改良Hodge试验对鲍曼不动杆菌产碳青霉烯酶检测效果的比较

目的比较改良Hodge试验采用三种不同纸片法对耐亚胺培南鲍曼不动杆菌产碳青霉烯酶的检测能力。方法改良Hodge试验采用三种不同纸片检测碳青霉烯酶;采用MicroScan WalkAway 96检测鲍曼不动杆菌的耐药性。结果改良Hodge试验(三种不同纸片法)同时检测33株耐亚胺培南鲍曼不动杆菌,其中应用改良Hodge试验(亚胺培南纸片法),阳性为22株,阳性率为66.7%;改良Hodge试验(厄他培南法),阳性为17株,阳性率为51.5%;改良Hodge试验(美罗培南法),阳性为8株,阳性率为24.2%。结论改良Hodge试验(三种不同纸片法)筛选耐亚胺培南鲍曼不动杆菌产碳青霉烯酶中,改良Hodge试验(亚胺培南纸片法)敏感性最高,而改良Hodge试验(美罗培南纸片法)敏感性最低。     

鲍曼不动杆菌和铜绿假单胞菌临床分离株对碳青霉烯抗生素和头孢他啶的耐药性和金属β内酰胺酶的检测

目的 :了解我院鲍曼不动杆菌和铜绿假单胞菌对碳青霉烯和头孢他啶的耐药性以及与金属 β内酰胺酶的关系。方法 :对 2 0 0 2年 4月～ 2 0 0 3年 1月我院临床分离的 1 0 1株鲍曼不动杆菌以及 2 0 0 3年 2月～ 4月我院临床分离的以MicroScanWalkAway～ 40全自动鉴定药敏仪确定的对亚胺培南和 (或 )对头孢他啶耐药的 69株鲍曼不动杆菌和 2 3株铜绿假单胞菌采用美国国家临床实验室标准委员会 (NCCLS)推荐的琼脂对倍稀释法测定了对亚胺培南、美罗培南和头孢他啶的最低抑菌浓度 (MICs) ,将对亚胺培南耐药和(或 )对头孢他啶高度耐药 (MIC >1 2…     

可利霉素对临床分离菌的体内外研究

目的:评价可利霉素对临床分离菌的体内外的抗菌作用.方法:应用最低有效浓度(Minimum inhibitory concentration,MIC)评价临床分离菌体外抗菌活性;通过小鼠生存率计算半数有效量(Median effective dose,ED50)了解可利霉素体内抗菌活性.结果:可利霉素对临床分离的200株鲍曼不动杆菌的MIC值在64-128μg?mL-1之间,对耐碳青霉烯的临床分离鲍曼不动杆菌的MIC值在128μg?mL-1,体外实验表明其抗菌活性不佳,但对耐碳青霉烯的临床分离鲍曼不动杆菌的半数有效量(ED50)153.2 mg?kg-1;耐碳青霉烯肺炎克雷伯菌ED50为112.2 mg?kg-1.结论:可利霉素对临床分离的鲍曼不动杆菌和耐碳青霉烯的细菌体外抗菌活性较弱,而在体内对耐碳青霉烯的临床分离鲍曼不动杆菌和肺炎克雷伯菌有一定的抗菌作用.     

5年间鲍曼不动杆菌产碳青霉烯酶特性与耐药相关性研究

目的 研究2002-2006年每年3-5月临床分离鲍曼不动杆菌中碳青霉烯酶的分布与变迁情况及其与碳青霉烯类抗生素耐药的相关性.方法 琼脂稀释法检测亚胺培南(IPM)和美罗培南(MEN)对174株鲍曼不动杆菌的最低抑菌浓度(MIC);2-巯基丙酸(2-MPA)和乙二胺四乙酸(EDTA)协同试验进行金属β-内酰胺酶表型检测;PCR扩增金属β-内酰胺酶(MBL)VIM、IMP和苯唑西林酶OXA-23、OXA-24、OXA-51、OXA-58相关基因.结果 2002-2006年每年3-5月临床分离的鲍曼不动杆菌对IPM的耐药率分别为0(0/20)、26%(1/38)、0(0/36)、34.9%(15/43)和59.5%(22/37),对MEN的耐药率分别为0(0/20)、5.3%(2/38)、0(0/36)、20.9%(9/43)和51.4%(19/37);15.5%(27/174)的菌株OXA-23阳性,72.4%(126/174)的菌株OXA-5I阳性,其中15.5%(27/174)菌株同时产OXA-51和OXA-23酶,OXA-23的阳性率从2002年的0上升到2006年的48.6%,OXA-51的阳性率从2002年的35.0%上升到2006年的89.2%;所有菌株均未检出OXA-24、OXA-58、IMP及VIM基因.结论 5年间鲍曼不动杆菌中OXA-23、OXA-5I的检出率及其对碳青霉烯类抗生素的耐药性均呈上升趋势;产OXA-23型B-内酰胺酶是本组鲍曼不动杆菌对碳青霉烯类抗生素产生耐药的重要原因,OXA61可能与鲍曼不动杆菌对碳青霉烯类抗生素的低水平耐药有关.     

体外联合用药对黏菌素异质性耐药鲍曼不动杆菌的抗菌活性研究北大核心CSCD

目的 评价黏菌素分别与美罗培南、左氧氟沙星和磷霉素联用对黏菌素异质性耐药鲍曼不动杆菌的体外抗菌活性.方法 收集2014—2015年温州医科大学附属第一医院临床分离的576株鲍曼不动杆菌,采用微量肉汤稀释法检测黏菌素对鲍曼不动杆菌最小抑菌浓度（MIC）,并采用菌谱分析法（PAPs）筛选黏菌素异质性耐药鲍曼不动杆菌.通过棋盘法设计和微量肉汤稀释法检测黏菌素分别与美罗培南、左氧氟沙星和磷霉素联用及各自单用时对黏菌素异质性耐药鲍曼不动杆菌的MIC值,并通过计算部分抑菌浓度指数（FICI）评价联合抑菌效果.结果 通过微量肉汤稀释法检测的576株鲍曼不动杆菌中,未获得黏菌素耐药菌株.通过PAPs筛选共获得9株黏菌素异质性耐药鲍曼不动杆菌,黏菌素与美罗培南、左氧氟沙星和磷霉素联用后对异质性耐药菌株的MIC值较单用时均降低.其中,与美罗培南联用后对黏菌素异质性耐药鲍曼不动杆菌的联合抗菌活性表现为协同作用的占55.6％,相加作用占33.3％,无关作用占11.1％,不存在拮抗作用;与左氧氟沙星联用后对黏菌素异质性耐药鲍曼不动杆菌的联合抗菌活性表现为协同作用的占55.6％,相加作用占22.2％,无关作用占22.2％,不存在拮抗作用;与磷霉素联用后对黏菌素异质性耐药鲍曼不动杆菌的联合抗菌活性表现为协同作用的占77.8％,相加作用占22.2％,不存在无关和拮抗作用.结论 黏菌素与美罗培南、左氧氟沙星或磷霉素联用对黏菌素异质性耐药鲍曼不动杆菌的体外抗菌活性主要表现为协同和相加作用,与美罗培南或左氧氟沙星联用的抗菌活性较少表现为无关作用,均无拮抗作用.     

醋酸钙-鲍曼不动杆菌复合体的精确鉴定与药敏分析

目的精确鉴定醋酸钙-鲍曼不动杆菌复合体菌株;检测菌株对氨基糖苷类抗生素和碳青霉烯类抗生素的敏感性。方法运用自动化分析仪VITEK 2试卡法对临床分离不动杆菌进行菌种鉴定,对鉴定为醋酸钙-鲍曼不动杆菌复合体的菌株进一步经16S rRNA序列分析确证其准确种属。分别用自动化分析仪VITEK 2和微稀释法测定精确鉴定后的醋酸钙-鲍曼不动杆菌复合体菌株对阿米卡星、庆大霉素、妥布霉素、亚胺培南和厄他培南五种抗生素的敏感性,分析药敏实验结果。结果共进行了232株不动杆菌的VITEK 2鉴定,其中195株鉴定为醋酸钙-鲍曼不动杆菌复合体。对195株醋酸钙-鲍曼不动杆菌复合体菌株进一步用16S rRNA序列分析确证其准确种属,结果显示173株为鲍曼不动杆菌,22株为醋酸钙不动杆菌。对173株鲍曼不动杆菌及22株醋酸钙不动杆菌分别用VITEK 2和微稀释法进行阿米卡星、庆大霉素、妥布霉素、亚胺培南和厄他培南五种抗生素的药敏检测。微稀释法药敏结果显示,受试鲍曼不动杆菌对三种氨基糖苷类抗生素均呈现高水平耐药,而对两种碳青霉烯类抗生素敏感度较高;受试醋酸钙不动杆菌对五种抗生素均呈现较高敏感度。与微稀释法药敏检测结果相比,VITEK 2试卡法药敏结果中受试鲍曼不动杆菌和醋酸钙不动杆菌对各抗生素的药敏检测结果均出现了不同程度的误差,鲍曼不动杆菌药敏检测结果中阿米卡星符合率最低,严重错误率高达34.10%;醋酸钙不动杆菌药敏检测结果中厄他培南符合率最低,重大错误率高达40.91%。结论 VITEK 2在不动杆菌种属鉴定中存在局限性,辅以16S rRNA序列分析,方可精确鉴定醋酸钙-鲍曼不动杆菌复合体。鲍曼不动杆菌对氨基糖苷类抗生素耐药现状严重。用VITEK 2进行鲍曼不动杆菌和醋酸钙不动杆菌对氨基糖苷类和碳青霉烯类的药敏测定时存在不同程度的误差,建议辅以微稀释法。     

重症监护病房标本中分离的鲍曼不动杆菌的耐药性分析

目的重症监护(ICU)病房标本分离出的鲍曼不动杆菌的耐药性,指导临床用药.方法回顾性调查2006年1月至2008年6月我院ICU病房标本分离的鲍曼不动杆菌的耐药性:用API鉴定系统鉴定和纸片扩散法检测耐药性.结果 203株鲍曼不动杆菌对亚胺培南、美罗培南、头孢哌酮/舒巴坦、哌拉西林/他唑巴坦的敏感率分别为:90%、89%、88%、52%:对氨曲南、哌拉西林、复方新诺明、头孢吡肟、阿米卡星的耐药率分别为:72%、63%、52%、40%、45%.结论 ICU病房标本分离的鲍曼不动杆菌有较严重的耐药性,应引起高度重视.     

医院泛耐药鲍曼不动杆菌对碳青霉烯抗生素的耐药机制

目的 探讨医院泛耐药鲍曼不动杆菌对碳青霉烯抗生素的耐药机制.方法 应用PCR方法对2010年12月至2012年3月期间本院从临床痰标本中分离的36株泛耐药鲍曼不动杆菌进行碳青霉烯酶IMP、OXA23基因和整合子基因检测;提取细菌膜蛋白行SDS-PAGE电泳分析其组成.结果 36株泛耐药鲍曼不动杆菌碳青霉烯酶OXA23基因扩增均为阳性;14株碳青霉烯酶IMP基因扩增阳性,22株阴性.12株整合子PCR产物约1200 bp,10株约3000 bp,14株整合子PCR产物约3500 bp.与碳青霉烯抗生素敏感鲍曼不动杆菌膜蛋白比较,22株泛耐药鲍曼不动杆菌存在相对分子质量为25 000、36 000的膜蛋白缺失.结论 医院泛耐药鲍曼不动杆菌耐碳青霉烯抗生素机制与产IMP、OXA23碳青霉烯酶及膜蛋白缺失有关.     

体内诱导耐碳青霉烯类鲍曼不动杆菌膜蛋白质组学研究

目的 研究膜蛋白在耐碳青霉烯类抗生素鲍曼不动杆菌中的作用.方法 从同一住院病人体内分别收集碳青霉烯类敏感和耐药的鲍曼不动杆菌各1株.经多序列位点测序分型(MIST)和细菌基因组外回文结构重复序列分型(REP-PCR)分析后,等电聚焦电泳检测其已知碳青霉烯类水解酶的表达,在此进行膜蛋白二维电泳和质谱鉴定分析,并最后应用PABN(Phe-Arg-β-naphthylamide)外排泵抑制剂检测其外排泵相关膜蛋白表达.结果 MIST和REP-PCR结果表明耐药株来源与敏感菌株属于同一型别;等电聚焦电泳在P17.6和P19.0处两株菌中检测到β-内酰胺酶,没有检测到任何已知的碳青霉烯类水解酶;耐约株和敏感株的差异膜蛋白组学鉴定出相对分子质量(M_r)为34×10~3外排泵膜蛋白和0prD与CarO膜孔蛋白,且后续的外排泵抑制剂试验表明,在PAβN存在的情况下,耐药株的亚胺培南最低抑菌浓度(MIC)由大于32 μg/ml下降到8 μg,/ml.结论 本研究发现外排泵膜蛋白的过度表达伴随OprD和CarO膜孔蛋白的下调是临床分离耐碳青霉烯类抗生素鲍曼不动杆菌主要耐药机制.     

2009—2011年某三甲医院鲍曼不动杆菌的耐药性分析

目的了解某三甲医院临床分离的鲍曼不动杆菌的分布及对各类抗菌药物的耐药性,以指导临床规范合理使用抗生素。方法收集常州市第一人民医院2009年1月至2011年12月临床分离的鲍曼不动杆菌,采用SPSS11．5统计软件统计分析鲍曼不动杆菌的检出率和耐药情况。结果2009—2011年共分离3360株鲍曼不动杆菌,均占全院分离病原菌的前三位。最常见的分离部位为下呼吸道,主要来源于ICU、呼吸内科、神经外科和神经内科,该菌对亚胺培南、美罗培南和哌拉西林-他唑巴坦的耐药率在2009年分别是55．52％、56．53％和70．01％,2011年分别上升至79．70％、77．61％和79．76％,差异有统计学意义。结论鲍曼不动杆菌对多种抗菌药物耐药率明显增高,泛耐药鲍曼不动杆菌比例明显增加。应加强耐药性监测,规范抗菌素的使用,防止鲍曼不动杆菌的暴发流行。     

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.     

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.     

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.     

HLA in North Colombia Chimila Amerindians

HLA-A,-B,-C,-DRB1 and -DQB1 alleles have been studied in Chimila Amerindians from Sabana de San Angel (North Colombian Coast) by using high resolution molecular typing. A frequent extended haplotype was found:HLA-A*24:02-B*51:10-C*15:02-BRB1*04:07-DQB1*03:02 (28.7%) which has also been described in Amerinndian Mayos Mexican population (Mexico, California Gulf, Pacific Ocean). Other haplotypes had already been found in Amerindians from Mexico (Pacific and Atlantic Coast), Peru (highlands and Amazon Basin), Bolivia and North USA. A geographic pattern according to HLA allele or haplotype frequencies is lacking in Amerindians, as already known. Also, five new extended haplotypes were found in Chimila Amerindians. Their HLA-A*24:02 high frequencies characteristic is shared with aboriginal populations of Taiwan; also, HLA-C*01:02 high frequencies are found in New Zealand Maoris, New Caledonians and Kimberly Aborigines from Australia. Finally, this study may show a model of evolutionary factors acting and rising one HLA allele frequency (-A*24:02), but not in others that belong to the same or different HLA loci.     

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.     

Functional role of fertility α2

Fertility α₂-microglobulin is one of the main proteins expressed between the late lutein phase of the menstrual cycle and the first gestation trimester. It is produced by endometrial secretory glandular epithelium and decidual membrane. It is believed to be involved in the preparation to gestation, conception, normal development of the fetoplacental system, and initiation of labor. The immunomodulating, effect of fertility α₂-microglobulin and its possible involvement in the regulation of fertilization by blocking the spermatozoon reaction with the ovocyte lucid membrane were demonstratedin vitro. The data of structural analysis (appurtenance to lipocalines and unique pattern of N-glycosylation) and analysis of the spatial and temporal parameters of the expression in connection with other events in the organism within the same system of coordinates propated us to investigate the probability of realization of other, so far unknown functions of α₂-microglobulin. The probable mechanisms of realization of the immunomodulating function are analyzed. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 10, pp. 364–373, October 1998