Notes

Affiliation Involving Genetic Hazards regarding Being overweight and Recollection in Children.
OBJECTIVE Humans use a complex system of protective cognitive biases or "positive illusions" that foster emotional well-being and subjective quality of life. This study examined the role of positive illusions in patient adjustment to drug-resistant epilepsy and its surgical treatment. METHODS One hundred fifty people participated, including 93 focal epilepsy patients being evaluated for surgery and 57 sociodemographically matched healthy controls. We purpose-built computer software, "Living With Epilepsy," to assess the impact of positive illusions on patient perceptions of their current life, and administered well-validated questionnaires of depression (Neurological Disorders Depression Inventory for Epilepsy), anxiety (Patient Health Questionnaire for Generalized Anxiety Disorder-7 items), and health-related quality of life (HRQOL; Epilepsy Surgery Inventory-55) before and at 3 and 12 months after surgery. RESULTS We identified two patient groups those with "high positive illusions" (53%) about their epilepsy and those with "low positive illusions" (47%), with no differences between sociodemographic or epilepsy variables (all P > .05). Before epilepsy surgery, patients with high positive illusions exhibited fewer symptoms of depression (P .05). SIGNIFICANCE These findings point to an active psychological process in drug-resistant patients, where approximately half generate strong positive illusions about their life with epilepsy, maintaining their mood and subjective well-being. Those who use this psychological mechanism show better adjustment 12 months postsurgery independent of seizure outcome, providing a potential new target for psychological treatment in patients with epilepsy. Wiley Periodicals, Inc. © 2020 International League Against Epilepsy.OBJECTIVE Individuals with epilepsy have poor bone development and preservation throughout the lifespan and are vulnerable to nontrauma fracture (NTFx) and post-NTFx complications. However, no studies have examined the contribution of NTFx to mortality among adults with epilepsy. The objective was to determine whether NTFx is a risk factor for mortality among adults with epilepsy. METHODS Data from 2011 to 2016 were obtained from Optum Clinformatics Data Mart, a nationwide claims database from a single private payer in the United States. Diagnosis codes were used to identify adults (≥18 years old) with epilepsy, NTFx, and covariates (demographics and pre-NTFx cardiovascular disease, respiratory disease, diabetes, chronic kidney disease, cancer). Crude mortality rate per 100 person-years was estimated. Cox regression estimated hazard ratios (HRs) and 95% confidence intervals (CIs) were determined for mortality, comparing epilepsy and NTFx (EP + NTFx; n = 11 471), epilepsy without NTFx (EP without NTFx; n = 50 h epilepsy and compared to adults without epilepsy, NTFx is associated with a higher 12-month mortality rate. Findings suggest that NTFx may be a robust risk factor for mortality among adults with epilepsy. Wiley Periodicals, Inc. https://www.selleckchem.com/products/apcin.html © 2020 International League Against Epilepsy.A critical tool in assessing ecosystem change is the analysis of long-term data sets, yet such information is generally sparse and often unavailable for many habitats. Kelp forests are an example of a rapidly changing ecosystem that are in most cases are data-poor. Because kelp forests are highly dynamic and have high intrinsic interannual variability, understanding how regional-scale drivers are driving kelp populations-and particularly how kelp populations are responding to climate change-requires long-term data sets. However, much of the work on kelp responses to climate change has focused on just a few, relatively long-lived perennial, canopy-forming species. To better understand how kelp populations with different life history traits are responding to climate related variability, we leverage 35 years of Landsat satellite imagery to track the population size of an annual, ruderal kelp, Nereocystis luetkeana, across Oregon. We found high levels of interannual variability in Nereocystis canopy area and varyd by copyright. All rights reserved.If a threat cannot be avoided, the organism has two defense options it can try to eliminate the threatening agent or boost physiological mechanisms to tolerate the challenge and its consequences. Both strategies can be (and usually are) used at the same time. Fighting an infection, for instance, requires mounting immune responses to control pathogen burden as well as physiologic adaptations to tolerate stress and damage. Thus, the two strategies are connected and interdependent. We are starting to understand how the regulation of host metabolic physiology during disease impacts both the ability to resist pathogens' burden and tolerate parenchymal tissue functional damage. Here, we review a number of recent publications that have begun to shed light on the physiological and immunological mechanisms that coordinate host defense and metabolic processes. In particular, we will cover the areas of energetic control, substrates utilization, and the regulatory signals that promote infectious disease tolerance. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.Repeated inhalation of airborne conidia derived from the fungus Aspergillus fumigatus (Af) can lead to a severe eosinophil-dominated inflammatory condition of the lung termed allergic bronchopulmonary aspergillosis (ABPA). ABPA affects about 5 million individuals worldwide and the mechanisms regulating lung pathology in ABPA are poorly understood. Here, we used a mouse model of ABPA to investigate the role of eosinophils and T cell-derived IL-4/IL-13 for induction of allergic lung inflammation. Selective deletion of IL-4/IL-13 in T cells blunted the Af-induced lung eosinophilia and further resulted in lower expression of STAT6-regulated chemokines and effector proteins such as Arginase 1, Relm-α, Relm-β, and Muc5a/c. Eosinophil-deficient ΔdblGata mice showed lower IL-4 expression in the lung and the number of Th2 cells in the lung parenchyma was reduced. However, expression of the goblet cell markers Clca1 and Muc5a/c, abundance of mucin-positive cells, as well as weight gain of lungs were comparable between Af-challenged ΔdblGata and WT mice.
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