Lutheran related antibodies.
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Biomedical subjects
Publications and source records attributed to G Daniels.
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Lungs from 153 calves with clinical signs of pneumonia were examined post-mortem (PM) for the presence of mycoplasmas and ureaplasmas during a 38-month period. Sixty-two percent of the cases were submitted during the months when wide fluctuations in climatic conditions occur. Using indirect fluorescent antibody tests (IFAT) and culture, mycoplasmas and/or ureaplasmas were detected in 63% of the lungs examined. Mycoplasma dispar was detected in 39%, M. bovis in 36%, Ureaplasma spp. in 22% and M. bovirhinis in 8.5% of the lungs. Thirty percent of the lungs were infected with more than one species; the most frequent combination was M. bovis, M. dispar and Ureaplasma spp. (10.5%). M. arginini, M. bovigenitalium and acholeplasmas were not cultured. M. dispar was shown to remain viable for up to 15 days PM in apical and cardiac lobes held at 4 degrees C and also was detected by IFAT in the same tissues for 49 days.
The effects of insulin and insulin-like growth factors (IGFs) on ovarian androgen production were examined in ovarian stroma obtained from four women with hyperandrogenism and three women without hyperandrogenism. In incubations of stroma obtained from all four hyperandrogenic patients, insulin alone (500 ng/ml) significantly stimulated androstenedione and testosterone release. LH alone (25 ng/ml) significantly stimulated androstenedione release in incubations of stroma obtained from three of the four hyperandrogenic patients and testosterone release in incubations of stroma obtained from one of the four hyperandrogenic patients. In stromal incubations from three of the four hyperandrogenic patients, insulin alone (500 ng/ml) resulted in a significantly greater release of androstenedione and testosterone than did LH alone (25 ng/ml). Dihydrotestosterone was released in measurable quantities in incubations of stromal tissue obtained from three of the four hyperandrogenic women. In all three instances in which dihydrotestosterone was detectable, insulin alone (500 ng/ml), but not LH alone (25 ng/ml), significantly stimulated dihydrostestosterone release. Incubations of stroma obtained from three nonhyperandrogenic, normally cycling women demonstrated low levels of androstenedione release and negligible testosterone and dihydrotestosterone release. Insulin alone (500 ng/ml) and LH alone (25 ng/ml) produced no significant increase in androstenedione release. Insulin (500 ng/ml) plus LH (25 ng/ml) significantly stimulated androstenedione accumulation in stroma obtained from two of the nonhyperandrogenic women. One insulin dose-response experiment was performed using stromal tissue obtained from a hyperandrogenic woman. In this experiment, insulin, at a dose of 50 ng/ml, was as effective as insulin at a dose of 500 ng/ml in stimulating androstenedione and testosterone release. In addition to insulin, IGF-I/somatomedin C (50 ng/ml) stimulated androstenedione and testosterone release. Relaxin (1 microgram/ml) and multiplication-stimulating activity (50 ng/ml) did not stimulate androstenedione and testosterone release. These studies suggest that human ovarian stroma may be a target tissue for insulin and IGF-I, and that hyperinsulinemia may be an important factor contributing to ovarian hyperandrogenism.
Selenium toxicosis was diagnosed as the cause of fatal paralytic disease in a group of feeder pigs. Lumbar poliomyelomalacia and coronary band necrosis were the principal lesions. High selenium concentrations were detected in liver and kidney. Excessive selenium was traced to the premix added to the complete ration.
The hyperthyroidism of Graves' disease may be caused by autoantibodies to thyrotropin (TSH) receptors. We have found that patients with this disease have autoantibodies to neutrophils as well, which can be displaced by TSH. Using a radiochemical opsonic assay, we found serum antibodies against homologous neutrophils in 6 of 11 Graves' patients. With a staphylococcal protein A-binding assay, we detected circulating antibodies to homologous neutrophils in 10 of 20 patients, while finding cell-bound antibody on autologous neutrophils in 7 of 8 (including 2 with negative serum tests). Use of human 125I-TSH in a radioligand binding assay revealed that TSH bound to neutrophils rapidly (maximum binding within 10 min at 22 degrees C, pH 7.4), specifically (less than 20% nonspecific binding), and reversibly. Adding TSH to the radiochemical assay resulted in a dose-dependent inhibition of opsonic antibody activity in serum from patients with Graves' disease. In contrast, TSH did not inhibit antibody activity of serum from patients with immune neutropenia not associated with thyroid disease. Our findings suggest a basis for the association of Graves' disease with neutropenia. Furthermore, the discovery of such antineutrophil antibodies in Graves' disease permits detection of cell-bound antibody when free antibody is not present.
Dantu, a previously undescribed low-incidence red cell antigen, is inherited as a Mendelian dominant character. The Dantu antigen is associated with very weak s antigen, protease resistant N antigen and either very weak or no U antigen. Two of the propositi had previously been shown to have an unusual hybrid MNSs sialoglycoprotein, and it is probably this which carries these unusual N, s and U antigens as well as the Dantu antigen. A study of the family of one propositus suggests, by conventional genetics, that Dantu is not controlled by the MNSs locus; a possible explanation is given. Several examples of anti-Dantu are known, one was found to cause a positive direct antiglobulin reaction on neonatal red cells.
Apparently identical twin boys are both XX/XY and have two populations, A1 and B, of cells in their peripheral blood. Chimerism in somatic tissue outside the blood cells can be demonstrated in only one of the twins. From analysis of chromosomes and many gene markers the mechanism of origin of the unusual twins remains unclear.
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After decades of studying the human blood groups by serological and, more recently, biochemical techniques, analysis of blood group genes at the molecular level has confirmed that a variety of different genetical events have given rise to the vast complexity of blood group systems. In order to illustrate this 4 blood group systems have been selected: ABO and H, involving carbohydrate determinants, and MNS and Rh, involving predominantly protein antigens. The molecular basis of the A1, A2, B, and O groups, and of the rare H-deficiency phenotypes will be described. The Sta antigen of the MNS system will be discussed in order to illustrate the variety of different genetic mechanisms that can give rise to a single rare antigen. Finally, recent work on the molecular basis of the polymorphic Rh antigens, D, C, c, E, and e, and on some rare Rh phenotypes, Rhnull, D--, and r's, will be explained briefly in order to emphasize the complexity of blood group genetics.
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