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  • 1.
    Archer, Trevor
    et al.
    Linnaeus University, Faculty of Health, Social Work and Behavioural Sciences, School of Education, Psychology and Sport Science. University of Gothenburg.
    Svensson, Kjell
    Linnaeus University, Faculty of Health, Social Work and Behavioural Sciences, School of Education, Psychology and Sport Science.
    Alricsson, Marie
    Linnaeus University, Faculty of Health, Social Work and Behavioural Sciences, School of Education, Psychology and Sport Science. Mittuniversitetet, Institutionen för hälsovetenskap.
    Physical exercise ameliorates deficits induced by traumatic brain injury2012In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 125, no 5, p. 293-302Article, review/survey (Refereed)
    Abstract [en]

    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.

  • 2.
    Bengtsson, D
    et al.
    Kalmar Cty Hosp, Sweden.
    Brudin, L
    Kalmar Cty Hosp, Sweden.
    Wanby, Pär
    Kalmar Cty Hosp, Sweden.
    Carlsson, Martin
    Kalmar Cty Hosp, Sweden.
    Previously unknown thyroid dysfunction in patients with acute ischemic stroke.2012In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 126, no 2, p. 98-102Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Opinions differ regarding the clinical significance of subclinical thyroid disorders. The aim of the present study was to evaluate the prevalence and influence of previously unknown overt or subclinical thyroid dysfunction in patients with acute ischemic stroke and to look for differences between cardio-embolic and non-embolic ischemic stroke.

    MATERIAL AND METHODS: A total of 153 Swedish patients diagnosed with first-time acute ischemic stroke were included in the study and categorized for suspected cardio-embolic (n = 30) or non-embolic (n = 123) ischemic stroke depending on the presence of atrial fibrillation (AF). Blood samples were taken 48 h or earlier after onset of stroke symptoms.

    RESULTS: Previously, unknown overt or subclinical thyroid dysfunction was found in 12%. Previously, unknown overt or subclinical hyperthyroidism was more common in the AF group (13%) compared to the non-AF group (3%), P = 0.048. Patients with AF had slightly higher concentrations of free T4 (15 vs 14 pm; P < 0.001), but there was no significant difference in concentrations of S-TSH or prevalence of thyroperoxidase (TPO) antibodies between the groups.

    CONCLUSIONS: In patients with first-time acute ischemic stroke, unknown thyroid dysfunction is common, and unknown overt or subclinical hyperthyroidism is associated with cardio-embolic stroke.

  • 3.
    Wanby, Pär
    et al.
    Region Kalmar län.
    Nilsson, I
    Brudin, L
    Nyhammar, I
    Gustafsson, I
    Carlsson, Martin
    Increased plasma levels of asymmetric dimethylarginine in patients with carotid stenosis: no evidence for the role of the common FABP2 A54T gene polymorphism.2007In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 115, no 2, p. 90-96Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Both asymmetric dimethylarginine (ADMA), which is an inhibitor of endothelial nitric oxide synthase and the fatty acid-binding protein 2 (FABP2) A54T gene polymorphism have been associated with cerebrovascular disease. The objective of the present study was to investigate the role of ADMA and the FABP2 A54T polymorphism in carotid atherosclerosis.

    MATERIAL AND METHODS: 54 patients with severe carotid stenosis and 54 matched controls without significant carotid stenosis were compared. ADMA was analysed with an ELISA method. The FABP2 A54T polymorphism was determined with a polymerase chain reaction-restriction fragment length polymorphism technique.

    RESULTS: Patients with carotid stenosis had higher ADMA levels (0.76 +/- 0.16 micromol/l) than the controls (0.70 +/- 0.14 micromol/l, P < 0,01). Allele and genotype frequencies of the FABP2 polymorphism did not differ between patients and controls.

    CONCLUSIONS: ADMA levels in subjects with carotid stenosis are increased which emphasize the role of ADMA as a novel risk factor for atherosclerosis and future cardiovascular risk. The FABP2 A54T polymorphism is not associated with severe carotid stenosis.

  • 4.
    Wanby, Pär
    et al.
    Region Kalmar län.
    Palmquist, P
    Rydén, I
    Brattström, L
    Carlsson, Martin
    The FABP2 gene polymorphism in cerebrovascular disease.2004In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 110, no 6, p. 355-360Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Earlier studies have shown that the fatty acid binding protein 2 (FABP2) T54 allele is associated with dyslipidemia, which in turn correlates with the incidence of cerebrovascular disease (CVD). To assess whether the FABP2 gene A54T polymorphism is associated with an increased risk of CVD we undertook a case-control study.

    MATERIALS AND METHODS: A total of 407 patients diagnosed with acute CVD and 158 control subjects were genotyped for the A54T polymorphism using a PCR-RFLP method.

    RESULTS: Allele and genotype frequencies of the FABP2 A54T polymorphism did not differ between subjects with acute CVD (TT, 9.6%; TA, 41.0%; AA, 49.4%) and controls (TT, 7.6%; TA, 41.1%; AA, 51.3%; P = ns) or in the following subgroups of CVD compared with controls: non-cardioembolic infarction (n = 252), intracerebral hemorrhage (n = 23), and cardioembolic infarction (n = 91). In transient ischemic attacks (TIAs) (n = 41) the combined TT and TA genotype frequency (TT + TA, 65.9%) was more frequent than in controls (48.7%) (P = 0.05). Furthermore, the TT genotype was more frequent in non-smoking patients under the age of 70 (n = 77) with a non-cardioembolic infarction (TT, 18.2%) compared with controls (7.6%) (P = 0.024).

    CONCLUSIONS: Our findings suggest an involvement of the FABP2 (A54T) gene polymorphism in the pathogenesis of CVD. The FABP2 T54 allele appears to be a genetic susceptibility marker for TIA and non-cardioembolic infarction at younger onset.

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