模拟心室驱动曲线变化对机械瓣流体动力学性能影响

目的 研究在生理条件下模拟心室驱动曲线变化对机械瓣流体动力学性能的影响,为合理评价机械瓣流体动力学性能提供实验依据. 方法 采用脉动流模拟循环装置,设定模拟心输出量为4 L/min,模拟心率为75次/分,观察5种心室驱动曲线对机械瓣平均跨瓣压差（△P）、有效瓣口面积（EOA）、关闭量（CLV）和泄漏量（LKV）的影响. 结果 生理范围内,心室驱动曲线形态上的改变,对测试瓣膜的△P可产生2.9%的变异,EOA的变异为1.5%,CLV为6.6%,LkV为3.6%. 结论 机械瓣的流体动力学性能受心室驱动曲线的影响,从而对瓣膜流体动力学性能评价的客观性和可比性产生不利作用.     

基于二尖瓣时变电阻模型的左心血液循环系统建模与仿真

改善传统血液循环系统数值仿真研究中关于二尖瓣流量的模拟仿真,充分考虑二尖瓣反流的客观存在性,并对二尖瓣动力学特性及二尖瓣运动在血液循环中的影响作用进行深入研究。根据血液动力学和电学网络的等效关系,提出基于时变电阻的二尖瓣电路模型,同时考虑血液在左心室的惯性及二尖瓣闭合的滞后性,建立改进型的左心血液循环系统等效电路模型。根据电学分析原理,求得该等效电路的状态微分方程数学模型。应用Matlab对数学模型进行建模仿真,结果得到更加符合生理要求的二尖瓣流量仿真曲线。二尖瓣流量分为3部分：舒张期的正向流量、收缩期关闭反流量和泄漏反流量。并且,二尖瓣流量充满心脏舒张的整个时期。在收缩期,可以明显看到正常反流延迟二尖瓣跨瓣压差,时间为50~80 ms。该研究揭示了二尖瓣在收缩期闭合速度和闭合质量对二尖瓣反流流量的影响。     

应用经食管实时三维超声评价缺血性二尖瓣反流及瓣叶形态功能变化的研究

目的应用经食管实时三维超声(RT-3D-TEE)和二尖瓣立体结构定量(MVQ)分析软件,对缺血性二尖瓣反流(IMR)的二尖瓣瓣环及瓣叶功能进行评价,筛选出对IMR机制有意义的参数。方法 25例IMR组患者,其中男性14例,女性11例;年龄41~72岁,平均年龄41.7岁。20例正常对照组,其中男性11例,女性9例;年龄37~69岁,平均年龄38.6岁。行RT-3D-TEE技术对2组患者进行检查,应用MVQ分析软件测量并分析2组二尖瓣瓣环及瓣叶几何形态学参数变化特点。结果 IMR组反流容积(46±11)m L,有限反流口面积(0.31±0.12)cm2,说明IMR组存在中度反流。与正常对照组相比,IMR组反映二尖瓣瓣环解剖结构参数如瓣环前外侧交界到后内侧交界的距离(DAIPm)、前叶瓣环中点到后叶瓣环中点的距离(DAP)、瓣环三维周长(C3DE)、绕环最小表面面积(A3Dmin)、环的椭圆度(E2D)及二尖瓣帆状区容积(Vtent)均有所增加(P﹤0.05);瓣环最高点所在平面与最低点所在平面的高(H)、环高度与联合直径的比率(H/DAIPm)、前后瓣叶对合的参数投影平面中的结合长度(L2DAIPm)及前后叶关闭时对合线的长度(LC3DLf)均有所减低(P﹤0.05)。与正常对照组相比,IMR组前小叶角度(θant)、后小叶角度(θpost)及小叶非平面角度(θnpa)未见明显变化。结论通过RT-3D-TEE能够为缺血性二尖瓣反流患者提供局部二尖瓣瓣环功能或形态异常的量化指标,为临床医生选择个性化治疗方案和疗效评价提供了依据。     

超声心动图评价重度子痫前期孕妇左室形态和功能的临床意义

目的评价重度子痫前期患者左室形态及功能变化,并探讨二尖瓣舒张早期E波峰值流速与舒张早期二尖瓣环心肌运动峰值速度之比(E/Ea)、收缩期二尖瓣环心肌运动峰值速度(Sa)评价重度子痫前期患者早期左室功能异常的临床意义及其与N-端脑利钠肽前体(NT-pro BNP)的相关性。方法 36例重度子痫前期患者和51例血压正常孕妇(对照组)。运用超声心动图测量左室形态参数,包括舒张末期左室前后径(LVDd)、舒张末期室间隔厚度(IVSd)、舒张末期左室后壁厚度(LVPWd);运用超声心动图测量左室功能参数,包括射血分数(LVEF)、二尖瓣瓣口舒张早期E波峰值流速与舒张晚期A波峰值流速比值(E/A)、收缩期二尖瓣环左室侧壁处心肌运动峰值速度(Sa),舒张早期二尖瓣环左室侧壁处心肌运动峰值速度(Ea),计算E与Ea比值(E/Ea)。同时检测血浆N-端脑利钠肽前体浓度。结果与对照组比较,重度子痫前期组左室形态各参数均明显增加,差异有统计学意义(P0.01);重度子痫前期组Sa明显降低,E/Ea明显增大,差异有统计学意义(P0.01),E/A减小,差异有统计学意义(P0.05)。NT-pro BNP与E/Ea呈正相关(r值为0.58,P0.05);NT-pro BNP与Sa呈负相关(r值为-0.69,P0.05)。结论重度子痫前期患者可以导致左室形态和功能发生变化,应用超声心动图测量E/Ea、Sa与NT-pro BNP相关性良好,可以作为评价左室功能的早期指标,     

可吸收羟基磷灰石/聚DL-乳酸骨折内固定材料机械强度和生物降解性研究

目的评价自行研制的可吸收羟基磷灰石/聚DL-乳酸(HA/PDLLA)复合骨折内固定材料的机械强度和生物降解性。方法体外降解实验是把相同分子量的HA/PDLLA和单纯PDLLA试件分别置于PBS缓冲液中,于2、4、6、8、10、12周取材,测试生物降解率、吸水率、失重率、机械强度及降解液pH值,并作扫描电镜(SEM)观察;体内实验是用一枚HA/PDLLA棒内固定兔股骨髁松质骨部横形截骨,作X线摄片、组织学、机械强度及材料骨界面SEM观察。结果HA/PDLLA复合材料较单纯PDLLA材料降解速度减慢,机械强度提高,骨折正常愈合。结论HA/PDLLA材料具有足够的强度保证实验性松质骨骨折正常愈合。     

小主动脉瓣环188例患者人工机械瓣换瓣术后疗效观察

目的回顾性分析188例成年人小主动脉瓣环(瓣环直径≤21 mm)人工机械瓣膜置换术后患者的疗效及心功能的变化,探讨3种机械瓣替换术后是否存在植入瓣膜与患者不匹配(PPM)现象。方法选择南京中医药大学附属医院心胸外科188例植入小主动脉瓣环(直径16~21 mm)成年患者(占所有主动脉瓣置换患者的45.83%),其中男性96例,女性92例;年龄17~72岁,平均年龄51.12岁。主动脉瓣二叶畸形10例,单纯主动脉瓣狭窄27例,单纯主动脉瓣关闭不全46例,二尖瓣联合主动脉瓣病变96例,感染性心内膜炎9例;其中20例置换17 mm SJ Regent机械瓣,45例置换19 mm SJ Regent机械瓣,30例置换21 mm SJ Regent机械瓣,31例置换Carbio-S 19 mm机械瓣,20例置换Carbio-S21 mm机械瓣,10例置换16 mm over-line Sorin机械瓣,16例置换18 mm over-line Sorin机械瓣,16例置换20 mm overline Sorin机械瓣。采用彩色多普勒超声心动图分别于术前、术后1周、术后3个月和1年,检测患者的左心室舒张末期内径、收缩末期内径、室间隔及左心室后壁厚度、左心室射血分数(LVEF)、左心室短轴缩短率(LVFS)和主动脉瓣跨瓣压差的变化,观察左心室质量指数变化情况,并进行各组比较分析。结果全组患者无手术死亡,围术期死亡2例,术后1年内不明原因猝死3例,其余183例患者均随访1年以上。参考各瓣膜厂家提供的有效瓣口面积指数(EOAI),该研究组无重度PPM,所有患者EOAI均大于0.65 cm~2/m~2,EOAI在0.65~0.85 cm~2/m~2(中度PPM)患者占35.14%,EOAI0.85 cm~2/m~2占64.86%,EOAI与主动脉瓣跨瓣压差之间无明显相关性;术后所有患者心功能均较术前提高2~3级。术后3个月至1年内平均LVEF和LVFS均在正常范围。术后各组患者3个月至1年左心室平均内径均恢复至正常范围。术后1周平均左心室质量指数为90.35 g/m~2,较术前(101.48 g/m~2)下降显著(P0.05),随访3个月到1年无显著变化;所有患者术后1周~1年内主动脉瓣跨瓣平均压差2.92 k Pa(21.92 mm Hg),各组患者术后1周随访至术后1年,主动脉瓣跨瓣压差均无显著变化。5组患者(16 mm over-line Sorin机械瓣组、20 mm over-line Sorin机械瓣组、17 mm SJ Regent机械瓣组、Carbio-S 19 mm机械瓣组、Carbio-S 21 mm机械瓣组)术后1年内主动脉瓣跨瓣压差与其他3组相比明显增大,组间差异有统计学意义(P0.05);其中16 mm over-line Sorin机械瓣组跨瓣压差最大。所有患者均未发现有PPM现象发生。结论采用中国市场上来自不同厂家的各种直径的主动脉瓣机械瓣膜置换术后未见明显PPM现象,左心室质量指数及主动脉跨瓣压差术后均在比较理想的范围;不同厂家的各种型号的人工主动脉机械瓣可以满足绝大多数成年小主动脉瓣环患者主动脉瓣置换的需求,大部分患者无须行主动脉瓣环扩大术或采用其他术式。     

纵向生理加压外固定器的生物力学分析

背景：目前骨外固定器大多为刚性结构,对骨折端存在过多的应力遮挡,影响骨折愈合速度及骨痂质量,甚至骨折发生不愈合。 目的：观察纵向生理加压外固定器固定胫骨中段横断骨折后与人体正常胫骨生物力学强度的差异。 方法：选取12根新鲜胫骨标本随机分为试验组和对照组,试验组分别用线锯造成胫骨中段横断骨折,纵向生理加压外固定器固定;对照组即正常胫骨。分别进行轴向载荷、弯曲载荷、扭转载荷作用下的力学实验,记录每一级加载后胫骨的位移及扭转角度,计算出轴向压缩刚度、弯曲刚度及扭转刚度。 结果与结论：在生理范围内加载下,试验左右应变略大于对照组,但其固定后整体刚度与对照组无显著性差异(P > 0.05);试验组的弯曲应变大于对照组,但其整体刚度与对照组无显著性差异(P > 0.05);两组整体扭转刚度无明显差异(P > 0.05);试验组极限弯曲载荷明显大于对照组(P < 0.05)。提示纵向生理加压外固定器能够达到足够的生物力学强度,有良好的稳定性,对骨折能起到生物学固定。     

载荷强度对受载胫骨中骨陷窝-骨小管系统内溶质输运速率影响

目的 利用有限元法研究载荷强度对受载胫骨中骨陷窝-骨小管系统（lacunar-canalicular system，LCS）内溶质输运速率的影响。方法 基于成年鼠胫骨的micro-CT扫描图像，利用Mimics、Hypermesh、FEBio等软件建立其胫骨有限元模型，且视为均质的两相-溶质材料。通过设置3组不同扩散率（3、15、30 μm2/s）的溶质和载荷强度（0.2、2.0、5.0 N），得到输运速率和溶质扩散率以及载荷强度之间的关系。对比光脱色荧光恢复（fluorescence recovery after photobleaching, FRAP）实验数据与有限元法得到的结果，分析载荷刺激对输运增强率的影响。结果 输运速率均随着扩散率和载荷强度的增大而增大。通过与FRAP实验的数据进行比对发现，有限元法得到的结果基本符合溶质运移规律。结论 研究结果可为研究皮质骨深层区域的力响应以及流动性提供一定基础，也为进一步揭示骨再生机制提供借鉴。     

二维纵向应变及应变率技术评价室间隔缺损修补术后室间隔功能变化

目的:应用二维斑点追踪技术评价室间隔缺损(VSD)修补术对室间隔局部功能的影响。方法:行室间隔修补术的儿童患者38例,于术前1周内、术后1周及术后6个月行超声检查,检测左室射血分数(LVEF)、二尖瓣口舒张早期血流速度(E)/二尖瓣环舒张早期速度(e')、左室整体收缩期纵向应变(LS)及应变率(LSRs)、舒张早期纵向应变率(LSRe)及舒张晚期纵向应变率(LSRa);室间隔心肌收缩期纵向应变(LS_(IVS))及应变率(LSRs_(IVS))、舒张早期纵向应变率(LSRe_(IVS))及舒张晚期纵向应变率(LSRa_(IVS))。同期30例正常儿童作为对照组。结果:术前VSD患者E/e'、LS、LSRs、LS_(IVS)及LSRs_(IVS)显著高于对照组(P0.05或P0.01),LSRe和LSRe_(IVS)减低(P0.05),而LVEF无差异(P0.05);修补术后1周,LVEF、LS、LSRs、LSRe、LS_(IVS)、LSRs_(IVS)及LSRe_(IVS)显著小于对照组(P0.05或P0.01),而E/e'较对照组增大(P0.05);术后6个月,LS_(IVS)、LSRs_(IVS)及LSRe_(IVS)仍显著低于对照组(P0.05),其余参数恢复正常。结论:VSD修补术后6个月,室间隔局部收缩、舒张功能仍减低;二维斑点追踪技术是准确评价室间隔局部功能的新方法。     

胰淀素对离体大鼠胰岛细胞内活性氧生成的影响

目的：观察高浓度胰淀素对胰岛细胞内活性氧（ROS）生成的影响。方法：以体外培养胰岛单层细胞为模型,应用ROS特异性荧光染料2′,7′-二氯二氢荧光素双醋酸盐（H₂DCF）进行标记，以粘附细胞仪570型测定10 μmol/L胰淀素作用2 h后胰岛细胞内DCF荧光强度变化。结果：10 μmol/L胰淀素作用2 h，胰岛细胞内DCF荧光强度在16.7 mmol/L葡萄糖刺激后，迅速急骤升高进入平台期，升高速度为28×10^-3/s，而正常细胞DCF荧光强度无明显变化。光镜下可见部分细胞胞体缩小，胞质发生空泡变性，少数细胞核固缩、裂解，胞膜突起。结论：10 μmol/L胰淀素作用后的胰岛细胞内ROS生成增多，细胞形态受损，这些活性氧基的生成可以反映胰淀素对胰岛细胞损害程度，推测活性氧可作为胰岛细胞毒性损伤指标之一。     

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.