负压封闭吸引对糖尿病溃疡愈合的促进作用

目的 在"创而床准备(WBP)"理论指导下,观察负压封闭吸引局部处理糖尿病溃疡的疗效.方法 收集2000年1月至2005年1月间收治的27例糖尿病溃疡患者作对照组,2005年1月至2007年6月的8例糖尿病溃疡患者为试验组.两组患者均经常规系统的治疗,试验组在创面的黑、黄期采用清创后负压吸引治疗.观察两组创而各分期间的演进情况.比较两组手术Ⅰ期修复率、入院首次及实施负压治疗后1、2、3周创面细菌学检查结果 .观察各期创面组织标本的HE染色和黄、红两期Ⅰ、Ⅲ型胶原纤维苦味酸-天狼猩红染色结果 及对其含量进行图像分析.结果 试验组患者创面各分期的演进速度、于术Ⅰ期修复率均优于以照组(100%比46%,P<0.05).治疗2周后试验组创面末检出致病菌,对照组检出率为66.7%(P<0.05).HE染色显示试验组各期间的演进类似于急性创面愈合过程,且试验组黄期Ⅰ、m型胶原总含量为12.28%,对照组为24.77%(P<0.01).结论 基于WBP方案的负压吸引治疗能促进糖尿病溃疡的创面愈合过程.     

Hemodynamic factors in the pathogenesis of diabetic nephropathy

Summary The pathogenesis of the diabetic glomerular lesion is unknown. However, cumulative indirect evidence favors hemodynamic factors associated with the abnormal endocrine environment as the cause of diabetic angiopathy. Experimental evidence suggests that the increased hydrostatic pressures in capillary beds, a hallmark of the early stages of insulin-dependent diabetes, are associated with macromolecular leakage leading to the typical thickening of glomerular capillary basement membrane and increased glomerular mesangial matrix even prior to the occurrence of systemic hypertension. Patients with renal or carotid artery stenosis seem to be protected against diabetic nephropathy and retinopathy on the stenosed side. The first signal of diabetic nephropathy even before deterioration of the renal function is microalbuminuria detected by sensitive methods such as radioimmunoassay. Not only in hypertensive, but even in normotensive diabetic patients with microalbuminuria antihypertensive therapy has been shown to reduce albumin excretion rate and to slow the progression of diabetic nephropathy. Once overt diabetic nephropathy has been established, hypertension is a constant accompaniment of the disease. Thus, hypertension may be a cause as well as a result of diabetic nephropathy. Tight control of blood sugar in close association with antihypertensive treatment reducing blood pressure to a lower normal limit, possibly with agents that specifically decrease glomerular capillary hydraulic pressure are the corner stone in protection against progression of the diabetic angiopathy.Abbreviations ECF extracellular fluid - ESRD end-stage renal disease     

Understanding the microbiome of diabetic foot osteomyelitis: insights from molecular and microscopic approaches

Objectives

Rigorous visual evidence on whether or not biofilms are involved in diabetic foot osteomyelitis (DFO) is lacking. We employed a suite of molecular and microscopic approaches to investigate the microbiome, and phenotypic state of microorganisms involved in DFO.

阿魏酸钠对糖尿病大鼠肾脏非酶糖基化和氧化的影响

目的:探讨阿魏酸钠(SF)对糖尿病(DM)大鼠肾脏非酶糖基化和氧化的影响。方法:对链脲佐菌素(STZ)诱导的DM大鼠灌胃给予SF 110 mg·kg^-1·d^-1,治疗8周,测定各组大鼠肾重／体重、肌酐清除率(Ccr)、24 h尿蛋白定量、血清和肾皮质果糖胺(FMN)、血清和肾皮质丙二醛(MDA)含量及抗氧化酶活性,并分别测定肾皮质糖基化终产物(AGEs)含量,观察肾脏病理改变。结果:糖尿病对照组(DM组)大鼠肾重／体重、Ccr、24 h尿蛋白定量、血清FMN、肾皮质FMN和AGEs显著高于正常对照组(N组);SF治疗组(SF组)肾重／体重、Ccr、24 h尿蛋白定量、血清FMN和肾皮质AGEs显著低于DM组;DM组大鼠肾皮质和血清超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性显著低于N组,MDA含量显著高于N组,SF治疗组大鼠肾皮质和血清SOD、CAT活性显著高于DM组,MDA含量显著低于DM组:DM组大鼠肾脏病理改变异常显著,SF组的肾脏病理学改变轻于DM组大鼠。结论: SF通过保护肾脏抗氧化酶,减轻氧化应激,抑制AGEs在肾脏的沉积对DM大鼠肾脏产生保护作用。     

2型糖尿病肾病患者血清胱抑素C的检测及意义

目的:检测糖尿病患者血清胱抑素C浓度变化,分析其在糖尿病患者早期肾损伤中的作用。方法:根据24h尿白蛋白排泄率(UAER)的测定结果,将104例糖尿病患者分为3组:单纯糖尿病组(SDM组)、早期糖尿病肾病组(EDN组)和临床糖尿病肾病组(CDN组);46名健康者作对照组;采用颗粒增强散射免疫比浊法测定血清胱抑素C水平,常规测定内生肌酐清除率、血肌酐和UAER,并对全部患者胱抑素C血清浓度与尿UAER进行直线相关分析。结果:SDM组,EDN组及CDN组间血清胱抑素C水平均有非常显著性统计学意义(P<0.01),血清胱抑素C与UAER、内生肌酐清除率及血肌酐值有良好相关性(r值分别为0.772,-0.754,0.785,P均<0.01)。结论:血清胱抑素C水平测定有助于2型糖尿病肾病的早期诊断,优于血肌酐和内生肌酐清除率,具有临床应用价值。     

SGK1在糖尿病小鼠肾脏皮质中时间差异性表达及意义

目的：研究血清和糖皮质激素诱导的蛋白激酶1（serum and glucocorticoid-inducible kinase 1,SGK1）在糖尿病（DM）小鼠肾脏皮质中时间上差异性表达及意义。方法: 采用链脲佐菌素（STZ）单次腹腔注射诱导小鼠糖尿病模型。将2月龄C57BL/6小鼠随机分成10组：第1、2、3、4、6、8、12周糖尿病小鼠组（DM₁、DM₂、DM₃、DM₄、DM₆、DM₈、DM₁₂）和相应的第1、4、8周正常对照组（N₁、N₄、N₈）。分别在DM模型制作成功后第1、2、3、4、6、8、12周末收集小鼠24 h尿量，检测24 h尿蛋白量；观察肾脏病理改变；半定量RT-PCR检测小鼠肾脏皮质SGK1及结缔组织生长因子（CTGF）mRNA的表达，Western blotting检测N₄、DM₄、DM₈组皮质SGK1、CTGF蛋白的表达。结果: 随着糖尿病病程的进展，DM组小鼠肾小球体积逐渐增大、系膜区逐渐增宽；DM组小鼠24h尿蛋白从第2周起开始逐渐增多，肾脏皮质SGK1 mRNA表达从第2周开始明显上调，在第４周达到峰值。CTGF随着糖尿病病程的进展表达逐渐递增。结论: SGK1在糖尿病早期肾脏表达峰值的出现及CTGF 持续递增的表达，提示SGK1在糖尿病肾病肾脏纤维化的发生发展过程中起重要作用。     

Alterations of glomerular matrix proteins in the pathogenesis of diabetic nephropathy

Summary Diabetic late complications are characterized by morphological and biochemical alterations of the extracellular matrix. In particular, longstanding diabetes causes quantitative and qualitative changes in basement membrane structure of retinal and renal capilleries. Immunohistochemical investigations of diabetic kidneys with diffuse glomerulosclerosis show increased collagen type IV deposition in the mesangial matrix and decreased heparan sulfate proteoglycan content in the mesangial matrix and glomerular basement membrane as well. In nodular glomerulosclerosis normal basement membrane components are decreased or absent while the occurrence of collagen type III in this stage has been interpreted as an irreversible alteration of the glomerular structure. These changes seem to be the underlying cause for the alterations in renal functions like persistent albuminuria and proteinuria. Increased intra- and extracellular levels of glucose and its derivatives are thought to be responsible for diabetic tissue dysfunction although there are reports on possible genetic defects causing increased susceptibility to develop diabetic nephropathy. Recent results, however, focuse on the role of glucose-induced cytokine secretion as mediator for altered metabolism of glomerular matrix proteins. In vitro studies with cultured kidney cells have shown that the glucose-induced dysregulation of the basement membrane synthesis may be mediated by a glucose dependent activation of protein kinase C. Alternatively or synergistically, the formation of AGE products formed after prolonged exposure of matrix proteins to elevated glucose may also lead to cytokine secretion subsequently inducing synthesis of extracellular matrix proteins. Studies in experimental animals confirm the diabetes induced dysregulation of the synthesis of extracellular matrix components on the molecular level.Abbreviations HSPG heparan sulfate proteoglycan - GBM glomerular basement membrane - ECM extracellular matrix - AGE advanced glucosylation end products - TNF tumor necrosis factor - bFGF basic fibroblast growth factor     

Eosinophilic pancreatitis in the newborn infant of a diabetic mother

Summary The authors have studied the pancreas of a premature female infant born to a diabetic mother. The findings included a peri-insular eosinophilic leucocyte infiltration, macropolinesia and a marked increase in B cells. In the exocrime parenchyma small B cells aggregates were also observed. B cells contained voluminous hypercromatic muclei and degranulated cytoplasm. Morphometric data demonstrated an increase in islet tissue. These morphological findings are indicative of excessive insulin secretion. The presence of eosinophilic leucocytes in pancreatic tissue and the pathogenic mechanism involved are discussed.     

Microangiopathy in human diabetic neuropathy

Summary Morphological change of endoneurial and perineurial vessels accompanied severe loss of myelinated axons in peripheral nerves of each of 17 patients with diabetic neuropathy. Vascular mural thickening averaged 18.9±9.9 m² in diabetic capillaries (n=11) vs. 6.9±4.1 m² in controls (n=7). Electron microscopy revealed vigorous endothelial proliferation as well as thickening and reduplication of basal lamina in each instance. Particular attention was paid to vessels which penetrate the perineurium en route to the endoneurial intertitium, since they provide a major portion of the endoneurial blood supply. Luminal narrowing and mural thickening of these vessels was compounded by basal laminar thickening of the perineurium. Fenestrated endoneurial capillary endothelium was noted in one case. Both demyelination and axonal degeneration were observed with intra-axonal glycogen accumulation in some axons. Morphometric analysis revealed extensive myelinated nerve fiber loss in diabetic nerves. These morphological findings emphasize the impact of diabetic microangiopathy on specialized endothelium and suggest that local anatomic factors in the perineurial sheath render the nerve vulnerable to chronic ischemia.Supported in part by the National Institute for Communicative Disorders and Stroke NS-14162 and by the Veterans Administration Research Service