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Biomedical subjects

O Bruserud

Publications and source records attributed to O Bruserud.

At least 91 records · Page 5Linked to original sources

Sudden death caused by heart block in a patient with multiple myeloma and cardiac amyloidosis.

A patient with multiple myeloma and amyloidosis was admitted to hospital following successful cardiopulmonary resuscitation at home. No disturbances in heart rhythm were seen during the first 48 hours of continuous telemetric ECG recording. The patient died from ventricular asystole due to complete atrioventricular block, while he was on a 24-hour Holter monitoring the fifth night in hospital. Patients with known cardiac amyloidosis and syncope should undergo long-term ECG recordings, preferably by telemetry. Repeated registrations may be necessary to discover disturbances in heart rhythm.

Amyloidosis↗

Combined intoxication with digitoxin and verapamil. The possible inhibition of sensitisation to digitalis-specific antiserum by toxic drug concentrations.

The clinical course in a patient with a combined intoxication with digitoxin (maximal serum level 357 nmol/l) and verapamil is described. The patient received two injections of digitalis-specific antiserum. No adverse reactions to the therapy was seen, and the antiserum markedly shortened the plasma half-life of digitoxin. In vitro studies indicate that digitoxin in concentrations seen during the intoxication may have an immunosuppressive effect, thereby reducing the risk of sensitisation to the antiserum.

Aged↗

Dipyridamol inhibits activation of human T lymphocytes in vitro.

The effect of dipyridamol on T-lymphocyte activation was investigated. The drug did not have an irreversible toxic effect on T lymphocytes. Dipyridamol inhibited both PHA- and mumps-stimulated proliferation and the proliferative response in mixed lymphocyte cultures. The drug inhibited PHA-stimulated proliferation independent of the time when it was added during the culture period. The PHA-stimulated expression of interleukin-2 (IL-2) receptors and IL-2 production (at least for low concentrations) was not inhibited. Dipyridamol inhibited IL-2-dependent growth of T cell lines. The drug caused no inhibition when present only during antigenic pulsing.

Cell Division↗

Genomic HLA-DQ beta polymorphism associated with insulin-dependent diabetes mellitus. Analysis of possible functional significance.

Twelve insulin-dependent diabetes mellitus (IDDM) patients and healthy controls, who all carried the serologically defined DR3 and DR4 antigens, were compared with respect to other HLA polymorphisms. No significant differences between patients and controls were found by typing for HLA-Dw determinants by homozygous cell typing, nor by studies of their genomic DR beta polymorphism using different restriction enzymes. In contrast, certain DR beta polymorphism using different restriction enzymes. In contrast, certain DR4-associated genomic DQ beta fragments had a significantly different distribution among the IDDM patients than among the controls. Furthermore, when the distribution of all DQ beta-specific fragments which demonstrated polymorphism in our material was taken into account, nine of the 12 DR3, 4 IDDM patients demonstrated a similar DQ beta polymorphism compared with only two out of the 12 DR3, 4 controls (P = 0.006; corrected P = 0.037). Cells from patients and controls who demonstrated this IDDM-associated DQ beta polymorphism stimulated each other significantly less in reciprocal MLC tests, compared with the responses seen when their cells were confronted with cells from the DR3, 4 individuals with other genomic DQ beta polymorphisms.

Adult↗

The mumps-specific T cell response in healthy individuals and insulin-dependent diabetics: preferential restriction by DR4-associated elements.

An increased frequency of mumps-specific T lymphocytes restricted by DR4-associated elements has previously been described in DR4 heterozygotes. Here we report that the preferential restriction elements may be present on DR4 molecules expressing either Dw4 or Dw14. No particular genomic DQ-beta-polymorphism was associated with the preferential restriction elements.

Diabetes Mellitus, Type 1↗

The effect of drugs used in anticoagulation therapy on T lymphocyte activation in vitro. II. Warfarin inhibits T lymphocyte activation.

The effect of warfarin on T lymphocyte activation in vitro was investigated. Warfarin was found to cause a dose-dependent inhibition of both antigen- and PHA-stimulated proliferation. The drug had to be present during the early steps in T lymphocyte activation to cause inhibition. Warfarin seemed to have no effect on antigen processing or presentation. Warfarin inhibited Interleukin 2 (IL-2) production, but had only minimal effects on expression of IL-2 receptors or IL-2 dependent proliferation. The inhibition in most in vitro models was found only at warfarin concentrations exceeding the therapeutic serum level.

Antigens, Viral↗

The effect of drugs used in anticoagulation therapy on T lymphocyte activation in vitro. I. Heparin inhibits activation by soluble antigen or allogeneic cells but not by phytohaemagglutinin.

Heparin in concentrations corresponding to the therapeutic serum level (0.5 IU/ml) was found to inhibit proliferative responses in MLC and antigen (mumps)-stimulated cultures. Heparin had to be present early during culture to exert this effect. Heparin did not inhibit antigen-induced expression of IL-2 receptors. No inhibition was seen when heparin was present only during antigen pulsing of antigen-presenting cells. Heparin had no effect on PHA-stimulated proliferation, IL-2 production or expression of IL-2 receptors. Heparin also inhibited the IL-2 dependent growth of long-time cultured T cell lines. The inhibitory effects of heparin were not caused by a toxic effect on the cells.

Antigens, Viral↗

The role of the CD8-positive subset of T cells in proliferative responses to soluble antigens. I. Studies of healthy subjects, type 1 diabetics, and coeliac disease patients.

Using magnetic monosized polymer particles (M 450) coated with a monoclonal mouse IgM anti-CD8 (ITI 5C2) antibody, we were able to selectively remove and isolate functionally active CD8+ T cells from human peripheral blood mononuclear cells. Isolated CD8+ cells did not respond by proliferation to soluble antigens, but proliferated in response to phytohaemagglutinin. However, in the presence of CD4+ T cells, CD8+ cells were able to mount a substantial proliferation when stimulated with soluble antigens. Depletion of CD8+ cells decreased rather than increased the T-cell responses to the antigens glyc-gli, Coxsackie B4, and mumps in healthy individuals. We therefore found no indication of involvement of functionally-active CD8+ suppressor cells in vitro. The T-cell responsiveness to these antigens has previously been shown to be influenced by HLA-DR-associated restriction elements, but the tendency for decreased responsiveness to these antigens by CD8 depletion seemed independent of the DR type of the cell donors. As in healthy subjects, CD8 depletion resulted in a decreased responsiveness to the gluten antigen glyc-gli in untreated and treated coeliac disease patients and to Coxsackie B4 and mumps antigens in Type 1 diabetics.

Antigens, Viral↗

Interleukin 2- and interferon-production and expression of interleukin 2 receptors by human mononuclear cells stimulated with mumps virus or phytohaemagglutinin.

Interleukin 2 (IL 2) production, expression of IL 2-receptors and interferon (IFN) production in vitro by human mononuclear cells stimulated with inactivated mumps-virus antigen and phytohaemagglutinin (PHA, a T lymphocyte mitogen) were characterized. The detectable level of the T-cell lymphokine IL 2 in culture supernatants peaked after 18-24 hours for PHA stimulation and after 48 hours for mumps stimulation. The expression of IL 2 receptors was maximal on day 3 of PHA stimulation and days 5-6 of mumps stimulation. The IFN-level in culture supernatants showed only small variations during the culture period, both for mumps- and PHA-stimulated cultures, and IFN-gamma was detected in both cultures.

Humans↗

The proliferative T-lymphocyte response to streptokinase.

Purified streptokinase was found to initiate a proliferative T-lymphocyte response. The response was characterized by dose-response and kinetics investigations. Streptokinase did not initiate any response when tested on T lymphocytes from newborns, thus indicating that the proliferative T-lymphocyte response to streptokinase in vitro is an antigen stimulated activation of T lymphocytes from individuals previously sensitized in vivo. Of healthy individuals, 40% (16 out of 40 tested) showed a significant proliferative response to streptokinase. Methylprednisolone, cyclosporin A, theophyllamine and verapamil all inhibited the streptokinase-stimulated proliferative T-lymphocyte responses in a dose-dependent manner.

Adult↗

The role of the CD8-positive subset of T cells in proliferative responses to soluble antigens. II. CD8-positive cells are not responsible for DR-associated differences in responsiveness to mumps and Coxsackie B4.

The role of CD8 (T8, Leu 2)-positive T lymphocytes in the proliferative T-lymphocyte response to mumps and Coxsackie B4 viral antigens in vitro was investigated. The frequency among enriched T-lymphocyte blasts of antigen-reactive T lymphocytes (ARTL) restricted by different DR-associated elements was investigated, using antigenic restimulation with allogeneic antigen-presenting cells in a limiting dilution assay. A decreased frequency of DR3-restricted and an increased frequency of DR4-restricted mumps and Coxsackie B4 ARTL were seen in the limiting dilution assay, whether or not HLA class I determinants were shared in the antigenic restimulation. Removal of CD8-positive cells did not increase the primary in vitro responsiveness to mumps and Coxsackie B4 viral antigens, and did not change the DR-associated differences in the frequency of ARTL seen in the limiting dilution assay.

Antigen-Presenting Cells↗

HLA-DR3 and -DR4 control T-lymphocyte responses to mumps and Coxsackie B4 virus: studies on patients with type 1 (insulin-dependent) diabetes and healthy subjects.

To study the relationships between the responses to viral antigens and the HLA-DR3 and -DR4 associations in Type 1 (insulin-dependent) diabetes mellitus, the frequency of T-lymphocyte proliferating in response to mumps, Coxsackie B4 and varicella-zoster antigens was determined. A decreased frequency was found in T lymphocytes able to respond to mumps or Coxsackie B4 when presented together with DR3, as compared with the frequency of T lymphocytes able to respond to these viruses together with other DR determinants. This was not found for varicella-zoster or purified protein derivative of tuberculin. In contrast, an increased frequency was found in T lymphocytes responding to mumps or Coxsackie B4 together with DR4, compared with other DR determinants. The results were similar in Type 1 diabetic and healthy individuals. The results suggest that elements on the DR3 and DR4 molecules may control T-lymphocyte responses to mumps and Coxsackie B4 viruses.

Adult↗

Effect of verapamil on T-lymphocyte activation in vitro.

Verapamil, a calcium-inhibitory drug, was found to inhibit T-lymphocyte proliferation in mixed lymphocyte culture and the proliferative response to phytohaemagglutinin and mumps antigen. It also inhibited production of interleukin 2 (IL-2). To exert inhibition, verapamil had to be added early in the culture period. Verapamil also had a relatively small inhibitory effect on IL-2-dependent growth. The effects were clearly seen only at concentrations exceeding the therapeutic serum level of verapamil.

Antigens, Viral↗