=3 μmole/l, the activity was 0.77±0.04 vs 0.93±0.02 μmole of orthophosphate per hour per ml of RRBC, for hypertensive and normotensive individuals respectively. The differences in the kinetics of inhibition of Na−K-ATPase activity when the Ca/ATP ratio in the RBC is decreased was apparently caused by the alteration of calcium binding ability of the inner part of the RBC membrane. It is suggested that the alteration of the RBC membrane function may be a manifestation of a more wide-spread defect of cell membrane in essential hypertension. The alteration of calcium binding in the membrane is probably one of the patterns of this defect.     

急性心肌缺血时红细胞变形性的变化及其机理

本实验观察了犬急性心肌缺血时体循环血与缺血区局部静脉血中红细胞变形性（ＲＣＤ）的变化。结果表明，阻断冠脉血流后高切变率下全血粘度（ηｂｈ）和红细胞刚性指数（ＥＲＩ）明显增高，而缺血区局部血液中此二者的变化明显大于体循环静脉血。事先切断内脏大神经，可使阻断冠脉后体循环血（而不是局部静脉血）的ηｂｈ和ＥＲＩ变化基本消失。缺血区局部血液ｐｈ和ｐＯ２明显降低，ｐＣＯ２明显增高，红细胞内ＡＴＰ含量减少和钙含     

缺血性中风红细胞变形能力与膜微粘度及膜生化改变的相关性研究

本文通过对脑梗塞患者及健康对照者进行红细胞变形能力与红细胞膜微粘度及膜生化成份的测定,发现两组有显著差异,且患者组红细胞变形能力与膜微粘度、胆固醇/磷脂比值、膜脂质过氧化物含量呈显著负相关,与膜唾液酸含量呈显著正相关,按影响程度大小排列依次为膜微粘度、脂质过氧化物含量、唾液酸、胆固醇/磷脂比值。     

脑梗塞患者红细胞变形能力与膜磷脂组分的关系

为探讨脑梗塞患者红细胞膜磷脂各组分对红细胞变形能力的影响，采用高效液相色谱法对58例脑梗塞患者和26名健康人的红细胞膜磷脂各组分进行了测定，并同时检测了其红细胞胆固醇含量及红细胞变形能力。结果表明，脑梗塞患者红细胞膜磷脂酸胆碱（PC）、磷脂酸乙醇胺（PE）含量降低，胆固醇（CHO）含量升高，红细胞变形能力降低。直线相关分析，膜PC与红细胞滤过指数呈显著负相关。结论：脑梗塞患者红细胞膜你在以PE、PC变化为主的磷脂代谢紊乱，膜PC异常可能是影响红细胞变形能力的一个重要因素。     

Studies of the lung in diabetes mellitus

Summary To evaluate the effects of chemically induced diabetes on lung tissue, we examined the ultrastructure of the lung of alloxan-induced diabetic rats. Fifty male Wistar rats were made diabetic by a single intraperitoneal injection of alloxan (200 mg/kg of body weight): they were sacrificed from one to four weeks later. The alloxan-induced diabetes produced significant morphological alterations in the lung. These include marked dilatation of the cisterna of the granular endoplasmic reticulum, dilation of the Golgi saccules and the appearance of glycogen granules as a cluster in the cytoplasm of the granular pneumocytes and the interstitium. These findings were well correlated with the severity of diabetes mellitus. The altered granular pneumocytes were observed in about 50% of animals and in most (87.5%) of the observed pneumocytes 2 weeks and 4 weeks after alloxan treatment respectively. The average number of lamellar inclusion bodies per granular pneumocyte decreased to about half of that of the control in diabetic rats 4 weeks after alloxan treatment, and minimum thickness of the capillary basement membrane was approximately 35% thicker than that of the control (diabetics; 879±189 Å, controls; 649±100 Å).The ultrastructural alterations of the lung in diabetic rats indicate disorders in the pulmonary capillaries and in the metabolism of pulmonary surfactant, which may cause pulmonary dysfunction in diabetic patients.     

长链非编码RNA与糖尿病关系的研究进展*

Long non-coding RNAs (lncRNAs) are a group of RNAs, which are longer than 200 nucleotides without containing functional open reading frame and cannot encode protein. The study of lncRNA will help to understand the multi-level expression regulatory network of the body, and is expected to provide the basis of prediction, diagnosis and treatment of complex diseases. Although the functions and mechanism of lncRNA remain unclear, some studies indicate that lncRNA is involved in the development of diabetes mellitus, and those lncRNAs may be new diagnostic markers and therapeutic targets.     

The effect of streptozotocin-induced diabetes mellitus on urinary excretion of sodium and renal Na+−K+-ATPase activity

Renal sodium handling and microsomal Na⁺–K⁺-ATPase activity in kidney cortex, medulla and papilla of rats with streptozotocin-induced diabetes mellitus (DM) was studied.During 7 days following the administration of streptozotocin GFR, urinary excretion, filtered load and tubular reabsorption of Na⁺ averaged (mean±SE) 1.18±0.016 ml/min, 1.74±0.14, 177.3±8.9 and 175.6±8.9 mEq/min respectively in experimental rats as compared to corresponding rates of 0.85±0.04 (P<0.001), 0.85±0.03 (P<0.001), 129.8±5.8 (P<0.001) and 129±5.8 (P<0.001) respectively in the control rats.The activity of microsomal Na–K-ATPase in the kidney cortex, medulla and papilla of the control group was (mean±SE) 44.7±1.7, 150±7.5 and 37.4±3.6 (moles Pi/mg prot/h) respectively. 24 h after DM induction Na–K-ATPase activity in the cortex rose to 59.3±2.4 (P<0.001) and remained high after 3 and 7 days. Medullary Na–K-ATPase activity was unchanged 24 h after streptozotocin administration but was markedly increased to 260±9 (P<0.001) after 3 days and remained high after 7 days.These findings show that stretozotocin-induced DM in rats causes a substantial increase in GFR which is associated with a net increase in filtered and reabsorbed load of Na⁺ and natriuresis. These alterations are accompanied by a marked increase in Na–K-ATPase activity in renal medulla and in the cortex.This study was supported by the Morton S. Kaufman Hemodialysis Foundation and by the Joint Research Fund of the Hebrew University and Hadassah     

Aggregate formation of erythrocytes and diabetic retinopathy in children,adolescents, and adults with diabetes mellitus (type I)

Summary In vitro measurements were carried out to study the aggregation of erythrocytes in 33 children and young adolescents, three older adolescents, and 38 adults with type I diabetes. The aggregate formation of erythrocytes in stasis was increased in adult patients with both good and poor metabolic control when compared to control values. The aggregation of red cells in all children and the younger adolescents, both those under good and poor metabolic control, did not statistically differ from those of controls. Each of the three older adolescents showed an increased aggregate formation of their erythrocytes compared to controls. All adult patients under poor metabolic control exhibited various stages of diabetic retinopathy as shown by fluorescence angiography. Only one child under poor metabolic control showed an early stage of retinopathy (stage I according to Malone). The three older adolescents showed an increased aggregate formation of their erythrocytes. These patients exhibited also stage I of retinopathy. We suggest that the increased aggregation of erythrocytes of both adult and older adolescent patients may be one of the reasons for the development of diabetic retinopathy. Moreover, the normal erythrocyte aggregation of the diabetic children and younger adolescents could help to explain the rare occurrence of microangiopathies in childhood diabetes.With support of the Deutsche Forschungsgemeinschaft, Bonn-Bad Godesberg, Ti 110/2-1