幕上、下乙状窦前入路的显微外科解剖学

目的:为幕上、幕下乙状窦前人路提供显微外科解剖学基础。方法:显微镜下对１５例成人尸体头部标本进行观察并测量有关数据。结果:迷路后、经迷路、经耳蜗入路骨质切除范围分别在后半规管最后点、内耳道、耳蜗和乙状窦沟之间。后半规管弓峰、内耳门后缘到乙状窦前缘的距离分别为(９．８±１．９)ｍｍ、(２２．０±２．４)ｍｍ,耳蜗到崖嵴最后点的距离为(２８．６±３．０)ｍｍ,岩嵴到颈静脉窝顶的距离为(１５．１±４．０)ｍｍ。结论:应用此入路能取得岩斜区病变手术治疗满意的结果。     

迷路后径路内镜下行脑桥小脑三角区手术的解剖学研究

目的 :为临床上保留迷路在内镜下行桥脑小脑三角区病变手术提供解剖学资料。方法 :在 2 0例 40侧成人尸头上模拟颞骨径路保留迷路内镜手术 ,测量乙状窦内侧至总骨脚、岩上窦下缘至外半规管在岩部后骨板延长线之间距离 ,对可操作范围进行评估 ,对内镜的导入角度进行研究。并就如何避免损伤半规管、颈静脉球、面神经、乙状窦、岩上窦等结构提出看法。结果 :岩上窦下缘至内淋巴囊上缘距离为(9 .5 3± 2 .64 )mm ,乙状窦内侧至总骨脚距离为 (13 .89± 2 .3 4)mm ,至内淋巴管距离为 (10 .62± 2 .0 9)mm ;由该三条线构成的上底为 13 .89mm ,下底为 10 .62mm ,高为 9.5 3mm的梯形为内镜操作范围。乙状窦距颞骨表面距离 (以乙状窦上膝为标准 )为 (5 .2 7± 1.60 )mm ,乙状窦宽度为 (11.97± 2 .10 )mm ,上下膝长度为 (2 4.78± 4.2 1)mm ,乙状窦与外耳道后壁距离为 (13 .5 9± 3 .0 3 )mm ,岩骨后骨板至后半规管后缘、总骨脚后缘距离分别为 (4 .0 7± 1.2 6)mm和 (5 .5 8± 1.49)mm ,内镜的导入角度应力争与岩部上嵴平行 ,这样的角度最便于观察和操作 ,且不易损伤内部重要结构。我们测得的岩部上嵴与矢状线之间角度为 (63 .87± 9.3 1)°。结论 :保留迷路所得到的操作范围完全可以满足在内镜下行脑桥小脑三角区     

内窥镜辅助颞下锁孔入路的应用解剖

目的 :为颞下锁孔入路提供解剖学基础。方法 :2 1例福尔马林固定尸体头部标本上进行入路相关解剖结构观察和测量 ,在 9例新鲜标本上模拟内窥镜辅助颞下锁孔入路手术 ,记录入路的显露范围及可利用的操作空间 ,尝试增加显露和操作空间的方法。结果 :圆孔、卵圆孔、棘孔、三叉神经压迹、弓状隆起、岩大神经裂孔到颞下颌关节处颧弓上缘和中线的距离分别为 :(4 5 .2± 3 .3 )mm和 (2 0 .1± 2 .3 )mm、(3 2 .6± 2 .1)mm和 (2 3 .7± 1.2 )mm、(2 8.9± 1.1)mm和 (3 1.2± 3 .1)mm、(4 0 .1± 1.2 )mm和 (15 .6±2 .7)mm、(2 5 .0± 2 .7)mm和 (3 3 .8± 0 .9)mm、(2 6.7± 2 .3 )mm和 (2 9.6± 0 .8)mm ,Kawase三角各边长度 :耳蜗至岩大神经与下颌神经交点 (18.6± 1.6)mm、耳蜗至三叉神经孔 (19.6± 1.5 )mm、三叉神经孔至岩大神经与下颌神经交点 (16.2± 0 .8)mm ;Day菱形区各边长度 :三叉神经孔至岩大神经与下颌神经交点(16.2± 0 .8)mm、弓状隆起至三叉神经孔 (2 1.7± 2 .5 )mm、岩大神经与下颌神经交点至膝状神经结 (7.2± 1.3 )mm、膝状神经结至弓状隆起 (12 .5± 2 .1)mm ;颞下锁孔入路最大控制范围前至视交叉 ,后到脑干腹外侧乳头体至中下斜坡的区域。结论 :颞下锁孔入路是治疗鞍上区和岩斜区病变     

内耳道的解剖学研究及其临床意义

目的:HTSS为内耳道手术定位提供解剖学依据。方法:对400块颞骨的内耳道及其有关结构进行解剖观察和测量。结果:内耳道与岩大神经管裂孔、弓状隆起等结构有较恒定的位置关系。内耳道底投影点至岩大神经管裂孔的距离,在左右两侧分别为8.85mm、7.95mm;至弓状隆起最高点的距离在左侧为7.89mm,右侧为8.50mm,内耳道上壁长左侧为8.41mm,右侧为8.61mm。结论:岩大神经管裂孔、弓状隆起等颞骨岩部结构是定位内耳道的重要标志。内耳道手术应避免损伤上半规管、耳蜗等结构。     

经乳突内窥镜下处理岩斜坡区病变两种硬脑膜切口的应用解剖

目的 :为颞骨径路在内窥镜下行岩斜坡区病变手术时因不同的手术目的采取不同的硬脑膜切口提供解剖学依据。方法 :在 2 0例 40侧成人尸头标本上采取不同的硬脑膜切口模拟颞骨径路内窥镜手术 ,比较两种切口对手术的影响 ;并测量相关数据。结果 :岩上窦下缘至内淋巴囊上缘为 ( 9.5 3± 2 .64 )mm、岩下窦上缘之间距离为 ( 2 3 .48± 2 .48)mm ,乙状窦内侧至共脚、内淋巴管、内淋巴囊外侧之间距离分为 :( 13 .89± 2 .3 4)mm、( 10 .62± 2 .0 9)mm和 ( 3 .73± 1.66)mm。结论 :两种切口各有优缺点 ,T形切口适应证稍广 ,但易损伤周围重要结构。     

骨性内耳道的解剖学观测

目的为内耳道手术定位提供解剖学依据。方法对400块颞骨的内耳道及其有关结构进行解剖观察和测量。结果内耳道与岩大神经管裂孔、弓状隆起等结构有较恒定的位置关系。内耳道底投影点至岩大神经管裂孔的距离,在左侧为8．85mm,在右侧为7．95mm;至弓状隆起最高点的距离在左侧为7．89mm,右侧为88．50mm,内耳道上壁长左侧为8．41mm,右侧为8．61mm。结论岩大神经管裂孔、弓状隆起等颞骨岩部结构是定位内耳道的重要标志。内耳道手术应避免损伤上半规管,耳蜗等结构。     

脑桥小脑三角的应用解剖学

目的为听神经瘤显微外科治疗提供解剖学参数.方法对35具甲醛固定的男性成人尸颅的脑桥小脑三角及毗邻结构进行解剖学测量.结果横窦乙状窦膝至内耳门后缘的距离约为(35.1±0.2)mm.乙状窦起始端最大宽为13.4 m.内耳门后缘至内淋巴囊裂孔的距离为(10.5±0.2)mm,内耳门至岩上窦的距离通常小于5 mm.内耳门至颈静脉孔的距离为5.4 mm.横窦乙状窦膝在小脑表面对应的膝点至绒球外侧缘的距离左侧为(31.3±0.5)mm,右侧为(30.4±0.5)m;至扁桃体内侧缘的距离左侧为(44.1±0.4)mm,右侧为(43.3±0.4)mm.结论这些数据是重要的解剖参数,是保证手术顺利进行、不损伤重要结构的解剖学依据.     

儿童颞骨岩部解剖学特征

目的 :了解儿童颞骨岩部的解剖特点 ,以利于儿童岩部的手术。方法 :对 8例 5～ 7岁的儿童头颅颞骨进行了骨性标志、面神经的走行、半规管的相对位置的观察 ,同时对 6例成人头颅进行了比较性的观察 ,测量了有关数据。结果 :儿童颞骨气房发育较成人差 ;65 %儿童后半规管下脚平面神经垂直段的中点 ,水平半规管更向下倾斜 ;岩部的上下径、面神经垂直段较成人短 [(3 6.3± 2 .6) <(4 5 .1± 3 .2 ) ]mm、[(9.3± 1.2 ) <(13 .9± 2 .3 ) ]。结论 :儿童颞骨结构与成人有较大区别 ,乳突部气房形成与否对半规管的位置影响较大 ;儿童经岩部手术应考虑到这些区别。     

经颞骨岩部乙状窦前入路处理岩斜区病变的应用解剖

目的 :研究经颞骨岩部乙状窦前入路进行岩斜区直接手术的方法 ,寻找出该入路的标志点和颞骨岩部的磨除方法 ,并观察手术的暴露范围和优缺点。方法 :用 15例血管经彩色乳胶灌注的成人尸头标本 ,显微镜下 (× 6～ 2 5 )解剖经颞骨岩部乙状窦前入路。结果 :岩乙状窦交叉点、内淋巴囊裂是磨除颞骨岩部后面的重要标志 ,用内淋巴囊裂可以初步定位前庭小管、总脚和后半规管。此入路能够暴露从鞍背到延髓中上部的区域 ,以暴露中岩斜区最佳。离断内淋巴囊 ,可扩大骨磨除的面积 ,增加手术的暴露。结论 :以岩乙状窦交叉点、内淋巴囊裂为标志为安全磨除颞骨岩部后面提供了保证。经颞骨岩部乙状窦前入路具有手术距离短、视野暴露充分的特点 ,特别适用于骑跨颅中、后窝而以颅后窝为主的岩斜区病变     

后鼓室手术入路的应用解剖学研究

目的　为后鼓室入路手术提供解剖学依据。方法　利用成人 6 0侧颞骨标本 ,用牙科钻磨开乳突腔 ,打开外耳道外侧壁和鼓室盾板 ,充分暴露后鼓室入路手术中有关的解剖结构。以外耳道上棘、面神经管锥曲为测量标志 ,在手术显微镜下 ,对在手术中遇到的解剖结构之间的距离进行了测量。结果　外耳道上棘至砧骨窝、锥隆起、鼓索隆起、面神经管锥曲、外侧半规管、后半规管、前庭窗、蜗窗、匙突、乙状窦垂直部前缘中点、窦膜角的距离分别是 17 19、18 0 2、15 2 2、14 4 9、15 39、17 35、19 5 8、2 0 0 9、2 0 32、15 6 8、18 76mm。面神经管锥曲至鼓索隆起、水平半规管、后半规管的距离分别是 3 33、1 5 3、2 15mm。结论　外耳道上棘、面神经管锥曲是后鼓室入路的重要手术标志 ,鼓索隆起向内 3mm是手术入路的安全区 ,面神经减压术时应避免损伤水平半规管及后半规管等结构     

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.