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Human Pregnancy (human + pregnancy)
Kinds of Human Pregnancy Selected AbstractsPlacental Trophoblast from Successful Human Pregnancies Expresses the Tolerance Signaling Molecule, CD200 (OX-2),AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2003David A. Clark Problem: Th1 cytokine-dependent abortions in the CBA × DBA/2 mouse model have been linked to down-regulation of expression of the CD200 (OX-2) ,tolerance' signal on trophoblast and in decidua prior to onset of the abortion process. Abortions could be prevented by administration of a soluble CD200. Is CD200 expressed on trophoblast in successful human pregnancy? Method of study: As one cannot easily obtain trophoblasts in large quantities from successful human pregnancies in the first trimester prior to the onset of the abortion process at 6 weeks gestation, we examined as a first step, trophoblast isolated from term placentae (i.e. successful pregnancies). CD9, trophoblasts were isolated by affinity column and stained for intracellular cytokeratin, and surface CD200 using PE-anti-human CD200 monoclonal antibody. mRNA was extracted from CD9+ and CD9, cells and tested by reverse transcription,polymerase chain reaction for CD200 mRNA. CD9, placental cells were separated by velocity sedimentation and test for CD200-dependent suppression of an allogeneic human mixed lymphocyte culture where cytotoxic T cell (CTL) generation, and Th1 , Th2 cytokine production shift were measured. Results: CD9, but not CD9+ placental cell populations contained cells with mRNA for CD200, both a normal length transcript and a truncated transcript. Flow cytometry showed a CD200+ cytokeratin+ moderate-to-large-sized cell population compatible with trophoblasts and a smaller subset of cytokeratin, cells that expressed CD200 at normal and at high levels. The moderate-sized population proved most potent at inhibiting CTL generation and caused a Th1,Th2 cytokine shift. These effects were blocked by monoclonal anti-CD200. Conclusions: A subpopulation of cytokeratin+ placental trophoblasts express bioactive CD200 able to alter maternal immune responses in a favorable (Th2 > Th1) direction. Two populations of CD200+ small- and medium-small-sized cytokeratin, placental cells remain to be identified. Studies of karyotyped first trimester elective termination and spontaneous miscarriage tissues are needed. [source] Leukocyte Pyruvate Kinase Expression is Reduced in Normal Human Pregnancy but not in Pre-eclampsiaAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2010Yi Xu Citation Xu Y, Madsen-Bouterse SA, Romero R, Hassan S, Mittal P, Elfline M, Zhu A, Petty HR. Leukocyte pyruvate kinase expression is reduced in normal human pregnancy but not in pre-eclampsia. Am J Reprod Immunol 2010; 64: 137,151 Problem, Emerging evidence suggests that metabolism influences immune cell signaling and immunoregulation. To examine the immunoregulatory role of glycolysis in pregnancy, we evaluated the properties of pyruvate kinase in leukocytes from non-pregnant women and those with normal pregnancy and pre-eclampsia. Method of study, We evaluated pyruvate kinase expression in lymphocytes and neutrophils from non-pregnant, pregnant, and pre-eclampsia patients using fluorescence microscopy and flow cytometry. Leukocyte pyruvate kinase activity and pyruvate concentrations were also evaluated. To study pyruvate's effect on signaling, we labeled Jurkat T cells with Ca2+ dyes and measured cell responses in the presence of agents influencing intracellular pyruvate. Results, The expression of pyruvate kinase is reduced in lymphocytes and neutrophils from normal pregnant women in comparison with those of non-pregnant women and pre-eclampsia patients. Similarly, the activity of pyruvate kinase and the intracellular pyruvate concentration are reduced in leukocytes of normal pregnant women in comparison with non-pregnant women and women with pre-eclampsia. Using Jurkat cells as a model of leukocyte signaling, we have shown that perturbations of intracellular pyruvate influence Ca2+ signals. Conclusion, Normal pregnancy is characterized by reduced pyruvate kinase expression within lymphocytes and neutrophils. We speculate that reduced pyruvate kinase expression modifies immune cell responses due to reduced pyruvate concentrations. [source] ORIGINAL ARTICLE: Hyperresistinemia , a Novel Feature in Systemic Infection During Human PregnancyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2010Shali Mazaki-Tovi Citation Mazaki-Tovi S, Vaisbuch E, Romero R, Kusanovic JP, Chaiworapongsa T, Kim SK, Ogge G, Yoon BH, Dong Z, Gonzalez JM, Gervasi MT, Hassan SS. Hyperresistinemia , a novel feature in systemic infection during human pregnancy. Am J Reprod Immunol 2010 Problem, Resistin, originally described as an adipokine, has emerged as a potent pro-inflammatory protein associated with both acute and chronic inflammation. Moreover, resistin has been proposed as a powerful marker of sepsis severity, as well as a predictor of survival of critically ill non-pregnant patients. The aim of this study was to determine whether pyelonephritis during pregnancy is associated with changes in maternal plasma resistin concentrations. Methods of study, This cross-sectional study included the following groups: (i) normal pregnant women (n = 85) and (ii) pregnant women with pyelonephritis (n = 40). Maternal plasma resistin concentrations were determined by ELISA. Non-parametric statistics was used for analyses. Results, (i) The median maternal plasma resistin concentration was higher in patients with pyelonephritis than in those with a normal pregnancy (P < 0.001); (ii) among patients with pyelonephritis, the median maternal resistin concentration did not differ significantly between those with and without a positive blood culture (P = 0.3); (iii) among patients with pyelonephritis who were diagnosed with systemic inflammatory response syndrome (SIRS), those who fulfilled ,3 criteria for SIRS had a significantly higher median maternal plasma resistin concentration than those who met only two criteria; and (iv) maternal WBC count positively correlated with circulating resistin concentration (r = 0.47, P = 0.02). Conclusion, Hyperresistinemia is a feature of acute pyelonephritis during pregnancy. The results of this study support the role of resistin as an acute-phase protein in the presence of bacterial infection during pregnancy. [source] A hierarchical analysis of transcriptome alterations in intrauterine growth restriction (IUGR) reveals common pathophysiological pathways in mammals,THE JOURNAL OF PATHOLOGY, Issue 3 2007C Buffat Abstract Intra-uterine growth restriction (IUGR) is a frequent disease, affecting up to 10% of human pregnancies and responsible for increased perinatal morbidity and mortality. Moreover, low birth weight is an important cause of the metabolic syndrome in the adult. Protein depletion during the gestation of rat females has been widely used as a model for human IUGR. By transcriptome analysis of control and protein-deprived rat placentas, we were able to identify 2543 transcripts modified more than 2.5 fold (1347 induced and 1196 repressed). Automatic functional classification enabled us to identify clusters of induced genes affecting chromosome structure, transcription, intracellular transport, protein modifications and apoptosis. In particular, we suggest the existence of a complex balance regulating apoptosis. Among repressed genes, we noted several groups of genes involved in immunity, signalling and degradation of noxious chemicals. These observations suggest that IUGR placentas have a decreased resistance to external aggression. The promoters of the most induced and most repressed genes were contrasted for their composition in putative transcription factor binding sites. There was an over-representation of Znfinger (ZNF) proteins and Pdx1 (pancreatic and duodenal homeobox protein 1) putative binding sites. Consistently, Pdx1 and a high proportion of ZNF genes were induced at the transcriptional level. A similar analysis of ZNF promoters showed an increased presence of putative binding sites for the Tata box binding protein (Tbp). Consistently again, we showed that the Tbp and TBP-associated factors (Tafs) were up-regulated in IUGR placentas. Also, samples of human IUGR and control placentas showed that human orthologous ZNFs and PDX1 were transcriptionnally induced, especially in non-vascular IUGR. Immunohistochemistry revealed increased expression of PDX1 in IUGR human placentas. In conclusion, our approach permitted the proposition of hypotheses on a hierarchy of gene inductions/repressions leading to massive transcriptional alterations in the IUGR placenta, in humans and in rodents. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Placental Trophoblast from Successful Human Pregnancies Expresses the Tolerance Signaling Molecule, CD200 (OX-2),AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2003David A. Clark Problem: Th1 cytokine-dependent abortions in the CBA × DBA/2 mouse model have been linked to down-regulation of expression of the CD200 (OX-2) ,tolerance' signal on trophoblast and in decidua prior to onset of the abortion process. Abortions could be prevented by administration of a soluble CD200. Is CD200 expressed on trophoblast in successful human pregnancy? Method of study: As one cannot easily obtain trophoblasts in large quantities from successful human pregnancies in the first trimester prior to the onset of the abortion process at 6 weeks gestation, we examined as a first step, trophoblast isolated from term placentae (i.e. successful pregnancies). CD9, trophoblasts were isolated by affinity column and stained for intracellular cytokeratin, and surface CD200 using PE-anti-human CD200 monoclonal antibody. mRNA was extracted from CD9+ and CD9, cells and tested by reverse transcription,polymerase chain reaction for CD200 mRNA. CD9, placental cells were separated by velocity sedimentation and test for CD200-dependent suppression of an allogeneic human mixed lymphocyte culture where cytotoxic T cell (CTL) generation, and Th1 , Th2 cytokine production shift were measured. Results: CD9, but not CD9+ placental cell populations contained cells with mRNA for CD200, both a normal length transcript and a truncated transcript. Flow cytometry showed a CD200+ cytokeratin+ moderate-to-large-sized cell population compatible with trophoblasts and a smaller subset of cytokeratin, cells that expressed CD200 at normal and at high levels. The moderate-sized population proved most potent at inhibiting CTL generation and caused a Th1,Th2 cytokine shift. These effects were blocked by monoclonal anti-CD200. Conclusions: A subpopulation of cytokeratin+ placental trophoblasts express bioactive CD200 able to alter maternal immune responses in a favorable (Th2 > Th1) direction. Two populations of CD200+ small- and medium-small-sized cytokeratin, placental cells remain to be identified. Studies of karyotyped first trimester elective termination and spontaneous miscarriage tissues are needed. [source] The Mechanisms and Regulation of Placental Amino Acid Transport to the Human FoetusJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2008J. K. Cleal The mechanisms by which amino acids are transferred across the human placenta are fundamental to our understanding of foetal nutrition. Amino acid transfer across the human placenta is dependent on transport across both the microvillous and basal plasma membranes of the placental syncytiotrophoblast, and on metabolism within the syncytiotrophoblast. Although the principles underlying uptake of amino acids across the microvillous plasma membrane are well understood, the extent to which amino acids are metabolised within human placenta and the mechanisms by which amino acids are transported out of the placenta across the basal plasma membrane are not well understood. Understanding the mechanisms and regulation of amino acid transport is necessary to understand the causes of intrauterine growth restriction in human pregnancy. [source] Ethanol Acutely Inhibits Ionotropic Glutamate Receptor-Mediated Responses and Long-Term Potentiation in the Developing CA1 HippocampusALCOHOLISM, Issue 4 2010Michael P. Puglia Background:, Developmental ethanol (EtOH) exposure damages the hippocampus, causing long-lasting alterations in learning and memory. Alterations in glutamatergic synaptic transmission and plasticity may play a role in the mechanism of action of EtOH. This signaling is fundamental for synaptogenesis, which occurs during the third trimester of human pregnancy (first 12 days of life in rats). Methods:, Acute coronal brain slices were prepared from 7- to 9-day-old rats. Extracellular and patch-clamp electrophysiological recording techniques were used to characterize the acute effects of EtOH on ,-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor (AMPAR)- and N -methyl- d -aspartate receptor (NMDAR)-mediated responses and long-term potentiation (LTP) in the CA1 hippocampal region. Results:, Ethanol (40 and 80 mM) inhibited AMPAR- and NMDAR-mediated field excitatory postsynaptic potentials (fEPSPs). EtOH (80 mM) also reduced AMPAR-mediated fEPSPs in the presence of an inhibitor of Ca2+ permeable AMPARs. The effect of 80 mM EtOH on NMDAR-mediated fEPSPs was significantly greater in the presence of Mg2+. EtOH (80 mM) neither affected the paired-pulse ratio of AMPAR-mediated fEPSPs nor the presynaptic volley. The paired-pulse ratio of AMPAR-mediated excitatory postsynaptic currents was not affected either, and the amplitude of these currents was inhibited to a lesser extent than that of fEPSPs. EtOH (80 mM) inhibited LTP of AMPAR-mediated fEPSPs. Conclusions:, Acute EtOH exposure during the third-trimester equivalent of human pregnancy inhibits hippocampal glutamatergic transmission and LTP induction, which could alter synapse refinement and ultimately contribute to the pathophysiology of fetal alcohol spectrum disorder. [source] Zinc Deficiency in Pregnancy and Fetal OutcomeNUTRITION REVIEWS, Issue 1 2006Dheeraj Shah MD Maternal zinc deficiency during pregnancy has been related to adverse effects on progeny, and there are data showing that mild to moderate zinc deficiency (as assessed by available indicators) is quite common in the developing world. Observational data relating zinc deficiency to adverse fetal outcome have produced conflicting results, mainly because of the lack of a valid indicator of zinc deficiency in pregnancy. Studies of human pregnancy and zinc supplementation, including those from developing countries, have failed to document a consistent beneficial effect on fetal growth, duration of gestation, and early neonatal survival. Preliminary results from unpublished studies in developing countries have also proven to be discouraging. However, recent data and some preliminary findings indicate a beneficial effect of maternal zinc supplementation on neonatal immune status and infant morbidity from infectious diseases, and there is also preliminary evidence that zinc supplementation may prevent congenital malformations (cleft lip/palate). With respect to neurobehavioral development, the evidence is conflicting, with only one study reporting a positive outcome. More research is required to assess the benefits of the large-scale introduction of zinc supplementation during pregnancy on congenital malformations, immune functions, neurobehavior, and overall neonatal survival in countries where zinc deficiency is a problem. Currently available information does not support the routine use of zinc supplementation to improve pregnancy outcome. [source] Functions of corticotropin-releasing hormone in anthropoid primates: From brain to placentaAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2006Michael L. Power Corticotropin-releasing hormone (CRH) is an ancient regulatory molecule. The CRH hormone family has at least four ligands, two receptors, and a binding protein. Its well-known role in the hypothalamic-pituitary-adrenal (HPA) axis is only one of many. The expression of CRH and its related peptides is widespread in peripheral tissue, with important functions in the immune system, energy metabolism, and female reproduction. For example, CRH is involved in the implantation of fertilized ova and in maternal tolerance to the fetus. An apparently unique adaptation has evolved in anthropoid primates: placental expression of CRH. Placental CRH stimulates the fetal adrenal zone, an adrenal structure unique to primates, to produce dehydroepiandrosterone sulfate (DHEAS), which is converted to estrogen by the placenta. Cortisol induced from the fetal and maternal adrenal glands by placental CRH induces further placental CRH expression, forming a positive feedback system that results in increasing placental production of estrogen. In humans, abnormally high placental expression of CRH is associated with pregnancy complications (e.g., preterm labor, intrauterine growth restriction (IUGR), and preeclampsia). Within anthropoid primates, there are at least two patterns of placental CRH expression over gestation: monkeys differ from great apes (and humans) by having a midgestational peak in CRH expression. The functional significance of these differences between monkeys and apes is not yet understood, but it supports the hypothesis that placental CRH performs multiple roles during gestation. A clearer understanding of the diversity of patterns of placental CRH expression among anthropoid primates would aid our understanding of its role in human pregnancy. Am. J. Hum. Biol. 18:431,447, 2006. © 2006 Wiley-Liss, Inc. [source] Comparative and evolutionary dimensions of the energetics of human pregnancy and lactationAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 5 2002D.L. Dufour The purpose of this article is to compare the energetics of reproduction for human and other primates in order to evaluate the extent to which human reproductive energetics are distinct from other primates and other large-bodied placental mammals. The article also evaluates the energetics of human and primate gestation and lactation using data from a variety of different populations living under different environmental circumstances. Energetics refers to energy intake and expenditure, and changes in body fat stores. Human and nonhuman primates have longer periods of gestation and lactation and slower prenatal and postnatal growth than other mammals of similar size. This reduces daily maternal energy costs. The development of sizable fat stores is not unique to humans, but fat stores are typically greater in human females and may play a greater role in reproduction. The strategies used to meet the energy costs of pregnancy vary among populations of humans and nonhuman primates and among humans interindividual variability is high. In pregnancy, some increase energy intake but others apparently do not. Increases in metabolic efficiency are evident in some human populations, whereas decreases in physical activity occur, but are not seen in all human or primate populations. Lactation is more energetically costly on a daily basis among humans and nonhuman primates, but has not been as well studied. It appears that both nonhuman and human primates tend to increase energy intake to meet in part the cost of lactation. They also use other strategies such as relying on body tissue stores, reductions in physical activity, and/or increases in metabolic efficiency to meet the remainder of the cost. It is also clear that human females in different populations and different women in the same population use a different combination of strategies to meet the cost of lactation. Am. J. Hum. Biol. 14:584,602, 2002. © 2002 Wiley-Liss, Inc. [source] PLAC1 (Placenta-specific 1): a novel, X-linked gene with roles in reproductive and cancer biologyPRENATAL DIAGNOSIS, Issue 6 2010Michael Fant Abstract Placenta-specific 1 (PLAC1) is a recently described X-linked gene with expression restricted primarily to cells derived from trophoblast lineage during embryonic development. PLAC1 localizes to a region of the X chromosome thought to be important in placental development although its role in this process has not been defined. This review summarizes our current understanding of its expression, regulation, and function. PLAC1 is expressed throughout human pregnancy by the differentiated trophoblast and localizes to membranous structures in the syncytiotrophoblast, including the microvillous plasma membrane surface. Recent studies have demonstrated that PLAC1 is also expressed by a wide variety of human cancers. Studies of the PLAC1 promoter regions indicate that its expression in both normal placenta and cancer cells is driven by specific interactions involving a combination of transcription factors. Although functional insight into PLAC1 in the normal trophoblast is lacking, preliminary studies suggest that cancer-derived PLAC1 has the potential to promote tumor growth and function. In addition, it also appears to elicit a specific immunologic response that may influence survival in some cancer patients, suggesting that it may provide a therapeutic target for the treatment of some cancers. We also discuss a potential role for PLAC1 as a biomarker predictive of specific pregnancy complications, such as preeclampsia. Copyright © 2010 John Wiley & Sons, Ltd. [source] PIBF: The Double Edged Sword.AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2010Pregnancy, Tumor Citation Szekeres-Bartho J, Polgar B. PIBF: The Double Edged Sword. Pregnancy and Tumor. Am J Reprod Immunol 2010; 64: 77,86 Problem, The role of progesterone-dependent immunomodulation in the maintenance of normal pregnancy. Methods,In vitro and in vivo data on the effect that progesterone and its mediator progesterone-induced blocking factor (PIBF) exert on the immune functions of pregnant women are reviewed, together with clinical findings. Results, Activated pregnancy lymphocytes express progesterone receptors, which enable progesterone to induce a protein called PIBF. PIBF increases Th2 type cytokine production by signaling via a novel type of IL-4 receptor and activating the Jak/STAT pathway. PIBF inhibits phosholipase A2, thus reduces prostaglandin synthesis. PIBF inhibits perforin release in human decidual lymphocytes and reduces the deleterious effect of high NK activity on murine pregnancy. PIBF production is a characteristic feature of normal human pregnancy, and its concentration is reduced in threatened pregnancies. PIBF mRNA and protein are expressed in a variety of malignant tumors. Inhibition of PIBF synthesis increases survival rates of leukemic mice. Conclusion, Progesterone-induced blocking factor is produced by pregnancy lymphocytes and also by malignant tumors. The PIBF-induced Th2-dominant immune response is favorable during pregnancy but might facilitate tumor growth by suppressing local antitumor immune responses. [source] Leukocyte Pyruvate Kinase Expression is Reduced in Normal Human Pregnancy but not in Pre-eclampsiaAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2010Yi Xu Citation Xu Y, Madsen-Bouterse SA, Romero R, Hassan S, Mittal P, Elfline M, Zhu A, Petty HR. Leukocyte pyruvate kinase expression is reduced in normal human pregnancy but not in pre-eclampsia. Am J Reprod Immunol 2010; 64: 137,151 Problem, Emerging evidence suggests that metabolism influences immune cell signaling and immunoregulation. To examine the immunoregulatory role of glycolysis in pregnancy, we evaluated the properties of pyruvate kinase in leukocytes from non-pregnant women and those with normal pregnancy and pre-eclampsia. Method of study, We evaluated pyruvate kinase expression in lymphocytes and neutrophils from non-pregnant, pregnant, and pre-eclampsia patients using fluorescence microscopy and flow cytometry. Leukocyte pyruvate kinase activity and pyruvate concentrations were also evaluated. To study pyruvate's effect on signaling, we labeled Jurkat T cells with Ca2+ dyes and measured cell responses in the presence of agents influencing intracellular pyruvate. Results, The expression of pyruvate kinase is reduced in lymphocytes and neutrophils from normal pregnant women in comparison with those of non-pregnant women and pre-eclampsia patients. Similarly, the activity of pyruvate kinase and the intracellular pyruvate concentration are reduced in leukocytes of normal pregnant women in comparison with non-pregnant women and women with pre-eclampsia. Using Jurkat cells as a model of leukocyte signaling, we have shown that perturbations of intracellular pyruvate influence Ca2+ signals. Conclusion, Normal pregnancy is characterized by reduced pyruvate kinase expression within lymphocytes and neutrophils. We speculate that reduced pyruvate kinase expression modifies immune cell responses due to reduced pyruvate concentrations. [source] ORIGINAL ARTICLE: Hyperresistinemia , a Novel Feature in Systemic Infection During Human PregnancyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2010Shali Mazaki-Tovi Citation Mazaki-Tovi S, Vaisbuch E, Romero R, Kusanovic JP, Chaiworapongsa T, Kim SK, Ogge G, Yoon BH, Dong Z, Gonzalez JM, Gervasi MT, Hassan SS. Hyperresistinemia , a novel feature in systemic infection during human pregnancy. Am J Reprod Immunol 2010 Problem, Resistin, originally described as an adipokine, has emerged as a potent pro-inflammatory protein associated with both acute and chronic inflammation. Moreover, resistin has been proposed as a powerful marker of sepsis severity, as well as a predictor of survival of critically ill non-pregnant patients. The aim of this study was to determine whether pyelonephritis during pregnancy is associated with changes in maternal plasma resistin concentrations. Methods of study, This cross-sectional study included the following groups: (i) normal pregnant women (n = 85) and (ii) pregnant women with pyelonephritis (n = 40). Maternal plasma resistin concentrations were determined by ELISA. Non-parametric statistics was used for analyses. Results, (i) The median maternal plasma resistin concentration was higher in patients with pyelonephritis than in those with a normal pregnancy (P < 0.001); (ii) among patients with pyelonephritis, the median maternal resistin concentration did not differ significantly between those with and without a positive blood culture (P = 0.3); (iii) among patients with pyelonephritis who were diagnosed with systemic inflammatory response syndrome (SIRS), those who fulfilled ,3 criteria for SIRS had a significantly higher median maternal plasma resistin concentration than those who met only two criteria; and (iv) maternal WBC count positively correlated with circulating resistin concentration (r = 0.47, P = 0.02). Conclusion, Hyperresistinemia is a feature of acute pyelonephritis during pregnancy. The results of this study support the role of resistin as an acute-phase protein in the presence of bacterial infection during pregnancy. [source] Mechanical ventilatory constraints during incremental cycle exercise in human pregnancy: implications for respiratory sensationTHE JOURNAL OF PHYSIOLOGY, Issue 19 2008Dennis Jensen The aim of this study was to identify the physiological mechanisms of exertional respiratory discomfort (breathlessness) in pregnancy by comparing ventilatory (breathing pattern, airway function, operating lung volumes, oesophageal pressure (Poes)-derived indices of respiratory mechanics) and perceptual (breathlessness intensity) responses to incremental cycle exercise in 15 young, healthy women in the third trimester (TM3; between 34 and 38 weeks gestation) and again 4,5 months postpartum (PP). During pregnancy, resting inspiratory capacity (IC) increased (P < 0.01) and end-expiratory lung volume decreased (P < 0.001), with no associated change in total lung capacity (TLC) or static respiratory muscle strength. This permitted greater tidal volume (VT) expansion throughout exercise in TM3, while preserving the relationship between contractile respiratory muscle effort (tidal Poes swing expressed as a percentage of maximum inspiratory pressure (PImax)) and thoracic volume displacement (VT expressed as a percentage of vital capacity) and between breathlessness and ventilation . At the highest equivalent work rate (HEWR = 128 ± 5 W) in TM3 compared with PP: , tidal Poes/PImax and breathlessness intensity ratings increased by 10.2 l min,1 (P < 0.001), 8.8%PImax (P < 0.05) and 0.9 Borg units (P < 0.05), respectively. Pulmonary resistance was not increased at rest or during exercise at the HEWR in TM3, despite marked increases in mean tidal inspiratory and expiratory flow rates, suggesting increased bronchodilatation. Dynamic mechanical constraints on VT expansion (P < 0.05) with associated increased breathlessness intensity ratings (P < 0.05) were observed near peak exercise in TM3 compared with PP. In conclusion: (1) pregnancy-induced increases in exertional breathlessness reflected the normal awareness of increased and contractile respiratory muscle effort; (2) mechanical adaptations of the respiratory system, including recruitment of resting IC and increased bronchodilatation, accommodated the increased VT while preserving effort,displacement and breathlessness, relationships; and (3) dynamic mechanical ventilatory constraints contributed to respiratory discomfort near the limits of tolerance in late gestation. [source] ORIGINAL ARTICLE: Glycation Endproducts, Soluble Receptor for Advanced Glycation Endproducts and Cytokines in Diabetic and Non-diabetic PregnanciesAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2009Magdalena Perty, ska-Marczewska Problem, Cytokines, advanced glycation end products (AGEs), and their receptor RAGE have been recently suggested to play a role in human pregnancy. In this study, we sought to determine the alterations of plasma AGEs, soluble RAGE (sRAGE), and proinflammatory cytokines in normal pregnancies and those complicated with type 1 diabetes mellitus. Method of study, These parameters were measured in samples from healthy non-pregnant (C), diabetic non-pregnant (D), healthy pregnant (HP), and pregnant diabetic (DP) women. Results, In the first trimester, DP showed lower sRAGE and higher AGEs compared to HP. In the DP group, significant negative correlations were seen between TNF-, and lipopolysaccharide (LPS)-stimulated ,L-6 in the first trimester and sRAGE in the third trimester. LPS-stimulated IL-12 was positively correlated with levels of AGEs in the third trimester. Conclusion, We detected several differences in the levels of AGEs, sRAGE, and proinflammatory cytokines between euglycemic and diabetic pregnancies. [source] P-3 Changes on pro-inflammatory cytokine responses in peripheral blood during normal human pregnancyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2004Article first published online: 12 NOV 200 Since publication it has come to our attention that the author names in the above abstract 1 were cited in the incorrect order. The correct order is as follows: [source] Placental Trophoblast from Successful Human Pregnancies Expresses the Tolerance Signaling Molecule, CD200 (OX-2),AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2003David A. Clark Problem: Th1 cytokine-dependent abortions in the CBA × DBA/2 mouse model have been linked to down-regulation of expression of the CD200 (OX-2) ,tolerance' signal on trophoblast and in decidua prior to onset of the abortion process. Abortions could be prevented by administration of a soluble CD200. Is CD200 expressed on trophoblast in successful human pregnancy? Method of study: As one cannot easily obtain trophoblasts in large quantities from successful human pregnancies in the first trimester prior to the onset of the abortion process at 6 weeks gestation, we examined as a first step, trophoblast isolated from term placentae (i.e. successful pregnancies). CD9, trophoblasts were isolated by affinity column and stained for intracellular cytokeratin, and surface CD200 using PE-anti-human CD200 monoclonal antibody. mRNA was extracted from CD9+ and CD9, cells and tested by reverse transcription,polymerase chain reaction for CD200 mRNA. CD9, placental cells were separated by velocity sedimentation and test for CD200-dependent suppression of an allogeneic human mixed lymphocyte culture where cytotoxic T cell (CTL) generation, and Th1 , Th2 cytokine production shift were measured. Results: CD9, but not CD9+ placental cell populations contained cells with mRNA for CD200, both a normal length transcript and a truncated transcript. Flow cytometry showed a CD200+ cytokeratin+ moderate-to-large-sized cell population compatible with trophoblasts and a smaller subset of cytokeratin, cells that expressed CD200 at normal and at high levels. The moderate-sized population proved most potent at inhibiting CTL generation and caused a Th1,Th2 cytokine shift. These effects were blocked by monoclonal anti-CD200. Conclusions: A subpopulation of cytokeratin+ placental trophoblasts express bioactive CD200 able to alter maternal immune responses in a favorable (Th2 > Th1) direction. Two populations of CD200+ small- and medium-small-sized cytokeratin, placental cells remain to be identified. Studies of karyotyped first trimester elective termination and spontaneous miscarriage tissues are needed. [source] Changes in Cytokine Production During and After Normal PregnancyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2000YUKI SHIMAOKA PROBLEM: The systemic T helper 1/T helper 2 (Th1/Th2) cytokine balance during normal human pregnancy is controversial, and observations about the balance in the postpartum period have only been reported for up to 3 months. METHOD: Whole-blood, from 83 healthy pregnant women, 80 healthy postpartum women, and 31 healthy non-pregnant women was stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin, and the levels of cytokines in the supernatant were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The production of all measured cytokines decreased during pregnancy, especially in the second trimester. After delivery, interferon-, (IFN-,) and interleukin-2 (IL-2) increased from 2 to 11 months postpartum, and IL-4 increased from 6 to 11 months postpartum. CONCLUSIONS: These data indicate that 1) decreases in production of both Th1- and Th2-type cytokines during pregnancy may be related to the pregnancy-induced amelioration of autoimmune diseases; 2) increases in production of both Th1- and Th2-type cytokines in the postpartum period may be related to the postpartum aggravation of autoimmune diseases. [source] A novel in vitro co-culture system for the study of maternal decidual endothelial cell,trophoblast interactions in human pregnancyBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 6 2001Eileen D.M. Gallery Investigation of the pathophysiology of pre-eclampsia (characterised by insufficient invasion of the intrauterine vasculature by cytotrophoblasts) has been hampered by the absence of a suitable animal model, and ethical constraints in clinical studies. We have developed a novel in vitro human cell co-culture system allowing direct assessment of cytotrophoblast invasion of a decidual endothelial cell monolayer from the abluminal side, as occurs in vivo. This model will facilitate detection, at the cellular level, of abnormal endothelial cell,trophoblast functional interactions in pre-eclampsia and other pregnancy disorders with abnormal placentation. [source] Placental endothelial nitric oxide synthase localization and expression in normal human pregnancy and pre-eclampsiaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2003SJ Orange Summary 1.,The aim of the present study was to investigate whether pre-eclampisa, a state of placental hypoxia, is associated with placental abnormalities in the amount, distribution and expression of enothelial nitric oxide synthase (eNOS). 2.,Localization and intensity of eNOS was determined by immunohistochemistry using an antibody specific for eNOS. The amount of eNOS mRNA expression was determined by reverse transcription,polymerase chain reaction (RT-PCR) and the densitometry of gel bands was expressed as a ratio of the band density of the housekeeping gene ,2 -microglobulin. 3.,Endothelial NOS staining was localized to syncytiotrophoblast cells within the villi and decidual trophoblast cells. It was not present in the endothelium of terminal villous vessels. There was no significant difference in eNOS villous or decidual staining intensity between normal pregnancy (NP; n = 12), pre-eclampsia (n = 14), or gestational hypertension (GH; n = 4). Staining for eNOS was not significantly different in the decidua compared with the villi in NP, GH or pre-eclampsia. Within the decidua, the depth of eNOS staining was similar in NP, pre-eclampisa and GH. 4.,There was no significant difference in eNOS mRNA expression between NP (0.70 ± 0.11), pre-eclampsia (0.5 ± 0.07) or GH (0.69 ± 0.26). 5.,These findings suggest that the amount of eNOS in the placenta is not deficient in pre-eclampsia, excluding a possible pathogenic role for eNOS in this disease. Furthermore, placental hypoxia, which is associated with pre-eclampsia, did not induce an upregulation of eNOS [source] | |||||||||||||