Ⅱ型糖尿病患者血、尿白介素-6变化的意义

目的 :探讨II型糖尿病 (DM)患者血、尿白介素 6 (interleukin 6 ,IL 6 )水平的变化 ,了解IL 6在糖尿病肾病中的发病学意义。方法 :用放射免疫法检测 4 5例II型糖尿病患者及 2 0例正常人血、尿IL 6水平并进行比较。结果 :(1)II型糖尿病患者血、尿IL 6水平明显高于正常人 (P <0 0 5或P <0 0 1)。 (2 )早期糖尿病肾病患者尿IL 6水平明显高于单纯糖尿病患者(P<0 0 5 )。 (3)患者血IL 6水平分别与病程和空腹胰岛素 (fastinginsulin ,FINS)水平呈正相关 (r=0 30 5和 0 32 9,P 均 <0 0 5 ) ,与胰岛素敏感指数 (insulinsensitiveindex ,ISI)呈负相关 (r =- 0 35 2 ,P <0 0 2 ) ,尿IL 6水平分别与病程和尿白蛋白排泄率 (urinealbuminexcretionrate ,UAER)呈正相关 (r =0 32 6 ,P <0 0 5 ;r =0 4 6 6 ,P <0 0 1)。结论 :患者体内高水平的血清IL 6可能是II型糖尿病胰岛素抵抗病理生理改变的一种表现 ,IL 6可能参与糖尿病肾病的发生发展 ,尿IL 6水平对糖尿病肾病的病情分析有重要临床意义。     

糖尿病视网膜病变患者血浆Hcy、CEC和ET水平的检测分析

目的:分析糖尿病视网膜病变患者血浆同型半胱氨酸(Hcy)、外周血循环内皮细胞(CEC)和血浆内皮素(ET)水平及其相互关系。方法:将80例2型糖尿病(T2DM)患者分为2组:无糖尿病视网膜病变(NDR)组50例,糖尿病视网膜病变(DR)组30例,以我院健康体检正常者30例为对照(NC)组。分别测定Hcy、CEC、ET水平。结果:T2DM患者Hcy、CEC和ET水平均明显高于对照组(P<0.01);DR组Hcy、CEC、ET明显高于NDR组(P<0.01)。DR组血浆CEC计数和ET浓度呈正相关(r=0.839,P<0.05),Hcy浓度与CEC计数呈正相关(r=0.615,P<0.05),Hcy与ET浓度亦呈正相关(r=0.642,P<0.05)。结论:T2DM患者血浆Hcy、CEC、ET水平升高与DR有密切关系,血浆Hcy升高及内皮损伤可能在糖尿病患者视网膜病变的发生和发展中起重要作用。     

超敏C反应蛋白、血小板活化与2型糖尿病血管并发症关系的临床探讨

目的探讨血超敏C反应蛋白(hs-CRP)和血小板活化指标PAC -1、CD62P与2型糖尿病 (2DM)血管病变之间的关系。方法采用免疫透射比浊法和流式细胞仪法分别测定68例2DM患者和60例对照组患者血浆中的hs -CRP和全血中PAC -1、CD62P。结果所有2DM组血中hs-CRP、CD62P水平显著高于对照组 (P<0.01)。2DM组中有血管病变组水平明显高于无血管病变组 (P<0.05)。同时血中hs-CRP、CD62P浓度在各组中呈正相关 (r=0.968,P<0.05)。结论2DM患者血管内处于炎症同时血小板活化度增强共同促进局部动脉粥样斑块的发展。对血液中hs-CRP和CD62P的联合检测对监测2DM患者的血管病变的发生、发展有重要的临床意义。     

尿IL-6与血IL-6、SOD、C1q联合检测在2型糖尿病肾病诊断中的应用价值

目的 探讨尿IL-6、血IL-6、超氧化歧化酶、补体C1 q四种炎性因子联合检测在2型糖尿病肾病诊断中的应用价值.方法 选取本院2020年1月至12月收治的154例糖尿病患者作为研究对象,按临床诊断标准分为单纯糖尿病组(T2DM)59例、早期DKD组52例、临床DKD组43例,选取60例健康体检者作为对照组.进行尿IL-6、血IL-6、SOD、C1 q检测,并对其结果进行分析.绘制单项及联合检测ROC工作曲线并计算曲线下面积(AUC),评价各指标的诊断性能.结果 与健康对照组比较,T2DM患者、早期和临床期DKD患者血IL-6、尿IL-6水平升高,C1q、SOD水平降低,差异有统计学意义(P<0.05);与T2DM组比较,早期DKD组、临床DKD组尿IL-6及血IL-6水平升高,C1q水平降低,差异有统计学意义(P<0.05),临床DKD组SOD水平降低,差异有统计学意义(P<0.05);与早期DKD组比较,临床DKD组四项指标差异均有统计学意义(P<0.05).四项指标联合诊断DKD的AUC值最高,为0.878,三项指标(C1q+SOD+尿IL-6)联合诊断DKD的特异性最高,为98.2％.结论 尿IL-6与血IL-6、SOD、C1q联合检测可提高2型糖尿病肾病的诊断价值,具有一定的临床意义.     

炎症相关因子水平联检在2型糖尿病肾病患者中的临床意义

目的:探讨2型糖尿病肾病(diabetic nephropathy,DN)患者的血清C反应蛋白(CRP)、白细胞介素6(IL-6)、白细胞介素8(IL-8)和肿瘤坏死因子-α(TNF-α)水平的变化在肾病发生、发展中的作用.方法:将112例2型DN患者根据24h尿微量白蛋白排泄率(UAER)分为:无蛋白尿组(n=41)、微量蛋白尿组(n=37)和大量蛋白尿组(n=34).观察患者CRP、IL-6、IL-8和TNF-α水平的改变,并与正常对照组(n=41)进行对比.结果:无蛋白尿组、微量蛋白尿组及大量蛋白尿组的CRP、IL-6、IL-8及TNF-α水平均明显高于正常对照组(P＜0.01);微量蛋白尿组的CRP 、IL-6、IL-8及TNF-α水平明显高于无蛋白尿组(P＜0.01);大量蛋白尿组的CRP、IL-6、IL-8及TNF-α水平明显高于微量蛋白尿组(P＜0.01).结论:早期检测血清CRP、IL-6、IL-8及TNF-α水平的变化可以作为临床观察DN病情及判断DM预后的参考指标.     

2型糖尿病患者血清F水平及Ins,FBG相关性探讨

目的 :探讨 2型糖尿病患者皮质醇水平的变化及其与血糖和胰岛素的相关性。方法 :测定 2 6例 2型糖尿病患者晨 8时的血糖、胰岛素及皮质醇水平。结果 :2型糖尿病患者血清皮质醇水平明显高于正常人 (P<0 0 1) ,且 2型糖尿病患者血皮质醇浓度与空腹血糖呈正相关 (r =0 .32 ,P <0 0 1) ,与胰岛素无直线相关性。结论 :2型糖尿病一定程度上存在皮质醇分泌的紊乱。     

2型糖尿病肾病患者血清 IL-2、SIL-2R 和 TNF-α 检测的临床意义

目的:探讨2型糖尿病肾病患者血清IL-2、SIL-2R和TNF-α水平变化在肾病发生、发展过程中的作用.方法:对42例2型糖尿病肾病患者采用放免法检测血清IL-2、SIL-2R和ELISA法检测TNF-α水平,并与35名正常人作比较.结果:2型糖尿病肾病患者血清SIL-2R和TNF-q水平显著高于正常人(P＜0.01),而IL-2水平则显著低于正常人(P＜0.01).结论:血清IL-2、SIL-2R和TNF-α水平的变化在2型糖尿病肾病的发生和发展中相互作用,观察其浓度的变化对探讨2型糖尿病肾病的发病机理、预防和指导用药均有十分重要的临床价值.     

2型糖尿病与细胞因子的相关性研究

目的:探讨2型糖尿病患者血浆白介素-6(IL-6)、白介素-8(IL-8)、肿瘤坏死因子(TNF-α)在糖尿病发生、发展过程中的浓度变化及相互关系。方法:用放射免疫分析检测45例2型糖尿病患者及33例年龄和性别相匹配的健康志愿者血清IL-6、IL-8、TNF-α的水平。结果:①2型糖尿病患者血中IL-6、IL-8、TNF-α水平明显高于对照组(P<0.01);②有合并症患者血清IL-8、TNF-α水平明显高于单纯糖尿病患者(P<0.02);③三种细胞因子间浓度呈正相关(P<0.01)。结论:细胞因子IL-6、IL-8、TNF-α在糖尿病的发生、发展过程中相互作用,观察其浓度变化对探讨糖尿病的发病机理、预防及指导用药均有重要价值。     

超氧化物歧化酶和氧磷脂酶-1在2型糖尿病肾病患者血清中的表达及临床意义

目的:探讨超氧化物歧化酶(SOD)和氧磷脂酶-1(PON-1)在2型糖尿病肾病(T2DM)中的作用及临床价值。方法:80例T2DM患者分为T2DM肾病组(肾病组)和T2DM非肾病组(非肾病组),测定患者血清中SOD和PON-1浓度及生化指标、计算胰胰岛素抵抗指数(HOMA-IR)。结果:肾病组SOD、PON-1水平显著低于非肾病组,相比较有显著性差异(P0.05);肾病组FINS、TG水平和HOMA-IR显著高于非肾病组,相比较有显著性差异(P0.05);而两组FBG、PBG2h、HbAlc水平比较差异无统计学意义;T2DM患者血清SOD、PON-1水平与HOMA-IR呈显著负相关(r=-0.287,-0.509;P=0.006,0.000),而血清SOD水平与PON-1水平无相关性(P0.05)。结论:SOD和PON-1参与了T2DM肾病的发生与发展,联合检测血清SOD、PON-1水平,对于T2DM肾病患者的早期诊断、预防、治疗及预后评价具有重要的临床意义。     

糖尿病肾病患者与相关细胞因子水平的变化

目的:探讨了糖尿病肾病患者的血清白介素-2、白介素-6、白介素-8和肿瘤坏死因子水平的变化在肾病发生、发展过程中的作用。方法:应用放射免疫分析对38例糖尿病肾病患者和36例正常人进行了血清IL-2、IL-6、IL-8和TNF水平的检测。结果:糖尿病肾病患者血清中IL-6、IL-8和TNF水平非常显著地高于正常人组(P<0.01),而IL-2水平则显著地低于正常人组(P<0.01)。结论:血清IL-2、IL-6、IL-8和TNF水平的变化在糖尿病肾病的发生和发展中相互作用,观察其浓度的变化对探讨其发病机理、预防和指导用药均有十分重要的临床价值。     

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.     

'Very sore nights and days': the child's experience of illness in early modern England, c.1580-1720

Sick children were ubiquitous in early modern England, and yet they have received very little attention from historians. Taking the elusive perspective of the child, this article explores the physical, emotional, and spiritual experience of illness in England between approximately 1580 and 1720. What was it like being ill and suffering pain? How did the young respond emotionally to the anticipation of death? It is argued that children’s experiences were characterised by profound ambivalence: illness could be terrifying and distressing, but also a source of emotional and spiritual fulfilment and joy. This interpretation challenges the common assumption amongst medical historians that the experiences of early modern patients were utterly miserable. It also sheds light on children’s emotional feelings for their parents, a subject often overlooked in the historiography of childhood. The primary sources used in this article include diaries, autobiographies, letters, the biographies of pious children, printed possession cases, doctors’ casebooks, and theological treatises concerning the afterlife.