51 research outputs found
Prescription Opioid Use Among Hispanics/Latinos With Arthritis Symptoms: Results From the Hispanic Community Health Study/Study of Latinos
Introduction: To determine the prevalence of prescription opioid (PO) use among Hispanics/Latinos with arthritis symptoms and to characterize how demographic and cultural factors are associated with PO use. Method: Cross-sectional analysis of baseline visit data during 2008 to 2011 from the Hispanic Community Health Study/Study of Latinos, a population-based cohort study of 16,415 Hispanics/Latinos living in Chicago, Illinois, Miami, Florida, Bronx, New York, and San Diego, California. Included participants self-reported painful inflammation or swelling in one or more joints. Multivariate models controlling for physical and mental health scores were constructed to assess how demographic and cultural factors were associated with PO use. Results: A total of 9.3% were using POs at the time of the baseline visit. In multivariate models, persons of Cuban background (adjusted odds ratio [AOR] = 0.42, 95% confidence interval [CI; 0.21, 0.81]) and of Dominican background (AOR = 0.38, 95% CI [0.18, 0.80]) were significantly less likely to use POs compared with a reference group of persons of Mexican background. Greater language acculturation was also negatively associated with PO use (AOR = 0.68, 95% CI [0.53, 0.87]). Conclusion: POs were used relatively uncommonly, and use showed marked variation between Hispanic/Latino groups. Future study should determine mechanisms for why greater use of English among Hispanics/Latinos might influence PO use
Interactions between the Nse3 and Nse4 Components of the SMC5-6 Complex Identify Evolutionarily Conserved Interactions between MAGE and EID Families
The SMC5-6 protein complex is involved in the cellular response to DNA damage. It is composed of 6-8 polypeptides, of which Nse1, Nse3 and Nse4 form a tight sub-complex. MAGEG1, the mammalian ortholog of Nse3, is the founding member of the MAGE (melanoma-associated antigen) protein family and Nse4 is related to the EID (E1A-like inhibitor of differentiation) family of transcriptional repressors.Using site-directed mutagenesis, protein-protein interaction analyses and molecular modelling, we have identified a conserved hydrophobic surface on the C-terminal domain of Nse3 that interacts with Nse4 and identified residues in its N-terminal domain that are essential for interaction with Nse1. We show that these interactions are conserved in the human orthologs. Furthermore, interaction of MAGEG1, the mammalian ortholog of Nse3, with NSE4b, one of the mammalian orthologs of Nse4, results in transcriptional co-activation of the nuclear receptor, steroidogenic factor 1 (SF1). In an examination of the evolutionary conservation of the Nse3-Nse4 interactions, we find that several MAGE proteins can interact with at least one of the NSE4/EID proteins.We have found that, despite the evolutionary diversification of the MAGE family, the characteristic hydrophobic surface shared by all MAGE proteins from yeast to humans mediates its binding to NSE4/EID proteins. Our work provides new insights into the interactions, evolution and functions of the enigmatic MAGE proteins
Atmospheric gas absorption knowledge in the submillimeter: Modeling, field measurements, and uncertainty quantification
Members of the atmospheric and astronomical science communities met to review the current state of the art of the submillimeter spectral region. Knowledge of gas spectroscopy is still questionable at these frequencies but is important to fully exploit upcoming
meteorological satellite measurements
Targeting physical activity interventions for adults: When should intervention occur?
Understanding demographic differences in transitions across physical activity (PA) levels is important for informing PA-promoting interventions, yet few studies have examined these transitions in contemporary multi-ethnic adult populations. We estimated age-, race/ethnicity-, and sex-specific 1-year net transition probabilities (NTPs) for National Health and Nutrition Examination Survey (2007–2012, n = 11,556) and Hispanic Community Health Study/Study of Latinos (2008–2011, n = 15,585) adult participants using novel Markov-type state transition models developed for cross-sectional data. Among populations with ideal PA (≥ 150 min/week; ranging from 56% (non-Hispanic black females) to 88% (non-Hispanic white males) at age 20), NTPs to intermediate PA (> 0–<149 min/week) generally increased with age, particularly for non-Hispanic black females for whom a net 0.0% (95% confidence interval (CI): 0.0, 0.2) transitioned from ideal to intermediate PA at age 20; by age 70, the NTP rose to 3.6% (95% CI: 2.3, 4.8). Heterogeneity in intermediate to poor (0 min/week) PA NTPs also was observed, with NTPs peaking at age 20 for Hispanic/Latino males and females [age 20 NTP = 3.7% (95% CI: 2.0, 5.5) for females and 5.0% (1.2, 8.7) for males], but increasing throughout adulthood for non-Hispanic blacks and whites [e.g. age 70 NTP = 7.8% (95% CI: 6.1, 9.6%) for black females and 8.1% (4.7, 11.6) for black males]. Demographic differences in PA net transitions across adulthood justify further development of tailored interventions. However, innovative efforts may be required for populations in which large proportions have already transitioned from ideal PA by early adulthood
Particulate air pollution and chronic ischemic heart disease in the eastern United States: a county level ecological study using satellite aerosol data
<p>Abstract</p> <p>Background</p> <p>There are several known factors that cause ischemic heart disease. However, the part played by air pollution still remains something of a mystery. Recent attention has focused on the chronic effect of particulate matter on heart disease. Satellite-derived aerosol optical depth (AOD) was found to be correlated with <it>PM</it><sub>2.5 </sub>in the eastern US. The objective of this study was to examine if there is an association between aerosol air pollution as indicated by AOD and chronic ischemic heart disease (CIHD) in the eastern US.</p> <p>Methods</p> <p>An ecological geographic study method was employed. Race and age standardized mortality rate (SMR) of CIHD was computed for each of the 2306 counties for the time period 2003–2004. A mean AOD raster grid for the same period was derived from Moderate Resolution Imaging Spectrometer (MODIS) aerosol data and the average AOD was calculated for each county. A bivariate Moran's I scatter plot, a map of local indicator of spatial association (LISA) clusters, and three regression models (ordinary least square, spatial lag, and spatial error) were used to analyze the relationship between AOD and CIHD SMR.</p> <p>Results</p> <p>The global Moran's I value is 0.2673 (<it>p </it>= 0.001), indicating an overall positive spatial correlation of CIHD SMR and AOD. The entire study area is dominated by spatial clusters of AOD against SMR (high AOD and high SMR in the east, and low AOD and low SMR in the west) (permutations = 999, <it>p </it>= 0.05). Of the three regression models, the spatial error model achieved the best fit (R<sup>2 </sup>= 0.28). The effect of AOD is positive and significant (beta = 0.7774, p = 0.01).</p> <p>Conclusion</p> <p>Aerosol particle pollution has adverse effect on CIHD mortality risk in the eastern US. High risk of CIHD mortality was found in areas with elevated levels of outdoor aerosol air pollution as indicated by satellite derived AOD. The evidence of the association would support targeting of policy interventions on such areas to reduce air pollution levels. Remote sensing AOD data could be used as an alternative health-related indictor of air quality.</p
Lysophosphatidate Induces Chemo-Resistance by Releasing Breast Cancer Cells from Taxol-Induced Mitotic Arrest
Taxol is a microtubule stabilizing agent that arrests cells in mitosis leading to cell death. Taxol is widely used to treat breast cancer, but resistance occurs in 25-69% of patients and it is vital to understand how Taxol resistance develops to improve chemotherapy. The effects of chemotherapeutic agents are overcome by survival signals that cancer cells receive. We focused our studies on autotaxin, which is a secreted protein that increases tumor growth, aggressiveness, angiogenesis and metastasis. We discovered that autotaxin strongly antagonizes the Taxol-induced killing of breast cancer and melanoma cells by converting the abundant extra-cellular lipid, lysophosphatidylcholine, into lysophosphatidate. This lipid stimulates specific G-protein coupled receptors that activate survival signals.In this study we determined the basis of these antagonistic actions of lysophosphatidate towards Taxol-induced G2/M arrest and cell death using cultured breast cancer cells. Lysophosphatidate does not antagonize Taxol action in MCF-7 cells by increasing Taxol metabolism or its expulsion through multi-drug resistance transporters. Lysophosphatidate does not lower the percentage of cells accumulating in G2/M by decreasing exit from S-phase or selective stimulation of cell death in G2/M. Instead, LPA had an unexpected and remarkable action in enabling MCF-7 and MDA-MB-468 cells, which had been arrested in G2/M by Taxol, to normalize spindle structure and divide, thus avoiding cell death. This action involves displacement of Taxol from the tubulin polymer fraction, which based on inhibitor studies, depends on activation of LPA receptors and phosphatidylinositol 3-kinase.This work demonstrates a previously unknown consequence of lysophosphatidate action that explains why autotaxin and lysophosphatidate protect against Taxol-induced cell death and promote resistance to the action of this important therapeutic agent
Bithionol inhibits ovarian cancer cell growth In Vitro- studies on mechanism(s) of action
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Trends in utilization of metabolic and bariatric surgery procedures by race-ethnicity: A state-wide analysis
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I know why the caged bird sings: Distress tolerant individuals show greater resting state connectivity between ventromedial prefrontal cortex and right amygdala as a function of higher vagal tone
Intolerance to psychological distress is associated with various forms of psychopathology, ranging from addiction to mood disturbance. The capacity to withstand aversive affective states is often explained by individual differences in cardiovagal tone as well as resting state connectivity of the ventromedial prefrontal cortex (vmPFC), a region involved in the regulation of emotions and cardio-autonomic tone. However, it is unclear which brain regions involved in distress tolerance show greater resting state functional connectivity (rsFC) as a function of resting heart rate variability (HRV).
One-hundred and twenty-six adults, aged 20 to 83.5Â years, were selected from a lifespan cohort at the Nathan Kline Institute-Rockland Sample. Participants' distress tolerance levels were assessed based upon performance on the Behavioral Indicator of Resiliency to Distress (BIRD) task. Artifact-free resting-state functional brain scans collected during separate sessions were used. While inside the scanner, a pulse oximeter was used to record beat-to-beat intervals to derive high-frequency heart rate variability (HF-HRV). The relationship between HF-HRV and vmPFC to whole brain functional connectivity was compared between distress tolerant (BIRD completers) and distress intolerant (BIRD non-completers).
Groups did not differ in their history of psychiatric diagnosis. Higher resting HF-HRV was associated with longer total time spent on the BIRD task for the entire sample (r = 0.255, p = 0.004). After controlling for age, gender, body mass index, head motion, and gray matter volume. Distress tolerant individuals showed greater rsFC (p < 0.005 (uncorrected), k = 20) between the vmPFC and default-mode network (DMN) hubs including posterior cingulate cortex/precuneus, medial temporal lobes, and the parahippocampal cortex. As a function of higher resting HF-HRV greater vmPFC connectivity was observed with sub-threshold regions in the right amygdala and left anterior prefrontal cortex, with the former passing small volume correction, in distress tolerant versus distress intolerant individuals.
In a lifespan sample of community-dwelling adults, distress tolerant individuals showed greater vmPFC connectivity with anterior and posterior hubs of the DMN compared to distress intolerant individuals. As a function of greater HF-HRV, distress tolerant individuals evidenced greater vmPFC with salience and executive control network hubs. These findings are consistent with deficits in neural resource allocation within a triple network resting amongst persons exhibiting behavioral intolerance to psychological distress
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