62 research outputs found

    Determinants of physical activity participation following traumatic brain injury

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    Aims The objective of the study described in this article was to establish the environmental, social, or personal determinants associated with physical activity participation in people with traumatic brain injury (TBI). Methods A multi-centre cross-sectional questionnaire survey using a convenience sample was used at eight community day centres for brain injured populations. The participants were 63 individuals with traumatic brain injury (51 male, 12 female). Physical activity participation was based on the proportion of participants achieving the level of physical activity recommended for health (30 mins moderate activity, most days of the week). Standardized measures were used to assess activities of daily living (Extended Activities of Daily Living Scale), self-efficacy (Self-Efficacy for Exercise Scale), social support (Social Support for Exercise Scale) and mood (General Health Questionnaire-12). Findings Over half the participants were not active enough for health benefit. Active participants were more independent in activities of daily living (t = -2.21, P < 0.05), had greater self-efficacy for exercise (t = -3.02, P < 0.05) and were more educated (χ2=5.61, P<0.05) than inactive participants. Logistic Regression showed self-efficacy for exercise to be the only significant predictor of physical activity participation (ÎČ = 0.32, OR 1.03, P < 0.05). Conclusions Self-efficacy predicted physical activity participation. Efforts to increase self-efficacy among brain injured participants may encourage activity participation in those who are able and this warrants further investigation

    Incidence trend and risk factors for campylobacter infections in humans in Norway

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    BACKGROUND: The objectives of the study were to evaluate whether the increase in incidence of campylobacteriosis observed in humans in Norway from 1995 to 2001 was statistically significant and whether different biologically plausible risk factors were associated with the incidence of campylobacteriosis in the different counties in Norway. METHODS: To model the incidence of domestically acquired campylobacteriosis from 1995 to 2001, a population average random effect poisson model was applied (the trend model). To case data and assumed risk-factor/protective data such as sale of chicken, receiving treated drinking water, density of dogs and grazing animals, occupation of people in the municipalities and climatic factors from 2000 and 2001, an equivalent model accounting for geographical clustering was applied (the ecological model). RESULTS: The increase in incidence of campylobacteriosis in humans in Norway from 1995 to 2001 was statistically significant from 1998. Treated water was a protective factor against Campylobacter infections in humans with an IRR of 0.78 per percentage increase in people supplied. The two-level modelling technique showed no evidence of clustering of campylobacteriosis in any particular county. Aggregation of data on municipality level makes interpretation of the results at the individual level difficult. CONCLUSION: The increase in incidence of Campylobacter infections in humans from 1995 to 2001 was statistically significant from 1998. Treated water was a protective factor against Campylobacter infections in humans with an IRR of 0.78 per percentage increase in people supplied. Campylobacter infections did not appear to be clustered in any particular county in Norway

    Levofloxacin versus placebo for the prevention of tuberculosis disease in child contacts of multidrug-resistant tuberculosis: study protocol for a phase III cluster randomised controlled trial (TB-CHAMP)

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    Background Multidrug-resistant (MDR) tuberculosis (TB) presents a challenge for global TB control. Treating individuals with MDR-TB infection to prevent progression to disease could be an effective public health strategy. Young children are at high risk of developing TB disease following infection and are commonly infected by an adult in their household. Identifying young children with household exposure to MDR-TB and providing them with MDR-TB preventive therapy could reduce the risk of disease progression. To date, no trials of MDR-TB preventive therapy have been completed and World Health Organization guidelines suggest close observation with no active treatment. Methods The tuberculosis child multidrug-resistant preventive therapy (TB-CHAMP) trial is a phase III cluster randomised placebo-controlled trial to assess the efficacy of levofloxacin in young child contacts of MDR-TB cases. The trial is taking place at three sites in South Africa where adults with MDR-TB are identified. If a child aged < 5 years lives in their household, we assess the adult index case, screen all household members for TB disease and evaluate any child aged < 5 years for trial eligibility. Eligible children are randomised by household to receive daily levofloxacin (15–20 mg/kg) or matching placebo for six months. Children are closely monitored for disease development, drug tolerability and adverse events. The primary endpoint is incident TB disease or TB death by one year after recruitment. We will enrol 1556 children from approximately 778 households with an average of two eligible children per household. Recruitment will run for 18–24 months with all children followed for 18 months after treatment. Qualitative and health economic evaluations are embedded in the trial. Discussion If the TB-CHAMP trial demonstrates that levofloxacin is effective in preventing TB disease in young children who have been exposed to MDR-TB and that it is safe, well tolerated, acceptable and cost-effective, we would expect that that this intervention would rapidly transfer into policy. Trial registration ISRCTN Registry, ISRCTN92634082. Registered on 31 March 2016

    Outcomes from elective colorectal cancer surgery during the SARS-CoV-2 pandemic

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    This study aimed to describe the change in surgical practice and the impact of SARS-CoV-2 on mortality after surgical resection of colorectal cancer during the initial phases of the SARS-CoV-2 pandemic

    Medicaid Enrollment among Elderly Medicare Beneficiaries: Individual Determinants, Effects of State Policy, and Impact on Service Use

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    OBJECTIVE: To better understand factors associated with Medicaid enrollment among low-income, community-dwelling elderly persons and to examine the effect of Medicaid enrollment on the use of health care services by elderly persons, taking into account selection in program participation. DATA SOURCES: 1996 Medicare Current Beneficiary Survey (MCBS) Access to Care and Cost and Use files. METHODS: Individual-level predictions of the probability of dual enrollment are obtained from equations that estimate jointly the residential status of Medicare beneficiaries (community versus institution) and the probability of Medicaid enrollment among community-dwelling eligible beneficiaries. Predicted values are then substituted into the service use equations, which are estimated via two-part models. PRINCIPAL FINDINGS: Less than half of all community-dwelling elderly persons with incomes at or below 100 percent of the Federal Poverty Level (FPL) were enrolled in Medicaid in 1996. Once selective enrollment was accounted for, there was limited evidence of a dual enrollment effect on service use. Although there were no effects of state Medicaid policy variables on the probability that beneficiaries lived in the community (as opposed to nursing homes), the effects of state's Medicaid generosity in home and community-based services had a sizeable and statistically significant effect on influencing the likelihood that eligible elderly persons enrolled in Medicaid. CONCLUSIONS: Our results provide compelling evidence that Medicaid participation can be influenced by state policy. The observation that “policy matters” provides new insights into how existing programs might reach a larger proportion of potentially eligible beneficiaries

    Reduced glucocerebrosidase is associated with increased &#945;-synuclein in sporadic Parkinsons disease

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    Heterozygous mutations in GBA1, the gene encoding lysosomal glucocerebrosidase, are the most frequent known genetic risk factor for Parkinsons disease. Reduced glucocerebrosidase and &#945;-synuclein accumulation are directly related in cell models of Parkinsons disease. We investigated relationships between Parkinsons disease-specific glucocerebrosidase deficits, glucocerebrosidase-related pathways, and &#945;-synuclein levels in brain tissue from subjects with sporadic Parkinsons disease without GBA1 mutations. Brain regions with and without a Parkinsons disease-related increase in &#945;-synuclein levels were assessed in autopsy samples from subjects with sporadic Parkinsons disease (n = 19) and age- and postmortem delay-matched controls (n = 10). Levels of glucocerebrosidase, &#945;-synuclein and related lysosomal and autophagic proteins were assessed by Western blotting. glucocerebrosidase enzyme activity was measured using a fluorimetric assay, and glucocerebrosidase and &#945;-synuclein mRNA expression determined by quantitative PCR. Related sphingolipids were analyzed by mass spectrometry. Multivariate statistical analyses were performed to identify differences between disease groups and regions, with non-parametric correlations used to identify relationships between variables. glucocerebrosidase protein levels and enzyme activity were selectively reduced in the early stages of Parkinsons disease in regions with increased &#945;-synuclein levels although limited inclusion formation, while GBA1 mRNA expression was non-selectively reduced in Parkinsons disease. The selective loss of lysosomal glucocerebrosidase was directly related to reduced lysosomal chaperone-mediated autophagy, increased &#945;-synuclein and decreased ceramide. glucocerebrosidase deficits in sporadic Parkinsons disease are related to the abnormal accumulation of &#945;-synuclein and are associated with substantial alterations in lysosomal chaperone-mediated autophagy pathways and lipid metabolism. Our data suggest that the early selective Parkinsons disease changes are likely due to the redistribution of cellular membrane proteins leading to a chronic reduction in lysosome function in brain regions vulnerable to Parkinsons disease pathology
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