74 research outputs found
Change in the direct cost of treatment for children and adolescents with hyperkinetic disorder in Germany over a period of four years
Gene Expression Changes in the Prefrontal Cortex, Anterior Cingulate Cortex and Nucleus Accumbens of Mood Disorders Subjects That Committed Suicide
Suicidal behaviors are frequent in mood disorders patients but only a subset of them ever complete suicide. Understanding predisposing factors for suicidal behaviors in high risk populations is of major importance for the prevention and treatment of suicidal behaviors. The objective of this project was to investigate gene expression changes associated with suicide in brains of mood disorder patients by microarrays (Affymetrix HG-U133 Plus2.0) in the dorsolateral prefrontal cortex (DLPFC: 6 Non-suicides, 15 suicides), the anterior cingulate cortex (ACC: 6NS, 9S) and the nucleus accumbens (NAcc: 8NS, 13S). ANCOVA was used to control for age, gender, pH and RNA degradation, with P≤0.01 and fold change±1.25 as criteria for significance. Pathway analysis revealed serotonergic signaling alterations in the DLPFC and glucocorticoid signaling alterations in the ACC and NAcc. The gene with the lowest p-value in the DLPFC was the 5-HT2A gene, previously associated both with suicide and mood disorders. In the ACC 6 metallothionein genes were down-regulated in suicide (MT1E, MT1F, MT1G, MT1H, MT1X, MT2A) and three were down-regulated in the NAcc (MT1F, MT1G, MT1H). Differential expression of selected genes was confirmed by qPCR, we confirmed the 5-HT2A alterations and the global down-regulation of members of the metallothionein subfamilies MT 1 and 2 in suicide completers. MTs 1 and 2 are neuro-protective following stress and glucocorticoid stimulations, suggesting that in suicide victims neuroprotective response to stress and cortisol may be diminished. Our results thus suggest that suicide-specific expression changes in mood disorders involve both glucocorticoids regulated metallothioneins and serotonergic signaling in different regions of the brain
Comment on 'Aeroelastic oscillations caused by transitional boundarylayers and their attenuation'
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Greater aridity increases the magnitude of urban nighttime vegetation-derived air cooling
High nighttime urban air temperatures increase health risks and economic vulnerability of people globally. While recent studies have highlighted nighttime heat mitigation effects of urban vegetation, the magnitude and variability of vegetation-derived urban nighttime cooling differs greatly among cities. We hypothesize that urban vegetation-derived nighttime air cooling is driven by vegetation density whose effect is regulated by aridity through increasing transpiration. We test this hypothesis by deploying microclimate sensors across eight United States cities and investigating relationships of nighttime air temperature and urban vegetation throughout a summer season. Urban vegetation decreased nighttime air temperature in all cities. Vegetation cooling magnitudes increased as a function of aridity, resulting in the lowest cooling magnitude of 1.4 °C in the most humid city, Miami, FL, and 5.6 °C in the most arid city, Las Vegas, NV. Consistent with the differences among cities, the cooling effect increased during heat waves in all cities. For cities that experience a summer monsoon, Phoenix and Tucson, AZ, the cooling magnitude was larger during the more arid pre-monsoon season than during the more humid monsoon period. Our results place the large differences among previous measurements of vegetation nighttime urban cooling into a coherent physiological framework dependent on plant transpiration. This work informs urban heat risk planning by providing a framework for using urban vegetation as an environmental justice tool and can help identify where and when urban vegetation has the largest effect on mitigating nighttime temperatures. © 2021 The Author(s). Published by IOP Publishing Ltd.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]
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