Search PubMed⌕ Search

Biomedical subjects

D Bennett

Publications and source records attributed to D Bennett.

At least 271 records · Page 15Linked to original sources
PubMed1981

Inhibition of complement-mediated cytotoxicity of antisera by fluid secreted by the seminal vesicle of the house mouse.

The fluid from the seminal vesicles of the house mouse inhibited complement-mediated cytotoxicity of antisera against both sperm and lymphocytes. This inhibition was not reduced by heating or by absorption with sperm. Fractionation of the seminal vesicle fluid on Sephadex G-100 columns revealed three peaks of inhibitory activity, one of which appeared in the void volume of the columns. This inhibitory action of the seminal vesicle fluid may protect sperm from immunological attack in the female reproductive tract. It could explain the observation that immunization of female house mice with sperm does not prevent pregnancy. The relationship between this activity in the seminal vesicles of house mice, which is directed against the cytotoxicity of antisera, and the inhibition of cell-mediated responses to sperm reported for human and bull semen have not been investigated.

Absorption↗
PubMed1981

Immunological studies of mouse decidual cells. II. Studies of cells in artificially induced decidua.

Cells from artificially induced decidual tissue (deciduoma) in the mouse were examined for Thy-1 surface antigen and receptors for the Fc portion of immunoglobulin G (FcR) and compared with cells of the normal decidua from 6 to day 9 of pregnancy. It was shown that (1) Thy-1 antigen is present on the same proportion of cells in decidua and deciduoma on day 6 and day 7, (2) FcR-bearing cells can be detected in similar numbers on day 6 and day 7 but this does not increase on day 8 in deciduoma as it does in decidua, and (3) progesterone treatment after induction of decidualization allowed further increase of FcR-bearing cells in deciduoma. These results present further evidence of the similarity between deciduoma and decidua in the mouse. They indicate that these two membrane markers are present in the early decidua, regardless of the presence of an embryo, and suggest that progesterone may play a part in the increase of FcR-bearing cells in the decidua during pregnancy.

Animals↗
PubMed1981

Observations on autoimmune orchitis in sterile mice carrying a recessive lethal mutation at the T/t complex exhibiting spontaneous allergic orchitis.

Electron microscopic observations of testes of sterile, backcross T/tw18 mice which spontaneously develop allergic orchitis have demonstrated accumulations of lymphocytes and occasional plasma cells between seminiferous tubules in affected mice. Many lymphocytes appeared to be insinuated amongst cytoplasmic processes of the peritubular adventitial cells which, in most samples, provided a barrier to direct infiltration of the germinal epithelium by lymphocytes. Although lymphocytes were rarely observed within the seminiferous epithelium, extensive degeneration of spermatogenic cells was observed within affected tubules. Sertoli cells phagocytosed degenerating germ cells at all stages of differentiation. In-vitro co-cultivation of syngeneic T/tw18 spleen and testicular cells revealed that testicular cells from sterile T/tw18 mice failed to activate suppressor T lymphocytes; consequently, the syngeneic splenocytes displayed a vigorous proliferative response to testicular autoantigens. Testicular cells from younger, fertile T/tw18 males, on the other hand, behaved like testicular cells from normal mice, triggering suppressor T cell activity and, thereby, abrogating proliferation of splenocytes. These results suggest genetic factors, introduced in the course of inbreeding and associated with chromosome 17, are responsible for the failure of spermatogenic cells from sterile T/tw18 males to maintain normal tolerance to their own antigens in vivo; allergic orchitis is an extreme manifestation of the inability of the defective germ cells to initiate normal T lymphocyte mediated suppression of an immune response.

Animals↗
PubMed1981

Immunoglobulins in the mouse uterus before implantation.

An indirect immunoperoxidase technique was used to study the distribution of IgA, IgG, IgM and albumin in the uterus of primigravid mice. As pregnancy proceeds from Days 2 to 6, IgA-containing plasma cells concentrate around the uterine glands, IgA is found in an increasing number of glands and then in the uterine lumen. At the same time the stroma is progressively invested by IgG, but IgG plasma cells are not present in significant numbers and IgG is very rarely found in glands. IgM remains in blood vessels until Day 5 when it is present in small amounts in the stroma. Albumin tends to follow a pattern similar to that of IgG but in addition is present in the lumen and in a few cells in the luminal epithelium. The growing decidua does not contain immunoglobulin. These results suggest that, as the embryo reaches the uterine lumen, IgA, produced locally by plasma cells, is secreted into the uterine lumen via uterine glands while IgG infiltrates the stroma as a result of increased permeability of the uterine capillaries at the time of implantation.

Albumins↗
PubMed1981

Erythrocyte deformability in the pathophysiology of the microcirculation.

The most commonly used technique for assessing the deformability of red cells, i.e. the filtration of the red cells through 5 mu pore filters, is discussed in regard to the criteria which have to be fulfilled in order to accept that an in vitro measurement truly reflects a valid physiological and pathological variable.

Animals↗
PubMed1981

The T/t-complex in the mouse: mutations that impair differentiation.

The T/t-complex in the mouse contains multiple genetic factors, capable of independent mutation and separable by recombination, that affect specific events of differentiation during embryonic development and spermatogenesis. Morphological and serological as well as biochemical studies have suggested that t-mutations are associated directly or indirectly with abnormalities of the cell surface. Recent efforts to identify the molecular nature of theses abnormalities gives evidence for at least two different types of molecules associated with complex lethal t-haplotypes. One molecule, a non-glycosylated protein of 63,000 daltons, is a direct gene product specified in apparently the same mutant form by each of over 30 independent t-haplotypes examined that contain the mutant gene responsible for tail interaction. On the other hand, the serologically defined antigenic determinants that define specific lethal t-haplotypes have been shown to reside on different oligosaccharides. The implication of these data with respect to the arrangement and function of mutant factors within the T/t-complex will be discussed.

Animals↗
PubMed1980

Molecular analysis of the genetic relationship of trans interacting factors at the T/t complex.

The T/t complex is an extensive genetic region proximal to the H-2 complex on mouse chromosome 17, with multiple effects on embryonic development, spermatogenesis and recombination. Recently, two-dimensional gel analysis of testicular cell proteins identified a gene within the T/t complex that codes for a major cell surface-associated protein, p63/6.9 (ref. 4). The wild-type gene, Tcp-1b, codes for a 63,000-molecular weight protein (p63/6.9b), whereas a mutant allele, Tcp-1a, which occurs in all intact t haplotypes, codes for a more acidic form of the protein (p63/6.9a). Analysis of partial t haplotypes obtained from rare recombination events showed that Tcp-1a correlated completely with the tail interaction factor tT, which is thought to be a genetic allele of T, thus raising the possibility that the locus of T codes for the p63/6.9 protein. We report here that the p63/6.9 proteins produced by seven chromosomes carrying independently derived dominant mutations at the locus of T are all indistinguishable from the wild-type form; thus, the cumulative data indicate that the Tcp-1 gene is most probably not at the locus of T.

Animals↗
PubMed1980

Early intravenous atenolol treatment in suspected acute myocardial infarction. Preliminary report of a randomised trial.

214 patients were studied in a randomised trial to determine whether administraiton of intravenous atenolol within 12 hours of chest pain reduced eventual infarct size, as estimated by cumulative enzyme release and by ECG changes. 135 patients already had ECG evidence of infarction at entry; 72 received atenolol which significantly decreased subsequent enzyme release (atenolol and control means = 121 IU, SE +/- 10 and 177 IU, SE +/- 17; 2p < 0.005) and enhanced R-wave preservation (atenolol and control means = 46% +/- 3 and 36% +/- 3; 2p < 0.02). 79 patients had no evidence of infarction at entry; 44 did not receive atenolol and 27 of these subsequently developed infarction, whereas only 11 of 35 treated patients infarcted during their hospital stay (2p < 0.01). In hospital, fewer atenolol patients died (4 vs 9), had non-fatal cardiac arrests (2 vs 6), or required therapy for heart-failure (36 vs 47). Unlike many previous trials which had negative results, in this trial we gave the drug intravenously and promptly (median of 4 hours from onset of pain to injecton), thereby achieving early beta-blockade.

Acute Disease↗
PubMed1980

Bullous autoimmune skin disease in the dog: (2) immunopathological assessment.

The immunological examinations of two cases of pemphigus vulgaris and four cases of bullous pemphigoid in the dog are reported. Deposits of immunoglobulin and complement were identified betweeen epithelial cells of the pemphigus cases and at the epithelial/connectivce tissue junction in the pemphigoid dogs. The bullous autoimmune diseases must be considered in the differential diagnosis of mucosal and skin ulceration in the dog.

Animals↗
PubMed1980

Bullous autoimmune skin disease in the dog: (1) clinical and pathological assessment.

The clinical and pathological findings of two cases of pemphigus vulgaris and four cases of bullous pemphigoid in the dog are reported. Clinically these cases were typified by ulcerative lesions of the oral mucous membranes, mucocutaneous junctions and skin. Pathologically there were intraepithelial separation and bulla formation in one of the cases of pemphigus and subepithelial separation and bulla formation in all cases of pemphigoid.

Animals↗
PubMed1980

Induction of tolerance in vitro by autologous murine testicular cells.

We have investigated the regulation of self tolerance in mice by examining lymphocyte reactivity in vitro against two subpopulations of autologous testicular cells: germ cells that were derived from the seminiferous tubules, and interstitial somatic cells. In the presence of germ cells, lymphocyte proliferation was strongly reduced. In contrast, somatic interstitial cells stimulated lymphocyte proliferation. In both cases, reactive lymphocytes were mostly T cells. Suppressor T cells activated by autologous germ cells were nonspecific and capable of inhibiting lymphocyte proliferation against autologous and allogeneic somatic testicular cells as well as against allogeneic spleen cells. Suppression was abrogated after treatment of the responder lymphocytes with anti-Ly-2.2 serum plus complement. Lymphocyte proliferation by autologous interstitial cells was considerably reduced, but not completely abolished, by complement-dependent lysis with anti-Thy-1.2 serum. This may indicate the participation in proliferation of a lymphoid cell population other than T cells.

Animals↗
PubMed1980

Nature of the antigenic determinants of T locus antigens.

The nature of the antigenic specificities of several antigens associated with the T/t complex in the mouse were analyzed by means of glycosidase and haptene inhibition studies. Results indicate that on testicular cells sugar residues are involved in at least six different T/t antigenic determinants. The immunodominant sugar appears to be different for each of the specificities. The specificity for the following T/t antigens resides predominantly in the sugars indicated: T:sialic acid; t12:beta-D-galactose; tw32:beta-D-galactose; t0:L-fucose; tw1:N-acetyl-D-galactosamine; tw18:L-fucose. It seems probable that these sugars are found at the terminal reducing ends of the carbohydrate portion of T/t-bearing moleculse. These studies imply that at least some of the genes in the T locus code for glycosyltransferases or regulators of glycosyltransferases which modigy oligosaccharide structures and impart specificity to the T/t antigens by alteration of their terminal sugar residues.

Acetylgalactosamine↗