考虑粘弹性性能的密质骨损伤本构模型的研究

本研究考虑密质骨的粘弹性性能,在连续损伤力学的框架范围内研究了密质骨的本构模型,分别就细观结构强度服从均匀分布和非均匀分布两种情况进行了讨论。实验研究表明,该损伤模型是可取的。     

用长骨密质骨推断年龄研究进展

本文概述了长骨密质骨的年龄变化规律 ,对利用密质骨判定骨骼年龄的磨片法、脱钙骨切片法、显微放射摄影法做了比较详细的介绍 ,并讨论了影响密质骨判定年龄准确性的因素。     

人密质骨的撞击实验研究

本文用分离式Hopkinson杆（SHBM）（应变率为7001/s)对人的密度骨进行撞击实验研究,得出了应力-时间、应变-时间、应变率-时间及应力-应变等曲线。用一维波传播理论分析实验数据。结果表明即使在高应变率下,人的密质骨也具有非线性粘弹性材料的特性,据此可得人密质骨的冲击特性可用三参数粘弹性力学模型描述,同时得出了高应变率下,人的密质骨也具有非线性粘弹性材料的特性。据此可得人密质骨的冲击特性可用三参数粘弹性力学模型描述,同时得出院高应变率下人密度骨的极限应力和残余应变值。     

密质骨各向异性性质的力学实验及细观分析

目的研究牛股骨密质骨的微观结构特征与其力学行为间的关系。方法对牛股骨密质骨纵向和横向试样分别进行压缩实验;对破坏后的纵向和横向试样进行断裂路径、断裂表面微结构特征观察;基于复合材料细观力学的理论,分析密质骨中骨单元方向对骨纵向和横向弹性模量及断裂极限强度的影响。结果纵向试样的压缩弹性模量和断裂极限强度均明显大于横向试样的压缩弹性模量和断裂极限强度;纵向试样的断裂路径与加载方向近似为0°,且比较平直,而横向试样的断裂路径与加载方向近似为45°,且比较曲折;纵向试样断面中存在许多与加载方向平行的条状结构,断面较为光滑,而横向试样断面存在许多圆弧形凹坑或凸起,断面较为粗糙。结论牛股骨密质骨具有各向异性的力学性质,其各向异性力学性质与骨单元方向密切相关。     

椎骨骨质增生的形态与组织学观察

目的：观察椎骨骨质增生与组织结构。方法：在３９０条干燥成人脊柱９７５０块椎骨标本，随机锯３０块增生骨唇经脱钙组织切片或骨磨片，光镜观察。结果：脊柱有骨质增生者２５８付占６６．１％，无骨质增生者１３２付占３３．９％。每块椎骨均可发生骨质增生。镜下观察，Ⅰ度和部分Ⅱ度较短增生骨唇只有骨密质。Ⅲ、Ⅳ和部分Ⅱ度较长的增生骨唇由上、下层骨密质和中层的骨松质三层结构组成，骨密质的骨板排列整齐，骨小梁排列不整齐，网眼大小不一。结论：椎体增生唇可累及其周围的血管神经，椎体增生骨唇可因载荷过重或椎间盘退行性变，椎间关节骨质增生可因椎关节不对称等因素。     

藏酋猴椎体骨质的解剖学观察

目的通过对藏酋猴各段椎体骨质的解剖学观察,比较不同节段椎体骨松质与骨密质的分布、排列规律及异同,为藏酋猴脊柱的应用研究提供形态学依据。方法对6具成年健康藏酋猴各段椎体标本进行正中冠状切、矢状切和水平切,并进行测量和观察。结果藏酋猴骨密质从颈部至腰部逐渐变薄;骨松质总体上在正中水平面和正中冠状面上排列紧密,在正中矢状面上排列较为稀疏。颈椎、胸椎和腰椎间骨密质除水平面上差异无统计学意义(P0.05)外,在冠状面、矢状面上差异均有统计学意义(P0.05或P0.01);骨松质在各切面的差异也均有统计学意义(P0.05或P0.01)。结论藏酋猴椎体骨密质和骨松质在颈、胸和腰椎的分布有显著的差异性,适用于对椎骨形态与功能及其病变的相关研究。     

女性骨盆三维有限元模型构建及其侧面碰撞分析

乘员骨盆损伤在车辆侧面碰撞中非常常见,研究骨盆在侧碰中的损伤机理,有助于优化汽车保护装置,提高乘员的安全性.本研究根据CT图片提取相关数据,利用逆向工程软件生成骨盆几何模型,用有限元前处理软件划分网格,构建一个中国50百分位女性骨盆的三维有限元模型,并用Guillemot尸体实验结果验证了模型的有效性.然后用该模型进行侧碰仿真模拟,研究骨盆在侧面碰撞中的响应及密质骨厚度对骨盆刚性的影响.结果表明,女性骨盆在侧面碰撞中发生骨折的临界撞击力为3.00kN;密质骨厚度不同,骨盆受到载荷时的响应也不同,密质骨厚度为l mm时,前下髂骨脊位移为9.75 mm,密质骨厚度为2 mm时,前下髂骨脊位移为5.35 mm.表明密质骨厚度越薄,骨盆刚性越低.     

密质骨的滑动界面细观力学模型

本文将粘合线作为骨单元和间板之间的粘弹性界面,建立了密质骨的细观力学模型,并给出了该模型在滑骨的轴线方向载荷作用下的应力响应和某些密质骨的宏观等效模量。还发现骨单元和间板的泊松比之差对密质骨的等效模量和内部横向应力的分布具有重要影响。     

人密质骨动态力学性能及莫电效应

本实验建立起用Ｈｏｐｋｉｎｓｏｎ压杆技术，测量骨动态力学性能及骨应变源电动势的实验方法，对新鲜人股骨密质进行测试。①低应变率下（２ｘ１０－３／ｓ）骨弹性模量值为１３．６ＧＰａ，与高应变率（６ｘ１０２／ｓ）下骨弹性模量值１８．３ＧＰａ之间差别显著，表明骨是一种粘弹性材料。②结合骨断面扫描电镜图象，讨论了静、动载荷下骨创伤发生的机制，证实骨单位粘合线处是密质骨力学性能薄弱点，骨单位断裂前发生骨板相对滑动。③湿骨试件应变源电动势（ＳＧＰｓ）峰值较干骨试件大，且时相滞后于骨应变时相约４４μｓ，干骨试件ＳＧＰｓ无明显滞后。④提出压电效应和流动电动势分别是干、湿骨试件ＳＧＰｓ产生的机制。实验结果为新型骨生物材料研制，临床骨伤病电刺激疗法的应用，以及骨折愈合质量的评价等，提供了理论依据。     

干牛骨拉伸弹性模量沿径向的分布

本文研究了干牛胫骨骨干密质骨部分沿生长轴方向的拉伸弹性模量沿径向的分布，发现此弹性模量沿径向呈非均匀分布，内外两侧的弹性模量值低于中间部分；提出了一种骨内疲劳裂纹的分布假设，并据此对测试结果进行了初步性的分析。     

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.     

'Very sore nights and days': the child's experience of illness in early modern England, c.1580-1720

Sick children were ubiquitous in early modern England, and yet they have received very little attention from historians. Taking the elusive perspective of the child, this article explores the physical, emotional, and spiritual experience of illness in England between approximately 1580 and 1720. What was it like being ill and suffering pain? How did the young respond emotionally to the anticipation of death? It is argued that children’s experiences were characterised by profound ambivalence: illness could be terrifying and distressing, but also a source of emotional and spiritual fulfilment and joy. This interpretation challenges the common assumption amongst medical historians that the experiences of early modern patients were utterly miserable. It also sheds light on children’s emotional feelings for their parents, a subject often overlooked in the historiography of childhood. The primary sources used in this article include diaries, autobiographies, letters, the biographies of pious children, printed possession cases, doctors’ casebooks, and theological treatises concerning the afterlife.