胺碘酮、美托洛尔对家兔急性心肌梗死血小板活化、纤溶活性、内皮血管活性物质的影响

目的 :探讨胺碘酮、美托洛尔对兔急性心肌梗死 (AMI)血小板活化、纤溶活性、内皮血管活性物质的影响。方法 :新西兰家兔 5 0只 ,随机分为 5组 ,每组 10只。Ⅰ组 :假手术组 ,Ⅱ组 :AMI组 ,Ⅲ组 :AMI+利多卡因组 ,Ⅳ组 :AMI+胺碘酮组 ,Ⅴ组 :AMI+美托洛尔组 ;Ⅱ、Ⅲ、Ⅳ、Ⅴ组分别结扎冠状动脉左室支中点后 ,4h取血分别测定血栓素B2 (TXB2 )、6 -酮 -前列腺素F1α( 6 -Keto-PGF1α)、内皮素 (ET)、一氧化氮 (NO)和组织型纤溶酶原激活剂 (t-PA)、纤溶酶原激活剂抑制物 (PAI)水平 ;摘取心脏 ,测定心肌梗死范围。结果 :Ⅱ、Ⅲ、Ⅳ、Ⅴ组血浆TXB2 、ET、NO浓度和PAI活性显著高于Ⅰ组 (P <0 0 1) ,6 -Keto-PGF1α浓度和t-PA活性显著低于Ⅰ组 (P <0 0 1) ,Ⅱ、Ⅲ、Ⅳ组之间比较 ,血浆TXB2 、6 -Keto-PGF1α浓度、t-PA活性及心肌梗塞范围无显著差异 (P >0 0 5 ) ,Ⅳ组血浆ET、NO浓度和PAI水平明显低于Ⅱ组 (P <0 0 1) ,Ⅴ组血浆TXB2 、ET、NO浓度和PAI水平明显低于Ⅱ组 (P <0 0 1) ,6 -Keto -PGF1α浓度、t-PA活性显著高于Ⅱ组 (P <0 0 1) ,心肌梗塞范围小于Ⅱ组 (P <0 0 1)。结论 :胺碘酮抑制AMI早期PAI活性 ,减少ET和NO的释放 ;美托洛尔抑制AMI早期血小板活化 ,改善纤溶活性 ,减少ET和NO的再释放 ,缩小     

COPD患者血浆TXB2和6-K-PGF1α含量变化及其与肺动脉高压的关系

目的 :探讨慢性阻塞性肺病 (COPD)患者血栓素A2 (TXA2 )和前列环素 (PGI2 )与肺动脉高压的关系。方法 :采用RIA对伴有和不伴有肺动脉高压的 30例缓解期COPD患者血浆中血栓素B2 (TXB2 )及 6 -酮-前列腺素F1α(6 -Keto -PGF1α)分别为TXA2 及PGI2 的代谢产物的含量变化进行了观察 ,还对 7例伴肺动脉高压的COPD患者不同时期的肺动脉平均压 (PaP)、血浆TXB2 及 6 -Keto -PGF1α水平作了对比分析。结果 :缓解期COPD患者中 ,伴肺动脉高压者血浆TXB2 明显增高 ,6 -Keto -PGF1α显著下降 ,TXB2 / 6 -Keto -PGF1α明显增大 ,与不伴肺动脉高压者比较 ,差异非常显著 (P均 <0 0 1) ,而不伴肺动脉高压者的这些指标与正常人的比较 ,则无统计学意义 (P均 >0 0 5 ) ;与急性期比较 ,COPD患者缓解期PaP明显下降 ,TXB2 亦显著降低 ,6 -Keto -PGF1α明显增高 ,TXB2 / 6 -Keto -PGF1α缩小 (P均 <0 0 1) ;相关分析发现 ,伴肺动脉高压者PaP与TXB2 呈明显正相关 ,与 6 -Keto -PGF1α呈负相关 (n =2 8,r = 0 .4 6 ,- 0 .39,p均 <0 0 5 )。 结论 :TXA2和PGI2 的代谢失常及两者之间的失衡与肺动脉高压的形成有非常密切的关系。     

153Sm-EDTMP对骨转移癌患者血浆TXB2,6-K-PGF1α水平的影响

目的 :观察153 Sm -EDTMP对骨转移癌患者血浆TXB2 、6 -K -PGF1α水平的影响。方法 :5 5例骨转移癌患者 ,肘静脉注射153 Sm -EDTMP ,剂量按 (18 5～ 37)MBq/kg ,放射免疫分析治疗前后不同时间血浆TXB2 、6 -K -PGF1α的浓度。结果 :血浆TXB2 治疗前、治疗 (1～ 2 )月与治疗 3月后无显著差异 ;6 -K -PGF1α治疗后 (1～ 2 )月较治疗前明显降低 ,3月后升高 ,骨痛缓解率高。结论 :153 Sm -EDTMP可调节 6 -K -PGF1α水平 ,这可能与其治疗骨转移癌骨痛的作用有关。     

心房颤动患者血浆TXB2,6-K-PGF1α浓度测定及意义

目的 :研究心房颤动 (房颤 )病人血浆血栓素B2 (TXB2 )、6 -酮 -前列腺素F1α(6 -K -PGF1α)浓度变化 ,探讨房颤引起血栓前状态 (Prethromboticstate ,PTS)的机制。方法 :用放射免疫分析对 2 1例孤立性阵发性房颤者 (IPAF)分别于房颤发作及终止后 1周测定外周静脉血浆TXB2 、6 -K -PGF1α浓度 ,并与 2 8例孤立性持续性房颤 (ISAF)、2 7例二尖瓣狭窄伴持续性房颤 (RHD)、32例阵发性室上性心动过速 (PSVT)及 35例健康志愿者相比较。结果 :IPAF房颤发作时 ,ISAF及RHD病人血浆TXB2 浓度和TXB2 / 6 -K -PGF1α比IPAF房颤终止后 1周、PSVT、正常对照组明显上升 ,而 6 -K -PGF1α无差别。TXB2 浓度及TXB2 / 6 -K -PGF1α比值与IPAF房颤发作时间呈正相关 ,而与患者年龄、性别及左心房内径等临床参数无关。结论 :房颤时血小板的激活和血管内皮细胞功能状况的改变参与房颤PTS的发生     

CCl4诱发肝损伤过程中血浆几种花生四烯酸代谢物和激素水平动态变化的研究

目的 :深入了解肝损伤对机体血浆花生四烯酸代谢、一些激素代谢以及肝脏功能变化产生的影响。方法 :选用 30只健康、1月龄SD大鼠 ,通过腹腔注射CCl4 诱发肝损伤后 ,第 2、4、6、8周观察血浆前列腺素E2(PGE2 )、6 -酮 -前列腺素F1α(6 -keto -PGF1α)、血栓素B2 (TXB2 )、谷 -草转氨酶 (AST)、碱性磷酸酶 (AKP)、皮质醇、胰岛素、生长激素 (GH)、甲状腺素 (T4 )和三碘甲腺原氨酸 (T3)水平变化。结果 :在整个实验期 ,大鼠血浆PGE2 水平在CCl4 注射后的第 2周高于对照组 ,TBX2 比对照组高 ,但二者t检验无显著性。而 6 -keto -PGF1α与对照组相近 ;血浆AST和AKP活力分别极显著高于对照组 ;皮质醇和胰岛素于 2、6、8周显著高于对照组 ;GH、T3均于第 8周显著低于对照组。T4 则于第 4、6、8周显著低于对照组。结论 :肝损伤影响血中花生四烯酸代谢物水平和代谢 ;并导致血中几种代谢激素水平的异常变化     

慢性房颤患者TXB2、6-K-PGF1α和PGE2的变化探讨

目的：研究慢性心房纤颤（CAF）患者血清血栓素B2（TXB2）、6-酮-前列腺素F1α（6-K-PGF1α）和前列腺素E2（PGE2）水平的变化及其临床意义。方法：放射免疫分析测定162例CAF患者、印例无CAF患者和40例对照组的血清TXB2、6-K-PGF1α和PGE2水平，并进行统计分析。结果：CAF组血清TXB2水平显著高于无CAF组和对照组（P均〈0．01），6-K-PGF1α显著低于对照组（P〈0．01），PGE2三组间无显著差异（P均〉0．05），CAF组中TXB2与6-K-PGF1α成显著正相关（P〈0．01）。CAF患者中Ⅰ、Ⅱ、Ⅲ、Ⅳ级心功能组间平均血清TXB2和6-K-PGF1α水平均呈依次显著性递增（P均〈0．01），PGE2无显著性改变（P〉0．05）；伴脑血栓组血清TXB2和6-K-PC-F1α水平均显著高于无脑血栓组（P均〈0．01）；住院死亡组血清TXB2水平显著高于好转出院组（P〈0．01）。结论：CAF患者血清TXB：水平显著增高，并随心功能分级依次递增，伴脑血栓组更高，死亡组TXB2也明显增高；CAF患者血清6-K-PGF1α水平明显降低；PGE2则无明显改变。     

153Sm-EDTMP对多发性骨转移癌骨痛作用机制的初步探讨

目的 :探讨153 Sm -EDTMP对多发性骨转移癌患者痛反应与体内疼痛因子的变化的关系。方法 :对5 5例多发性骨转移癌患者153 Sm -EDTMP治疗前与治疗 (1～ 2 )个月及 3个月后血浆内皮素 (ET)、降钙素基因相关肽 (CGRP)、血栓素B2 (TXB2 )与 6酮 -前列腺素F1α(6 -k -PGF1α)含量变化进行了测定。结果 :治疗 3月后 6 9 1% (38/ 5 5 )患者疼痛缓解。TXB2 水平治疗前、治疗 1月～ 2月与治疗 3月后 ,差异均无显著意义 (P均>0 0 5 ) ;6 -k -PGF1α含量治疗 1月～ 2月与治疗前相比显著降低 (P <0 0 1) ,治疗 3月后显著高于治疗前 (P<0 0 1)及治疗 1月～ 2月 (P <0 0 1)。治疗 1月～ 2月血浆ET水平与治疗前相比无显著降低 (P >0 0 5 ) ,治疗 3月后与治疗 1月～ 2月、治疗前相比显著升高 (P均 <0 0 1) ;CGRP含量治疗 1月～ 2月与治疗前相比显著升高 (P <0 0 5 ) ,治疗 3月后较治疗 1月～ 2月显著减低 (P <0 0 1)、与治疗前相比无显著性差异 (P >0 0 5 )。ET/CGRP值治疗 3月后显著高于治疗 1月～ 2月及治疗前 (P均 <0 0 1)。结论 :多发性骨转移癌患者治疗后骨痛反应与疼痛因子 6 -k -PGF1α含量密切相关 ,与体内的ET含量以及ET和CGRP之间的平衡变化有关。     

永久性心房颤动患者血清TXB2、6-K-PGF1α和PGE2改变的探讨

目的:探讨永久性心房颤动(PAF)患者血清血栓素B2(TXB2)、6-酮-前列腺素F1α(6-K-PGF1α)和前列腺素E2(PGE2)水平的变化及其临床意义.方法:采用放射免疫分析158例PAF患者和40例健康对照组的血清TXB2、6-K-PGF1α和PGE2水平,进行对照统计分析.结果:PAF组血清TXB2水平[(80.89±18.86)ng/L vs (51.38±7.66)ng/L]和 PGE2水平[(11.48±4.20)ng/L vs (7.15±1.26)ng/L]显著高于健康对照组( P<0.01;P<0.01),6-K-PGF1α水平[(49.81±7.53_ng/L vs (81.12±9.02)ng/L]显著低于健康对照组(P<0.01),三者之间均无显著相关性(P均＞0.05).NYHA心功能Ⅰ、Ⅱ、Ⅲ和Ⅳ级组PAF患者血清TXB2和PGE2水平依次升高,具有统计学意义(P均<0.01),6-K-PGF1α水平变化无统计学差异(P>0.05)(方差检验F TXB2=52.75,P<0.01;F 6-K-PGF1α=0.949,P>0.05;F PGE2=62.04;P<0.01).合并脑梗死组血清TXB2水平显著高于无合并组(P<0.01),但6-K-PGF1α和PGE2无统计学差异(P均>0.05).结论:PAF组血清TXB2和PGE2水平显著高于健康对照组,6-K-PGF1α水平显著低于健康对照组;心功能Ⅰ、Ⅱ、Ⅲ和Ⅳ级组PAF患者血清TXB2和PGE2水平依次升高,合并脑梗死组血清TXB2水平显著升高.     

康赛宁联合IL-2对C57BL/6小鼠Lewis肺癌原发瘤生长的影响

目的 :选择具有协同免疫调节作用的生物制剂进行联合治疗是提高肿瘤生物治疗 ,减少抗癌药物的副作用。方法 :40只Ｃ57ＢＬ/6小鼠右侧腋下皮下接种Ｌｅｗｉｓ肺癌瘤株 (ＬＬＣ) 1 5× 1 0 6实验分 4组 ,每组 1 0只小鼠 ,Ⅰ组为对照组 ,注射生理盐水 ;Ⅱ组注射康赛宁 ;Ⅲ组为注射ＩＬ - 2 ;Ⅳ组为康赛宁 白细胞介素Ⅱ剂量减半。接种肿瘤第 2ｄ开始用药 ,间日注射 ,5次为一疗程 ,进行二个疗程 ,中间间隔 4ｄ。结果 :1 Ⅱ、Ⅲ组较对照组Ⅰ肿瘤潜伏期延长 ,肿瘤体积与重量都明显减少 (Ｐ <0 0 5)。第二个疗程结束时 ,抑瘤率分别为 40 %、30 %…     

心肌缺血程度与ET-1、TXB2、6-keto-PGF1α水平相关性分析

为了解不同缺血程度冠心病（CHD）患者血浆中内皮素-1（ET-1）和血栓素B2（TXB2）、6-酮-前列腺素F1α（6-keto—PGF1α）水平，现经检测后将结果报道如下。     

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