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Biomedical subjects

R Hällgren

Publications and source records attributed to R Hällgren.

At least 181 records · Page 10Linked to original sources
PubMed1985

Raised serum hyaluronate levels in scleroderma: an effect of growth factor induced activation of connective tissue cells?

The circulating levels of hyaluronate were determined in 36 patients with scleroderma and in 36 control subjects matched for age and sex. The mean serum hyaluronate concentration in patients with progressive systemic sclerosis (n = 25) was 131 +/- 67 (SD) microgram/l and significantly greater (p less than 0.001) than that of the controls (mean level 49 +/- 21 (SD) microgram/l). Hyaluronate levels in patients with localised scleroderma (n = 4) were 141 +/- 47 (SEM) microgram/l and in patients with scleroderma-associated overlap syndromes (n = 7) 202 +/- 54 (SEM) microgram/l. The increase in serum hyaluronate probably reflected an enhanced synthesis or outflow of hyaluronate from the connective tissue, or both; it could not be explained by affection of the liver, which is the catabolic site of hyaluronate. The hyaluronate values were not related to certain serological indicators of inflammatory activity or to the extent of the skin lesions or the severity of internal organ manifestations. A positive correlation was noted between circulating platelet counts and hyaluronate levels (p less than 0.001). Plasma beta-thromboglobulin was measured in 15 of the patients with systemic sclerosis and found to correlate positively with platelet counts. Raised levels of beta-thromboglobulin were associated with the highest hyaluronate values. Platelet-derived growth factor, which stimulates connective tissue cells and is stored in the alpha-granules of platelets together with beta-thromboglobulin, was shown to enhance hyaluronate synthesis in fibroblast cultures. The results suggest an involvement in scleroderma of connective tissue activating substances released from platelets.

Cells, Cultured↗
PubMed1985

C3b receptor-mediated phagocytosis in sarcoidosis with extra-thoracic manifestations.

Two groups of sarcoidosis patients were studied. One group of 24 patients had previously had erythema nodosum (EN+), and the other group of 54 patients had never had any such extrathoracic manifestation of the disease (EN-). The two groups were similar with respect to age, disease duration, chest radiographic appearance, and granuloma mass as estimated from the serum concentration of lysozyme. Neutrophil phagocytic function was studied by a kinetic method which allows distinction between Fc- and C3b-receptor-mediated uptake. Fc-receptor function was normal in both groups. The function of C3b receptors was normal in the EN+ groups but significantly reduced in the EN- group. This observation indicates that sarcoidosis associated with erythema nodosum may represent a separate disease entity with respect to the pathogenetic mechanism involved in granuloma formation.

Adult↗
PubMed1985

Neutrophil phagocytosis in sarcoidosis. Reduced C3b receptor-mediated phagocytosis in active and silent sarcoidosis.

The phagocytic and complement receptor function of polymorphonuclear neutrophils (PMN) from patients with sarcoidosis was studied using a kinetic assay which allows the distinction to be made between Fc receptor-mediated and C3b receptor-mediated particle uptake. The study included one group (A) of patients with active disease (n = 20), and one group (B) with silent or inactive disease who since 10 years had no symptoms or radiological signs of sarcoidosis (n = 11). Abnormal C3b receptor function was observed in both groups but the impairment was most pronounced in the A group. The presence of C3b receptor dysfunction in both groups with a quantitative difference between the groups, is compatible with C3b receptor dysfunction being a primary causal factor of sarcoidosis.

Adult↗
PubMed1985

The dual action of glucose on the cytosolic Ca2+ activity in pancreatic beta-cells. Demonstration of an inhibitory effect of glucose on insulin release in the mouse and man.

The cytosolic Ca2+ activity was measured with the fluorescent indicator quin-2 in pancreatic beta-cells obtained from obese-hyperglycemic mice. When present at a concentration of 20 mmol/l in a medium physiologically balanced in cations, glucose induced a rise of cytosolic Ca2+ after a delay of 1--3 min. At lower concentrations of extracellular Ca2+ this effect was not only prevented but the sugar promptly reduced the cytosolic Ca2+ activity. The dual effect of glucose on cytosolic Ca2+ had its counterpart in the release of insulin. Whereas 20 mmol/l of glucose stimulated the release of insulin from mouse islets previously stored in a Ca2+-deficient medium, the sugar was clearly inhibitory when present at a concentration of 6 mmol/l. Intravenous glucose tolerance tests revealed a temporary glucose depression of the serum concentrations of insulin and C-peptide in several patients with diabetes. In a mentally retarded girl with hyperinsulinemia associated with acanthosis nigricans the glucose suppression of circulating insulin was prolonged and sufficiently pronounced to suggest an almost complete inhibition of the secretory activity of the pancreatic B-cells.

Aminoquinolines↗
PubMed1985

Eosinophil involvement in rheumatoid arthritis as reflected by elevated serum levels of eosinophil cationic protein.

Circulating levels of eosinophil cationic protein (ECP), an eosinophil specific granule protein, and numbers of peripheral eosinophils were determined in 42 patients with rheumatoid arthritis. At the time of the investigation the patients were without drug treatment. They had normal blood counts of eosinophils but on average a five-fold increase of the serum ECP values compared with healthy subjects. The intracellular content of ECP in eosinophils isolated from 14 patients was normal. High serum levels of ECP were particularly observed in patients with a disease of rather short duration but with a more aggressive course. Other factors associated with high ECP values were blood eosinophil counts in the upper normal range, high rheumatoid factor titre and increased inflammatory activity as defined by elevated serum haptoglobin and blood platelet counts. No relation was found between serum ECP and circulating immune complexes or serum total IgE. Synovial fluids obtained from 14 patients with rheumatoid arthritis contained very high concentration of ECP; on average nine times higher than those in the circulation of the patients. During corticosteroid but not NSAID therapy serum ECP decreased on average about 50% compared with pre-treatment values. Although eosinophils are not a notable feature of the synovial membrane infiltrate or cellular joint exudate, data obtained indirectly indicates their participation in the inflammatory reaction in RA.

Anti-Inflammatory Agents↗
PubMed1985

Elevated granulocyte manganese in rheumatoid arthritis and other connective tissue diseases.

Higher than normal amounts (p less than 0.001) of manganese were found in granulocytes isolated from patients with rheumatoid arthritis, other inflammatory arthritides, and scleroderma, while erythrocytes and platelets contained normal amounts of manganese. The cause of manganese accumulation is not known but evidently is linked to the intensity of the inflammatory process since significant positive correlations (p less than 0.001) were seen between erythrocyte sedimentation rate or serum haptoglobin and granulocyte manganese. During corticosteroid therapy granulocyte manganese started to return to normal levels but the relative changes were modest. Strong positive correlations (p less than 0.001) were found between granulocyte manganese and granulocyte stores of calcium and iron, suggesting a close relationship in the cellular regulation of these elements in chronic inflammatory conditions.

Adult↗
PubMed1984

Signs of neutrophil and eosinophil activation in adult respiratory distress syndrome.

Circulating levels of lactoferrin, a specific granule protein of neutrophilic leukocytes, and eosinophil cationic protein (ECP), a specific granule protein of eosinophilic leukocytes, were serially measured in 19 patients at risk for adult respiratory distress syndrome (ARDS). Those patients who developed ARDS had significantly higher concentrations of both proteins than the patients without signs of ARDS. High ECP levels were observed in spite of peripheral eosinopenia. The lactoferrin levels were also increased in relation to circulating numbers of neutrophils. These findings are consistent with an enhanced turnover and/or activity of eosinophils and neutrophils in ARDS and thereby support other clinical and experimental observations suggesting a central pathophysiologic role for granulocytes in ARDS. No relation was found between ARDS or serum concentrations of lactoferrin or ECP and degree of complement consumption, suggesting that other mechanisms besides complement activation may underlie granulocyte activation in ARDS.

Adolescent↗
PubMed1984

Complement activation and its relationship to adult respiratory distress syndrome. An experimental study in pigs.

Pulmonary leucostasis induced by complement activation has been considered an important pathogenic factor in adult respiratory distress syndrome (ARDS). To determine whether complement activation per se could evoke pulmonary dysfunction similar to ARDS, pigs were repeatedly infused with complement-activated plasma (CAP). Complement activation was produced by incubation of plasma with zymosan. Three groups of animals were investigated. Control animals received non-activated plasma. Nine animals (Group II) were given four infusions of CAP at a rate of 7 ml X min-1, and another nine animals (Group III) received two CAP infusions at a rate of 7 ml X min-1 followed by two at a rate of 14 ml X min-1. In the control animals there were no changes in gas exchange or haemodynamic variables and the leucocyte counts gradually increased. Infusion of CAP resulted in transient peripheral leucopenia and a dose-rate-dependent reversible increase in pulmonary vascular resistance in all animals. In one animal of Group II and in six of Group III there was a significant infusion-related decrease in Pao2 due to increased venous admixture. These animals were characterized by an enhanced pulmonary vascular tone before the start of the first CAP infusion. They also displayed a more pronounced pulmonary vascular response to infusion of CAP. The changes in gas exchange variables and pulmonary haemodynamics showed no relation to the degree of leucopenia or decrease in platelet count. The increased venous admixture was caused by "dry" ventilation/perfusion mismatching and not by oedema. These results suggest that additional factors besides complement activation and pulmonary leucostasis are required for the development of increased microvascular permeability and the pulmonary oedema characterizing ARDS.

Animals↗
PubMed1984

Eosinophil cationic protein in inflammatory synovial effusions as evidence of eosinophil involvement.

Eosinophils are seldom noted in inflammatory synovial fluids but are reported to infiltrate the synovial tissue in inflammatory arthritides. To elucidate a possible role for eosinophils in inflammatory joint reactions the concentrations of eosinophil cationic protein (ECP)--a specific granule protein from eosinophils--were measured by radioimmunoassay in 90 synovial fluids from patients with various inflammatory arthritides (rheumatoid arthritis, reactive and crystal arthritides, Reiter's disease and psoriatic arthropathy). In the same specimens lactoferrin was measured as an indicator of neutrophil-involved inflammation. In comparison with the normal circulating levels of ECP and lactoferrin the measured synovial fluid concentrations of both proteins were considerably raised in all patient groups with inflammatory joint diseases in contrast to patients with non-inflammatory arthritides. There was a striking positive correlation between the ECP and lactoferrin synovial fluid concentrations. These data indicate that eosinophil activation is prominent in inflammatory joint reactions and is linked to the activation of neutrophils. The regulation of degranulation or secretion by eosinophils is unknown. Our in-vitro studies showed that peripheral blood isolated neutrophils as well as eosinophils degranulated when exposed to IgG complexes. However, eosinophil degranulation was modest compared with neutrophil degranulation. These data suggest that neutrophil phagocytosis of, for example, immune complexes may be one major mechanism in neutrophil degranulation but that other factors determine the appearance of eosinophil products in inflammatory synovial effusions. The possible modulatory or harmful role of eosinophils in inflammatory joint disease can at present only be speculated on.

Adolescent↗
PubMed1984

Elevated circulating levels of eosinophil cationic protein in uremia as signs of abnormal eosinophil homeostasis.

Circulating levels of eosinophil cationic protein (ECP), an eosinophil-specific granule protein, and peripheral eosinophils were determined in 56 patients with uremia. The patients were on a chronic hemodialysis or CAPD program or treated with diet only. They had normal counts of peripheral eosinophils but on average a threefold increase of the serum ECP concentrations compared with healthy subjects. The intracellular content of ECP in eosinophils isolated from 6 patients on maintenance hemodialysis was normal. The management or duration of the uremic condition did not influence the circulating ECP levels or eosinophil counts. Neither was any relation found between total IgE levels and peripheral eosinophils or serum ECP. The present results are compatible with an accelerated turnover of peripheral eosinophils in uremia. Such a proposed abnormal eosinophil homeostasis should demand an accelerated marrow eosinophil production, thereby explaining the previously reported marrow eosinophilia in azotemic patients.

Adult↗
PubMed1984

Elevated granulocyte strontium in inflammatory arthritides is related to the inflammatory activity.

Total cellular strontium and calcium were measured by the nuclear microprobe technique. Increased mass fraction of both elements was found in granulocytes isolated from patients with active rheumatoid arthritis and other kinds of inflammatory arthritides. Increased granulocyte calcium but only marginally elevated granulocyte strontium was demonstrated in patients with scleroderma. The granulocyte accumulation of strontium and calcium seems to be linked to the degree of inflammatory activity, because the granulocyte content of both elements was positively correlated to the plasma concentration of acute-phase proteins. Corticosteroid therapy induced a marked reduction of granulocyte strontium but a more modest decrease of granulocyte calcium. The serum levels of strontium and calcium were within the normal ranges in all patients and were not significantly altered by corticosteroids.

Adolescent↗
PubMed1984

Serum-mediated stimulation and inhibition of neutrophil locomotion in sarcoidosis.

Chemotactic and chemokinetic activity was studied in sera from 57 patients with various stages of sarcoidosis. Reduced chemotactic activity was observed in 39% of the sera, mainly in sera from patients with parenchymal densities on chest radiographs. Increased chemokinetic activity was noted in more than one third of the fresh sarcoid sera. Asymptomatic patients showed higher chemokinetic activity in their sera than patients with symptoms. The presence of heat-stable chemokinetic inhibitors was suggested in one third of the cases. No relationship was found between these inhibitors and the inhibitors of neutrophil phagocytosis previously demonstrated in sarcoid sera. Although many of the findings show minor differences to those of normal sera, the liability in sarcoidosis to produce a variety of inhibitors directed against various functions of neutrophils would theoretically hamper the elimination of putative antigens. The presence of serum mediated stimulation and inhibition of neutrophil locomotion could be significant for the pathogenesis of the disease.

Aminopeptidases↗
PubMed1983

Beta-thromboglobulin in inflammatory synovial fluid.

Activated platelets release substances which potentially can contribute to joint lesions in inflammatory arthritides. To elucidate a possible participation of platelets in inflammatory joint reactions, the concentrations of the platelet protein beta-thromboglobulin (beta-TG) were measured in 90 inflammatory synovial fluids. Seven percent of the patients with rheumatoid arthritis and none of the patients with other inflammatory joint diseases (e.g., Reiter's disease, reactive or crystal arthritides) had beta-TG concentrations in synovial fluid exceeding the upper normal range of plasma beta-TG. The absent or very modest signs of local platelet activation were contrasted by the pronounced neutrophilic and monocytic activation, as assessed by the measurements of some granule proteins: lactoferrin, myeloperoxidase, lysozyme, and ferritin. No correlation was found between these inflammatory cell markers and beta-TG. A positive correlation (p less than 0.001) was noted between beta-TG and beta 2-microglobulin, which appeared in particularly high amounts in rheumatoid arthritis. This correlation may reflect a disturbed permeability of synovial membrane for LMW proteins or a related activation of platelets and lymphocytes. The present results do not give any evidence of platelet activation playing a major role in proliferative or destructive processes in arthritis.

Adolescent↗
PubMed1983

Eosinophil cationic protein (ECP) in the cerebrospinal fluid.

ECP (eosinophil cationic protein) has been measured by means of a specific radioimmunoassay in the cerebrospinal fluid (CSF) from 210 individuals with various diseases affecting the central nervous system. In the same specimens lactoferrin and albumin were measured as well, as indicators of neutrophil-involved inflammation and damage to the blood-brain barrier. From a patient reference group (n = 39) the upper "normal" limit for ECP was estimated to 1.7 microgram/l. In patients with acute cerebrovascular disease (n = 108) ECP levels were elevated in 38% of the cases which was a significantly (P less than 0.001) greater proportion than seen for lactoferrin (7%). In patients with acute infections of the CNS (n = 30) 67% had raised ECP levels with significantly higher levels (P less than 0.001) in those having bacterial infections. The ECP levels were significantly correlated (P less than 0.001) to the lactoferrin-levels in the whole infectious group. In patients with tumours (n = 25) raised levels of ECP were found in 67% of those with malignant and in 6% of those having benign tumours. This difference was statistically significant (P = 0.001). The ECP levels were closely related to those of lactoferrin (P less than 0.001) and albumin (P less than 0.005). Of the patients with multiple sclerosis (n = 19) 25% had raised ECP levels. This proportion was not significantly different from those having raised lactoferrin levels. In three patients extremely high ECP levels (70-455 micrograms/l) were found and a causal relationship between ECP and the brain tissue damage in these patients is suggested. In comparison with the neutrophil-related data the findings suggest a preferential involvement of eosinophils in some diseases affecting the central nervous system.

Adolescent↗
PubMed1983

Brain purinergic activity linked with depressive symptomatology: hypoxanthine and xanthine in CSF of patients with major depressive disorders.

The purine metabolites hypoxanthine and xanthine were analyzed in cerebrospinal fluid (CSF) of 70 patients with major depressive disorders (diagnosed according to Research Diagnostic Criteria) and, for reference, in 26 nonpsychiatric individuals. In the patient group, levels adjusted by analysis of covariance to same sex, age, height, and weight were univariately and multivariately correlated with both depressive subdiagnoses and individual depressive symptoms. Results indicate that raw CSF levels in depressed patients are significantly correlated with the four variables used in adjustment (for hypoxanthine mainly negatively with height; for xanthine mainly positively with age). Hypoxanthine and xanthine both appear to be linked with the expression of depressive symptomatology: lower levels of hypoxanthine are associated with anger and suicidal tendencies, and higher levels are related to memory disturbance; lower xanthine levels characterize patients with subjective feelings of depression, and in patients with higher levels appetite is poor.

Adult↗
PubMed1983

Increased total serum IgE in alcoholics.

Total serum IgE concentrations were measured in 106 male alcoholics with current alcohol abstinence of varying duration. The influence of smoking habits and clinical atopy on IgE levels was considered. The majority (91%) of the alcoholics were smokers and 26% suffered from possible clinical atopy. The geometric mean IgE in non-atopic, smoking alcoholics was 42 kU/l and significantly higher than the mean IgE level, 19 kU/l, in age-matched, smoking, non-atopic male participants in a general health survey (p less than 0.001). The IgE levels declined with the length of the alcohol abstinence period. Alcoholics, serially followed after a heavy drinking spree, showed a uniform pattern of declining IgE levels during a fortnight of abstinence (p less than 0.001). No link was noted between total IgE levels and the extent of liver affection as estimated by various serum variables (bilirubin, aminotransferases, gamma-GT, IgG, IgA and IgM) or galactose tolerance test. The increased IgE levels in alcoholics are suggested to reflect an influence of ethanol on T lymphocytes regulating the IgE synthesis. Such a proposed effect of ethanol on cellular immunity may contribute to certain organic alcohol diseases, but does not appear to influence the frequency of clinical atopy, being similar in our patient group and in the general population of the same geographic area.

Adult↗