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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Neurology) "

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

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61.
  • Midlöv, Patrik, et al. (författare)
  • Medication report reduces number of medication errors when elderly patients are discharged from hospital
  • 2008
  • Ingår i: PHARMACY WORLD & SCIENCE. - : Springer Science and Business Media LLC. - 0928-1231 .- 1573-739X. ; 30:1, s. 92-98
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To investigate whether a Medication Report can reduce the number of medication errors when elderly patients are discharged from hospital. Method We conducted a prospective intervention with retrospective controls on patients at three departments at Lund University Hospital, Sweden that where transferred to primary care. The intervention group, where patients received a Medication Report at discharge, was compared with a control group with patients of the same age, who were not given a Medication Report when discharged from the same ward one year earlier. Main outcome measures The main outcome measure was the number of medication errors when elderly patients were discharged from hospital. Results Among 248 patients in the intervention group 79 (32%) had at least one medication error as compared with 118 (66%) among the 179 patients in the control group. In the intervention group 15% of the patients had errors that were considered to have moderate or high risk of clinical consequences compared with 32% in the control group. The differences were statistically significant (P < 0.001). Conclusion Medication errors are common when elderly patients are discharged from hospital. The Medication Report is a simple tool that reduces the number of medication errors.
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62.
  • Bäckryd, Emmanuel, et al. (författare)
  • High levels of cerebrospinal fluid chemokines point to the presence of neuroinflammation in peripheral neuropathic pain : a cross-sectional study of 2 cohorts of patients compared with healthy controls
  • 2017
  • Ingår i: Pain. - : Ovid Technologies (Wolters Kluwer Health). - 0304-3959 .- 1872-6623. ; 158:12, s. 2487-2495
  • Tidskriftsartikel (refereegranskat)abstract
    • Animal models suggest that chemokines are important mediators in the pathophysiology of neuropathic pain. Indeed, these substances have been called “gliotransmitters,” a term that illustrates the close interplay between glial cells and neurons in the context of neuroinflammation and pain. However, evidence in humans is scarce. The aim of the study was to determine a comprehensive cerebrospinal fluid (CSF) inflammatory profile of patients with neuropathic pain. Our hypothesis was that we would thereby find indications of a postulated on-going process of central neuroinflammation. Samples of CSF were collected from 2 cohorts of patients with neuropathic pain (n = 11 and n = 16, respectively) and healthy control subjects (n = 11). The samples were analyzed with a multiplex proximity extension assay in which 92 inflammation-related proteins were measured simultaneously (Proseek Multiplex Inflammation I; Olink Bioscience, Uppsala, Sweden). Univariate testing with control of false discovery rate, as well as orthogonal partial least squares discriminant analysis, were used for statistical analyses. Levels of chemokines CXCL6, CXCL10, CCL8, CCL11, CCL23 in CSF, as well as protein LAPTGF-beta-1, were significantly higher in both neuropathic pain cohorts compared with healthy controls, pointing to neuroinflammation in patients. These 6 proteins were also major results in a recent similar study in patients with fibromyalgia. The findings need to be confirmed in larger cohorts, and the question of causality remains to be settled. Because it has been suggested that prevalent comorbidities to chronic pain (eg, depression, anxiety, poor sleep, and tiredness) also are associated with neuroinflammation, it will be important to determine whether neuroinflammation is a common mediator.
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63.
  • Pourhamidi, Kaveh, et al. (författare)
  • No difference in small or large nerve fiber function between individuals with normal glucose tolerance and impaired glucose tolerance
  • 2013
  • Ingår i: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 36:4, s. 962-964
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE To assess small and large nerve fiber function in people with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes (T2D).RESEARCH DESIGN AND METHODS Participants were recruited consecutively from a population-based cohort: NGT (n = 39), IGT (n = 29), and T2D (n = 51). Electrophysiological measures included nerve conduction studies and thermal thresholds. Intraepidermal nerve fiber density (IENFD) in skin biopsies was calculated.RESULTS There was no difference between IGT and NGT in sural nerve conduction, IENFD, and thermal thresholds. IENFD was significantly lower in T2D (median = 2.8 fibers/mm [Interquartile range 1.1–4.7 fibers/mm]) than NGT individuals (4.5 fibers/mm [3.4–6.1 fibers/mm]; P < 0.05). T2D participants had poorer nerve conduction and higher heat thresholds than NGT and IGT.CONCLUSIONS Large and small nerve function in people with IGT did not differ from those with NGT. Our finding does not support the existence of neuropathy in a prediabetic stage.
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64.
  • Peny-Dahlstrand, Marie, 1953, et al. (författare)
  • Patterns of participation in school-related activities and settings in children with spina bifida
  • 2013
  • Ingår i: Disability and Rehabilitation. - : Informa UK Limited. - 0963-8288 .- 1464-5165. ; 35:21, s. 1821-1827
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: To evaluate how children with spina bifida (SB) participate in school-related activities and to explore if their motor and process skills in task performance were related to their level of active participation in school. Method: Fifty children from a geographical cohort of children with SB (aged 6-14 years) and their teachers rated the children's frequency of participation in school-related activities using a Swedish adaptation of the Availability and Participation Scale. The teachers also rated each child's level of active participation with the School Function Assessment, part one. Each child's motor and process skills were evaluated with the Assessment of Motor and Process Skills. The relation between levels of active participation and motor and process skills was subjected to binary logistic regression analysis. Results: The children participated very frequently in school activities, but their level of active participation was restricted, particularly in the recess/playground setting. There was a highly significant relation between full active participation in most school settings and the children's motor and process skills. Conclusion: Children with SB need support to become more actively involved, particularly in unstructured peer activities. The school staff need to be informed that not only the motor skills but also the process skills have an impact on the children's active participation.
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65.
  • Ingre, Caroline, 1977-, et al. (författare)
  • A novel phosphorylation site mutation in profilin 1 revealed in a large screen of US, Nordic and German amyotrophic lateral sclerosis/frontotemporal dementia cohorts
  • 2013
  • Ingår i: Neurobiology of Aging. - New York : Elsevier. - 0197-4580 .- 1558-1497. ; 34:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Profilin 1 is a central regulator of actin dynamics. Mutations in the gene profilin 1 (PFN1) have veryrecently been shown to be the cause of a subgroup of amyotrophic lateral sclerosis (ALS). Here, weperformed a large screen of US, Nordic, and German familial and sporadic ALS and frontotemporaldementia (FTLD) patients for PFN1 mutations to get further insight into the spectrum and pathogenicrelevance of this gene for the complete ALS/FTLD continuum. Four hundred twelve familial and 260sporadic ALS cases and 16 ALS/FTLD cases from Germany, the Nordic countries, and the United Stateswere screened for PFN1 mutations. Phenotypes of patients carrying PFN1 mutations were studied. Ina German ALS family we identified the novel heterozygous PFN1 mutation p.Thr109Met, which wasabsent in controls. This novel mutation abrogates a phosphorylation site in profilin 1. The recentlydescribed p.Gln117Gly sequence variant was found in another familial ALS patient from the United States.The ALS patients with mutations in PFN1 displayed spinal onset motor neuron disease without overtcognitive involvement. PFN1 mutations were absent in patients with motor neuron disease anddementia, and in patients with only FTLD. We provide further evidence that PFN1 mutations can causeALS as a Mendelian dominant trait. Patients carrying PFN1 mutations reported so far represent the“classic” ALS end of the ALS-FTLD spectrum. The novel p.Thr109Met mutation provides additional proofof-principle that mutant proteins involved in the regulation of cytoskeletal dynamics can cause motorneuron degeneration. Moreover, this new mutation suggests that fine-tuning of actin polymerization byphosphorylation of profilin 1 might be necessary for motor neuron survival.
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66.
  • Ohlsson, Monica, et al. (författare)
  • Hereditary myopathy with early respiratory failure associated with a mutation in A-band titin
  • 2012
  • Ingår i: Brain. - : Oxford University Press (OUP). - 0006-8950 .- 1460-2156. ; 135:6, s. 1682-1694
  • Tidskriftsartikel (refereegranskat)abstract
    • Hereditary myopathy with early respiratory failure and extensive myofibrillar lesions has been described in sporadic and familial cases and linked to various chromosomal regions. The mutated gene is unknown in most cases. We studied eight individuals, from three apparently unrelated families, with clinical and pathological features of hereditary myopathy with early respiratory failure. The investigations included clinical examination, muscle histopathology and genetic analysis by whole exome sequencing and single nucleotide polymorphism arrays. All patients had adult onset muscle weakness in the pelvic girdle, neck flexors, respiratory and trunk muscles, and the majority had prominent calf hypertrophy. Examination of pulmonary function showed decreased vital capacity. No signs of cardiac muscle involvement were found. Muscle histopathological features included marked muscle fibre size variation, fibre splitting, numerous internal nuclei and fatty infiltration. Frequent groups of fibres showed eosinophilic inclusions and deposits. At the ultrastructural level, there were extensive myofibrillar lesions with marked Z-disc alterations. Whole exome sequencing in four individuals from one family revealed a missense mutation, g.274375T > C; p.Cys30071Arg, in the titin gene (TTN). The mutation, which changes a highly conserved residue in the myosin binding A-band titin, was demonstrated to segregate with the disease in all three families. High density single nucleotide polymorphism arrays covering the entire genome demonstrated sharing of a 6.99 Mb haplotype, located in chromosome region 2q31 including TTN, indicating common ancestry. Our results demonstrate a novel and the first disease-causing mutation in A-band titin associated with hereditary myopathy with early respiratory failure. The typical histopathological features with prominent myofibrillar lesions and inclusions in muscle and respiratory failure early in the clinical course should be incentives for analysis of TTN mutations.
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67.
  • Olivo, G., et al. (författare)
  • Immediate effects of a single session of physical exercise on cognition and cerebral blood flow: A randomized controlled study of older adults
  • 2021
  • Ingår i: Neuroimage. - : Elsevier BV. - 1053-8119 .- 1095-9572. ; 225
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Regular physical activity is beneficial for cognitive performance in older age. A single bout of aerobic physical exercise can transiently improve cognitive performance. Researchers have advanced improvements in cerebral circulation as a mediator of long-term effects of aerobic physical exercise on cognition, but the immediate effects of exercise on cognition and cerebral perfusion are not well characterized and the effects in older adults are largely unknown. Methods: Forty-nine older adults were randomized to a 30-min aerobic exercise at moderate intensity or relaxation. Groups were matched on age and cardiovascular fitness (VO2 max). Average Grey Matter Blood Flow (GMBF), measured by a pulsed arterial-spin labeling (pASL) magnetic resonance imaging (MRI) acquisition, and working memory performance, measured by figurative n-back tasks with increasing loads were assessed before and 7 min after exercising/resting. Results: Accuracy on the n-back task increased from before to after exercising/resting regardless of the type of activity. GMBF decreased after exercise, relative to the control (resting) group. In the exercise group, higher n-back performance after exercise was associated with lower GMBF in the right hippocampus, left medial frontal cortex and right orbitofrontal cortex, and higher cardiovascular fitness was associated with lower GMBF. Conclusion: The decrease of GMBF reported in younger adults shortly after exercise also occurs in older adults and relates to cardiovascular fitness, potentially supporting the link between cardiovascular fitness and cerebrovascular reactivity in older age.
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68.
  • Johansson, Åsa, et al. (författare)
  • Precision medicine in complex diseases - : Molecular subgrouping for improved prediction and treatment stratification
  • 2023
  • Ingår i: Journal of Internal Medicine. - : John Wiley & Sons. - 1365-2796 .- 0954-6820. ; 294:4, s. 378-396
  • Forskningsöversikt (refereegranskat)abstract
    • Complex diseases are caused by a combination of genetic, lifestyle, and environmental factors and comprise common noncommunicable diseases, including allergies, cardiovascular disease, and psychiatric and metabolic disorders. More than 25% of Europeans suffer from a complex disease, and together these diseases account for 70% of all deaths. The use of genomic, molecular, or imaging data to develop accurate diagnostic tools for treatment recommendations and preventive strategies, and for disease prognosis and prediction, is an important step toward precision medicine. However, for complex diseases, precision medicine is associated with several challenges. There is a significant heterogeneity between patients of a specific disease-both with regards to symptoms and underlying causal mechanisms-and the number of underlying genetic and nongenetic risk factors is often high. Here, we summarize precision medicine approaches for complex diseases and highlight the current breakthroughs as well as the challenges. We conclude that genomic-based precision medicine has been used mainly for patients with highly penetrant monogenic disease forms, such as cardiomyopathies. However, for most complex diseases-including psychiatric disorders and allergies-available polygenic risk scores are more probabilistic than deterministic and have not yet been validated for clinical utility. However, subclassifying patients of a specific disease into discrete homogenous subtypes based on molecular or phenotypic data is a promising strategy for improving diagnosis, prediction, treatment, prevention, and prognosis. The availability of high-throughput molecular technologies, together with large collections of health data and novel data-driven approaches, offers promise toward improved individual health through precision medicine.
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69.
  • Munoz-Novoa, Maria, et al. (författare)
  • Upper Limb Stroke Rehabilitation Using Surface Electromyography: A Systematic Review and Meta-Analysis
  • 2022
  • Ingår i: Frontiers in Human Neuroscience. - : Frontiers Media SA. - 1662-5161. ; 16
  • Forskningsöversikt (refereegranskat)abstract
    • Background: Upper limb impairment is common after stroke, and many will not regain full upper limb function. Different technologies based on surface electromyography (sEMG) have been used in stroke rehabilitation, but there is no collated evidence on the different sEMG-driven interventions and their effect on upper limb function in people with stroke. Aim: Synthesize existing evidence and perform a meta-analysis on the effect of different types of sEMG-driven interventions on upper limb function in people with stroke. Methods: PubMed, SCOPUS, and PEDro databases were systematically searched for eligible randomized clinical trials that utilize sEMG-driven interventions to improve upper limb function assessed by Fugl-Meyer Assessment (FMA-UE) in stroke. The PEDro scale was used to evaluate the methodological quality and the risk of bias of the included studies. In addition, a meta-analysis utilizing a random effect model was performed for studies comparing sEMG interventions to non-sEMG interventions and for studies comparing different sEMG interventions protocols. Results: Twenty-four studies comprising 808 participants were included in this review. The methodological quality was good to fair. The meta-analysis showed no differences in the total effect, assessed by total FMA-UE score, comparing sEMG interventions to non-sEMG interventions (14 studies, 509 participants, SMD 0.14, P 0.37, 95% CI –0.18 to 0.46, I2 55%). Similarly, no difference in the overall effect was found for the meta-analysis comparing different types of sEMG interventions (7 studies, 213 participants, SMD 0.42, P 0.23, 95% CI –0.34 to 1.18, I2 73%). Twenty out of the twenty-four studies, including participants with varying impairment levels at all stages of stroke recovery, reported statistically significant improvements in upper limb function at post-sEMG intervention compared to baseline. Conclusion: This review and meta-analysis could not discern the effect of sEMG in comparison to a non-sEMG intervention or the most effective type of sEMG intervention for improving upper limb function in stroke populations. Current evidence suggests that sEMG is a promising tool to further improve functional recovery, but randomized clinical trials with larger sample sizes are needed to verify whether the effect on upper extremity function of a specific sEMG intervention is superior compared to other non-sEMG or other type of sEMG interventions.
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70.
  • Thacher, Jesse D., et al. (författare)
  • Occupational noise exposure and risk of incident stroke: a pooled study of five Scandinavian cohorts
  • 2022
  • Ingår i: OCCUPATIONAL AND ENVIRONMENTAL MEDICINE. - : BMJ. - 1351-0711 .- 1470-7926. ; 79:9, s. 594-601
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives To investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND). Methods We pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (L-Aeq8h): <70, 70-74, 75-79, 80-84, >= 85 dB(A). We identified residential address history and estimated 1-year average road traffic noise at baseline. Using national patient and mortality registers, we identified 7777 stroke cases with a median follow-up of 20.2 years. Analyses were conducted using Cox proportional hazards models adjusting for individual and area-level potential confounders. Results Exposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75-79, 80-84 and >= 85 dB(A) exposure groups, compared with <70 dB(A), respectively. In subanalyses using time-varying occupational noise exposure, we observed an indication of higher stroke risk among the most exposed (>= 85 dB(A)), particularly when restricting analyses to people exposed to occupational noise within the last year (HR: 1.27; 95% CI: 0.99 to 1.63). Conclusions We found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation.
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