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Träfflista för sökning "WFRF:(Mona S) srt2:(2005-2009)"

Sökning: WFRF:(Mona S) > (2005-2009)

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1.
  • Laj, P., et al. (författare)
  • Measuring Atmospheric Composition Change
  • 2009
  • Ingår i: Atmospheric Environment. - : Elsevier BV. - 1873-2844 .- 1352-2310. ; 43:33, s. 5351-5414
  • Tidskriftsartikel (refereegranskat)abstract
    • Scientific findings from the last decades have clearly highlighted the need for a more comprehensive approach to atmospheric change processes. In fact, observation of atmospheric composition variables has been an important activity of atmospheric research that has developed instrumental tools (advanced analytical techniques) and platforms (instrumented passenger aircrafts, ground-based in-situ and remote sensing stations, earth observation satellite instruments) providing essential information on the composition of the atmosphere. The variability of the atmospheric system and the extreme complexity of the atmospheric cycles for short-lived gaseous and aerosol species have led to the development of complex models to interpret observations, test our theoretical understanding of atmospheric chemistry and predict future atmospheric composition. The validation of numerical models requires accurate information concerning the variability of atmospheric composition for targeted species via comparison with observations and measurements. In this paper, we provide an overview of recent advances in instrumentation and methodologies for measuring atmospheric composition changes from space, aircraft and the surface as well as recent improvements in laboratory techniques that permitted scientific advance in the field of atmospheric chemistry. Emphasis is given to the most promising and innovative technologies that will become operational in the near future to improve knowledge of atmospheric composition. Our current observation capacity, however, is not satisfactory to understand and predict future atmospheric composition changes, in relation to predicted climate warming. Based on the limitation of the current European observing system, we address the major gaps in a second part of the paper to explain why further developments in current observation strategies are still needed to strengthen and optimise an observing system not only capable of responding to the requirements of atmospheric services but also to newly open scientific questions.
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2.
  • Sedimbi, S. K., et al. (författare)
  • SUMO4 M55V polymorphism affects susceptibility to type I diabetes in HLA DR3- and DR4-positive Swedish patients
  • 2007
  • Ingår i: Genes Immun. - : Springer Science and Business Media LLC. - 1466-4879 .- 1476-5470. ; 8:6, s. 518-21
  • Tidskriftsartikel (refereegranskat)abstract
    • SUMO4 M55V, located in IDDM5, has been a focus for debate because of its association to type I diabetes (TIDM) in Asians but not in Caucasians. The current study aims to test the significance of M55V association to TIDM in a large cohort of Swedish Caucasians, and to test whether M55V is associated in those carrying human leukocyte antigen (HLA) class II molecules. A total of 673 TIDM patients and 535 age- and sex-matched healthy controls were included in the study. PCR-RFLP was performed to identify the genotype and allele variations. Our data suggest that SUMO4 M55V is not associated with susceptibility to TIDM by itself. When we stratified our patients and controls based on heterozygosity for HLA-DR3/DR4 and SUMO4 genotypes, we found that presence of SUMO4 GG increased further the relative risk conferred by HLA-DR3/DR4 to TIDM, whereas SUMO4 AA decreased the risk. From the current study, we conclude that SUMO4 M55V is associated with TIDM in association with high-risk HLA-DR3 and DR4, but not by itself.
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4.
  • Bakhtadze, Ekaterine, et al. (författare)
  • Common variants in the TCF7L2 gene help to differentiate autoimmune from non-autoimmune diabetes in young (15-34 years) but not in middle-aged (40-59 years) diabetic patients
  • 2008
  • Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 51:12, s. 2224-2232
  • Tidskriftsartikel (refereegranskat)abstract
    • Type 1 diabetes in children is characterised by autoimmune destruction of pancreatic beta cells and the presence of certain risk genotypes. In adults the same situation is often referred to as latent autoimmune diabetes in adults (LADA). We tested whether genetic markers associated with type 1 or type 2 diabetes could help to discriminate between autoimmune and non-autoimmune diabetes in young (15-34 years) and middle-aged (40-59 years) diabetic patients. In 1,642 young and 1,619 middle-aged patients we determined: (1) HLA-DQB1 genotypes; (2) PTPN22 and INS variable-number tandem repeat (VNTR) polymorphisms; (3) two single nucleotide polymorphisms (rs7903146 and rs10885406) in the TCF7L2 gene; (4) glutamic acid decarboxylase (GAD) and IA-2-protein tyrosine phosphatase-like protein (IA-2) antibodies; and (5) fasting plasma C-peptide. Frequency of risk genotypes HLA-DQB1 (60% vs 25%, p =9.4x10(-34); 45% vs 18%, p= 1.4x10(-16)), PTPN22 CT/TT (34% vs 26%, p=0.0023; 31% vs 23%, p=0.034), INS VNTR class I/I (69% vs 53%, p=1.3x10(-8); 69% vs 51%, p=8.5x10(-5)) and INS VNTR class IIIA/IIIA (75% vs 63%, p=4.3x10(-6); 73% vs 60%, p=0.008) was increased in young and middle-aged GAD antibodies (GADA)-positive compared with GADA-negative patients. The type 2 diabetes-associated genotypes of TCF7L2 CT/TT of rs7903146 were significantly more common in young GADA-negative than in GADA-positive patients (53% vs 43%; p=0.0004). No such difference was seen in middle-aged patients, in whom the frequency of the CT/TT genotypes of TCF7L2 was similarly increased in GADA-negative and GADA-positive groups (55% vs 56%). Common variants in the TCF7L2 gene help to differentiate young but not middle-aged GADA-positive and GADA-negative diabetic patients, suggesting that young GADA-negative patients have type 2 diabetes and that middle-aged GADA-positive patients are different from their young GADA-positive counterparts and share genetic features with type 2 diabetes.
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5.
  • Boman, Kurt, et al. (författare)
  • Exercise and cardiovascular outcomes in hypertensive patients in relation to structure and function of left ventricular hypertrophy : the LIFE study.
  • 2009
  • Ingår i: European Journal of Cardiovascular Prevention & Rehabilitation. - 1741-8267 .- 1741-8275. ; 16:2, s. 242-248
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Exercise lowers blood pressure and improves cardiovascular function, but little is known about whether exercise impacts cardiovascular morbidity and mortality independent of left ventricular hypertrophy (LVH) and LV geometry. DESIGN: Observational analysis of prospectively obtained echocardiographic data within the context of a randomized trial of antihypertensive treatment. METHODS: A total of 937 hypertensive patients with ECG LVH were studied by echocardiography in the Losartan Intervention For Endpoint reduction in hypertension study. Baseline exercise status was categorized as sedentary (never exercise), intermediate (30 min twice/week). During 4.8-year follow-up, 105 patients suffered the primary composite endpoint of myocardial infarction (MI), stroke, or cardiovascular death. MI occurred in 39, stroke in 60, and cardiovascular death in 33 patients. RESULTS: Sedentary individuals (n = 212) had, compared with those physically active (n = 511), higher heart rate (P<0.001), weight (P<0.001), body surface area (P = 0.02), body mass index (P<0.001), LV mass (LVM, P = 0.04), LVM indexed for height or body surface area (P = 0.004); thicker ventricular septum (P = 0.012) and posterior wall (P = 0.016); and larger left atrium (P = 0.006). Systolic variables did not differ. In Cox regression analysis, physically active compared with sedentary patients had lower risk of primary composite endpoint [odds ratio (OR): 0.42, 95% confidence interval (CI): 0.26-0.68, P < 0.001], cardiovascular death (OR: 0.50, 95% CI: 0.22-0.1.10, NS), and stroke (OR: 0.26, 95% CI: 0.13-0.49, P < 0.001) without significant difference for MI (OR: 0.79, 95% CI: 0.35-1.75, NS) independent of systolic blood pressure, LVM index, or treatment. CONCLUSION: In hypertensive patients with LVH, physically active patients had improved prognosis for cardiovascular endpoints, mortality, and stroke that was independent of LVM.
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6.
  • Eklund, Mona, et al. (författare)
  • Subjective quality of life in relation to psychiatric rehabilitation and daily life
  • 2007
  • Ingår i: Quality of Life Impairment in Schizophrenia, Mood and Anxiety Disorders : New Perspectives on Research and Treatment - New Perspectives on Research and Treatment. - Dordrecht : Springer Netherlands. - 9781402057779 ; , s. 355-372
  • Bokkapitel (refereegranskat)abstract
    • Due to the great variation in approaches to psychiatric rehabilitation, the literature does not provide a uniform description of these methods. In this review, outcomes in terms of subjective quality of life are discussed in relation to vocational training, activity-based rehabilitation, case management, and social skills training. Relationships between aspects of daily life and subjective quality of life are also illuminated. In all the rehabilitation approaches studied, clients have shown an improved quality of life during the rehabilitation period, but no more than the respective comparison group receiving some other form of intervention. Concerning daily life, having employment, being engaged in and satisfied with daily activities, having a supportive social network, and living in the community have consistently been shown to be related to a better quality of life. The reasons why subjective quality of life has not been shown to improve to any substantial degree as a result of psychiatric rehabilitation are probably manifold, and research so far has left many questions unanswered. More, well-designed studies, including multi-methodological approaches and long follow-up periods, are needed to elucidate how subjective quality of life is affected by various rehabilitation strategies
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7.
  • Gladman, Dafna D., et al. (författare)
  • Clinical and genetic registries in psoriatic disease
  • 2008
  • Ingår i: Journal of Rheumatology. - 0315-162X .- 1499-2752. ; 35:7, s. 1458-1463
  • Tidskriftsartikel (refereegranskat)abstract
    • Clinical and genetic registries are an important tool in studying psoriasis and psoriatic arthritis (PsA). They assist in delineating disease features and are crucial in defining phenotype and identifying genetic and other markers of disease expression. At the 2007 Annual Meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA), members of the clinical registries and genetics committees described several ongoing registries, including their construction, protocols, and some results from their analyses. In breakout groups, members discussed data issues, including identification of core datasets, ownership, and how to share data; and ethical issues and possible sources of funding for registries. Proceedings of these meetings are summarized.
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8.
  • Hall, T. R., et al. (författare)
  • Longitudinal epitope analysis of insulin-binding antibodies in type 1 diabetes
  • 2006
  • Ingår i: Clinical and Experimental Immunology. - : Oxford University Press (OUP). - 0009-9104 .- 1365-2249. ; 146:1, s. 41531-41531
  • Tidskriftsartikel (refereegranskat)abstract
    • Autoantibodies to insulin (IAA) are one of the first markers of the autoimmune process leading to type 1 diabetes (T1D). While other autoantibodies in T1D have been studied extensively, relatively little is known about IAA and their binding specificities, especially after insulin treatment is initiated. We hypothesize that insulin antibodies (IA) that develop upon initiation of insulin treatment differ in their epitope specificities from IAA. We analysed insulin antibody binding specificities in longitudinal samples of T1D patients (n = 49). Samples were taken at clinical diagnosis of disease and after insulin treatment was initiated. The epitope specificities were analysed using recombinant Fab (rFab) derived from insulin-specific monoclonal antibodies AE9D6 and CG7C7. Binding of radiolabelled insulin by samples taken at onset of the disease was significantly reduced in the presence of rFab CG7C7 and AE9D6. rFab AE9D6 competed sera binding to insulin significantly better than rFab CG7C7 (P = 0.02). Binding to the AE9D6-defined epitope in the initial sample was correlated inversely with age at onset (P = 0.005). The binding to the AE9D6-defined epitope increased significantly (P < 0.0001) after 3 months of insulin treatment. Binding to the CG7C7-defined epitope did not change during the analysed period of 12 months. We conclude that epitopes recognized by insulin binding antibodies can be identified using monoclonal insulin-specific rFab as competitors. Using this approach we observed that insulin treatment is accompanied by a change in epitope specificities in the emerging IA.
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9.
  • Hutchinson, Dana S., et al. (författare)
  • Diphenylene iodonium stimulates glucose uptake in skeletal muscle cells through mitochondrial complex I inhibition and activation of AMP-activated protein kinase
  • 2007
  • Ingår i: Cellular Signalling. - : Elsevier BV. - 0898-6568 .- 1873-3913. ; 19:7, s. 1610-1620
  • Tidskriftsartikel (refereegranskat)abstract
    • NADPH oxidase inhibitors such as diphenylene iodonium (DPI) and apocynin lower whole body and blood glucose levels and improve diabetes when administered to rodents. Skeletal muscle has an important role in managing glucose homeostasis and we have used L6 cells, C2C12 cells and primary muscle cells as model systems to investigate whether these drugs regulate glucose uptake in skeletal muscle cells. The data presented in this study show that apocynin does not affect glucose uptake in skeletal muscle cells in culture. Tat gp91ds, a chimeric peptide that inhibits NADPH oxidase activity, also failed to affect glucose uptake and we found no significant evidence of NADPH oxidase (subunits tested were Nox4, p22phox, gp91phox and p47phox mRNA) in skeletal muscle cells in culture. However, DPI increases basal and insulin-stimulated glucose uptake in L6 cells, C2C12 cells and primary muscle cells. Detailed studies on L6 cells demonstrate that the increase of glucose uptake is via a mechanism independent of phosphoinositide-3 kinase (PI3K)/Akt but dependent on AMP-activated protein kinase (AMPK). We postulate that DPI through inhibition of mitochondrial complex 1 and decreases in oxygen consumption, leading to decreases of ATP and activation of AMPK, stimulates glucose uptake in skeletal muscle cells.
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10.
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