To examine prospective associations between chronic stress in the parent-child and family systems and subsequent rates of illnesses and the activity of natural killer (NK) cells in children.
Design
Prospective cohort study.
Setting
The Golisano Children's Hospital at Strong, Rochester, NY, from July 1, 2001, to June 30, 2003.
Participants
One hundred sixty-nine socioeconomically and racially diverse children (aged 5-10 years) and their parents. Parents completed measures of their psychiatric symptoms and stress in the family every 6 months. Children's blood samples were obtained for NK cytotoxicity assays every 6 months.
Main Outcome Measures
Parent-reported total child illnesses and febrile illnesses and results of NK cell cytotoxicity assays. We estimated adjusted illness rate ratios and adjusted mean differences in NK activity.
Results
Elevated parental psychiatric symptoms occurring with family stressors were associated with more total illnesses (rate ratio, 1.11; 95% confidence interval [CI], 1.00-1.22) and febrile illnesses (rate ratio, 1.36; 95% CI, 1.13-1.64) in children. Natural killer cell function was enhanced in children whose parents reported more chronic stress (estimate, 0.15; 95% CI, 0.05-0.26). Natural killer cell function was not associated with short-term changes in stress. Stress-illness relationships were not associated with stress-related alterations in NK cell function.
Conclusions
Chronic family stress was associated with increased illnesses in children. Unlike older adults, children living with elevated chronic stress had enhanced rather than decreased NK cytotoxicity, suggesting chronic stress may have different effects on the developing immune system. Impaired parental functioning may be a mechanism linking family stress with adverse effects on children's health.
We hypothesized that specific mutations in the β-glucocerebrosidase gene (GBA) causing neuropathic Gaucher's disease (GD) in homozygotes lead to aggressive cognitive decline in heterozygous Parkinson's disease (PD) patients, whereas non-neuropathic GD mutations confer intermediate progression rates.
Background. Dust control is recommended as one of the primary strategies to prevent or control children's exposure to residential lead hazards, but the effect of dust control on children's blood lead levels is poorly understood. Objective. To determine the effectiveness of dust control in preventing children's exposure to lead, as measured by blood lead levels, during their peak age of susceptibility. Design. A randomized, controlled trial. Setting. Rochester, NY. Participants. A total of 275 urban children were randomized at 6 months of age, of whom 246 (90%) were available for the 24-month-old follow-up visit. Interventions. Children and their families were randomly assigned to an intervention group (n = 140), which received cleaning equipment and up to eight visits by a dust control advisor, or a control group (n = 135). Outcome Measures. Geometric mean blood lead levels and prevalence of elevated blood lead levels (ie, >10 μg/dL, 15 μg/dL, and 20 μg/dL). Results. At baseline, children's geometric mean blood lead levels were 2.9 μg/dL (95% confidence interval [CI] = 2.7, 3.1); there were no significant differences in characteristics or lead exposure by group assignment, with the exception of water lead levels. For children in the intervention group, the mean number of visits by a dust control advisor during the 18-month study period was 6.2; 51 (36%) had 4 to 7 visits, and 69 (49%) had 8 visits. At 24 months of age, the geometric mean blood lead was 7.3 μg/dL (95% CI = 6.6, 8.2) for the intervention group and 7.8 μg/dL (95% CI = 6.9, 8.7) for the control group. The percentage of children with a 24-month blood lead ≥10 μg/dL, ≥15 μg/dL, and ≥20 μg/dL was 31% versus 36%, 12% versus 14%, and 5% versus 7% in the intervention and control groups, respectively. Conclusions. We conclude that dust control, as performed by families and in the absence of lead hazard controls to reduce ongoing contamination from lead-based paint, is not effective in the primary prevention of childhood lead exposure. blood lead, lead-contaminated house dust, randomized trial, children, environmental exposure, lead poisoning, primary prevention, prevention.
Suicidal ideation (SI) and attempts are increased in Huntington's disease (HD), making risk factor assessment a priority.To determine whether, hopelessness, irritability, aggression, anxiety, CAG expansion status, depression, and motor signs/symptoms were associated with Suicidal Ideation (SI) in those at risk for HD.Behavioral and neurological data were collected from subjects in an observational study. Subject characteristics were calculated by CAG status and SI. Logistic regression models were adjusted for demographics. Separate logistic regressions were used to compare SI and non-SI subjects. A combined logistic regression model, including 4 pre-specified predictors, (hopelessness, irritability, aggression, anxiety) was used to assess the relationship of SI to these predictors.801 subjects were assessed, 40 were classified as having SI, 6.3% of CAG mutation expansion carriers had SI, compared with 4.3% of non- CAG mutation expansion carriers (p = 0.2275). SI subjects had significantly increased depression (p < 0.0001), hopelessness (p < 0.0001), irritability (p < 0.0001), aggression (p = 0.0089), and anxiety (p < 0.0001), and an elevated motor score (p = 0.0098). Impulsivity, assessed in a subgroup of subjects, was also associated with SI (p = 0.0267). Hopelessness and anxiety remained significant in combined model (p < 0.001; p < 0.0198, respectively) even when motor score was included.Behavioral symptoms were significantly higher in those reporting SI. Hopelessness and anxiety showed a particularly strong association with SI. Risk identification could assist in assessment of suicidality in this group.
The objective of this study was to determine the effects of rasagiline as monotherapy on quality of life (QOL) in patients with early Parkinson's disease (PD). Rasagiline, a potent, second-generation, irreversible, selective monoamine oxidase B inhibitor improves PD symptoms in patients with early PD. Patients with early untreated PD were randomly assigned to once-daily rasagiline 1 mg/day, rasagiline 2 mg/day, or placebo in a 6-month, double-blind trial (n=404). At the end of 6 months, patients entered the preplanned, active-treatment phase in which those receiving 1 mg/day and 2 mg/day of rasagiline continued on their previously assigned dosages and those receiving placebo switched to rasagiline 2 mg/day, while maintaining blinding to treatment assignments. QOL was measured with the Parkinson's Disease Quality of Life questionnaire (PDQUALIF) at 0, 14, 26, and 52 weeks after randomization. Analysis of the change in PDQUALIF scores from baseline to 6 months showed adjusted treatment effects (with 95% confidence interval) favoring rasagiline over placebo of -2.91 units (-5.19, -0.64, P=0.01) for the 1 mg/day group and -2.74 units (-5.02, -0.45, P=0.02) for the 2 mg/day. Subscore analysis attributed most of this benefit to the self-image/sexuality domain. At 12 months (n=266), with all groups receiving rasagiline for at least 6 months, no significant differences in PDQUALIF scores were seen between groups. Rasagiline improved QOL compared with placebo. This QOL improvement appears to be accounted for primarily by the symptomatic benefit of rasagiline.
Alison Eldera*, Jean-Philippe Coudercb, Robert Geleina, Shirley Eberlyc, Christopher Coxc, Xiaojuang Xiab, Wojciech Zarebab, Philip Hopked, Winthrop Wattse, David Kittelsone, Mark Framptonf, Mark Utellf & Günter Oberdörsteraa Department of Environmental Medicine, University of Rochester, Rochester, New Yorkb Department of Cardiology, University of Rochester, Rochester, New Yorkc Department of Biostatistics, University of Rochester, Rochester, New Yorkd Department of Chemical Engineering, Clarkson University, Potsdam, New Yorke Department of Mechanical Engineering, University of Minnesota, Minneapolis, Minnesota, USAf Department of Pulmonary and Critical Care Medicine, University of Rochester, Rochester, New York
