溃疡性结肠炎患者血清性激素及脂蛋白测定的临床意义

目的：研究溃疡性结肠炎（ulcerative colitis,UC）患者血清蛋白质和脂代谢异常与性激素水平异常的关系。方法：分别测定72例UC组和72例健康对照组血清雌二醇（E2）、睾酮（T）、孕酮（P）、泌乳素（PRL）、促黄体生成素（LH）、促卵泡激素（FSH）及血清总蛋白（TP）、白蛋白（Alb）、球蛋白（G）、白球比（A/G）、总胆固醇（TC）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）水平,并对其进行相关分析。性激素测定时对照组采用年龄、性别和卵巢周期与病例组1 1配对的原则。结果：UC患者血清T、LH、FSH、TB、Alb、A/G、TC、LDL-C水平显著低于正常对照组（P〈0.01）;血清E2、PRL水平显著高于正常对照组（P〈0.01）。相关分析表明,UC患者E2与TB、A/G、TC之间存在高度负相关（P〈0.01）;T与TC、TB之间存在高度正相关（P〈0.01）。女性E2与LH、FSH之间无相关性（P〉0.05）,男性T与LH、FSH之间亦无相关性（P〉0.05）。结论：UC患者存在脂蛋白及性激素水平代谢异常,血清性激素水平异常影响患者脂蛋白的水平代谢。测定血清性激素水平可为临床提供新的治疗思路。     

少、弱精子症与生殖激素水平关系的研究

目的探讨少、弱精子症与生殖激素血清泌乳素（PRL）、卵泡刺激素（FSH）、黄体生成素（LH）、睾酮（T）、雌二醇（E2）的关系。方法采用化学发光免疫分析仪检测健康对照组和少、弱精子症患者血清PRL、LH、FSH、E2和T。结果少精子症组与对照组相比,FSH、LH值均明显升高（P〈0．01,P〈0．05）,但T值却明显降低（P〈0．01）,PRL和E2水平没有明显变化（P〉0．05）;弱精子症组与对照组比较,弱精子症组PRL、FSH、E2、T／LH水平统计学差异均有意义（P〈0．01,P〈0．05）,其中PRL、FSH和E2均显著增高,而T／LH则显著降低（P〈0．05）,T和LH水平没有明显变化（P〉0．05）。结论少、弱精子症与生殖激素水平有一定的相关性,激素测定对睾丸生精功能的判断有指导意义。     

男性肝硬化患者血清性激素水平变化

目的：探讨男性肝硬化患者血清性激素水平的变化及其临床意义。方法：采用放射免疫分析测定118例肝硬化患者和108例正常健康人的血清卵泡刺激素（FSH）、黄体生成素（LH）、雌二醇（E2）、睾酮（T）及泌乳素（PRL）,以进行比较。结果：肝硬化患者血清T、E2水平较正常对照组显著降低（P〈0.01）,血清PRL含量则高于对照组（P〈0.01）,而FSH、LH变化不大。结论：男性肝硬化患者体内存在性激素水平的失衡和紊乱,联检血清T、E2、PRL含量对估测肝硬化的严重程度及预后具有实用价值。     

PCOS患者血浆leptin和血清T、E2、FSH、LH、PRL检测的临床意义

目的：探讨多囊卵巢综合征（PCOS）患者血浆leptin和血清T、E2、FSH、LH、PRL水平的变化及临床意义。方法：应用放射免疫分析和发光法对31例PCOS患者进行了血浆leptin和血清T、E2、FSH、LH、PRL测定,并以正常妇女作对照。结果：PCOS患者血浆leptin和血清T、LH、PRL水平非常显著地高于正常妇女组（P〈0.01）,FSH、E2水平与正常妇女组比较无显著性差异（P〉0.05）,且血浆leptin水平与血清T、LH、PRL水平呈正相关（r=0.5784、0.5411、0.6082,P〈0.01）。结论：检测PCOS患者血浆leptin和血清T、E2、FSH、LH、PRL水平的变化与疾病的发生和发展密切相关。     

男性勃起功能障碍患者体内生殖激素水平分析

目的：探讨男性勃起功能障碍（ED）患者生殖激素水平的改变和相互间关系。方法：应用化学发光免疫分析测定患者血清生殖激素（LH、FSH、T、P、E2和PRL）水平。结果：ED患者体内的LH、FSH、PRL、E2水平明显高于正常对照组（P〈0．01），T水平有显著降低（P〈0．01），P水平在两者间变化不明显。结论：睾丸存在病变可能是大多数ED患者的主病因。ED患者存在下丘脑-垂体-性腺轴功能紊乱。生殖激素检测在男性性功能评价上有着十分重要的意义，尤其是对ED患者病因诊断和治疗。     

两种SD大鼠多囊卵巢综合征模型的比较研究

目的比较两种SD大鼠多囊卵巢综合征动物模型的建模效果。方法建立两种PCOS动物模型。观察各组大鼠卵巢形态学、性激素及空腹血糖和胰岛素的变化。结果DHEA建模组大鼠的体重显著低于对照组（P〈0．05）;hCG建模组大鼠卵巢重量和体积均显著高于对照组（P〈0．05）。两建模组大鼠卵巢卵泡多呈囊性扩张,颗粒细胞层数减少,卵泡膜细胞、间质细胞增生。两建模组大鼠血清T、FINS、FBG和HOMA指数均显著高于对照组（P〈0．05）;DHEA建模组LH水平较对照组无显著性差异;hCG建模组大鼠血清LH、LH／FSH比值均显著高于对照组（P〈0．05）。DHEA建模组FSH水平显著高于对照组（P〈0．05）。结论利用hCG诱导SD幼年雌性大鼠出现了与PCOS患者极为相似的卵巢病理改变及LH、雄激素水平升高和胰岛素抵抗等典型内分泌变化,其建模效果优于DHEA。     

更年期综合征妇女雌激素替代治疗的研究

目的：探讨更年期综合征妇女激素替代治疗相关指标的变化及其临床意义。方法：采用放射免疫分析法、离子电极法及酶法测定了50例更年期综合征患者血清E2、FSH、LH、TC、TG、LDL、HDL、ALP水平及尿Ca/Cr比值。结果：经激素替代治疗，患者改良Kuppormen评分显著下降（P＜0．05，P＜0．01）TC、TG及LDL亦显著下降（P＜0．05），HDL略有上升，但统计差异无显著性（P＞0．05）；E2水平明显升高（P＜0．05），FSH及LH则显著下降（P＜0．05），ALP治疗前后无显著差异（P＞0．05），Ca/Cr比值显著下降（P＜0．05）。结论：研究证实，激素替代治疗更年期综合征有满意疗效。     

男性Graves’病患者血清性激素与Th1/Th2细胞因子相关性研究

目的：观察男性Graves’病（GD）患者治疗前后血清性激素及干扰素γ（IFN-γ）、白介素-4（IL-4）的动态变化,探讨男性GD患者血清性激素与Th1/Th2细胞因子的相关性。方法：选取初发未治的男性Graves’病患者42例为治疗组,经抗甲状腺药物治疗12周后均临床缓解。治疗前后分别应用放免法（RIA）检测血清雌二醇（E2）、睾酮（T）、黄体生成素（LH）、卵泡刺激素（FSH）水平,应用酶联免疫吸附法（ELISA）检测血清干扰素γ（IFN-γ）、白介素-4（IL-4）水平。健康男性体检合格者40例作为正常对照组。结果：男性GD患者治疗前血清E2、T、LH、FSH水平均较正常对照组明显升高（P〈0.05）,治疗后均接近正常对照组。治疗前血清IL-4、IFN-γ水平较正常对照组均升高（P〈0.05）,治疗后IL-4水平下降,接近正常对照组,而IFN-γ水平仍较高。经多元逐步回归分析,血清E2水平是影响IL-4水平的独立因素,呈正相关;血清T水平是影响IFN-γ水平的独立因素,呈正相关;IL-4与IFN-γ水平是相互的独立因素,呈负相关。结论：初发未治的男性GD患者存在性激素水平的变化及Th1/Th2细胞因子失衡,性激素在男性Graves’病患者Th1/Th2平衡方面起着一定的作用。     

不孕症患者性激素水平的变化

为了解性激素的变化在不孕症发病过程中的作用,将84例患不孕症的妇女,分为四组,在卵泡期对血清六项激素：FSH、LH、PRL、E2、T、P进行了放射检测。检测结果表明：四组患者的六项指标均高于标准值,除E2（P＜0．05）外,其他各项指标的组均数间无显著性差别,在被检病例中E2、P含量增高的患者所占的百分比与LH／FSH比值增高患者所占的百分比基本一致。     

绝经后女性冠心病性激素与冠状动脉病变关系探讨

目的研究绝经后妇女性激素水平失衡与冠状动脉病变的关系。方法选取121例行双源CT（DSCT）冠状动脉成像的绝经后女性住院病人为研究对象,分为冠心病（coronary heart disease,CHD）组70例和非冠心病组51例。按照DSCT结果对冠状动脉狭窄病变程度进行定量Gensim评分,计算冠脉病变支数;缺血相关病变根据Ambrose分类方法分为两组：简单病变和复杂病变;同时测定血清雌二醇（E2）、睾酮（T）、孕酮（P）含量,血脂。结果①冠心痛组和非冠．心病组比较,E2、HDL—C低于非冠心病组,有显著差异（P〈0．05）,LDL—C、TG、TC、T、T／E2高于非冠心病组,有显著差异（P〈005）,P、P／E2无明显差异（P〉0．05）。②冠状动脉病变积分与性激素及性激素比值无明显相关性（P〉0．05）。③不同冠状动脉病变支数的患者,性激素及性激素比值比较,差异无统计学意义（P〉0．05）。④复杂病变与简单病变之间比较,E2水平降低,T、P、T／E2、P／E2水平增加,但无显著性差异（P〉005）。⑤多因素分析结果显示T／E2、LDL—C是冠心病复杂病变发生的独立危险因素;线性相关分析表明T／E2与TC、LDL—C呈正相关,与HDL—C呈负相关。结论①性激素比值与冠状动脉病变支数及狭窄程度无关;与病变类型有关。②T／E2是女性冠心病复杂病变发生的独立危险因素,性激素水平失衡可能通过血脂代谢紊乱导致冠状动脉粥样硬化病理生理改变及斑块不稳定性的发生。     

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.