骨性关节炎动物模型内侧副韧带的应力松弛

背景：韧带和其他生物软组织一样,具有黏弹性特性,其应力松弛和蠕变黏弹性特性是为适应人的生理功能需要而存在的。研究说明骨性关节炎对韧带力学性能具有一定影响。 目的：比较正常和骨性关节炎动物模型内侧副韧带的应力松弛流变特性,确定骨性关节炎对内侧副韧带应力松弛特性的影响。 方法：以闭合关节刻痕法复制骨性关节炎动物模型,取正常和骨性关节炎动物模型大鼠膝关节内侧副韧带各10个试样,进行应力松弛实验。应力松弛实验的应变增加速度为5%/s。设定实验时间为7 200 s,采集100个数据,观察应力松弛数据和曲线、应力与时间的变化规律,以一元线性回归分析的方法处理实验数据。 结果与结论：正常组和病态组试样应力松弛最初600 s变化较快,之后应力缓慢下降,正常组7 200 s应力松弛量0.47 MPa,病态组7 200 s应力松弛量0.29 MPa。模型组7 200 s应力松弛量显著低于正常组(P < 0.05),且应力松弛曲线是以对数关系变化的。说明骨性关节炎时可以使膝关节对内侧副韧带应力松弛量降低,对膝关节应力松弛特性具有一定影响。     

人脊柱棘间韧带与黄韧带应力松弛实验的研究

从应力松弛力学特性角度对棘间韧带和黄韧带进行定量分析,为人工韧带材料研究和韧带损伤吻合手术提供应力松弛力学参数。将标本装夹于软组织夹具中,之后装夹于电子万能试验机夹头内,驱动机器以1%/s的应变增加速度对标本施加拉应变,在36.5℃温度场下进行实验,采集90个数据,实验结束后计算机自动输出7 200 s之间应力松弛数据和曲线。棘间韧带组7 200 s应力松弛量为1.06 MPa,黄韧带组7 200s应力松弛量为1.62 MPa。棘间韧带和黄韧带具有不同的应力松弛力学特性。     

髂股韧带与股骨头韧带黏弹性实验研究

目的 研究新鲜成人尸体髋关节髂股韧带和股骨头韧带的黏弹性力学性质,为临床提供生物力学参数.方法 取正常国人髂股韧带和股骨头韧带各10个试样进行应力松弛、蠕变实验.结果 得出了应力松弛、蠕变实验曲线,以回归分析的方法处理实验数据,得出了回归系数.结论 髂股韧带7200s应力松弛蠕变量显著大于股骨头韧带.     

去卵巢骨质疏松模型大鼠L4脊椎骨的应力松弛与蠕变

背景：去卵巢大鼠脊椎骨会发生哪些应力松弛与蠕变及时间的变化规律？ 目的：观察去卵巢骨质疏松对雌性大鼠承重骨黏弹性特性的影响。 方法：Wistar雌性大鼠44只随机等分为对去卵巢骨质疏松动物模型组和对照组。模型组大鼠于0周摘除卵巢,14周后对大鼠L4椎骨进行应变增加速度为1%/s的应力松弛实验和应力增加速度为0.01 MPa/s的蠕变实验,在7 200 s采集100个数据。 结果与结论：大鼠L4椎骨对照组7 200 s应力松弛量和蠕变量大于模型组(P < 0.05);同时大鼠L4椎骨应力松弛曲线是以对数关系变化的,蠕变曲线是以指数关系变化的。提示去卵巢骨质疏松大鼠椎骨黏弹性力学特性发生了改变。     

骨性关节炎动物模型外侧副韧带应力松弛特性的研究

比较正常和骨性关节炎动物模型外侧副韧带的应力松弛流变特性,确定骨性关节炎对外侧副韧带应力松弛特性的影响.在日本岛津电子万能试验机上对正常和病态各8个试样进行应力松驰实验.应力松弛实验的应变增加速度为5%/s.设定实验时间为7 200 s,采集100个数,以一元线性回归分析的方法处理实验数据.结果表明:正常和病态组试样应力松弛最初600 s变化较快,之后应力缓慢下降,正常组7 200 s应力松弛量为2.231 Mpa,病态组7 200 s应力松弛量为2.458 Mpa.表明应力松弛曲线是以对数关系变化的,骨性关节炎对外侧副韧带应力松弛特性具有一定影响.     

改性玻璃离子水门汀应力松弛蠕变实验

文题释义：黏弹性力学：连续介质力学的重要分支,又称黏弹性理论,研究黏弹性物质的力学行为、本构关系及其破坏规律,以及黏弹性体在外力和其他因素作用下的变形和应力分布。聚合物、混凝土、金属、岩石、土壤、石油、肌肉、血液和骨骼等,在一定条件下既具有弹性性质又具有黏性性质,这种兼具弹性和黏性性质的材料称为黏弹性材料,含黏弹性固体与黏弹性流体,又可分为线性黏弹性体和非线性黏弹性体。线性黏弹性体的两种极端情况即为胡克体(遵循胡克定律)和牛顿流体(遵循牛顿粘性定律)。 生物力学：是应用力学原理和方法对生物体中的力学问题定量研究的生物物理学分支,其研究范围从生物整体到系统、器官(包括血液、体液、脏器、骨骼等),从鸟飞、鱼游、鞭毛和纤毛运动到植物体液的输运等。 物力学的基础是能量守恒、动量定律、质量守恒三定律并加上描写物性的本构方程。生物力学研究的重点是与生理学、医学有关的力学问题,依研究对象的不同可分为生物流体力学、生物固体力学和运动生物力学等。 背景：以往对改性玻璃离子水门汀的力学性能研究多以压缩、弯曲实验居多,关于玻璃离子水门汀加入锶羟基磷灰石后的应力松弛、蠕变实验研究鲜有报道。 目的：对比分析传统玻璃离子水门汀、复合树脂釉质粘接剂、改性玻璃离子水门汀的应力松弛、蠕变特性。 方法：按质量比15%向玻璃离子水门汀中加入掺锶羟基磷灰石,制备改性玻璃离子水门汀。制作改性玻璃离子水门汀、复合树脂釉质粘接剂与传统玻璃离子水门汀试样,3组各取10个试样进行应力松弛实验,另取10个试样进行蠕变实验。 结果与结论：①应力松弛实验7 200 s时,传统玻璃离子水门汀组应力下降了1.18 MPa,复合树脂釉质粘接剂组应力下降了1.39 MPa,掺锶羟基磷灰石复合玻璃离子水门汀组应力下降了1.38 MPa;传统玻璃离子水门汀组应力下降量小于掺锶羟基磷灰石复合玻璃离子水门汀组、复合树脂釉质粘接剂组(P < 0.05),掺锶羟基磷灰石复合玻璃离子水门汀组和复合树脂釉质粘接剂组应力下降量无差异(P > 0.05)。②蠕变实验7 200 s时,传统玻璃离子水门汀组应变上升了0.24%,复合树脂釉质粘接剂组应变上升了0.33%,掺锶羟基磷灰石复合玻璃离子水门汀组应变上升了0.32%;传统玻璃离子水门汀组应变上升量小于掺锶羟基磷灰石复合玻璃离子水门汀组、复合树脂釉质粘接剂组(P < 0.05),掺锶羟基磷灰石复合玻璃离子水门汀组试和复合树脂釉质粘接剂组应变上升量无差异(P > 0.05)。③结果表明,15%掺锶羟基磷灰石提高和改善了玻璃离子水门汀的黏弹特性,有利于其与黏结物体的黏结,有利于提高黏结强度。 ORCID: 0000-0003-1024-5733(丁洁) 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     

前交叉韧带粘弹性特性的实验研究

目的 探讨前交叉韧带的力学性能和粘弹性行为与时间的变化规律，为研究人工韧带提供生物力学参数。方法 对正常国人新鲜尸体膝关节前交叉韧带进行系统的拉伸、应力松驰、蠕变实验，得出最大载荷、强度极限、最大应变、弹性模量等；还得出了应力松驰、蠕变实验数据和曲线，归一化应力松驰函数、蠕变函数数据和曲线。并得到7200s时的蠕变量和应力松驰量。结果 ①前交叉韧带在实验中表现出典型的松弛、蠕变现象，说明其粘弹性性质在膝关节运动中起着重要的缓冲作用。②最初600s时应力应变的变化幅度较大，之后应力缓慢下降，应变缓慢上升，前交叉韧带7200s时应力松弛量1．05Mp，蠕变量为6．82％。结论 前交叉韧带具有良好的粘弹性力学性质。其粘弹性力学行为是为了适应其所在解剖部位的功能需要。     

正常与病态股骨头应力松弛特性的对比分析

比较正常股骨头和股骨头坏死后股骨头应力松弛性质,为人工关节研究和髋关节置换术提供应力松弛参数。在日本岛津电子万能试验机上对正常与病态股骨头各8个试样进行应力松弛实验。模拟人体温在36.5℃的温度场下进行实验,以5%/s的应变增加速度对标本施加应变,设定时间为7 200 s,采集100个实验数据。采用三参数模型计算应力松弛方程。观察应力松弛曲线和7 200 s应力松弛量。股骨头在最初600 s变化较快,之后应力缓慢下降,正常组7 200 s应力松弛量为0.31 MPa,病态组7 200 s应力松弛量为0.22 MPa,病态组7 200 s应力松弛量显著低于正常组(P<0.05)。股骨头坏死后打乱了松质骨头骨小梁的正常排列,骨量丢失,从而对应力松弛特性造成影响。应力松弛数据可以定量地说明坏死股骨头应力松弛特性差。     

正常与病态股骨头应力松弛特性的对比分析

比较正常股骨头和股骨头坏死后股骨头应力松弛性质,为人工关节研究和髋关节置换术提供应力松弛参数。在日本岛津电子万能试验机上对正常与病态股骨头各8个试样进行应力松弛实验。模拟人体温在36.5℃的温度场下进行实验,以5%/s的应变增加速度对标本施加应变,设定时间为7 200 s,采集100个实验数据。采用三参数模型计算应力松弛方程。观察应力松弛曲线和7 200 s应力松弛量。股骨头在最初600 s变化较快,之后应力缓慢下降,正常组7 200 s应力松弛量为0.31 MPa,病态组7 200 s应力松弛量为0.22 MPa,病态组7 200 s应力松弛量显著低于正常组(P<0.05)。股骨头坏死后打乱了松质骨头骨小梁的正常排列,骨量丢失,从而对应力松弛特性造成影响。应力松弛数据可以定量地说明坏死股骨头应力松弛特性差。     

膝关节前交叉韧带与后交叉韧带粘弹性实验研究

研究了10具新鲜成人尸体膝关节前交叉韧带和后交叉韧带的拉伸力学性质和粘弹性力学性质,对前交叉韧带和后交叉韧带进行单向拉伸实验,得出了破坏载荷,强度极限、最大应变、伸长比、弹性模量.对前交叉韧带和后交叉韧带进行应力松弛,蠕变实验,得出了应力松弛、蠕变实验数据和曲线.对实验数据进行归一化处理,得出了归一化应力松弛函数,蠕变函数,以回归分析的方法处理实验数据,得出了回归系数,很好的拟合了实验曲线.实验结果表明:前交叉韧带的拉伸强度极限、最大应变等大于后交叉韧带,后交叉韧带7200s应力松弛、蠕变量小于前交叉韧带.     

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.