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Biomedical subjects

C Koch

Publications and source records attributed to C Koch.

At least 487 records · Page 27Linked to original sources
PubMed1976

[Development of the internal ear in albino rat embryos subjected to transverse acceleration at + 3 G. Note 3: First observations on the ultrastructural picture of the labyrinth. 1st ultrastructural studies of the labyrinth].

Marked body size reduction (minus 50.5%), and delayed head and body skeletal development were noted in albino rat embryos following exposure of the mother to +/- 3 G acceleration for 3 hr/day between the 10th and 19th day of pregnancy. In addition, electron microscope examination of the inner ear showed signs of greater functional activity of the labyrinth, unaccompanied by reduction of development. Semicircular canal cells and size, in fact, were normal in the crests and at a distance from the latter. There was a marked increase in the number of mitochondria in the cells, in ER area and volume, and A and B glycogen granule richness compared with the controls, these being all signs of considerable activity. The findings substantiate prior histological and histochemical observations: the physiological stimulus offered by acceleration is highly specific for the inner ear structure, particularly that of the labyrinth, to the point where the handicap imposed by the circulatory hypoxia caused by such acceleration, by disturbing the mother-foetus circulation, is overcome.

Acceleration↗
PubMed1976

Sequential studies of lymphocytes, neutrophils and serum proteins during prednisone treatment.

Seven patients (6 with connective tissue diseases, 1 with bronchial asthma) have been studied before, during, and after prednisone therapy. Maximum dose was 15 mg daily, which was tapered off to zero within three months. All patients showed striking subjective improvement during therapy. The ESR reflected this improvement but the acute phase proteins did not. The serum concentration of prealbumin rose significantly during the period of most intensive steroid treatment. IgE decreased in the patient with bronchial asthma, but otherwise the immunoglobulins did not change, and positive serological tests remained unchanged. Contact sensitization to haptens was induced without impairment during therapy. Prednisone induced rises in blood lymphocyte and neutrophil concentrations. Lymphocyte transformation, both mitogen- and antigen-induced, was not influenced by therapy, but PPD-induced inhibition of leucocyte migration decreased. Neutrophil phagocytosis was unimparied, but bactericidal capacity, stimulated nitroblue tetrazolium reduction, and neutrophil and plasma lysozyme concentrations were all depressed during treatment with prednisone.

Adult↗
PubMed1976

Genetic control of antibody responses to PHA in inbred rats.

Phytohemagglutinin (PHA-P; Difco) contains four immunogenic components. The antibody response in rats to two of these components is shown to be genetically determined: AS rats are high responders and BN rats are low responders to both antigens. Responsiveness to the two components segregates independently as autosomal, dominant traits in a manner that is compatible with a one-gene hypothesis for both responses. The antibody response to the mitogenic fraction of PHA segregates together with the in vitro mitogenic response to PHA and to other mitogens. These responses are not linked to the major histocompatibility complex (MHC) of the rat. The antibody response to a nonmitogenic fraction from PHA is, however, linked to the MHC.

Animals↗
PubMed1976

Genetic control of the in vitro responses of rat blood lymphocytes. II. Number of loci involved and linkage with in vivo antibody formation.

Blood lymphocytes from the inbred rat strains AS and BN differ in the magnitude both of their in vitro proliferative response to different mitogens and of their in vivo antibody response to the mitogenic fraction of phytohemagglutinin (PHA). We have examined the segregation of in vitro responsiveness to PHA in (AS X BN)F1 X BN backcross rats and have tried to correlate it with other characters that vary in backcross rats. In vitro responsiveness is regulated by one or a few loci, is linked to the in vitro responsiveness to B lymphocyte mitogens and the in vivo antibody response to the mitogenic fraction of PHA, but is not linked to the major histocompatibility locus (Ag-B) nor to the frequency of short-lived small Ig-negative lymphocytes in blood. Lymphocytes from high-responder rats have a shorter lag period before the onset of DNA synthesis in vitro than low-responder rats, and possibly also a higher number of in vitro responsing cells. To explain our findings, that the same gene og genes regulate in vitro responsiveness to different mitogens and in vivo antibody response to the mitogenic fraction of PHA, we suggest that the gene or genes act in an immunologically unspecific manner on the regulation of lymphocyte proliferation in vitro as well as in vivo.

Animals↗
PubMed1975

Genetic control of the in vitro responses of rat blood lymphocytes. I. Comparison of in vitro and in vivo responses.

Nielsen, H. E. & Koch, C. Genetic Control of the In Vitro Responses of Rat Blood Lymphocytes. I. Comparison of In Vitro and In Vivo Responses, Scand. J. Immunol. 4, 31-36, 1975. In vitro DNA synthetic responses of blood lymphocytes from the inbred rat strains BN, Lewis, and AS were compared with each other after stimulation with allogeneic lymphocytes, human lymphocytes, phytohemagglutinin, and anti-Ig antibodies. BN lymphocytes responded less well than AS and Lewis lymphocytes regardless of the stimulus used. The responses of the congenic strains Lewis and Lewis. BN were identical, suggesting that H-1 (Ag-B)-linked loci do not determine in vitro responsiveness in these strains. In vivo, AS and BN rats were equally able to reject third-party skin grafts and to induce graft-versus-host reactions in F1 hybrids. We conclude that the interstrain differences found in vitro reflect genetically determined differences in in vitro kinetics, possibly related to the fraction of short-lived lymphocytes present rather than to demonstrable differences in the frequency of reactive lymphocytes.

Animals↗
PubMed1975

Antigen binding by non-bursa-derived chicken leukocytes.

Antigen-binding peripheral blood leukocytes (PBL) from normal and bursectomized agammaglobulinemic chickens were labeled by incubation in vitro with radioiodinated antigen at 4 degrees C in the presence of sodium azide. [125I]TGAL-binding cells could be detected by autoradiography of PBL from normal, unimmunized chickens at a frequency of 1 to 4 labeled cells per 10(4) leukocytes. No [125I]TGAL-binding cells were found in PBL from bursectomized chickens, even after incubation with 25 mug/ml of labeled antigen followed by prolonged autoradiographic exposure. The binding to normal PBL was specific as judged by inhibition with unlabeled TGAL but not with unlabeled TIGAL. The binding was, furthermore, inhibited by preincubation with rabbit anti-chicken L chain antibody but unaffected by normal rabbit IgG. [125I]TIGAL was, in contrast, found to bind to PBL from both normal and bursectomized chickens at a frequency of 6 to 80 labeled cells per 10(4) leukocytes. The labeling was specific, since it was inhibited by cold TIGAL but not by cold TGAL. The binding of [125I]TIGAL to PBL from bursectomized chickens showed from none to slight inhibition on preincubation of the cells with anti-L chain antibody, whereas preincubation with normal rabbit IgG resulted in almost complete inhibition. To our knowledge this is the first demonstration of antigen binding to PBL from agammaglobulinemic chickens.

Agammaglobulinemia↗