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Adrian K Charles

Publications and source records attributed to Adrian K Charles.

6 recordsLinked to original sources

Placenta and fetal growth restriction.

The placenta, as the vector for all maternal-fetal oxygen and nutrient exchange, is a principal influence on birthweight. Placental weight summarizes laterally expanding growth of the chorionic disc, and villous arborization yielding the nutrient exchange surface. These different growth dimensions alter fetoplacental weight ratio and ponderal index, and thus may modify placental functional efficiency. The placenta may show a range of histopathologies, some of which are also associated with fetal growth restriction. Different fetal intrinsic abilities to compensate for gross and histo-pathology may clarify the imperfect relationships between fetal growth and both intrauterine pathology, and the long-term health risks associated with poor fetal growth.

Birth Weight↗

Discordant fetal infection for parvovirus B19 in a dichorionic twin pregnancy.

There are only a few reports of fetal parvovirus infection in the circumstance of a twin pregnancy. We report a case of differential fetal infection following maternal parvovirus B19 infection in a dichorionic twin pregnancy culminating in a dual live-birth. A 32-year-old woman was diagnosed with parvovirus infection following exposure to her infected child at 19 weeks' gestation in a dichorionic twin gestation. Maternal IgG seroconversion was documented and maternal blood parvovirus B19 DNA was detected by PCR testing. Fetal monitoring with serial ultrasound assessment was instituted. At 25 weeks' gestation Twin I (male) displayed minor ascites, small pericardial effusion, placentomegaly and oligohydramnios. Middle cerebral artery peak systolic velocity (MCA PSV) studies were abnormal. Twin II (female) was sonographically unremarkable. A single fetal intravascular transfusion for Twin I was performed (pretransfusion Hb 80 g/L). Twin I fetal blood parvovirus B19 DNA was detected by polymerase chain reaction (PCR) and serum demonstrated both B19 IgG and IgM. Following fetal transfusion the hydrops resolved, although the placentomegaly persisted. Two live infants were delivered at 37 weeks' gestation. Individual neonatal venepuncture detected B19 DNA by PCR in Twin I but not in Twin II. B19 IgM was present in Twin I but not Twin II. Both neonates had B19 IgG antibodies. Placental histopathology demonstrated mild edema for Twin I but no inclusion cells. The placenta of Twin II was unremarkable. This case demonstrates the ability for differential transplacental infection of this virus and the assistance of fetal MCA flow studies to guide therapy in a multiple pregnancy at risk of parvovirus infection.

Blood Flow Velocity↗

Morphometry of the basal plate superficial uteroplacental vasculature in normal midtrimester and at term.

Uteroplacental (UP) vascular arterial pathology has been associated with pregnancy complications. UP arterial structure has been characterized in placental bed biopsies, at the decidual-myometrial junction. Basal plate UP arteries, which are delivered with the placenta and thus routinely available, are not well characterized. We compared basal plate UP arterial segment morphometry in cases of elective termination of a clinically normal pregnancy at 11 to 24 weeks and of term birth. This study was done in a community-based obstetric service in New York City. UP arteries were identified in placentas of 20 midtrimester (MT) cases and 17 term (TERM) cases. We measured 336 UP artery cross-sections from 46 TERM and 290 MT cases. The basal plate UP artery path length was calculated as the distance between (x,y) coordinates of estimated centers of lumen cross-sections. Basal plate thickness near UP arteries, UP artery cross-sectional areas, vascular luminal eccentricity, and radial standard deviation were directly measured off digital images. Nonparametric and parametric methods compared groups, with P < 0.05 considered statistically significant. In TERM cases, the basal plate thickness near UP arteries was 1.8-fold thinner (P = 0.002) and mean basal plate path lengths were 2.13-fold shorter (P < 0.0001) than in MT cases. Mean TERM UP artery cross-sectional area was 3.15-fold larger, the major axis was 1.95-fold larger, and the minor axis was 1.75-fold larger than in MT arteries (P = 0.001 to 0.008). Our data demonstrate that basal plate UP arteries (delivered with the placenta) are less tortuous, with shorter path lengths and larger areas as gestation advances. Normative morphometric data may allow improved diagnostics of placentas from complicated pregnancies.

Arteries↗

Caspase-14 expression in the human placenta.

Caspase-14 is involved in epidermal differentiation, and previous studies demonstrated abundant expression in the skin. However, the expression of caspase-14 in the human placenta has not been reported. The aims of this study were to determine whether caspase-14 is expressed in the first trimester and term human placenta, and if it is associated with apoptosis in the placenta. Caspase-14 is expressed in the trophoblast cells, and in lower amounts in the mesenchyme. Western blot analysis demonstrated increased expression in the first trimester compared with term placentae. Immunohistochemistry for caspase-14 showed diffuse expression in the trophoblast layer, and not only in occasional cells that are identified by TUNEL staining. Using an explant model in which apoptosis was inhibited with superoxide dismutase (SOD), no significant differences in caspase-14 protein concentrations were seen with differing levels of apoptosis. Caspase-14 is present in the human placenta, primarily in the trophoblast, but its function is not clear, and appears not to be related purely to apoptosis.

Apoptosis↗

Advanced abdominal pregnancy: still an occurrence in modern medicine.

In a world bewildered by spectacular advances in imaging technology, the early detection of an abdominal pregnancy should be a feasible objective. A case of an advanced abdominal pregnancy is presented. Although the pregnancy was the result of in vitro fertilisation technology, the diagnosis was not suspected until 35 weeks gestation. Both ultrasound and magnetic resonance imaging (MRI) were used to achieve a diagnosis prior to delivery. The placenta was left within the peritoneal cavity but removal was necessitated for maternal symptomatology 4 months postdelivery. This case illustrates that despite the almost ubiquitous usage of prenatal ultrasound, extrauterine pregnancies may not be detected in a timely manner unless attention to basic ultrasound techniques is followed.

Adult↗

Functional deletion of the calcium-sensing receptor in a case of neonatal severe hyperparathyroidism.

Heterozygous inactivating mutations of the calcium-sensing receptor (CaR) cause familial hypocalciuric hypercalcemia, whereas homozygous or compound heterozygous inactivating mutations normally cause neonatal severe hyperparathyroidism. In a case of neonatal severe hyperparathyroidism characterized by moderately severe hypercalcemia and very high PTH levels, coupled with evidence of hyperparathyroidism and effects on brain development not previously demonstrated, we detected point mutations on separate alleles of the CaR, resulting in premature stop codon substitutions at G94 and R648. This led to severely truncated receptors and an effective so-called knockout of functional CaR. FLAG-tagged, truncated receptors were expressed in HEK293 cells for functional analysis. Confocal microscopy demonstrated cytoplasmic localization of the G94stop receptor, whereas the R648stop receptor was present both in the cytoplasm and associated with the cell membrane. Only the R648stop receptor could be detected by Western analysis. Functional assays in which R648stop and wild-type receptor were cotransfected into HEK293 cells demonstrated a reduction in wild-type Ca(2+)-responsiveness by the R648stop receptor, even at physiological Ca(2+) levels, thus simulating familial hypocalciuric hypercalcemia in relatives of the infant who were heterozygous for the R648stop mutation. The R648stop receptor alone was nonresponsive to Ca(2+). This case contributes to our understanding of the clinical manifestation of a CaR knockout.

Alleles↗