血管内皮损伤标志物在2型糖尿病患者中的变化

目的:探讨2型糖尿病(DM)患者血管内皮损伤标志物的变化。方法:分别测定89例2型DM患者和76例正常对照者血浆可溶性血管内皮细胞蛋白C受体(sEPCR),血管性血友病因子(v WF)和可溶性血栓调节蛋白(sTM),并测定DM患者24h尿白蛋白排泄(UAE),根据尿UAE水平和病程分组进行比较分析。结果:2型DM患者血浆sEPCR、v WF及sTM水平高于正常对照组(P<0.05),并且与其尿UAE水平和病程呈显著正相关。结论:血浆sEPCR、v WF及sTM水平可作为观察2型DM并发血管病变以及严重程度的指标。     

抗CD3单克隆抗体在预防肾移植术后急性排斥反应中的作用

目的 :观察抗CD3单克隆抗体在预防肾移植术后急性排斥反应的作用。方法 :16 4例肾移植患者分为两组 ,4 2例移植术后应用抗CD3单克隆抗体 (5mg d)为治疗组 ;其它 12 2例为对照组。观察移植术后人 肾存活率、急性排斥反应及CMV感染的发生率。结果 :治疗组 1年、2年及 3年人存活率与对照组无显著差异 ,而治疗组移植肾存活率明显高于对照组(P <0 0 5 )。治疗组急性排斥反应发生率 (18 6 % )比对照组 (2 8 7% )低 ,P <0 0 5 ,且首次急性排斥反应发生时间明显延长 ,对MP冲击治疗效果好。治疗组CMV感染的发生率 (33 3% )高于对照组 ,P <0 0 5。结论 :肾移植术后预防性使用抗CD3单克隆抗体对提高移植肾存活率 ,降低急性排斥反应发生率有较好的作用 ;用药期间应注意预防及治疗CMV感染。     

肾移植患者肿瘤坏死因子-α动态检测的临床意义

目的 :动态观察肾移植患者肿瘤坏死因子 -α(TNF -α)水平的变化 ,探讨TNF -α对肾移植预后的意义。方法 :采用放射免疫分析检测 4 5例肾移植患者术前及术后两天血清及尿液中TNF -α的水平 ,并与 4 5例正常对照者进行对比分析。对 33例术后稳定者 ,动态检测术后 2d、7d、14d、2 1d及 2 8d血清及尿液中TNF -α的水平。结果 :术前组、术后稳定组、术后排斥组、CsA中毒组血清TNF -α水平均显著高于正常对照组 (P <0 0 1) ,术后排斥组显著高于术前组及术后其他各组 (P <0 0 1) ;术前组和术后稳定组尿液TNF -α水平均显著高于正常对照组 (P <0 0 1) ,术后排斥组尿液TNF -α水平高于正常对照组 (P <0 0 5 ) ,术后两天排斥组与稳定组间尿液TNF -α水平无显著性差异 (P >0 0 5 )。 33例肾移植术后稳定者血清TNF -α水平术后 7天开始下降 ,至 2 1天时已降至与正常对照组无显著性差异 (P >0 0 5 ) ;尿液TNF -α水平下降较血清快 ,术后 7天即降至与正常对照组无显著性差异 (P >0 0 5 )。结论 :动态检测TNF -α水平可作为观察肾移植患者排斥反应的一项重要指标。     

尿CD54+淋巴细胞在肾移植急性排斥反应中的变化

背景：正常肾脏、肾小管上皮和血管内皮细胞仅有少量CD54表达,当发生急性排斥反应时,肾小管上皮细胞和血管内皮细胞CD54表达明显增加,同时大量白细胞浸润;间质浸润细胞和肾小管上皮细胞CD54表达增加。 目的：探讨流式细胞仪检测尿CD54⁺淋巴细胞对移植肾急性排斥反应的诊断价值。 方法：来自解放军成都军区总医院的肾移植后恢复正常者(n=18)、出现急性排斥反应者(n=8)、移植肾功不全者(n=9)以及健康志愿者(n=10)。流式细胞仪比较各组移植前后尿液中CD54⁺淋巴细胞比率变化。 结果与结论：尿CD54⁺淋巴细胞在肾移植患者出现排斥反应时明显增加(P < 0.01),抗排斥治疗后逐渐下降。移植肾功能正常者和移植肾功不全者CD54轻度升高。提示尿液中CD54⁺淋巴细胞水平能准确反映肾移植物移植后患者的免疫状态,可作为肾移植后急性排斥反应的特异标志。     

肾移植群体反应性抗体的检测及其临床应用

目的 :探讨人类白细胞抗原 (HLA)群体反应性抗体 (PRA)对肾移植效果的影响。方法 :采用酶联免疫吸附法 (ELISA)对 2 0 6例肾移植受者的血清PRA进行检测。同时对 14 0份血清分成四组包括首次移植术前及术后 1个月 ,半年至 1年肾功能稳定期病人 ,第一次尸肾移植失功恢复血透病人进行PRA检测。结果 :PRA阴性组受者移植术后排斥发生率为 11 85 % ,阳性组受者平均PRA高达 4 6 5 % ,两组比较差异显著 (P <0 0 0 1)。首次移植术前A组PRA阳性率 17 1% ,术后B组PRA阳性率 31 4 % ,肾功能稳定组 (C组 )PRA阳性率 14 3%。而移植失功恢复血透者 (D组 )PRA阳性率达 77 1%。结论 :PRA的检测是肾脏移植术前筛选致敏受者的重要指标 ,对肾脏移植后排斥反应和移植物存活率关系密切。     

检测尿MCP-1诊断移植肾急性排斥反应的研究

目的　动态检测肾移植受者尿液单核细胞趋化性肽 1(MCP 1)的含量 ,了解其变化规律 ,探讨其在肾移植急性排斥反应中的意义。方法　应用酶联免疫吸附法 (ELISA) ,测定了 74例肾移植受者和 10例无肾脏疾病患者尿液单核细胞趋化性肽 1(MCP 1)的含量。结果　肾功能稳定的肾移植受者尿液MCP 1水平 (412± 2 5 )ng mL ,正常对照组为 (40 7+12 )ng mL ,二者无明显差异 (P >0 .0 5 )。发生急性排斥反应时尿液MCP 1水平为 (1193+5 6 )ng mL ,明显高于正常对照和肾功能稳定组(P <0 .0 1)。经抗排斥治疗后 ,对治疗有反应的受者尿液MCP 1浓度明显降低。结论　尿液MCP 1水平与肾移植急性排斥反应有密切关系 ;检测尿液MCP 1水平有助于急性排斥反应的早期诊断及预后判断     

肾移植排斥反应中细胞毒性T淋巴细胞相关抗原4的作用

背景：细胞毒性T淋巴细胞相关抗原4是新近发现的共刺激分子,在肿瘤及自身免疫性疾病中研究较多,在肾移植领域缺少研究。目的：探讨细胞毒性T淋巴细胞相关抗原4在肾移植排斥反应中的作用。方法：纳入肾移植患者50例,根据移植后肾功能分为2组,急性排斥组20例,移植肾功能稳定组30例。同时选择30例健康查体者作为健康对照组。分别抽取外周静脉血,采用ELISA法及流式细胞术检测观察对象血清及外周血淋巴细胞中的细胞毒性T淋巴细胞相关抗原4水平。结果与结论：细胞毒性T淋巴细胞相关抗原4在肾移植后急性排斥组、肾功能稳定组及健康对照组血清中的表达水平差异有显著性意义(F=70.008 1,P=0.000 0)。肾功能稳定组显著低于健康对照组(P=0.000 0),急性排斥组显著低于健康对照组(P=0.000 0),急性排斥组显著低于肾功能稳定组(P=0.000 0)。细胞毒性T淋巴细胞相关抗原4在肾移植后急性排斥组、肾功能稳定组及健康对照组淋巴细胞中的表达水平差异无显著性意义(F=1.865 6,P=0.161 7)。提示细胞毒性T淋巴细胞相关抗原4在肾移植患者发生排斥反应时血清中表达减低,具有一定的相关性,可能参与了排斥反应的发生。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

急性脑梗死患者血清sICAM-1含量变化的研究

目的 :探讨人类脑缺血后血流中可溶性细胞间粘附分子 1(sICAM 1)含量与疾病转归、脑血管病危险因素及病变体积的关系。方法 :采用酶联免疫吸附法 ,测定 35例脑梗死患者血清sICAM 1的含量 ,与 2 0例正常人对照比较。结果 :脑梗死4 8h内和 14d血清sICAM 1含量明显高于正常对照组 (P <0 0 5 ,P <0 0 0 5 )。脑梗死 4 8h内 ,合并高血压、糖尿病患者血清sICAM 1明显高于非高血压、糖尿病患者 (P <0 0 5 ;P<0 0 0 1) ,且血清sICAM 1的含量与血糖水平有明显相关性 (r=0 8857,P <0 0 5 )。动态观察显示 ,脑梗死 4 8h内与 14d血清sICAM 1含量比较无明显变化 ,但血清sICAM 1含量与单发梗死体积有明显相关性 (r=0 4 38,P <0 0 5 ;r=0 5 37,P <0 0 5 )。结论 :ICAM 1与脑梗死的发生发展密切相关 ,其含量受脑血管病危险因素、梗死体积等多种因素影响     

大鼠肾移植急性排斥反应过程中 IL-17 表达及其意义

目的:探讨IL-17在大鼠肾移植急性排斥反应过程中的表达特点及其意义。方法:将大鼠随机分为正常对照组、同系基因对照组、同种异体移植组、免疫抑制剂干预组,并建立肾移植急性排斥反应模型,用RT-PCR及免疫组织化学方法检测急性排斥时IL-17在肾组织中的表达。结果:同种异体移植组在移植后第3天、5天和7天,移植肾IL-17均明显升高,与其他组相比,均有统计学意义(P0. 05),其中以第5天为最高,差异具有统计学有意义(P0. 05)。结论:IL-17参与了大鼠肾移植急性排斥反应的发生,并为早期事件,IL-17检测可能为人类肾移植早期急性排斥反应的诊断和治疗提供理论依据。     

Ⅱ型糖尿病患者血浆可溶性凝血酶调节蛋白的变化及临床意义

目的 评价血浆可溶性凝血酶调节蛋白与Ⅱ型糖尿病患者凝血和纤溶系统之间的关系。方法 我们检测了50例Ⅱ型糖尿病患者血浆中可溶性凝血酶调节蛋白、蛋白C(PC)(由凝血酶-TM复合物诱导产生的抗凝物质)、凝血酶原片段F1+2(一种凝血酶生成的直接标志物)、纤溶酶-α2-抗纤溶酶复合物(PAP)和D二聚体(DD)。结果 患者血浆中的sTM(P<0.01)、PAP(P<0.01)、PC(P<0.05)和F1+2(P<0.05)较50例正常对照组明显增高,糖尿病肾病患者的sTM和PAP升高更加显著。在糖尿病患者中,sTM与PC呈负相关(r=-0.50,P<0.001),而与PAP呈正相关(r=0.47,P=0.01)。结论 结果表明糖尿病患者的凝血和纤溶系统均是活化的,血浆中的可溶性凝血酶调节蛋白升高与糖尿病患者凝血和纤溶系统活化相关。     

Renal dysplasia and asplenia in two sibs

A family is reported in which two sibs, one male and the other female, both died within 24 hours of birth with enlarged polycystic kidneys. Postmortem histology in the second child showed gross renal dysplasia. In both children the pancreas was enlarged, nodular and cystic but the liver appeared macroscopically normal. In the second child, histological examination confirmed pancreatic fibrosis with cystic dilation of ducts, but showed portal fibrosis with bile duct proliferation in the liver.
This combination of findings is very reminiscent of those in a girl and her brother reported by Ivemark et al. (1959). The children reported here also showed absence or hypoplasia of the spleen, cardiac anomalies and other features of the Ivemark syndrome (Ivemark 1955), a quite different, usually sporadic, congenital disorder. It is suggested that the children described here have a distinct lethal congenital disorder, probably inherited in an autosomal recessive manner.     

Schizophrenia in a North Swedish geographical isolate, 1900–1977. Epidemiology, genetics and biochemistry

Over 200 schizophrenic patients belonging to three major and interrelated pedigree complexes have been investigated over the past 30 years in a North Swedish geographically isolated population, presently numbering about 6,000. An intensive investigation of a number of biochemical correlates and genetic markers in a few selected families belonging to one of the major pedigrees has indicated new strategies for the current research program.
Schizophrenia, as defined operationally, is significantly associated with decreased activities of two enzymes (1) blood platelet monoamine oxidase, (2) plasma dopamine-β-hydroxylase, and (3) with the genetic marker Gc² (group specific antigen). Both enzymes are subject to genetic variation. A positive score for linkage between schizophrenia and low plasma DBH activity has been calculated, but, so far, available data are insufficient for discrimination between linkage and partial contribution of genetically controlled low plasma DBH to the pathogenesis of the disease. Alternatively, both mechanisms could be involved.
As a model for continued research, schizophrenia is explained as based on a double dominant-recessive genotype (Aabb), representing a vulnerability which in about 50 % of cases develops into clinical schizophrenia. It is suggested that the dominant mutation (A) operates on or affects MAO activity, and that the recessive genotype (bb) is instrumental in low variates of DBH activity and very likely such variates within the normal range of physiological variation. Moreover, it is suggested that the combined effects of MAO- and DBH-reduced efficiency on the metabolism of e.g. dopamine could be an essential pathogenic mechanism for the schizophrenic illness which is segregating in this population.     

What will studies of Fulani individuals naturally exposed to malaria teach us about protective immunity to malaria?

There are an estimated over 200 million yearly cases of malaria worldwide. Despite concerted international effort to combat the disease, it still causes approximately half a million deaths every year, the majority of which are young children with Plasmodium falciparum infection in sub-Saharan Africa. Successes are largely attributed to malaria prevention strategies, such as insecticide-treated mosquito nets and indoor spraying, as well as improved access to existing treatments. One important hurdle to new approaches for the treatment and prevention of malaria is our limited understanding of the biology of Plasmodium infection and its complex interaction with the immune system of its human host. Therefore, the elimination of malaria in Africa not only relies on existing tools to reduce malaria burden, but also requires fundamental research to develop innovative approaches. Here, we summarize our discoveries from investigations of ethnic groups of West Africa who have different susceptibility to malaria.     

The universal muscular chain reaction,muscle spasm,Torsions, ruptures and extravasations. Chameleons of pathology and some manifestations of simple muscular disorders

Most bodily functions require the coordinated actions of complementary and supplementary paired muscle groups. Where this essential muscular cooperation is lacking, hollow organs may burst and others become literally screwed up, giving rise to many similar spastic diseases such as Torticollis, Twisted ovarian cyst, Torsion of the Testis, Volvulus of the intestines, Varicose Veins, Megacolon, Aortamegaly, Scoliosis, Erb's Palsy, Peyronie's Disease, Main-en-Griffe, Undescended Foot (Pes Cavus), Talipes, Strabismus. Spasm is “panenepidemic” and unclassified examples of Torsion Dystonia and Dyskinesia really are as common as debt and taxes.     

Class II HLA in Georgia Caucasus Tbilisi Georgians and their Mediterranean ancestry: The Usko Mediterranean languages

Georgia (or Sakartvelo in its own language) is a South Caucasus Mts. country with its easternmost part is enigmatically named Iberia, like the Iberian Peninsula, which may refer to rivers “Kura” and “Ebro” or their valleys respectively. Most of their inhabitants speak Georgian which is included within Dene-Caucasian group and Usko-Mediterranean subgroup of languages. The latter includes Basque, Berber, ancient Iberian-Tartessian, Etruscan, Hittite, Minoan Lineal A and others. In the present paper, HLA class II -DRB1 and -DQB1 alleles has been studied and extended haplotypes calculated. Most frequent haplotypes are also of Mediterranean origin (i. e.: (A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*51)-DRB1*13:01-DQB1*06:03, or (A*24-B*35)-DRB1*01:01-DQB1*05:01) and DA genetic distances show that closest world populations to Georgians are Mediterraneans. Georgians also show common extended haplotypes ((A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*13)-DRB1*07:01-DQB1*02:01 and (A*03-B*35)-DRB1*11:01-DQB1*03:01) with Svan people, a secluded population in North Georgia mountains. We can conclude that Georgians belong to a very old Mediterranean substratum according to both linguistics (Usko Mediterranean languages) and HLA genetics.     

Hypo- und Hypermagnesämie aus kardiologischer Sicht

Zusammenfassung Eine Reihe pathologischer Zustände bedingen Magnesiummangel. Zustände mit Hypermagnesämie sind ebenfalls bekannt, doch wesentlich seltener. Für den Kardiologen beachtenswert ist, daß unter Therapie mit bestimmten Diuretica bei Herzinsuffizienz, bei Herzinfarkt, Kardiomyopathie, Digitalisintoxikation und bestimmten Herzrhythmusstörungen Hypomagnesämie beobachtet wurde. Leider kann in der klinischen Routine nur ein extracelluläres Magnesiumdefizit durch Serumbestimmungen gemessen werden; über Magnesiummangel einzelner Organe kann nichts ausgesagt werden. Hinweise für Magnesiummangel geben aber neben der Messung des Serumspiegels Anamnese, klinischer Befund, bestimmte EKG-Veränderungen wie auch evtl. Hypokalämie, ein Zustand, bei dem sich oft — besonders bei Aldosteronismus — parallele Veränderungen zeigten.Tierexperimente deuten darauf hin, daß infarktähnliche Läsionen unter Magnesiummangel entstehen, doch ob Herzinfarkt beim Menschen durch Magnesiummangel ausgelöst werden kann, ist noch ungeklärt. In Leichenherzen zeigte sich im Infarktgebiet neben Calciumakkumulation signifikanter Magnesiumverlust, wobei unklar blieb, ob sich Ursache oder Folge des Infarktes widerspiegelten. Falls ein ursächlicher Zusammenhang besteht, ist er im Myokardstoffwechsel selbst zu suchen, wie bei der Alkoholkardiomyopathie, wo myokardialer Magnesiummangel zumindest als pathogenetischer Teilfaktor anerkannt wird. Andererseits versucht man aber auch Beziehungen zwischen Atherosklerose, Blutgerinnung und Hypomagnesämie herzustellen, in der Meinung, daß Magnesiummangel auch über den coronaren Pathomechanismus des Herzinfarktes wirken könnte. Sicher scheint, daß gewisse EKG-Veränderungen und Herzrhythmusstörungen durch einen irritierten Magnesiumhaushalt bedingt sein können, da sie bei Gabe bzw. Entzug von Magnesium verschwinden. Daß Magnesiummangel die Glykosidtoleranz verringert, wird tierexperimentell bestätigt. Unter Hypomagnesämie bewirkt Acetylstrophanthidin eher und länger Rhythmusstörungen als ohne, außerdem lassen diese sich durch Magnesiumgaben eliminieren. Da in gewissen Fällen spontane und digitalisinduzierte Herzrythmusstörungen durch Magnesiuminjektionen beseitigt wurden, scheint Magnesium als Therapeuticum angebracht. Einsatz verschiedener Magnesiumsalze bei Angina pectoris, degenerativen Herzerkrankungen und Herzinsuffizienz ohne geprüften und offensichtlich gestörten Magnesiumhaushalt ist fragwürdig, weil keine eindeutigen klinischen Erfolgsbeweise vorliegen. Immerhin mag es aber larvierte, durch Serumbestimmungen nicht erfaßbare Mangelzustände geben. Allgemein erscheint es aus kardiologischer Sicht ratsam, den Magnesiumhaushalt zu überwachen und in entsprechenden Fällen auszugleichen, um möglichen Myokardläsionen oder fatalen Herzrhythmusstörungen entgegenzuwirken.     

HLA in North Colombia Chimila Amerindians

HLA-A,-B,-C,-DRB1 and -DQB1 alleles have been studied in Chimila Amerindians from Sabana de San Angel (North Colombian Coast) by using high resolution molecular typing. A frequent extended haplotype was found:HLA-A*24:02-B*51:10-C*15:02-BRB1*04:07-DQB1*03:02 (28.7%) which has also been described in Amerinndian Mayos Mexican population (Mexico, California Gulf, Pacific Ocean). Other haplotypes had already been found in Amerindians from Mexico (Pacific and Atlantic Coast), Peru (highlands and Amazon Basin), Bolivia and North USA. A geographic pattern according to HLA allele or haplotype frequencies is lacking in Amerindians, as already known. Also, five new extended haplotypes were found in Chimila Amerindians. Their HLA-A*24:02 high frequencies characteristic is shared with aboriginal populations of Taiwan; also, HLA-C*01:02 high frequencies are found in New Zealand Maoris, New Caledonians and Kimberly Aborigines from Australia. Finally, this study may show a model of evolutionary factors acting and rising one HLA allele frequency (-A*24:02), but not in others that belong to the same or different HLA loci.     

Environmental risk factors and their role in the management of atopic dermatitis

Introduction: The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.

Areas covered: We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.

Expert commentary: The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.     

Functional role of fertility α2

Fertility α₂-microglobulin is one of the main proteins expressed between the late lutein phase of the menstrual cycle and the first gestation trimester. It is produced by endometrial secretory glandular epithelium and decidual membrane. It is believed to be involved in the preparation to gestation, conception, normal development of the fetoplacental system, and initiation of labor. The immunomodulating, effect of fertility α₂-microglobulin and its possible involvement in the regulation of fertilization by blocking the spermatozoon reaction with the ovocyte lucid membrane were demonstratedin vitro. The data of structural analysis (appurtenance to lipocalines and unique pattern of N-glycosylation) and analysis of the spatial and temporal parameters of the expression in connection with other events in the organism within the same system of coordinates propated us to investigate the probability of realization of other, so far unknown functions of α₂-microglobulin. The probable mechanisms of realization of the immunomodulating function are analyzed. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 10, pp. 364–373, October 1998