人类巨细胞病毒感染与胰岛功能的临床研究

目的探讨人类巨细胞病毒（HCMV）感染与胰岛功能的关系，以明确HMCV作为糖尿病致病因素的可能性。方法利用ELISA技术检测血清HCMV-IgG、IgM，免疫组化技术检外周血单个核细胞中HCMV pp65的表达水平，同时测定空腹血糖及C肽水平，对HCMV感染状况及血糖和C肽水平进行分析。结果空腹血糖增高组HCMV pp65阳性率明显高于正常对照组，HCMV-IgG、IgM及PBMC HCMV DNA在两组中阳性率无显著性差异，但空腹血糖增高组HCMV-IgG的相对含量明显高于正常对照组，且HCMV-IgG的相对含量与空腹血糖及C肽水平存在明显的相关关系。结论HCMV感染与糖尿病的发病密切相关，HCVM感染可能是糖尿病的始发因素。     

1型糖尿病与成人隐匿性自身免疫糖尿病

主要探讨自身免疫糖尿病（包括1型糖尿病和LADA）的临床以及致病谱。遗传易感因素影响了自身免疫糖尿病的发病年龄。1型糖尿病和LADA的最主要的易感基因位于HLA区域。由于年龄相关的遗传影响因素,目前还不能用遗传学的方法来区分LADA和1型糖尿病。非遗传因素在1型糖尿病中有很大的作用,但关于LADA还知之甚少。在低龄儿童中就可有糖尿病相关的免疫过程,这可预测β细胞毁损过程。对于LADA的治疗和预防还需进一步研究以确定最佳方案。     

人类巨细胞病毒感染的临床检测方法

人类巨细胞病毒(HCMV)在人群中的感染率极高．绝大多感染者不出现任何临床症状，而当宿主免疫力降低时，即诱发严重临床疾病，因而人类巨细胞病毒感染的临床检测就显得很重要。病毒的分离与鉴定虽是临床诊断的金标准，但受各种条件的制约不能得到广泛的应用。随着医学检测手段与技术的提高，人类巨细胞病毒感染的临床检测也出现了更多更好的检测方法。     

人类巨细胞病毒感染与优生优育

人类巨细胞病毒（HCMV）是一种人体的疱疹病毒,在人群中普遍隐性感染。HCMV感染与机体免疫状态密切相关,许多免疫缺陷或患免疫抑制性疾病都伴有HCMV感染。如器官移植、妊娠、新生儿、恶性肿瘤等在机体抵抗力下降时均可引起严重的感染,死亡率较高。     

Ⅱ型糖尿病肾病患者治疗前后巨细胞病毒感染分析

目的分析Ⅱ型糖尿病肾病患者治疗前后尿巨细胞病毒DNA（HVMV-DNA）含量及其临床意义。方法选取进行治疗的Ⅱ型糖尿病肾病患者52例作为观察组,同时选取在门诊进行健康体检的健康成人52例作为对照组,依据观察组患者的肾功能对其进行分组,并比较患者治疗前后尿HCMV—DNA含量水平。结果观察组患者治疗前的HCMV阳性例数为5例,高于对照组的0例,差异有统计学意义（P〈0．05）;治疗后轻度肾功能不全患者的尿HCMV阳性率为3．70％,中度肾功能不全为37．50％,重度肾功能不全为44．44％,不同组别比较差异有统计学意义（P〈0．05）。结论Ⅱ型糖尿病肾病患者容易发生HCMV感染,除了和自身抵抗力及免疫抑制荆治疗有关外,还与患者自身病情严重程度有关。     

巨细胞病毒感染与2型糖尿病患者动脉粥样硬化

心血管病变仍是糖尿病最主要的致死和致残的原因。２型糖尿病的冠心病发病危险性较普通人群高２～３倍。然而 ,迄今为止 ,２型糖尿病患者发生动脉粥样硬化 (ＡＳ)的原因及其可能机制尚未完全阐明。自从Ｆａｂｒｉｃａｎｔ等 ［１］用禽类疱疹病毒 (ＭＤＶ)在鸡体内成功诱发ＡＳ以来 ,大量研究表明人类巨细胞病毒 (ＨＣＭＶ)感染与ＡＳ形成有关。在许多方面 ,ＨＣＭＶ的生物学特征与ＡＳ发生机制相一致 :ＨＣＭＶ感染系全身感染 ;ＨＣＭＶ感染内皮细胞 ;多形核白细胞吸附于受感染的血管内皮细胞表面 ,造成细胞损伤 ;受感染的内皮细胞释放病毒…     

谷氨酸脱羧酶抗体和胰岛细胞抗体对1型糖尿病的诊断价值

目的 探讨谷氨酸脱羧酶抗体(GAD-Ab)、胰岛细胞抗体(ICA)对1型糖尿病诊断的敏感度和特异度。方法 应用酶联免疫方法检测45例l型糖尿病患者和50例健康人血清GAD-Ab与ICA。结果 测量GAD-Ab的敏感度是48．9％，特异度94％；测量ICA的敏感度是26．7％，特异度96％；而GAD-Ab与ICA平行试验的敏感度62．5％。结论 GAD-Ab与ICA联合检测对1型糖尿病的诊断更敏感。     

特发性1型糖尿病的发病机制进展

根据1型糖尿病发病机制,可分为自身免疫性(1A型)和特发性(1B型)两种类型.1A型患者体内有多种胰岛自身抗体存在,主要包括胰岛细胞抗体(ICA)、胰岛素自身抗体(IAA)、谷氨酸脱羧酶抗体(GADA)和酪氨酸磷酸酶抗体(IA 2A)等;1B型病因未明,但目前发现在这些患者中存在数种少见型胰岛自身抗体,如羧基肽酶H抗体(CPHAb)和SOX13(ICA12)抗体等.随着这些抗体本质逐渐被揭示,不仅被用于特发性1型糖尿病的诊断和筛查,而且在对本病病因和防治的研究中都起到了很大作用.     

特发性1型糖尿病的发病机制进展

根据1型糖尿病发病机制,可分为自身免疫性(1A型)和特发性(1B型)两种类型。1A型患者体内有多种胰岛自身抗体存在,主要包括胰岛细胞抗体(ICA)、胰岛素自身抗体(IAA)、谷氨酸脱羧酶抗体(GADA)和酪氨酸磷酸酶抗体(IA-2A)等;1B型病因未明,但目前发现在这些患者中存在数种少见型胰岛自身抗体,如羧基肽酶H抗体(CPHAb)和SOX13(ICA12)抗体等。随着这些抗体本质逐渐被揭示,不仅被用于特发性1型糖尿病的诊断和筛查,而且在对本病病因和防治的研究中都起到了很大作用。     

胰岛自身抗体联合测定与1型糖尿病相关性研究

目的:探讨胰岛自身抗体联合测定对早期诊断1型糖尿病的相关互补性及临床意义。方法:对686例糖尿病患者采用ELISA法定性检测ICA、IAA及定量检测GAD,用放射免疫法空腹和餐后2h检测C肽。结果:自身抗体双阳性者(ICA+GAD、GAD+IAA、ICA+IAA)68例,为受检人数的9.94％;单一ICA阳性者28例(4.08％),GAD阳性者24例(3.5％),IAA阳性者14例(1.98％),自身抗体双阳性检出率明显高于单一抗体阳性,有显著差异(P<0.01)。自身抗体双阳性组年龄为36.2±18.4岁,明显低于胰岛自身抗体阴性组(54.6±17.2岁),两组年龄有显著差异(P<0.01)。IAA+ICA阳性组平均年龄为32.6±18.4岁,低于ICA+GAD阳性组(40.4±19.6)和GAD+IAA阳性组(38.8±18.6),(P<0.001)。自身抗体双阳性组及单一GAD阳性组、ICA阳性组空腹和餐后2hC肽明显低于抗体阴性组(P<0.001)。单一IAA阳性组与抗体阴性组无明显差异(P>0.05)。结论:胰岛自身抗体阳性糖尿病患者胰岛细胞功能明显低于阴性患者,提示自身抗体阳性患者(单一IAA阳性除外)胰岛功能有明显损伤;单一IAA阳性患者不能反映胰岛功能受损程度。成年糖尿病患者GAD阳性率较高,青少年糖尿病患者ICA、IAA阳性率较高,三种抗体联合检测可提高对1型糖尿病患者诊断的敏感性和特异性,对1型糖尿病患者的早期诊断和治疗有重?     

儿童1型糖尿病合并肺毛霉菌病死亡1例

患儿,男,6岁,以精神差5 d ,呼吸困难伴紫绀1 d入院.查体:意识不清,压眶反应弱,双眼窝稍凹陷,双瞳孔对光反射迟钝,口唇干燥伴紫绀,呼吸深大不规则,四肢温度凉,毛细血管再充盈时间2 s.血气分析示pH 7. 122,PCO218. 9 mmHg,PO282 mmHg,BE-21. 8 mmol/L,Na+ 129...     

Implication of epigenetic factors in the pathogenesis of type 1 diabetes

Type 1 diabetes (T1D) is an autoimmune disease that resulted from the severe destruction of the insulin-producing β cells in the pancreases of individuals with a genetic predisposition. Genome-wide studies have identified HLA and other risk genes associated with T1D susceptibility in humans. However, evidence obtained from the incomplete concordance of diabetes incidence among monozygotic twins suggests that environmental factors also play critical roles in T1D pathogenesis. Epigenetics is a rapidly growing field that serves as a bridge to link T1D risk genes and environmental exposures, thereby modulating the expression of critical genes relevant to T1D development beyond the changes of DNA sequences. Indeed, there is compelling evidence that epigenetic changes induced by environmental insults are implicated in T1D pathogenesis. Herein, we sought to summarize the recent progress in terms of epigenetic mechanisms in T1D initiation and progression, and discuss their potential as biomarkers and therapeutic targets in the T1D setting.     

1-脱氧野尻霉素减轻2型糖尿病小鼠的肝纤维化

Objective To investigate the effect of 1-deoxynojirimycin (DNJ) for improving diabetic liver fibrosis and explore the underlying mechanism. Methods Mouse models of type 2 diabetes were established in 10 Kunming mice by high-fat diet feeding for 8 weeks and intraperitoneal injection of STZ, with 5 mice receiving intraperitoneal injection of citrate buffer solution with normal feeding as the control group. The mouse models were randomized into two groups (n=5) for further high-fat feeding (model group) and additional treatment with 10% DNJ in drinking water (200 mg · kg- 1 per day; DNJ group) for 8 weeks. The mice were monitored for changes in body weight (BW), blood glucose, serum total cholesterol (TC), triglyceride (TG) and superoxide dismutase (SOD) levels. The pathological changes in the liver tissue were observed using HE and Sirius Red staining, and the solubility of collagens in the liver tissues was determined. The expression levels of MCP-1, TNF-α, IL-1β and TGF-β1 mRNA were detected with real-time PCR, and the protein expressions of α-SMA and collagen2 (ColA2) were determined with Western blotting. In the in vitro experiment, mouse fibroblasts L929 cells were pretreated with DNJ (10 μg/ mL) or PBS for 30 min followed by culture in high-glucose medium for 24 h, and the level of ROS production was measured using dihydroethidium (DHE) staining. Results In the mouse model of type 2 diabetes, DNJ treatment significantly lowered serum level of glucose, TC, and TG (P<0.05) and increased serum SOD activity (P<0.05). DNJ obviously attenuated liver fibrosis in the diabetic mice, as shown by alleviated cross-linking of collagens and reduced contents of pepsin-solubilized collagen (PSC) and total collagen (P<0.05). DNJ treatment also significantly reduced the overexpression of the pro-inflammatory cytokines and fibrosis-related cytokines induced by diabetes (P<0.05). In L929 cells exposed to high glucose, pretreatment with DNJ significantly lowered the intensity of red fluorescence in DHE staining. Conclusion DNJ can attenuate type 2 diabetes-induced liver fibrosis in mice through its hypoglycemic, anti-inflammatory and anti-oxidative effects.     

人巨细胞病毒感染致血管内皮细胞损伤机制的研究

摘要：目的观察人巨细胞病毒（HCMV）感染对人血管内皮细胞氧化应激的影响及对血管细胞粘附分子-1（VCAM-1）和糖基化终产物受体（RAGE）时序性表达的影响,研究HCMV感染致动脉粥样硬化（AS）的作用机制。方法用HCMV感染血管内皮细胞,用激光共聚焦显微镜检测细胞内活性氧（ROS）的改变;采用RT-PCR方法检测不同感染时段细胞VCAM-1及RAGEmRNA的表达。结果HCMV感染血管内皮细胞后,HCMV组荧光强度显著高于对照组（P＜0.01）。感染0h时,VCAM-1mRNA有基础水平的表达,4h开始升高,8h时达高峰,12h开始回落,24h回落更明显,与0h比较,均有统计学意义（P＜0.01）,48h接近0h表达水平（P＞0.05）。感染0h时,RAGEmRNA有基础水平的表达,4h开始升高,8h时表达水平明显升高,随感染时间延长,表达量逐渐增高,感染24h时达高峰,48h开始回落,仍维持在较高的水平,各时段与0h比较,均有统计学意义(P＜0.01)。结论HCMV感染血管内皮细胞后能够增强氧化应激,促进VCAM-1及RAGE的mRNA表达,并且呈时间依赖性。HCMV有可能通过增强氧化应激、上调VCAM-1及RAGE的表达介导血管内皮细胞的炎症反应,促进动脉粥样硬化的发生、发展。     

燥邪对2型糖尿病发病机制的影响

糖尿病是多种原因引起的因胰岛素分泌不足和/或胰岛素抵抗所致的以高血糖为基本病理生理改变的糖、脂肪、蛋白质代谢紊乱的综合征.流行病学调查发现2型糖尿病占本病90%以上.其发病机制目前尚未完全清楚,多与遗传、自身免疫及环境因素有关.2型糖尿病与中医对消渴的认识、记载、描述极为相似,属于中医消渴病范畴.其典型症状为多饮、多食、多尿,或消瘦.历代医家认为其基本病机是热烁津液化燥,或气机阻滞、津液失布.     

1型糖尿病(T1D)的细胞免疫学发病机制的研究进展

 近年来,1型糖尿病(type 1 diabetes,T1D)的发病率不断上升,其发病是遗传、环境、免疫等因素共同作用引发了胰岛β细胞为主体的自身免疫损害反应。T1D的发病机制涉及免疫应答及调节等免疫过程,其中细胞免疫在T1D的发病过程中起着重要作用,CD4+及CD8+ T淋巴细胞的浸润,B淋巴细胞、自然杀伤细胞(natural killer cells,NK)、树突状细胞(dendritic cells,DC)等免疫细胞共同参与了β细胞的损伤,最终引起T1D的发病。     

Autoantibodies,human T lymphotropic virus type 1 and type 1 diabetes mellitus in Jamaicans

The clinical characteristics, autoantibody profiles and seroprevalence of human T lymphotropic virus Type 1 (HTLV-1) were assessed in 30 Jamaican patients with Type 1 diabetes mellitus. Two hundred and fifty-two blood donors and 108 patients with Graves' disease were included as controls for the HTLV-1 component of the study. The mean age of onset of diabetes mellitus was 20.5 +/- 9.2 years and the mean duration of diabetes mellitus was 10.5 +/- 6.1 years. The remarkable clinical data included an absence of other associated organ-specific autoimmune diseases, and clinical evidence and history of congenital rubella in one patient. Islet cell cytoplasmic antibodies (ICA) were absent but 17% (5/30) of the diabetic patients tested positive for glutamic acid decarboxylase (GAD) antibodies. No other organ-specific autoantibodies were detected but non-organ-specific autoantibodies were present in 9 (30%) of the sera of diabetic patients. The seroprevalence of HTLV-1 in the patients with diabetes mellitus was significantly higher than that in the healthy controls (17% (5/30) versus 4% (11/252), p = 0.05). Autoantibodies were found in the sera of 4/5 (80%) of the diabetic patients who were positive for HTLV-1. None of the patients with onset of diabetes mellitus below age 15 years was HTLV-1 positive. The likely polyaetiological nature of Type 1 diabetes mellitus in Jamaicans is being further investigated at the molecular level.     

2型糖尿病所致认知功能障碍的研究进展

2型糖尿病和认知功能障碍是严重威胁人类生存质量的慢性疾病,是老年人群中严重的健康问题,世界大部分地区这2种疾病的发病率都在增加。2型糖尿病引起的认知功能障碍的发病机制尚不清楚。可能的因素和相关机制包括胰岛素抵抗、高胰岛素血症因素、胰岛素与β-淀粉样蛋白（Aβ）代谢之间的关系、高血糖因素导致的晚期糖基化终末产物（AGEs）生成增多、低血糖因素、脑血管病因素、脂代谢紊乱、炎症因子等有关。本文就2型糖尿病致认知功能障碍的多种因素及机制进行综述,以期为认知功能障碍包括阿尔茨海默病的防控及早期干预提供思路。