糖尿病患者尿路感染病原菌分布及耐药性分析

目的探讨糖尿病患者合并尿路感染的病原菌分布和耐药性,指导临床合理应用抗生素。方法回顾性分析2003年1月￣2005年9月81例2型糖尿病合并尿路感染患者细菌学培养及病原菌的菌群分布和耐药性。结果①740例糖尿病患者中合并尿路感染的81例,尿路感染发生率占10.95%,其中女性占82.7%,年龄60岁以上占65.4%;②细菌学检查率为77.8%,尿细菌培养阳性率为44.4%,尿细菌培养阴性率为33.4%;③尿细菌培养阳性36例,G-菌株占65.8%,大肠杆菌占52.6%,G 菌株占28.9%,粪肠球菌及葡萄球菌属各占10.5%,真菌2株占5.3%;④大肠杆菌对氨苄青霉素、头孢噻吩、培氟沙星、复方新诺明、阿莫西林/棒酸耐药率较高,粪肠球菌对喹诺酮类及四环素耐药率较高,葡萄球菌属对青霉素G、头孢唑啉、复方新诺明、红霉素、氨苄青霉素、阿莫西林/棒酸、左氧氟沙星、培氟沙星、庆大霉素耐药率较高。结论糖尿病患者由于免疫力低下,局部组织结构功能受损易于被病原菌侵袭和繁殖,故合并尿路感染应重视病原菌及其耐药性检测,对控制尿路感染、合理使用抗生素十分重要。     

Effects of combined renovascular hypertension and diabetes mellitus on myocardial cells,non-vascular interstitium and capillaries: a stereological study on rat hearts

Summary The effects of combined renovascular hypertension and diabetes mellitus on the rat heart were investigated in order to detect possible synergistic effects of the two conditions. Hypertensive diabetic and hypertensive non-diabetic animals were compared to diabetic and non-diabetic controls. Hypertension was established for 12 weeks by a surgical stenosis of the left renal artery; diabetes mellitus was maintained for 8 weeks by a single intraperitoneal injection of 60 mg/kg streptozotocin. Light microscopic stereology did not reveal significant divergences between diabetic hypertensives and non-diabetic hypertensives. Hypertension induced a focal perivascular and interstitial fibrosis with increased volume densities of non-vascular interstitium and fibrosis (P<0.001). Capillary density (Q_A) was decreased in transverse sections (P<0.01) and increased in longitudinal sections (P<0.01). This indicates a three-dimensional remodelling of the capillary bed with an increased number of obliquely running capillaries. At least the length density (L_V) of capillaries (mm/mm³) tends to be normalized in long-term renovascular hypertension. At the ultrastructural level, a synergism of hypertension and diabetes mellitus was observed: the volume ratio of mitochondria to myofibrils was significantly decreased in hypertensive diabetics, but not in non-diabetic hypertensives or in diabetics. This may enhance the risk of cardiac deterioration. We conclude that the primary target of the synergistic damage in hypertensive diabetic heart muscle disease is the myocardial cell and not the cardiac interstitium.Preliminary results of this study have been published in: Mall G (1991) Morphometric study on the rat heart in combined renovascular hypertension and diabetes mellitus. In: Nagano N, Dhalla NS (eds) The diabetic heart. Raven Press, New York, pp 115–124Dedicated to Prof. Dr. med. G. Seifert on the occasion of his 70th birthday     

妊娠糖尿病对母婴影响的分析

目的探讨妊娠糖尿病（GDM）对母婴影响。方法观察妊娠糖尿病患者36例及健康孕妇36例,分析其妊娠结局。结果GDM组妊娠期高血压疾病、早产、巨大儿及剖宫产发生率分别为41.7%、27.7%、25%及58.3%,明显高于对照组16.7%、8.3%、5.5%及27.7%,差异有显著性（P〈0.05）。结论GDM是危害孕产妇和围产儿的妊娠并发症,早期诊断GDM及控制血糖是减少母婴并发症的关键。     

T Cells Recognize Multiple GAD65 and Proinsulin Epitopes in Human Type 1 Diabetes, Suggesting Determinant Spreading

Human type 1 diabetes is thought to be mediated by autoreactive T cells specific for antigens expressed by pancreatic beta cells. However, it is unclear which autoantigens and determinants thereof are the targets of the autoimmune attack. Using comprehensive peptide libraries that cover the entire sequence of two major candidate autoantigens, GAD65 and proinsulin, we measured the in vivo frequencies of peptide-specific, IFN-gamma-producing memory T cells in 27 diabetic patients, 14 high risk individuals, and 15 partially HLA-matched healthy controls. Compared to the controls, both a higher number of determinants on the islet cell antigens were recognized and the frequencies of peptide specific cells were increased in patients and high risk individuals. Inclusion of signal enhancing anti-CD28 antibody further accentuated this difference. Considerable heterogeneity in peptide recognition was seen even in DRB1*04, DQB1*0302 matched individuals. Unlike its peptides, the GAD protein antigen did not recall a T cell memory response. The highly heterogeneous recognition of a multitude of peptide determinants on both autoantigens, occurring in the absence of protein recognition, and the low functional avidity of the memory cells involved jointly suggest that the autoimmune T cell repertoire in human type 1 diabetes primarily targets cryptic determinants engaged by determinant spreading.     

1型糖尿病及肥胖儿童血清瘦素水平及与其它常用指标相关性分析

目的比较1型糖尿病及肥胖儿童血清瘦素水平。方法以EL1SA方法测定35例1型糖尿病、32例肥胖及35例健康儿童的血清瘦素水平。35例1型糖尿病患者中 ,7例为新患糖尿病伴酮症酸中毒的患者。通过测定C -肽水平来评估胰岛素的分泌。C -肽、血糖、糖化血红蛋白按常规方法测定。结果糖尿病患者血清瘦素水平低于对照组 (P<0.001)。肥胖儿童血清瘦素及C -肽水平高于糖尿病组及对照组。在糖尿病新患者中 ,经1个月的胰岛素治疗后 ,血清瘦素水平未有任何变化 (P>0.05)。在联合组中 ,瘦素与体重指数 (bodymassindex,BMI)及C -肽呈正相关(P<0.001) ,而与血糖及糖化血红蛋白呈负相关(P<0.05)。结论1型糖尿病患儿血清瘦素水平低可能与代谢控制有关的慢性胰岛素缺乏引起的。瘦素及胰岛素在保持身体体重稳定的过程中可能起着补充作用。     

Dissimilar background genes control susceptibility to autoimmune disease in the context of different MHC haplotypes: NOD.H-2(s) congenic mice are relatively resistant to both experimental autoimmune encephalomyelitis and type I diabetes

Nonobese diabetic (NOD) mice develop multi-organ autoimmune diseases, including type 1 diabetes. We hypothesized that backcrossing the MHC region from SJL (H-2(s)) mice, which have an endogenous PLP(139-151)-reactive repertoire, onto the background of autoimmune-prone NOD mice would result in a mouse strain that is highly susceptible to experimental autoimmune encephalomyelitis (EAE). Unexpectedly, although we detected an endogenous PLP(139-151) repertoire in the NOD.S mice, they did not develop spontaneous EAE and were relatively resistant to PLP(139-151)-induced EAE when compared to SJL mice. This resistance was associated with lower production of proinflammatory cytokines and a decreased expansion of PLP(139-151)-specific CD4(+) T cells after immunization and restimulation with PLP peptide in vitro. V(beta) chain usage among PLP(139-151)-reactive T cells differed between SJL and NOD.S mice. Furthermore, NOD.S mice were resistant to the development of insulitis and cyclophosphamide-induced diabetes, but not sialadenitis. Altogether, even though NOD mice develop spontaneous autoimmune diseases, they become relatively resistant to induction of EAE even when they express the EAE-permissive class II molecule I-A(s). Our data show that certain combinations of otherwise susceptibility-conferring MHC and non-MHC genes can mediate autoimmune-disease resistance when they are paired together. These findings do not support the "shared autoimmune gene" hypothesis.     

急性胰腺炎患者空腹高血糖发生率及其危险因素分析

目的:回顾性分析急性胰腺炎(AP)患者空腹高血糖发生率及其危险因素。方法:收集2018-01—2018-12武汉大学人民医院胰腺外科133例AP且无糖尿病(DM)病史的住院患者病历资料,按照不同性别、年龄、AP临床分型、病因、CT指数评分(CISI)等分组,χ2检验分析各组临床因素与空腹高血糖(FPG≥6.1mmol/L)发生率的关系,多因素二元logistic回归分析空腹高血糖独立危险因素。结果:AP临床分型(χ2=5.494,P=0.019)和CTSI(χ2=6.236,P=0.013)与AP患者空腹高血糖相关(P<0.05)。CTSI≥6分(P=0.015,OR=2.920,95%Cl=1.234—6.905)为AP患者空腹高血糖的独立危险因素(P<0.05)。结论:临床分型中重症+重症及CTSI≥6分的AP患者易发生空腹高血糖,尤其CTSI≥6分是AP后空腹高血糖的独立危险因素,临床应高度关注。     

Pervanadate对大鼠类I型糖尿病的影响

钒盐衍生物 (ｐｅｒｖａｎａｄａｔｅ)在离体研究中表现出多种明显的类胰岛素效应 ,包括促脂质生成 ,促蛋白合成和抗脂质分解等 ,但其在体研究的报道并不多见。本研究旨在观察ｐｅｒｖａｎａｄａｔｅ对链脲菌素 (ｓｔｒｅｐｔｏｚｏｃｉｎ ,ＳＴＺ)所致大鼠类Ｉ型糖尿病的血糖水平的影响 ,并探讨其可能机制 ,以期为糖尿病的研究和治疗提供新的资料。材　料　和　方　法1　动物模型雌性Ｗｉｓｔａｒ大鼠 ,体重 1 4 0 - 1 60ｇ ,ＳＴＺ(Ｓｉｇｍａ)溶于 0 1ｍｏｌ/Ｌ柠檬酸缓冲液 (ｐＨ 4 5)中 ,按 65ｍｇ/ｋｇ体重尾静脉一次注射复制类Ｉ型…     

TNF-alpha impairs peripheral tolerance towards beta-cells,and local costimulation by B7.1 enhances the effector function of diabetogenic T cells

Maintenance of peripheral tolerance and inactivation of autoreactive T cells is based on a delicate balance between pro-inflammatory and protective cytokines that is poorly understood. We have here addressed how the local expression of the inflammatory cytokine TNF-alpha can impair peripheral tolerance and lead to autoreactivity. After transplantation of pancreata that are immunogenic due to beta-cell expression of B7.1 and TNF-alpha, into thymectomized and euthymic syngeneic mice, we found that only euthymic mice rejected the grafts. This result suggests that under normal circumstances autoreactive T cells are functionally inactivated, and initiation of an autoreactive response requires de-novo generation of T cells. By contrast, thymectomized mice expressing TNF-alpha on the endogenous islets rejected the grafts, showing that expression of TNF-alpha prevents functional silencing of the autoreactive T cells. Thus, this study provides a mechanism by which TNF-alpha and possibly chronic inflammatory responses may promote autoimmune diseases. Furthermore, we have investigated whether B7.1 can enhance T cell responses of already activated T cells leading to islet rejection. By transplantation of wild-type and B7.1-expressing islets into overtly diabetic mice we found that only the wild-type islets could restore normoglycemia, suggesting that costimulation by B7.1 is required in the expansion or effector phase of the response.     

Diet selection and metabolic fuels in three models of diabetes mellitus

Dietary self-selection and circulating metabolic fuels (glucose, free fatty acids, ketones) were examined in three forms of experimental diabetes mellitus in rats: pancreatectomy and streptozotocin treatment in adult and neonatal rats. Changes in diet selection resulting from insulin replacement also were examined. Differences were found in diet selection and circulating metabolic fuels between these types of diabetes. Mildly diabetic rats selected large amounts of fat while more severely diabetic rats primarily selected protein. Insulin treatment enhanced carbohydrate intake of diabetic rats and nearly normalized diet selection and circulating metabolic fuels. All diabetic groups exhibited severe glucose intolerance. These results support the observations of the beneficial effects of low-carbohydrate diets, question the generality of the use of high-fat diets, and suggest a more important role for high-protein diets in energy regulation in severely diabetic rats.