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- Gomez Real, F., et al.
(författare)
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Hormone replacement therapy, body mass index and asthma in perimenopausal women: a cross sectional survey
- 2006
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Ingår i: Thorax.. ; 61:1
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Hormone replacement therapy (HRT) and obesity both appear to increase the risk of asthma. A study was undertaken to investigate the association of HRT with asthma and hay fever in a population of perimenopausal women, focusing on a possible interaction with body mass index (BMI). METHODS: A postal questionnaire was sent to population based samples in Denmark, Estonia, Iceland, Norway, and Sweden in 1999-2001, and 8588 women aged 25-54 years responded (77%). Pregnant women, women using oral contraceptives, and women <46 years were excluded. Analyses included 2206 women aged 46-54 years of which 884 were menopausal and 540 used HRT. Stratified analyses by BMI in tertiles were performed. RESULTS: HRT was associated with an increased risk for asthma (OR 1.57 (95% CI 1.07 to 2.30)), wheeze (OR 1.60 (95% CI 1.22 to 2.10)), and hay fever (OR 1.48 (95% CI 1.15 to 1.90)). The associations with asthma and wheeze were significantly stronger among women with BMI in the lower tertile (asthma OR 2.41 (95% CI 1.21 to 4.77); wheeze OR 2.04 (95% CI 1.23 to 3.36)) than in heavier women (asthma: p(interaction) = 0.030; wheeze: p(interaction) = 0.042). Increasing BMI was associated with more asthma (OR 1.08 (95% CI 1.05 to 1.12) per kg/m(2)). This effect was only found in women not taking HRT (OR 1.10 (95% CI 1.05 to 1.14) per kg/m(2)); no such association was detected in HRT users (OR 1.00 (95% CI 0.92 to 1.08) per kg/m(2)) (p(interaction) = 0.046). Menopause was not significantly associated with asthma, wheeze, or hay fever. CONCLUSIONS: In perimenopausal women there is an interaction between HRT and BMI in the effects on asthma. Lean women who were HRT users had as high a risk for asthma as overweight women not taking HRT. It is suggested that HRT and overweight increase the risk of asthma through partly common pathways.
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- Janson, C., et al.
(författare)
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Insomnia is more common among subjects living in damp buildings
- 2005
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Ingår i: Occup Environ Med. ; 62:2
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Insomnia is a condition with a high prevalence and a great impact on quality of life. Little is known about the relation between and sleep disturbances and the home environment. AIM: To analyse the association between insomnia and building dampness. METHODS: In a cross-sectional, multicentre, population study, 16 190 subjects (mean age 40 years, 53% women) were studied from Reykjavik in Iceland, Bergen in Norway, Umea, Uppsala, and Goteborg in Sweden, Aarhus in Denmark, and Tartu in Estonia. Symptoms related to insomnia were assessed by questionnaire. RESULTS: Subjects living in houses with reported signs of building dampness (n = 2873) had a higher prevalence of insomnia (29.4 v 23.6%; crude odds ratio 1.35, 95% CI 1.23 to 1.48). The association between insomnia and different indicators of building dampness was strongest for floor dampness: "bubbles or discoloration on plastic floor covering or discoloration of parquet floor" (crude odds ratio 1.96, 95% CI 1.66 to 2.32). The associations remained significant after adjusting for possible confounders such as sex, age, smoking history, housing, body mass index, and respiratory diseases. There was no significant difference between the centres in the association between insomnia and building dampness. CONCLUSION: Insomnia is more common in subjects living in damp buildings. This indicates that avoiding dampness in building constructions and improving ventilation in homes may possibly have a positive effect on the quality of sleep.
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- Janson, Christer, et al.
(författare)
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The effect of infectious burden on the prevalence of atopy and respiratory allergies in Iceland, Estonia, and Sweden
- 2007
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Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier BV. - 0091-6749 .- 1097-6825. ; 120:3, s. 673-679
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Tidskriftsartikel (refereegranskat)abstract
- Background: Epidemiologic reports on the effect of microbe exposure on the development of atopy and allergic asthma are inconsistent. Objectives: The study investigates the association between serologic markers of infections and occurrence of atopy, allergic asthma, and rhinitis among adults in Iceland, Sweden, and Estonia. Methods: Individuals (n = 1249; mean age, 42 years) from Iceland, Sweden, and Estonia underwent a structured interview and blood sampling. Specific IgE was measured against 4 allergens, and IgG antibodies were measured against Helicobacter pylori, Toxoplasmosis gondii, hepatitis A virus, herpes simplex virus 1, Chlamydia pneumoniae, EBV, and cytomegalovirus. Results: Nonatopic subjects more often had positive serology for Helicobacter pylori, herpes simplex virus 1, Chlamydia pneumoniae, and cytomegalovirus. Having a low number (≤3) of IgG antibodies against the various infectious agents was an independent risk factor for atopy (odds ratio [OR], 1.43; 95% CI, 1.06-1.93), allergic asthma (OR, 1.82; 95% CI, 1.12-2.98), and allergic rhinitis (OR, 1.69; 95% CI, 1.21-2.37). The proportion of atopy that can be explained by a lower number (≤3) of infections was 6.7% in Iceland, 9.2% in Estonia, and 16.4% in Sweden, and 6.7%, 48.2%, and 33.4% for allergic asthma, respectively. Conclusion: Our data are consistent with cumulative protective effect of infections against atopy and respiratory allergies irrespective of route of infection. Clinical implications: The study indicates what microbes or combination of microbes play a role in the complex interplay between hygiene and allergy and may contribute toward the understanding of the allergy epidemic.Background: Epidemiologic reports on the effect of microbe exposure on the development of atopy and allergic asthma are inconsistent. Objectives: The study investigates the association between serologic markers of infections and occurrence of atopy, allergic asthma, and rhinitis among adults in Iceland, Sweden, and Estonia. Methods: Individuals (n = 1249; mean age, 42 years) from Iceland, Sweden, and Estonia underwent a structured interview and blood sampling. Specific IgE was measured against 4 allergens, and IgG antibodies were measured against Helicobacter pylori, Toxoplasmosis gondii, hepatitis A virus, herpes simplex virus 1, Chlamydia pneumoniae, EBV, and cytomegalovirus. Results: Nonatopic subjects more often had positive serology for Helicobacter pylori, herpes simplex virus 1, Chlamydia pneumoniae, and cytomegalovirus. Having a low number (≤3) of IgG antibodies against the various infectious agents was an independent risk factor for atopy (odds ratio [OR], 1.43; 95% CI, 1.06-1.93), allergic asthma (OR, 1.82; 95% CI, 1.12-2.98), and allergic rhinitis (OR, 1.69; 95% CI, 1.21-2.37). The proportion of atopy that can be explained by a lower number (≤3) of infections was 6.7% in Iceland, 9.2% in Estonia, and 16.4% in Sweden, and 6.7%, 48.2%, and 33.4% for allergic asthma, respectively. Conclusion: Our data are consistent with cumulative protective effect of infections against atopy and respiratory allergies irrespective of route of infection. Clinical implications: The study indicates what microbes or combination of microbes play a role in the complex interplay between hygiene and allergy and may contribute toward the understanding of the allergy epidemic.
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- Jögi, Annika, et al.
(författare)
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Systemic administration of anti-urokinase plasminogen activator receptor monoclonal antibodies induces hepatic fibrin deposition in tissue-type plasminogen activator deficient mice
- 2007
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Ingår i: Journal of Thrombosis and Haemostasis. - : Elsevier BV. - 1538-7933 .- 1538-7836. ; 5:9, s. 1936-1944
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Degradation of extracellular matrix proteins, such as fibrin, is pivotal to tumor invasion. Inhibition of the interaction between urokinase plasminogen activator (u-PA) and its receptor (u-PAR), and hence pro-u-PA activation, is an attractive approach to anti-invasive cancer therapy. A number of inhibitors exist for the human system, but because of species specificity none of these are efficient in mice. We have recently generated an inhibitory monoclonal antibody (mAb) against mouse u-PAR (mR1) by immunization of u-PAR-deficient mice. OBJECTIVES: To evaluate the effect of mR1 in vivo in a physiological setting sensitive to deregulated fibrinolysis, we have administered mR1 systemically and quantitated the effect on liver fibrin accumulation. METHODS: Wild-type and tissue-type plasminogen activator (t-PA) deficient mice were administered with mR1, or control antibody, during 6 weeks. Thereafter, the livers were retrieved and the amount of liver fibrin measured by unbiased morphometrical analysis of immunofluorescence signal. RESULTS: Systemic administration of mR1 caused significantly increased fibrin signal in anti-u-PAR treated t-PA-deficient mice compared to mock-treated, which mimics the phenotype of u-PAR;t-PA double-deficient mice. Fibrin and fibronectin accumulated within the sinusoidal space and was infiltrated by inflammatory cells. Analysis of small and rare hepatic fibrin plaques observed in t-PA-deficient mice showed infiltrating macrophages that, contrary to surrounding Kuppfer cells, expressed u-PAR. CONCLUSION: We show that u-PAR-expressing macrophages are involved in cell-mediated fibrinolysis of liver fibrin deposits, and that the antimouse-u-PAR mAb is effective in vivo and thus suited for studies of the effect of targeting the u-PA/u-PAR interaction in mouse cancer models.
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| 8. |
- Pass, Jesper, et al.
(författare)
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Murine monoclonal antibodies against murine uPA receptor produced in gene-deficient mice: inhibitory effects on receptor-mediated uPA activity in vitro and in vivo
- 2007
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Ingår i: Thrombosis and Haemostasis. - 0340-6245. ; 97:6, s. 1013-1022
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Tidskriftsartikel (refereegranskat)abstract
- Binding of urokinase plasminogen activator (uPA) to its cellular receptor, uPAR, potentiates plasminogen activation and localizes it to the cell surface. Focal plasminogen activation is involved in both normal and pathological tissue remodeling processes including cancer invasion. The interaction between uPA and uPAR therefore represents a potential target for anti-invasive cancer therapy. Inhibitors of the human uPA-uPAR interaction have no effect in the murine system. To enable in-vivo studies in murine cancer models we have now generated murine monoclonal antibodies (mAbs) against murine uPAR (muPAR) by immunizing uPAR-deficient mice with recombinant muPAR and screened for antibodies, which inhibit the muPA-muPAR interaction. Two of the twelve mAbs obtained, mR1 and mR2, interfered with the interaction between muPAR and the amino-terminal fragment of muPA (mATF) when analyzed by surface plasmon resonance. The epitope for mR1 is located on domain I of muPAR, while that of mR2 is on domains (II-III). In cell binding experiments using radiolabelled mATF, the maximal inhibition obtained with mR1 was 85% while that obtained with mR2 was 50%. The IC(50) value for mR1 was 0.67 nM compared to 0.14 nM for mATF. In an assay based on modified anthrax toxins, requiring cell-bound muPA activity for its cytotoxity, an approximately 50% rescue of the cells could be obtained by addition of mR1. Importantly, in-vivo efficacy of mR1 was demonstrated by the ability of mR1 to rescue mice treated with a lethal dose of uPA-activatable anthrax toxins.
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| 9. |
- Thjodleifsson, Bjarni, et al.
(författare)
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Seroprevalence of Helicobacter pylori and cagA antibodies in Iceland, Estonia and Sweden
- 2007
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Ingår i: Scandinavian Journal of Infectious Diseases. - : Informa UK Limited. - 0036-5548 .- 1651-1980. ; 39:8, s. 683-689
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Tidskriftsartikel (refereegranskat)abstract
- The public health implications from H. pylori infection are considerable but the transmission routes are largely unknown. In this study, the prevalence, patient characteristics and risk factors for Helicobacter pylori infection were comparatively investigated in Iceland, Sweden and Estonia. Blood samples were collected from 1046 subjects aged≈25-50 y (447 in Reykjavik, 359 in Uppsala and 240 in Tartu) for determination of antibodies to H. pylori and its cagA protein. The prevalence of H. pylori antibodies was 69% in Tartu, 36% in Reykjavik and 11% in Uppsala (p<0.0001). There was an increase in prevalence with age in Iceland and Sweden but not in Estonia. The prevalence of antibodies to the cagA protein in subjects seroreactive to H. pylori was lower in Reykjavik (36%) than in Uppsala (69%) and Tartu (62%) (p<0.0001). H. pylori infection, as determined by seroreactivity, was positively associated with smoking and BMI. Overall, socioeconomic development during the childhood period seems to be the most important factor for the prevalence of H. pylori infection. In adults, smoking may be a contributory factor.
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