Noonanpaul2061

Dementia was increasingly assigned as underlying cause of death in Western Europe, but rarely in eastern European countries. find more Ill-defined causes accounted for between  less then  1% and 53% of all cardiovascular deaths. CHD mortality rates were closely linked to a countries' proportion of cardiovascular deaths assigned to CHD (R2 = 0.95 for 2000 and 0.99 for 2013). We show that CHD mortality is considerably influenced by national particularities in certifying death. Changes in CHD mortality rates reflect changes in certifying competing underlying causes of death. This must be accounted for when discussing reasons for the CHD mortality decline.We aimed to study the effects of hypothetical interventions on systolic blood pressure (SBP) and smoking on risk of stroke and dementia using data from 15 years of follow-up in the Rotterdam Study. We used data from 4930 individuals, aged 55-80 years, with no prior history of stroke, dementia or cognitive impairment, followed for 15 years within the Rotterdam Study, a population-based cohort. We defined the following sustained interventions on SBP (1) maintaining SBP below 120 mmHg, (2) maintaining SBP below 140 mmHg, (3) reducing SBP by 10% if above 140 mmHg, (4) reducing SBP by 20% if above 140 mmHg, and a combined intervention of quitting smoking with each of these SBP-lowering strategies. We considered incident stroke and incident dementia diagnoses as outcomes. We applied the parametric g-formula to adjust for baseline and time-varying confounding. The observed 15-year risk for stroke was 10.7%. Compared to no specified intervention (i.e., the "natural course"), all interventions that involved reducing SBP were associated with a stroke risk reduction of about 10% (e.g., reducing SBP by 20% if above 140 mmHg risk ratio 0.89; 95% CI 0.76, 1). Jointly intervening on SBP and smoking status further decreased the risk of stroke (e.g., risk ratio 0.83; 95% CI 0.71, 0.94). None of the specified interventions were associated with a substantive change in dementia risk. Our study suggests that a joint intervention on SBP and smoking cessation during later life may reduce stroke risk, while the potential for reducing dementia risk were not observed.

There is limited evidence about prevalence and odds of adverse birth outcomes among Arab American women in the United States. We estimated the prevalence of low birth weight (LBW < 2500g) and preterm birth (PTB < 37 completed weeks' gestation) among Arab American women in Ohio and studied the association between ethnicity, Arab American nativity (foreign or US born) and odds of LBW and PTB.

We identified Arab American women based on birth certificate data from live singleton births from 2007-2010 to 2013-2015 and a name algorithm. We compared the prevalence of LBW and PTB by ethnicity (Arab American vs. non-Hispanic White) and by nativity (foreign-born Arab American vs. US-born Arab American). Logistic regression models were used to estimate the unadjusted and adjusted effects of ethnicity and mother's nativity on study outcomes.

31,744 Arab American women (2.5% of all births in Ohio) were identified over a 7-year period. 24,129 Arab American women with complete data were included in the analysis influenced by nativity among Arab American women. These findings may be informative for developing and implementing strategies for adverse birth outcomes for a growing US ethnic minority population.This study examined the role of autonomy support from adults' informal health supporters (family or friends) in diabetes-specific health behaviors and health outcomes. Using baseline data from 239 Veterans with type 2 diabetes at risk of complications enrolled in behavioral trial, we examined associations between autonomy support from a support person and that support person's co-residence with the participant's diabetes self-care activities, patient activation, cardiometabolic measures, and predicted risk of a cardiac event. Autonomy support from supporters was associated with significantly increased adherence to healthy lifestyle behaviors (diet, p  less then  .001 and exercise, p = .003); higher patient activation (p  less then  .001); greater patient efficacy in interacting with healthcare providers, and lower 5-year (p = .044) and 10-year (p = .027) predicted cardiac risk. Autonomy support was not significantly associated with diabetes-specific behaviors (checking blood glucose, foot care, or medication taking); or hemoglobin A1c, systolic blood pressure, or non-HDL cholesterol. There was a significant interaction of autonomy support and supporter residence in one model such that lack of autonomy support was associated with lower patient activation only among individuals with in-home supporters. No other interactions were significant. Findings suggest that autonomy support from family and friends may play a role in patient self-management, patient activation, and lower cardiac risk.Four genes associated with isolated dystonia are currently well replicated and validated. DYT-THAP1 manifests as young-onset generalized dystonia with predominant craniocervical symptoms; and is associated with mostly deleterious missense variation in the THAP1 gene. De novo and inherited missense and protein truncating variation in GNAL as well as primarily missense variation in ANO3 cause isolated focal and/or segmental dystonia with preference for the upper half of the body and older ages at onset. The GAG deletion in TOR1A is associated with generalized dystonia with onset in childhood in the lower limbs. Rare variation in these genes causes monogenic sporadic and inherited forms of isolated dystonia; common variation may confer risk and imply that dystonia is a polygenic trait in a subset of cases. Although candidate gene screens have been successful in the past in detecting gene-disease associations, recent application of whole-genome and whole-exome sequencing methods enable unbiased capture of all genetic variation that may explain the phenotype. However, careful variant-level evaluation is necessary in every case, even in genes that have previously been associated with disease. We review the genetic architecture and phenotype of DYT-THAP1, DYT-GNAL, DYT-ANO3, and DYT-TOR1A by collecting case reports from the literature and performing variant classification using pathogenicity criteria.