心交感神经反射在阻断冠脉血流后血液流变学变化中的作用

本实验在21只狗身上观察了阻断冠脉血流后缺血区局部静脉血与体循环静脉血流变特性的变化及心交感神经反射在这一变化中的作用。主要结果如下:1.心肌缺血时血液流变学出现明显异常变化,且缺血区局部静脉血高切变率下全血粘度变化大于体循环静脉血;2.阻断冠脉血流后用利多卡因浸润缺血区心肌,可使心肌缺血时体循环血液流变学变化明显减轻,但缺血区局部静脉血高切变率下全血粘度仍明显升高;3.阻断冠脉前切除双侧星状神经节对心肌缺血时血液流变学变化无明显影响。上述结果提示,阻断冠脉血流后起源于缺血区内的传入神经活动增强是诱发血液流变学变化的重要因素。     

油酸型呼吸窘迫综合征家兔的血液流变性改变及山莨菪碱的作用

对家兔油酸型呼吸窘迫综合征（ＲＤＳ）组、油酸型ＲＤＳ６５４－２治疗组和生理盐水治疗组的血液流变性进行了研究。结果表明油酸型ＲＤＳ和生理盐水治疗组ηａ、ＲＩ、ＴＫ均明显增高，ＯＤ、ＨＣＴ显著降低；而６５４－２治疗组ηａ、ＲＩ和ηｐ等均无明显变化。提示油酸型ＲＤＳ存在高全血粘度血症。６５４－２可能通过抑制红细胞、血小板聚集等而降低全血粘度、减轻肺损伤     

血库存血不同时间内流变性的变化

通过血液流变性实验，初步探讨了血库存血（４℃）在不同时间内（２４ｈ、３天、７天、１４天）其血液流变学指标红细胞电泳时间（ＥｐＴ）、全血（比）粘度（ηｂ）、血浆（比）粘度（ηｐ）的变化，结果分别为存放１天（２４ｈ），ＥｐＴ值有非常显著延长，存放３天加值有非常显著性增高，Ｐ＜０．０１，储存时间越长其值越高；存放３天内ηｂ值无明显变化，Ｐ＞０．０５；７天与１４天有显著性和非常显著性变化，Ｐ＜０．０５和Ｐ＜０．０１；存放时间越长，其ηｐ值顺次变小。     

阻断冠脉血流后体循环与缺血区局部静脉血液流变学变化的对比研究

阻断狗冠脉左前降支血流后,缺血区局部静脉血流变特性出现明显、稳定的异常变化。缺血40min时低切变率(r=1.15s~(-1))全血粘度已明显升高(从对照值的39±7.9mPa.s增加到58±8.4mPa.s),这一变化出现在血浆纤维蛋白原浓度与HCT明显变化之前,提示急性心肌缺血早期血液粘度的异常增高除血浆纤维蛋白原与HCT的影响外,可能还有另外一些尚未阐明的快速调节机制参与。缺血区局部血液高切变率下(r=230s~(-1))全血粘度升高程度明显大于体循环静脉血,这可能与缺血区酸性代谢产物蓄积、H~ 浓度增高以及氧分压降低有关。     

汉防已甲素对大鼠实验性脑梗塞的影响

目的和方法：选用热凝造成大脑中动脉阻断（ＭＣＡＯ）而致实验性大鼠脑局灶性缺血模型，观察汉防己甲素（ｔｅｔｒａｎｄｒｉｎｅ，ＴＥＴ）对大鼠脑局灶性缺血的防治作用。结果：ＴＥＴ组用药七天，脑梗塞范围明显小于缺血组，缺血区脑组织Ｃａ２＋、Ｎａ＋、过氧化脂质（ＬＰＯ）、血浆血栓素Ｂ２（ＴＸＢ２）明显低于缺血组，而超氧化物歧化酶（ＳＯＤ）明显高于缺血组，６－酮－前列腺素Ｆ１α（６－ｋｅｔｏＰＧＦ１α）无显著改变，ＴＸＢ２／６－酮（Ｔ／Ｋ）比值明显低于缺血组。结论：ＴＥＴ具有对大鼠ＭＣＡＯ局灶性脑缺血有效的防治作用，其机制可能与减少脑组织缺血区Ｃａ２＋、Ｎａ＋、ＬＰＯ含量，降低ＴＸＢ２，使Ｔ／Ｋ比值趋于正常有关。     

老年性疾病患者的血液流变学研究

目的探讨脑梗塞、冠心病、高血压病、糖尿病和肺心病等几种常见老年性疾病的发生发展与血液流变学的关系。方法采用ＬＢＹ—Ｎ６Ａ全自动旋转式血液粘度计，分别检测几种老年性疾病患者和正常对照组３个切变率下的全血粘度（ηｂ）及血浆粘度（ηｐ），并以温氏法、魏氏法和凝固法分别测定红细胞比积（ＨＣＴ）、血沉（ＥＳＲ）和纤维蛋白原（Ｆｉｂ）含量，计算出全血还原粘度（ηｒｅ）、红细胞聚集指数（ＲＡＩ）、红细胞刚性指数（ＩＲ）、红细胞变形指数（ＤＩ）和血沉方程Ｋ值（ＥＳＲＫ）与正常对照组比较。结果几种老年性疾病患者的 ηｈ、ηＰ、ＨＣＴ、Ｆｉｂ、ＥＳＲＫ均有不同程度增高（Ｐ＜０． ０５～０． ００１），红细胞聚集性、刚性明显增强，变形能力降低。研究表明，几种老年性疾病患者存在高粘滞、高聚集状态之共性。结论老年性疾病患者血液流变性的异常改变，特别是红细胞聚集性增强，红细胞变形性降低（即红细胞刚性增强）是体内微循环障碍、血液淤滞、血栓形成的危险因素之一。故认为老年性疾病患者需要做血液流变学检查。血液流变性特点可作为早期诊断和监测指标，为疾病的发展、转归和预后提供重要信息。     

小儿肺炎时血液流变学的变化

本实验对１７例小儿肺炎患者进行了血液流变学指标的检测。结果表明：肺炎组高切变率（２ｏｏｓ－１）下校正全血粘度（ｃｏｒｒｅｃｔｗｈｏｌｅｂｌｏｏｄｖｉｓｃｏｓｉｔｙ，ＣＷＢＶ）和相对全血粘度（ｒｅｌａｔｉｖｅｗｈｏｌｅｂｌｏｏｄｖｉｓｃｏｓｉｔｙ，ＲＷＢＶ）均明显高于正常对照组；低切变率（１０ｓ￣（－１））下ＣＷＢＶ和ＲＷＢＶ也高于正常对照组，校正ＥＳＲ值下降，血沉方程Ｋ值减小，纤维蛋白原（ｆｉｂｒｉｎｏｇｅｎ，Ｆｇ）含量与高、低切变率下ＣＷＢＶ和ＲＷＢＶ显著相关，与血浆粘度（ηｐ）也显著相关；红细胞聚集指数（ｒｅｄｃｅｌｌａｇｇｒｅｇａｔｉｏｎｉｎ－ｄｅｘ，ＲＡＩ）与高、低切变率下ＣＷＢＶ也显著相关。提示小儿肺炎时全血及血浆粘度均增高，红细胞刚性增加，聚集性增强。     

红细胞生成素3‘—增强子片段对内皮细胞缺氧时环加氧酶—2？…

目的和方法：体外合成红细胞生成素（Ｅｐｏ）３‘－增强子野生型及突变型片段，借助脂质全，转入内皮细胞用半定量ＲＴ－ＰＣＲ方法测定分离细胞在常氧或缺氧条件下培养４ｈ的环加氧酶２（ＣＯＸ－２）ｍＲＮＡ。结果：（１）大鼠主主动脉内皮细胞、肺微血管内皮细胞在常氧下培养，有ＣＯＸ－２基因表达；（２）缺氧能诱导这两种细胞ＣＯＸ－２基因表达增加；（３）野生型Ｅｐｏ３’－增强子片段能阻断缺氧地内皮细胞ＣＯＸ－２基因     

pCO2,pH对兔离体肺动脉缺氧性收缩的影响

观察了二氧化碳（ＣＯ＿２）和ｐＨ对兔离体肺动脉缺氧性收缩（ｈｙｐｏｘｉｃｐｕｌｍｏｎａｒｙｖａｓｏ－ｃｏｎｓｔｒｉｃｔｉｏｎ，ＨＰＶ）反应的影响。浴槽内ＣＯ＿２浓度降低（ｐＣＯ＿２＝１．３３ｋＰａ）使ＨＰＶ加强，Ｋ％为４２．６３±３．１１；而ＣＯ＿２浓度增高则抑制ＨＰＶ（ｐＣＯ＿２＝９．３３ｋＰａ），Ｋ％为１８．４７±２．３１，均与对照值（ｐＣＯ＿２＝５．３３ｋＰａ，Ｋ％为３１．５４±２．６６）有显著差异。相关分析表明ｐＣＯ２与ＨＰＶ的改变呈负相关（ｒ＝一０．４８１，Ｐ＜０．０１，ｎ＝８２）。浴槽内ｐＨ的增高或降低均有使ＨＰＶ增高的趋势，但ｐＨ低至７．１０时ＨＰＶ被抑制。一氧化氮（ＮＯ）合成酶抑制剂ＮＧ一硝基左旋精氨酸抑制了ＨＰＶ，也抑制了低ＣＯ＿２加强ＨＰＶ的作用。结果提示ＣＯ＿２可经对ＮＯ的影响而改变肺血管对缺氧的反应。     

人红细胞急性出血性结膜炎病毒受体的研究

本文在首次证明ＣＡ２４ｖ具有血凝性的基础上，用受体破坏酶（即霍乱滤液）、胰蛋白酶处理人Ｏ型红细胞观察对ＥＶ７０、ＣＡ２４ｖ血凝的影响，发现两病毒的受体是相似的；进一步用Ｄｏｄｇｅ氏法从成人Ｏ型血获得红细胞膜，再用酚抽提、氯仿甲醇说明得到的可溶性糖蛋白，能阻断ＥＶ７０和ＣＡ２４ｖ的血凝，而不阻断ＥＣＨＯ７的血凝，证明是ＥＶ７０和ＣＡ２４ｖ的受体蛋白，该蛋白的受体活性在４℃￣６０℃基本保持稳定，提示人     

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.