冠心病患者血清BNP测定的临床意义

目的:探讨了冠心病患者血清脑钠素(BNP)水平测定的临床意义.方法:应用化学发光法对78例冠心病患者进行血清BNP水平检测(其中稳定型心绞痛33例,不稳定型心绞痛30例,急性心肌梗死15例).并与35名正常健康人作比较.结果:冠心病患者血清BNP水平均非常显著地高于正常人组(P＜0.01),急性心肌梗死组和不稳定型心绞痛组又高于稳定型心绞痛组(P＜0.01).结论:检测冠心病患者血清BNP水平对疾病的预后观察具有重要的临床价值.     

CHD患者治疗前后血清IL-6、TNF-α、IFN-γ检测的临床意义

目的:探讨冠心病(CHD)患者治疗前后血清IL-6、TNF-α、IFN-γ水平的变化及临床意义.方法:应用放射免疫分析对66例CHD患者进行了血清IL-6、TNF-α、IFN-γ水平检测[其中稳定型心绞痛(SAP)31例,不稳定型心绞痛(UAP)22例,急性心肌梗死(AMI)13例],并与35名正常健康人作比较.结果:...     

CHD患者血清可溶性CD40L检测的临床意义

目的:探讨冠心病(CHD)患者血清可溶性CD40L(sCD40L)水平变化的临床意义.方法:应用酶联免疫吸附法(ELISA)对入选的90例CHD患者[急性心梗(AMI)患者28例,不稳定型心绞痛(UAP)患者35例,稳定型心绞痛(SAP)患者27例]的外周血sCD40L进行检测,并与30例正常对照者血清sCD40L的浓...     

冠心病患者血清hs-CRP和E-Selectin检测的临床意义

目的:探讨了冠心病患者血清超敏C反应蛋白(hs-CRP)和E-选择素(E-Selectin)水平的变化及意义.方法:应用免疫比浊法检测hs-CRP,ELISA法检测E-Selectin水平对58例冠心病患者进行了血清hs-CRP,E-Selectin水平检测.其中稳定型心绞痛25例,不稳定型心绞痛20例,急性心肌梗死13例,并以35名正常健康人作比较.结果:冠心病患者血清hs-CRP和E-Selectin水平明显高于正常人组(P＜0.01),急性心肌梗死组和不稳定型心绞痛组有明显高于稳定型心绞痛组(P＜0.01),冠心病组血清hs-CRP、E-Selectin水平与冠状动脉狭窄程度无明显相关性(P＞0.05).结论:血清hs-CRP和E-Selectin水平的变化与冠心病的发生、发展有关,但与冠状动脉狭窄程度无关.     

血清新蝶呤与急性冠状动脉综合征之间的关系

目的 :探讨急性冠状动脉综合征 (ACS)患者血清新蝶呤浓度的变化。方法 :对 4 7例ACS患者 ,其中急性心肌梗死 (AMI) 2 4例 ,不稳定型心绞痛 (UAP) 2 3例和 30例稳定型心绞痛 (SAP)患者 ,以酶联免疫法测定其血清新蝶呤水平 ,所有患者均为接受冠状动脉造影。结果 :血清新蝶呤浓度 ,在ACS病人中 ,AMI组 (1 1 88±3 0 9)nmol/L和UAP组 (9 85± 2 2 7)nmol/L ,均显著高于稳定型心绞痛患者的水平 (8 2 0± 1 5 2 )nmol/L ,(P <0 .0 0 0 1 ,P <0 .0 1 )同为ACS病人 ,AMI组与UAP之间其血清新蝶呤水平有显著差异 (P <0 .0 5 )。ACS的血清新喋呤水平与其不稳定斑块病变的数量有明显相关性。结果 :ACS病人血清新蝶呤浓度显著升高 ,可作为不稳定性动脉粥样硬化斑块的炎性标志     

胰岛素样生长因子-1与急性冠脉综合症的关系

目的 探讨胰岛素样生长因子-1(IGF-1)与急性冠脉综合症的关系.方法 采用酶联免疫吸附法(ELIsA)分别对急性心肌梗死(AMI),不稳定型心绞痛(UAP),稳定型心绞痛(SAP)患者及正常对照组,进行血清IGF-1水平测定.结果 AMI和UAP组中IGF-1明显高于SAP和对照组(P＜0.01).SAP组IGF-1明显低于对照组(P＜0.01).结论 IGF-1参与动脉硬化粥样斑块的发生发展过程.可作为预测斑块稳定性的标志物.     

血清胱抑素C、超敏C反应蛋白表达水平对急性冠脉综合征的临床诊断价值

目的 探讨血清超敏C反应蛋白（hs-CRP）、胱抑素（Cys-C）表达水平对急性冠脉综合征（ACS）的临床诊断价值.方法 选取入住我院心内科134例ACS患者,其中稳定型心绞痛患者（SA）60例,不稳定型心绞痛患者（UAP）52例,急性心肌梗死（AMI）患者22例,同时健康体检者62例,测定各组hs-CRP、Cys-C l以及相关性因子的水平,并进行统计学分析.结果 ①ACS患者hs-CRP（mg/L）（SA组：4.87 ±0.65、UAP组：9.81 ±1.13、AMI组：20.27±2.36、对照组1.24±0.52）、Cys-C （mg/L）（SA组：0.76±0.13、UAP组：1.03±0.17、AMI组：1.39±0.36、对照组0.46±0.07、基质金属蛋白酶（MMP）-9（μg/mL）（SA组：308.43±35.52、UAP组：379.86±27.90、AMI组：420.13±50.16、对照组112.07±10.18）以及IL-6 （pg/L）（SA组：62.37±5.18、UAP组：69.05±7.18、AMI组：72.53±6.95、对照组27.19±3.96）表达水平明显升高,差异具有统计学意义（P＜0.05）,内皮细胞一氧化氮合酶（eNOS）（μmol/L）（SA组：22.84±2.65、UAP组：19.43±1.79、AMI组：7.93±1.17、对照组30.19±3.53）水平相对于对照组降低,差异有统计学意义（P＜0.05）;②ACS血清hs-CRP表达与Cys-C,MMP-9,eNOS相关（P＜0.05）,Cys-C与MMP-9、eNOS、IL-6表达具有相关性（P＜0.05）;③SA组、UAP组以及AMI组血清hs-CRP、Cys-C表达水平依次升高,差异具有统计学意义（P＜0.05）.结论 血清hs-CRP、Cys-C表达对于诊断ACS可能具有临床意义.     

冠心病患者血清hs-CRP、IL-18和IL-1β检测的临床意义

目的：探讨冠心病患者血清hs-CRP、IL-18和IL-1β水平的变化及意义。方法：应用免疫比浊法和ELISA对62例冠心病患者进行了血清hs-CRP、IL-18和IL-1β检测,其中稳定型心绞痛26例,不稳定型心绞痛22例,急性心肌梗死14例,并以35名正常健康人作比较。结果：冠心病患者血清hs-CRP、IL-18和IL-1β水平明显地高于正常人组（P〈0.01）,急性心肌梗死组和不稳定型心绞痛组又明显地高于稳定型心绞痛组（P〈0.01）。结论：血清hs-CRP、IL-18和IL-1β水平的变化与冠心病的发生和发展有关。     

急诊就诊的不稳定型心绞痛患者外周血T细胞亚群表达变化分析

目的:分析急诊就诊的不稳定型心绞痛患者(UAP)外周血T细胞亚群表达变化。方法:连续选择近期急诊就诊的UAP患者(UAP组,19例),入选对象接受了外周血T细胞亚群(CD3+,CD4+,CD8+,CD4+/CD8+)指标检测,并与同期住院稳定心绞痛患者(SAP组,17例)以及健康体检者(对照组,20例)相同指标测试结果比较。结果:UAP组血清CD3+、CD4+、CD4+/CD8+指标明显高于SAP组和对照组,而CD8+水平则明显低于后两者(P均<0.05～0.01)。结论:UAP患者存在明确的外周血T细胞亚群指标表达异常。     

血清新蝶呤与冠状动脉斑块形态的关系的临床研究

目的 探讨冠心病患者新蝶呤与冠状动脉斑块形态的关系.方法 86例冠心病患者分为急性心肌梗死(AMI)组21例,不稳定型心绞痛(UAP)组35例,稳定型心绞痛(SAP)组30例,均经冠状动脉造影(CAG)确诊,30例CAG结果正常者为对照组.采用酶联免疫吸附法(ELISA)测定其新蝶呤水平,分析与冠状动脉斑块形态的关系.结果 新蝶呤浓度在AMI和UAP组中均高于SAP(P＜0.01);但在AMI组与UAP组,SAP和对照组之间差异无统计学意义(P＞0.05).新蝶呤浓度在Ⅱ型斑块组中高Ⅰ型、Ⅲ型斑块组(P＜0.05).结论 新蝶呤参与动脉硬化粥样斑块的发生发展过程,可作为预测斑块稳定性的标志物.     

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.     

The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: Substrate beriberi

About 1900, modern food selection and processing caused widespread $\text{epidemics}$ of the B vitamin deficiency diseases of beriberi and pellagra which, for genetic reasons, often expressed as different diseases ranging from bowel and heart disease to dermatoses and psychoses. But the B vitamins merely help convert essential fatty acids (EFA) into the prostaglandin (PG) tissue regulators and it now turns out that, through hydrogenation, milling and selection of w3-poor southern foods, we have also been systematically depleting, by as much as 90%, a newly discovered trace Nordic EFA (w3) of special importance to primates and sole precursor of the PG3(4) series, even as a concurrent fiber deficiency increases body demand for EFA. Since substrate EFA is processed by many B vitamin catalysts, an EFA deficiency will mimic a $\text{panh}$ypovitaminosis B, i.e., a mixture of $\text{substrate}$ beriberi and $\text{substrate}$ pellagra resembling vitamin beriberi and pellagra but exhibiting as even more diverse $\text{endemic}$ disease. This would consitute a second stage of the Modern Malnutrition and explain why some workers now hold the dominant diseases of modermized societies to be new, nutritionally based, pellagraform yet lipid-related and to range, once again, from heart disease to psychosis. It is an assumption that our dominant diseases are unrelated to each other or are merely revealed by our diagnostic acumen and therapeutic success; and that hydrogenating millions of tons of food oils annually, to destroy the rancidity producing w3-EFA, is safe for $\text{primates}$. Extensive beriberiform disease is reported here in 32 typical cases taken from medical practice which responds strikingly to linseed oil supplements (60% w3-EFA) in confirmation of identical results in Capuchins.     

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.     

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.     

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.     

HLA genes in Amerindians from Mexico San Vicente Tancuayalab Teenek/Huastecos

Huastecos or Teenek Amerindians are presently living at North East Mexico (San Luis Potosi State). They have probably one of the most ancient culture of Mexico and Central America together with Mayas and Olmec groups with which also show close relationships. Proximity to Atlantic Ocean/Mexican Gulf originated that Spaniards had very early contact with them at about 1519 CE or before. In the present paper we have aimed to study HLA gene profile which may be useful for HLA and disease epidemiology and transplant programs in Teeneks. HLA-DRB1*04:07, -DRB1*14:06 and -DRB1*04:11 have been found in high frequency like in other Amerindian groups. High frequency typical Amerindians HLA extended haplotypes have been found, such as A*02-B*35-DRB1*04:07-DQB1*03:02; A*68-B*39-DRB1*04:07-DQB1*03:02 and A*02-B*39-DRB1*04:07-DQB1*03:02; also new haplotypes have been described, like A*02-B*52-DRB1*04:11-DQB1*03:02, A*68-B*35-DRB1*14:02-DQB1*03:01 and A*68-B*40-DRB1*16:02-DQB1*03:01. Genetic proximity is observed not only to linguistically close Mayans, but also to Mazatecans, Mixtecans and Zapotecans, who speak an altogether different languages; it shows once more that genes and languages do not correlate. This population was greatly diminished after European contact between 1500 and 1600 years CE; in fact, North and South America First Inhabitants population was brought from 80 down to 8 million people because of diseases (i.e.: measles, smallpox or influenza), slavery and war.