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Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Neurology) > Mittuniversitetet

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1.
  • Jonsdottir, Ingibjörg H, 1966, et al. (författare)
  • Cognitive impairment in patients with stress-related exhaustion
  • 2013
  • Ingår i: Stress-the International Journal on the Biology of Stress. - : Informa UK Limited. - 1025-3890 .- 1607-8888. ; 16:2, s. 181-190
  • Tidskriftsartikel (refereegranskat)abstract
    • Patients who seek medical care for stress-related mental health problems frequently report cognitive impairments as the most pronounced symptom. The purpose of the present study was to compare cognitive function in patients with stress-related exhaustion with that in healthy controls, using a comprehensive battery of cognitive tests. We also explored whether neuropsychological findings were related to severity of illness measured using the Shirom–Melamed burnout questionnaire and hospital anxiety and depression scale. Thirty-three patients (15 males) and 37 healthy controls (11 males), mean age 46 years [standard deviation (SD) 3.9] and 47 years (SD 4.3), respectively, were included in the final analysis. Five cognitive domains were assessed: (1) speed, attention and working memory, (2) learning and episodic memory, (3) executive functions, (4) visuospatial functions and (5) language. The most pronounced difference between patients and controls was seen on executive function, when tested with a multidimensional test, including aspects of speed, control and working memory. The patients also performed poorer on Digit span, measuring attention span and working memory as well as on learning and episodic memory, when measured as delayed recall and the difference between immediate and delayed recall. Delayed recall was the only test that was significantly related to severity of burnout symptoms among the patients. This could reflect poor cognitive sustainability in the patients with the highest burnout scores, as this particular test was the last one performed during the test session. This study clearly shows that cognitive impairment should be considered when evaluating and treating patients who seek medical care for stress-related exhaustion.
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2.
  • Styrke, Johan, 1980-, et al. (författare)
  • Sex-differences in symptoms, disability, and life satisfaction three years after mild traumatic brain injury : a population-based cohort study
  • 2013
  • Ingår i: Journal of Rehabilitation Medicine. - : Stiftelsen Rehabiliteringsinformation. - 1650-1977 .- 1651-2081. ; 45:8, s. 749-757
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate sex differences in symptoms, structure of symptoms, disability and life satisfaction 3 years after mild traumatic brain injury. Secondary aims were to find risk factors for adverse outcome.DESIGN: Population-based cohort study.Patients: The cohort comprised 137,000 inhabitants at risk in a defined population served by a single hospital in northern Sweden. Patients attending the emergency department following a mild traumatic brain injury in 2001 were included.METHODS: Of 214 patients aged 18–64 years, 163 answered a questionnaire on symptoms, disability, and life-satisfaction 3 years post-injury. The instruments were analysed with descriptive statistics. A principal component analysis of the Rivermead Post-Concussion Symptoms Questionnaire was conducted. Risk factors were identified using logistic regression.RESULTS: Post-concussion syndrome was found in 50% of the women and 30% of the men. Disability was found in 52% of the women and 37% of the men, and 57% of the women and 56% of the men were satisfied with their lives. For both genders, high frequency of symptoms was a risk factor for disability and low life satisfaction. Back pain was a risk factor for disability. Living alone was a risk factor for low levels of life satisfaction. The principal component analysis revealed differences between the sexes.CONCLUSION: There are sex differences in outcome 3 years after mild traumatic brain injury. Women and men should be analysed separately.
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3.
  • Fransson, Eleonor I, et al. (författare)
  • Job strain and the risk of stroke : an individual-participant data meta-analysis
  • 2015
  • Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 46:2, s. 557-559
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND PURPOSE: Psychosocial stress at work has been proposed to be a risk factor for cardiovascular disease. However, its role as a risk factor for stroke is uncertain.METHODS: We conducted an individual-participant-data meta-analysis of 196 380 males and females from 14 European cohort studies to investigate the association between job strain, a measure of work-related stress, and incident stroke.RESULTS: In 1.8 million person-years at risk (mean follow-up 9.2 years), 2023 first-time stroke events were recorded. The age- and sex-adjusted hazard ratio for job strain relative to no job strain was 1.24 (95% confidence interval, 1.05;1.47) for ischemic stroke, 1.01 (95% confidence interval, 0.75;1.36) for hemorrhagic stroke, and 1.09 (95% confidence interval, 0.94;1.26) for overall stroke. The association with ischemic stroke was robust to further adjustment for socioeconomic status.CONCLUSION: Job strain may be associated with an increased risk of ischemic stroke, but further research is needed to determine whether interventions targeting job strain would reduce stroke risk beyond existing preventive strategies.
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4.
  • Kivimäki, Mika, et al. (författare)
  • Body mass index and risk of dementia : Analysis of individual-level data from 1.3 million individuals
  • 2018
  • Ingår i: Alzheimer's & Dementia. - : Elsevier. - 1552-5260 .- 1552-5279. ; 14:5, s. 601-609
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. Methods: We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Results: Hazard ratios per 5-kg/m(2) increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. Conclusions: The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. (C) 2017 The Authors. Published by Elsevier Inc. on behalf of the Alzheimer's Association.
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5.
  • Archer, Trevor, et al. (författare)
  • Physical exercise ameliorates deficits induced by traumatic brain injury
  • 2012
  • Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 125:5, s. 293-302
  • Forskningsöversikt (refereegranskat)abstract
    • The extent and depth of traumatic brain injury (TBI) remains a major determining factor together with the type of structural insult and its location, whether mild, moderate or severe, as well as the distribution and magnitude of inflammation and loss of cerebrovascular integrity, and the eventual efficacy of intervention. The influence of exercise intervention in TBI is multiple, ranging from anti-apoptotic effects to the augmentation of neuroplasticity. Physical exercise diminishes cerebral inflammation by elevating factors and agents involved in immunomodulatory function, and buttresses glial cell, cerebrovascular, and blood-brain barrier intactness. It provides unique non-pharmacologic intervention that incorporate different physical activity regimes, whether dynamic or static, endurance or resistance. Physical training regimes ought necessarily to be adapted to the specific demands of diagnosis, type and degree of injury and prognosis for individuals who have suffered TBI. © 2012 John Wiley & Sons A/S.
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6.
  • Carlsson, Lena, et al. (författare)
  • Myotilin - a prominent marker of myofibrillar remodelling
  • 2007
  • Ingår i: Neuromuscular Disorders. - : Elsevier BV. - 0960-8966 .- 1873-2364. ; 17:1, s. 61-68
  • Tidskriftsartikel (refereegranskat)abstract
    • Myofibrillar remodelling with insertion of sarcomeres is a typical feature of biopsies taken from persons suffering of exercise-induced delayed onset muscle soreness. Here we studied the presence of the sarcomeric protein myotilin in eccentric exercise related lesions. Myotilin is a component of sarcomeric Z-discs and it binds several other Z-disc proteins, i.e. alpha-actinin, filamin C, F-actin and FATZ. Myotilin has previously been shown to be present in nemaline rods and central cores and to be mutated in limb girdle muscular dystrophy 1A (LGMD1A) and in a subset of myofibrillar myopathies, indicating an important role in Z-disc maintenance. Our findings on non-diseased muscle affected by eccentric exercise give new information on how myotilin is associated to myofibrillar components upon remodelling. We show that myotilin was present in increased amount in lesions related to Z-disc streaming and events leading to insertion of new sarcomeres in pre-existing myofibrils and can therefore be used as a marker for myofibrillar remodelling. Interestingly, myotilin is preferentially associated with F-actin rather than with the core Z-disc protein alpha-actinin during these events. This suggests that myotilin has a key role in the dynamic molecular events mediating myofibrillar assembly in normal and diseased skeletal muscle.
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7.
  • Hsiung, Nai-Huan, et al. (författare)
  • Translation, adaptation, and validation of the behavioral pain scale and the critical-care pain observational tools in Taiwan
  • 2016
  • Ingår i: Journal of Pain Research. - Auckland, New Zealand : Dove Medical Press. - 1178-7090. ; 9, s. 661-669
  • Tidskriftsartikel (refereegranskat)abstract
    • This study describes the cultural adaptation and testing of the behavioral pain scale (BPS) and the critical-care pain observation tools (CPOT) for pain assessment in Taiwan. The cross-cultural adaptation followed the steps of translation, including forward translation, back-translation, evaluation of the translations by a committee of experts, adjustments, and then piloting of the prefinal versions of the BPS and the CPOT. A content validity index was used to assess content validities of the BPS and the CPOT, with 0.80 preset as the level that would be regarded as acceptable. The principal investigator then made adjustments when the content validity index was,0.80. The pilot test was performed with a sample of ten purposively selected patients by 2 medical staff from a medical care center in Taiwan. The BPS and the CPOT are adequate instruments for the assessment of pain levels in patients who cannot communicate due to sedation and ventilation treatments.
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8.
  • Naghavi, Mohsen, et al. (författare)
  • Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013
  • 2015
  • Ingår i: The Lancet. - 1474-547X .- 0140-6736. ; 385:9963, s. 117-171
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Up-to-date evidence on levels and trends for age-sex-specifi c all-cause and cause-specifi c mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specifi c all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specifi c causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-year group to sum to all-cause mortality based on draws from the uncertainty distributions. Findings Global life expectancy for both sexes increased from 65.3 years (UI 65.0-65.6) in 1990, to 71.5 years (UI 71.0-71.9) in 2013, while the number of deaths increased from 47.5 million (UI 46.8-48.2) to 54.9 million (UI 53.6-56.3) over the same interval. Global progress masked variation by age and sex: for children, average absolute diff erences between countries decreased but relative diff erences increased. For women aged 25-39 years and older than 75 years and for men aged 20-49 years and 65 years and older, both absolute and relative diff erences increased. Decomposition of global and regional life expectancy showed the prominent role of reductions in age-standardised death rates for cardiovascular diseases and cancers in high-income regions, and reductions in child deaths from diarrhoea, lower respiratory infections, and neonatal causes in low-income regions. HIV/AIDS reduced life expectancy in southern sub-Saharan Africa. For most communicable causes of death both numbers of deaths and age-standardised death rates fell whereas for most non-communicable causes, demographic shifts have increased numbers of deaths but decreased age-standardised death rates. Global deaths from injury increased by 10.7%, from 4.3 million deaths in 1990 to 4.8 million in 2013; but age-standardised rates declined over the same period by 21%. For some causes of more than 100 000 deaths per year in 2013, age-standardised death rates increased between 1990 and 2013, including HIV/AIDS, pancreatic cancer, atrial fibrillation and flutter, drug use disorders, diabetes, chronic kidney disease, and sickle-cell anaemias. Diarrhoeal diseases, lower respiratory infections, neonatal causes, and malaria are still in the top five causes of death in children younger than 5 years. The most important pathogens are rotavirus for diarrhoea and pneumococcus for lower respiratory infections. Country-specific probabilities of death over three phases of life were substantially varied between and within regions. Interpretation For most countries, the general pattern of reductions in age-sex specifi c mortality has been associated with a progressive shift towards a larger share of the remaining deaths caused by non-communicable disease and injuries. Assessing epidemiological convergence across countries depends on whether an absolute or relative measure of inequality is used. Nevertheless, age-standardised death rates for seven substantial causes are increasing, suggesting the potential for reversals in some countries. Important gaps exist in the empirical data for cause of death estimates for some countries; for example, no national data for India are available for the past decade.
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9.
  • Yang, Fei, et al. (författare)
  • Moist smokeless tobacco (Snus) use and risk of Parkinson's disease
  • 2017
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 46:3, s. 872-880
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Cigarette smoking is associated with a lower risk of Parkinson's disease. It is unclear what constituent of tobacco smoke may lower the risk. Use of Swedish moist smokeless tobacco (snus) can serve as a model to disentangle what constituent of tobacco smoke may lower the risk. The aim of this study was to determine whether snus use was associated with a lower risk of Parkinson's disease.METHODS: Individual participant data were collected from seven prospective cohort studies, including 348 601 men. We used survival analysis with multivariable Cox regression to estimate study-specific relative risk of Parkinson's disease due to snus use, and random-effects models to pool estimates in a meta-analysis. The primary analyses were restricted to never-smokers to eliminate the potential confounding effect of tobacco smoking.RESULTS: During a mean follow-up time of 16.1 years, 1199 incident Parkinson's disease cases were identified. Among men who never smoked, ever-snus users had about 60% lower Parkinson's disease risk compared with never-snus users [pooled hazard ratio (HR) 0.41, 95% confidence interval (CI) 0.28-0.61]. The inverse association between snus use and Parkinson's disease risk was more pronounced in current (pooled HR 0.38, 95% CI 0.23-0.63), moderate-heavy amount (pooled HR 0.41, 95% CI 0.19-0.90) and long-term snus users (pooled HR 0.44, 95% CI 0.24-0.83).CONCLUSIONS: Non-smoking men who used snus had a substantially lower risk of Parkinson's disease. Results also indicated an inverse dose-response relationship between snus use and Parkinson's disease risk. Our findings suggest that nicotine or other components of tobacco leaves may influence the development of Parkinson's disease.
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10.
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