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Biomedical subjects

B Huber

Publications and source records attributed to B Huber.

At least 73 records · Page 4Linked to original sources
PubMed1978

Traumatic rupture of the aorta and paraplegia.

During the past 10 years, 15 traumatic ruptures of the aorta isthmus have been diagnosed. The most likely mechanism is that of a brutal deceleration. Three patients developed a complete mid-thoracic flaccid paraplegia. One died in a few hours of a complete rupture, the second after a few days from renal insufficiency, the third 12 days after, having been operated upon on the same day of the accident. All had associated lesions. Diagnosis can be very difficult in these patients, especially in the first few hours. Paraplegia is here considered as an aggravation ischaemic symptom with anuria and loss of blood circulation in the lower limbs. In delayed cases the vascular mechanism of the infarction of the spinal cord is discussed, either by compression of the intercostal arteries or by direct compression of the aorta itself. In our cases, the most likely mechanism is that of an obstruction of the lumen of the aorta by a torn inner coat. These patients must be transferred as quickly as possible to a cardiovascular surgical unit and operated upon immediately. Three cases of preoperative, rapidly progressive paraplegia with neurological recovery after the operation, have been reported in the literature.

Accidents, Traffic↗
PubMed1978

Molecular identification of a surface structure on B cells (Lyb-3) and its relationship to B cell triggering.

Lactoperoxidase-catalyzed radioiodination of cell surface proteins and immunochemical procedures are used to identify murine splenic lymphocyte membrane components bound by anti-Lyb-3 serum. This antiserum defines membrane components (Lyb-3) on a subpopulation of murine B cells that may function as a receptor for T cell signals. SDS-PAGE analysis of surface-labeled membrane components bound by anti-Lyb-3 serum demonstrated a single molecular species of 68,000 d. The polypeptides recognized by anti-Lyb-3 are not composed of disulfide-linked subunits and bear no antigenic relationship with known membrane immunoglobulins (IgM or IgD). Absorption of anti-Lyb-3 serum with the 68,000 d polypeptides removed the ability of anti-Lyb-3 serum to augment the in vivo immune response of mice to low doses of sheep erythrocytes. The latter provides formal proof that the 68,000 d polypeptide bound by anti-Lyb-3 serum is the target on the B cell membrane for the immunoenhancing activity of the antiserum.

Animals↗
PubMed1977

Identification of a B-cell surface structure involved in antigen-dependent triggering: absence of this structure on B cells from CBA/N mutant mice.

CBA/N mice have an X-linked B-cell maturation defect which is reflected in part in an absence or dysfunction of a subclass of mature B cells. We have immunized the defective male offspring of the mating (CBA/N female X BALB/c male) with BALB/c spleen cells. The resulting antiserum (alphaLyb3) selectively reacts with a component on the surface of a portion of B cells from a panel of H-2 different mouse strains. Binding of alphaLyb3 serum to this B-cell subclass results in substantial (10- to 20-fold) enhancement of the antibody response to low doses of SRBC. Both binding and enhancing activity are removed by absorption with B cells from B6 and BALB/c, but not CBA/N mice. Absorption of the serum with bone marrow cells, T cells, or thymocytes from Lyb3+ strains does not remove activity. Since the enhanced plaque-forming cell (PFC) responses are specific for the immunizing antigen, and since no PFC response is produced by injection of the antiserum alone, this enhancement probably reflects a second signal produced by specific interaction between antibody and the surface Lyb3 component. Moreover, this signal can partially replace the requirement for T cells in the production of antibody to a "thymus-dependent" antigen. These findings (taken in conjunction with the previously described immune defects in CBA/N mice and other studies of B-cell maturation) suggest to us that Lyb3 is a cell surface component expressed selectively on a mature B-cell subclass. This component is important in B-cell triggering by antigen and fails to develop in CBA/N mice, due to a dysfunction of a regulatory gene on the CBA/N X chromosome.

Animals↗
PubMed1976

Independent differentiative pathways of Ly1 and Ly23 subclasses of T cells. Experimental production of mice deprived of selected T-cell subclasses.

When B mice are supplied with Ly1 or Ly23 cells they acquire, over the next 6 mo, only the immune functions associated with each of these T-cell subclasses, respectively. The T-cell population of these "B-Ly1" and "B-Ly23" mice mice also remains restricted to the Ly1 and Ly23 subclass phenotypes. Thus the Ly1 and Ly23 populations are derived from two separate lines of differentiation and are not sequential stages of a single differentiative pathway.

Animals↗
PubMed1976

Cell-mediated immunity: delayed-type hypersensitivity and cytotoxic responses are mediated by different T-cell subclasses.

Cell-mediated immunity includes both the generation of cytotoxic cells and initiation of delayed-type hypersensitivity (DTH). The resting T-cell population, before stimulation by antigen, already contains cells of the Lyl subclass that are programmed to initiate DTH (and helper function) but not cytotoxic responses, as well as Ly23 cells which can generate killer activity (and suppressive function) but not DTH. The central implication of these findings is that the broad division between humoral and cell-mediated immune responses does not precisely correspond to the division of labor among T-cell subclasses. The relative contribution of DTH-competent Lyl cells and cytotoxic Ly23 cells to the classical homograft response remains to be determined.

Animals↗