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Biomedical subjects

B H Waksman

Publications and source records attributed to B H Waksman.

At least 19 recordsLinked to original sources
PubMed1991

Science training for European journalists.

"Immunology", it was stated recently in a leading European national newspaper, "is a complicated and obscure discipline...that immunologists don't understand much about themselves". Set against this background, Byron Waksman reports on a recent meeting*, which was attended by journalists and scientists from all over Europe, on the attitude of the general public towards science and the need for scientific training among journalists.

Europe↗
PubMed1990

Astrocytes: auxiliary cells for immune responses in the central nervous system?

Active and replicating astrocytes are prominent in multiple sclerosis (MS) lesions and in experimental demyelinating diseases resembling MS. As evidence is amassed supporting an autoimmune etiology for MS, the possible contribution of astrocytes as auxiliary/effector cells in the generation of tissue damage and subsequent scar formation has attracted considerable attention. A recent workshop fostered interaction between neurobiologists interested in astrocytes and investigators interested in demyelinative diseases. Key issues were attempts to relate the behavior of astrocytes in demyelinative lesions to findings in model systems in vitro, to distinguish various astrocyte functions (auxiliary, effector, scar formation) and to identify the regulatory mechanisms associated with each function.

Antigen-Presenting Cells↗
PubMed1990

Psychoneuroimmunology.

Complex interactions among the nervous, endocrine, and immune systems have been documented and these are currently being studied at the cellular and molecular levels with ever more powerful tools. They have an important impact on diseases affecting the three systems, in particular on autoimmune and infectious diseases of the nervous system. In time neuroimmunological diseases and psychoneuroimmunological relationships may become as "respectable" as the more familiar neuroendocrine diseases and relationships.

Humans↗
PubMed1989

Multiple sclerosis.

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Autoimmune Diseases↗
PubMed1988

Autoimmunity in demyelinating diseases.

Demyelinative diseases of the CNS and peripheral nervous system can be distinguished on the basis of primary mediation by antibody or T lymphocytes (or failure of the T-cell-mediated response) and on the basis of chronicity. The principal mechanisms are autoimmunization to myelin antigens after actual immunization with tissue or infection with cross-reactive viruses or, alternatively, persistent infection of the nervous system (viral or spirochetal) with an associated immune response to the pathogen.

Animals↗
PubMed1979

Catheptic carboxypeptidase B as a major component in "T-cell activating factor" of macrophages.

TAF (T-cell activating factor), produced by peritoneal macrophages and assayed by its ability to potentiate DNA synthesis in macrophage-depleted lymph node cells stimulated with Phytochemagglutinin-concanavalin A, was shown to contain catheptic carboxypeptidase B (CPB) which accounted almost quantitatively for its potentiating activity. TAF action was inhibited by CPB inhibitors and could be mimicked by commercial pig pancreas CPB. The activity was absorbed from active supernatants on EACA-Sepharose and could be eluted with free EACA (epsilon aminocaproic acid).

Animals↗
PubMed1978

Regulatory substances produced by lymphocytes. VI. Cell cycle specificity of inhibitor of DNA synthesis action in L cells.

IDS inhibits DNA synthesis and mitosis of L cells only when present during the late G1 phase of the cell cycle, as shown with L cells synchronized by a variety of methods. This corresponds well with earlier findings that IDS inhibits DNA synthesis in mitogen-stimulated lymphocytes when present between 16 and 24 h after adding mitogen. In both cell types, the inhibition produced by IDS appears to be totally the result of elevation of cAMP level. Thus, inhibitors of cAMP phosphodiesterase work synergistically with IDS, and activators of cAMP phosphodiesterase overcome the inhibition by IDS. This paper shows that IDS raises cAMP levels in L cells only within a narrow interval of the cell cycle, around 6-8 h after mitosis. This cell cycle specificity, which may be related to appearance of receptors for IDS only at discrete times, may be important in limiting IDS action to suppression, as elevated cAMP levels have a variety of other effects during other phases of the cell cycle.

Animals↗