磁性纳米多孔复合支架材料的细胞相容性研究

目的研究磁性纳米多孔复合(n-HA/PLLA/Fe2O3)材料的细胞相容性,探讨细胞在材料表面黏附、增殖、表达等生物学行为,为其医学应用提供实验依据。方法将大鼠成骨细胞与磁性纳米多孔复合材料共培养,采用CCK-8法检测细胞增殖、扫描电镜观察细胞在材料上的黏附、RT-PCR检测I型胶原和骨钙素基因的表达。结果 CCK-8检测显示实验组磁性纳米多孔复合材料上细胞的增殖与空白对照组没有差异性(0.05);扫描电镜观察到细胞在磁性纳米多孔复合材料的表面和孔隙内大量黏附、增殖和生长,随着共培养时间的增加,材料表面的细胞数量明显增多;RT-PCR显示随着共培养时间的增加,I型胶原基因的表达增强(0.05),骨钙素的表达无明显差异(0.05)。结论磁性纳米多孔复合支架材料适于成骨细胞的黏附、生长和分化,具有良好的细胞相容性。     

天冬氨酸修饰纳米羟基磷灰石/聚乳酸复合物制备软骨组织工程支架及其生物性能研究

目的:通过天冬氨酸修饰的纳米羟基磷灰石（Asp-nHA）和左旋聚乳酸（PLLA）复合,制备软骨组织工程支架,并进行体外实验研究,探索其作为软骨组织工程支架的可行性。 方法:以碳二亚胺盐酸盐/N-羟基琥珀酰亚胺偶联法制备Asp-nHA,并与PLLA复合,获得新型Asp-nHA/PLLA纳米复合支架。比较成骨细胞在该新型材料表面的粘附、生长和增殖的情况。 结果:加入nHA后,Asp-nHA/PLLA复合材料可显著增强细胞的粘附、生长、增殖;Asp-nHA/PLLA的生物学性能明显优于PLLA及HA/PLLA,且Asp-nHA/PLLA具有最强的体外诱导成骨细胞分化能力。 结论:Asp-nHA/PLLA制备简单,具有良好的生物相容性和成骨活性,是一种性能良好的骨组织工程支架材料。     

胶原-纳米羟基磷灰石复合支架的细胞相容性

背景：观察成骨细胞在生物材料上的形态、增殖和分化等项目,可评估生物支架材料的生物相容性。 目的：观察复合支架材料纳米羟基磷灰石/胶原对成骨细胞增殖、分化的影响。 方法：取新生24 h内Wistar大鼠的颅盖骨,采用改良胶原酶消化法进行成骨细胞原代培养,取第3代细胞与纳米羟基磷灰石/胶原支架或普通羟基磷灰石材料体外复合培养。培养3,6,9 d后,观察材料周边的细胞形态及支架材料对细胞分化、增殖的影响。 结果与结论：纳米羟基磷灰石/胶原材料较普通的羟基磷灰石材料更有利于成骨细胞的黏附、生长、分化、增殖,证实其生物相容性更好,有望成为一种新型的骨组织工程支架材料。     

多孔碳酸钙陶瓷与干细胞源性成骨细胞的相容性

背景：国内外的研究证实普通碳酸钙陶瓷作为骨替代材料时具有细胞支架作用。 目的：观察多孔碳酸钙陶瓷与成骨细胞的相容性,及作为骨组织工程支架的可能性。 方法：SD大鼠骨髓基质干细胞经矿化诱导培养、扩增并检测证实其已具成骨细胞表型后,分别与多孔碳酸钙陶瓷支架、普通羟基磷灰石陶瓷支架体外复合培养。 结果与结论：骨髓基质干细胞经体外诱导形成成骨细胞,钙结节、Ⅰ型胶原和碱性磷酸酶免疫染色结果阳性。多孔碳酸钙陶瓷支架材料与羟基磷灰石陶瓷材料皆有细胞附着生长,但多孔碳酸钙陶瓷支架材料细胞的黏附能力、增殖活力及成骨活性均强于羟基磷灰石陶瓷材料。提示多孔碳酸钙陶瓷支架材料与SD大鼠骨髓基质干细胞源性成骨细胞有良好相容性。     

不同比例的β-TCP/PLLA复合材料的体外生物相容性研究

为了挑选最适比例的β-TCP/PLLA多孔支架材料,我们选用生物相容性好、降解性能优异的β-磷酸三钙(β-TCP)与聚乳酸(PLLA)复合,制备成不同比例的β-TCP/PLLA(β-TCP/PLLA=11,1 2,21)多孔支架材料,将其与体外培养的大鼠骨髓间充质干细胞复合,通过扫描电镜、荧光显微镜以及MTT等方法初步比较了三种不同比例的β-TCP/PLLA多孔支架材料的生物相容性,结果表明三种材料均具有一定的生物相容性,细胞生长良好.但以β-TCP/PLLA=21的材料最好,对细胞生长影响最小.     

重组骨脱细胞细外基复合Wistar大鼠成骨细胞体外培养的形态学观察

目的新型重组骨脱细胞细胞外基质(REAECM)的制备及其细胞相容性的初步检测,为骨组织工程寻找一种新型的细胞外支架提供实验依据。方法应用体外细胞培养技术,对鼠成骨细胞和REAECM体外进行联合培养1-4周,通过相差显微镜、光镜、电镜观察细胞在材料中的生长情况。结果成骨细胞可以在REAECM上发生良好的黏附、增殖,并且可以长入REAECM的孔隙内。结论REAECM可作为构建组织工程骨的一种较好的支架材料,具有网状孔隙结构;在体外和成骨细胞复合培养时表现出良好的细胞相容性,可以作为一种天然的骨组织替代材料。     

大鼠成骨细胞与壳聚糖/羟基磷灰石复合支架降解产物的生物相容性

背景：人们对壳聚糖/羟基磷灰石复合多孔生物支架在体内的降解过程并非十分清楚,而且有关其降解产物对成骨细胞的影响研究也较少。 目的：分析大鼠成骨细胞与壳聚糖/羟基磷灰石复合多孔生物支架降解产物的生物相容性。 方法：将培养的第2代大鼠成骨细胞分别在壳聚糖/羟基磷灰石复合支架降解产物浸提液和含体积分数10%胎牛血清的DMEM培养液中培养,培养第2,4,6,8,10天分别对两组细胞做MTT细胞计数,采用联合会推荐法测定细胞碱性磷酸酶活性,采用BCA蛋白定量法测定总蛋白。 结果与结论：在壳聚糖/羟基磷灰石复合多孔生物支架降解产物浸提液中培养的大鼠成骨细胞增殖速度、细胞碱性磷酸酶活性、细胞总蛋白合成及碱性磷酸酶与总蛋白的比值明显高于在体积分数为10%胎牛血清DMEM培养液中培养的细胞(P < 0.05)。表明壳聚糖/羟基磷灰石复合多孔生物支架的降解产物不仅可促进大鼠成骨细胞的黏附、生长和增殖,还可增强其骨化功能,具有较好的生物相容性。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;组织工程全文链接：     

超临界流体技术合成的复合型骨替代生物材料:体内外生物学评价

背景:在复合材料内部增加细胞黏附性较好的高分子材料或同骨组织羟基磷灰石成分相似的无机材料,可以改善材料的表面化学结构。过去的十几年,产生和发展了许多合成生物降解支架材料的新技术,虽然超临界流体技术应用在合成支架中时间尚短,但有着其他技术不可比拟的众多优点,目前越发受到学者的重视。目的:以聚乳酸和同种异体骨粉为原材料,通过超临界流体技术合成复合型骨替代生物材料,评价其生物学特性。方法:首先将同种异体皮质骨粉与聚乳酸在超临界二氧化碳作用下合成多孔复合型骨生物替代材料。将材料浸提液与成骨细胞系复合培养,体外观察细胞形态、增殖情况;通过材料浸提液皮内注射实验和材料肌袋内埋入实验,体内观察动物的致敏、组织炎症发生情况。结果与结论:体外大体观察该种复合材料形状、大小、孔隙可控,孔径适中,有较好的硬度,体外实验表明细胞相容性良好,对细胞的增殖无毒副作用;体内实验表明材料植入动物体内未发生致敏反应,组织相容性良好,但无异位成骨作用。说明制备的新型复合骨组织生物材料在细胞学和生物相容性检测上可以满足组织工程支架和骨组织替代的要求,该种合成技术及多孔生物材料有广阔发展前景。     

骨髓间充质干细胞与纳米羟基磷灰石支架材料的体外相容性研究

目的　探讨兔骨髓间充质干细胞(rBMSCs)与纳米羟基磷灰石(nano-HA)支架材料的相容性,进一步验证nano-HA材料作为骨组织工程支架材料的可行性。 方法　将rBMSCs与nano-HA支架材料在体外复合培养,通过倒置显微镜、扫描电镜观察细胞与材料的复合情况,用MTT法、碱性磷酸酶活性检测法检测材料对细胞增殖、分化的影响。 结果　rBMSCs可以在nano-HA支架材料表面及孔隙中良好的黏附、迁移、增殖和分化,复合培养5 d后nano-HA支架材料对rBMSCs的增殖分化表现出一定的促进作用。 结论　rBMSCs与nano-HA支架材料具有良好的生物相容性, nano-HA支架材料可以作为rBMSCs良好的载体。     

成骨诱导人脐带间充质干细胞与纳米羟基磷灰石/聚酰胺66支架材料的生物相容性☆

背景：纳米羟基磷灰石/聚酰胺66材料有利于成骨细胞的长入和新生骨的形成、且抗弯强度、抗压强度等各项参数与正常骨组织的力学性能相接近,能满足实验动物硬组织修复的要求。 目的：分析成骨诱导后人脐带间充质干细胞与纳米羟基磷灰石/聚酰胺66复合支架的生物相容性。 方法：体外培养人脐带间充质干细胞,纯化增殖,成骨诱导。取成骨诱导后的第3代人脐带间充质干细胞接种于纳米羟基磷灰石/聚酰胺66支架材料上,观察细胞的生长、增殖情况及材料细胞毒性。 结果与结论：成骨诱导后人脐带间充质干细胞在复合支架上生长分化良好,增殖活性不受材料影响。成骨诱导14 d内,可见碱性磷酸酶活性随着培养时间延长而逐渐增高。MTT法检测细胞无毒性。扫描电镜观察,1 d后可见细胞在支架表面附着生长;7 d后可见细胞在材料上生长良好,材料空隙有大量充填。说明纳米羟基磷灰石/聚酰胺66支架可作为骨组织工程中人脐带间充质干细胞的细胞载体,具有良好的生物相容性,能满足骨组织工程的需要。关键词：羟基磷灰石/聚酰胺66;人脐带间充质干细胞;细胞培养;骨组织工程;支架;生物相容性 缩略语注释：nHA/PA66：nano-hydroxyapatite crystals and pnolyamide 66,羟基磷灰石/聚酰胺66;hUCMSCs：human umbilical cord mesenchymal stem cells,人脐带间充质干细胞 doi:10.3969/j.issn.1673-8225.2012.16.019     

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.