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- Jokinen, H, et al.
(author)
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Incident lacunes influence cognitive decline: the LADIS study.
- 2011
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In: Neurology. - 0028-3878 .- 1526-632X. ; 76:22, s. 1872-8
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Journal article (peer-reviewed)abstract
- In cerebral small vessel disease, the core MRI findings include white matter lesions (WML) and lacunar infarcts. While the clinical significance of WML is better understood, the contribution of lacunes to the rate of cognitive decline has not been established. This study investigated whether incident lacunes on MRI determine longitudinal cognitive change in elderly subjects with WML.
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- Austeng, Dordi, et al.
(author)
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Treatment for retinopathy of prematurity in infants born before 27 weeks of gestation in Sweden
- 2010
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In: British Journal of Ophthalmology. - : BMJ. - 0007-1161 .- 1468-2079. ; 94:9, s. 1136-1139
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Journal article (peer-reviewed)abstract
- AIMS: To study various aspects of treatment for retinopathy of prematurity (ROP) in a Swedish population of extremely preterm infants born before 27 weeks of gestation. METHODS: A national, prospective and population-based study was performed in Sweden from April 1, 2004 to March 31, 2007. The criteria for treatment of ROP accorded with the recommendations of the Early Treatment for Retinopathy of Prematurity Cooperative Group. RESULTS: Twenty percent of the infants (99/506) were treated for ROP. The likelihood of reaching treatment criteria nearly doubled for each week of reduction in gestational age (GA) at birth. The first treatment was performed at an earlier postmenstrual age in the most immature infants. One third of the infants had more than one session of laser treatment. CONCLUSIONS: A high percentage of these extremely preterm infants required treatment for ROP. The likelihood of reaching treatment criteria increased with a decline in GA at birth. Although only a few infants progressed to ROP Stages 4 and 5, our findings indicate a potential for improvement of the treatment routines, both regarding timing and number of laser spots at the first treatment.
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- Barnes, J. N., et al.
(author)
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Aging enhances autonomic support of blood pressure in women
- 2014
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In: Hypertension. - 0194-911X .- 1524-4563. ; 63:2, s. 303-308
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Journal article (peer-reviewed)abstract
- The autonomic nervous system plays a central role in both acute and chronic blood pressure regulation in humans. The activity of the sympathetic branch of the autonomic nervous system is positively associated with peripheral resistance, an important determinant of mean arterial pressure in men. In contrast, there is no association between sympathetic nerve activity and peripheral resistance in women before menopause, yet a positive association after menopause. We hypothesized that autonomic support of blood pressure is higher after menopause in women. We examined the effect of ganglionic blockade on arterial blood pressure and how this relates to baseline muscle sympathetic nerve activity in 12 young (25±1 years) and 12 older postmenopausal (61±2 years) women. The women were studied before and during autonomic blockade using trimethaphan camsylate. At baseline, muscle sympathetic nerve activity burst frequency and burst incidence were higher in the older women (33±3 versus 15±1 bursts/min; 57±5 versus 25±2 bursts/100 heartbeats, respectively; P<0.05). Muscle sympathetic nerve activity bursts were abolished by trimethaphan within minutes. Older women had a greater decrease in mean arterial pressure (-29±2 versus-9±2 mm Hg; P<0.01) and total peripheral resistance (-10±1 versus-5±1 mm Hg/L per minute; P<0.01) during trimethaphan. Baseline muscle sympathetic nerve activity was associated with the decrease in mean arterial pressure during trimethaphan (r=-0.74; P<0.05). In summary, our results suggest that autonomic support of blood pressure is greater in older women compared with young women and that elevated sympathetic nerve activity in older women contributes importantly to the increased incidence of hypertension after menopause. © 2013 American Heart Association, Inc.
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- Curtin, W. A., et al.
(author)
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Hybrid discrete dislocation models for fatigue crack growth
- 2010
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In: International Journal of Fatigue. - : Elsevier BV. - 1879-3452 .- 0142-1123. ; 32:9, s. 1511-1520
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Journal article (peer-reviewed)abstract
- A framework for accurately modeling fatigue crack growth in ductile crystalline solids is necessarily multiscale The creation of new free surface occurs at the atomistic scale, where the material's cohesive strength is controlled by the local chemistry On the other hand, significant dissipation during fatigue crack growth takes place at a size scale that can be modeled appropriately by conventional continuum mechanics. The intermediate size scale where the discreteness of dislocations comes Into play is the main origin of the hysteresis needed for fatigue and of the high stresses required for atomistic separation to take place. We focus on recent developments which permit analyses of fatigue crack growth involving the direct coupling of disparate size scales. Although no analyses have been carried out directly coupling size scales from the atomic to the conventional continuum, the ingredients to do so are in place. We provide background that illustrates the key role played by the intermediate discrete dislocation size scale and review steps that have been taken to permit direct size scale coupling. The prospects and modeling needs for further developments are also discussed (C) 2009 Elsevier Ltd All rights reserved.
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- Firbank, M. J., et al.
(author)
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Relationship between progression of brain white matter changes and late-life depression: 3-year results from the LADIS study
- 2012
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In: British Journal of Psychiatry. - : Royal College of Psychiatrists. - 0007-1250 .- 1472-1465. ; 201:1, s. 40-45
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Journal article (peer-reviewed)abstract
- Background Brain white matter changes (WMC) and depressive symptoms are linked, but the directionality of this association remains unclear. Aims To investigate the relationship between baseline and incident depression and progression of white matter changes. Method In a longitudinal multicentre pan-European study (Leukoaraiosis and Disability in the elderly, LADIS), participants aged over 64 underwent baseline magnetic resonance imaging (MRI) and clinical assessments. Repeat scans were obtained at 3 years. Depressive outcomes were assessed in terms of depressive episodes and the Geriatric Depression Scale (GDS). Progression of WMC was measured using the modified Rotterdam Progression scale. Results Progression of WMC was significantly associated with incident depression during year 3 of the study (P = 0.002) and remained significant after controlling for transition to disability, baseline WMC and baseline history of depression. There was no significant association between progression of WMC and GDS score, and no significant relationship between progression of WMC and history of depression at baseline. Conclusions Our results support the vascular depression hypothesis and implicate WMC as causal in the pathogenesis of late-life depression.
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- Jokinen, H., et al.
(author)
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Brain atrophy accelerates cognitive decline in cerebral small vessel disease The LADIS study
- 2012
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In: Neurology. - 0028-3878. ; 78:22, s. 1785-1792
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Journal article (peer-reviewed)abstract
- Objective: To examine the independent contributions and combined interactions of medial temporal lobe atrophy (MTA), cortical and subcortical atrophy, and white matter lesion (WML) volume in longitudinal cognitive performance. Methods: A total of 477 subjects with age-related WML were evaluated with brain MRI and annual neuropsychological examinations in 3-year follow-up. Baseline MRI determinants of cognitive decline were analyzed with linear mixed models controlling for multiple confounders. Results: MTA and subcortical atrophy predicted significantly steeper rate of decline in global cognitive measures as well as compound scores for psychomotor speed, executive functions, and memory after adjusting for age, gender, education, lacunes/infarcts, and WML volume. Cortical atrophy independently predicted decline in psychomotor speed. WML volume remained significantly associated with cognitive decline even after controlling for the atrophy scores. Moreover, significant synergistic interactions were found between WML and atrophy measures in overall cognitive performance across time and the rate of cognitive decline. Synergistic effects were also observed between baseline lacunar infarcts and all atrophy measures on change in psychomotor speed. The main results remained robust after exclusion of subjects with clinical stroke or incident dementia, and after additional adjustments for progression of WML and lacunes. Conclusions: Brain atrophy and WML are independently related to longitudinal cognitive decline in small vessel disease. MTA, subcortical, and cortical atrophy seem to potentiate the effect of WML and lacunes on cognitive decline. Neurology (R) 2012;78:1785-1792
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- Lawlor, B., et al.
(author)
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NILVAD protocol: A European multicentre double-blind placebo-controlled trial of nilvadipine in mild-to-moderate Alzheimer's disease
- 2014
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In: BMJ Open. - : BMJ Publishing Group. - 2044-6055. ; 4:10
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Journal article (peer-reviewed)abstract
- Introduction: This study is a European multicentre, randomised, double-blind, placebo-controlled trial investigating the efficacy and safety of nilvadipine as a disease course modifying treatment for mild-to-moderate Alzheimer's disease (AD) in a phase III study that will run for a period of 82 weeks with a treatment period of 78 weeks. Methods and analysis: Adult patients, males and females over 50 years with mild-to-moderate AD as defined by the National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's disease and Related Disorders Association (NINCDSADRDA) criteria, will be included in the study. It aims to recruit a total of 500 patients with AD; 250 in the nilvadipine group and 250 in the placebo group. Participants will be randomised to receive nilvadipine, an 8 mg overencapsulated, sustained release capsule, or a matching overencapsulated placebo (sugar pill) for a period of 78 weeks of treatment. The primary efficacy outcome measure in this study is the change in cognitive function as assessed by the Alzheimer's disease Assessment Scale (ADASCog 12) from baseline to the end of treatment duration (78 weeks). There are two key secondary outcome measures, the Clinical Dementia Rating Scale Sum of Boxes (CDRsb) and the Disability Assessment for Dementia (DAD). If a statistically significant effect is seen in the primary outcome, CDRsb will be considered to be a coprimary end point and only the DAD will contribute to the secondary outcome analysis. Ethics and dissemination: The study and all subsequent amendments have received ethical approval within each participating country according to national regulations. Each participant will provide written consent to participate in the study. All participants will remain anonymised throughout and the results of the study will be published in an international peerreviewed journal. Trial registration number EUDRACT Reference Number: 201200276427.
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10. |
- Poggesi, A., et al.
(author)
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Cerebral white matter changes are associated with abnormalities on neurological examination in non-disabled elderly: the LADIS study
- 2013
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In: Journal of Neurology. - : Springer Science and Business Media LLC. - 0340-5354 .- 1432-1459. ; 260:4, s. 1014-1021
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Journal article (peer-reviewed)abstract
- Cerebral white matter changes (WMC) are associated with motor, cognitive, mood, urinary disturbances, and disability, but little is known about the prevalence of neurological signs in patients with these brain lesions. We assessed the presence and occurrence of neurological abnormalities over a 3-year period and their possible associations with WMC in a cohort of initially non-disabled elderly subjects. Data from the multicenter Leukoaraiosis And DISability study were used. A standard neurological examination was performed at baseline and at each of the annual follow-up visits. A standard MRI scan was performed at baseline and after 3-years. WMC severity was graded as mild, moderate, or severe on the Fazekas scale, while the Rotterdam scale was used to assess progression. Infarcts and their occurrence were also assessed. Six hundred and thirty-nine non-disabled subjects were enrolled (mean age 74.1 +/- A 5.0, M/F: 288/351). Severe WMC at baseline were associated with gait and stance abnormalities, upper motor signs, and fingertap slowing. This effect was independent of age, sex, lacunar and non-lacunar infarcts. The occurrence of stance abnormalities, upper motor signs, primitive reflexes and fingertap slowing during the 3-year follow-up period was associated with both baseline WMC load and their progression. The occurrence of the same abnormalities plus extrapyramidal and primitive reflexes was associated with incident lacunar infarcts. In our cohort of non-disabled elders, severe WMC were associated with the presence and the occurrence of neurological signs, independently of other vascular brain lesions, confirming that these lesions have clinical relevance.
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