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Biomedical subjects

G M Stirrat

Publications and source records attributed to G M Stirrat.

At least 73 records · Page 4Linked to original sources

Radioimmunoassay of thyroxine and 3,3',5'-triiodothyronine (reverse T3) in human amniotic fluid.

Measurement of amniotic fluid iodothyronine concentrations may enable antenatal detection of fetal thyroid abnormalities; however, the delineation of normal ranges is complicated by methodological problems associated with strong and highly variable protein-binding, and specificity of antisera. Improved radioimmunoassays of thyroxine (T4) and 3,3',5-triiodothyronine (reverse T3, rT3) have been developed to overcome these problems. In normal pregnancy, mean rT3 concentrations at less than 17 weeks, 17-22 weeks and 35-42 weeks gestation were 3.6 nmol/l (n = 21), 6.1 nmol/1 (n = 14) and 0.66 nmol/1 (n = 39) respectively; corresponding mean T4 concentrations were 2.4 nmol/1, 6.5 nmol/1 and 3.6 nmol/1. rT3 concentrations showed a strong positive correlation with T4 concentration in each age range; however, the molar ratio of rT3:T4 decreased progressively with gestational age, from 1.69 at less than 17 weeks to 0.19 at 35-42 weeks. In both mid- and late gestation, rT3 and T4 concentrations were strongly correlated with total amniotic fluid protein concentrations.

Amniotic Fluid↗

Maternal serum alpha-fetoprotein and low birth weight in relation to gestational age.

To determine when in the first and second trimester a raised serum alpha-fetoprotein (AFP) level best predicts low birth weight a case-control study was performed on 157 singleton low birth-weight (less than or equal to 2.5 kg) and 314 singleton control pregnancies (birth weight greater than 2.5 kg). The association between raised maternal serum AFP and low birth weight was confirmed, but there was no special time in pregnancy before 29 weeks gestation when a raised AFP level predicted low birth weight materially better than at any other time.

Female↗

Maternal cell-mediated immunity in normal and pre-eclamptic pregnancy.

Maternal cell-mediated immunity (CMI) to fetal (paternal) HLA was studied in both normal and pre-eclamptic pregnancies. Maternal-paternal mixed lymphocyte reactivity (MLR) was assessed using macrophage migration inhibitory factor (MIF), leucocyte migration inhibitory factor (LIF) and blast transformation assays. Primary and secondary responses were differentiated by studying 6 day MLR time courses. Maternal lymphocytes (normal pregnancies) did not show an early, (i.e. secondary), proliferative response, nor did the pattern of LIF release suggest maternal CMI to fetal (paternal) HLA. However, the lymphocyte responses between pre-eclamptic couples, in terms of both proliferation and LIF release, were consistently and significantly different from those of normal couples; a finding which may reflect an abnormal immune response.

Female↗

The expression of major histocompatibility antigens by human chorionic villi.

Frozen sections of human placentae taken at selected stages throughout gestation were stained with monoclonal antibodies to HLA-A, B, C and DR antigens, using an indirect immunoperoxidase technique. No staining of villous trophoblastic tissue was detected. Antibody to HLA-A, B, and C antigens clearly stained membranous elements of the villous stroma. Antibody to HLA-DR antigens stained rare, elongated cells of the villous stroma in the term placenta. Monoclonal antibodies to syncytiotrophoblast membrane were used as a control. This antigen distribution was confirmed by absorption of these monoclonal antibodies in an indirect radioimmunoassay. Adult spleen homogenate gave much stronger absorption than a trophoblast membrane preparation with antibodies to HLA-A, B, C or DR antigens. The opposite absorption pattern was observed with the anti-trophoblast monoclonal antibodies. Detergent solubilisation did not affect the absorption capacity of trophoblast membrane for HLA-A, B, C or DR antigens. Maternal antibody could be eluted from trophoblastic areas of term placental sections by washing at physiological pH, but this did not effect the binding of monoclonal antibodies. Thus the HLA antigens were not masked by preformed maternal alloantibody. These observations confirm that chorionic villous trophoblast does not express detectable HLA antigen. This may be the principal reason for the lack of rejection of the fetal allograft.

Absorption↗

Raised maternal serum AFP, oligohydramnios and poor fetal outcome.

Six women who had an ultrasound scan examination in early pregnancy on account of a high serum alpha-fetoprotein level were noted to have little or no amniotic fluid. This paper gives details of the six pregnancies, two of which were extrauterine; only one of the six infants survived.

Adolescent↗

Monoclonal antibodies to human syncytiotrophoblast.

Two monoclonal antibodies, NDOG1 and NDOG2, have been produced which are directed towards human syncytiotrophoblast. The antigens detected by these antibodies are absent from human liver, heart, kidney, brain and from normal human sera. The NDOG1 antigen but not NDOG2 antigen is a component of pregnancy sera and falls to undetectable levels within 6 hours of placental delivery. This molecule is not human chorionic gonadotrophin, human placental lactogen, placental alkaline phosphatase. SP1 or PAPP-A. Immunoperoxidase staining shows that both antigens are on apical aspects of the syncytiotrophoblast and not in the villous stroma.

Antibodies, Monoclonal↗

HLA A, B, C antigens are expressed on nonvillous trophoblast of the early human placenta.

Samples were taken from the human chorionic sac at 6 wk postconception and were stained with monoclonal antibodies to trophoblast and to HLA antigens by means of an indirect immunoperoxidase technique. Antibody to HLA A, B, C antigens did not stain chorionic villous trophoblast in accordance with previous studies, but did stain nonvillous trophoblast of the cytotrophoblast cell columns and cytotrophoblastic shell. Antibody to HLA DR antigens showed no staining of trophoblast. This is the first demonstration of HLA antigens on a human fetal tissue in direct maternal contact. We have discussed the immunologic implications of this finding.

Abortion, Induced↗

Amniotic-fluid acetylcholinesterase as a possible diagnostic test for neural-tube defects in early pregnancy.

Raised levels (greater than or equal to 4.5 munits/ml) of acetylcholinesterase (AChE) activity in amniotic fluid at 14--23 weeks of pregnancy were significantly associated with open fetal neural-tube defects. Out of 72 pregnancies correctly classified by the amniotic-fluid alpha-fetoprotein (A.F.P.) test, 2 of 56 without neural-tube defects and all 16 with open neural-tube defects (8 with anencephaly and 8awith open spina bifida) had raised levels of AChE. Out of 5 pregnancies misclassified by the A.F.P. test (4 without neural-tube defects and 1 with open spina bifida), only 1 was misclassified by the AChE test--namely, one of those without a neural-tube defect. Thus, only 3 of the 77 pregnancies tested were misclassified by the quantitative AChE test. A qualitative test for an isoenzyme of AChE found in cerebrospinal fluid correctly classified these 3 pregnancies. These findings suggest that the analysis of AChE in amniotic fluid may be a useful test in the diagnosis of open neural-tube defects.

Acetylcholinesterase↗