Blood platelets are the central players in thrombosis and blood coagulation. Moreover, they also exhibit immunoregulatory properties and bridge hemostasis and immunity. Morphological and functional characteristics of the platelets ensure continuous surveillance for the vascular system, recognition of different hazards, development of appropriate response and recruitment of immune cells. Indirect platelet-leukocyte interactions are mediated by immunoregulatory molecules that are released, along with coagulation and thrombosis factors in the course of platelet activation and degranulation. Chemokines, cytokines, growth factors, some of which are synthesized de novo , are released from activated platelets and modulate cellular functions, thus modulating both innate and adaptive immune response. Activated platelets enter contacts with immune cells to form heterotypic aggregates, i.e., platelet-leukocyte complexes that reside in blood circulation along with other blood cells. The aggregate formation and stabilization is mediated by interaction between the molecules expressed on the surface of platelets and leukocytes, in particular, P-selectin (CD62P) and PSGL-1 (CD162). Platelet-monocyte and platelet-neutrophil complexes are most abundant, with platelet-monocyte aggregates being most stable. Moreover, the platelet-derived microvesicles also interact with leukocytes to form heterotypic aggregates, thus, probably, modulating the immune cell functions via transfer of non-coding RNA molecules. Formation of platelet-leukocyte complexes results into mutual activation of platelets and leukocytes. Platelets and platelet-derived microvesicles stimulate phagocytic activity, cytokine secretion, and generation of reactive oxygen species in monocytes and neutrophils, inducing formation of neutrophilic extracellular traps and procoagulant phenotype in monocytes. The blood platelets regulate monocyte differentiation, promote adhesion, as well as transmigration of lymphocytes and NK cells. At the sites of inflammation, platelets enhance extravasation and infiltration of leukocytes into the damaged tissue. Impaired interactions of platelets with endothelial layer and immune cells may underlie pathogenic conditions. Increased level of circulating plateletleukocyte complexes is observed in various disorders including cardiovascular diseases, acute ischemic stroke, respiratory disorders, renal pathologies, liver diseases, diabetes, reproductive disorders, bacterial and viral infections. Further studies of platelet-leukocyte interactions are warranted to unveil pathogenic mechanisms and to develop new therapeutic approaches.

Введение. Адекватный контроль функциональной активности тромбоцитов, в том числе при воздействии антиагре­гантных препаратов, является нерешенной проблемой лабораторной диагностики. К наиболее часто используемым методам определения функциональной активности тромбоцитов относятся оптическая агрегатометрия и проточная цитометрия. Цель исследования: оценить изменения функциональной активности тромбоцитов под влиянием антиагрегантных препаратов, используя методы оптической агрегатометрии и проточной цитометрии. Материалы и методы. В проспективном исследовании приняли участие 22 здоровые женщины фертильного возраста (26,0 ± 4,7 лет). Кровь отбирали из локтевой вены в вакутейнер с антикоагулянтом – цитратом натрия в соотношении кровь: антикоагулянт = 9:1. В качестве антиагрегантов использовали ацетилсалициловую кислоту (АСК) и эптифибатид. С помощью метода оптической агрегатометрии оцени­вали степень и скорость агрегации тромбоцитов (АТ). Методом проточной цитометрии оценивали экспрессию P-селектина (CD62P), гликопротеина GPIIb/IIIa (CD41а) и образование тромбоцитарно-лейкоцитарных комплексов. Результаты. Определение функциональной активности АДФ-индуцированных тромбоцитов под действием АСК выявило снижение скорости и степени их агрегационной активности и снижение уровня экспрессии CD41a и CD62P. При обработке тромбоцитов препаратом эптифибатид установлено увеличение экспрессии CD62P и CD41a и выраженное подавление скорости и степени АТ. Добавление АСК не оказывало заметного влияния на АДФ-индуцированное образование комплексов тромбоцитов с лейко­цитами. Напротив, в присутствии эптифибатида наблюдали более интенсивную АТ с лейкоцитами. Заключение. Оценку функциональной активности тромбоцитарного звена гемостаза необходимо проводить с учетом всех этапов активации тромбоцитов и их участия в межклеточных взаимодействиях. Расширение подходов к оценке эффективности антиагрегантной терапии лабораторными методами имеет большое значение для поиска безопасных и эффективных методов лечения пациентов с тромбофилическими состояниями на различных этапах их развития. Background. Adequate control of platelet functional activity, including exposure to antiplatelet drugs, is an unresolved problem in laboratory diagnostics. Optical aggregation and flow cytometry are the most commonly used methods for determining of platelet functional activity. Objective: to assess changes in platelet functional activity under the influence of antiplatelet drugs using optical aggregation and flow cytometry methods. Patients/Methods. The prospective study involved 22 healthy women of fertile age (26.0 ± 4.7 years). Blood was taken from the cubital vein into a vacutainer with an anticoagulant – sodium citrate in ratio blood: anticoagulant = 9:1. Acetylsalicylic acid (ASA) and eptifibatide were used as antiplatelet agents. The degree and rate of platelet aggregation (РA) were accessed by optical aggregation. Flow cytometry was used to assess the expression of P-selectin (CD62P), glycoprotein GPIIb/IIIa (CD41a) and the formation of platelet-leukocyte complexes. Results. Determination of the functional activity of ADP-induced platelets under ASA action revealed a decrease in the rate and degree of РA activity and a decrease in the level of CD41a and CD62P expression. Platelet processing with eptifibatide caused an increase of CD62P and CD41a expression anda pronounced suppression of РA rate and degree. ASA addition had no significant effect on ADP-induced formation of platelet-leukocyte complexes. On the contrary, more intense РA with leukocytes was observed in the presence of eptifibatide. Conclusions. Assessment of platelet functional activity should take into account all stages of platelet activation and their participation in intercellular interactions. Expansion of approaches for assessing of antiplatelet therapy effectiveness by laboratory methods is of great importance for searching safe and effective methods of treating patients with thrombophilic conditions at various stages of their development.

The article presents the results of the investigation of cytokine production by endometrioid heterotopias in organotypic cultivation in comparison with the cell secretory activity of peritoneal fluid and endometrial tissue in women with external genital endometriosis. The obtained results show systemic changes of regulation of cytokine production in the process of external genital endometriosis development.

Activated platelets aggregate with monocytes by binding membrane bound molecules. Platelet-monocyte interaction is considered to underlie pathophysiological mechanisms bridging thrombosis and inflammation. Detection and analysis of platelet-monocyte complexes (PMC) provide means for revealing their physiological and pathogenetic roles and are instrumental in the diagnostics of various pathological conditions including obstetric complications. The aim of the study was to develop the method of quantitative determination of peripheral blood PMC, that preserve phenotypic features of platelets and monocytes, and to reveal their changes by ex vivo analysis. The suggested procedure includes immediate fixation of blood sample, immunocytochemical staining with fluorochrome-conjugated specific antibodies against markers of activation and differentiation followed by lysis of erythrocytes, and flow cytometric analysis. Fourteen samples of peripheral blood from patients with history of pregnancy complication were obtained in first trimester of ongoing pregnancy and analyzed. It was demonstrated that quantitative and qualitative in vivo characteristics of PMC remained unchanged in fixed samples, whereas the number of PMC and expression levels of the markers of platelet and monocyte activation dramatically increased in the unfixed blood. The set of monoclonal antibodies and gating strategies, used in this study, ensure phenotyping and evaluation of percentage/absolute count of PMC in the total monocyte population (CD45+CD14+) and in the subpopulations of classical (CD14+CD16-), intermediate (CD14+CD16+), and non-classical (CD14lowCD16+) monocytes. This approach provides insight into the participation of different monocyte subsets in the formation of PMC and their roles in physiological and pathophysiological processes. In some samples, elevated PMC proportion was observed, accompanied by significant increase in the expression of platelet activation marker CD62P and decrease in the expression of its monocytic ligand CD162. These changes suggested altered activation of PMC and their participation in the pathophysiological mechanisms of some pregnancy complications. Immunophenotyping of PMC affords an opportunity to characterize their proinflammatory, procoagulant and adhesive properties; these results can be used for research and diagnostics. In particular, the method is suitable for detection and phenotyping of PMC in pregnancy complications and other pathological conditions associated with the disorders of hemostasis and thrombosis.

Introduction: Macrophages participate in the regulation immune and morphogenetic events in the placenta. However, these roles remain unclear for placental macrophages (Hofbauer cells). The aims of this study were to characterize the consecutive steps of cytokine production (intracellular synthesis and secretion) in placental macrophages in early and late gestation and to compare the secretory profiles of placental macrophages and villous tissue. Methods: Macrophages and villous tissue were isolated from placentas obtained from normal pregnancies at either 9-12 or 38-40 weeks of gestation. Intracellular cytokines were determined by flow cytometry after staining with monoclonal antibodies. Secreted cytokines were quantified by cytometric bead array and ELISA. Results: Two patterns of cytokine production were revealed in placental macrophages. Cytokines in the first group (IL-1, IL-6, IL-8, IL-10, TNF alpha) demonstrated low basal production and were stimulated by bacterial endotoxin. Cytokines in the second group (IL-11, IL-17A, IL-17F, TGF-beta, VEGF) were characterized by constitutive production and did not respond to stimulation. Gestational age-dependent changes were observed: basal secretion of TNF alpha and IL-8 increased whereas IL-11 and IL-17 secretion decreased in third-trimester macrophages compared with the first-trimester cells. Comparison of cytokine production at the cellular and tissue levels suggested the contribution of the placental macrophages both in intraplacental and extraplacental cytokine production. Discussion: It would be safe to assume that the two patterns of cytokine production, revealed in our study, correspond to two regulatory roles of placental macrophages: "immune" and "morphogenetic". The inflammatory phenotype of macrophages is attenuated in early gestation and increases with the progression of pregnancy. The cytokines of the first group supposedly contribute to both local and extraplacental levels, whereas the cytokine effects of the second group are more likely confined to the placental tissue.

Recurrent pregnancy loss is a significant clinical problem affecting 1-5% of the population, while in more than half of the cases the cause of premature loss of pregnancy remains unknown. Changes in the morphofunctional properties of monocytes can be factors leading to various pregnancy complications, in particular, to miscarriage. However, the role of monocytes in the pathogenesis of recurrent pregnancy loss has not been sufficiently studied. The aim of the study was to determine the quantitative changes in the content and antigenic phenotype of platelet-free (not bound to platelets) monocytes at the level of the entire population and individual subpopulations of peripheral blood monocytes in recurrent miscarriage compared to uncomplicated pregnancy. The study groups included 6-12-week pregnant women aged 24-42 years diagnosed with recurrent pregnancy loss and women with uncomplicated pregnancy (7-12 weeks). Monocyte content and expression of CD11b, CD86, CD162, HLA-DR, TREM-1 were determined in the total population and subpopulations of peripheral blood monocytes using cytofluorimetric analysis. It was found that the proportion of platelet-free monocytes decreased (74.6%) compared to uncomplicated pregnancy (83.4%), with all three subpopulations of monocytes (classical, intermediate and non-classical) contributed to the decrease. Decrease in HLA-DR expression and increase in CD11b expression was observed in total PMC, caused by the fraction of classical monocytes, while the expression of CD162, CD86 and TREM-1 did not change significantly. Subpopulations of monocytes contributed differently to the changes in the expression levels of activation markers, associated with recurrent miscarriage, and these changes were not always manifested in the total monocyte population. The results obtained suggest that recurrent pregnancy loss is accompanied by a decrease in the content of free monocytes in the peripheral blood and changes in the antigenic phenotype of monocytes, characterizing a weakening of the proinflammatory properties and an increase in the adhesive properties of these cells. These changes may underlie the pathophysiological processes leading to premature termination of early pregnancy. Determination of the expression patterns ofactivation markers characteristic of a particular obstetric pathology contributes not only to the identification of pathophysiological mechanisms of reproductive disorders, but also to the improvement of methods for their diagnosis and the development of pathogenetically reasoned methods of therapy.

Abstract. Pregnancy represents the state with particularly activated constituents of hemostasis and immune systems. Hyperactivation of platelets and monocytes may be a causative factor for pregnancy complications including preeclampsia. The pathogenetic role of platelet-monocyte complexes (PMC), recognized as diagnostic marker and therapeutic target, is poorly investigated. The aim of the study was to determine quantitative changes in the peripheral blood PMC level and antigenic phenotype in preeclampsia, and to evaluate effects of platelets on the expression of monocyte surface marker proteins in normal and pathological pregnancy. The tested groups included third trimester pregnant women diagnosed with severe preeclampsia (35-41 weeks of gestation) and women with uncomplicated (physiological) pregnancies (33-41 weeks of gestation). All participants were between the age of 24 and 42 years. PMC levels and CD62P, CD11b, CD86, CD162, HLA-DR, TREM-1 expressed by PMC and free circulating cells were determined by flow cytometry in the peripheral blood total monocytes and monocyte subpopulations.It was found that PMC level increased (29.2% of total monocyte population) when compared to uncomplicated pregnancy (17.5%), and this augmentation was ensured by two PMC-forming monocyte subpopulations: classical and intermediate. Moreover, expression levels of platelet and monocyte activation markers CD62P, CD162, HLA-DR, CD86, TREM-1, CD11b were significantly higher in preeclampsia. The fractions of classical, intermediate and non-classical monocytes differently contributed to preeclampsia-associated changes in the expression levels of monocyte activation markers. Comparison of PMC and free circulating monocytes demonstrated that observed changes in the surface antigenic phenotype of monocytes within PMC were ensured by platelets and other factors. In preeclampsia, platelet-induced augmentation of monocyte inflammatory and adhesive capacities displayed itself in the increased TREM-1 and CD11b expression. In contrast, increased levels of HLA-DR and CD86 in monocytes were not induced by the interaction with platelets. The results of the study suggest that preeclampsia is accompanied by increased peripheral blood PMC levels and activation of monocytes within PMC, demonstrate immunomodulatory effect of platelets, and provide a rationale for the evaluation of expression patterns of PMC surface antigenic markers with diagnostic and therapeutic purposes.

Recurrent pregnancy loss is a significant clinical problem that affects 1-5% of the population, and in more than half of cases the cause of premature pregnancy loss remains unknown. One of the possible reasons is an imbalance in the maternal hemostatic system, leading to thrombosis of the uteroplacental vessels, decreased placental perfusion and hypoxia. Changes in the morphofunctional features of monocytes and the aggregates formed by them and activated platelets can be factors causing various complications of pregnancy, in particular, miscarriage. However, the role of platelet-monocyte complexes (PMC), which are of interest as a diagnostic marker and as a therapeutic target, is virtually unknown in the pathogenesis of recurrent pregnancy loss. The purpose of the study was to determine quantitative changes in the content and phenotypic characteristics of the peripheral blood PMC in patients with recurrent miscarriage, and to assess the effect of platelets on the expression of monocyte surface marker proteins during the physiological and pathological pregnancy. The study groups consisted of women aged 24-42 years diagnosed with recurrent miscarriage, having a current pregnancy of 6-12 weeks, and women with an uncomplicated (physiological) pregnancy of 7-12 weeks. In the total population and subpopulations of peripheral blood monocytes, the PMC content and expression of platelet and monocyte surface antigens CD62P, CD11b, CD86, CD162, HLA-DR, TREM-1 were determined using cytoflorimetric analysis. It was found that in recurrent pregnancy loss, the level of PMC was increased (26.5%) compared to uncomplicated pregnancy (15.3%), and all three subpopulations of monocytes (classical, intermediate and non-classical) contributed to the increase. At the same time, a decrease in HLA-DR expression and increase in CD11b expression was observed in the total PMC, while the expression of CD62P, CD162, CD86 and TREM-1 did not change significantly. Monocyte subpopulations differently contributed to the changes in the expression of activation markers associated with recurrent miscarriage, and the changes seen in subpopulations were not always evident in the toatl monocyte population. A comparison of PMC and free monocytes showed that changes in the surface phenotype of monocytes aggregated with platelets, were caused by both the influence of platelets and other factors. In cases of recurrent miscarriage, a platelet-induced increase in the adhesive properties of monocytes was observed, which was manifested in an increase in CD11b expression. In contrast, the decrease in the level of HLA-DR expression in monocytes was not associated with their interaction with platelets. The results obtained suggest that recurrent miscarriage is accompanied by an increase in the content of peripheral blood PMC and changes in the antigenic phenotype of platelet-associated and free monocytes, demonstrate the immunomodulatory effect of platelets, and also provide justification for the importance of determining the expression patterns of surface antigenic markers of PMC for diagnostic and therapeutic purposes.

PROBLEM:To determine if placental macrophages (Hofbauer cells) can synthesize and secrete cytokines of the IL-17 family throughout pregnancy and to reveal the patterns of cytokine expression in early and late gestation.METHODS OF STUDY:Macrophages were isolated from the first-trimester and term placental villous tissues from normal pregnancies. Basal and stimulated intracellular production of IL-17A, IL-17E, IL-17F as well as IL-17A secretion was quantified by flow cytometry and cytometric bead array, respectively. The expression of IL-17 and IL-23 receptors was determined on the surface of the placental macrophages by flow cytometry after antibody staining.RESULTS:In early and late gestation, a substantial proportion of the placental macrophages synthesized IL-17A and IL-17F, but not IL-17E, as determined by intracellular staining of the cytokines. Neither the intracellular production nor the secretion of IL-17 was significantly affected by LPS stimulation and spontaneous labour. The level of secretion decreased slightly but significantly at term. The IL-23 receptor was absent on the surface of cells, whereas variable expression of the IL-17 receptor was observed.CONCLUSION:Placental macrophages constitutively produced IL-17 at different gestational ages and represent thus a source of this cytokine in the human placenta. Patterns of the cytokine and receptor expression suggest that this cell population may participate in non-immune processes and contribute to the regulation of placental development and function.

Introduction: Mononuclear phagocytes are thought to significantly contribute to cytokine regulation at the maternal-foetal interface, but the role of placental macrophages has been poorly investigated. TNF alpha and VEGF were demonstrated to have regulatory effects on basic structures of the placenta, particularly the trophoblast and blood vessels. The aims of this study were to determine the expression of TNF alpha, VEGF and related receptors in placental macrophages, and how does the participation of placental macrophages alter with gestational age in TNF alpha-and VEGF-mediated signaling.Methods: Macrophages were isolated from placental villous tissue from normal pregnancies at either 9 -12 or 38-40 weeks gestation. Cell surface receptors (TNFR1, TNFR2, VEGFR1, and VEGFR2) and intracellular TNF alpha and VEGF were quantified by flow cytometry after antibody staining. Basal and stimulated secretion of both cytokines and soluble TNF receptors was quantified by cytometric bead arrays. Secreted VEGFR1 was measured by ELISA.Results: The expression of TNFR1 and VEGFR1 was remarkably variable and did not change from first to third trimester. There was minimal basal TNF alpha production in the placental macrophages, but nearly all cells in the population produced VEGF. TNF alpha and VEGF secretion increased with gestational age accompanied by decreased secretion of the antagonists sTNFR1 and sVEGFR. Macrophages isolated from early term placentas were less effective in responding to bacterial endotoxin. Lipopolysaccharide induced increases in the secretion of TNF alpha, TNFR1, TNFR2, and VEGFR1 but did not affect the production of VEGF. In late pregnancy, a significant correlation was observed between TNFR1 and VEGFR1.Discussion: The progression of pregnancy is accompanied by the concerted increase in TNF alpha and VEGF secretion and decrease in the production of their soluble receptors, but the expression of cell surface receptors does not depend on gestational age. The observed patterns of basal and stimulated expression of TNF alpha and VEGF may reflect the dual immune and morphogenetic roles of placental macrophages in gestation. Compatible patterns of TNFR1 and VEGFR1 expression suggest common regulatory pathways for these receptors. (C) 2016 Elsevier Ltd. All rights reserved.

The expression of surface molecules in cord blood monocytes and placental macrophages was studied using flow cytometry. When compared with monocytes, macrophages presented a decrease in HLA-DR and LAP/TGF-β1 levels and increased expression of alternative activation markers, especially CD206. No difference in the production of the apoptotic factors TRAIL and TWEAK was observed, whereas the levels of cytokine receptors in monocytes were significantly higher than in macrophages. Most remarkable was the difference in the expression of IL-17 and TNFα receptors. A strong correlation between VEGF and TNFα receptors was revealed in both cell populations. The results obtained in this study provide antigenic phenotypes for two related cell populations and outline the feasible functional alterations during tissue macrophage differentiation.

The expression of VEGF and membrane-bound and soluble forms of the VEGF-R1 receptor in cultured placental macrophages (trimesters I and III of pregnancy) was studied by flow cytometry, cytometric bead array, and ELISA. Nearly all population of placental macrophages (98%) was capable of producing VEGF during the early and late gestational periods. However, the expression of cellular VEGF-R1 varied from 3.4 to 92%. VEGF secretion was relatively low in the first and third trimesters (0.5 and 1.1 pg/10(5) cells, respectively). Cultured placental macrophages produced soluble receptor sVEGF-R1 in the first and third trimesters (86.4 and 36.4 pg/10(5) cells, respectively). Stimulation with LPS was followed by a 4-fold increase in sVEGF-R1 secretion. Our results indicate that placental macrophages are involved in the autocrine and paracrine regulation in chorionic villi. The data suggest that these cells have a physiological and pathogenetic role in gestation.

PROBLEM:IL-11 is a cytokine with pleiotropic activities, including gestational effects. Whereas IL-11 production by maternal reproductive tissues is extensively studied, there is poor information about IL-11 sources in the fetal counterpart of the maternal-fetal unit.METHOD OF STUDY:We investigated the expression of IL-11 in the purified human term placenta macrophages, using flow cytometry and immunoenzyme assay.RESULTS:Intracellular IL-11 was detected in a substantial proportion of cultured CD68(+) cells (median 38%). IL-11 secretion by the placental macrophages was observed after 23-hr cultivation (median 4.3 pg/10(5) cells). Stimulation with lipopolysaccharide did not significantly change both intracellular expression and secretion of the cytokine.CONCLUSION:Demonstrated IL-11 expression by placental macrophages suggests that non-trophoblast cells contribute to IL-11 production at the maternal-fetal interface and thus account for the reproductive effects of the cytokine.

MERIT is a proof‐of‐principle experiment of a target station suitable as source for future muon colliders or neutrino factories. When installed at the CERN (European Organization for Nuclear Research) PS (Proton Synchrotron) complex fast‐extracted high‐intensity proton beams intercepted a free mercury jet inside a normal‐conducting, pulsed 15‐T capture solenoid magnet cooled with liquid nitrogen. Up to 25 MJ of Joule heat was dissipated in the magnet during a pulse. The fully automated, remotely controlled cryogenic system of novel design permitted the transfer of nitrogen by the sole means of differential pressures inside the vessels. This fast cycling system permitted several hundred tests in less than three weeks during the 2007 data taking campaign.

The ATLAS detector at the CERN LHC is equipped with a superconducting magnet system consisting of three large toroids and a solenoid. The 2.3m diameter, 5.3m long solenoid is located at the heart of the experiment where it provides a 2T field for spectrometry of the particles emanating from the interaction of the counter-rotating beams of hadrons. As the electromagnetic calorimeter of the experiment is situated outside the solenoid, the coil must be as transparent as possible to traversing particles. The magnet, which was designed at KEK, incorporates progress in technology coming from the development of previous solenoids of this type, in particular that of a new type of reinforced superconductor addressing the requirement of transparency. Special attention has been paid to ensuring reliability and ease of operation of the magnet, through the application of sufficiently conservative guidelines for the mechanical and electrical design, stringent testing during manufacture, and a comprehensive commissioning program. This report gives an overview of the design, manufacture, test, installation and commissioning of the ATLAS central solenoid.

PROBLEMMacrophages are apparently the only immune cells within placenta villi, yet functions of these cells remain obscure. It has been postulated that placental macrophages accomplish regulatory roles at the fetal-maternal interface by means of wide variety of secreted cytokines. We attempt to analyze the patterns of cytokine production in an isolated population of placental macrophages.METHOD OF STUDYMacrophages were obtained from term placentas in the absence of spontaneous labor. The basal and lipopolysaccharide (LPS)-stimulated levels of intracellular cytokines were detected by flow cytometry. The basal cytokine secretion was determined by BD Cytometry Bead Array (BD Biosciences, San Diego, CA, USA).RESULTSIntracellular IL-1alpha, IL-1beta, IL-6, and TNFalpha were detected in 31, 27, 4, and 3% CD68+ cells, respectively. Stimulation with LPS increased the proportions of cytokine-producing CD68+ cells to 48, 50, 28, and 49%, respectively. Under basal conditions, levels of released TNFalpha and IL-6, respectively, were 20- and 25-fold higher when compared with IL-1b while IL-10 was secreted in small but detectable amounts. When a secretory activity was estimated for cytokine-producing cells, the secretion rate for TNFalpha and IL-6 overwhelmingly surpassed that for IL-1beta (TNFalpha:IL-6:IL-1beta ratio was 192:145:1).CONCLUSIONThese results suggest functional heterogeneity of the placental macrophage population and contribute to the elucidation of regulatory roles of these cells in gestation.

Problem Macrophages are apparently the only immune cells within placenta villi, yet functions of these cells remain obscure. It has been postulated that placental macrophages accomplish regulatory roles at the fetal–maternal interface by means of wide variety of secreted cytokines. We attempt to analyze the patterns of cytokine production in an isolated population of placental macrophages. Method of study Macrophages were obtained from term placentas in the absence of spontaneous labor. The basal and lipopolysaccharide (LPS)-stimulated levels of intracellular cytokines were detected by flow cytometry. The basal cytokine secretion was determined by BD ™ Cytometry Bead Array (BD Biosciences, San Diego, CA, USA). Results Intracellular IL-1α, IL-1β, IL-6, and TNFα were detected in 31, 27, 4, and 3% CD68+ cells, respectively. Stimulation with LPS increased the proportions of cytokine-producing CD68+ cells to 48, 50, 28, and 49%, respectively. Under basal conditions, levels of released TNFα and IL-6, respectively, were 20- and 25-fold higher when compared with IL-1β while IL-10 was secreted in small but detectable amounts. When a secretory activity was estimated for cytokine-producing cells, the secretion rate for TNFα and IL-6 overwhelmingly surpassed that for IL-1β (TNFα:IL-6:IL-1β ratio was 192:145:1). Conclusion These results suggest functional heterogeneity of the placental macrophage population and contribute to the elucidation of regulatory roles of these cells in gestation.

Secretion of IL-1α, IL-1α, IL-6, IL-10, and TNF-α cytokines by villous chorion cultures (7–14 weeks) during normal pregnancy and in spontaneous abortions was studied. Secretion of IL-1α and IL-6 increased 4.5 and 7.3 times in miscarriages, while secretion of IL-1α, IL-10, and TNF-α decreased. LPS stimulated the production of IL-1α and IL-6 in samples obtained during surgical abortion. LPS stimulated IL-1α and TNF-α secretion in miscarriages, while the level of IL-6 production decreased significantly. It is hypothesized that increased production of IL-1α and IL-6 and attenuation of the antiinflammatory effect of IL-10 play an important role in the pathogenesis of miscarriages at early stages of gestation. The results suggest that cytokine regulation of the fetus rejection is different at early and late stages of gestation.

The ATLAS detector is presently under construction as one of the five LHC experiment set-ups. It relies on a sophisticated magnet system for the momentum measurement of charged particle tracks. The superconducting solenoid is at the center of the detector, the magnet system part nearest to the proton-proton collision point. It is designed for a 2 Tesla strong axial magnetic field at the collision point, while its thin-walled construction of 0.66 radiation lengths avoids degradation of energy measurements in the outer calorimeters. The solenoid and calorimeter have been integrated in their common cryostat, cooled down and tested on-surface. We review the on-surface set-up and report the performance test results.

The central solenoid is part of the superconducting magnet system of the ATLAS experiment at the CERN LHC collider. It provides a 2 tesla axial magnetic field for the inner 24 m 3 volume centre particle tracker. Design and construction was done in Japan by KEK and Toshiba in collaboration with CERN. Factory tests were made in Japan with the proximity cryogenics in a geometrical arrangement corresponding to the final installation and, a full magnet test. After shipment to CERN the proximity cryogenics has been installed at a surface hall and recommissioning with load simulations and the instrumentation adapted for radiation hard requirements at the final underground area. The solenoid has recently been integrated in the common cryostat vessel of the liquid argon barrel. Cool down for final surface testing has started. The final control systems architecture and process logics are applied which is tested.