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  • Book
    Eduardo E. Benarroch.
    Contents:
    Central autonomic network
    Anatomy and function of the peripheral autonomic system
    Autonomic neurotransmission
    Autonomic pharmacology
    Evaluation of autonomic disorders
    Neurogenic orthostatic hypotension
    Postural tachycardia syndrome
    Baroreflex failure
    Syncope and other causes of transient loss of consciousness
    Disorders of sweating
    Neurogenic bladder and sexual dysfunction
    Gastrointestinal dysmotility
    Autonomic hyperactivity
    Neurodegenerative autonomic disorders
    Autonomic neuropathies
    Neuropathic pain disorders with autonomic component
    Autoimmune autonomic disorders
    Focal disorders of the cerebral hemispheres and brainstem
    Focal disorders of the spinal cord
    Chronic pain disorders with autonomic features.
    Print Access Request
    Location
    Version
    Call Number
    Items
    Books: General Collection (Downstairs)
    2014
    RC346 .B46 2014
    1
  • Article
    Pierce SK, Cancro MP, Klinman NR.
    J Exp Med. 1978 Sep 01;148(3):759-65.
    In recent years antigen-specific T cells have been shown to be capable of mediating a number of diverse functions in collaboration with B cells in humoral immune responses. One of the more intriguing roles attributed to helper T cells is the promotion of the synthesis of multiple immunoglobulin isotypes by B cells in T-dependent antibody responses. The experiments presented in this report were carried out to determine if an individual antigen-specific T lymphocyte has the capability to enable the production of antibodies of multiple immunoglobulin heavy chain isotypes. We describe an experimental system which allows for the isolation and antigenic stimulation of individual helper T cells in a splenic environment which provides an excess of primary B cells for collaboration with isolated T lymphocytes. Employing this system we have demonstrated that an individual antigen-specific T lymphocyte, specific for the PR8 strain of influenza virus, has the capacity to enable primary B-cell PR8-specific antibody responses of more than a single immunoglobulin isotype. The implications made by these studies regarding the problem of genetic restrictions regulating T-cell-B-cell interaction is discussed.
    Digital Access Access Options