呼吸道感染患儿血清心肌酶谱的模糊聚类分析

统计了4组（上感组、支哮组、肺炎组、心衰组）共276例呼吸道感染患儿及30例正常的血清心肌酶谱（AST,LDH,CK）,运用基于区间值模糊集的聚类方法对其进行了聚类分析.结果:上呼吸道感染患儿的心肌酶大致正常,大多支气管哮喘患儿的心肌酶谱升高,但不显著,多数肺炎或心衰患儿的心肌酶谱明显升高.提示呼吸道感染可伴有不同程度的心肌损害,治疗中应注意保护心脏功能.     

米力农对心脏搭桥术后心力衰竭患者血管内皮生长因子、心肌酶谱与心功能的影响

选择2017年2月至2019年10月在我院接受治疗的心脏搭桥术后心力衰竭患者84例进行研究.探讨米力农对心脏搭桥术后心力衰竭患者血管内皮生长因子、心肌酶谱与心功能的影响.采用随机数字表法将患者分为2组,每组各42例.对照组行常规治疗,观察组在此基础上加以米力农治疗.比较2组患者临床疗效、血管内皮生长因子、心肌酶谱、心功...     

慢性肾脏病患者血清及尿胱氨酸蛋白酶抑制剂C测定的临床意义

目的：探讨慢性肾脏病（CKD）患者不同分期血清及尿胱氨酸蛋白酶抑制剂C（CYS—c）水平测定及临床意义。方法：应用乳胶增强免疫比浊法及速率法测定99例CKD（1～5期）患者血清及尿CYS—C指标水平,采用不同分组,并与正常对照组作比较。结果99例CKD患者各期的血清及尿CYS—C指标均有不同程度的升高（P〈O．05）,其水平与肾小球滤过率（GFR）呈显著负相关,与血肌酐（Scr）、尿素氮（BUN）水平呈正相关,与CKD的进程呈正相关（P〈0．05）,与24h尿蛋白定量（u-TP）量呈正相关（P〈O．05）,与患者的年龄段似无直接关联。结论：检测血清及尿CYS—C浓度可以准确、灵敏的反映肾小球滤过功能的改变,在临床上可作CKD患者理想的肾小球滤过功能评估指标,具有很高的临床应用价值。     

磷酸肌酸钠治疗手足口病合并心肌损伤疗效观察

目的:观察磷酸肌酸钠治疗手足口病合并心肌损伤的疗效.方法:选择2011年在兴安盟人民医院儿科就诊的符合手足口病合并心肌损伤5岁以下患儿40例,分为磷酸肌酸钠组、对照组.通过7d治疗后复查心肌酶,观察治疗的效果.结果:在40例手足口病合并心肌损伤的患儿中,磷酸肌酸钠组心肌酶谱改善明显优于对照组,差异有统计学意义(P＜0.05).结论:磷酸肌酸钠治疗手足口病并发心肌损伤疗效显著.     

198例新生儿窒息患儿心肌酶的临床研究

目的:探讨新生儿窒息患儿心肌酶变化与病情的关系.方法:对2002年1月-2004年6月住我科198例新生儿窒息患儿进行心肌酶监测.结果:新生儿重度窒息患儿心肌酶异常发生率高于轻度窒息;新生儿窒息发生心肌损伤与窒息的严重程度相关.结论:新生儿窒息患儿易并发心肌缺血缺氧性损伤,我们在治疗原发病的同时,应注意保护心肌细胞,以避免心肌细胞损伤.     

急性心肌梗塞国产重组链激酶静脉溶栓的疗效和安全性

目的观察国产重组链激酶(r-SK)静脉溶栓治疗急性心肌梗塞(AMI)的疗效及安全性.方法选择12例AMI患者应用r-SK静脉溶栓治疗,观察临床症状、心电图、心肌酶谱的变化,判断血管再通率.结果 12例AMI患者溶栓再通率85.7%,5例发病6～24h溶栓再通1例,再通率20%,两者相比差异有显著性(P＜0.05).结论 AMI患者选用国产r-SK静脉溶栓是安全、有效的治疗方法.     

慢性阻塞性肺疾病患者低氧血症对血清肌钙蛋白Ⅰ的影响

目的探讨慢性阻塞性肺疾病(COPD)患者低氧血症对血清肌钙蛋白I(CTnI)的影响.方法对137例急性发作期的COPD患者的血氧分压p(O2)和血清CTnI及心肌酶谱进行检测,按氧分压的水平分成3组,观察CTnI及心肌酶谱的变化,并分析COPD患者p(O2)与CTnI及各种心肌酶的相关关系.结果轻、中、重度低氧血症组的CTnI分别为(0.15±0.08)μg/L,(0.87±0.92)μg/L和(2.24±0.97)μg/L,3组间均有显著差异(P＜0.05).而3组p(O2)水平与相对应的CTnI水平呈显著的负相关关系(r=0.968 1,P＜0.05).死亡患者8例,平均CTnI为(3.62±1.08)μg/L,与存活病例比较显著升高(P＜0.05).结论低氧血症可导致COPD患者血清CTnI显著升高,且与氧分压p(O2)呈显著负相关关系.当CTnI明显升高时,提示患者病情危重.     

重症脑卒中患者的心肌酶观察

目的:探讨重症脑卒中患者急性期不同时段的心肌酶变化及心肌酶变化与预后有无关系.方法:选取108例重症脑卒中病人,同期非重症脑卒中病人85例的心肌酶进行观察,均选择入院即刻、入院后24h、72h、7d的不同时段观察心肌酶变化.选观察组中死亡患者在以上时段的心肌酶变化与生存患者在以上时段的心肌酶变化.结果:重症脑卒中患者多有心肌酶的改变,早期心肌酶改变的重症脑卒中患者,其心肌酶升高持续时间越长,预后越差.结论:重症脑卒中患者大多有心肌酶升高,且心肌酶升高出现越早,持续时间越长者,死亡率更高.     

慢性阻塞性肺疾病患者低氧血症对血清肌钙蛋白I的影响

目的　探讨慢性阻塞性肺疾病 (COPD)患者低氧血症对血清肌钙蛋白I(CTnI)的影响 .方法　对 137例急性发作期的COPD患者的血氧分压p(O2 )和血清CTnI及心肌酶谱进行检测 ,按氧分压的水平分成 3组 ,观察CTnI及心肌酶谱的变化 ,并分析COPD患者 p(O2 )与CTnI及各种心肌酶的相关关系 .结果　轻、中、重度低氧血症组的CTnI分别为 (0 .15± 0 .0 8) μg/L ,(0 .87± 0 .92 ) μg/L和 (2 .2 4± 0 .97) μg/L ,3组间均有显著差异 (P <0 .0 5 ) .而 3组 p(O2 )水平与相对应的CTnI水平呈显著的负相关关系 (r =0 .96 81,P <0 .0 5 ) .死亡患者 8例 ,平均CTnI为 (3.6 2± 1.0 8) μg/L ,与存活病例比较显著升高 (P <0 .0 5 ) .结论　低氧血症可导致COPD患者血清CTnI显著升高 ,且与氧分压p(O2 )呈显著负相关关系 .当CTnI明显升高时 ,提示患者病情危重     

150例慢性肾炎患者99mTC-DTPA肾功测定GFR分析

以放射性核素进行肾脏功能的测定检查在临床已广泛开展,本文对150例慢性肾炎患者进行了99mTC-DTPA肾小球滤过率(GFR)测定,同时获得肾动态显像及DTPA肾功能曲线. 1 资料与方法     

Atrial natriuretic peptide causes pre-glomerular vasodilatation and post-glomerular vasoconstriction in rat kidney

Atrial natriuretic peptide (ANP) can be extracted from rat hearts, and is found to increase fluid excretion by the kidneys when injected into test animals. The mechanism of ANP action is still unclear. ANP may reduce sodium reabsorption in the renal tubules, but it is also known that it increases the rate of glomerular filtration in the kidney, and relaxes preparations of smooth muscle, including one made from arteries that supply the kidney. To clarify its mode of action, we have studied directly the effects of semi-purified and synthetic ANP on blood vessels in the kidney of anaesthetized rats. We found that ANP causes a vasodilatation of the blood vessels which supply the glomeruli and a vasoconstriction of the arterioles which drain them. This substantiates the finding that increased filtration pressure participates in the natriuretic response.     

血液灌流联合血液滤过治疗急性重症白毒伞蕈中毒临床分析

目的：探讨血液灌流联合血液滤过治疗白毒伞蕈中毒的临床价值。方法：对我院2004年6月至8月集中收治的进行血液灌流联合血液滤过治疗的13例急性重症白毒伞蕈中毒患者进行回顾性分析。对13例患者治疗前后肝、肾功能、心肌酶及临床症状进行对比观察。结果：13例患者在应用血液灌流联合血液滤过治疗后,血液中血尿素氮（BUN）、血肌酐（SCr）、肌酸激酶同工酶（CK—MB）、丙氨酸氨基转移酶（ALT）、天门冬酸氨基转移酶（AST）、乳酸脱氢酶（LDH）明显下降,其中BUN、SCr、CK—MB具有统计学意义（P〈0．05）。临床症状明显改善,除2例患者由于经济原因未坚持治疗自动出院、1例因多器官功能衰竭死亡外,其余10例全部治愈出院。结论：对于急性重症白毒伞蕈中毒的救治,早期及时行血液灌流联合血液滤过治疗,可有效地清除和吸附血液中BUN、SCr、CK—MB、ALT、AST、LDH毒性物质,是避免白毒伞蕈中毒发生致死性肝损害的有效措施之一。     

改良肾大部切除大鼠诱发慢性肾衰模型的建立

对5/6切除大鼠肾脏诱发其慢性肾功能衰竭的动物模型进行改良,该方法省时省力,可以减少麻药用量不当造成的大鼠死亡,随差血肌酐(Scr)、尿素氮(BUN)的增加,肾衰逐渐加重,为药理研究及筛选治疗慢性肾衰的有效药物提供了一种实验对象。     

Nck adaptor proteins link nephrin to the actin cytoskeleton of kidney podocytes

The glomerular filtration barrier in the kidney is formed in part by a specialized intercellular junction known as the slit diaphragm, which connects adjacent actin-based foot processes of kidney epithelial cells (podocytes). Mutations affecting a number of slit diaphragm proteins, including nephrin (encoded by NPHS1), lead to renal disease owing to disruption of the filtration barrier and rearrangement of the actin cytoskeleton, although the molecular basis for this is unclear. Here we show that nephrin selectively binds the Src homology 2 (SH2)/SH3 domain-containing Nck adaptor proteins, which in turn control the podocyte cytoskeleton in vivo. The cytoplasmic tail of nephrin has multiple YDxV sites that form preferred binding motifs for the Nck SH2 domain once phosphorylated by Src-family kinases. We show that this Nck-nephrin interaction is required for nephrin-dependent actin reorganization. Selective deletion of Nck from podocytes of transgenic mice results in defects in the formation of foot processes and in congenital nephrotic syndrome. Together, these findings identify a physiological signalling pathway in which nephrin is linked through phosphotyrosine-based interactions to Nck adaptors, and thus to the underlying actin cytoskeleton in podocytes. Simple and widely expressed SH2/SH3 adaptor proteins can therefore direct the formation of a specialized cellular morphology in vivo.     

Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1

Glomerulonephritis is an inflammation of the kidney characterized by the accumulation of extracellular matrix within the damaged glomeruli, impaired filtration and proteinuria. In its progressive form, the disease destroys kidney function leading to uraemia and death, unless dialysis therapy or kidney transplantation is available. The pathogenesis of glomerulonephritis is incompletely understood, but the eliciting factor is thought often to be an immunological injury to mesangial and/or other resident cells in the glomeruli. We have used an animal model of acute mesangial proliferative glomerulonephritis to show that this disease is associated with increased production and activity of transforming growth factor beta 1 (TGF-beta 1), an inducer of extracellular matrix production. Here we report that administration of anti-TGF-beta 1 at the time of induction of the glomerular disease suppresses the increased production of extracellular matrix and dramatically attenuates histological manifestations of the disease. These results provide direct evidence for a causal role of TGF-beta 1 in the pathogenesis of the experimental disease and suggest a new approach to the therapy of glomerulonephritis.     

Biocompatibility of bio-Mg-Zn alloy within bone with heart, liver, kidney and spleen

A magnesium-zinc alloy rod was implanted into the marrow cavity of the distal femur in New Zealand rabbits. The femur with the implanted alloy was compared with the contralateral femur in which a bone tunnel without implant was formed as a control. Degradation of the magnesium-zinc alloy was analyzed via X-ray, scanning electron microscopy, and element energy spectrum analysis. Serum magnesium, liver and kidney function tests, and myocardial enzymes were measured. Heart, liver, kidney and spleen were sectioned for pathological analysis, and the effects of the implanted material on the histology and function of important organs were analyzed. Magnesium-zinc alloy was resorbed from the bone marrow cavity of the femur; 87% of the alloy was degraded within 14 weeks after the surgery. There were no significant differences in serum magnesium, liver or kidney function tests, or myocardial enzymes before the surgery and after degradation of the magnesium-zinc alloy. Histology of the heart, liver, kidney, and spleen did not change. This study demonstrated that magnesium-zinc alloy can be resorbed in bone, and that the degradation products have good biocompatibility with heart, liver, kidney, and spleen. Supported by the National Natural Science Foundation of China (Grant No. 30772182, and the Medical-Industial intersect study in Shanghai Jiaotong University (Grant No. YG2007MS26)     

The insect nephrocyte is a podocyte-like cell with a filtration slit diaphragm

The nephron is the basic structural and functional unit of the vertebrate kidney. It is composed of a glomerulus, the site of ultrafiltration, and a renal tubule, along which the filtrate is modified. Although widely regarded as a vertebrate adaptation, 'nephron-like' features can be found in the excretory systems of many invertebrates, raising the possibility that components of the vertebrate excretory system were inherited from their invertebrate ancestors. Here we show that the insect nephrocyte has remarkable anatomical, molecular and functional similarity to the glomerular podocyte, a cell in the vertebrate kidney that forms the main size-selective barrier as blood is ultrafiltered to make urine. In particular, both cell types possess a specialized filtration diaphragm, known as the slit diaphragm in podocytes or the nephrocyte diaphragm in nephrocytes. We find that fly (Drosophila melanogaster) orthologues of the major constituents of the slit diaphragm, including nephrin, NEPH1 (also known as KIRREL), CD2AP, ZO-1 (TJP1) and podocin, are expressed in the nephrocyte and form a complex of interacting proteins that closely mirrors the vertebrate slit diaphragm complex. Furthermore, we find that the nephrocyte diaphragm is completely lost in flies lacking the orthologues of nephrin or NEPH1-a phenotype resembling loss of the slit diaphragm in the absence of either nephrin (as in human congenital nephrotic syndrome of the Finnish type, NPHS1) or NEPH1. These changes markedly impair filtration function in the nephrocyte. The similarities we describe between invertebrate nephrocytes and vertebrate podocytes provide evidence suggesting that the two cell types are evolutionarily related, and establish the nephrocyte as a simple model in which to study podocyte biology and podocyte-associated diseases.     

短期有氧运动对糖尿病大鼠肾功能的影响

糖尿病肾病是非常严重的糖尿病并发症,其可以导致终末期肾衰,也是心血管疾病的一个危险因素。糖尿病肾病引起的重要的临床问题是尿蛋白和肾功能减退。运动作为糖尿病管理中的一个手段得到广泛共识。但急性运动引起尿蛋白和降低肾小球滤过率,所以运动对糖尿病肾病的影响存在争议。研究的目的是调查有氧运动对糖尿病大鼠微白蛋白尿和肾小球滤过率的影响。链脲霉素建立糖尿病大鼠模型,跑台上进行8周的有氧运动。大鼠分为4组：坐式对照组（ZD）;运动对照组（YD）;坐式糖尿病组（ZT）和运动糖尿病组（YT）。分别取建模成功稳定期（第四周末）和运动8周后的血样测定血糖水平。测定肌酐清除率（CCr）和微白蛋白尿（MA）评价肾功能。数据分析显示,与ZT组相比,有氧运动显著降低YT组血糖水平（p〈0.05）;与ZT组相比,有氧运动显著降低YT组微白蛋白尿水平（p〈0.01）;与ZD组相比,YD组和YT组肌酐清除率显著降低。研究结果表明,尽管肌酐清除率下降,有氧运动对微白蛋白尿的发生有预防作用。因此可能延迟糖尿病大鼠肾病的发生。     

青年男性尿液中多环芳烃代谢物与肾功能指标的关联研究

为了解青年男性多环芳烃暴露浓度与肾功能指标之间的关联,征集郑州地区121名志愿者进行了问卷调查和血液及尿液样品采集,分析了血肌酐、血尿素和血尿酸以及尿液中1-羟基芘(1-OHP),并在此基础上计算了估算肾小球滤过率(eGFR)和内生肌酐清除率(Ccr)。采用相关系数、线性回归模型和逻辑斯蒂回归模型进行分析。结果发现郑州地区青年男性体内普遍存在多环芳烃暴露,尿液1-OHP浓度与血尿素之间存在弱正相关,未在PAHs暴露与eGFR、Ccr和血尿酸等肾功能指标之间发现显著关联。     

Renal conservation of antifreeze peptide in Antarctic eelpout, Rhigophila dearborni.

In Antarctic notothenioid fishes large amounts (3% w/v) of small molecular weights of 2,600-23,500 and would be expected to be filtered into the urine, they remain in the blood because the kidneys of these fishes contain only aglomerular nephrons. Unlike the situation in most fishes, urine formation is the result of secretion rather than filtration and reabsorption. On the other hand, the peptide antifreezes in Northern Hemisphere fishes such as the winter flounder. Pseudopleuronectes americanus, are retained by the glomerular kidney even though inulin, of comparable weight, is rapidly filtered from the blood into the urine. The Antarctic eelpout (zoarcid), Rhigophila dearborni, which is unrelated to either the Antarctic notothenioids or P. americanus, also uses a peptide antifreeze (molecular weight 6,000) which is maintained at a concentration of 3% (w/v) in the blood plasma. We report here that the lack of antifreeze in the urine of R. dearborni probably reflects the fact that the glomeruli are not functional and cannot filter. We support this conclusion with morphological and physiological evidence and relate our findings to the conservation of biological antifreeze necessary for life in ice-laden polar waters.