高糖状态对大鼠肺泡巨噬细胞释放NO和TNF的影响

从正常Ｗｉｓｔａｒ大鼠肺中分离出肺泡巨噬细胞，在体外正常和高糖状态下培养并分别以干扰素（ＩＦＮａ－２ｂ、卡介苗（ＢＣＧ）以及干扰素和卡介苗联合刺激肺泡巨噬细胞，测定其释放一氧化氮（ＮＯ）和肿瘤坏死因子－ａ（ＴＮＦ－ａ）量。结果显示，高糖状态下ＢＣＧ刺激肺泡巨噬细胞时。其ＮＯ和ＴＮＦ－ａ释放量明显低于对照组（Ｐ＜０．０１）：ＩＦＮａ－２ｂ刺激肺泡巨噬细胞时，其ＮＯ和ＴＮＦ－ａ释放量与对照组无差别（Ｐ＞０．０５）：ＩＦＮａ－２ｂ与ＢＣＧ协同刺激肺泡巨噬细胞时，其ＮＯ和ＴＮＦ－ａ释放量明显低于对照组（Ｐ＜０．０１）。由此表明高糖状态下。肺泡巨噬细胞释放ＮＯ和ＴＮＦ－ａ减少，可能是导致糖尿病患者肺部易感染的一个重要原因。     

2型糖尿病患者T淋巴细胞活化与颈动脉内中膜厚度的相关性

目的探讨2型糖尿病患者T淋巴细胞活化与颈动脉内中膜厚度（IMT）的关系。方法121例2型糖尿病患者根据IMT水平分为IMT正常组与IMT增厚和斑块形成组,测定淋巴细胞活化水平、生化指标及基本临床资料。结果（1）CD3^＋HLA-DR^＋细胞比率在IMT增厚和斑块形成组显著高于对照组[（11．16±6．88 vs 6．91±3．33）％,P〈0．05],IMT正常组与对照组的差异无统计学意义;（2）偏相关分析显示,CD3^＋HLA-DR^＋细胞比率与IMT呈正相关;CD3^＋HLA-DR^＋细胞比率、年龄、SBP为影响颈动脉IMT水平的独立相关因素。结论T淋巴细胞活化正相关于颈动脉IMT,可能参与T2DM大动脉硬化的发病机制。     

肥胖2型糖尿病患者血清E-选择素水平与氧化应激的关系

目的： 探讨肥胖2型糖尿病（DM）患者血清E-选择素及氧化应激变化的关系。 方法： 检测肥胖2型DM患者血清E-选择素、氧化低密度脂蛋白胆固醇（ox-LDL）、血清丙二醛(MDA)含量和血清超氧化物歧化酶（SOD）活性。 结果： 非肥胖和肥胖2型DM患者E-选择素、ox-LDL和MDA含量均显著高于正常对照组（P<0.05），HDL-C、HDL2-C和HDL3-C含量均显著低于正常对照组（P<0.01），肥胖2型DM患者SOD活性显著低于正常对照组（P<0.01）。肥胖2型DM患者的E-选择素和MDA含量均明显高于非肥胖2型DM患者（P<0.05）,而SOD活性明显低于2型DM患者（P<0.01）。肥胖2型DM患者E-选择素与HbA1c、腰围、TC、ox-LDL和MDA正相关（r=0.352, P<0.05；r=0.634，P<0.05；r=0.517，P<0.05；r=0.480，P<0.05;r=0.572，P<0.05），与HDL3-C呈负相关（r=-0.374，P<0.05）。 结论： 肥胖2型DM患者血清E-选择素含量明显增加，氧化应激可能参与其变化。     

Graves'病患者血清GAD-Ab含量的测定

目的：研究谷氨酸脱羧酶抗体（GAD-Ab）与Graves'病病程及浸润性突眼的关系。方法：用ELISA法测定51例Graves'病患者血清中的GAD-Ab。结果：20例阳性,阳性率39.2%,其中病程＜6月组,GAD-Ab阳性率7.7%,明显低于病程＞6月组（Ｐ＜0.01）,Graves'病并浸润性突眼组,阳性率为57.7%,明显高于非浸润性突眼组（Ｐ＜0.01）。结论：GAD-Ab的测定有助于了解Graves'病病程及监测浸润性突眼。     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

血管紧张素Ⅱ受体拮抗剂对糖尿病肾病患者微量白蛋白尿的作用不受血压影响

目的研究血管紧张素Ⅱ受体拮抗剂(ARB)氯沙坦对2型糖尿病、糖尿病肾病患者微量白蛋白尿的治疗效果。方法血压正常的2型糖尿病患者43例,其尿白蛋白排泄率(UAER)在20~200μg/min之间,其血糖控制在可接受水平[空腹血糖(FBG)≤7mmol/L,餐后2h血糖(P2hBG)≤10mmol/L]。随机分为治疗组23例,对照组20例,对照组在控制血糖基础上加用安慰剂,治疗组加用ARB氯沙坦50mg/d。两组患者在治疗前和治疗12周后复查FBG、P2hBG、糖化血红蛋白(HbA1c)和UAER。结果治疗12周后,治疗组UAER为(76±11)μg/min,与治疗前(119±14)μg/min相比明显下降(P<0·05),与对照组(125±13)μg/min比较,差异有显著性(P<0·05)。结论对血压正常的2型糖尿病早期糖尿病肾病患者,ARB氯沙坦在对血压无影响的情况下具有独特的降低尿微量白蛋白水平,延缓糖尿病肾病进展的作用。     

糖尿病高糖危象患者氧化应激与细胞黏附因子变化的关系

血浆细胞黏附分子(CAM)增加被认为是全身内皮细胞功能和白细胞损害或激活的标志,也是早期动脉粥样硬化的分子标记.自由基增加与糖尿病大血管和微血管并发症存在明显相关性,同时,CAM与细胞所处的氧化还原状态密切相关.     

成人迟发性自身免疫性糖尿病患者血清CD30水平变化及其意义

CD30分子主要表达于活化的 T/ B细胞 ,诱导 T细胞膜分泌 TH2类型的细胞因子参与自身免疫疾病的发病机制 [1 ] 。成人迟发性自身免疫性糖尿病 (latent autoimm une diabetesin adults,L ADA)乃由免疫因素引起的β细胞破坏所致 ,具体发病机制尚不清楚 ,本研究拟通过对 L ADA患者血清CD30水平的测定 ,探讨 CD30分子在 L ADA中的意义。一、对象和方法1.研究对象 :选取本院 31例确诊为 L ADA的患者 ,男性 19例 ,女性 12例 ,平均年龄 4 7(2 7～ 6 8)岁。正常对照组30例 ,男 16例 ,女 14例 ,平均年龄 4 8(2 6～ 70 )岁。2 .方法 :送检空…     

自我管理网络支持模式在初发中青年2型糖尿病患者中的应用

目的探讨自我管理网络支持模式在初发中青年2型糖尿病患者中应用效果。方法将在医院糖尿病教育门诊就诊的200例初发中青年2型糖尿病患者按时间顺序分为对照组和干预组各100例,对照组入组后按常规进行糖尿病自我管理知识和技能教育及门诊随访管理;干预组在对照组基础上对患者进行自我管理网络支持干预。观察两组自我管理知识、心理状态以及糖化血红蛋白等指标变化情况。结果干预6个月后,干预组自我管理知识显著高于对照组,糖化血红蛋白显著低于对照组;干预组抑郁症状发生率显著低于对照组(均P0.05)。结论开展自我管理网络支持模式有利于提高初发中青年2型糖尿病患者自我管理知识,减轻抑郁症状,控制血糖水平,是一种有效的健康管理手段。     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.