空腹血糖受损患者脂联素水平的临床观察

目的探讨空腹血糖受损（IFG）患者脂联素水平的变化。方法入选糖耐量正常（NGT）、孤立性空腹血糖受损（I-IFG）、孤立性糖耐量低减（I-IGT）、空腹血糖受损并糖耐量低减（IFG／IGT）、新发2型糖尿病（T2DM）各30例，采用酶联免疫吸附法（ELISA）测定血清脂联素，同时检测胰岛素水平及血糖、血脂，计算胰岛素抵抗指数（HOMA．IR）。结果I-IFG组、1-IGT组、IFG／IGT组及新发T2DM组脂联素均明显低于NGT组（P均〈0．01）；新发T2DM组和IFG／IGT组的HOMA-IR均〉I-IGT组〉I-IFG组〉NGT组，各组间差异有统计学意义（P均〈0．05或P〈0．01）；脂联素与空腹血糖（FBG）、餐后2h血糖（2HBG）及HOMA-IR呈负相关（Pa〈0．01）。结论在I-IFG阶段已存在脂联素水平降低，胰岛素抵抗增加，具有向糖尿病转化及并发大血管病变的风险，提高脂联素水平可为糖尿病及其并发症的防治提供一条新的思路。     

多囊卵巢综合征患者血清IL-18、IL-6及CRP的变化及意义

目的探讨血清IL-18、IL-6及CRP水平在多囊卵巢综合征患者（PCOS）患者中的变化及其临床意义。方法分别应用酶联免疫吸附法和免疫透射比浊法检测64例PCOS患者血清IL-18、IL-6及CRP含量,并与64例正常对照组比较分析。结果PCOS患者血清IL-18、IL-6、CRP及HOMA—IR水平较健康对照组升高（P〈0．05）;且PCOS肥胖型患者血清IL—18、IL-6、CRP及HOMA—IR水平较非肥胖型明显升高（P〈0．05）;血清IL-18、IL-6、CRP水平与HOMA—IR均呈明显正相关（r=0．639,r=0．657,r=0．708,均P〈0．01）。结论PCOS可能是一种慢性亚临床炎症反应状态,炎症因子的明显增加,导致炎症损伤,并和胰岛素抵抗关系密切,而肥胖可能作为一种慢性亚临床炎症反应加重P—COS的异常。     

初诊DM2患者脂联素、炎性因子与胰岛素抵抗的相关分析

目的：分析初诊2型糖尿病（DM2）患者脂联素、IL-6、TNF-α水平变化及其与胰岛素抵抗（IR）、肥胖的相关性。方法：选择初诊DM292例,分为肥胖组（体重指数BMI≥25kg/m^2）42例、非肥胖组（BMI〈25kg/m^2）50例、正常对照组40例,测定血清脂联素、IL-6、TNF-α、体重、身高、血脂、空腹血糖（fPG）、餐后2h血糖（2hPG）、空腹胰岛素（fINS）、餐后2h胰岛素（2hINS）、计算胰岛素抵抗指数（HOMA-IR）,做相关性分析。结果：肥胖组脂联素低于非肥胖组（P〈0.05）及正常对照组（P〈0.01）,非肥胖组又低于正常对照组（P〈0.05）。而肥胖组IL-6、TNF-α高于非肥胖组（P〈0.05）及正常对照组（P〈0.01）,非肥胖组又高于正常对照组（P〈0.05）。脂联素与BMI、HOMA-IR呈负相关,IL-6、TNF-α与BMI、HOMA-IR呈正相关。结论：脂联素、IL-6、TNF-α与IR密切相关,参与了糖脂代谢紊乱。     

妊娠期糖尿病患者CRP、PAI-1与IR相关性的初步探讨

目的探讨C-反应蛋白（CRP）、纤溶酶原激活物抑制剂-1（PAI—1）与胰岛素抵抗（IR）的关系及在GDM发病机制中的作用。方法分别测定29例妊娠糖尿病患者（GDM）、31例糖耐量异常（IGT）孕妇和35例糖耐量正常（NGT）孕妇的CRP、PAI-1及葡萄糖耐量试验（OGTT）的4点血糖和对应的胰岛素水平,同时计算胰岛素抵抗指数（HOMA—IR）和胰岛β细胞功能指数（HOMA—HBCI）,分析比较各组的差异与关系。结果①NGT组HOMA—IR低于IGT和GDM组,均有统计学差异（P〈0．05）,NGT组的HOMA—HBCI高于IGT和GDM组,均有统计学差异（P〈0．05）②GDM组的CRP、PAI—1水平显著高于NGT和IGT组,差异有统计学意义（P〈0．05）。③相关性分析：血清CRP与空腹血糖（FPG）（r=0．331,P=0．01）、HOMA—IR（r=0．303,P=0．035）、孕前BMI（r=0．283,P=0．040）正相关;血浆PAI-1分别与HOMA—IR、空腹胰岛素（Flns）、孕前BMI正相关,相关系数分别为：r=0．525,P=0．001;r=0．550,P=0．001;r=0．625,P=0．000。结论GDM患者IR增加,但胰岛细胞分泌功能却下降,两者共同导致GDM的发生：炎症因子CRP、PAI—1都与IR有关．可能参与GDM的发生和发展。     

IGT患者IL-6、TNF-α与胰岛素抵抗的相关性分析

胰岛素抵抗（IR）是2型糖尿病（DM2）和糖耐量低减（IGT）的主要病因之一。近年来发现多种炎性因子如白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、C反应蛋白（CRP）等都参与了糖脂代谢紊乱及动脉硬化的过程，并与胰岛素抵抗的发生发展有密切关系。本文检测了IGT患者血清IL-6、TNF-α水平的变化，并探讨炎性因子与胰岛素抵抗的相关性。     

不同糖代谢阶段非特异性炎性标志物水平变化与动脉粥样硬化的相关性研究

目的通过观察不同糖代谢阶段患者非特异性炎性标志物水平以及颈动脉内膜中层厚度，研究炎症反应与糖尿病及动脉粥样硬化的相互关系。方法测定正常糖耐量（NGT）组25例，糖耐量减低（IGT）组50例，2型糖尿病无大血管并发症（T2DM）组53例，2型糖尿病伴大血管并发症组46例的血糖、血脂、胰岛素、HbA1c、超敏C反应蛋白（hs-CRP）、白细胞介素-1（IL-1）、肿瘤坏死因子-α（TNF-α）水平以及颈动脉内膜中层厚度（IMT）。结果①IGT组及T2DM合并大血管并发症组的血清IL-1、TNF-α水平均显著高于NGT组及T2DM组（P〈0．05或P〈0．01），而IGT组与T2DM合并大血管并发症组间的血清IL-1、TNF-α水平无显著性差异（P〉0．05）；②T2DM组及2型糖尿病合并大血管并发症组的IMT均显著高于NGT组及IGT组（均P〈0．05），而NGT组与IGT组间的IMT无显著性差异（P〉0．05）；③相关分析显示，IMT与年龄及LDL-C均呈正相关（分别为r=0．314，P〈0．01；r=0．250，P〈0．01），而与hs-CRP、IL-1、TNF-α无明显相关性；IL-1与TNF-α及hs-CRP均呈正相关（分别为r=0．230，P〈0．01；r=0．261，P〈0．01）。结论不同糖代谢阶段中IGT阶段炎症反应最强，而糖尿病出现大血管并发症后炎症反应可能较无大血管并发症时有所增强。各种非特异性炎性标志物可能联合影响不同糖代谢阶段的炎症反应，但与动脉粥样硬化无明显相关性。     

多囊卵巢综合征患者血清中瘦素水平与胰岛素抵抗关系的研究

目的探讨多囊卵巢综合征（PCOS）患者血清中瘦素（Leptin）与胰岛素抵抗的关系。方法测定了56例PCOS患者和30例正常妇女血清中的瘦素、血糖和胰岛素水平；用胰岛素抵抗指数（IR）和胰岛素敏感指数（ISI）以及胰岛素曲线下面积（AUC）作为评价患者胰岛素抵抗的指标，相关性分析探讨瘦素与胰岛素抵抗的关系。结果PCOS组患者血糖、胰岛素及Leptin水平明显高于对照组（P〈0．05）；PCOS纽中瘦素与FINS（r=0．655，P〈0．0I）、IR（r=0．442，P〈0．01）、AUC（r=0．520，P〈0．01）、ISI（r=0．458，P〈0．05）均呈正相关关系。结论瘦素可能参与PCOS发生、发展有关，PCOS患者血清中瘦素水平与胰岛素抵抗存在一定的相关性。     

2型糖尿病患者血清瘦素水平及临床意义

目的：观察2型糖尿病（DM2）患者血清瘦素（leptin）水平及其与肥胖、血糖、血脂的关系。方法：采用放射免疫分析（RIA）测定42例DM2患者和38例正常对照组的血清leptin水平。结果：DM2组血清leptin水平明显高于对照组（P〈0．01）;血清leptin与体重指数（BMI）、血清胰岛素（INS）、总胆固醇（TC）、甘油三酯（TG）、脂蛋白LDL-C呈正相关。结论：DM2患者的高leptin血症与肥胖、血脂异常及胰岛素抵抗（IR）密切相关。     

吡格列酮和二甲双胍治疗对2型糖尿病患者血清抵抗素的影响

探讨吡格列酮和二甲双胍治疗对2型糖尿病患者血清抵抗素和胰岛素抵抗的不同影响。将48例初诊肥胖2型糖尿病患者随机分两组,分别给予二甲双胍（M组）和二甲双胍联合吡格列酮（MP组）治疗12周,于治疗前后测定受试者空腹血清抵抗素、血糖（FBS）、血脂、胰岛素（FINS）,测量身高、体重,计算体重指数（BMI）、胰岛素抵抗指数（HOMA-IR）。结果显示,与治疗前相比,MP组FBS、FINS、HOMA-IR、抵抗素水平明显降低（P〈0.01）;M组抵抗素水平没有明显改变（P〉0.05）,BMI、FINS、HOMA-IR水平明显降低（P〈0.01）。结论：吡格列酮治疗能有效降低肥胖2型糖尿病患者血清抵抗素水平。     

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.