Biomedical subjects

A K Rasmussen

Publications and source records attributed to A K Rasmussen.

18 recordsLinked to original sources

PubMed1994

[Chronic fatigue syndrome--a defined unity?].

Chronic fatigue syndrome (CFS) is characterized by a sudden onset of an influenza-like illness followed by marked chronic fatigue and abnormal exercise-induced exhaustion. The precise pathogenesis of this disorder is unknown, but viral infection triggering immune imbalance has been suggested. The literature on CFS is reviewed. We find no consistent support for chronic viral infection or immunological dysfunction. The data in the published studies are rather conflicting, and further research in order to identify parameters that differentiate CFS from other disorders is necessary.

Diagnosis, Differential↗

PubMed1994

[Chronic fatigue syndrome--a controlled cross-sectional study].

Twenty-one patients fulfilling the Center for Disease Control criteria for chronic fatigue syndrome (CFS) were examined in a controlled study. Viral antibodies and tests evaluating the immune system were investigated in the patients and in a control group of 21 sex- and age-matched individuals. Production in vitro of the predominantly T-cell-derived cytokines interleukin-2 and interferon-gamma was significantly higher in patients with CFS compared the control group. Furthermore, the serum concentrations of IgA and IgE were significantly lower in patients with CFS; however, the values were within the normal reference range. All other variables were similar in the two groups. This study does not suggest a clearly disordered immune system or a chronic viral infection as a major pathogenetic factor in CFS. Longitudinal studies of immunological and virological parameters in CFS are warranted as are studies on patients that are severely handicapped.

Adolescent↗

PubMed1994

Influence of tumour necrosis factor-alpha, tumour necrosis factor-beta and interferon-gamma, separately and added together with interleukin-1 beta, on the function of cultured human thyroid cells.

Interleukin (IL)-1, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma have been demonstrated in thyroid tissue. We have previously shown that high concentrations of IL-1 inhibit and low concentrations stimulate human thyroid cell function in vitro. In the present study, TNF-alpha, TNF-beta and IFN-gamma all inhibited thyroglobulin (Tg) and cAMP production from cultured human thyroid cells. When TNF-alpha was added simultaneously with IL-1 beta, the highest concentration of TNF-alpha (10(6) U/l) enhanced the inhibition of Tg and cAMP induced by IL-1 beta (1-10(5) U/l). TNF-beta had no influence on IL-1 beta-induced inhibition. IFN-gamma (10(4) U/l) added together with IL-1 beta in lower concentrations (1-10(2) U/l) stimulated cAMP production, while at high concentrations of IL-1 beta (10(5) U/l), IFN-gamma enhanced the inhibitory influence of IL-1 beta on Tg production. The hormones of the immune system, IL-1, TNF and IFN-gamma, may thus contribute to the decreased thyroid function characteristic of some thyroid inflammatory diseases.

Cells, Cultured↗

PubMed1994

Nitric oxide production is not involved in the effects of interleukin-1 beta on cAMP, thyroglobulin and interleukin-6 in TSH-stimulated human thyroid cells.

Interleukin (IL)-1 inhibits the function of insulin-producing rat pancreatic beta-cells in vitro and in vivo, and it has been postulated that the IL-1 effect is mediated through the cytokine inducible nitric oxide (NO) synthase. IL-1 inhibits the function of cultured human thyroid cells too, and in this study human thyroid cell production of NO in response to the TSH-stimulated influence of IL-1 beta (10(5) U/l) and TNF-alpha (10(6) U/l), alone or in combination was measured. IL-1 beta, but not TNF-alpha, induced an increase in nitrite production, which was significantly reduced by the competitive inhibitor of nitric oxide synthase L-NG-monomethyl-arginine (L-NMMA) (0.1 mmol/L and 0.5 mmol/L). However, the nitrite production was unrelated to the IL-1 beta-induced inhibition of thyroglobulin (Tg) and cyclic AMP (cAMP) and the IL-1 beta-induced IL-6 production. Thus, it is unlikely that NO is a second mediator of the demonstrated effects of IL-1 beta and TNF-alpha on human thyroid cells in culture.

Cells, Cultured↗

PubMed1992

Effects of human anti-IL-1 alpha autoantibodies on receptor binding and biological activities of IL-1.

Immunoglobulin G (IgG) antibodies to interleukin 1 alpha (IL-1 alpha) are frequently found in the sera of healthy human individuals. The effects of these autoantibodies on receptor binding and biological activities of human IL-1 were tested. Using the murine T-lymphocyte line NOB-1, human thyrocytes and human foreskin fibroblasts, the antibodies competitively inhibited the biological activity of human recombinant IL-1 alpha (rIL-1 alpha). The degree of inhibition correlated with 125I-rIL-1 alpha binding to IgG in different immunoglobulin preparations and in individual sera. These antibodies also neutralized the IL-1 activity of isolated membrane fragments and lysates of human blood monocytes activated by lipopolysaccharide. In contrast, the supernatant IL-1 activity was not affected. Stronger inhibition of biological activity and cell binding of 125I-rIL-1 alpha was obtained with NOB-1 cells than with human thyrocytes. The antibodies failed to interfere with the biological activity of rIL-1 beta. It is concluded that IgG autoantibodies of IL-1 alpha in the sera of healthy humans selectively inhibit the biological activity of the soluble and membrane-associated forms of IL-1 alpha in vitro, and that the degree of biological inhibition afforded by these antibodies depends upon the target cell.

Animals↗

PubMed1991

Interleukin-1 receptors on human thyroid cells and on the rat thyroid cell line FRTL-5.

Cellular binding of interleukin-1 (IL-1) was tested on monolayers of human thyrocytes in secondary culture, on long-term cultures of human thyrocytes, and on the rat thyroid cell line FRTL-5. The human thyrocytes in secondary culture showed specific binding of human 125I-rIL-1 alpha. Scatchard plots of data obtained at 4 degrees C indicated the presence of a single population of receptors with a Kd of 30 to 170 pM and 2,000 to 6,000 receptors per cell. Incubation at room temperature resulted in internalization of the receptor-ligand complex. Parallel experiments were performed with the IL-1 receptor-positive murine T-cell lines EL-4 and NOB-1. The IL-1 receptors on these cells had Kd values one fifth to one tenth those on human thyroid cells in secondary culture. Both rIL-1 alpha and rIL-1 beta inhibited 125I-rIL-1 alpha binding to human thyrocytes and the murine T cells. In contrast to the cells in secondary culture, there was no specific binding of 125I-rIL-1 alpha to long-term cultivated human thyroid cells or to the FRTL-5 cells. We concluded that recently described differences in the response to IL-1 of different thyroid cell culture systems are most likely caused by differences in expression of IL-1 receptors.

Animals↗

PubMed1991

Interleukin-6 production by thyroid epithelial cells. Enhancement by interleukin-1.

Interleukin-1 is a potent inhibitor of thyroglobulin and cAMP production in human thyroid cells and the inhibitory effect is enhanced by tumor necrosis factor-alpha and interferon-gamma. In the present study secondary cultures of human thyroid cells produced interleukin-6 and the production was significantly increased after exposure of the cells to recombinant interleukin-1 alpha and -1 beta. This increase was dose-dependent and concomitant of the IL-1 induced decrease in cAMP and thyroglobulin production. Both tumor necrosis factor-alpha and -beta also augmented interleukin-6 production, but less potently than interleukin-1. Interferon-gamma did not affect the production of interleukin-6. The rat thyroid cell line FRTL-5 produced interleukin-6 spontaneously, and the production was enhanced after addition of recombinant interleukin-1 beta. A pathogenetic role of interleukin-6 in autoimmune thyroid disease is suggested.

Animals↗

PubMed1990

[Treatment of patients with lumbar disc prolapse with ibuprofen. A controlled clinical trial].

The justification of employing the anti-inflammatory agent, ibuprofen, in the conservative treatment of lumbar disc prolapse was investigated. Forty-two patients admitted with clinical symptoms compatible with lumbar disc prolapse participated in the investigation. They were allotted double blindly at random to treatment with a placebo or ibuprofen as a supplement to the conservative treatment consisting of rest in bed, traction and mild analgesics. The analgesic effect of treatment in the two groups was assessed with the aid of a visual analogue scale and also the amounts of supplementary analgesics necessary. No significant difference in the pain experienced or employment of supplementary analgesics in the two groups could be registered. This investigation has thus not demonstrated further analgesic effect of ibuprofen administered as a supplement to the conservative treatment otherwise employed for lumbar disc prolapse.

Adolescent↗

PubMed1990

Differential effects of interleukin 1 alpha and 1 beta on cultured human and rat thyroid epithelial cells.

The effects of human recombinant interleukin 1 alpha (20 pg/1-2 micrograms/l) and 1 beta (200 pg/1-20 micrograms/l) on two systems of thyroid cells have been compared. The thyroglobulin and cAMP secretion and the DNA content of human thyroid cells cultured in monolayer and of continuously grown rat thyroid cells, Fischer rat thyroid cell line have been studied. The growth of the rat thyroid cell line was inhibited by interleukin 1 beta (20 ng/1-20 micrograms/l), but not by interleukin 1 alpha. None of the cytokines changed the cAMP production of the rat thyroid cells. In contrast, both cAMP production and thyroglobulin secretion were inhibited dose-dependently by the cytokines in human thyroid cells in secondary cultures. These results caution the interpretation and extrapolation of changes induced by interleukin 1 from one cell system to the other.

Animals↗

PubMed1989

[Legal rights for the aged on admission to a psychiatric clinic or transfer to a psychiatric nursing home. Forms of admission, compulsory admission and incapacitation].

The legal position of elderly persons on transfer to a psychiatric department must be improved. The proportion of elderly persons in the population is increasing and, parallel with this, there are increasing problems concerning incapacity to manage their own affairs on account of various forms of dementia. Conditions of dementia may cause inability to make decisions about transfer to a psychiatric department. The extent of this problem is illustrated in this article. On referral to a psychiatric nursing home, it is necessary to declare these persons incapable of managing their own affairs for legal reasons. To avoid this form of intervention, the present authors suggest appointment of a personal advisor instead. It is recommended that directives for solving this problem should be incorporated in the new Danish legislation concerning mental illness.

Aged↗

PubMed1989