Moderating Effects of Cortisol on Neural-Cognitive Association in Cognitively Normal Elderly Subjects

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PM2.5 Exposure Suppresses Dendritic Maturation in Subgranular Zone in Aged Rats

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Meditation-induced neuroplastic changes in amygdala activity during negative affective processing

Recent evidence suggests that the effects of meditation practice on affective processing and resilience have the potential to induce neuroplastic changes within the amygdala. Notably, literature speculates that meditation training may reduce amygdala activity during negative affective processing. Nonetheless, studies have thus far not verified this speculation. In this longitudinal study, participants (N = 21, 9 men) were trained in awareness-based compassion meditation (ABCM) or matched relaxation training. The effects of meditation training on amygdala activity were examined during passive viewing of affective and neutral stimuli in a non-meditative state. We found that the ABCM group exhibited significantly reduced anxiety and right amygdala activity during negative emotion processing than the relaxation group. Furthermore, ABCM participants who performed more compassion practice had stronger right amygdala activity reduction during negative emotion processing. The lower right amygdala activity after ABCM training may be associated with a general reduction in reactivity and distress. As all participants performed the emotion processing task in a non-meditative state, it appears likely that the changes in right amygdala activity are carried over from the meditation practice into the non-meditative state. These findings suggest that the distress-reducing effects of meditation practice on affective processing may transfer to ordinary states, which have important implications on stress management.Department of Rehabilitation Sciences2016-2017 > Academic research: refereed > Publication in refereed journalbcr

Search for large missing transverse momentum in association with one top-quark in proton-proton collisions at s√=13 TeV with the ATLAS detector

This paper describes a search for events with one top-quark and large missing transverse momentum in the final state. Data collected during 2015 and 2016 by the ATLAS experiment from 13 TeV proton–proton collisions at the LHC corresponding to an integrated luminosity of 36.1 fb−1 are used. Two channels are considered, depending on the leptonic or the hadronic decays of the W boson from the top quark. The obtained results are interpreted in the context of simplified models for dark-matter production and for the single production of a vector-like T quark. In the absence of significant deviations from the Standard Model background expectation, 95% confidence-level upper limits on the corresponding production cross-sections are obtained and these limits are translated into constraints on the parameter space of the models considered

Endothelin-1 induced cofilin rod formation in hippocampal neurons via endothelin type B receptor and NADPH oxidase-mediated oxidative stress pathway

Poster Presentation: no. P57High expression level of endothelin-1 (ET-1) has been detected in the post-mortem brains of Alzheimer’s disease (AD) patients. Two ET receptor (ET rec) subtypes are expressed in neurons. However, the direct effects of ET-1 on mature neurons have remained elusive. ET-1 mediated oxidative stress production via NADPH oxidase (NOX) in endothelial cells, and regulated actin in astrocytes. Previously, oxidative stress-mediated aggregation of cofilin was identified as a key mediator of neuronal degeneration in AD models. Formation of cofilin rods was proposed to mediate the loss of synapses and distal dendrites in primary neurons. Here, this study investigated the effect of ET-1 in mediating cofilin rod formation in 14 days in vitro primary mouse hippocampal neurons. The 24h treatment of ET-1 significantly increased the percentage of neurons with cofilin rods, which was inhibited by pre-treatment of ETB rec antagonist (BQ788), but not by ETA rec antagonist (BQ123). Neurons treated with ETB rec agonist (IRL1620) formed cofilin rods and showed significant reduction of distal dendritic extension. Co- or pre-treatment of antioxidant (N-acetylcysteine) or NOX inhibitor (VAS2870), respectively, inhibited IRL1620-induced cofilin rod formation, indicating ETB rec activation mediated cofilin rod formation via oxidative stress pathway. In short, our findings presented a novel neurotoxic role of ETB rec, associating the ET-1 system dysregulation with AD pathogenesis