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Biomedical subjects

L Lindholm

Publications and source records attributed to L Lindholm.

At least 19 recordsLinked to original sources
PubMed1992

Angio-oedema in relation to treatment with angiotensin converting enzyme inhibitors.

OBJECTIVE: To evaluate and describe the clinical course of angio-oedema reactions induced by angiotensin converting enzyme inhibitors. DESIGN AND METHODS: All reports of angio-oedema reactions associated with angiotensin converting enzyme inhibitors submitted to Swedish Adverse Reactions Advisory Committee were reviewed and the clinical courses summarised. Numbers of cases judged to be induced by angiotensin converting enzyme inhibitors were related to their annual usage, estimated from total sales of defined daily doses, as well as to the estimated number of new patients. All cases of angio-oedema associated with angiotensin converting enzyme inhibitors reported to the World Health Organisation's international drug information system were also summarised. RESULTS: 36 of the 38 reported cases in Sweden between 1981 and 1990 were judged to be related to angiotensin converting enzyme inhibitors. During 1981 through 1990, altogether 1309 cases of angio-oedema associated with angiotensin converting enzyme inhibitors were registered with the international drug information system. The incidence of reported cases of angio-oedema increased largely in parallel with the increased sales (usage) of angiotensin converting enzyme inhibitors. Of the 36 Swedish patients, 77% experienced the reaction within the first three weeks after starting treatment. 10 patients needed hospitalisation, two of whom had life threatening laryngeal obstruction. With one exception all 36 patients were free of symptoms within one week after discontinuing the drug. CONCLUSIONS: Angio-oedema induced by angiotensin converting enzyme inhibitors is a rare but potentially life threatening reaction, which in most instances occurs shortly after the start of treatment. Any patient in whom the reaction is suspected should have the treatment interrupted and, if necessary, be admitted for observation.

Adult↗
PubMed1992

Comparison of the biodistribution of 75Se- and 131I-labelled monoclonal antibodies in nude mice.

A monoclonal antibody, C-215, against colon cancer, was internally labelled with [75Se]methionine. The biodistribution was studied in tumour-bearing nude mice and compared with the biodistribution of [131I]C-215. The tissue uptake was divided into three parts: antibody bound to the antigen, antibody in the extracellular space and uptake of the released radionuclide. [75Se]C-215 showed a greater amount of antigen-bound antibody in the tumour, but also a greater unspecific uptake both in tumour and normal tissue.

Animals↗
PubMed1992

Coexpression of ganglioside antigen Fuc-GM1, neural-cell adhesion molecule, carcinoembryonic antigen, and carbohydrate tumor-associated antigen CA 50 in lung cancer.

With the aid of specific monoclonal antibodies, tumor tissues from 68 patients with lung cancer were examined for their expression of two small cell lung carcinoma (SCLC) antigens, Fuc-GM1 (fucosyl GM1; IV2FucII3NeuAc GgOse4) and neural-cell adhesion molecule (NCAM), and two broader tumor antigens, carcinoembryonic antigen (CEA) and carbohydrate cancer-associated antigen CA 50. Expression of Fuc-GM1 was seen in 75% and NCAM in 78% of the SCLC specimens, but also in 12 and 20% of non-SCLC. Either or both of these antigens were expressed in more than 90% of SCLC and in 25% of non-SCLC. CEA was found in more than 80% of SCLC and non-SCLC. Expression of CA 50 was seen in 65-68% of non-SCLC and SCLC, showing preference for SCLC and lung adenocarcinoma. In SCLC, cellular expression of Fuc-GM1 was generally seen together with NCAM and CA 50, but rarely with CEA. There was considerable inter- and intratumor heterogeneity in the expression of all four antigens. The results suggest that CEA is the antigen of choice for the detection of lung cancer regardless of histotype. In combined analysis of CEA, CA 50, Fuc-GM1 and NCAM, two patterns of antigen expression were recognized that appear to discriminate between SCLC and non-SCLC tumors, respectively. A considerable fraction of SCLC and non-SCLC tumors, however, exhibited similar patterns of antigen expression. The biological and clinical significance of these observations remains to be investigated.

Antibodies, Monoclonal↗
PubMed1979

Demonstration of a thymus derived, splenic suppressor cell responsible for the age-dependent decrease in contact hypersensitivity in the adult mouse.

A suppression of contact hypersensitivity to picryl chloride has been demonstrated in adult thymectomized, 4 and 5 1/2 mo-old CBA mice after i.v. injection of spleen cells from intact CBA mice of the same age. The cells signifcantly suppressed the elicitation of the allergic contact sensitivity reaction and this effect could be inhibited by pretreating the cells with anti-Thy 1 serum and complements. The induction phase was found to be unaffected. However, spleen cells from donors which had received an i.v. injection of picryl sulfonic acid suppressed the induction as well as the elicitation phase of the contact dermatitis. On the basis of these results it appears reasonable to conclude that the decline in the ability to develop contact hypersensitivity in aging mice may be due to the development of a splenic suppressor T cell, mainly affecting the elicitation of the contact hypersensitivity reaction.

Age Factors↗
PubMed1978

Depressed non-specific lymphocyte reactivity in psoriasis.

T-lymphocyte number and functions were studied in 24 patients with psoriasis guttata as compared to healthy controls. A decrease was found of the in vitro ability to synthetize DNA in response to stimulation with phytohemagglutinin (PHA), concanavalin A, poke weed mitogen and PPD, which was statistically significant for PHA. The percentage and absolute numbers of both T and B peripheral blood lymphocytes were not altered.

Adolescent↗
PubMed1978

Stimulation of immune reactivity by methoxy-substituted glycerol ethers incorporated into the feed.

In mice, the plaque-forming cell response to sheep red blood cells was stimulated by a mixture of methoxy-substituted glycerol ethers isolated from Greenland shark liver oil and by synthetic 1-0-(2-methoxyhexadecyl)-glycerol, given in the diet. In preliminary experiments, this synthetic compound also increased the ability of parental spleen cells to induce graft-vs.-host reactions in F1 hybrid mice. Glycerol ethers occur in the bone marrow fat of mammals and in the membrane phospholipids. It is postulated that the methoxy-substituted glycerol ethers supplied in the diet may stimulate the bone marrow and/or may be incorporated into membrane lipids, thereby changing the structure and function of the membranes.

Animals↗
PubMed1978

Interaction of cholera toxin and toxin derivatives with lymphocytes. III. Modulating effects in vivo by cholera toxin on the graft-versus-host reactivity of lymphoid cells: suggested inhibition of suppressor cells.

The influence of cholera toxin (CT), and thus probably of cyclic AMP, on the capacity of parental lymphoid cells to elicit a graft-versus-host reaction (GVHR) was studied. Toxin-treated DBA/1 mice were used as cell donors and untreated DBA/1xC57B1/6 F1 hybrid mice as recipients, and the GVHR reactivity of the transferred cells was estimated by their ability to induce spleen enlargement or stimulation of antibody formation ('allogenic effect') in the recipients. Spleen cells from donors intravenously injected with 1 microgram CT 1-3 days earlier, gave a significantly stronger GVHR than did spleen cells of untreated mice. Choleragenoid, a toxin analog devoid of the toxin's ability to activate plasma membrane adenylate cyclase even though it binds efficiently to cells, had no effect on the GVHR-inducing capacity of the spleen cells. The enhanced GVHR by spleen cells from toxin-treated DBA/1 animals was reduced to the normal level when the donor cells were transferred along with lymphoid cells from untreated animals of the same strain. Spleen was the most powerful source of the suppressive influence. No evidence for a redistribution of suppressor cells following administration of CT was found. Spleen cells from mice syngeneic with the recipients had no suppressive effect. The results suggest that parenterally administered CT, directly or indirectly, can inhibit a cell population in spleen which normally exerts an antigen-specific suppressive regulatory influence on the development of GVHR.

Cholera Toxin↗
PubMed1977

Enhancement of the allogeneic effect by irradiation of transferred cells.

Hot-pulse treatment of parental thymus or spleen cells increased their ability to simulate antibody synthesis in F1 hybrid recipient mice. A similar effect was obtained after treatment of the cells with low doses of X-irradiation. Likewise, irradiation of syngeneic unprimed cells made them stimulatory on antibody production. The production of IgG, IgM as well as IgE antibodies was enhanced after transfer of irradiated cells. The results suggest that irradiation preferentially inactivates suppressor cells, that are present in the thymus and the spleen.

Animals↗
PubMed1977

Immune suppression induced by acetoacetylated antigen.

Injection of acetoacetylated antigen into rabbits with an ongoing reagin response abrogated this response. The possibility that this phenomenon might be due to activation of suppressor cells was studied in mice. Thymus or spleen cells from animals which had been primed with acetoacetylated antigen were able to suppress the IgG and IgM antibody response upon transfer to syngeneic mice. Maximal suppressive effect was observed 12-14 days after priming with native as well as acetoacetylated antigen. The IgG and IgM responses were equally affected by the transferred suppressor cells.

Acetoacetates↗
PubMed1977

Deficient neutrophil function in a patient with chronic mucocutaneous candidiasis, thymoma and myasthenia gravis.

The case of a 68-year-old man who suffered the onset of chronic mucocutaneous candidiasis, thymoma, myasthenia gravis and a reversible neutrophil dysfunction during adult life is reported. All tests for humoral and cellular immunity proved normal. Thymectomy and the administration of transfer factor had no effect on the skin disease. Long-term oral administration of 5-fluorocytosine almost cleared the skin lesions; the neutrophil defect disappeared.

Aged↗
PubMed1976

Suppressor cell activity in a male infant with T-and B-lymphocyte dysfunction treated with thymosin.

A male infant with bilateral iris coloboma who had had repeated infections and malabsorption was studied. The levels of total lymphocytes and of T and B cells were normal or high, but IgA became undectable and IgG low, whereas IgM was normal. His lymphocytes did not respond to phytohemagglutinin (PHA), concanavalin A, pokeweed mitogen (PWM) or in mixed lymphocyte reactions (MLR), nor did they respond in vitro when thymosin was included in the test systems. He was skin-test-negative, even to dinitrochlorobenzene. His crudely isolated T lymphocytes and the supernatant of his PHA-stimulated lymphocytes inhibit the response of normal lymphocytes to PHA, PWM, and in MLR. During thymosin treatment skin test and lymphocyte reactivity to mitogen remained negative. He became faintly positive in MLR, and the suppressor activity in the supernatant of his PHA-stimulated lymphocytes no longer inhibited the response of normal lymphocytes to PHA, PWM, or in MLR. In parallel with thymosin treatment he showed quite marked clinical improvement.

B-Lymphocytes↗
PubMed1976

T lymphocytes in atopic children.

The number of circulating T and B cells and the sensitivity of lymphocytes to stimulation with phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweek mitogen (PWM) was studied in 233 atopic children. The number of T lymphocytes was found to be decreased in cases of rhinoconjunctivitis, asthma as well as atopic eczema. Levels of B lymphocytes were normal. Sensitivity to stimulation with PHA and to a lesser degree, Con A, was significantly decreased whereas stimulation with PWM was unaffected. The severity of the atopic eczema was inversely correlated to T cell numbers. Several lines of evidence indicated that the abnormalities observed were intrinsically associated with the atopic conditions and not evoked by corticosteroid treatment. The results are compatible with the hypothesis that atopy is associated with a defect of a subpopulation of T cells. The possibility that this subpopulation has a suppressor function on reagin formation is discussed.

Adolescent↗
PubMed1976

Interaction of cholera toxin and toxin derivatives with lymphocytes. II. Modulating effects of cholera toxin on in vivo humoral and cellular immune responses.

The in vivo effects of cholera toxin on lymphoid organ structure and function in mice were investigated. It was found that within a day following intravenous injection of 1 mug of toxin, thymus as well as spleen weight decreased but the animals remained healthy. Histological studies suggested that the involution of lymphoid organs was due to cell death. Injection of cholera toxin into adrenalectomized mice was lethal within 36 h. In these animals no decrease in lymphoid organ weight was noted. Thymus cells from toxin-treated mice were found to be much inferior to thymocytes of untreated animals in their in vitro response to Concanavalin A, whereas the response of spleen cells from toxin-treated animals to mitogens was slightly increased. 1 mug of cholera toxin increased primary antibody formation when given to mice together with antigen (sheep erythrocytes) and decreased primary antibody formation when given before or after the antigen. The toxin also increased secondary antibody formation when injected simultaneously with or after the booster antigen dose, and decreased the antibody formation when given a few days before the booster injection. Treatment of mice with toxin was found to increase the capacity of spleen cells from these animals to induce the parental effect on antibody formation and to induce graft-versus-host reactions. The mechanisms behind the observed effects are discussed. It is suggested that cholera toxin affects different types of cells involved in immune responses primarily by a direct inhibitory action on cellular proliferation but also indirectly by causing release of adrenal gland hormones.

Adrenalectomy↗