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Träfflista för sökning "WFRF:(Janson Peter) srt2:(2010-2014)"

Sökning: WFRF:(Janson Peter) > (2010-2014)

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1.
  • Burney, Peter, et al. (författare)
  • Chronic obstructive pulmonary disease mortality and prevalence : the associations with smoking and poverty-a BOLD analysis
  • 2014
  • Ingår i: Thorax. - : BMJ. - 0040-6376 .- 1468-3296. ; 69:5, s. 465-473
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Chronic obstructive pulmonary disease (COPD) is a commonly reported cause of death and associated with smoking. However, COPD mortality is high in poor countries with low smoking rates. Spirometric restriction predicts mortality better than airflow obstruction, suggesting that the prevalence of restriction could explain mortality rates attributed to COPD. We have studied associations between mortality from COPD and low lung function, and between both lung function and death rates and cigarette consumption and gross national income per capita (GNI). Methods National COPD mortality rates were regressed against the prevalence of airflow obstruction and spirometric restriction in 22 Burden of Obstructive Lung Disease (BOLD) study sites and against GNI, and national smoking prevalence. The prevalence of airflow obstruction and spirometric restriction in the BOLD sites were regressed against GNI and mean pack years smoked. Results National COPD mortality rates were more strongly associated with spirometric restriction in the BOLD sites (<60 years: men r(s)=0.73, p=0.0001; women r(s)=0.90, p<0.0001; 60+ years: men r(s)=0.63, p=0.0022; women r(s)=0.37, p=0.1) than obstruction (<60 years: men r(s)=0.28, p=0.20; women r(s)=0.17, p<0.46; 60+ years: men r(s)=0.28, p=0.23; women r(s)=0.22, p=0.33). Obstruction increased with mean pack years smoked, but COPD mortality fell with increased cigarette consumption and rose rapidly as GNI fell below US$ 15 000. Prevalence of restriction was not associated with smoking but also increased rapidly as GNI fell below US$ 15 000. Conclusions Smoking remains the single most important cause of obstruction but a high prevalence of restriction associated with poverty could explain the high 'COPD' mortality in poor countries.
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  • de Marco, Roberto, et al. (författare)
  • Risk Factors for Chronic Obstructive Pulmonary Disease in a European Cohort of Young Adults
  • 2011
  • Ingår i: American Journal of Respiratory and Critical Care Medicine. - 1073-449X .- 1535-4970. ; 183:7, s. 891-897
  • Tidskriftsartikel (refereegranskat)abstract
    • Rationale: Few studies have investigated the factors associated with the early inception of chronic obstructive pulmonary disease (COPD). Objectives: We investigated COPD risk factors in an international cohort of young adults using different spirometric definitions of the disease. Methods. We studied 4,636 subjects without asthma who had prebronchodilator FEV1/FVC measured in the European Community Respiratory Health Survey both in 1991 to 1993 (when they were 20-44 yr old) and in 1999 to 2002. COPD was defined according to the Global Initiative for Chronic Obstructive Lung Disease fixed cut-off criterion (FEV1/FVC < 0.70), and two criteria based on the Quanjer and LuftiBus reference equations (FEV1/FVC less than lower limit of normal). COPD determinants were studied using two-level Poisson regression models. Measurements and Main Results: COPD incidence ranged from 1.85 (lower limit of normal [Quanjer]) to 2.88 (Global Initiative for Chronic Obstructive Lung Disease) cases/1,000/yr. Although about half of the cases had smoked less than 20 pack-years, smoking was the main risk factor for COPD, and it accounted for 29 to 39% of the new cases during the follow-up. Airway hyperresponsiveness was the second strongest risk factor (15-17% of new cases). Other determinants were respiratory infections in childhood and a family history of asthma, whereas the role of sex, age, and of being underweight largely depended on the definition of COPD used. Conclusions: COPD may start early in life. Smoking prevention should be given the highest priority to reduce COPD occurrence. Airway hyperresponsiveness, a family history of asthma, and respiratory infections in childhood are other important determinants of COPD. We suggest the need for a definition of COPD that is not exclusively based on spirometry.
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  • Edfeldt, Katarina, et al. (författare)
  • TCEB3C a putative tumor suppressor gene of small intestine neuroendocrine tumors
  • 2014
  • Ingår i: Endocrine-Related Cancer. - 1351-0088 .- 1479-6821. ; 21:2, s. 275-284
  • Tidskriftsartikel (refereegranskat)abstract
    • Small intestinal neuroendocrine tumors (SI-NETs), formerly midgut carcinoids, are rare and slow-growing neoplasms. Frequent loss of one copy of chromosome 18 in primary tumors and metastases has been observed. The aim of the study was to investigate a possible role of TCEB3C (Elongin A3), currently the only imprinted gene on chromosome 18, as a tumor suppressor gene in SI-NETs, and whether its expression is epigenetically regulated. Primary tumors, metastases, the human SI-NET cell line CNDT2.5, and two other cell lines were included. Immunohistochemistry, gene copy number determination by PCR, colony formation assay, Western blotting, real-time quantitative RT-PCR, RNA interference, and quantitative CpG methylation analysis by pyrosequencing were performed. The large majority of tumors (33/43) showed very low to undetectable Elongin A3 expression and as expected 89% (40/45) displayed one TCEB3C gene copy. The DNA hypomethylating agent 5-aza-2'-deoxycytidine induced TCEB3C expression in CNDT2.5 cells, in primary SI-NET cells prepared directly after surgery, but not in two other cell lines. Also siRNA to DNMT1 and treatment with the general histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in a cell type-specific way. CpG methylation at the TCEB3C promoter was observed in all analyzed tissues and thus not related to expression. Overexpression of TCEB3C resulted in a 50% decrease of clonogenic survival of CNDT2.5 cells, but not of control cells. The results support a putative role of TCEB3C as a tumor suppressor gene in SI-NETs. Epigenetic repression of TCEB3C seems to be tumor cell type-specific and involves both DNA and histone methylation.
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  • Fjalldal, Sigridur B., et al. (författare)
  • Smoking, stages of change and decisional balance in Iceland and Sweden
  • 2011
  • Ingår i: The Clinical Respiratory Journal. - 1752-6981. ; 5:2, s. 76-83
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Smoking remains a significant health problem. Smoking interventions are important but selection of successful quitters can be difficult. Objective: To characterise smokers with emphasis on two constructs of the transtheoretical model, the stages of change and decisional balance. Methods: A random sample from adults aged 40 and over in Reykjavik, Iceland, and Uppsala, Sweden. Smokers were defined as being in the stage of pre-contemplation (not thinking of quitting within the next 6 months), contemplation (thinking of quitting within the next 6 months) or preparation (thinking of quitting within the next 30 days, having managed to quit for at least 24 h within the last 12 months). Results: A total of 226 participants were smokers: 72 (32%) were in the pre-contemplation stage, 126 (56%) in the contemplation stage and 28 (12%) in the preparation stage. A younger age, higher body mass index (BMI) and higher educational level were significantly related to being in a more advanced stage. A significant association was observed between decisional balance and stages of change such that decreased importance of the positive aspects of smoking and increased importance of the negative aspects of smoking were independently associated with an increased readiness to quit. Conclusion: The motivated smoker is likely to be young and educated with an above average BMI. A smoker in the contemplation stage is likely to maintain the negative aspects of smoking at a high level. Decreasing the value of the pros of smoking may facilitate the shift towards the stage of preparation.
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8.
  • Gilbert, Ruth, et al. (författare)
  • Child maltreatment : variation in trends and policies in six developed countries
  • 2012
  • Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 379:9817, s. 758-772
  • Forskningsöversikt (refereegranskat)abstract
    • We explored trends in six developed countries in three types of indicators of child maltreatment for children younger than 11 years, since the inception of modern child protection systems in the 1970s. Despite several policy initiatives for child protection, we recorded no consistent evidence for a decrease in all types of indicators of child maltreatment. We noted falling rates of violent death in a few age and country groups, but these decreases coincided with reductions in admissions to hospital for maltreatment-related injury only in Sweden and Manitoba (Canada). One or more child protection agency indicators increased in five of six countries, particularly in infants, possibly as a result of early intervention policies. Comparisons of mean rates between countries showed five-fold to ten-fold differences in rates of agency indicators, but less than two-fold variation in violent deaths or maltreatment-related injury, apart from high rates of violent child death in the USA. These analyses draw attention to the need for robust research to establish whether the high and rising rates of agency contacts and out-of-home care in some settings are effectively reducing child maltreatment.
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  • Goemans, Nathalie M, et al. (författare)
  • Systemic administration of PRO051 in Duchenne's muscular dystrophy.
  • 2011
  • Ingår i: The New England journal of medicine. - 1533-4406. ; 364:16, s. 1513-22
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Local intramuscular administration of the antisense oligonucleotide PRO051 in patients with Duchenne's muscular dystrophy with relevant mutations was previously reported to induce the skipping of exon 51 during pre-messenger RNA splicing of the dystrophin gene and to facilitate new dystrophin expression in muscle-fiber membranes. The present phase 1-2a study aimed to assess the safety, pharmacokinetics, and molecular and clinical effects of systemically administered PRO051.
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