334 research outputs found

    Calcium Intake From Diet and Supplements and the Risk of Coronary Artery Calcification and its Progression Among Older Adults: 10‐Year Follow‐up of the Multi‐Ethnic Study of Atherosclerosis (MESA)

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    BACKGROUND: Recent randomized data suggest that calcium supplements may be associated with increased risk of cardiovascular disease (CVD) events. Using a longitudinal cohort study, we assessed the association between calcium intake, from both foods and supplements, and atherosclerosis, as measured by coronary artery calcification (CAC). METHODS AND RESULTS: We studied 5448 adults free of clinically diagnosed CVD (52% female; aged 45-84 years) from the Multi-Ethnic Study of Atherosclerosis. Baseline total calcium intake was assessed from diet (using a food frequency questionnaire) and calcium supplements (by a medication inventory) and categorized into quintiles. Baseline CAC was measured by computed tomography, and CAC measurements were repeated in 2742 participants ≈10 years later. At baseline, mean calcium intakes across quintiles were 313.3, 540.3, 783.0, 1168.9, and 2157.4 mg/day. Women had higher calcium intakes than men. After adjustment for potential confounders, among 1567 participants without baseline CAC, the relative risk (RR) of developing incident CAC over 10 years, by quintile 1 to 5 of calcium intake, were 1 (reference), 0.95 (0.79-1.14), 1.02 (0.85-1.23), 0.86 (0.69-1.05), and 0.73 (0.57-0.93). After accounting for total calcium intake, calcium supplement use was associated with increased risk for incident CAC (RR=1.22 [1.07-1.39]). No relation was found between baseline calcium intake and 10-year changes in log-transformed CAC among those participants with baseline CAC >0. CONCLUSIONS: High total calcium intake was associated with a decreased risk of incident atherosclerosis over long-term follow-up, particularly if achieved without supplement use. However, calcium supplement use may increase the risk for incident CAC

    Towards reliability centred maintenance of wind turbines

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    Reliability centred maintenance applied to a fleet of wind turbines is presented in this paper. The key components and failure modes are identified via analysis of maintenance records. Corrective actions which an operator can take to mitigate such failures are discussed, together with implementation issues. By developing a robust set of RCM tools, wind farm operators can better quantify and minimise operational expenditure of wind farm fleets

    Women, lipids, and atherosclerotic cardiovascular disease:a call to action from the European Atherosclerosis Society

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    Cardiovascular disease is the leading cause of death in women and men globally, with most due to atherosclerotic cardiovascular disease (ASCVD). Despite progress during the last 30 years, ASCVD mortality is now increasing, with the fastest relative increase in middle-aged women. Missed or delayed diagnosis and undertreatment do not fully explain this burden of disease. Sex-specific factors, such as hypertensive disorders of pregnancy, premature menopause (especially primary ovarian insufficiency), and polycystic ovary syndrome are also relevant, with good evidence that these are associated with greater cardiovascular risk. This position statement from the European Atherosclerosis Society focuses on these factors, as well as sex-specific effects on lipids, including lipoprotein(a), over the life course in women which impact ASCVD risk. Women are also disproportionately impacted (in relative terms) by diabetes, chronic kidney disease, and auto-immune inflammatory disease. All these effects are compounded by sociocultural components related to gender. This panel stresses the need to identify and treat modifiable cardiovascular risk factors earlier in women, especially for those at risk due to sex-specific conditions, to reduce the unacceptably high burden of ASCVD in women

    Relationship between age at menopause, obesity, and incident heart failure: The Atherosclerosis Risk in Communities Study

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    Background The mechanisms linking menopausal age and heart failure (HF) incidence are controversial. We investigated for heterogeneity by obesity on the relationship between menopausal age and HF incidence. Methods and Results Using postmenopausal women who attended the Atherosclerosis Risk in Communities Study Visit 4, we estimated hazard ratios of incident HF associated with menopausal age using Cox proportional hazards models, testing for effect modification by obesity and adjusting for HF risk factors. Women were categorized by menopausal age: \u3c45 years, 45 to 49 years, 50 to 54 years, and ≥55 years. Among 4441 postmenopausal women, aged 63.5±5.5 years, there were 903 incident HF events over a mean follow-up of 16.5 years. The attributable risk of generalized and central obesity for HF incidence was greatest among women who experienced menopause at age ≥55 years: 11.09/1000 person-years and 7.38/1000 person-years, respectively. There were significant interactions of menopausal age with body mass index and waist circumference for HF incidence

    Readmission and processes of care across weekend and weekday hospitalisation for acute myocardial infarction, heart failure or stroke: an observational study of the National Readmission Database.

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    OBJECTIVES: Variation in hospital resource allocations across weekdays and weekends have led to studies of the 'weekend effect' for ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), heart failure (HF) and stroke. However, few studies have explored the 'weekend effect' on unplanned readmission. We aimed to investigate 30-day unplanned readmissions and processes of care across weekend and weekday hospitalisations for STEMI, NSTEMI, HF and stroke. DESIGN: We grouped hospitalisations for STEMI, NSTEMI, HF or stroke into weekday or weekend admissions. Multivariable adjusted ORs for binary outcomes across weekend versus weekday (reference) groups were estimated using logistic regression. SETTING: We included all non-elective hospitalisations for STEMI, NSTEMI, HF or stroke, which were recorded in the US Nationwide Readmissions Database between 2010 and 2014. PARTICIPANTS: The analysis sample included 659 906 hospitalisations for STEMI, 1 420 600 hospitalisations for NSTEMI, 3 027 699 hospitalisations for HF, and 2 574 168 hospitalisations for stroke. MAIN OUTCOME MEASURES: The primary outcome was unplanned 30-day readmission. As secondary outcomes, we considered length of stay and the following processes of care: coronary angiography, primary percutaneous coronary intervention, coronary artery bypass graft, thrombolysis, brain scan/imaging, thrombectomy, echocardiography and cardiac resynchronisation therapy/implantable cardioverter-defibrillator. RESULTS: Unplanned 30-day readmission rates were 11.0%, 15.1%, 23.0% and 10.9% for STEMI, NSTEMI, HF and stroke, respectively. Weekend hospitalisations for HF were associated with a statistically significant but modest increase in 30-day readmissions (OR of 1.045, 95% CI 1.033 to 1.058). Weekend hospitalisation for STEMI, NSTEMI or stroke was not associated with increased risk of 30-day readmission. CONCLUSION: There was no clinically meaningful evidence against the supposition that weekend and weekday hospitalisations have the same 30-day unplanned readmissions. Thirty-day readmission rates were high, especially for HF, which has implications for service provision. Strategies to reduce readmission rates should be explored, regardless of day of hospitalisation

    Progression of atherosclerosis with carnitine supplementation: a randomized controlled trial in the metabolic syndrome

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    Background: L-carnitine (L-C), a ubiquitous nutritional supplement, has been investigated as a potential therapy for cardiovascular disease, but its effects on human atherosclerosis are unknown. Clinical studies suggest improvement of some cardiovascular risk factors, whereas others show increased plasma levels of pro-atherogenic trimethylamine N-oxide. The primary aim was to determine whether L-C therapy led to progression or regression of carotid total plaque volume (TPV) in participants with metabolic syndrome (MetS). Methods: This was a phase 2, prospective, double blinded, randomized, placebo-controlled, two-center trial. MetS was defined as ≥ 3/5 cardiac risk factors: elevated waist circumference; elevated triglycerides; reduced HDL-cholesterol; elevated blood pressure; elevated glucose or HbA1c; or on treatment. Participants with a baseline TPV ≥ 50 mm3 were randomized to placebo or 2 g L-C daily for 6 months. Results: The primary outcome was the percent change in TPV over 6 months. In 157 participants (L-C N = 76, placebo N = 81), no difference in TPV change between arms was found. The L-C group had a greater increase in carotid atherosclerotic stenosis of 9.3% (p = 0.02) than the placebo group. There was a greater increase in total cholesterol and LDL-C levels in the L-C arm. Conclusions: Though total carotid plaque volume did not change in MetS participants taking L-C over 6-months, there was a concerning progression of carotid plaque stenosis. The potential harm of L-C in MetS and its association with pro-atherogenic metabolites raises concerns for its further use as a potential therapy and its widespread availability as a nutritional supplement. Trial registration: ClinicalTrials.gov, NCT02117661, Registered April 21, 2014, https://clinicaltrials.gov/ct2/show/NCT02117661

    Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA)*

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    Stereo imaging is an important area of image and video processing, with exploding progress in the last decades. An open issue in this field is the understanding of the conditions under which the straightforward application of a given image processing operator to both the left and right image of a stereo pair preserves the stereoscopic perception. In this paper, we explore this problem with application to artistic imaging and we prove that, unlike other methods, artistic operators based on edge preserving smoothing have this desirable property. We also present a novel multiresolution artistic operator, purposely designed for stereo images, which enhances the perception of three-dimensionality by means of a depth driven local scale control.

    Kidney Development in the Absence of Gdnf and Spry1 Requires Fgf10

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    GDNF signaling through the Ret receptor tyrosine kinase (RTK) is required for ureteric bud (UB) branching morphogenesis during kidney development in mice and humans. Furthermore, many other mutant genes that cause renal agenesis exert their effects via the GDNF/RET pathway. Therefore, RET signaling is believed to play a central role in renal organogenesis. Here, we re-examine the extent to which the functions of Gdnf and Ret are unique, by seeking conditions in which a kidney can develop in their absence. We find that in the absence of the negative regulator Spry1, Gdnf, and Ret are no longer required for extensive kidney development. Gdnf−/−;Spry1−/− or Ret−/−;Spry1−/− double mutants develop large kidneys with normal ureters, highly branched collecting ducts, extensive nephrogenesis, and normal histoarchitecture. However, despite extensive branching, the UB displays alterations in branch spacing, angle, and frequency. UB branching in the absence of Gdnf and Spry1 requires Fgf10 (which normally plays a minor role), as removal of even one copy of Fgf10 in Gdnf−/−;Spry1−/− mutants causes a complete failure of ureter and kidney development. In contrast to Gdnf or Ret mutations, renal agenesis caused by concomitant lack of the transcription factors ETV4 and ETV5 is not rescued by removing Spry1, consistent with their role downstream of both RET and FGFRs. This shows that, for many aspects of renal development, the balance between positive signaling by RTKs and negative regulation of this signaling by SPRY1 is more critical than the specific role of GDNF. Other signals, including FGF10, can perform many of the functions of GDNF, when SPRY1 is absent. But GDNF/RET signaling has an apparently unique function in determining normal branching pattern. In contrast to GDNF or FGF10, Etv4 and Etv5 represent a critical node in the RTK signaling network that cannot by bypassed by reducing the negative regulation of upstream signals
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