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M Shade

Publications and source records attributed to M Shade.

9 recordsLinked to original sources
PubMed1999

Clinical follow-up of high mid-trimester maternal serum intact human chorionic gonadotrophin concentrations in singleton pregnancies.

Mid-trimester biochemical screening of 38 143 pregnancies in south-east Scotland revealed 127 cases (0.34 per cent) in which the maternal serum (MS) intact human chorionic gonadotrophin (hCG) concentration was > or = 4 multiples of the median in singleton pregnancies (MOM). Three were lost to follow-up but in 72 (58 per cent) complications developed or there were associated fetal abnormalities. This percentage was greatest at very high hCG concentrations, 92 per cent with hCG > or = 10 MOM (n = 12) compared with 48 per cent with hCG concentrations of 4-4.99 MOM (n=69). 22 cases had an MS alpha-fetoprotein > or = 2 MOM in addition to an MS hCG > or = 4 MOM, and in only 3 of these was the pregnancy uneventful; 86 per cent were associated with abnormalities or pregnancy complications.

Chorionic Gonadotropin↗
PubMed1999

Amniotic fluid levels of dimeric inhibins, pro-alpha C inhibin, activin A and follistatin in Down's syndrome.

OBJECTIVE: In the second trimester of pregnancy, inhibin A is significantly increased in maternal serum and decreased in amniotic fluid in Down's syndrome pregnancies compared to normal. We wished to further evaluate the levels of inhibin A, inhibin B, pro-alpha C inhibin, activin A and the binding protein follistatin in amniotic fluid in Down's syndrome and control pregnancies. DESIGN: Case-matched control study. PATIENTS: 29 Down's syndrome and 290 chromosomally normal control pregnancies were identified from records and amniotic fluid, collected at second trimester amniocentesis, retrieved from routine storage for analysis. MEASUREMENTS: Inhibin A, inhibin B, pro-alpha C inhibin, total activin A and follistatin were measured using sensitive and specific enzyme linked immunosorbent assays. RESULTS: The median (10th-90th percentiles) amniotic fluid inhibin A level in the control pregnancies increased from 334 (122-553) ng/l at 14 weeks' to 695 (316-1475) ng/l at 19 weeks' gestation. The corresponding figures for inhibin B and the alpha-subunit precursor inhibin pro-alpha C were 632 (185-1354) and 2062 (1237-3381) ng/l, respectively at 14 weeks' and 2439 (748-5307) and 3115 (2021-6567) ng/l, respectively at 19 weeks' gestation. Total activin A increased from 3795 (1554-5296) at 14 weeks' to 5086 (3059-8224) at 18 weeks' gestation. Expressed as multiples of the median (MoM) the median (95% CI) amniotic fluid levels of inhibin A, inhibin B, pro-alpha C inhibin and acitivin A in the Down's syndrome samples were 0.77 (0.59-0.85), 0.94 (0.63-1.23), 0.77 (0.49-0.84) and 0.77 (0.53-0.87), respectively. Compared to controls the levels of inhibin A, pro-alpha C inhibin and activin A were significantly lower in Down's syndrome pregnancies (P < 0.01, Mann-Whitney U test). Follistatin levels in the controls declined slightly from 2106 (1421-3538) ng/l at 14 weeks' to 1600 (1281-2543) ng/l at 18 weeks' gestation. Levels in the Downs' syndrome pregnancies were similar to controls. CONCLUSIONS: The data suggest that the production, secretion or metabolism of the inhibin alpha- and beta A-subunits is altered in Down's syndrome pregnancies in the second trimester.

Activins↗
PubMed1997

Dimeric inhibins in amniotic fluid, maternal serum, and fetal serum in human pregnancy.

Using new specific and sensitive enzyme-linked immunosorbent assays for inhibin A and inhibin B, we measured these proteins in amniotic fluid (AF), maternal serum (MS), and umbilical cord serum in normal pregnancies. Inhibin A levels in AF rose from a median (10-90th percentile) level of 615 (158.2-1124.6) pg/mL at 14 weeks to 1336.0 (489.4-2084.1) pg/mL at 20 weeks, and inhibin B rose from 216.6 (67.4-554.6) to 1078.2 (439.3-2482.2) pg/mL over the same period. In MS, inhibin A levels fell from a median (10-90th percentile) level of 177.5 (101.4-290.7) pg/mL at 10 weeks to a nadir of 111.9 (59.5-200.3) pg/mL at 17 weeks, rising again to 180.3 (74.1-327.2) pg/mL at 20 weeks. No inhibin B was detectable in MS. In 47 pairs of matched samples (14-16 weeks gestation) there was no correlation of inhibin A levels in AF with those in MS (r = 0.19; P > 0.05). In 45 term umbilical cord serum samples, no dimeric inhibin was detectable in serum from female babies, but inhibin B was detectable in male sera; the median (10-90th percentile) concentration was 167.4 (111.2-224.8) pg/mL. These data suggest that for the gestation periods studied, although the placenta secretes inhibin A, another source, probably the fetal membranes, secretes both inhibin A and inhibin B. Further, the presence of inhibin B in male fetuses is consistent with a testicular origin, suggesting that inhibin B may be important in the development of the fetal hypothalamo-pituitary-testicular axis.

Amniocentesis↗
PubMed1984

Phorbol esters enhance spontaneous cytotoxicity of human lymphocytes, abrogate Fc receptor expression, and inhibit antibody-dependent lymphocyte-mediated cytotoxicity.

Phorbol esters with tumor promoter activity enhance the spontaneous cytotoxicity of human lymphocytes against a variety of target cell lines, with an efficiency that correlates with their potency as tumor promoters or skin irritants. Analysis of surface marker expression of the lymphocytes cytotoxic after treatment with phorbol ester identified the cytotoxic cell subset as that containing natural killer cells. Although gamma-interferon (IFN gamma) is produced by T cells treated with phorbol esters, IFN gamma is probably not the mediator of enhancement of natural killer cell activity, because anti-IFN gamma antibodies failed to block this enhancement. Spontaneous cell-mediated cytotoxicity is inhibited when phorbol esters are present during the cytotoxic assay, but is enhanced when the effector cells are pretreated with these agents. On the other hand, antibody-dependent cytotoxicity mediated by lymphocytes is inhibited by phorbol ester pretreatment of the effector cells or by phorbol esters present during the cytotoxic assay. Treatment of lymphocytes with phorbol esters at 37 degrees C, but not at 4 degrees C, completely abrogates in 1 to 2 hr the expression of the receptor for the Fc fragment of IgG, as detected by rosette formation with IgG-sensitized erythrocytes and by reactivity with anti-Fc receptor antibodies. The inhibition of antibody-dependent cytotoxicity by phorbol esters is probably secondary to their effect on the Fc receptor.

Animals↗
PubMed1982

Further studies on the natriuretic activity of p-hydroxytriamterene.

p-Hydroxytriamterene, the phase I metabolite of triamterene, increased sodium excretion without affecting urinary volume or potassium when administered orally to rats on sodium deficient diets at doses of 15 and 30 mg/kg. The urine of these animals also contained p-hydroxytriamterene sulfuric acid ester, the phase II metabolite of triamterene but did not contain p-hydroxytriamterene. This evidence indicates that p-hydroxytriamterene is orally active as a potassium-sparing natriuretic in rats.

Animals↗
PubMed1981

Mapping by gene dosage, using aneuploid human lymphoid cell lines.

Human lymphoblastoid cell lines evolve in vitro by the emergence of successive waves of clones which are often chromosomally marked. This offers the opportunity to compare tissue samples of the same genetic origin but differing in certain defined parts of the karyotype. Using selected sets of lines in which the members of genetically matched pairs differed in the number of copies of 8p or of 12p, levels of GSR and LDH B respectively have been shown to correlate with the specific chromosome aberrations, supporting existing data on the regional assignment of these two structural loci. This approach represents a useful addition to established methods for human gene mapping.

Aneuploidy↗
PubMed1980

Chromosome aberrations acquired in vitro by human B-cell lines. II. Distribution of break points.

Among 165 human B-cell lines examined, 57 were found to have karyotypic abnormalities that involved chromosome breakage. The sites of breakage were identified with quinacrine-, Giemsa-, and reverse-banding techniques, and the distribution of 239 break points was plotted. A pronounced excess of telomeric and, to a lesser extent, centromeric breaks was observed. Chromosomes No. 7, 8, 9, 11, and 14 were involved in structural rearrangements more often and chromosomes No. 2, 5, 10, 20, and X less often than was predicted on the basis of their relative lengths. Lines derived from patients with different categories of disorders varied in the distribution of break points throughout the karyotype. In this sample of cell lines, No. 8q; 14q translocations were found only in cultures derived from patients with Burkitt's lymphoma and were never observed to arise among other Epstein-Barr virus-carrying lines even after several hundred cell generations in vitro. An additional feature, which was evidently restricted to lines derived from leukemia or lymphoma patients, was the presence of interstitial insertion, deletion, or reduplication, particularly involving the long arm of chromosome No. 1.

B-Lymphocytes↗
PubMed1980

Chromosome aberrations acquired in vitro by human B-cell lines. I. Gains and losses of material.

Gains and losses of chromosomes or chromosome arms were recorded in 45 of 165 human B-cell lines. Most aberrations were acquired in vitro, and their frequency was related to duration of culture. Gains occurred more frequently than losses and their distribution was nonrandom. Chromosomes most commonly affected were No. 3, 7, 8 (particularly 8q), 9, 12, and 21. Certain differences in the frequency of particular aberrations appeared to be related to the clinical conditions of the patients from whom the lines were derived. The distribution of chromosome gains in this material was correlated with those detected in direct preparations from human tumors.

Aneuploidy↗