18 research outputs found

    Social and emotional support as a protective factor against current depression among individuals with adverse childhood experiences

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    Depression is one of the most prevalent mental health disorders among adults with adverse childhood experiences (ACE). Several studies have well documented the protective role of social support against depression in other populations. However, the impact of perceived social and emotional support (PSES) on current depression in a large community sample of adults with ACE has not been studied yet. This study tests the hypothesis that PSES is a protective factor against current depression among adults with ACE. Data from the 2010 Behavioral Risk Factor Surveillance System (BRFSS) involving adults with at least one ACE were used for the purpose of this study (n = 12.487). PSES had three categories: Always, Usually/Sometimes, and Rarely/Never. Current depression, defined based on the responses to the eight-item Patient Health Questionnaire (PHQ-8) depression scale, was treated as a binary outcome of interest: Present or absent. Logistic regression models were used for the analysis adjusting for all potential confounders. When compared to individuals who reported that they rarely/never received social and emotional support, individuals who reported that they always received were 87% less likely to report current depression (AOR: 0.13 [95% CI: 0.08–0.21]); and those who reported that they usually/sometimes received social and emotional support were 69% less likely to report current depression (AOR: 0.31 [95% CI: 0.20–0.46]). The results of this study highlight the importance of social and emotional support as a protective factor against depression in individuals with ACE. Health care providers should routinely screen for ACE to be able to facilitate the necessary social and emotional support

    Clinical and Individual Factors Associated with Smoking Quit Attempts among Adults with COPD: Do Factors Vary with Regard to Race?

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    Only half of adults with chronic obstructive pulmonary disease (COPD) report a smoking quit attempt in the past year. Adults with COPD have frequent encounters with the healthcare system that are opportunities for health behavior interventions that support quit attempts. The purpose of this research was to examine individual- and clinical-level factors associated with smoking quit attempts in adults with COPD. Cross-sectional data were from the 2011 Behavioral Risk Factor Surveillance System. Race-stratified, weighted logistic regression examined factors associated with quit attempt among current smokers with COPD. Overall, quit attempt was reported by 65% (95% confidence interval (CI): 61.9, 67.5) of adults and was more likely among blacks than whites (p < 0.0001). Among whites with COPD quit attempt was associated with: Female gender (adjusted odds ratio (AOR) = 1.3; CI: 1.0, 1.7), exercise (AOR = 2.0; CI: 1.5, 2.5), and medications for COPD (AOR = 1.6; CI: 1.3, 2.2). Among black adults with COPD quit attempt was associated with: Having a partner (AOR = 4.5; CI: 1.3, 15.0), exercise (AOR = 3.7; CI: 1.6, 8.7), spirometry (AOR = 9.5; CI: 3.2, 28.7), and having a personal doctor (AOR = 6.4; CI: 1.8, 22.5). Individual and clinical-factors associated with quit attempt varied by race. These findings suggest an impact of the healthcare system that supports quit attempts in blacks but not whites with COPD.</p

    Stimulation of glucose transport in response to activation of distinct AMPK signaling pathways

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    AMP-activated protein kinase (AMPK) plays a critical role in the stimulation of glucose transport in response to hypoxia and inhibition of oxidative phosphorylation. In the present study, we examined the signaling pathway(s) mediating the glucose transport response following activation of AMPK. Using mouse fibroblasts of AMPK wild type and AMPK knockout, we documented that the expression of AMPK is essential for the glucose transport response to both azide and 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR). In Clone 9 cells, the stimulation of glucose transport by a combination of azide and AICAR was not additive, whereas there was an additive increase in the abundance of phosphorylated AMPK (p-AMPK). In Clone 9 cells, AMPK wild-type fibroblasts, and H9c2 heart cells, azide or hypoxia selectively increased p-ERK1/2, whereas, in contrast, AICAR selectively stimulated p-p38; phosphorylation of JNK was unaffected. Azide's effect on p-ERK1/2 abundance and glucose transport in Clone 9 cells was partially abolished by the MEK1/2 inhibitor U0126. SB 203580, an inhibitor of p38, prevented the phosphorylation of p38 and the glucose transport response to AICAR and, unexpectedly, to azide. Hypoxia, azide, and AICAR all led to increased phosphorylation of Akt substrate of 160 kDa (AS160) in Clone 9 cells. Employing small interference RNA directed against AS160 did not inhibit the glucose transport response to azide or AICAR, whereas the content of P-AS160 was reduced by ∼80%. Finally, we found no evidence for coimmunoprecipitation of Glut1 and p-AS160. We conclude that although azide, hypoxia, and AICAR all activate AMPK, the downstream signaling pathways are distinct, with azide and hypoxia stimulating ERK1/2 and AICAR stimulating the p38 pathway

    Influenza vaccination in adults with chronic obstructive pulmonary disease: the impact of a diagnostic breathing test on vaccination rates.

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    INTRODUCTION: Influenza vaccination rates are low in adults with chronic obstructive pulmonary disease (COPD). A diagnostic breathing test in adults with COPD may increase vaccination rates; however, research has not demonstrated this relationship. The purpose of this research was to determine if adults with COPD diagnosed by a breathing test were more likely to have had an influenza vaccination during the past 12 months when compared to those with COPD diagnosed without a breathing test. METHODS: This was a cross-sectional study using data from the 2011 Behavioral Risk Factor Surveillance System. Logistic regression examined the relationship between influenza vaccination among adults with COPD diagnosed with a breathing test (n = 13,201) compared to those diagnosed without a breathing test (n = 3,108), after controlling for all potential confounders. RESULTS: Overall, 49% of respondents with COPD received an influenza vaccination within the past 12 months and 78% reported their COPD was diagnosed by a breathing test. The prevalence of influenza vaccination in the past 12 months was greater in those with COPD diagnosed by a breathing test (53%) compared to those diagnosed without a breathing test (36%). In adjusted analysis, adults with COPD who had a breathing test were 31% (confidence interval 1.1, 1.6) more likely to have received an influenza vaccination in the past 12 months compared to those without a breathing test. DISCUSSION: A diagnostic breathing test for COPD was associated with increased likelihood of having had an influenza vaccination in the past 12 months. This may be an indicator of the relationship between knowledge of lung function and the need for preventative care, a sign of quality healthcare, or good health-seeking behaviors in patients with COPD. This research is the first to use a nationally representative sample to suggest that spirometry diagnosis of COPD may increase rates of influenza vaccination

    Characteristics of respondents with COPD: frequency, weighted prevalence, and 95% confidence intervals, overall and by breathing test to diagnose COPD, 2011 BRFSS, n = 16,309.

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    <p>COPD = chronic obstructive pulmonary disease; BRFSS = Behavioral Risk Factor Surveillance System; SD = standard deviation; CHD = coronary heart disease; MI = myocardial infarction.</p

    Unadjusted and adjusted weighted prevalence odds ratios and 95% confidence intervals for ever had a seasonal flu vaccination among persons with COPD in the 2011 BRFSS, n = 16,309.

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    <p>COPD = Chronic Obstructive Pulmonary Disease; BRFSS = Behavioral Risk Factor Surveillance System; UOR = unadjusted odds ratio; AOR = adjusted odds ratio; CHD = coronary heart disease; MI = myocardial infarction.</p
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