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- Janaudis-Ferreira, Tania, et al.
(författare)
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Relationship and responsiveness of three upper-limb tests in patients with chronic obstructive pulmonary disease
- 2013
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Ingår i: Physiotherapy Canada. - : University of Toronto Press Inc. (UTPress). - 0300-0508 .- 1708-8313. ; 65:1, s. 40-43
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: To determine (1) the relationship among three common upper-limb tests for patients with chronic obstructive pulmonary disease (COPD): unsupported upper limb exercise test (UULEX), 6-minute pegboard and ring test (6PBRT), and a muscle-strength test using a hand-held dynamometer; and (2) the responsiveness of these three tests to changes after pulmonary rehabilitation that included a resistance arm-training programme.Methods: The study was a secondary analysis of a randomized controlled trial (RCT). The UULEX and the 6PBRT were used to measure peak arm exercise capacity and arm function, respectively. A handheld dynamometer was used to measure elbow and shoulder flexion force. We analyzed baseline data for all participants in the ACT, as well as baseline and post-PR data for those who completed 6-week follow-up testing.Results: 36 patients with COPD (mean forced expiratory volume in 1 second [FEV1] = 35% [SD 15%] predicted; age 66 [9] y) participated, of whom 13 completed an arm-training programme. The correlations among the test results ranged from 0.41 to 0.81 (p < 0.0001). Standardized response means were 1.0 for muscle force of elbow flexion, 1.2 for shoulder flexion, and 1.8 for the 6PBRT and UULEX.Conclusions: Although the three tests (UULEX, 6PBRT, and muscle-strength test using a hand-held dynamometer) are intended to measure different constructs, they were moderately to highly correlated with one another. The 6PBRT, UULEX, and muscle-strength test were demonstrated to be responsive to the resistance arm-training programme.
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- Janaudis-Ferreira, Tania, 1976-, et al.
(författare)
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Resistance arm training in patients with chronic obstructive pulmonary disease : a randomized controlled trial
- 2011
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Ingår i: Chest. - : American College of Chest Physicians. - 0012-3692 .- 1931-3543. ; 139:1, s. 151-158
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The study aimed to evaluate the effect of upper extremity resistance training for patients with COPD on dyspnea during activity of daily living (ADL), arm function, arm exercise capacity, muscle strength and health related quality of life (HRQL)METHODS: Patients were randomly assigned to an intervention or control group. The intervention group underwent arm resistance training. The control group performed a sham. Both groups exercised 3 times a week for 6 weeks. Dyspnea during ADL and HRQL were measured using the chronic respiratory disease questionnaire (CRDQ). Arm function and exercise capacity were measured using the 6-minute pegboard and ring test (6PBRT) and the unsupported upper limb exercise test (UULEX), respectively. Muscle strength for the biceps, triceps, anterior and middle deltoids was obtained using an isometric dynamometer.RESULTS: Thirty-six patients with COPD (66 +/- 9 yrs) participated in the study. Compared with the control group, the magnitude of change in the intervention group was greater for the 6PBRT (p = 0.03), UULEX (p = 0.01) and elbow flexion force (p = 0.01); elbow extension force (p = 0.02), shoulder flexion force (p = 0.029) and shoulder abduction force (p = 0.01). There was no between-group difference in dyspnea during ADL, HRQL or symptoms during the 6PBRT or UULEX (all p values greater than 0.08).CONCLUSIONS: Resistance based arm training improved arm function, arm exercise capacity and muscle strength in patients with COPD. No improvement in dyspnea during ADL, HRQL or symptoms was demonstrated.
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- Jansen, Willemijn J, et al.
(författare)
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Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum.
- 2022
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Ingår i: JAMA neurology. - : American Medical Association (AMA). - 2168-6157 .- 2168-6149. ; 79:3, s. 228-243
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Tidskriftsartikel (refereegranskat)abstract
- One characteristic histopathological event in Alzheimer disease (AD) is cerebral amyloid aggregation, which can be detected by biomarkers in cerebrospinal fluid (CSF) and on positron emission tomography (PET) scans. Prevalence estimates of amyloid pathology are important for health care planning and clinical trial design.To estimate the prevalence of amyloid abnormality in persons with normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia and to examine the potential implications of cutoff methods, biomarker modality (CSF or PET), age, sex, APOE genotype, educational level, geographical region, and dementia severity for these estimates.This cross-sectional, individual-participant pooled study included participants from 85 Amyloid Biomarker Study cohorts. Data collection was performed from January 1, 2013, to December 31, 2020. Participants had normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia. Normal cognition and subjective cognitive decline were defined by normal scores on cognitive tests, with the presence of cognitive complaints defining subjective cognitive decline. Mild cognitive impairment and clinical AD dementia were diagnosed according to published criteria.Alzheimer disease biomarkers detected on PET or in CSF.Amyloid measurements were dichotomized as normal or abnormal using cohort-provided cutoffs for CSF or PET or by visual reading for PET. Adjusted data-driven cutoffs for abnormal amyloid were calculated using gaussian mixture modeling. Prevalence of amyloid abnormality was estimated according to age, sex, cognitive status, biomarker modality, APOE carrier status, educational level, geographical location, and dementia severity using generalized estimating equations.Among the 19097 participants (mean [SD] age, 69.1 [9.8] years; 10148 women [53.1%]) included, 10139 (53.1%) underwent an amyloid PET scan and 8958 (46.9%) had an amyloid CSF measurement. Using cohort-provided cutoffs, amyloid abnormality prevalences were similar to 2015 estimates for individuals without dementia and were similar across PET- and CSF-based estimates (24%; 95% CI, 21%-28%) in participants with normal cognition, 27% (95% CI, 21%-33%) in participants with subjective cognitive decline, and 51% (95% CI, 46%-56%) in participants with mild cognitive impairment, whereas for clinical AD dementia the estimates were higher for PET than CSF (87% vs 79%; mean difference, 8%; 95% CI, 0%-16%; P=.04). Gaussian mixture modeling-based cutoffs for amyloid measures on PET scans were similar to cohort-provided cutoffs and were not adjusted. Adjusted CSF cutoffs resulted in a 10% higher amyloid abnormality prevalence than PET-based estimates in persons with normal cognition (mean difference, 9%; 95% CI, 3%-15%; P=.004), subjective cognitive decline (9%; 95% CI, 3%-15%; P=.005), and mild cognitive impairment (10%; 95% CI, 3%-17%; P=.004), whereas the estimates were comparable in persons with clinical AD dementia (mean difference, 4%; 95% CI, -2% to 9%; P=.18).This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. This finding suggests that preclinical and prodromal AD may be more prevalent than previously estimated, which has important implications for clinical trial recruitment strategies and health care planning policies.
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- Sampson, Joshua N., et al.
(författare)
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Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
- 2015
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 107:12
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Tidskriftsartikel (refereegranskat)abstract
- Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
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