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Biomedical subjects

A M Denman

Publications and source records attributed to A M Denman.

At least 109 records · Page 6Linked to original sources
PubMed1978

Chronic myelocytic leukemia. Origin of some lymphocytes from leukemic stem cells.

In three patients with chronic myelocytic leukemia who were heterozygous at the X-linked glucose-6-phospháte dehydrogenase locus, lymphocytes were studied to determine if they had the same stem cell origin as the leukemic myeloid cells. Normal tissues such as skin had both B and A glucose-6-phosphate dehydrogenase isoenzymes, but the leukemic myelogenous cells displayed only one isoenzyme type, consistent with their clonal origin. A population of cells with undoubted thymus-derived (T)-lymphocyte characteristics had both isoenzymes. Presumably, then, these T cells did not arise from the leukemic stem cell, either because they antedated the development of leukemia in that stem cell or, more likely, because they arose from progenitors not involved by the disease. In contrast, another population of lymphocytes showed only one isoenzyme type, suggesting that it arose from the chronic myelocytic leukemia stem cell. However, although this population contained many cells with the characteristics of bone marrow-derived (B) lymphocytes, it is not certain that the single enzyme produced by the cells over all can be attributed to B lymphocytes rather than to contaminating non-B-lymphoid cells.

Adult↗
PubMed1976

Abnormal lymphocyte function is secondary to drug-induced autoimmunity.

Abnormal lymphocyte function has been frequently reported in patients with connective tissue diseases but its significance has been uncertain. Sequential studies of lymphocyte function were carried out in patients receiving the beta-adrenergic blocking drug practolol (Eraldin) both before and during the development of autoimmune complications. No evidence was obtained that abnormal lymphocyte function presaged the onset of autoimmunity, and when these tests did show deficient responses these could be correlated with disease activity in general.

Adult↗
PubMed1976

[The aetiology of rheumatoid arthritis (author's transl)].

An ineffective aetiology for rheumatoid arthritis and other connective tissue diseases has been frequently postulated but never proven. Despite the failure to obtain firm evidence of viral infection in most patients with these disorders for several reasons this theory should not be discarded. Firstly several mechanisms have been discovered by which virus infections can persist in lymphocytes and other tissue thereby provoking inflammation without the production of complete readily detectable virus particles. Secondly there are numerous ways in which host resistance to virus can be subverted with the perpetuation of an ineffective or inappropriate immune response. Thirdly the immunopathological features of these diseases are entirely compatible with an infective aetiology. The main problem is likely to prove the difficulty in attributing a primary pathogenetic role to any isolated virus rather than regarding it as a passenger virus which has been non-specifically activated by the disease process. However preoccupation with a viral aetiology should not blind one to other possibilities since many environmental allergens can produce immunopathological disease of highly protean nature.

Antibodies, Viral↗
PubMed1976

The treatment of connective tissue diseases with antilymphocyte globulin.

Immunosupprissive therapy was carried out using steroids, azathiprine and antilymphocyte globulin in one patient with systemic lupus erythematosus (SLE) and four with dermatomyositis. Response to treatment was based upon clinical evaluation. The patients with SLE and two of the four with dermatomyositis responded favourably to the regime. It is suggested that this preliminary study is sufficiently promising to warrant the creation of a rigidly controlled investigation.

Aged↗
PubMed1975

The viral theory of connective tissue diseases: a review.

For many years evidence for a viral aetiology of connective tissue diseases such as systemic lupus erythematosus and rheumatoid arthritis has been sought by a variety of methods, including attempts at direct isolation, the study of rheumatoid synovial cells, ultrastructural examination of pathological material and assays of anti-viral antibody. No convincing proof has yet been obtained. However, a better understanding of the mechanisms of viral persistence, and the ways in which host defences can be subverted by viral infections has prompted other ways of approaching this problem. A viral aetiology for this group of diseases remains an attractive but unsubstantiated hypothesis.

Animals↗
PubMed1974

Replication or inactivation of different viruses by human lymphocyte preparations.

Cultures of phytohemagglutinin-stimulated, unstimulated, and frozen and thawed mononuclear (as controls) cells from normal human donors were infected with different viruses. A variable pattern of virus infectivity was noted, and influenza and Coxsackie virus were rapidly inactivated even by stimulated lymphocytes. Direct inactivation by lymphocytes may be one form of host defense in infection by some viruses.

Adenoviridae↗