长径比差异对牙种植体-颌骨界面的应力分布影响

目的探讨不同长径比下牙种植体-颌骨界面的应力分布差异,为新型牙种植体结构的设计提供依据。方法运用Geomagic studio、SolidWorks和ANSYS Workbench软件建立下颌骨三维有限元模型,并根据种植体颈部有、无螺纹分成A、B两组进行仿真实验,对下颌磨牙分别施加不同的斜向咬合力和垂直向咬合力,对比分析牙种植体和周围骨组织的应力分布情况。结果长径比相同的情况下,同一种植体模型在斜向载荷作用下的等效应力峰值明显高于垂直载荷;在斜向和垂直两种载荷作用下,A、B组种植体模型应力主要集中于种植体颈部。斜向载荷作用下,A、B组种植体应力变化范围分别为144.74～374.67、161.52～475.38 MPa;垂直载荷作用下,A、B组种植体应力变化范围分别为101.28～187.40、110.08～210.32 MPa,A组种植体模型最大应力显著小于B组。结论临床上医生可根据长径比2.67初步选择标准种植体,同时结合患者颌骨状况进行选择。     

不同载荷条件对后牙单种植体义齿下颌骨应力的影响

目的探讨垂直和斜向载荷作用于下颌后牙单种植体支持式义齿不同载荷点对下颌骨应力分布的影响。方法应用部分下颌骨CT扫描图像建立下颌骨的三维有限元模型,根据测量数据建立种植体的三维有限元模型,建立半解剖式种植义齿牙冠的三维有限元模型;在下颌第一恒磨牙种植体义齿各咬合点分别加垂直和斜向载荷,计算下颌骨所受的最大等效应力。结果在垂直和斜向载荷作用下,下颌骨的最大等效应力位于颈周骨皮质的上方;在相同的垂直斜向载荷下,不同咬合点加载时,下颌骨上所产生的最大等效应力有明显差异;同一载荷点在大小相同、方向不同的载荷作用下,下颌骨的最大等效应力有明显差异。结论在垂直和斜向载荷作用下,下颌骨的最大等效应力位于颈周骨皮质的上方,向根尖部递减;远中尖斜向加载时颈周骨皮质的上方的等效应力最大;载荷方式是影响颈周骨皮质应力分布的重要因素。     

TM种植体骨界面应力分布的有限元分析

背景：种植体形态是决定种植体骨界面应力分布的重要因素之一。探讨顺应人体正常颌骨解剖形态的TM种植体骨界面的应力分布特征对临床医生选择和设计种植体有指导意义。 目的：观察集中荷载作用下TM种植体及其周围骨组织应力分布的特征。 方法：通过逆向工程技术,将二维下颌骨CT图片转化为三维实体模型,并建立3种包含不同锥度的TM种植体真实下颌骨B/2类骨质的有限元模型,利用有限元技术研究两种加载方式下TM种植体骨界面应力分布特征。 结果与结论：垂直加载时,对于锥度较大的TM种植体周边密质骨承受较小的应力;斜向加载时,对于锥度较大的TM种植体周边密质骨和松质骨承受较大的应力;种植体颈部,密质骨上缘与种植体接触处和种植体底部松质骨出现明显应力集中现象,斜向荷载下种植体骨界面的应力分布显著高于垂直荷载下的应力分布。从1/2长度开始变化的TM种植体骨界面在垂直荷载下表现出较好的应力分布特征。     

牙科即刻种植中不同螺纹形态及深度设计参数种植体的生物力学性能

目的分析牙科即刻种植中不同螺纹形态和螺纹深度种植体周围骨质应力分布情况,为种植体的设计和选择提供依据。方法利用Geomagic Studio、Solid Works和ANSYS Workbench建立下颌骨骨块、种植体及下颌磨牙简化模型,施加垂直载荷和斜向载荷,观察不同螺纹形态和螺纹深度的种植体及其周围骨组织应力分布情况。结果垂直载荷作用下,种植体、皮质骨、松质骨应力峰值变化范围分别为120. 51～129. 63 MPa、9. 94～13. 25 MPa、3. 92～8. 01 MPa,V形、矩形、支撑形、反支撑形种植体周围皮质骨在螺纹深度0. 40～0. 45 mm范围内应力变化平稳;斜向载荷作用下,种植体、皮质骨、松质骨应力峰值变化范围分别为220. 23～286. 51 MPa、33. 39～45. 08 MPa、4. 96～12. 5 MPa。螺纹深度为0. 45 mm,V形、支撑形、反支撑形种植体应力最小。结论 V形、支撑形、反支撑形螺纹种植体选择螺纹深度为0. 45 mm,矩形种植体选择螺纹深度0. 40 mm,呈现出较好的生物力学特性。     

种植体不同设计参数对下颌骨牙齿种植的影响

目的 建立不同设计参数的种植体-下颌骨模型,观测种植体及周围骨质应力分布,分析不同设计参数对下颌骨牙齿种植的影响。方法 基于结构特征参数（种植体直径、螺纹深度、基台穿龈高度、螺纹形态）,设计8组种植体模型,并分别进行下颌骨整体模型的装配。对模型施加静态150 N垂直、斜向45°两种载荷,分析骨组织和种植体von Mises应力峰值,探讨对von Mises应力峰值最敏感的种植体结构参数变量。结果 斜向载荷比垂直载荷对颌骨会产生更大的应力峰值。种植体直径是影响皮质骨von Mises应力峰值的关键因素;螺纹深度是影响松质骨von Mises应力峰值的关键因素;基台穿龈高度也会对颌骨von Mises应力峰值产生影响,但影响程度不如螺纹深度和种植体直径明显;螺纹形态对颌骨von Mises应力峰值几乎没有影响。结论 不同的种植体设计参数会影响颌骨不同组织的应力峰值,对于个性化种植需要慎重考虑种植体参数的选择。研究结果为口腔种植体的结构参数设计提供理论指导,为口腔种植手术精准预测提供参考。     

上颌前牙区不同种植修复体在不同咬合受力下的三维有限元分析

文题释义：口腔种植修复体：是一种以植入骨组织内的结构为基础来支持、固位上部牙修复体的缺牙修复方式,它包括种植体、固位螺丝、修复基台及上部修复体,故以上各结构良好的生物力学性能决定着种植修复体的长期稳定性。 三维有限元分析：通过单元格划分将连续的模型划分为有限个单元,后期根据研究的需要赋予其不同的材料性能,模拟生物力学环境,计算其所受应力。自1980年运用于口腔医学研究以来,有限元法已涉口腔种植的各个领域,如通过三维有限元法分析螺纹形态、基台角度、植体类型、颈部设计等因素对种植修复体的影响,目前经过国内外学者的大量研究,三维有限元模型的精确度也已得到了较大提升。 背景：在口腔种植修复治疗中,修复因素与咬合因素影响着植体内部结构及植体-骨界面处应力的分布,植体内部结构及植体-骨界面处应力分布是否平衡决定着种植体的长期寿命与周围骨质水平的稳定性。 目的：探讨与分析二氧化锆全瓷冠与钴铬合金烤瓷冠修复体在3种咬合关系中对植体-骨界面处、种植体、修复基台、固位螺丝及修复体内部应力分布的影响。 方法：参照1例上颌中切牙区行种植体植入修复患者的锥形束CT影像资料,运用Mimics17.0软件建立上颌中切牙种植修复体模型,分别构建二氧化锆全瓷冠与钴铬合金烤瓷冠两种三维有限元模型,模拟对刃合、正常合、深覆合3种咬合状况进行加载,分析在2种修复体与3种加载方式影响下种植体内部各结构与种植体-骨界面的应力分布情况。 结果与结论：①在钴铬合金烤瓷冠组中,当咬合关系由对刃合转变为正常合及深覆合时,修复体咬合位点处应力相应增加,而修复基台、种植体边缘及植体-骨界面处的应力减小;正常咬合关系中固位螺丝处的应力较其他两种咬合方式更为集中,等效应力峰值更高。②在二氧化锆全瓷冠组中,当咬合关系由对刃合转变为正常合及深覆合时,修复基台、种植体及种植体-骨界面的应力峰值呈逐渐下降趋势;正常合时修复体咬合位点及固位螺丝处的应力峰值高于其他两种咬合关系。③对刃合时,钴铬合金烤瓷冠组修复体咬合位点处的等效应力峰值略高于二氧化锆全瓷冠组,修复基台、固位螺丝、种植体与种植体-骨界面的等效应力峰值略低于二氧化锆全瓷冠组;正常合时,钴铬合金烤瓷冠组种植体颈部处的等效应力峰值略高于二氧化锆全瓷冠组,修复体、修复基台、固位螺丝、种植体-骨界面的等效应力峰值略低于二氧化锆全瓷冠组;深覆合时,钴铬合金烤瓷冠组修复体咬合位点处及种植体颈部处的等效应力峰值均高于二氧化锆全瓷冠组,修复基台、固位螺丝、种植体-骨界面的等效应力峰值略低于二氧化锆全瓷冠组。④结果表明,咬合关系与上部修复体的不同影响着应力在种植修复体各结构及植体-骨界面的分布,此结论或许能为种植修复体远期并发症的预测提供参考依据。 ORCID: 0000-0001-8522-5337(安尼卡尔•安尼瓦尔) 中国组织工程研究杂志出版内容重点：生物材料;骨生物材料; 口腔生物材料; 纳米材料; 缓释材料; 材料相容性;组织工程     

植体弹性模量变化对牙种植体和骨组织应力分布的影响

目的通过三维有限元法分析,探讨植体弹性模量变化对牙种植体和骨组织应力分布的影响,为新型牙种植系统的研究提供实验依据。方法应用螺旋CT数据,建立下颌骨和种植体模型。设定植体弹性模量分别为110、90、70、55和40 GPa,模拟咬合状态,在垂直、水平、斜向分别施加300、100、130 N静止载荷,计算并分析各组在3种载荷下植体周围骨组织和牙种植体各部分的应力。结果随着植体弹性模量的降低,水平和斜向载荷下牙种植体周围皮质骨受到的应力会随之降低,种植体的应力也呈逐渐减小趋势。结论降低牙种植体材料的弹性模量有利于载荷在种植体和周围骨组织中的传导,降低种植义齿晚期失败的风险。     

上颌中切牙角度基台不同载荷的三维有限元优化分析

背景：口腔种植修复中,种植体中基台角度的优化设计对骨吸收有重要影响,同时患者的高用力也对骨质的吸收重建有着重要影响。 目的：利用Ansys Workbench 13.0软件对上颌骨前牙区进行优化设计模型,探讨中切牙角度基台不同载荷对皮质骨和松质骨应力大小的影响。 方法：建立圆柱状V形螺纹种植体的上颌骨骨块三维有限元模型,设定基台角度为0°,5°,10°,15°,20°、25°,30°,设定加载应力为90,105,120,135,150,165,180,195,210 N。在种植体上模拟中切牙咬合,在修复体正中进行颊舌向力学加载,观察基台角度和加载应力变化对颌骨Von Mises应力峰值的影响。 结果与结论：单因素影响下,以基台角度为变量逐渐增加时,在唇腭侧向加载中皮质骨和松质骨的Von Mises应力峰值增幅分别为60.63%和69.30%;以加载应力为变量逐渐增加时,在颊舌向加载中皮质骨和松质骨的Von Mises应力峰值增幅分别为68.74%和69.30%。在基台角度和加载应力交互作用下,当加载应力小于  150 N,同时基台角度小于25°时,对颌骨Von Mises应力峰值响应曲线的切线斜率位于-1至0之间。所以从力学分析看来,松质骨的应力大小更易受到基台角度和加载应力的影响,螺纹种植体最佳的基台角度设计应小于25°,咬合力应小于150 N。中国组织工程研究杂志出版内容重点：生物材料;骨生物材料; 口腔生物材料; 纳米材料; 缓释材料; 材料相容性;组织工程     

动态加载下3种基台材料对上颌角度植入种植修复体周围骨应力的影响北大核心

背景:在口腔种植修复中,上颌前牙区单颗缺失的患者缺牙区常因不同原因导致牙槽骨吸收、缺损,为了避免植骨的风险,往往采用倾斜植入种植体的方式避开牙槽骨吸收区域,并使用角度基台恢复患者正常覆合覆盖关系,不同的基台材料传递咬合力时影响力在种植体及周围骨的大小及分布。目的:比较模拟动态加载下使用3种基台材料的种植修复体在3种植入条件下对周围骨应力峰值随时间变化关系的影响。方法:选取1例行上颌中切牙区种植修复患者的锥形束CT资料,运用Minics软件对颌骨进行切割,运用Solidworks 2018建立种植体、颌骨、角度基台(角度分别为0°,15°,25°,基台材料分别为纯钛、氧化锆、氧化铝)、中央螺丝、二氧化锆全瓷冠等模型,装配完成,以原上颌中切牙牙根方向为植入0°角,然后分别模拟腭向倾斜15°,25°植入,种植体螺纹均无暴露,按照不同植入角度分为0°组、15°组、25°组,分别进行动态加载,加载时间为0.2 s,得出各组各材料基台种植修复体周围骨等效应力峰值随时间变化的关系。结果与结论:①所有基台种植修复体在受咬合力时周围骨应力峰值分布一致,均位于种植体颈部骨皮质,各材料基台种植修复体周围骨应力上升幅度最快时间段均为0.025-0.05 s内,15°组骨皮质高应力值范围较0°组更大,25°组种植体骨皮质初始应力值明显高于其余两组,且加载结束后骨皮质残留较高应力值;钛基台种植修复体周围骨应力上升幅度最大,高应力值范围较为集中;②在15°组中,3种材料基台种植修复体周围骨应力峰值均位于种植体颈部,应力上升幅度钛基台种植修复体周围骨应力上升幅度较大但并不明显,高应力分布范围较为一致;25°组相较于其余两组应力高值较为集中,应力起始值高且变化幅度更大,其中氧化铝基台种植修复体周围骨应力在0-0.1 s内上升幅度最大,在0.2 s时氧化锆基台种植修复体骨等效应力峰值降为0,其余两种材料基台种植修复体周围骨内均残留较高应力;③结果提示,植入角度及基台材料的不同影响应力在种植体骨界面的分布,采用氧化锆材料基台的种植修复体各时间点骨应力均较为稳定。     

前牙区平台转换种植体不同种植深度的生物力学分析

目的采用三维有限元方法建立平台转换种植系统的模型,分析平台转换种植系统应用于前牙时,不同加载时种植体植入不同深度的应力分布情况。方法利用Solidwork2007设计软件和Ansys Workbench有限元分析软件,分析平台转换种植体分别在植入牙槽嵴水平、牙槽嵴下1 mm(minus1)、牙槽嵴下2 mm(minus2)时的应力分布情况,以常规种植体为对照组。结果平台转换种植体中牙槽嵴顶骨质的应力值随种植体植入深度加深而有效降低,且比常规组小,而常规组随种植体深入种植应力没有发生明显变化。垂直加载下,各个模型中平台转换基台的应力分布基本相似,与种植深度无明显的相关性,而常规基台的应力分布随着种植深度的下移呈逐渐上移的趋势;各个种植深度中两组种植体、松质骨的应力分布情况基本相似,与种植深度无明显的相关性;在平台转换组中,皮质骨的应力分布随种植深度的下移而下移,而常规组中应力始终集中于牙槽嵴顶与基台相接处没有变化,且其应力分布比平台转换组集中。水平加载下各模型的应力分布规律与垂直组相似,不同的是基台、种植体的最大应力值主要集中在他们相应部位的唇侧。皮质骨中,唇侧的应力明显较垂直加载组集中。结论平台转换种植体植于牙槽嵴顶下水平可以改善牙槽嵴顶应力分布情况,比常规种植体有明显的优势,水平方向的分力将增加牙槽嵴顶骨组织受力,应尽量避免。     

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.