子痫前期患者外周及胎盘血循环中瘦素水平的比较

目的探讨妊娠期高血压疾病子痫前期患者血中瘦素水平的变化,及胎盘在这一变化中的作用.方法行剖宫产时,取孕妇肘前静脉及胎盘附着部位子宫静脉血.其中妊娠期高血压疾病子痫前期患者(研究组)15例,正常妊娠妇女(对照组)20例.应用放射免疫分析法测定血清瘦素水平.结果研究组外周血瘦素水平为23.29±3.32μg/L,对照组为13.87±1.24μg/L,两组比较差异有极显著性(P<0.01).研究组子宫静脉血瘦素水平为16.44±2.23μg/L,对照组为11.2±0.94μg/L,两组比较有显著性(P<0.05).研究组外周血和子宫静脉血比较有极显著性(P<0.01).对照组外周血和子宫静脉血比较有极显著性(P<0.01).结论妊娠期高血压疾病子痫前期患者外周血瘦素水平高于正常妊娠,提示瘦素可能参与妊娠期高血压疾病的发病.妊娠期高血压疾病子痫前期患者子宫静脉血瘦素水平高于正常妊娠,提示妊娠期高血压疾病患者胎盘中瘦素的合成增加.妊娠期高血压疾病子痫前期患者及正常妊娠孕妇外周血瘦素水平均高于子宫静脉血,提示胎盘只是正常妊娠孕妇及妊娠期高血压疾病患者血中瘦素增加来源之一.     

可溶性血管内皮生长因子受体-1的mRNA在妊娠高血压胎盘组织中的表达及意义

目的探讨妊娠高血压疾病患者中可溶性血管内皮生长因子受体-1mRNA在胎盘组织中的表达。方法23例妊娠高血压疾病孕妇(其中妊娠期高血压7例,轻度子痫前期3例,重度子痫前期9例,子痫4例)为妊娠高血压疾病组,足月妊娠血压正常孕妇作为对照组。应用半定量逆转录-聚合酶链反应(RT-PCR)技术检测两组孕妇分娩后胎盘组织中sF lt-1的表达强度。结果妊娠高血压疾病组sF lt-1mRNA(1.45±1.47),与对照组(1.04±0.69)比较,差异无显著性(P>0.05)。子痫组(2.99±2.47),明显高于对照组(P<0.01)。结论sF lt-1是维持正常妊娠所必需的因子。它表达水平的高低与妊娠高血压的发病相关,在子痫患者它的表达明显增高。     

sICAM-1在妊娠期高血压疾病患者的变化和临床意义

目的探讨可溶性细胞间粘附分子-1(sICAM-1)在妊娠期高血压疾病(HDCP)患者血浆中的变化及其临床意义。方法研究对象包括33例妊娠期高血压疾病患者(其中子痫前期13例、妊娠期高血压20例),20例正常妊娠妇女(均为孕32-35周)和25例正常未孕妇女,应用酶联免疫吸附试验(ELISA)测定各组研究对象血浆中的sICAM-1水平。结果 sIACM-1未孕组443.68±235.17ng/ml,正常妊娠组664.67±287.33 ng/ml,两者性比差异有统计学意义(P<0.05);与正常妊娠组比较,妊娠期高血压组1145.46±326.67 ng/ml,差异有统计学意义(P<0.05);子痫前期组1402.89±354.67 ng/ml,明显高于正常妊娠组,差异均具有统计学意义(P<0.01);与妊娠高血压组比较差异有显著性(P<0.05)。结论外周血中sICAM-1水平变化与妊娠期高血压疾病(HDCP)密切相关,随着病情加重sICAM-1值明显升高,提示sICAM-1水平上调与妊娠期高血压疾病的发生有关。     

孕妇红细胞叶酸水平与妊娠期高血压疾病的发病关系

目的探讨孕妇红细胞叶酸水平与妊娠期高血压疾病的发病关系。方法选择2007年9月至2008年12月在北京市海淀区妇幼保健院行常规产检的孕妇作为研究对象,初检孕周12～15w,其中妊娠期高血压孕妇组33例(轻度子痫前期26例,重度子痫前期7例),对照组(正常妊娠组)462例;在孕妇初诊时抽取外周血检测红细胞叶酸水平,比较组间叶酸水平有无差异。结果①妊娠期高血压疾病组红细胞叶酸水平(601.10±153.26)nmol/L,对照组红细胞叶酸水平为(608.23±222.67)nmol/L,两组比较,差异无显著性。②轻度子痫前期孕妇组红细胞叶酸水平(605.01±200.36)nmol/L,与对照组比较,差异无显著性;重度子痫前期孕妇组红细胞叶酸水平(512.30±122.34)nmol/L,与对照组比较,差异有显著性(P<0.05)。结论妊娠期补充叶酸可能降低妊娠期高血压疾病的发生或者减轻妊娠期高血压疾病的病情严重程度。     

细胞因子IL-6及TNF-α在妊娠期高血压风险预测价值中的研究

目的探讨联合检测孕妇外周血中细胞因子(cytokines)白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)的表达水平对妊娠期高血压发病风险的预测价值。方法选择妊娠期高血压患者30例(子痫前期患者24例)为妊娠期高血压组,同期正常中、晚孕产检孕妇36例为对照组。采用流式荧光法检测两组孕妇外周血清中IL-2、IL-4、IL-6、IL-10、TNF-α和γ干扰素(IFN-γ)的表达水平,分析各细胞因子在两组患者中表达水平的差异及意义,并采用多因素Logistic回归方法分析各细胞因子表达水平与妊娠期高血压及子痫前期发病风险的相关性。结果妊娠期高血压组患者外周血中IL-6、TNF-α水平分别为18.29±19.47 pg/mL、9.92±11.04 pg/mL,正常组孕妇外周血中IL-6、TNF-α的表达水平分别为4.91±0.73pg/mL、4.28±0.51pg/mL,经统计学分析,两组IL-6、TNF-α水平相比较,差异均有显著性意义(P0.05)。而两组其它细胞因子水平相比较则均无显著性差异(P0.05)。采用多因素logistic回归分析显示细胞因子IL-6、TNF-α表达水平增高均是影响妊娠期高血压发生风险的独立因素。同时,依据上述分析结果,建立了在中、晚孕期联合检测孕妇外周血中细胞因子IL-6、TNF-α水平来预测妊娠期高血压发生概率的模型。结论孕、中晚期联合检测细胞因子IL-6、TNF-α表达水平在妊娠期高血压风险预测中具有较高价值。     

瘦素、脂联素与TNF-α在子痫前期患者血清中的表达及相关性研究

目的检测子痫前期患者血清瘦素、脂联素及TNF-α的表达并探讨TNF-α与瘦素、脂联素的相关性。方法采用酶联免疫吸附法(ELISA)检测44例子痫前期患者及24例正常孕妇血清中瘦素、脂联素及TNF-α的表达水平。结果(1)轻、重度子痫前期患者血清瘦素水平分别为4308.60±378.83pg/ml、4476.39±115.18pg/ml,明显高于对照组4041.97±455.39pg/ml,差异有统计学意义(P<0.05,P<0.01);(2)轻度、重度子痫前期患者血清TNF-α水平分别为73.33±57.91pg/ml及538.50±551.25pg/ml,明显高于对照组62.89±82.85pg/ml,而血清脂联素水平分别为8.06±5.06pg/ml、5.28±1.47pg/ml,明显低于对照组12.73±2.90pg/ml,重度组与对照组之间的差异有统计学意义(P<0.05);(3)重度组瘦素与TNF-α成正相关(r=0.478),脂联素与TNF-α成负相关(r=-0.536),轻度组及对照组中TNF-α与瘦素、脂联素均无相关性。结论瘦素、脂联素及TNF-α参与子痫前期的发病,且TNF-α可以调节瘦素及脂联素的水平。     

孕前BMI和孕期血浆同型半胱氨酸对妊娠高血压疾病的影响

目的研究孕前体重指数和孕期血浆同型半胱氨酸水平对妊娠高血压疾病发生的影响。方法研究对象为56例妊娠高血压疾病的单胎初产妇(病例组)及56例孕晚期正常妊娠单胎初产妇(对照组),用荧光偏振免疫分析法检测其血浆同型半胱氨酸水平,并统计两组孕妇孕前年龄、孕周、身高、体重并分析其BMI。结果妊娠高血压疾病组血浆同型半胱氨酸水平(13.61±5.3)μmol/L,明显高于正常妊娠组(11.14±3.31)μmol/L,差别有统计学意义(P﹤0.05)。病例组体重指数(BMI)(23.68±2.82)kg/m2,也明显高于对照组(22.60±2.6)kg/m2,差别有统计学意义(P﹤0.05)。结论孕前体重指数、血浆同型半胱氨酸水平偏高可增加妊娠高血压疾病的发生风险,早期检测血浆同型半胱氨酸水平可预测妊娠高血压疾病的发生。     

较小剂量~(131)I联合中药治疗Graves病后血清sFas/sFasL变化及其与TRAb关系的探讨

目的:探讨Graves病(GD)用较小剂量131I联合中药治疗前后血清sFas/sFasL(可溶性细胞凋亡因子-1 /sFas配体)变化的规律及其与TRAb的关系。方法: 31例GD患者,用较小剂量131I(85 1~207 2MBq,平均140 6MBq)联合中药进行治疗,用酶联免疫吸附试验(ELISA)检测GD患者治疗前及治疗后不同时期血清sFas与sFasL含量,求出sFas/sFasL,并与正常对照组对比,分析GD患者血清sFas和sFasL含量,求出sFas/sFasL,并与正常对照组对比,分析GD患者血清sFas和sFasL与TRAb的相关关系。结果:①GD患者治疗前sFas(179. 8±64. 2)pg/ml明显高于临床治愈期(104. 2±23. 5)pg/ml,P<0 05和正常对照组(110 6±18. 1)pg/ml,P<0 05,甲低时的sFas(117 0±20. 6)pg/ml与正常对照比无显著性差异。sFasL治疗前(353 8±92 8)pg/ml同样明显高于临床治愈期(261 1±85 3)pg/ml,P<0 05和正常对照组(265 6±62 1)pg/ml,P<0 05。甲低时的sFasL(257 1±55 3)pg/ml与正常对照比无显著性差异。②GD患者治疗前的sFas/sFasL(0 51±0 23)和甲低时(0 46±0 13)皆大于正常对照( 0 41±0 16,P<0 05 )。sFas和sFasL皆与TRAb呈正相关(r分别为0 52和0 49,P<0. 05)。③较小剂量131I联合中药治疗GD近期疗效良好,有效率100% (31 /31),一次性治愈率74 2% (23 /31),总治愈率8     

外周血中血管内皮生长因子、内皮抑素水平与流产发病的关系

目的通过检测外周血中血管内皮生长因子（vascular endotrelial growth factor,VEGF）、内皮抑素（endostatin,ES）浓度水平,探讨与先兆流产、难免流产发病的关系。方法（1）取90例孕妇外周血,其中正常妊娠要求流产组30例;先兆流产组30例;难免流产组30例。（2）清宫或治疗前采集前臂肘静脉血3ml,离心取血清于-70℃保存待测。（3）采用酶联免疫吸附测定法（ELISA）检测血清中血管内皮生长因子、内皮抑素的浓度水平。结果（1）血清VEGF浓度先兆流产组为（153.7±48.3）pg/ml,明显高于正常妊娠要求流产组的（39.7±22.8）pg/ml和难免流产组的（86.3±27.5）pg/ml,差异均有显著性（P〈0.01,P〈0.05）。（2）血清ES浓度先兆流产组为（46.3±26.4）ng/ml,明显高于正常妊娠要求流产组的（10.8±4.5）ng/ml和难免流产组的（23.4±10.7）ng/ml,差异均有显著性（P〈0.01,P〈0.05）。（3）在先兆流产组、难免流产组和正常对照组中,血管内皮生长因子与内皮抑素之间存在关联关系,呈显著正相关（r=0.560P〈0.05;r=0.563P〈0.05;r=0.572P〈0.05）。结论VEGF、ES水平变化反应了不良妊娠的不同结局,两者共同参与了先兆流产及难免流产的发生和发展。     

肾病综合征型妊娠期高血压疾病临床分析

目的探讨肾病综合征型高血压疾病的发病特点及对孕妇和胎儿的影响。方法回顾性分析9例肾病综合征型高血压疾病(肾病组)和52例重度子痫前期(对照组)的临床资料。结果NSP占分娩总数的0.024%,占重度子痫前期的14.75%。肾病组血浆白蛋白、胆固醇、围产儿死亡及FGR发生率两组均有极显著性差异(P<0.01),两组之间收缩压、总蛋白、肌酐、尿素氮的差异有显著性(P<0.05)。但是发病孕周、终止妊娠周数、病程、发病年龄、舒张压、腹水及重度水肿的发生率无显著性差异(P>0.05)。结论肾病综合征型妊娠期高血压疾病对母婴影响大,适时终止妊娠可减少妊娠期并发症和围产儿发病率及死亡率。     

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.