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Biomedical subjects

J Andersson

Publications and source records attributed to J Andersson.

At least 289 records · Page 16Linked to original sources
PubMed1984

Haemodynamic effects of prenaterol and cardiac glycosides in patients with recent myocardial infarction.

Prenalterol was given to twenty five patients with acute myocardial infarction. Thirteen patients (group B) had signs of cardiac decompensation while twelve (group A) had not. Ejection fraction was determined with 99mTc-labelled red blood cells before and after prenalterol (50 micrograms kg-1 body weight), intravenously. In group B this procedure was repeated after digitalization 2 days later. The ejection fraction increased significantly in group A after prenalterol injection. In group B, prenalterol produced an increase, but this was not significant. After digitalis the ejection fraction increased significantly and prenalterol produced an additional significant rise. No significant changes in blood pressure occurred. Heart rate increased significantly in both groups after prenalterol injection and decreased significantly after digitalis.

Adrenergic beta-Agonists↗
PubMed1984

Secretion of gamma-interferon at the cellular level. Induction by Epstein-Barr virus.

Using a haemolytic plaque assay for gamma-interferon (IFN-gamma) secretion we found that in vitro Epstein-Barr virus (EBV) exposure of peripheral blood mononuclear cells from EBV immune individuals led to IFN-gamma secretion, which was apparent within 6 h after virus contact and peaked 12-24 h after induction. Live, ultraviolet-light-irradiated and heat-inactivated virions all caused IFN-gamma secretion. In contrast, blood mononuclear cells from EBV non-immune adults or neonates could not be activated to IFN-gamma production by EBV.

Cells, Cultured↗
PubMed1984

Mode of inhalation for trained and untrained asthmatics using a pressurized aerosol.

A pressurized inhalation aerosol should be actuated at the beginning of a slow and deep inhalation, followed by a long pause of breathholding. In this study a registration was performed on the mode of inhalation. The flow-volume curve and the moment of actuation were obtained from an aerosol actuator provided with sensors, and the breathholding pause was measured. Data were obtained from 34 asthmatic patients, regularly trained to use the pressurized aerosol, and these data were compared with those from 44 untrained patients. When the subjects used a terbutaline sulfate aerosol in their usual fashion, most of the trained subjects succeeded well. Further improvements could possibly be made regarding the depth of inhalation and, after control with the recording device, regarding the flow rate at actuation. Most of the untrained subjects did not use a deep enough inhalation with respect to their vital capacity, and their breath-holding pause was very short. It only seems possible to improve these parameters by regular training. In order to reach optimal results the asthmatic patients must be regularly controlled and instructed regarding their use of a pressurized inhalation aerosol. A recording device is useful in demonstrating to each subject which parameter can be improved.

Adolescent↗
PubMed1984

Multiple low-dose streptozotocin-induced diabetes in the mouse. Evidence for stimulation of a cytotoxic cellular immune response against an insulin-producing beta cell line.

Mice were examined for the presence of splenocytes specifically cytotoxic for a rat insulinoma cell line (RIN) during the induction of diabetes by streptozotocin (SZ) in multiple low doses (Multi-Strep). Cytotoxicity was quantitated by the release of 51Cr from damaged cells. A low but statistically significant level of cytolysis (5%) by splenocytes was first detectable on day 8 after the first dose of SZ. The cytotoxicity reached a maximum of approximately 9% on day 10 and slowly decreased thereafter, becoming undetectable 42 d after SZ was first given. The time course of the in vitro cytotoxic response correlated with the degree of insulitis demonstrable in the pancreata of the Multi-Strep mice. The degree of cytotoxicity after Multi-Strep was related to the number of effector splenocytes to which the target RIN cells were exposed and was comparable to that detectable after immunization by intraperitoneal injection of RIN cells in normal mice. The cytotoxicity was specific for insulin-producing cells; syngeneic, allogeneic, and xenogeneic lymphocytes and lymphoblasts, 3T3 cells, and a human keratinocyte cell line were not specifically lysed by the splenocytes of the Multi-Strep mice. This phenomenon was limited to the Multi-Strep mice. Splenocytes from mice made diabetic by a single, high dose of SZ exhibited a very low level of cytotoxicity against the RIN cells. The cytotoxic response was also quantitated in splenocytes from control and Multi-Strep mice (10 d after the first dose of SZ) before and after culture with mitomycin-treated RIN cells in the presence of T cell growth factor (TCGF). The cytotoxicity of the Multi-Strep splenocytes was enhanced more than fivefold after such culture, suggesting the proliferation of an effector cell that could be stimulated and supported in vitro by TCGF. These results support the hypothesis that cell-mediated anti-beta cell autoimmunity may play a role in the destruction of the beta cells in this animal model. The stimulation of this response by TCGF may provide a tool by which enough cytotoxic effector cells could be obtained to establish their possible direct pathogenetic role in the induction of insulin-dependent diabetes. In addition, such cells will be a valuable tool to define the specific beta-cell antigens that may direct the highly selective cell-mediated destruction of these cells in experimental models and, perhaps, in human insulin-dependent diabetes mellitus.

Adenoma, Islet Cell↗
PubMed1984

Spontaneous production of interferon-gamma in adult and newborn humans.

By using a hemolytic plaque assay for IFN-gamma secretion by single cells, we found that one to three IFN-gamma secreting cells per 1 X 10(3) mononuclear cells were present in the blood from normal adult and newborn humans, without in vitro culture or stimulation by antigens or mitogens. The frequency of such cells was higher in newborns. These spontaneous IFN-gamma-secreting cells were predominantly T cells of the helper/inducer phenotype, as defined by treatment with monoclonal antibody and complement. By using indirect immunofluorescence staining, it was seen that 1% of blood mononuclear cells from adults and 3.5% from newborns contained cytoplasmic IFN-gamma. These cytoplasmic IFN-gamma-positive cells belonged to a heterogeneous population by morphology and by staining with monoclonal antibody. The majority of these cells were DR-positive T cells. We propose that these IFN-gamma-producing cells were activated in vivo, and that they possibly mediate antiviral or lymphokine activities.

Adult↗
PubMed1983

Epidermal Langerhans cells as accessory cells in con A stimulation of T lymphocytes in the guinea-pig.

Stimulation of guinea-pig T cells by concanavalin A (Con A) requires Ia-antigen expressing accessory cells. Such functional accessory cells were identified among the normal epidermal cells and could be fractionated and enriched by centrifugation on discontinuous Percoll density gradients. Epidermal cells collecting at a density of 1.08 g/ml were the most effective in mediating Con A-dependent T cell proliferation, induced the highest activity of T cell growth factors (TCGF) and were enriched fivefold for Ia antigen expressing cells. A monolayer immunosorbent technique yielded a 35-fold enrichment of Ia antigen expressing epidermal cells. This cell fraction induced high levels of TCGF in the culture supernatants. Since the only cells in the normal epidermis expressing Ia antigens are the Langerhans cells, we conclude that the Langerhans cells may act as accessory cells for Con A stimulation of T cells.

Animals↗
PubMed1983

T-cell growth factor contains activity that supports natural killer activity in vitro.

Lymphocytes from athymic and normal mice were tested and compared for cytotoxic activity after in vitro cultures supplemented with concanavalin A or T-cell growth factor (TCGF). Our results indicate that, in addition to cytotoxic T cells, natural killer (NK) activity can be recovered from lymphocytes cultured in the presence of TCGF and that this is not the result of contaminating interferon in the TCGF preparations. The NK nature of the effector cells was established by means of a panel of target cells, including a teratocarcinoma tumour cell, which enabled the distinction of T-cell- and NK-cell-mediated lysis.

Animals↗
PubMed1981

Cellular interaction and the environment in lymphocyte development: the roles of antigen, histocompatibility, and growth factors in T cell-dependent B cell stimulation.

T cell-dependent B cell stimulation depends on cellular interactions between macrophages, T cells, and B cells. T cells recognize antigen in the context of Ia determinants on macrophages. This leads to the activation of helper T cells and to the production of helper factor(s) either by the activated helper T cells or by the macrophages. Cloned lines of helper T cells produce factors("help') for B cell replication and Ig secretion in the presence of histocompatible macrophages and of specific antigen. These factors stimulate histocompatible, as well as histoincompatible, mitogen-activated B cell blasts polyclonally. Thus, neither antigen nor histocompatibility, but antigen-unspecific, soluble factors are required to stimulate an activated B cell blast through the next round of division. Small resting B cells, however, are not stimulated to replication by these factors, but only to polyclonal, H-2-unrestricted maturation to Ig-secreting cells. Replication (and Ig secretion) of small resting B cells, however, is only induced when antigen-specific small B cells bind their specific antigen via surface Ig molecules and interact with histocompatible helper T cells. The preference of the resting B cells for such collaboration with T cell help is mapped to the K-end of the H-2 locus and probably constitutes the antigen expressed on B cells by the I region. It appears that a resting B cell is excited by the binding of specific antigen to surface Ig and by the interaction of its surface Ia with helper T cells. After this dual recognition the excited B cell can be stimulated by the antigen-unspecific factor(s) generated by the interaction of helper T cells, adherent cells and antigen to initiate growth. Immune induction of a B cell thus involves three controlling elements: Ig, Ia, and B cell growth factor receptors.

Animals↗
PubMed1980

Antigen-specific T-helper cells stimulate H-2-compatible and H-2-incompatible B-cell blasts polyclonally.

Lipopolysaccharide (LPS)-activated B-cell blasts from C57BL/6J nu/nu spleen cells develop into IgM-secreting clones after stimulation by antigen-specific T-helper cells of C57BL/6J origin. Although induction of help is antigen-dependent, help itself acts polyclonally. 1 of 1--3 B-cell blasts is restimulated in a homologous fashion by LPS, or in a heterologous fashion by sheep erythrocyte (SRC)- or horse erythrocyte (HRC)-activated T-helper cells. The repertoire of activated B-cell blasts reflects the polyclonal nature of activation: approximately 1 in 1,000--3,000 restimulated B-cell blasts is specific for SRC, 1 in 300--1,000 is specific for HRC, and 1 in 100--300 specific for trinitrophenylated SRC (TNP30-SRC). B-cell blasts that are either H-2 compatible or H-2 incompatible with the antigen-activated T-cell help are stimulated polyclonally in similar high frequencies. Thus, neither antigen nor H-2 compatibility are required to stimulate a B-cell blast into the next cell cycle.

Animals↗