新生儿血清瘦素水平变化与胰岛素和生长激素关系的研究

目的　探讨新生儿血清瘦素来源及其与胰岛素和生长激素的关系。方法　采用放射免疫法检测 80例新生儿静脉血和脐血瘦素水平 ,根据不同胎龄新生儿出生体重值分为大于胎龄儿 (LGA)组 2 8例 ,适于胎龄儿 (AGA)组 36例 ,小于胎龄儿 (SGA)组 16例 ;采用Rohrer′s指数 =出生体重 (g)× 10 0 /身长 (cm) 3 估测新生儿营养状态。结果　早产儿血清瘦素水平明显低于足月儿 (0 6 6± 1 0 3ng/mlvs 3 5 9± 2 16ng/ml,P <0 0 1) ;AGA儿血清瘦素水平 (3 0 6± 0 96ng/m1)明显低于LGA儿(4 0 3± 2 2 2ng/m1) ,而高于SGA儿 (1 13± 1 98ng/m1) ;足月新生儿血清瘦素水平与Rohrer′s指数、新生儿体重、胎龄 ,血清胰岛素、生长激素水平呈显著正相关。结论　新生儿体内瘦素主要来源于自身脂肪组织 ,它反映新生儿的生长营养状态 ,推测瘦素可能通过胰岛素、生长激素共同调节新生儿的生长发育 ,在胎儿和新生儿生长发育中起重要作用。     

血浆神经肽Y水平在不同甲状腺功能状态的意义

目的 :研究不同甲状腺功能状态 (甲亢、甲减及正常 )神经肽Y的水平。方法 :选取甲亢患者 5 5例 ,甲减患者 4 7例和正常对照 5 7例 ,放射免疫分析其NPY水平。结果 :甲亢患者 (无论性别 )NPY水平 (71 5±14 7)ng/L较正常对照组 (5 2 3± 11 8)ng/L呈显著性增高 (0 0 0 1

0 0 5 ) ;甲亢组 (71 5± 14 7)ng/L较甲减组 (4 2 2± 2 4 3)ng/L呈显著性增高 (P <0 0 0 1) ;所有样本NPY与瘦素 (Leptin)关系分析呈负相关 (r =-0 5 8,P =0 .0 15 )。结论 :甲状腺激素与NPY是影响人体正常能量代谢的激素 ;甲状腺激素与NPY可能存在相互影响的关系。     

肺瘤坏死因子和神经肽Y与急性心肌梗塞的关系

动态测定76例临床明确诊断的急性心肌梗塞患者和15例正常对照组肿瘤坏死因子和血浆神经肽Y的水平。结果显示,正常对照组NPY为93.3±10.6ng/L,急性心肌梗塞组在发病后1天NPY异常升高,为160.2±26.3ng/L,发病后第7天为121.3±24.7ng/L,均高于正常对照组(p<0.05);与NPY不同,正常对照组的TNF为0.97±0.38μg/L,在急性心肌梗塞发病后第1天升高至2.48±0.89μg/L(p<0.01),但发病后第3天降至1.12±0.37μg/L,已接近正常(p>0.05)。提示,TNF在急性心肌梗塞的发生中有重要作用,但与患者预后无直接关系;而血浆神经肽Y的水平不仅与急性心肌梗塞患者的发生有关,而且在急性心肌梗塞的病程和预后中有重要价值。     

糖尿病视网膜病变患者瘦素水平的变化

目的 :探讨糖尿病视网膜病变患者血清瘦素水平变化规律。方法 :受试对象 12 0例 ,分为对照组 30例 (男 18,女 12 )、糖尿病无视网膜病变组 30例 (男 18,女 12 ) ,非增殖性视网膜病变组 30例 (男 18,女 12 )及增殖性视网膜病变组 30例 (男 18,女 12 ) ,检测血清瘦素、胰岛素、Ⅳ型胶原及血糖浓度 ,分析瘦素水平与其它指标的相关性。结果 :对照组、无视网膜病变组、NPDR组及PDR组血清瘦素浓度分别为 6 91± 1 87μg/L ,7 83± 2 11μg/L ,9 5 6± 2 4 3μg/L和 11 6 9± 2 5 7μg/L ,经协方差分析排除体重指数的影响 ,PDR组血清瘦素浓度高于NPDR组 (t=2 15 ,p<0 0 5 )、无视网膜病变组 (t=2 71,p <0 0 1)及对照组 (t =3 5 0 ,p <0 0 0 1) ;NPDR组高于无视网膜病变组 (t=2 2 3,p <0 0 5 )及对照组 (t=2 75 ,p<0 0 1)。血清瘦素浓度与体重指数、胰岛素呈正相关 (r=0 2 2 ,p <0 0 5 ;r=0 2 8,p<0 0 1)。结论 :糖尿病视网膜病变患者血清瘦素浓度升高 ,且增高的幅度与病情的严重程度正相关     

急性脑梗死患者血浆NPY水平变化

目的 :观察脑梗死 (ACI)急性期血浆神经肽Y(NPY)的变化及临床意义。方法 :采用放射免疫分析法检测 5 0例急性脑梗死 (CI)患者血浆神经肽Y(NPY)浓度 ,并以 30例健康人作为对照。结果 :ACI患者血浆中NPY含量为 431.0 3± 142 .0ng/L显著高于正常对照组 145 .1± 44 .1ng/L(P <0 .0 0 1)。结论 :检测结果表明 ,NPY作为一种具有强烈收缩血管的神经多肽与急性脑梗死的发病机理有密切的关系     

新生儿血清瘦素水平变化与IGF—I、生长激素等相关因素的分析

目的　探讨新生儿血清瘦素来源及其与胰岛素样生长因子 -I(IGF -I)和生长激素的关系。方法　采用放射免疫法检测 80例新生儿静脉血和脐血瘦素水平 ,根据不同胎龄新生儿出生体重值分为大于胎龄儿组 2 8例 ,适于胎龄儿组 36例 ,小于胎龄儿组 16例 ;采用Rohrer’s指数 =出生体重 (g)× 10 /身长 (cm) 3 估测新生儿营养状态。结果　早产儿血清瘦素水平明显低于足月儿 (0 .6 6± 1.0 3ng/mlvs 3.5 9± 2 .16ng/ml,P <0 .0 1=;适于胎龄儿血清瘦素水平 (3.0 6± 0 .96ng/ml明显低于大于胎龄儿 (4.0 3± 2 .2 2ng/ml) ,而高于小于胎龄儿 (1.13± 1.98ng/ml) ;足月新生儿血清瘦素水平与Rohrer’s指数、新生儿体重、胎龄、血清IGF -I、生长激素水平呈显著正相关。结论　新生儿体内瘦素主要来源于自身脂肪组织 ,它反映新生儿的生长营养状态 ,推测瘦素可能通过IGF -I、生长激素共同调节新生儿的生长发育 ,在胎儿和新生儿生长发育中起重要作用     

妊高征患者血清瘦素水平的初步研究

目的　探讨妊娠高血压综合征 (妊高征 )血清瘦素水平及其与血压间的关系。方法　采用放射免疫法 ,测定 32例妊高征患者 (妊高征组 )及 30例正常妊娠妇女 (对照组 )血清瘦素水平 ,分析瘦素与收缩压 (SBP)、舒张压 (DBP)的相关性。结果　⑴妊高征组血清瘦素水平为 (16 .5 1± 4 .4 7)ng/mL ,高于正常妊娠组的 (14 .14± 3.79)ng/mL ,差异具有显著性 (P <0 .0 5 ) ;(2 )产后妊高征组瘦素水平为 (8.6 2± 2 .2 3)ng/mL ,较产前明显降低 (P <0 .0 1) ,与对照组产后瘦素水平 (7.97± 2 .2 2 )ng/mL相比 ,差异无显著 (P >0 .0 5 ) ;(3)正常妊娠组与妊高征组产前血清瘦素水平与SBP、DBP的相关系数分别为 (0 .2 5 8,0 .0 74 )及 (0 .0 91,0 .0 6 5 ) ,均无显著相关 (P >0 .0 5 )。结论　妊高征患者血清瘦素水平升高 ,它与血压不相关 ,妊高征血压升高与血清瘦素水平间无明确的因果关系。     

血浆与血小板中NPY、NT在慢性肾功能衰竭患者血液透析中的变化及意义

采用RIA法检测40例慢性肾功能衰竭(CRF)患者血液透析(以下简称血透)过程中,血浆和血小板中神经肽Y(NPY)、神经降压素(NT)的含量变化及其临床意义。并以30例健康人作为对照。结果显示,①CRF患者血透前血浆NPY、NT含量分别为432.34±52.27ng/L、138.44±80.35ng/L;血透后分别为324.52±48.16ng/L、211.6±124.69ng/L。②CRF患者血透前血小板中NPY、NT含量分别为34.86±18.82ng/L、41.12±24.12ng/L;血透后分别为66.97±21.81ng/L、14.89±12.56ng/L。结果表明,CRF患者存在NPY及NT分泌异常。NPY与NT作为体内重要的神经递质,参与了肾脏病及其并发高血压的病理生理过程。     

自然流产患者血清瘦素水平的改变

目的　探讨自然流产患者瘦素水平的变化及其临床意义。方法　用ELISA法测定 2 3名自然流产患者、2 1名正常妊娠者及 2 0名正常未孕者血清瘦素水平。结果　自然流产者血清瘦素水平平均为 875 3± 4 2 5 0ng/ml,正常妊娠者为1185 9± 4 0 3 2ng/ml,正常未孕者为 6 14 7± 15 0 2ng/ml,两两比较差异均有显著性。结论　自然流产患者血清瘦素水平明显降低 ,低瘦素水平可能是自然流产发生的又一原因。     

急性颅脑损伤早期C型利钠多肽的实验研究

目的 :探讨C -型利钠多肽 (CNP)在急性颅脑损伤早期的病理生理作用。方法 :用放免法测定了 2 9例急性颅脑损伤患者在损伤后 1天内、治疗后 3天、14天三种状态下血浆CNP含量。结果 :急性颅脑损伤后 1天内及治疗后 3天患者血浆CNP水平 (4 8± 4 0ng/L ,5 4± 4 3ng/L)较正常对照组 (15 5± 7 4ng/L)明显减少 (p <0 0 1) ,治疗后 14天血浆CNP含量 (15 7± 9 4ng/L)已上升至正常对照组水平 (p >0 0 5 )。结论 :观察CNP的含量变化对探讨急性颅脑损伤早期的病理生理机制、判断疗效及预测预后具有重要意义。     

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.     

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.     

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.     

'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.