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Sökning: L773:0785 3890 OR L773:1365 2060 > (2010-2014)

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  • de Boer, Rudolf A, et al. (författare)
  • Predictive value of plasma galectin-3 levels in heart failure with reduced and preserved ejection fraction
  • 2011
  • Ingår i: Annals of Medicine. - : Informa UK Limited. - 0785-3890 .- 1365-2060. ; 43:1, s. 60-68
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS: galectin-3 is an emerging biomarker which has been studied in relatively small heart failure (HF) cohorts with predominantly systolic HF. We studied the prognostic value of base-line galectin-3 in a large HF cohort, with preserved and reduced left ventricular ejection fraction (LVEF), and compared this to other biomarkers. METHODS: we studied 592 HF patients who had been hospitalized for HF and were followed for 18 months. The primary end-point was a composite of all-cause mortality and HF hospitalization. RESULTS: a doubling of galectin-3 levels was associated with a hazard ratio (HR) of 1.97 (1.62-2.42) for the primary outcome (P < 0.001). After correction for age, gender, BNP, eGFR, and diabetes the HR was 1.38 (1.07-1.78; P = 0.015). Galectin-3 levels were correlated with higher IL-6 and CRP levels (P < 0.002). Changes of galectin-3 levels after 6 months did not add prognostic information to the base-line value (n = 291); however, combining plasma galectin-3 and BNP levels increased prognostic value over either biomarker alone (ROC analysis, P < 0.05). The predictive value of galectin-3 was stronger in patients with preserved LVEF (n = 114) compared to patients with reduced LVEF (P < 0.001). CONCLUSIONS: galectin-3 is an independent marker for outcome in HF and appears to be particularly useful in HF patients with preserved LVEF.
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3.
  • Fava, Cristiano, et al. (författare)
  • From circulating biomarkers to genomics and imaging in the prediction of cardiovascular events in the general population.
  • 2012
  • Ingår i: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 44:5, s. 433-447
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. In the last decades numerous markers have been considered and investigated for the prediction of CV events, but only a few of them resulted in improved global risk assessment beyond traditional risk factors when incorporated into coronary evaluation scores. Recent genetic studies have pointed out a few but consistent loci or genes which are independently associated with CV risk. The idea is fascinating that these genetic markers could lead to improved individual CV risk assessment and tailored pharmacological interventions. In this brief review we will not make a systematic review of all non-genetic and genetic markers of CV risk but we will try to make a brief overview of the most interesting ones with the aim to underline potential 'pros' and 'cons' of their implementation in clinical practice.
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  • Hemminki, Kari, et al. (författare)
  • Risk of asthma and autoimmune diseases and related conditions in patients hospitalized for obesity
  • 2012
  • Ingår i: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 44:3, s. 289-295
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Although there are putative mechanistic links between obesity and autoimmune diseases, obesity is not considered a risk factor for most autoimmune diseases. Methods. Using the nation-wide Hospital Discharge Register we defined a cohort of 29,665 patients hospitalized for obesity since year 1964. The patients were followed for hospitalization for any of 34 autoimmune or related conditions through year 2007. Standardized incidence ratios (SIRs) were calculated for autoimmune diseases in obese individuals compared to those who had not been hospitalized for obesity. Results. Among 22 immune diseases diagnosed after hospitalization for obesity and in at least 5 patients, the overall SIR was 2.05. Of the individual diseases studied, the risk of 16 was significantly increased; none displayed a decreased risk. Psoriasis (4.54) and Behcet's disease (4.49) exhibited the highest risks, followed by Hashimoto's disease/hypothyroidism (4.12) and asthma (3.39). Small but significant increases in SIRs were also noted for the common autoimmune diseases Graves' sdisease/hyperthyroidism (1.28) and rheumatoid arthritis (1.37). Conclusions. The present population of obese individuals, subsequently diagnosed with a number of autoimmune diseases and related conditions, was hospitalized at a relatively young age. Further studies are needed to describe the morbidity in the obese population at large.
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  • Jonasson, Lena, et al. (författare)
  • Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2 diabetes compared with advice to follow a low-fat diet
  • 2014
  • Ingår i: Annals of Medicine. - : Informa Healthcare. - 0785-3890 .- 1365-2060. ; 46:3, s. 182-187
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Inflammation may play an important role in type 2 diabetes. It has been proposed that dietary strategies can modulate inflammatory activity.METHODS: We investigated the effects of diet on inflammation in type 2 diabetes by comparing a traditional low-fat diet (LFD) with a low-carbohydrate diet (LCD). Patients with type 2 diabetes were randomized to follow either LFD aiming for 55-60 energy per cent (E%) from carbohydrates (n = 30) or LCD aiming for 20 E% from carbohydrates (n = 29). Plasma was collected at baseline and after 6 months. C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra), IL-6, tumour necrosis factor receptor (TNFR) 1 and TNFR2 were determined.RESULTS: Both LFD and LCD led to similar reductions in body weight, while beneficial effects on glycaemic control were observed in the LCD group only. After 6 months, the levels of IL-1Ra and IL-6 were significantly lower in the LCD group than in the LFD group, 978 (664-1385) versus 1216 (974-1822) pg/mL and 2.15 (1.65-4.27) versus 3.39 (2.25-4.79) pg/mL, both P < 0.05.CONCLUSIONS: To conclude, advice to follow LCD or LFD had similar effects on weight reduction while effects on inflammation differed. Only LCD was found significantly to improve the subclinical inflammatory state in type 2 diabetes.
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10.
  • Kechagias, Stergios, et al. (författare)
  • Effects of moderate red wine consumption on liver fat and blood lipids : a prospective randomized study
  • 2011
  • Ingår i: Annals of Medicine. - : Informa Healthcare. - 0785-3890 .- 1365-2060. ; 43:7, s. 545-554
  • Tidskriftsartikel (refereegranskat)abstract
    • Background : There have been no human prospective randomized studies of the amount of alcohol that can induce hepatic steatosis. less thanbrgreater than less thanbrgreater thanMethods : Thirty-two healthy women and twelve healthy men (34 +/- 9 years of age) were randomized to consume 150 ml of red wine/day for women (16 g ethanol/day) or double that amount for men (33 g ethanol/day), or to alcohol abstention for 90 days. Participants underwent proton-nuclear magnetic-resonance spectroscopy for measurement of hepatic triglyceride content (HTGC). Blood samples for assessment of cardiovascular risk were drawn before and after the intervention. less thanbrgreater than less thanbrgreater thanResults: After exclusion of three subjects with steatosis at baseline a trend towards increased HTGC was apparent for red wine (before median: 1.1%, range 0.2-3.9%, after median: 1.1%, range 0.5-5.2%, P = 0.059) a difference that was statistically significant compared with abstainers (p = 0.02). However, no subject developed hepatic steatosis. Low-density lipoprotein (LDL)-cholesterol was lowered by red wine (-0.3 mmol/l, SE-0.1, 95% CI-0.6 to -0.04). less thanbrgreater than less thanbrgreater thanConclusions: Moderate consumption of red wine during three months increased HTGC in subjects without steatosis at baseline. However, since not a single participant developed steatosis we suggest that the threshold of alcohol consumption to define nonalcoholic fatty liver disease should not be lower than the amount in our study.
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