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The objectives of this study were to describe and evaluate potential drivers of genetic structure in Canadian breeding populations of the Ovenbird, Seiurus aurocapilla. We performed genetic analyses on feather samples of individuals from six study sites using nuclear microsatellites. We also assessed species identity and population genetic structure of quill mites (Acariformes, Syringophilidae). For male Ovenbirds breeding in three study sites, we collected light-level geolocator data to document migratory paths and identify the wintering grounds. We also generated paleohindcast projections from bioclimatic models of Ovenbird distribution to identify potential refugia during the last glacial maximum ( LGM, 21,000 years before present) as a factor explaining population genetic structure. Birds breeding in the Cypress Hills (Alberta/Saskatchewan) may be considered a distinct genetic unit, but there was no evidence for genetic differentiation among any other populations. We found relatively strong migratory connectivity in both western and eastern populations, but some evidence of mixing among populations on the wintering grounds. There was also little genetic variation among syringophilid mites from the different Ovenbird populations. These results are consistent with paleohindcast distribution predictions derived from two different global climate models indicating a continuous single LGM refugium, with the possibility of two refugia. Our results suggest that Ovenbird populations breeding in boreal and hemiboreal regions are panmictic, whereas the population breeding in Cypress Hills should be considered a distinct management unit. [ABSTRACT FROM AUTHOR]

Aim The aim of this study was to examine the role of hereditary thrombophilia in the development of fetal growth retardation (FGR) in the population of Central Russia. Methods The case-control study sample included 497 women in the third trimester of pregnancy recruited during 2009-2013. The participants were enrolled into two groups: patients with FGR ( n = 250) and controls without FGR ( n = 247). The participants were genotyped for four genetic markers of hereditary thrombophilia: factor V Leiden ( G > A FV, rs6025), prothrombin ( G > A FII, rs1799963), factor VII ( G > A FVII, rs6046), and fibrinogen ( G > A FI, rs1800790). Results The genetic factors for an increased risk of FGR were allele G of rs6046 (odds ratio [OR] = 2.34) and genotype GG of rs6046 (OR = 2.64), whereas genotype GA of rs6046 had the protective value (OR = 0.42). A combination of alleles G of rs1799963, A of rs6046, and G of rs1800790 (OR = 0.31) reduces the risk of FGR. Conclusion Polymorphism rs6046 of the FVII gene is associated with the development of FGR. [ABSTRACT FROM AUTHOR]

This paper considers influence of elevated irradiation temperature on structure and properties of 15Kh2NMFAA reactor pressure vessel (RPV) steel. The steel is investigated after accelerated irradiation at 300°C (operating temperature of VVER-1000-type RPV) and 400°C supposed to be the operating temperature of advanced RPVs. Irradiation at 300°C leads to formation of radiation-induced precipitates and radiation defects-dislocation loops, while no carbide phase transformation is observed. Irradiation at a higher temperature (400°C) neither causes formation of radiation-induced precipitates nor provides formation of dislocation loops, but it does increase the number density of the main initial hardening phase—of the carbonitrides. Increase of phosphorus concentration in grain boundaries is more pronounced for irradiation at 400°C as compared to irradiation at 300°C due to influence of thermally enhanced diffusion at a higher temperature. The structural-phase changes determine the changes of mechanical properties: at both irradiation temperatures irradiation embrittlement is mainly due to the hardening mechanism with some contribution of the nonhardening one for irradiation at 400°C. Lack of formation of radiation-induced precipitates at T = 400°C provides a small ΔTK shift (17°C). The obtained results demonstrate that the investigated 15Kh2NMFAA steel may be a promising material for advanced reactors with an elevated operating temperature. [ABSTRACT FROM AUTHOR]

Problem Risk factors for preterm birth include placental abruption, giving rise to excessive decidual thrombin, and intrauterine bacterial infection. Human endometrial endothelial cells (HEECs) express Toll-like receptors (TLRs), and infection-derived agonists trigger HEECs to generate specific inflammatory responses. As thrombin, in addition to inducing coagulation, can contribute to inflammation, its effect on HEEC inflammatory responses to the TLR4 agonist, bacterial lipopolysaccharide (LPS), was investigated. Method of study HEECs were pre-treated with or without thrombin or specific protease-activated receptor (PAR) agonists, followed by treatment with or without LPS. Supernatants were measured for cytokines and chemokines by ELISA and multiplex analysis. Results Thrombin significantly and synergistically augmented LPS-induced HEEC secretion of interleukin (IL)-6, IL-8, granulocyte colony-stimulating factor (G-CSF), and growth-regulated oncogene-alpha (GRO-α), and significantly augmented monocyte chemotactic protein (MCP)-1, tumor necrosis factor-alpha (TNF-α), and vascular endothelial growth factor (VEGF) secretion additively. Similar to thrombin, a PAR1 agonist synergistically augmented the LPS-induced HEEC secretion of inflammatory IL-6, IL-8, G-CSF, and GRO-α. Conclusion Thrombin, via PAR1 activation, synergistically augments LPS-induced HEEC production of chemokines involved in immune cell recruitment and survival, suggesting a mechanism by which intrauterine abruption and bacterial infection may together be associated with an aggravated uterine inflammatory response. [ABSTRACT FROM AUTHOR]

Problem Microbial-driven responses in placenta are linked with adverse pregnancy outcomes. The role of Toll-like receptor ( TLR) function in Hofbauer cells ( HBCs) and fetal macrophages of the placental villous core remains understudied. Method of Study Flow cytometry and immunohistochemistry (IHC) were used to establish the phenotype of HBCs. Regulation of cytokine secretion in response to treatment with TLR agonists and expression levels of TLRs and co-activators were compared in HBCs, placental fibroblasts (FIBs), and human umbilical vein endothelial cells (HUVECs) using ELISA and qPCR. Results Although flow cytometry and IHC revealed HBCs to be M2 (anti-inflammatory) macrophages, LPS and polyinosinic: polycytidylic acid [poly (I:C)] treatments markedly enhanced IL-6 secretion by HBCs, and expression of TLR-2, TLR-3, TLR-4, CD14, and MD-2 was the highest in HBCs. Conclusion These results indicate that although HBCs are M2 macrophages, inflammatory responses are induced through TLR-3 and TLR-4 in this cell type, suggesting a role in microbial-driven placental/fetal inflammation. [ABSTRACT FROM AUTHOR]

Problem Human endometrial endothelial cell ( HEEC) innate immunity remains poorly characterized. Based on their direct contact with the circulation, HEECs are uniquely positioned to be exposed to viral infections. This study evaluated the innate immune response generated by HEECs after exposure to the TLR3 agonist, Poly(I:C) and the TLR8 agonist, viral ss RNA. Method of Study HEECs were treated with or without Poly(I:C) or ss RNA. Culture supernatants were measured for cytokines by multiplex analysis. RNA was analyzed by qRT- PCR for type I interferons and antiviral factors. Results Treatment of HEECs with Poly(I:C) rapidly upregulated the secretion of IL-2, IL-6, IL-8, IFN-γ, G- CSF, GM- CSF, MCP-1, MIP-1β, RANTES, and GRO-α after 12 hr, while ss RNA treatment induced the slower secretion of IL-6, IL-8, IFN-γ, G- CSF, VEGF, and GRO-α after 24 hr. Both viral components induced HEEC IFN-α and IFN-β expression. While treatment with Poly(I:C) induced APOBEC3G and OAS expression, treatment with ssRNA upregulated APOBEC3 G and M×A mRNA. Conclusion Our findings demonstrate that HEECs can differentially sense and respond to viral components by generating distinct inflammatory and antiviral immune responses, indicating that these cells likely play an active role in the immune protection of the uterus toward viral infections. [ABSTRACT FROM AUTHOR]

This paper reviews the basic physical notions underlying microwave sintering and the theoretical and numerical models of the microwave sintering process. The propagation and absorption of electromagnetic waves in materials, and the distribution of electromagnetic field in cavity resonators that serve as applicators for microwave processing are discussed and the electromagnetic modeling of such applicators is reviewed. The microwave absorption properties of ceramic and metal powder materials and the methods of their description are addressed. Self-consistent electromagnetic and thermal models that are capable of predicting the temperature distribution in the microwave-heated materials and dynamic effects such as thermal runaway instabilities are reviewed. The multiphysics simulations that combine electromagnetic, thermal, and sintering models and result in predicting densification, shrinkage, and grain structure evolution are discussed in detail. The significance of microwave nonthermal effects in sintering is demonstrated based on the experimental results, and the models of such effects are reviewed. [ABSTRACT FROM AUTHOR]

Problem Uterine innate immunity remains poorly characterized, and while endometrial endothelial cells are known to express Toll-like receptors ( TLRs), little is known about their function in these cells. The present study evaluated the effect of Gram-negative bacterial lipopolysaccharide ( LPS) on human endometrial endothelial cell ( HEECs) cytokine secretion and tissue factor expression, and the role of TLR-4 in these responses. Methods Human endometrial endothelial cells were treated with or without LPS ± LPS- RS, a TLR-4 antagonist, via the binding of MD-2. After 24 hr, cell-free supernatants were evaluated for cytokines by multiplex analysis and cell lysates were analyzed for tissue factor expression by Western blot. Results Treatment of HEECs with LPS significantly upregulated the secretion of IL-6, IL-8, and G- CSF, and this was prevented by LPS- RS. LPS also induced tissue factor expression by the HEECs; however, this was unaffected by LPS- RS. Conclusion These findings suggest that TLR-4 is functional in HEECs and its activation by bacterial LPS induces a specific cytokine/chemokine response. However, bacterial LPS also induced tissue factor expression in what seemed to be a TLR-4-independent fashion, suggesting that this bacterial component can act on the HEECs through TLR-4-dependent and TLR-4-independent pathways. These findings indicate that endometrial endothelial cells may play an active role in uterine innate immunity. [ABSTRACT FROM AUTHOR]

Problem Toll-like receptor-4 ( TLR-4) protects against Gram-negative bacteria expressed lipopolysaccharide and 'danger signals' from injured or dying cells. Although decidual cells ( DCs) and interstitial trophoblasts ( ITs) are in close contact, TLR-4 has been studied extensively only in ITs. Method of study Formalin-fixed, paraffin-embedded serial sections of endometrium in follicular and luteal phases and deciduas from first and second trimester elective terminations and third trimester normal deliveries were immunostained for TLR-4, trophoblast-specific cytokeratin, and DC-specific vimentin. HSCORE assessed TLR-4 immunostaining in DCs versus ITs. Results TLR-4 HSCORES were significantly higher in: (i) first trimester DCs than luteal phase pre-decidual stromal cells; (ii) first and third versus second trimester DCs, but similar between third trimester deciduas parietalis and basalis; (iii) first versus second trimester ITs; (iv) DCs versus ITs across gestation. Conclusion Higher TLR-4 in DCs than ITs suggests DCs as primary targets for Gram-negative bacteria and/or inflammation-related danger signals. [ABSTRACT FROM AUTHOR]

Tissue factor (TF), is a cellular receptor that binds the factor VII/VIIa to initiate the blood coagulation cascade. In addition to its role as the initiator of the hemostatic cascade, TF is known to be involved in angiogenesis via intracellular signaling that utilizes the protease activated receptor-2 (PAR-2). We now review the physiologic expression of TF in the endometrium and its altered expression in multiple cell types derived from eutopic and ectopic endometrium from women with endometriosis compared with normal endometrium. Our findings suggest that TF might be an ideal target for therapeutic intervention in endometriosis. We have employed a novel immunoconjugate molecule known as Icon and were able to eradicate endometrial lesions in a mouse model of endometriosis without affecting fertility. These findings have major implications for potential treatment in humans. [ABSTRACT FROM AUTHOR]

Reductions in uteroplacental flow initiate a cascade of molecular effects leading to hypoxia, thrombosis, inflammation, and endothelial cell dysfunction resulting in untoward pregnancy outcomes. In this review, we detail these effects and their relationship to preeclampsia (PE) and intrauterine growth restriction (IUGR). [ABSTRACT FROM AUTHOR]

Toti P, Arcuri F, Tang Z, Schatz F, Zambrano E, Mor G, Niven-Fairchild T, Abrahams VM, Krikun G, Lockwood CJ, Guller S. Focal increases of fetal macrophages in placentas from pregnancies with histological chorioamnionitis: potential role of fibroblast monocyte chemotactic protein-1. Am J Reprod Immunol 2011; 65: 470-479 Histopathological chorioamnionitis (HCA) is caused by microbial-driven infiltration of leukocytes to the maternal-fetal interface resulting in adverse neonatal outcomes in a subset of pregnancies. The role of placental villus macrophages (i.e. Hofbauer cells, HBCs) in the pathophysiology of HCA is unelucidated. The number of HBCs in human term placental villi in HCA and control groups was compared using immunohistochemistry. Levels of monocyte chemotactic protein (MCP-1) expression were measured in primary cultures of syncytioytrophoblasts (SCTs) and fibroblasts (FIBs) treated with bacterial compounds [lipopolysaccharide (LPS) and peptidoglycan] and pro-inflammatory cytokines (TNF-α and IL-1β) using ELISA and quantitative real-time PCR. Immunohistochemistry revealed a focal increase in HBCs in HCA. Treatment of FIBs with LPS, IL-1β, and TNF-α significantly increased MCP-1 mRNA and protein expression. Conversely, MCP-1 mRNA and protein levels were virtually undetectable in treated and untreated SCTs. These results demonstrate cell-type-specific regulation of MCP-1 expression in human placenta. A model is presented in which bacterial products and inflammatory cytokines initiate a fibroblast-driven cytokine cascade resulting in recruitment of fetal monocytes to placenta which focally increases levels of HBCs in pregnancies complicated by HCA. [ABSTRACT FROM AUTHOR]

Abnormal uterine bleeding is the leading indication for discontinuation of long-term progestin-only contraceptives. Histological sections of endometria from long-term progestin-treated patients display abnormally enlarged blood vessels that are prone to bleed in a nonuniform manner. Because it has been complex to attain patients willing to complete long-term studies, and good quality endometrial tissues have proven difficult to obtain, animal models have been used to obviate this problem. In this review, we describe these models including the guinea pig, an animal model we have previously investigated, to assess the mechanisms involved in abnormal uterine bleeding following long-term progestin-only contraception. [ABSTRACT FROM AUTHOR]

The human endometrium is a dynamic tissue that undergoes cycles of growth and regression with each menstrual cycle. Adult progenitor stem cells are likely responsible for this remarkable regenerative capacity; these same progenitor stem cells may also have an enhanced capacity to generate endometriosis if shed in a retrograde fashion. The progenitor stem cells reside in the uterus; however, less-committed mesenchymal stem cells may also travel from other tissues such as bone marrow to repopulate the progenitor population. Mesenchymal stem cells are also involved in the pathogenesis of endometriosis and may be the principle source of endometriosis outside of the peritoneal cavity when they differentiate into endometriosis in ectopic locations. Finally, besides progenitor stem cells, recent publications have identified multipotent stem cells in the endometrium. These multipotent stem cells are a readily available source of cells that are useful in tissue engineering and regenerative medicine. Endometrial stem cells have been used to generate chondrocytes, myocytes, neurons, and adiposites in vitro as well as to replace dopaminergic neurons in a murine model of Parkinson's disease. [ABSTRACT FROM AUTHOR]

The article discusses the issues encompassing the teaching and learning of popular music in higher education in Memphis, Tennessee. The author describes two issues facing the contemporary music educators, the lack of popular music pedagogy in music teacher education and the difficulty of acquiring a rock music curriculum. Moreover, he highlights on the "Tribute to Stax Records" project, an educational concert intended as a teaching model performed at Bergen Community College.

Tissue factor (TF), is a cellular receptor that binds the ligand factor VII/VIIa to initiate the blood coagulation cascade. In addition to its role as the initiator of the hemostatic cascade, TF is known to be involved in angiogenesis via an interaction with factor VIIa and protease-activated receptor-2 (PAR-2). In this article we review previous studies from our laboratory demonstrating that the pattern and level of TF expression is altered in multiple cell types derived from eutopic and ectopic endometrium from women with endometriosis compared with normal endometrium. We posit that the inflammatory environment that occurs in ectopic and eutopic endometrium from patients with disease results in high TF expression that in turn, signals via PAR-2 to further produce inflammatory cytokine or chemokine production and macrophage recruitment. Thus, our studies suggest that TF might be an ideal target for therapeutic intervention in endometriosis. [ABSTRACT FROM AUTHOR]

During extravascular trophoblast (EVT) invasion of the decidua, thrombin generated from decidual cell–expressed tissue factor (TF) forms a “hemostatic envelope” that protects against hemorrhage during the initial breaching of capillaries by EVTs and subsequent invasion and remodeling of the spiral arteries and arterioles. Preeclampsia, the world's leading cause of fetal and maternal morbidity and mortality, stems from shallow trophoblast invasion leading to incomplete vascular remodeling that impairs uteroplacental blood flow. A considerable subset of cases of preeclampsia is associated with decidual hemorrhage and maternal thrombophilias, which form excess thrombin from decidual cell–expressed TF. Thrombin affects several cell functions by binding to protease-activated receptors. In first-trimester decidual cells, thrombin enhances expression of sFlt-1, which can block the angiogenic effects of vascular endothelial growth factor (VEGF) and placental growth factor. By contrast, thrombin does not affect decidual cell VEGF expression. Thrombin-enhanced sFlt-1 expression by decidual cells, the predominant cell type encountered by invading cytotrophoblasts, could promote preeclampsia by interfering with angiogenesis-dependent vascular remodeling to reduce uteroplacental blood flow. [ABSTRACT FROM AUTHOR]

Preeclampsia is associated with an increased release of factors from the placental syncytium into maternal blood, including the antiangiogenic factors soluble fms-like tyrosine kinase-1 and soluable endoglin, the antifibrinolytic factor plasminogen activator inhibitor-1, prostanoids, lipoperoxides, cytokines, and microparticles. These factors are suggested to promote maternal endothelium dysfunction and are associated with placental damage in pregnancies also complicated with intrauterine growth restriction (IUGR). In this report, we briefly describe the interaction of syncytial factors with hypoxia, reactive oxygen species, and apoptosis in the pathophysiology of preeclampsia and IUGR. Given the critical role of the syncytium in these complications of pregnancy, we also present a novel methodology in which laser capture microdissection followed by Western blotting is used to assess levels of syncytial Fas ligand, a key protein in the apoptotic cascade. [ABSTRACT FROM AUTHOR]

Introduction Pregnancy complications have been linked to improper trophoblast migration and failure of spiral artery transformation. Endothelial cells play an essential role in directing trophoblast migration and transformation, although by an unknown mechanism. We describe a novel in vitro model to evaluate endothelial–trophoblast interaction and signaling in a three-dimensional system. Method of study Immortalized human endometrial endothelial cell line and first trimester trophoblast cells were co-cultured. Endothelial transformation into vessel-like structures occurred in MatrigelTM OpenLab Image Analysis software was used to monitor labeled trophoblast migration and endothelium transformation. Cytokine/chemokine production was determined using Multiplex. Results Trophoblast migrates toward endothelial cells in Matrigel, aligns on top of the endothelium within 4–8 hr and achieves complete replacement of the endothelium by 72–96 hr. Lipopolysaccharide treatment damages the endothelium and disrupts endothelium–trophoblast interaction. Conclusion We report a novel three-dimensional in vitro and in vivo system of trophoblast–endothelium cell interaction. Significant changes in endothelial cells’ phenotype are observed upon differentiation in Matrigel. These changes may be necessary for endothelium to direct trophoblast migration and transformation. [ABSTRACT FROM AUTHOR]

Numerous factors have been implicated in angiogenesis. This article concentrates on the expression of the major angiogenic factors, namely, vascular endothelial growth factor (VEGF) and the angiopoietins in the human endometrium. Particular emphasis is placed on the expression of the angiopoietins and their physiological and pathological expression. [ABSTRACT FROM AUTHOR]

Isolates of Glomus macrocarpum Tul. & Tul. grown in soil cultures from single spores were tested at known numbers of propagules ml[SUP-1] soil for their efficacy in promoting growth of bell pepper (Capsicum annuum L.) seedlings. The soil cultures, propagated under similar growth conditions, had from 0.02 to 25 propagules ml[SUP-1] as measured by the most probable number technique. Seven cultures with similar levels of inoculum density (a median of 7 propagules mi[SUP-]l) were used undiluted, and at 10[SUP1] and at 10[SUP-2] dilutions to test efficacy of the isolates. Also, cultures with originally dissimilar propagule levels (0.02 to 15 ml[SUP-l] ) were diluted to uniform inoculum density levels and tested for efficacy. Large intra-species variation in efficacy occurred in isolates collected from different soils and in those isolated from the same soil. Differences in the growth enhancement ability of isolates were evident from four weeks after seeding until harvest. The best isolates were superior at all inoculum levels tested but the ranking of isolates differed with the inoculum density. A significant positive correlation was found between initial G. macrocarpum propagules ml[SUP-1] soil and all plant height and weight parameters measured. Growth of mycorrhizal plants was significantly greater than that of non-mycorrhizal plants when more than 0.5 propagule ml[SUP4] was present. With more than 5 ml[SUP-1], 70% of the isolates were effective. A minimum level of I propagule ml[SUP-1] is suggested for infestation of pepper seed beds; greater benefits can be expected from higher levels up to at least 10 to 15 propagules ml[SUP-1]. [ABSTRACT FROM AUTHOR]

Recovery from water stress was studied on similarly sized VA mycorrhizal and non-mycorrhizal rough lemon seedlings (Citrus jambhiri Lush). VA mycorrhiza affected stomatal conductance, photosynthesis and proline accumulation, but not leaf water potential, suggesting that most of the effect of the mycorrhizal association is on stomatal regulation rather than on root resistances. [ABSTRACT FROM AUTHOR]

The effects of rootstock, irrigation regime and water salinity on the vertical distribution of vesicular-arbuscular mycorrhiza (VAM) of citrus roots were investigated in the field. Rootstocks differed in the uniformity of the vertical distribution of VAM, notably, Rough lemon exhibited a uniform vertical distribution and Sour orange a non-uniform distribution with decreased VAM infection at depth. Decreasing the interval between irrigations reduced VAM infection of Sour orange, especially in the upper layers of soil. Increased salinity of irrigation-water reduced VAM in deep layers of soil. [ABSTRACT FROM AUTHOR]

Initial studies on the chemokine stromal derived factor 1 (now referred to as CXCL12) were proposed to be enhanced in several diseases including those which affect the female reproductive tract. These include endometriosis, Asherman's syndrome, endometrial cancers, and ovarian cancers. Additionally, recent studies from our laboratory suggest that CXCL12 signaling is involved in leiomyomas (fibroids). These diseases present an inflammatory/hypoxic environment which further promotes pathology. At first, studies focused on signaling by CXCL12 via its well‐known receptor, CXCR4. However, the discovery of CXCR7 as another receptor for CXCL12 with rather high binding affinity and recent reports about its involvement in endometrial disease and cancer progression has questioned the potential of "selective blockade"' of CXCR4 to treat these ailments. This review will focus on the signaling and effects of the potent chemokine CXCL12, and its long‐known G protein‐coupled receptor CXCR4, as well as the alternate receptor CXCR7 on the female reproductive tract and related diseases such as endometriosis, Asherman's syndrome, leiomyomas, endometrial cancer, and ovarian cancer. Although several other mechanisms are inherent to these diseases such as gene mutations, differential expression of miRNAs and epigenetics, for this review, we will focus on the CXCL12/CXCR4/CXCR7 axis as a novel target. [ABSTRACT FROM AUTHOR]

Introduction: Preeclampsia and IUGR have been linked to improper trophoblast migration that impairs maternal spiral artery transformation minimizing vessel dilation and therefore restricting blood flow to the developing fetus. Endothelial cells are thought to play an essential role in directing trophoblast migration and transformation, although the mechanism by which this occurs is not fully understood. We have developed a novel in vitro system that evaluates endothelial-trophoblast interaction and signaling in a three-dimensional environment. Methods: An immortalized human endometrial endothelial cell line (HEEC) (Krikun et al., 2004) and first trimester trophoblast cell lines HTR-8 and Swan.71 were used. Endothelial transformation into vessel-like structures occurred in Matrigel Basement Membrane Matrix. Cell membrane linker dye and OpenLab Image Analysis software were used to monitor trophoblast migration and transformation. Cytokine and chemokine production was determined using a multiplex bead assay. Results: Upon differentiation in matrigel, endothelial cells undergo a shift in cytokine production characterized by an increased secretion of chemokines. First trimester trophoblast cells migrate toward the differentiated endothelium, and reach it within 4–8 hr. Complete replacement of the endothelium is seen by 48 hr. The transformed tubes maintain structure and remain functional for several weeks allowing for further co-culture studies. Conclusion: We report the characterization of a novel three-dimensional in vitro system of trophoblast–endothelium cell interaction. We found significant changes in the phenotype (cytokine expression and LPS responses) of endothelial cells upon differentiation in matrigel as compared to the monolayer culture. These changes may be necessary for the endothelium to direct trophoblast migration. Furthermore, this model represents an ideal co-culture system to evaluate the role of additional cell types, e.g. immune cells, involved in the process of spiral artery transformation. [ABSTRACT FROM AUTHOR]