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Sökning: L773:0021 9150 OR L773:1879 1484

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  • Carlson, Lars A., et al. (författare)
  • A case of massive hypertriglyceridemia corrected by nicotinic acid or nicotinamide therapy
  • 1972
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 16:3, s. 359-368
  • Tidskriftsartikel (refereegranskat)abstract
    • A case of massive hypertriglyceridemia with fasting plasma triglycerides around 100 mmoles/l is described. Large amounts of chylomicra were present in fasting plasma and the amounts of low-density and high-density lipoproteins were very low. Postheparin plasma lipolytic activity was normal and intravenous heparin rapidly cleared the patient's abnormally prolonged alimentary lipemia with a concomitant rise in plasma free fatty acid levels.Nicotinic acid or nictotinamide given in doses of 3 g or more daily reduced plasma triglyceride levels to about 2–3 mmoles/1 and raised the reduced levels of low and high-density lipoproteins. The mode of onset of this therapeutic effect was slow and the effect persisted for several weeks after withdrawal of either nicotinic acid or nicotinamide.The pathogenesis of the hypertriglyceridemia as well as the mode of action of nicotinic acid and nicotinamide is discussed.
  • Carlson, Lars A., et al. (författare)
  • Effect of chlorophenoxyisobutyric acid (CPIB) on fat-mobilizing lipolysis and cyclic AMP levels in rat epididymal fat
  • 1972
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 16:3, s. 349-357
  • Tidskriftsartikel (refereegranskat)abstract
    • High concentrations of chlorophenoxyisobutyric acid (CPIB) reduced basal glycerol release from rat epididymal fat pads in vitro and antagonized the lipolytic effects of noradrenaline. Furthermore, very high concentrations of CPIB significantly antagonized the effects or noradrenaline or ACTH on cyclic AMP accumulation by isolated rat adipocytes. These data are not incompatible with the hypothesis that a primary mechanism in the hypolipidemic action of CPIB is to lower the levels of cyclic AMP in adipose tissue, resulting in decreased hormone-sensitive lipase activity and/or increased lipoprotein lipase activity.
  • Holmlund, A., et al. (författare)
  • Soluble intercellular adhesion molecule-1 is related to endothelial vasodilatory function in healthy individuals
  • 2002
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 165:2, s. 271-276
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate the associations between markers of systemic and vascular inflammation, and indicators of vascular morphology and function. METHODS: In 59 apparently healthy individuals, we measured serum levels of highly sensitive C-reactive protein (hsCRP), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. Endothelium-dependent (EDV) and -independent (EIDV) vasodilatation was evaluated in the forearm by venous occlusion plethysmography and local infusions of methacholine and sodium nitroprussid. Endothelial function index (EFI) was expressed as the EDV/EIDV ratio. The intima-media thickness (IMT) of the common carotid artery was investigated with ultrasound (far wall). RESULTS: EFI was inversely related only to ICAM-1 (r=-0.31, P<0.02) by univariate analysis. This association remained significant after adjustment for age, sex, blood pressure, smoking and serum cholesterol. EFI did not relate to hsCRP, VCAM-1 or E-selectin. Neither hsCRP, nor the adhesion molecules were significantly related to carotid artery IMT. CONCLUSION: ICAM-1 was related to endothelial vasodilatory function, but not to IMT, suggesting that endothelial inflammatory activation is related to an impaired vascular relaxation in apparently healthy individuals.
  • Sarabi, Mahziar, et al. (författare)
  • Endothelium-dependent vasodilation is related to the fatty acid composition of serum lipids in healthy subjects
  • 2001
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 156:2, s. 349-355
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • The fatty acid (FA) composition of the serum lipids has been associated with cardiovascular disease (CVD). As an attenuated endothelium-dependent vasodilation (EDV) has been suggested as an early marker of atherosclerosis, we investigated the relationships between the proportion of FA in serum lipids (cholesterol esters and phospholipids) together with the levels of serum LDL- and HDL-cholesterol and triglycerides and EDV, as well as endothelium-independent vasodilation (EIDV). Fifty-six healthy subjects (31 men and 25 women), aged between 20 and 69 years, underwent measurements of forearm blood flow (FBF) at rest and during local infusion of 2 and 4 microg/min of metacholine (Mch, evaluating EDV), 5 and 10 microg/min of sodium nitroprusside (SNP, evaluating endothelium-independent vasodilation, EIDV) using venous occlusion plethysmography. An index of endothelial function was calculated as the ratio between EDV and EIDV. The proportion of palmitic (16:0) and palmitoleic (16:1) acids were inversely related (r=-0.35 and -0.35, P<0.01 for both), while linoleic acid (18:2 n6) and the HDL-cholesterol concentration were positively related (r=0.35 and 0.36, P<0.01 for both) to the endothelial function index. In multiple regression analysis also including age and gender, palmitoleic acid and HDL-cholesterol were significant independent predictors of endothelial function. Alfa-linolenic acid (18:3 n3) was positively correlated to both EDV and EIDV (r=0.40 and 0.43, P<0.01 for both), indicating a protective effect of this essential FA on vasodilation in general. It is concluded that the FA composition of serum lipids, partly reflecting the composition of dietary fat and previously associated with the development of CVD, was associated with endothelial function in apparently healthy subjects.
  • Steer, Peter, et al. (författare)
  • Vitamin C, diclophenac and L-arginine protect endothelium-dependent vasodilation against elevated circulating fatty acid levels in humans
  • 2003
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 168:1, s. 65-72
  • Tidskriftsartikel (refereegranskat)abstract
    • An acute elevation of circulating non-esterified fatty acids (NEFAs) has previously been shown to impair endothelium-dependent vasodilation (EDV). In this study, we investigated if local administration of vitamin C (n=8, 18 mg/min), L-arginine (n=8, 12.5 mg/min), or the cyclooxygenase (COX) inhibitor diclophenac (n=8, 0.5 mg/min) can counteract the endothelial dysfunction seen during infusion of Intralipid plus heparin (n=10). EDV and endothelium-independent vasodilation (EIDV) were studied in the forearm after local administration of methacholine chloride (Mch; 2 and 4 microg/min) and sodium nitroprusside (SNP; 5 and 10 microg/min). Forearm blood flow (FBF) was determined with venous occlusion plethysmography. Intralipid and heparin increased circulating NEFA levels sevenfold and impaired EDV (P<0.001 vs baseline). Concomitant administration of L-arginine or diclophenac abolished the NEFA-induced impairment in EDV. Concomitant vitamin C administration actually improved EDV (P<0.05 vs baseline). NEFA elevation increased EIDV (P<0.01), but this effect was not significant after L-arginine or diclophenac infusions. In conclusion, an acute elevation of circulating NEFAs led to impaired EDV. Administration of L-arginine, vitamin C or COX inhibition abolished this effect, suggesting that NEFAs might interact with endothelial vasodilatory function through multiple mechanisms.
  • Bennet, A. M., et al. (författare)
  • Association of TNF-α serum levels and TNFA promoter polymorohisms with risk of myocardial infarction
  • 2006
  • Ingår i: Atherosclerosis. - Elsevier. - 0021-9150 .- 1879-1484. ; 187:2, s. 408-414
  • Tidskriftsartikel (refereegranskat)abstract
    • Elevated levels of tumor necrosis factor-alpha (TNF-α), and presence of polymorphisms of the TNFA gene have been implicated in cardiovascular disease pathogenesis. We explored the relationship between polymorphisms in the TNFA gene (−1031C/T, −863C/A −857T/C, −308G/A, −238G/A), protein levels of TNF-α and their association to myocardial infarction (MI) using a sample of 1213 post-MI patients and 1561 healthy controls. MI risk was higher among men with elevated TNF-α levels, with the highest compared to the lowest TNF-α quartile giving a 70% risk increase (OR [95% CI]: 1.7 [1.1; 2.6]). Obese subjects who also had elevated TNF-α levels were at even higher risk for MI (OR [95% CI]: 3.4 [2.1; 5.6]). Higher TNF-α levels were seen among smokers (but not among non-smokers) carrying the −857T allele. Furthermore, a rare haplotype occurred more frequently among the cases than the controls. Elevated TNF-α levels are associated with increased MI risk. Obese subjects with elevated TNF-a levels, and carriers of polymorphisms in or near TNFA are particularly susceptible to the hazards of smoking, results which may have implications for cardiovascular preventive measures.
  • Bernberg, Evelina, 1981-, et al. (författare)
  • Repeated exposure to stressors do not accelerate atherosclerosis in ApoE-/- mice
  • 2009
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 204:1, s. 90-95
  • Tidskriftsartikel (refereegranskat)abstract
    • Psychosocial stress is suggested to play a significant role in development of cardiovascular disease. To evaluate the effects of repeated exposure to stress on atherosclerosis in atherosclerosis-prone ApoE(-/-) mice we used five different stressors. We further sought to determine whether stress combined with high salt diet induces dysfunctional neurohormonal regulation and impaired salt excretion, thus amplifying the atherogenic potential of salt. The five stressors were evaluated in male C57BL/6 mice and ApoE(-/-) mice (studies I and II) and then used in female ApoE(-/-) mice to study their effect on atherosclerosis (study III). The mice in study III received standard or high salt diet (8%) alone or in combination with stress for 12 weeks. Urine and plasma were collected for corticosterone and lipid analysis, respectively. Acute blood pressure (BP) and heart rate (HR) responses to stress were measured using telemetry. Plaque burden was assessed in the thoracic aorta and aortic root. Plaque morphology was investigated regarding macrophages and collagen content. Urinary corticosterone chronically increased in stressed mice (P<0.05 control vs. stress, P<0.05 control salt vs. stress salt). BP and HR increased acutely during all stressors (P<0.05). Body weight gain decreased significantly in the stress group (P<0.05 vs. control). However, stress did not alter plasma lipid levels, plaque area or plaque morphology. Increased BP and HR suggest an acute stress-related response in ApoE(-/-) mice. Furthermore, stress chronically decreased body weight gain and increased urinary corticosterone levels. Notably, despite an apparent stress effect, stress affected neither atherogenesis nor plaque morphology.
  • Bernberg, Evelina, 1981-, et al. (författare)
  • Social disruption stress increases IL-6 levels and accelerates atherosclerosis in ApoE-/- mice.
  • 2012
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 221:2, s. 359-65
  • Tidskriftsartikel (refereegranskat)abstract
    • We have previously shown that different forms of stress have distinctive effects on atherogenesis in mice. We showed that social stress increase atherosclerosis in ApoE(-/-) mice, while more physical forms of stress do not. Here we evaluated the effect of social disruption (SDR) stress on atherogenesis and evaluated cytokine release after SDR-stress and five more physical stressors.
  • Carlsson, Axel C, et al. (författare)
  • Levels of soluble tumor necrosis factor receptor 1 and 2, gender, and risk of myocardial infarction in Northern Sweden
  • 2018
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 272, s. 41-46
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND AIMS:Soluble receptors for tumor necrosis factor alpha (sTNFR1 and sTNFR2) have been associated with cardiovascular diseases, and some evidence points towards a difference in associated risk between men and women. We aimed to study the association between sTNFR1 and sTNFR2 and incident myocardial infarctions (MI) and to explore the influence of established cardiovascular risk factors in men and women.METHODS:We conducted a nested case control study in three large Swedish cohorts, including 533 myocardial infarction cases, and 1003 age-, sex- and cohort-matched controls. Odds ratios (OR) with 95% confidence intervals (CI) were calculated.RESULTS:An association between circulating sTNFR1 and sTNFR2 and an increased risk for MI was found when comparing cases and controls. The odds ratios were significant after adjustment for established cardiovascular risk factors and C-reactive protein in women (OR 1.44, 95% CI 1.08-1.93 for TNFR1, and 1.61, 95% CI 1.11-2.34 for TNFR2), but was abolished in men. Women with a combination of elevated CRP and values in the upper quartile of TNFR1 or TNFR2 had a 5-fold higher risk of myocardial infarction versus those with normal CRP and values in the lower three quartiles of TNFR1 or TNFR2.CONCLUSIONS:As the risk estimates for TNFR1 and TNFR2 were higher and remained significant after adjustments for established cardiovascular risk factors in women but not in men, a potential role for TNFR1 and TNFR2 in identifying women with a higher MI risk is possible. The future clinical role of TNFR1 and TNFR2 in combination with CRP to identify high risk patients for coronary heart disease has yet to be determined.
  • Carlsson, Axel C, et al. (författare)
  • Soluble tumor necrosis factor receptor 1 (sTNFR1) is associated with increased total mortality due to cancer and cardiovascular causes Findings from two community based cohorts of elderly
  • 2014
  • Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 237:1, s. 236-242
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Experimental evidence support soluble receptors for tumor necrosis factor alpha as important mediators of the underlying pathology leading to cardiovascular disease and cancer. However, prospective data concerning the relation between circulating soluble tumor necrosis factor receptor-1 (sTNFR1) and mortality in humans are lacking. We aimed to explore and validate the association between sTNFR1 and mortality, and to explore the influence of other established risk factors for mortality, including other inflammatory markers.METHODS: The association between serum sTNFR1and the risk for mortality was investigated in two community-based cohorts of elderly: the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS; women 50%, n = 1005, mean age 70 years, median follow-up 7.9 years) and the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 775, mean age 77 years, median follow-up 8.1 years).RESULTS: In total, 101 participants in PIVUS and 274 in ULSAM died during follow-up. In multivariable Cox regression models adjusted for inflammation, lifestyle and established cardiovascular risk factors, one standard deviation (SD) higher sTNFR1 was associated with a hazard ratio (HR) for mortality of 1.37, 95% confidence interval (CI) 1.17-1.60, in PIVUS and HR 1.22, 95% CI 1.10-1.37 in ULSAM. Moreover, circulatingsTNFR1 was associated with cardiovascular mortality (HR per SD of sTNFR1, 1.24, 95% CI 1.07-1.44) and cancer mortality (HR per SD of sTNFR1, 1.32, 95% CI 1.11-1.57) in the ULSAM cohort. High levels of sTNFR1 identified individuals with increased risk of mortality among those with high as well as low levels of systemic inflammation.CONCLUSIONS: An association between circulating sTNFR1 and an increased risk for mortality was found and validated in two independent community-based cohorts. The future clinical role of sTNFR1 to identify high risk patients for adverse outcomes and mortality has yet to be determined.
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