利他林对注意缺陷多动障碍患儿注意能力影响的ERP研究

目的:探讨注意缺陷多动障碍(ADHD)患儿的视觉空间注意刺激诱发的事件相关电位(ERP)特征,并研究利他林(MPH)对其影响。方法:采用有效提示、无效提示刺激模块对22名ADHD患儿和22名年龄匹配的正常儿童进行ERP检测和记录其行为学表现。ADHD患儿在服MPH前和服MPH后2 h分别接受两次ERP检测。结果:与正常对照组相比,ADHD组在服MPH前,额部N2波潜伏期显著延长(P<0．05),各导联P2、N2波波幅显著降低(P<0．05);服MPH后2 h额部N2波潜伏期显著缩短(P<0．05),各导联波幅显著增高(P<0．05);服MPH后2 h各导联P2、N2波的潜伏期及波幅与正常对照组比较差异无显著意义(P>0．05)。结论:视觉空间注意ERP可以客观检测ADHD患儿注意缺陷的存在及程度,为临床诊断和评价MPH疗效提供了客观依据。     

注意缺陷多动障碍儿童服用单剂量哌甲酯后脑电α波的变化

目的:通过观察注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)儿童服用单剂量哌甲酯后其脑电α波的变化,及其用药后是否达到正常水平,探讨ADHD的神经病理机制.方法:本研究为自身对照研究.所有ADHD儿童来自于北京大学精神卫生研究所门诊,正常儿童来自北京大学精神卫生研究所附近学校,各110例.应用脑电超慢涨落分析技术(encephaloflutuographtechnology,ET) ,对符合DSM-Ⅳ中ADHD 诊断的患儿在服用哌甲酯前及服药后(10 mg)2 h 及性别、年龄与之匹配的健康对照的脑电信号进行分析处理.结果:(1)用药后:主频明显变快[(8.97±0.94)Hz vs.(9.40±0.99)Hz ,P=0.000];各导联8 Hz优势几率明显下降[(27.08±13.04)%vs.(23.50±13.66)%,P<0.05];全脑10 Hz平均优势几率呈上升趋势[(28.83±14.90)% vs.(30.64±16.66)%,P=0.06];全脑11 Hz平均优势几率明显上升[(12.35±10.50)% vs.(13.90±12.73),P=0.047];全脑平均熵值(Qm)明显降低 [(0.72±0.11)vs.(0.69±0.12),P<0.001].(2)用药后,主频仍明显低于健康对照 [(9.40±0.99)Hz vs.(9.67±0.92)Hz,P<0.001],8 Hz全脑平均优势几率仍高于健康对照 [(23.50±13.66)% vs.(18.19±12.27)%,P<0.001],10Hz各脑区平均优势几率与健康对照差异无统计学意义[(30.64±16.66)% vs.(34.24±17.13),P>0.05],总熵值仍明显高于健康对照 [(0.69±0.12)vs.(0.65±0.11),P<0.05].结论:通过观察ADHD患儿单次服用哌甲酯前后两种状态脑功能的变化,提示单剂量哌甲酯可使ADHD患儿脑电图趋向正常,可使其脑有序度提高、低功效状态改善.     

注意缺陷多动障碍儿童在不同情绪面孔刺激下的持续注意任务事件相关电位

目的:了解不同情绪面孔刺激下注意缺陷多动障碍(ADHD)患儿执行持续注意任务时的事件相关电位特征。方法:选取符合美国精神障碍诊断与统计手册第4版(DSM-IV)诊断标准的混合型ADHD患儿32例(年龄9~15岁)及年龄、性别匹配的正常对照组儿童32例,要求被试在高兴、中性、恐惧和愤怒等4种情绪面孔刺激随机呈现后执行注意与选择任务,同时记录事件相关电位。观察ADHD患者和正常对照组儿童面孔诱发的N170电位及靶刺激诱发的P300电位的特征。结果:ADHD组患儿在4种不同情绪面孔刺激下颞枕区面孔特异性N170波波幅均低于对照组[如恐惧面孔,(17.7±9.5)μv vs.(25.8±14.0)μv,P0.05],顶枕区P300潜伏期长于对照组[如恐惧面孔,[(454.2±51.3)ms vs.(433.0±29.8)ms,P0.05]。ADHD患儿组在四情绪面孔诱发的N170波幅和潜伏期差异无统计学意义(P0.05),诱发的P300在四种情绪刺激中以恐惧面孔刺激后执行注意任务的P300波幅最低,潜伏期最长。结论:ADHD儿童在4种不同情绪面孔刺激下,以恐惧面孔刺激引起的P300波幅最低,且P300潜伏期延长最明显。提示恐惧面孔可能影响ADHD患儿情绪调节,并影响其持续注意过程。     

正常儿童视觉空间注意ERP的研究

目的：研究正常儿童空间视觉注意刺激诱发的事件相关电位（Event-Related Potentials ERP）的特征.方法：采用有效提示、无效提示刺激模块（即Posner Cue）对30名8岁儿童进行检测.刺激信号同步触发,数字化脑电图（EEG）同步记录,使用德国的Besa软件从中提取ERP进行分析.结果：同一导联脑枕后部同一导联有效提示的N1、P2波幅大于无效提示（P＜0.05）,潜伏期无差异（P＞0.05）;脑顶前部有效提示的P1波幅大于无效提示,N1波幅则小于无效提示（P＜0.05）,潜伏期无差异（P＞0.05）;脑顶前部导联的N1潜伏期长于枕后部导联（P＜0.05）.结论：处理有效刺激的投入大收益也大,处理无效刺激的投入小收益也小,但儿童易受差异信息的干扰使得收益发生改变：二者的处理时程相似.     

精神分裂症患者事件相关电位N2-P3的波幅及潜伏期研究

目的:通过追踪观察精神分裂症患者治疗前后事件相关电位(ERP)检测靶刺激N2-P2峰峰波幅及N2-P3峰峰潜伏期的变化情况,进一步探讨其深入意义。方法:对71例正常对照组和71例首发或复发但停药半年以上的精神分裂症患者在药物治疗前及42例患者在瑞思哌酮(维思通)治疗1、3、6个月后分别进行ERP检测,以及进行阳性和阴性综合征量表(PANSS)评定。ERP检测仪器采用美国NicoletBravo脑电生理仪。结果:患者组治疗前与对照组比较N2-P3峰峰波幅减小,并且在Cz、Pz点记录的N2-P3波幅两组间比较差异有统计学意义(P&lt;0.01或P&lt;0.05),N2-P3峰峰潜伏期两组间比较差异则无统计学意义(P&gt;0.05)。维思通治疗后Fz、Cz、Pz三个记录点记录的N2-P3峰峰波幅无明显改变(P&gt;0.05),但N2-P3峰峰潜伏期增大,并在Fz、Pz点记录的N2-P3潜伏期两组间比较差异有统计学意义(P&lt;0.01)。治疗6个月后N2-P3峰峰波幅及N2-P3峰间潜伏期的减分率与PANSS分的减分率无相关性(P&gt;0.05)。结论:N2-P3峰峰波幅可能是精神分裂症的属性指标,虽目前尚不能用作临床诊断指标,但可试用于...     

特质焦虑人群应激条件下ERP中P3的变化

目的：探讨不同特质焦虑大学生应激条件下的ERP特点。方法：以大学英语四级考试为应激源，应用特质-状态焦虑量表在200名考生中，筛选高特质焦虑和低特质焦虑各15人，使用NeuroScan 32 Channel ERP System观察应激期和应激后P3变化。结果：①低特质焦虑组应激后P3波幅大于应激期（P〈0．05），潜伏期小于应激期。②高特质焦虑组应激期和应激后相比，P3波幅、潜伏期无变化。③应激时，高、低特质焦虑组P3波幅、潜伏期无明显差异。④应激后，低特质焦虑组P3波幅大于高特质焦虑组、潜伏期小于高特质焦虑组（P〈0．05）。结论：高、低特质人群的P3差异提示不同人格特质群体在相同应激事件中，认知功能有差异。     

阿米替林治疗无效的抑郁症患者P_(300)研究

目的：探讨抑郁症患者在治疗前后P３００特点及其变化。方法：比较25例抑郁症和25例正常对照者P３００的测量数值，并根据临床疗效分为阿米替林治疗有效和治疗无效组，用配对t检验比较治疗前后P３００成分变化。结果：抑郁症与对照组比较，N２潜伏期延长(P＜005)，P３潜伏期延长(P＜001)，P3波幅降低(P＜001)，治疗无效组治疗后比治疗前P３波幅增高(P＜005)，P３潜伏期未见明显差异，治疗有效组治疗后P３潜伏期显著缩短(P＜001)，波幅增高，但无显著性。讨论：P３００主要成分的异常，反映了抑郁症患者认知功能存在障碍，并可用其作为评定抑郁症疗效的参考指标。     

强迫症患者GO/NOGO任务的事件相关电位研究

目的:探讨强迫症患者执行GO/NOGO任务时所诱发的事件相关电位(ERPs)特点,初步探讨GO/NOGO任务所诱发的ERP成分与脑反应抑制过程的关系.方法:记录22名强迫症患者和21名正常对照在执行线索引导的视觉GO/NOGO任务时诱发的ERPs.该任务序列包括400个刺激,需要被试作出反应的GO刺激及需要被试抑制反应的NOGO刺激各占10%.结果:强迫症患者在GO任务中的平均反应时长于正常对照组(351.0±56.8/307.1±53.5 ms,t=2.605,P=0.013),但反应错误数与正常对照组差异不显著(2.5±2.3/1.5±1.7,t=1.626,P=0.112).强迫症患者的GO-P3波幅与对照组差异无统计学意义(P＞0.05),但NOGO-P3波幅在FZ、FCZ、FC3、FC4点较对照组降低(16.0±7.6/20.1±5.7,19.2±8.6/24.7±6.3,14.6±6.3/18.4±5.6,15.7±6.8/20.8±5.7,t=-2.01～-2.65,均P＜0.05),强迫症患者的GO/NOGO-P3潜伏期与正常对照组差异无统计学意义(P＞0.05).强迫症患者颅脑电位分布范围小于正常对照,其中以NOGO任务额区脑电活动减弱为明显.结论:强迫症患者GO/NOGO任务所诱发的事件相关电位表现异常.NOGO-P3可能是反应额叶反应抑制过程的重要成分.     

哌甲酯控释剂对注意缺陷多动障碍儿童抑制功能的影响

目的:探讨哌甲酯控释剂对注意缺陷多动障碍(Attention Deficit/Hyperactivity Disorder,ADHD)儿童临床症状、不同维度(操作性神经心理测查和生态学)抑制功能的影响以及临床症状改善与不同维度抑制功能改善之间的关系.方法:采用自身对照研究,对符合DSM-IV诊断标准的28名ADHD患者[年龄(10.8±1.8)岁],使用哌甲酯控释剂(18～54mg/d)治疗4～6周,以ADHD症状评定问卷(父母问卷)为主要临床疗效评价指标,以自编的计算机版本的Go/No Go任务评定ADHD患者操作性神经心理测查的抑制功能,以执行功能行为评定量表(BRIEF)中的抑制因子得分评价ADHD患者生态学抑制功能的情况.结果:经哌甲酯控释剂治疗后,ADHD患者临床症状的总分[(32.8±9.2) vs. (20.7±11.9)],注意缺陷[(18.6±4.1) vs.(11.5±6.1)]及多动冲动评分[(14.2±6.6) vs. (9.1±6.6)]、Go/No Go任务虚报数[(22.0±10.9) vs. (14.8±10.4)],以及BRIEF量表中抑制因子的得分[(2.0±0.5) vs. (1.7±0.4)]较服药前均显著下降(P<0.05);相关性分析发现,ADHD注意缺陷分的改善率与Go/No Go任务虚报数的改善率呈正相关(r=0.42,P<0.05),多动冲动症状的改善率与BRIEF量表中抑制因子的改善率呈正相关(r=0.50,P<0.01).结论:哌甲酯控释剂能有效地改善ADHD患者的临床症状及不同维度的抑制功能.BRIEF量表中抑制因子得分的改善与ADHD多动冲动症状的改善相关,操作性神经心理测查的执行功能测定是对临床实践的必要补充.     

哌甲酯治疗后注意缺陷多动障碍核心症状与执行功能改善的关系

目的:探索哌甲酯治疗对注意缺陷多动障碍(ADHD)患者核心症状与执行功能改善的关系。方法:选取85例符合美国精神障碍诊断与统计手册第4版(DSM-IV)ADHD诊断标准的门诊患儿,用哌甲酯控释剂开放治疗,经1～3周的剂量调整,以最适剂量继续治疗4周。采用ADHD评定量表(ADHD-RS-IV)评估核心症状,操作性测查Stroop色词命名测验、Rey复杂图形记忆任务、数字广度、汉诺塔任务、连线测验、言语流畅性和生态学行为评定量表(BRIEF)评估执行功能,分析ADHD-RS-IV减分与执行功能改善分的相关关系。结果:ADHD-RS-IV总分和分量表减分与Rey复杂图形记忆任务延迟结构得分改善分呈低度相关(r=0.19～0.24,均P0.05);与BRIEF量表减分呈低至中度相关(r=0.19～0.66,均P0.05),注意缺陷分量表减分与BRIEF量表的总分、元认知指数(MI)及4个因子减分、BRI及抑制因子减分呈中度相关(r=0.51～0.69,均P0.05),多动冲动分量表减分与BRIEF量表的BRI及抑制因子和中度相关(r=0.54～0.64,均P0.05)。结论:哌甲酯治疗后ADHD核心症状与执行功能的改善存在相关关系。     

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.