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Biomedical subjects

O Bäck

Publications and source records attributed to O Bäck.

At least 19 recordsLinked to original sources
PubMed1992

Binding of tissue plasminogen activator to human endothelial cells. Importance of the B-chain as a ligand.

The aim of the present study was to investigate the binding of tissue plasminogen activator (tPA) to cultured endothelial cells and to characterize binding structures present in the cultures. Studies on the binding of 125I-tPA to cultured endothelial cells from human umbilical-cord veins (HUVEC) indicated that the number of sites for specific binding of tPA is 8 x 10(5) per cell. Treatment with an excess of antibodies against plasminogen-activator inhibitor type 1 (PAI-1) caused an 80% decrease in the binding, leaving about 1.6 x 10(5) unoccupied binding sites per cell, which appeared to be different from PAI-1. About 1.9 x 10(5) binding sites/cell for tPA were found on the surface of HUVEC that had been detached from the matrix. This indicates that only minor amounts of PAI-1 occur on the surface of the cells. In addition, immunocytochemical analysis showed that PAI-1 antigen is present almost exclusively in the cytoplasm but was not observed on the surface of the cells, whereas tPA antigen is abundant on the plasma membrane of tPA-treated cells as well as intracellularly. Competition studies using unlabelled compounds showed that native tPA and tPA B-chain (the proteinase domain), as well as the inactive derivatives, B-chain inactivated with D-Phe-Pro-Arg-chloromethane and tPA-PAI-1 complex, caused a considerable quenching of the binding of 125I-tPA to HUVEC, whereas the isolated A-chain had no demonstrable effect. Two components (apparent molecular masses 38 kDa and 56 kDa) reacting with tPA but lacking PAI-1 antigen determinants were identified. Thus the data suggest that tPA binds to HUVEC by two principally different mechanisms. One is mediated by PAI-1, which binds and inactivates tPA with a functional active site. The other binding is achieved by components which react with sites on the activator molecule other than structures of the A-chain or the active site.

Cell Membrane↗
PubMed1992

In-vivo administration of interleukin 1 both enhances and suppresses contact sensitivity in the mouse.

The in-vivo effects of systemic administration of recombinant human interleukin 1 beta (rIL-1 beta) were studied in the mouse contact-sensitivity model. rIL-1 beta in a single dose of 20 micrograms injected intraperitoneally 72-48 h before or 2-24 h after sensitization suppressed contact sensitivity. Given before challenge rIL-1 beta modulated the response in a biphasic way with an enhancement at 48 h and a suppression at 2 h before challenge. Only microgram doses of rIL-1 beta could enhance the contact sensitivity at 48 h, while microgram doses of rIL-1 beta at 2 h before challenge suppressed and nanogram doses enhanced the response. Treatment with indomethacin could only abrogate the effects of nanogram doses of rIL-1 beta. Measurements of the thickness of unchallenged control ears revealed that rIL-1 beta by itself could cause a small but significant increase in thickness depending on the dose and the time of administration.

Animals↗
PubMed1990

Plasma levels of endothelial-derived haemostatic factors in autoimmune thrombocytopenia and haemolytic anaemia.

The endothelial cell-synthesized haemostatic factors tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI) and von Willebrand factor (vWF) were assayed in a cross-sectional study of patients with immune thrombocytopenia (ITP) (n = 12) and autoimmune haemolytic anaemia (AIHA) (n = 3), and compared with a simultaneously selected contrast group of other hospitalized patients with obscure blood cytopenia at the time of sampling. All three factors were grossly elevated in both the study group and the contrast group. In the autoimmune patient group, the three haemostatic variables were significantly correlated with orosomucoid levels, demonstrating the acute-phase nature of the increased levels of vWF, tPA and PAI. These findings support the view that haemostatic factors of the vessel wall are implicated in the pathophysiology of a wide spectrum of diseases.

Adult↗
PubMed1990

Interleukin-1 decreases the number of Ia+ epidermal dendritic cells but increases their expression of Ia antigen.

It is generally accepted that ETAF/IL-1 is produced in epidermis by both keratinocytes and Langerhans' cells. We have studied the density and morphology of Ia+ epidermal dendritic cells in mice after systemic or intracutaneous injection of recombinant IL-1 beta. We found that rIL-1 beta decreased the density of Ia+ dendritic cells in the time period 2-7 days after rIL-1 beta administration. However, the remaining dendritic cells were enlarged and more arborized with increased expression of Ia antigen 1-4 days after injection of rIL-1 beta. The implication of the results is that ETAF/IL-1 modulates the function of Langerhans' cells through autocrine and paracrine regulation.

Animals↗
PubMed1989

Systemic interleukin I administration suppresses arachidonic acid-induced ear oedema in the mouse.

Recombinant human interleukin 1 beta (IL-1 beta), given intraperitoneally to mice as a single injection, significantly suppressed the development of arachidonic acid (AA)-induced ear oedema. This effect was noted 2 h after administration and for at least 5 days afterwards. IL-1 beta was effective in the dose range of 250 ng-20 micrograms/mouse. Injection of IL-1 beta per se resulted in erythema of the ears, and thus, IL-1 beta has the capacity not only to induce and augment but also to suppress inflammatory responses. Indomethacin administered as subcutaneously-implanted pellets did not influence the IL-1 beta induced-ear erythema, but suppressed to some extent the effect of IL-1 beta on the AA-induced ear oedema.

Animals↗
PubMed1988

Decreased peripheral beta-adrenergic reactivity in asthmatics treated with oral beta 2-agonists.

Peripheral beta-adrenoceptor reactivity, measured as the dermal erythematous reaction to iontophoretically administered isoprenaline was studied in 41 asthmatics, 13 patients with allergic rhinoconjunctivitis and 21 healthy control subjects. The response of intact superficial dermal blood vessels to isoprenaline, which has previously been demonstrated to be beta 2-adrenoceptor mediated, was reduced in asthmatics treated with high dose, oral, slow-release beta 2-agonists compared to healthy controls. The response in asthmatics not treated with oral beta 2-agonists and in patients with allergic rhinoconjunctivitis did not differ from controls. Thus, the peripheral beta 2-adrenergic reactivity of intact human superficial blood vessels is affected by oral, slow-release beta 2-agonists.

Administration, Inhalation↗
PubMed1988

Iontophoretic study of skin vessel reactivity in atopic dermatitis and its correlation to serum IgE levels.

Skin vessel reactivity was studied by means of an iontophoretic technique in 19 adult patients with atopic dermatitis. Fifteen patients were available for reinvestigation some 6 months later in winter. Compared with a control group, we found a significantly increased sensitivity in summer of dermal skin vessels toward the alpha 1-agonist phenylephrine. Patients with elevated serum IgE levels seemed to be more sensitive to phenylephrine. However, the difference was not significant. Isoproterenol, the beta-adrenoceptor agonist, induced blanching (as opposed to erythema) in 7 of 19 (37%) atopic dermatitis patients in summer and in 9 of 15 (60%) in winter compared with 1 of 36 in the control groups. This blanching was antagonized by the alpha-blocker phentolamine. From the results we concluded that there may be an increased alpha-adrenoceptor reactivity and/or a decreased beta-adrenoceptor reactivity in atopic dermatitis patients, which might be a primary defect.

Adult↗
PubMed1988

Increased peripheral alpha-adrenoceptor response in allergic asthmatics.

The peripheral alpha-adrenoceptor reactivity, measured as dermal blanching response to iontophoretically administered phenylephrine, was studied in 28 allergic asthmatics, 13 patients with allergic rhinoconjunctivitis and 21 healthy controls. The blanching response, which has previously been demonstrated to be mediated via alpha 1-adrenoceptors, was found to be significantly increased in allergic asthmatics compared with controls. It is suggested that there is an increased peripheral alpha-adrenoceptor reactivity in allergic asthma.

Adolescent↗
PubMed1987

Iontophoretic study of adrenergic and cholinergic skin vessel reactivity in normal ageing and Alzheimer's disease.

Iontophoresis was used to evaluate the peripheral reactivity of phenylephrine (alpha 1-agonist), isoproterenol (beta-agonist) and metacholine (cholinergic agonist) in patients with Alzheimer's disease (AD). The cutaneous responses--erythema and blanching--were visually recorded. Healthy personnel, medical students and patients with various dermatoses served as controls. A reduced response towards the adrenergic agonists was seen in AD. The reduced sensitivity was highly significant for the beta-agonist isoproterenol (p less than 0.001), in contradistinction the metacholine response did not differ between AD and age-matched controls. Furthermore, increasing age did not seem to significantly influence the cutaneous responses in mentally healthy controls. Thus, a reduced peripheral adrenergic reactivity was observed in the patients suffering from AD.

Adolescent↗
PubMed1986

An immunologic and cultural study of Pityrosporum folliculitis.

In patients with Pityrosporum folliculitis the mean serum antibody titer against Pityrosporum orbiculare was significantly higher than in healthy control subjects (p less than 0.01). The mean number of P. orbiculare organisms per square centimeter cultured from normal-looking skin in patients was not significantly higher than the number cultured from normal-looking skin in control subjects. Results of prick tests against P. orbiculare extract were negative or weak, indicating that patients with Pityrosporum folliculitis had no type I hypersensitivity against P. orbiculare. Immunohistochemical staining of skin lesions showed perivascular dermal cell infiltrates near the hair follicles dominated by anti-Leu 3a-reactive T lymphocytes. Human lymphocyte antigens with the DR locus, but not those with the DQ locus, on keratinocytes were observed in one case.

Adult↗
PubMed1986

Mast cells and lysozyme positive macrophages in bronchoalveolar lavage from patients with sarcoidosis. Valuable prognostic and activity marking parameters of disease?

In the deteriorating group of sarcoidosis patients, progress towards pulmonary fibrosis is a major problem. In order to benefit from corticosteroids, it is important for the treatment to start early. We studied a group of 45 patients with sarcoidosis. Most of them were newly detected patients and none were under or had currently received corticosteroid therapy. The patients were followed for at least six months. We found that increased amounts of polymorphonuclear neutrophils (PMN) or lysozyme-positive macrophages (Lys+MF) and mast cells (MC) in bronchoalveolar lavage (BAL) could implicate a bad prognosis.

Bronchi↗
PubMed1986

Long-term oral acyclovir treatment prevents recurrent genital herpes.

Thirty-three patients with frequently recurring genital herpes completed a randomized double-blind, crossover trial with oral acyclovir 200 mg 4 times a day and placebo for periods of 12 weeks. Five patients (15%) had full recurrence during acyclovir treatment and 31 (94%) while receiving placebo. The median time to first recurrence was 20 days for placebo and more than 84 days for acyclovir. It was concluded that acyclovir was well tolerated and an effective treatment to suppress the disease in selected cases of severe and frequently recurring genital herpes. However, the relapses seem to occur with the same rate as before, when the suppressive acyclovir treatment is stopped.

Acyclovir↗
PubMed1986

The importance of anamnestic information of atopy, metal dermatitis and earlier hand eczema for the development of hand dermatitis in women in wet hospital work.

By means of a prospective study design and multivariate regression analyses we have studied the relative importance of atopy, metal dermatitis and earlier hand eczema as risk factors for the development of hand eczema in women during 20 months of "wet" hospital work. The population consisted of 1857 women. The prevalence of hand eczema during the observation period was 41%. The risk of developing hand eczema was calculated as predicted relative odds ratios. The interrelationship of the risk factors was analysed. A summarized description of this analysis shows that a history of earlier hand eczema increased the odds by 12.9 times, a history of metal dermatitis by 1.8 times and atopic dermatitis and atopic mucosal symptoms by 1.3 times. Thus a history of earlier hand eczema seems of crucial importance for the occurrence of hand eczema in women in 'wet' hospital work. Our hypothesis is that a history of earlier hand eczema may be considered a major indicator of a skin vulnerability factor predisposing the individual to hand eczema. If the hypothesis is true, this factor may be present approximately in one half of the subjects with atopic dermatitis, in one fourth of the subjects with atopic mucosal symptoms and in one fifth of the non-atopics.

Asthma↗
PubMed1985

Elevated plasmin-alpha 2-antiplasmin complex levels in hereditary angioedema: evidence for the in vivo efficiency of the intrinsic fibrinolytic system.

The contact activation and fibrinolytic systems were assessed in 5 patients with hereditary angioedema (HAE). Reductions in F XII levels and increase in kallikrein-like activity in some patients indicated activation of the contact (intrinsic) system of coagulation. A great increase in plasmin-alpha 2-antiplasmin complex in all subjects indicated that in this disease, there is a constantly ongoing fibrinolysis. Since C1-inhibitor, the deficient protein in HAE, is a poor inhibitor of the well-known extrinsic (tissue-type) plasminogen activator, but the major inhibitor of the contact activation system and a related in vitro phenomenon termed intrinsic fibrinolysis, our data show that this fibrinolytic system is also sometimes operating efficiently in vivo. Furthermore, the known clinical data on HAE are compatible with a role of intrinsic fibrinolysis in the pathophysiology of this disease.

Angioedema↗
PubMed1985

Dermatitis herpetiformis: 'pH optimum' for the release of potentially antigen-binding IgA fragments from papillary dermis of uninvolved skin by peptic digestion.

In preparations of papillary dermis taken from clinically normal skin of patients with dermatitis herpetiformis (DH), the disappearance of granular IgA deposits induced by peptic digestion was partial at pH 4.5 and total at pH 4.1, as visualized by immunofluorescence microscopy. In a model system in which human monomeric IgA was digested by pepsin using a pepsin-IgA ratio of 100:0.3, an IgA concentration of 3 lambda g/ml and a pH range of 5.1-4.1, the degradation of IgA molecules did not appear to proceed beyond the formation of fragments corresponding to F (ab)'. When supernatants after peptic digestion of papillary dermis at pH 4.1 were analysed by sodium-dodecylsulphate (SDS)-polyacrylamide gel electrophoresis after reduction and alkylation followed by electrophoretic transfer to nitrocellulose membranes and subsequent immunochemical detection, IgA-like material corresponding to the alpha-chain part of F (ab)' fragments was found in preparations from DH patients but not in those from controls.

Dermatitis Herpetiformis↗