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Träfflista för sökning "WFRF:(Miao Jonasson Junmei) "

Sökning: WFRF:(Miao Jonasson Junmei)

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  • [1]23Nästa
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1.
  • Eriksson, Erik M, et al. (författare)
  • Participation in a Swedish cervical cancer screening program among women with psychiatric diagnoses: a population-based cohort study.
  • 2019
  • Ingår i: BMC public health. - 1471-2458. ; 19:1
  • Tidskriftsartikel (refereegranskat)abstract
    • In Sweden, organized screening programs have significantly reduced the incidence of cervical cancer. For cancers overall, however, women with psychiatric diagnoses have lower survival rates than other women. This study explores whether women with psychiatric diagnoses participate in cervical cancer screening programs to a lesser extent than women on average, and whether there are disparities between psychiatric diagnostic groups based on grades of severity.Between 2000 and 2010, 65,292 women within screening ages of 23-60 had at least two ICD-10 (International Statistical Classification of Diseases and Related Health Problems - Tenth Revision) codes F20*-F40* registered at visits in primary care or psychiatric care in Region Västra Götaland, Sweden. Participation in the cervical cancer screening program during 2010-2014 was compared with the general female population using logistic regression adjusted for age.Relative risk for participation (RR) for women diagnosed within psychiatric specialist care RR was 0.94 compared with the general population, adjusted for age. RR for diagnoses outside specialist care was 0.99. RR for psychoses (F20*) was 0.81.Women with less-severe psychiatric diagnoses participate in the screening program to the same extent as women overall. Women who have received psychiatric specialist care participate to a lesser extent than women overall. The lowest participation rates were found among women diagnosed with psychoses.
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2.
  • Miao Jonasson, Junmei, et al. (författare)
  • Social Support, Social Network Size, Social Strain, Stressful Life Events, and Coronary Heart Disease in Women With Type 2 Diabetes: A Cohort Study Based on the Women's Health Initiative
  • 2020
  • Ingår i: Diabetes care. - : AMER DIABETES ASSOC. - 0149-5992 .- 1935-5548. ; 43:8, s. 1759-1766
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE We studied associations between social support, social network size, social strain, or stressful life events and risk of coronary heart disease (CHD) in postmenopausal women with type 2 diabetes. RESEARCH DESIGN AND METHODS From the Women's Health Initiative, 5,262 postmenopausal women with type 2 diabetes at baseline were included. Cox proportional hazards regression models adjusted for demographics, depressive symptoms, anthropometric variables, and lifestyle factors were used to examine associations between social factors and CHD. RESULTS A total of 672 case subjects with CHD were observed during an average 12.79 (SD 6.29) years of follow-up. There was a significant linear trend toward higher risk of CHD as the number of stressful life events increased (Pfor trend = 0.01; hazard ratio [HR] [95% CI] for the third and fourth quartiles compared with first quartile: 1.27 [1.03-1.56] and 1.30 [1.04-1.64]). Being married or in an intimate relationship was related to decreased risk of CHD (HR 0.82 [95% CI 0.69-0.97]). CONCLUSIONS Among postmenopausal women with type 2 diabetes, higher levels of stressful life events were associated with higher risk of CHD. Experience of stressful life events might be considered as a risk factor for CHD among women with type 2 diabetes.
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  • Nemes, Szilard, 1977, et al. (författare)
  • A diagnostic algorithm to identify paired tumors with clonal origin.
  • 2013
  • Ingår i: Genes, chromosomes & cancer. - 1098-2264. ; 52:11, s. 1007-16
  • Tidskriftsartikel (refereegranskat)abstract
    • Despite practical implications we still lack standardized methods for clonality testing of tumor pairs. Each tumor is characterized by a set of chromosomal abnormalities, nonrandom changes preferentially involving specific chromosomes and chromosomal regions. Although tumors accumulate chromosomal abnormalities during their development, the majority of these alterations is specific and characteristic for each individual tumor is not exhibited at the population level. Assumingly, secondary tumors that develop from disseminated cells from the primary tumor inherit not only chromosomal changes specific for the cancerous process but also random chromosomal changes that accumulate during tumor development. Based on this assumption, we adopted an intuitive index for genomic similarities of paired tumors, which ranges between zero (completely different genomic profiles) and one (identical genomic profiles). To test the assumption that two tumors have clonal origins if they share a higher degree of genomic similarity than two randomly paired tumors, we built a permutation-based null-hypothesis procedure. The procedure is demonstrated using two publicly available data sets. The article highlights the complexities of clonality testing and aims to offer an easy to follow blueprint that will allow researchers to test genomic similarities of paired tumors, with the proposed index or any other index that fits their need. © 2013 Wiley Periodicals, Inc.
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8.
  • Nemes, Szilard, 1977, et al. (författare)
  • Bias in odds ratios by logistic regression modelling and sample size.
  • 2009
  • Ingår i: BMC medical research methodology. - 1471-2288. ; 9
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: In epidemiological studies researchers use logistic regression as an analytical tool to study the association of a binary outcome to a set of possible exposures. Methods: Using a simulation study we illustrate how the analytically derived bias of odds ratios modelling in logistic regression varies as a function of the sample size. Results: Logistic regression overestimates odds ratios in studies with small to moderate samples size. The small sample size induced bias is a systematic one, bias away from null. Regression coefficient estimates shifts away from zero, odds ratios from one. Conclusion: If several small studies are pooled without consideration of the bias introduced by the inherent mathematical properties of the logistic regression model, researchers may be mislead to erroneous interpretation of the results.
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  • Nemes, Szilard, 1977, et al. (författare)
  • Segmented regression, a versatile tool to analyze mRNA levels in relation to DNA copy number aberrations.
  • 2012
  • Ingår i: Genes, chromosomes & cancer. - 1098-2264. ; 51:1, s. 77-82
  • Tidskriftsartikel (refereegranskat)abstract
    • DNA copy number aberrations (CNA) and subsequent altered gene expression profiles (mRNA levels) are characteristic features of cancerous cells. Integrative genomic analysis aims to identify recurrent CNA that may have a potential role in cancer development, assuming that gene amplification is accompanied by overexpression, while deletions give rise to downregulation of gene expression. We propose a segmented regression-based approach to identify CNA-driven alteration of gene expression profiles. Segmented regression allows to fit piecewise linear models in different domains of CNA joined by a change-point, where the mRNA-CNA relationship undergoes structural changes. Here, we illustrate the implementation and applicability of the proposed model using 1,161 chromosome fragments detected as DNA CNA in primary tumors from 97 breast cancer patients. We identified significant CNA-driven changes in gene expression levels for 341 chromosome fragments, of which 72 showed a nonlinear relationship to CNA. For 59 of 72 chromosome fragments (82%), we observed an initial increase in mRNA levels due to changes in CNA. After the change-point was passed, the mRNA levels reached a plateau, and a further increase in DNA copy numbers did not induce further elevation in mRNA levels. In contrast, for 13 chromosome fragments, the change-point marked the point where mRNA production accelerated. We conclude that segmented regression modeling may provide valuable insights into the impact CNA have on gene expression in cancer cells. © 2011 Wiley Periodicals, Inc.
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