Changes in Toxoplasma diagnosis.

The serological laboratory workload in detecting toxoplasma infection may be expected to change with changes in the clinical profile of patient populations. We have examined the clinical information and laboratory results for patients referred to the Scottish Toxoplasma Reference Laboratory in April-March 1999-2000 and 2009-2010. Numbers of patient sera submitted for testing were similar (1624 and 1552) but there was a change in the clinical profile, with a significant fall in patients with symptoms of current infection (612 versus 335; P<0.

Antibody treatment promotes compensation for human cytomegalovirus-induced pathogenesis and a hypoxia-like condition in placentas with congenital infection.

Human cytomegalovirus (HCMV) is the major viral cause of birth defects worldwide. Affected infants can have temporary symptoms that resolve soon after birth, such as growth restriction, and permanent disabilities, including neurological impairment. Passive immunization of pregnant women with primary HCMV infection is a promising treatment to prevent congenital disease.

More specific bands in the IgG western blot in sera from Scottish patients with suspected Lyme borreliosis.

Aims: To identify further Western blot bands that may be specific in the diagnosis of Lyme borreliosis.

Methods: The Borrelia burgdorferi antibody profiles of 270 western blot positive patients and 241 western blot negative patients from 2008 were examined.

Results: 27 different non-specific bands were detected in both groups.

Toxoplasma tachyzoites from cell culture are more appropriate in some situations.

Background: Laboratories traditionally culture toxoplasma tachyzoites in animals for testing and experimental use. This article considers why available cell culture methods are not used more often.

Aim: To compare HeLa cell culture and animal culture for production of toxoplasma tachyzoites.

Gene expression profiling of the human maternal-fetal interface reveals dramatic changes between midgestation and term.

Human placentation entails the remarkable integration of fetal and maternal cells into a single functional unit. In the basal plate region (the maternal-fetal interface) of the placenta, fetal cytotrophoblasts from the placenta invade the uterus and remodel the resident vasculature and avoid maternal immune rejection. Knowing the molecular bases for these unique cell-cell interactions is important for understanding how this specialized region functions during normal pregnancy with implications for tumor biology and transplantation immunology.

Maternal antibodies enhance or prevent cytomegalovirus infection in the placenta by neonatal Fc receptor-mediated transcytosis.

How human cytomegalovirus (CMV) reaches the fetus across the placenta is unknown. The major viral cause of congenital disease, CMV infects the uterine-placental interface with varied outcomes depending on the strength of maternal humoral immunity and gestational age. Covering the surface of villi that float in blood, syncytiotrophoblasts express the neonatal Fc receptor (FcRn) that transports IgG for passive immunity.

Patterns of human cytomegalovirus infection in term placentas: a preliminary analysis.

Background: Primary maternal CMV infection is the major risk factor for symptomatic congenital infection as maternal immunity reduces the risk of transmission to the fetus. Analysis of first trimester placentas showed that virus replicates in the uterus and is transmitted to the placenta causing focal infection.

Objectives And Study Design: We examined 78 term placentas from uncomplicated deliveries for the presence of CMV DNA and evaluated evidence of infection by means of immunohistological and serological analysis.

Serum-free derivation of human embryonic stem cell lines on human placental fibroblast feeders.

Objective: To derive new human embryonic stem cell (hESC) lines on pathogen-free human placental fibroblast feeders under serum-free conditions. Because the embryo develops in close contact with extraembryonic membranes, we hypothesized that placental mesenchyme might replicate the stem cell niche in situ.

Design: We isolated and characterized human placental fibroblast lines from individual donors and tested their ability to support growth of federally registered hESC lines.

Insights into viral transmission at the uterine-placental interface.

During human gestation, viruses can cause intrauterine infections associated with pregnancy complications and fetal abnormalities. The ability of viruses to spread from the infected mother to the fetus arises from the architecture of the placenta, which anchors the fetus to the uterus. Placental cytotrophoblasts differentiate, assume an endothelial phenotype, breach uterine blood vessels and form a hybrid vasculature that amplifies the maternal blood supply for fetal development.

Viral and bacterial pathogens at the maternal-fetal interface.

We studied the incidence of pathogenic bacteria and concurrent infections with human cytomegalovirus (CMV) and herpes simplex virus (HSV) type 1 and 2 in biopsy samples from the placenta and decidua of women with healthy pregnancies. By polymerase chain reaction analysis, we found that 38% of placental samples were positive for selected bacteria and viruses. CMV, HSV-1, and HSV-2 were detected in isolation or with bacteria in first- and second-trimester samples.

Human cytomegalovirus interleukin-10 downregulates metalloproteinase activity and impairs endothelial cell migration and placental cytotrophoblast invasiveness in vitro.

At the uterine-placental interface, fetal cytotrophoblasts invade the decidua, breach maternal blood vessels, and form heterotypic contacts with uterine microvascular endothelial cells. In early gestation, differentiating- invading cytotrophoblasts produce high levels of matrix metalloproteinase 9 (MMP-9), which degrades the extracellular matrix and increases the invasion depth. By midgestation, when invasion is complete, MMP levels are reduced.

Human cytomegalovirus transmission from the uterus to the placenta correlates with the presence of pathogenic bacteria and maternal immunity.

Prenatal cytomegalovirus infection may cause pregnancy complications such as intrauterine growth restriction and birth defects. How virus from the mother traverses the placenta is unknown. PCR analysis of biopsy specimens of the maternal-fetal interface revealed that DNA sequences from cytomegalovirus were commonly found with those of herpes simplex viruses and pathogenic bacteria.

Focal adhesion kinase is required for blood vessel morphogenesis.

The nonreceptor tyrosine kinase focal adhesion kinase (FAK) is a point of convergence for signals from extracellular matrix, soluble factors, and mechanical stimuli. Targeted disruption of the fak gene in mice leads to death at embryonic day 8.5 (E8.

Association of antiretroviral resistance genotypes with response to therapy--comparison of three models.

Genotype-based resistance assays are commonly used to aid treatment in HIV-infected individuals failing antiretroviral therapy. The relationship between genotype and antiretroviral therapy comes mostly from in vitro assays of the response to a single drugs although there is a need for a prediction of clinical response to combination therapy. We have compared three different methods of analysing genotype data as a predictor of clinical response in a small clinical cohort of highly antiretroviral-experienced individuals failing therapy.