脑源性神经营养因子在成年猴脑的分布

采用免疫组织化学方法探讨了 BDNF在成年猴脑的分布。结果显示 ,脑源性神经营养因子阳性反应产物主要分布于下列结构 :大脑皮层 III～ V层的锥体细胞及突起 ;小脑皮质篮状细胞、Purkinje细胞、Golgi细胞及小脑顶核的神经元及其突起 ;海马各区的神经元、纤维和齿状核的颗粒细胞 ;尾状核、豆状核和室旁核部分神经元和纤维 ;脑干脑桥核、舌下神经核、迷走神经背核、前庭神经核、下橄榄核及网状结构的神经元及纤维或膨体。此外 ,在大、小脑的白质也可见到部分脑源性神经营养因子阳性胶质细胞。脑源性神经营养因子阳性反应产物广泛地分布于猴脑的多种区域和细胞 ,提示其功能可能涉及不同类型的神经元及可能的非神经细胞。本研究结果为探讨脑源性神经营养因子在成年猴脑的分布规律及其功能特点提供了有用的形态学依据。     

Caspase-3在成年大鼠中枢神经系统分布的免疫组织化学研究

采用免疫组织化学ABC法观察caspase3在成年大鼠中枢神经系统不同区域内的分布。caspase3阳性反应产物主要分布于脊髓前角和侧角大型运动神经元及中型神经元的胞浆、胞核及突起;脊髓后角及灰质连合的中、小型神经元的胞核及胞浆亦可见caspase3阳性反应产物;脊髓白质内的星形胶质细胞、小胶质细胞及少突胶质细胞的胞核和胞浆,caspase3阳性反应产物呈强阳性反应。在延髓内,caspase3阳性反应产物定位于中央灰质、三叉神经尾侧亚核和中央网状核内中型神经元的胞浆。大脑皮层各区内的caspase3阳性反应产物集中分布于ⅢⅤ层锥体细胞的胞浆,呈弱阳性反应。海马的CA1、CA2、CA3、CA4区的锥体细胞层的细胞,胞浆亦呈弱阳性反应。小脑内,以Purkinje细胞胞浆着色为主。乳头体核、尾状核、豆状核、嗅前核后部、嗅结节及丘脑等部位亦可见caspase3阳性神经元。本研究的结果说明caspase3在中枢神经系统内广泛分布,且在不同部位神经元的亚细胞分布存在差异。     

甘草对大鼠杏仁中央核肽能神经元年龄变化的影响

目的:验证甘草具有抗衰老作用。方法:选用Wistar大鼠,实验组喂饲甘草粉,用免疫组织化学法观察大鼠杏仁中央核(CA)神经紧张肽(NT)和亮氨酸脑啡肽(LENK)标记神经元的分布及其变化。结果:NT和LENK标记神经元在CA的外侧亚区(CL)分布最密集,在CL还观察到NT—LENK双标神经元。老龄大鼠标记神经元树突分枝增多、突起伸长、弯曲,梭形细胞明显增多,NT标记和NT—LENK双标记神经元更加明显。NT和LENK标记神经元的灰度值和平均面积分别在9~12月开始明显增加。喂饲甘草大鼠与同月龄正常大鼠相比在细胞数、灰度值、平均面积等方面均有显著改善。结论:甘草具有抗衰老作用。     

大鼠脊髓神经肽Y、神经降压肽免疫反应神经元向结合臂旁核的投射

用HRP逆行束路追踪法结合免疫细胞化学双标记技术,研究了大鼠颈、胸、腰、骶各段脊髓神经肽Y(NPY)、神经降压肽(NT)免疫反应神经元向结合臂旁核的投射。HRP逆行标记细胞分布于两侧脊髓灰质第Ⅰ、Ⅱ、Ⅳ、Ⅴ、Ⅶ层、中央管背侧灰质连合及外侧颈核、外侧脊髓核中,以对侧为主。NPY免疫反应阳性神经元分布于两侧后角第Ⅰ层、第Ⅱ层浅部、外侧颈核、外侧脊髓核及骶髓后连合核中。NT免疫阳性神经元分布于两侧后角第Ⅰ层及第Ⅱ层中。在后角第Ⅰ层、外侧颈核和外侧脊髓核中,可观察到部分NPY-HRP双标记神经元;在后角第Ⅰ层可观察到部分NT-HRP双标记神经元。本研究结果提示,NPY和NT神经元可能参与脊髓-结合臂旁核的痛觉传递。     

大鼠下丘脑室旁核对脾脏免疫功能神经调控的研究

目的 探讨PVN不同亚核在调控脾脏免疫功能中的作用。方法 4只SD大鼠脾脏内注射假狂犬病毒（PRV）96h后,采用免疫组化法和体视学方法研究被假犬病毒跨突触感染的神经元在PVN不同亚核内的分布特点及其与PVN内AVP神经元位置配布间的相互关系。结果 PRV感染的神经元主要聚集于PVN段的尾侧大细胞亚核（ＰＭ）和外侧小细胞亚核（LP）（占总面积的73.49%),少量分布于喙段的前小细胞亚核（LP）、中段的背侧小细胞亚核（DP）和室周小细胞亚核内（PP）。其中LP及PM内的部分PRV感染神经元分布在AVP阳性神经元聚集的区域内。结论 PVN对脾脏免疫功能的调控除了传统神经内分泌途径外,还可能存在下列途径：PM内的AVP阳性神经元和LP、DP及AP内的神经元通过向延髓背侧及脊髓中间外侧柱的投射,然后再通过副交感和交感神经的直接神经支配途径调控脾脏的功能。     

T-激肽原在大鼠腰骶髓及背根节的分布

<正> T-激肽原(T-kininogen,T-Kg)是属于血管舒缓素-激肽系统(Kallikrein-kininsystem,Kks)的蛋白多肽.为进一步探讨T-Kg在神经系统的定位和作用,本文应用免疫细胞化学ABC法,研究了T-激肽原在大鼠腰骶髓及L_(46)背根节的分布.研究发现T-激肽原分布于L_(46)背根节及腰骶髓灰质的第Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅸ层神经元及脊髓白质的神经胶质细胞和神经纤维.结果提示:在背根节的感觉神经元、腰骶髓白质的神经胶质细胞和神经纤维以及灰质的第Ⅱ、Ⅲ、Ⅸ层神经元内T-Kg和Hkg、Lkg及Bk等可能共存.这进一步提示,在神经元和神经胶质细胞存在内源性的Kks.它们     

NGF在成年猴脑的分布

为了解NGF在成年猴脑的分布,采用免疫组化SP法对成年猴脑多个冠状位切片进行免疫组化反应。结果证明,NGF阳性反应神经元主要分布于大脑皮质Ⅲ、V层,小脑Purkinje细胞,海马,齿状回,纹状体,脑干网状结构等处。此外,在黑质、舌下神经核、迷走神经背核、前庭神经核、三叉神经核、疑核、下橄榄核也出现NGF阳性反应。在大脑和脑干还观察到NGF阳性胶质细胞。本实验结果表明,在成年猴脑的多个脑区有NGF表达,提示NGF可能涉及猴脑某些神经元及胶质细胞的生理过程。     

同一心内神经元酪氨酸羟化酶、生长抑素的各自基因表达与贮存——原位杂交和/或免疫组织化学法光镜观察

目的　在转录与翻译水平同时证明 1 部分心内神经节的单一细胞内既出现酪氨酸羟化酶 (TH)的基因表达 ,又储存TH ;2 部分心内神经节的单一细胞内既出现生长抑素 (SS)的基因表达 ,又储存SS。　方法　在中华蟾蜍心房后壁腔静脉窦部位的冰冻切片 (30 μm)上 ,分两组以原位杂交、免疫组织化学及原位杂交 免疫组织化学结合双标方法分别进行心内神经节细胞的THmRNA、TH 免疫反应 (TH IR)及SSmRNA、SS 免疫反应 (SS IR)染色观察。　结果　在两组心内神经节切片分别发现下述标记细胞 :TH IR阳性神经元、THmRNA阳性神经元、THmRNA TH IR双阳性神经元 ;以及SS IR阳性神经元、SSmRNA阳性神经元、SSmRNA SS IR双阳性神经元。　结论　 1 证明部分心内神经节的细胞内既出现TH的基因表达 ,同时又有TH ,可能是肾上腺素能的交感神经细胞 ;2 SS系心内神经节细胞的一种内源性神经递质。本研究为心内SS能神经结构参与心功能 (兴奋传导、心肌分泌及收缩 )的局部神经调节提供直接的化学神经解剖学证据。     

产前应激对发育海马神经元及其超微结构的影响

目的:观察产前应激(PS)对子鼠海马神经元和神经元超微结构是否有损伤作用, 以及这种损伤是否与氧化物的过度生成有关。方法:采用束缚应激模型, 观察出生后1个月雄性子鼠的海马神经元数量、神经元超微结构及神经型一氧化氮合酶(nNOS)表达的变化。结果:晚期应激(LS)引起子鼠海马CA1和CA4区的细胞数量明显减少;电镜可见PS使子鼠海马CA1区神经元超微结构发生改变, 表现为线粒体肿大、边界不清、电子密度不均, 脂褐素增多, 偶见核变形;中期应激(MS)使子鼠海马CA1、CA2、CA3区和DG内nNOS阳性表达量显著升高, LS使子鼠海马CA1、CA2、CA3、CA4区和DG内nNOS阳性表达量也显著升高。结论:结果提示, PS对子鼠海马神经元及神经元超微结构有损伤作用, 这种损伤可能由氧化物过度生成引起。     

雌激素β受体免疫阳性神经元在成年雌性大鼠脑内的分布

目的　探讨雌激素对神经系统的作用 ,研究雌激素 β受体 (ER β)免疫阳性细胞在雌性大鼠脑内的分布。　方法　应用硫酸镍铵增强显色的免疫组织化学技术。　结果　ER β免疫阳性物质主要位于神经元的细胞核内。最强的免疫阳性信号见于前嗅核、大脑皮质、小脑浦肯野细胞、斜角带垂直部、前庭上核、梨状内核、杏仁外侧核、红核和蓝斑 ;中等强度的染色见于隔内侧核、杏仁皮质后核、海马CA3、CA4区、齿状回、终纹床核、视上核等部位 ;较弱的阳性细胞见于下丘脑核团、屏状核、动眼神经核以及杏仁复合体的部分核团。　结论　雌激素 β受体免疫阳性神经元在成年雌性大鼠脑组织内有较广泛的分布 ,可能参与了雌激素对多种脑功能如学习记忆等的调控     

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.     

HLA genes in Amerindians from Mexico San Vicente Tancuayalab Teenek/Huastecos

Huastecos or Teenek Amerindians are presently living at North East Mexico (San Luis Potosi State). They have probably one of the most ancient culture of Mexico and Central America together with Mayas and Olmec groups with which also show close relationships. Proximity to Atlantic Ocean/Mexican Gulf originated that Spaniards had very early contact with them at about 1519 CE or before. In the present paper we have aimed to study HLA gene profile which may be useful for HLA and disease epidemiology and transplant programs in Teeneks. HLA-DRB1*04:07, -DRB1*14:06 and -DRB1*04:11 have been found in high frequency like in other Amerindian groups. High frequency typical Amerindians HLA extended haplotypes have been found, such as A*02-B*35-DRB1*04:07-DQB1*03:02; A*68-B*39-DRB1*04:07-DQB1*03:02 and A*02-B*39-DRB1*04:07-DQB1*03:02; also new haplotypes have been described, like A*02-B*52-DRB1*04:11-DQB1*03:02, A*68-B*35-DRB1*14:02-DQB1*03:01 and A*68-B*40-DRB1*16:02-DQB1*03:01. Genetic proximity is observed not only to linguistically close Mayans, but also to Mazatecans, Mixtecans and Zapotecans, who speak an altogether different languages; it shows once more that genes and languages do not correlate. This population was greatly diminished after European contact between 1500 and 1600 years CE; in fact, North and South America First Inhabitants population was brought from 80 down to 8 million people because of diseases (i.e.: measles, smallpox or influenza), slavery and war.