糖尿病微血管病变的分子学研究进展

糖尿病是一组全身性的内分泌代谢性疾病,其慢性并发症几乎涉及到全身各器官组织。微血管病变作为糖尿病的特征性并发症,是多种器官损害的病理生理基础,其主要改变为毛细血管基底膜增厚,微血管屏障功能破坏及进行性闭塞,组织缺氧。早期糖尿病以相关组织中微血管血流量增加和由此引起的血压增高为特点。微血管内皮细胞压力增加,引起更多的细胞外基质蛋白产生,其作为一种损伤性反应,必然引起微血管硬化症。糖尿病微血管改变主要引起糖尿病视网膜病变(DR)、糖尿病肾病(DN)、糖尿病心肌病变等。现将近几年糖尿病微血管病变的分子学研究进展作一综述。     

糖尿病患者微循环改变的观察

本文观察108例Ⅱ型糖尿病患者治疗一年前、后球结合膜和甲皱襞微循环改变,并比较临床有、无微血管病变和病情控制情况与之的关系。治疗后,仅在临床无微血管病变以及糖尿病控制良好的患者中才见到微循环的改善,提示早期严格控制糖尿病对微血管病变防治的重要性。     

血管生成素与糖尿病肾病

<正>糖尿病肾病(diabetic nephropathy,DN)是糖尿病(diabetes mellitus,DM)主要的微血管并发症之一,近年研究发现DN与DM视网膜病变都存在血管生成异常,DN早期肾小球肥大、毛细血管袢扩张,尿白蛋白排泄增多;晚期微血管大量退缩,肾组织缺血缺氧,最终导致肾小球硬化和肾间质纤维化。动物实验研究证实,早期给予血     

递法明对早期糖尿病肾病患者的疗效观察

糖尿病肾病(DN)是糖尿病常见的并发症，也是糖尿病(DM)患者的主要死亡原因之一。早期糖尿病肾病是DN得以完全恢复的最后机会，再向前发展，DN就无法完全治愈。所以在DN早期应积极进行治疗。糖尿病眼病及糖尿病肾病均属于糖尿病性微血管并发症，两者具有毛细血管高渗透性的共同发病机制；递法明是目前新公认的治疗糖尿病毛细血管病变的理想药物，其对于糖尿病视网膜病变有良好的疗效，但国内关于递法明用于糖尿病肾病的报道较少，所以本研究中笔者选择了本院60例早期DN患者，     

E-选择素与糖尿病视网膜病变

糖尿病视网膜病变是进展性的微血管病变 ,而E 选择素介导的白细胞与内皮细胞的相互作用是内皮细胞损伤、血管闭塞、新生毛细血管形成的重要原因。粘附、聚集于毛细血管内的白细胞释放自由基、酶及血管活性物质 ,增加血管通透性 ,破坏毛细血管结构 ;同时白细胞释放的血管生长物质及SE 选择素自身又都可刺激新生血管形成。E 选择素及其单克隆抗体的研究将为糖尿病视网膜病变的诊断和治疗提供新的思路。     

糖尿病人为什么会出现靶器官损害？

问：糖尿病微血管病变发生的机制？答：糖尿病微血管病变在临床上表现为：视网膜病变、肾脏病与周围神经炎。主要病理生理机制如下：细胞内高血糖引起血管通透性加大，NO减少，血管扩张减弱，血管收缩加强。AngⅡ、内皮素、血管内皮生长因子（VEGF）增加。时间越长，微血管内皮细胞丧失，血管外TGF-β生成增多，血管外基质蛋白沉积，毛细血管进行性闭塞。再加上局部组织水肿、缺血、缺O2引起视网膜血管新生，蛋白尿，肾小球膜扩张，肾小球硬化，周围神经退行性变。     

糖尿病与肺部疾病的关系

糖尿病是一种并发多器官病变的疾病,肾脏、视网膜、神经系统、微血管以及心血管系统均可受累,特别是糖尿病微血管病变也会累及肺泡一毛细血管网,从而对肺部产生影响,部分学者认为肺脏是糖尿病的靶向器官。本文就糖尿病对肺部的生理病理基础影响、肺功能的损害以及与肺部常见疾病的关系等方面进行综合阐述和分析。     

糖尿病患者保护视力三大着眼点

糖尿病的并发症主要是微血管病变，如脑部、肾脏、眼底视网膜的微血管病变等。视网膜的微血管病变是人体唯一可以通过医生的肉眼观察到的病变。有糖尿病视网膜病变的存在说明身体其他器官或脏器的微血管病变也存在。临床已证实眼内视网膜的微血管病变与肾脏微血管病变相符，即糖尿病性视网膜病变的严重程度与肾脏微血管病变的严重程度基本一致。所以我们通过了解糖尿病患者的视网膜病变情况，     

糖尿病合并血管病变的护理

糖尿病可以并发多种血管病变，如心血管．脑血管、肾脏．视网膜及皮肤的微血管等，是目前糖尿病病人死亡和致残的主要原因之一。对血管病的护理，除按糖尿病的一般护理外，还要根据不同部位的血管病变进行护理。     

E—选择素与糖尿病视网膜病变

糖尿病视网膜病变是进展性的微血管病变，而E－选择素介导的白细胞与内皮细胞的相互作用是内皮细胞损伤、血管闭塞、新生毛细血管形成的重要原因。粘附、聚集于毛细血管内的白细胞释放自由基、酶及血管活性物质，增加血管通透性，破坏毛细血管结构；同时白细胞释放的血管生长物质及SE－选择素自身又都可刺激新生血管形成。E－选择素及其单克隆抗体的研究将为糖尿病视网膜病变的诊断和治疗提供新的思路。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

CagA-Hp抗体IgG与胃炎的组织学分析

研究幽门螺杆菌(Hp)感染与胃炎的关系。方法对204例慢性胃炎患者胃粘膜进行观察分析,并测定其中137例Hp阳性患者血清CagA-Hp抗体IgG水平,与组织学对照。结果慢性萎缩性胃炎伴肠上皮化生患者血清CagA抗体IgG明显高于对照组(P＜0.01);其他类型胃炎患者血清CagA抗体IgG水平无明显增高(P＞0.05)。结论CagA-Hp可能是导致慢性萎缩性胃炎伴肠上皮化生的因素之一,对这类患者应密切随访观察。     

慢阻肺急性加重期患者预后的影响因素分析

目的探讨慢性阻塞性肺病急性加重期(AECOPD)患者预后的相关危险因素。方法回顾性调查、收集58例AECOPD患者可能影响其预后的相关因素,并对其分别进行单因素分析。并进行Logistic多元逐步回归进行多因素分析,筛选影响AECOPD患者预后的独立危险因素。结果单因素分析后将结果 P0.1的因素纳入多因素Logistic回归,分析发现是否合并呼吸衰竭、气促程度、白细胞计数、APACHEⅡ、应用抗氧化剂、慢阻肺治疗依从性为影响AECOPD患者预后不佳的独立因素(P0.05)。结论根据AECOPD患者预后的独立危险因素,及早判断,选择合适的后续治疗方案,对提高其生存率及生存质量具有重要意义。