Fetal umbilical artery flow velocity waveforms and placental resistance: pathological correlation.

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(97)08357-8.pdf

Microchimerism and HLA-compatible relationships of pregnancy in scleroderma

Recent studies indicate that fetal cells persist in maternal blood for decades after pregnancy. Maternal cells are known to engraft and persist in infants with immunodeficiency, but whether maternal cells persist long-term in immunocompetent offspring has not specifically been investigated. We developed sensitive human leukocyte antigen-specific (HLA-specific) PCR assays and targeted nonshared maternal HLA genes to test for persistent maternal microchimerism in subjects with scleroderma and in healthy normal subjects. Nonshared maternal-specific DNA was found in 6 of 9 scleroderma patients. In situ hybridization with double labeling for X and Y chromosome-specific sequences revealed female cells in peripheral blood samples from 2 male scleroderma patients. HLA-specific PCR also frequently revealed persistent maternal microchimerism in healthy control subjects. The mean age of all subjects with maternal microchimerism was 28 years (range: 9-49 years). With few exceptions, mothers of subjects with persistent maternal microchimerism were HLA incompatible with subjects for class I and class II alleles. These results clearly indicate that HLA-disparate maternal cells can persist in immunocompetent offspring well into adult life. The biological significance of maternal microchimerism and whether it might contribute to autoimmune disease requires further investigation.

/pdf/microchimerism-of-maternal-origin-persists-into-adult-life-4apjjv2uks.pdf

Microchimerism of maternal origin persists into adult life

Classification of placental lesions.

Prenatal removal of frontal association cortex in the fetal rhesus monkey: anatomical and functional consequences in postnatal life.

The syndrome of chronic abruptio placentae, hydrorrhea, and circumvallate placenta

Persistence of donor cells in neonates after fetal and exchange transfusion.

Experiments performed at 130 days gestation in 11 rhesus monkeys revealed a positive correlation between pituitary prolactin concentrations in maternal plasma, but not fetal plasma, and those in amniotic fluid. Minute amounts of radioactively-labeled prolactin passed between maternal and fetal circulation. Small amounts of labeled hormone also passed from the mother, but not from the fetus, to the amniotic cavity. Fetal plasma prolactin was elevated by fetalinjection of thyrotropin-releasing factor (TRF), but not to an extent comparable to maternal plasma rises seen after the hypothalamic hormone was injected into the mother. Fetal tissues andthe placenta acquired protein-bound radioactivity when l25I-labeled prolactin was injected intothe amniotic fluid, the 125I in the former organ being displaced by incubation with nonlabeled prolactin. It was concluded that the maternal circulation may be a major source of amniotic fluid prolactin, while fetal and maternal circulations show mutually, essentially indep...

Sources and Disposition of Pituitary Prolactin in Maternal Circulation, AmnioticFluid, Fetus and Placenta in the Pregnant Rhesus Monkey

The clinical outcome from 461 Rh-sensitized pregnancies whose infants received fetal and/or neonatal blood transfusion have been observed over a period of 7 years. 23 of 124 (19.5 %) infants receiving intrauterine transfusion showed persistence of donor white blood cells at birth. 34 of 82 (41.5 %) peripheral blood samples taken one day following exchange transfusion of the neonate displayed metaphase figures of donor cells. Donor cells could be identified in only 15 of 57 (26.3 %) of these infants on the day of hospital discharge. At four months of age, only one infant maintained a donor cell line which subsequently disappeared at one year of age. In contrast, 5 of 65 infants surviving fetal transfusion have consistently demonstrated the persistence of circulating donor white cells beyond one year of age. One of these infants has developed acute lymphocytic leukaemia at 4 1/2 years of age, and one of these presumably chimeric children demonstrated hybrid cells in its peripheral blood. No evidence of morbid conditions relating to the transfusion(s) have been noted in the infants who received transfusions only after birth.

Donald L. Hutchinson

Papers

The syndrome of chronic abruptio placentae, hydrorrhea, and circumvallate placenta

Persistence of donor cells in neonates after fetal and exchange transfusion.

Sources and Disposition of Pituitary Prolactin in Maternal Circulation, AmnioticFluid, Fetus and Placenta in the Pregnant Rhesus Monkey

Chimerism following fetal transfusion. Report of leucocyte hybridization and infant with acute lymphocytic leukaemia.

The pathogenesis of placental infarction. II. An experimental study in the rhesus monkey placenta.