Cognitive control over conflicting information has been studied extensively using tasks such as the color-word Stroop, flanker, and spatial conflict task. Neuroimaging studies typically identify a ...fronto-parietal network engaged in conflict processing, but numerous additional regions are also reported. Ascribing putative functional roles to these regions is problematic because some may have less to do with conflict processing per se, but could be engaged in specific processes related to the chosen stimulus modality, stimulus feature, or type of conflict task. In addition, some studies contrast activation on incongruent and congruent trials, even though a neutral baseline is needed to separate the effect of inhibition from that of facilitation. In the first part of this article, we report a systematic review of 34 neuroimaging publications, which reveals that conflict-related activity is reliably reported in the anterior cingulate cortex and bilaterally in the lateral prefrontal cortex, the anterior insula, and the parietal lobe. In the second part, we further explore these candidate “conflict” regions through a novel functional magnetic resonance imaging experiment, in which the same group of subjects perform related visual and auditory Stroop tasks. By carefully controlling for the same task (Stroop), the same to-be-ignored stimulus dimension (word meaning), and by separating out inhibitory processes from those of facilitation, we attempt to minimize the potential differences between the two tasks. The results provide converging evidence that the regions identified by the systematic review are reliably engaged in conflict processing. Despite carefully matching the Stroop tasks, some regions of differential activity remained, particularly in the parietal cortex. We discuss some of the task-specific processes which might account for this finding.
Background and objective
Deafferentation caused by cochlear pathology (which can be hidden from the audiogram) activates forms of neural plasticity in auditory pathways, generating tinnitus and its ...associated conditions including hyperacusis. This article discusses tinnitus mechanisms and suggests how these mechanisms may relate to those involved in normal auditory information processing.
Materials and methods
Research findings from animal models of tinnitus and from electromagnetic imaging of tinnitus patients are reviewed which pertain to the role of deafferentation and neural plasticity in tinnitus and hyperacusis.
Results
Auditory neurons compensate for deafferentation by increasing their input/output functions (gain) at multiple levels of the auditory system. Forms of homeostatic plasticity are believed to be responsible for this neural change, which increases the spontaneous and driven activity of neurons in central auditory structures in animals expressing behavioral evidence of tinnitus. Another tinnitus correlate, increased neural synchrony among the affected neurons, is forged by spike-timing-dependent neural plasticity in auditory pathways. Slow oscillations generated by bursting thalamic neurons verified in tinnitus animals appear to modulate neural plasticity in the cortex, integrating tinnitus neural activity with information in brain regions supporting memory, emotion, and consciousness which exhibit increased metabolic activity in tinnitus patients.
Discussion and conclusion
The latter process may be induced by transient auditory events in normal processing but it persists in tinnitus, driven by phantom signals from the auditory pathway. Several tinnitus therapies attempt to suppress tinnitus through plasticity, but repeated sessions will likely be needed to prevent tinnitus activity from returning owing to deafferentation as its initiating condition.
The global use of online communities has exploded to involve hundreds of millions of users. Despite the tremendous social impact and business opportunities afforded by these communities, little ...information systems (IS) research has addressed them - especially in a cross-cultural context. Our research proposes an online community self-disclosure model, tested in a cross-cultural setting using data provided by French and British working professionals. Our model is based on social exchange theory (SET) and social penetration theory (SPT), as well as on cross-cultural theory related to individualism-collectivism. SET explains that individuals engage in relationships when the perceived costs associated with the relationship are less than the expected benefits. SPT extends SET to explain that individuals participate in self-disclosure to foster relationships - reciprocation is the primary benefit of self-disclosure, whereas risk is the foundational cost of self-disclosure. Our study established several important findings: positive social influence to use an online community increases online community self-disclosure; reciprocity increases self-disclosure; online community trust increases self-disclosure; and privacy risk beliefs decrease self-disclosure. Meanwhile, a tendency toward collectivism increases self-disclosure. We further found that French participants had higher scores on horizontal individualism than British participants. Several other findings and their implications for practice are also discussed.
Cardiopulmonary bypass (CPB) lyses erythrocytes and induces lipid peroxidation, indicated by increasing plasma concentrations of free hemoglobin, F2-isoprostanes, and isofurans. Acetaminophen ...attenuates hemeprotein-mediated lipid peroxidation, reduces plasma and urine concentrations of F2-isoprostanes, and preserves kidney function in an animal model of rhabdomyolysis. Acetaminophen also attenuates plasma concentrations of isofurans in children undergoing CPB. The effect of acetaminophen on lipid peroxidation in adults has not been studied. This was a pilot study designed to test the hypothesis that acetaminophen attenuates lipid peroxidation in adults undergoing CPB and to generate data for a clinical trial aimed to reduce acute kidney injury following cardiac surgery.
In a prospective double-blind placebo-controlled clinical trial, sixty adult patients were randomized to receive intravenous acetaminophen or placebo starting prior to initiation of CPB and for every 6 hours for 4 doses. Acetaminophen concentrations measured 30 min into CPB and post-CPB were 11.9 ± 0.6 μg/mL (78.9 ± 3.9 μM) and 8.7 ± 0.3 μg/mL (57.6 ± 2.0 μM), respectively. Plasma free hemoglobin increased more than 15-fold during CPB, and haptoglobin decreased 73%, indicating hemolysis. Plasma and urinary markers of lipid peroxidation also increased during CPB but returned to baseline by the first postoperative day. Acetaminophen reduced plasma isofuran concentrations over the duration of the study (P = 0.05), and the intraoperative plasma isofuran concentrations that corresponded to peak hemolysis were attenuated in those subjects randomized to acetaminophen (P = 0.03). Perioperative acetaminophen did not affect plasma concentrations of F2-isoprostanes or urinary markers of lipid peroxidation.
Intravenous acetaminophen attenuates the increase in intraoperative plasma isofuran concentrations that occurs during CPB, while urinary markers were unaffected.
ClinicalTrials.gov NCT01366976.
Deficits in a wide array of functional outcome areas (eg, social functioning, social skills, independent living skills, etc) are marked in schizophrenia. Consequently, much recent research has ...attempted to identify factors that may contribute to functional outcome; social cognition is one such domain. The purpose of this article is to review research examining the relationship between social cognition and functional outcome. Comprehensive searches of PsycINFO and MEDLINE/PUBMED were conducted to identify relevant published manuscripts to include in the current review. It is concluded that the relationship between social cognition and functional outcome depends on the specific domains of each construct examined; however, it can generally be concluded that there are clear and consistent relationships between aspects of functional outcome and social cognition. These findings are discussed in light of treatment implications for schizophrenia.
Background and purpose: Acute activation of P2X7 receptors rapidly opens a non‐selective cation channel. Sustained P2X7 receptor activation leads to the formation of cytolytic pores, mediated by ...downstream recruitment of hemichannels to the cell surface. Species‐ and single‐nucleotide polymorphism‐mediated differences in P2X7 receptor activation have been reported that complicate understanding of the physiological role of P2X7 receptors. Studies were conducted to determine pharmacological differences between human, rat and mouse P2X7 receptors.
Experimental approach: Receptor‐mediated changes in calcium influx and Yo‐Pro uptake were compared between recombinant mouse, rat and human P2X7 receptors. For mouse P2X7 receptors, wild‐type (BALB/c) and a reported loss of function (C57BL/6) P2X7 receptor were also compared.
Key results: BzATP 2,3‐O‐(4‐benzoylbenzoyl)‐ATP was more potent than ATP in stimulating calcium influx and Yo‐Pro uptake at rat, human, BALB/c and C57BL/6 mouse P2X7 receptors. Two selective P2X7 receptor antagonists, A‐740003 and A‐438079, potently blocked P2X7 receptor activation across mammalian species. Several reported P2X1 receptor antagonists e.g. MRS 2159 (4‐(4‐formyl‐5‐hydroxy‐6‐methyl‐3‐(phosphonooxy)methyl}‐2‐pyridinyl)azo‐benzoic acid), PPNDS and NF279 blocked P2X7 receptors. NF279 fully blocked human P2X7 receptors, but only partially blocked BALB/c P2X7 receptors and was inactive at C57BL/6 P2X7 receptors.
Conclusions and implications: These data provide new insights into P2X7 receptor antagonist pharmacology across mammalian species. P2X7 receptor pharmacology in a widely used knockout background mouse strain (C57BL/6) was similar to wild‐type mouse P2X7 receptors. Several structurally novel, selective and competitive P2X7 receptor antagonists show less species differences compared with earlier non‐selective antagonists.
Aim
Wildfires increasingly create large high‐severity patches with interior areas far from less disturbed habitats. We evaluated how these trends impact bird communities by investigating the effect ...of internal distance from lower‐severity areas, high‐severity patch size, and years since fire on avian alpha and beta diversity.
Location
Sierra Nevada, California, USA.
Methods
Bird occurrence data were collected during 2009–2017 within high‐severity patches of 27 wildfires representing 1–30 years since disturbance. A two‐step multispecies occupancy method was used to account for imperfect detection of 94 species and estimate effects of patch characteristics on community richness and dissimilarity.
Results
Community richness decreased with distance from patch edge and with patch size. Richness increased with years since fire, but this pattern was dependent on distance from edge with higher peak richness (23 species) near edges than interiors (18 species). Community dissimilarity was not associated with distance, indicating that large high‐severity patch interiors contain subsets of, rather than complements to, edge communities. Dissimilarity peaked later with increasing patch size. Guild richness of tree and primary cavity nesters was negatively associated with distance and patch size. Richness of ground and shrub nesters was insensitive to distance, while shrub nester richness increased somewhat with patch size. Due to declines among other species, ground and shrub nesters made up a greater percentage of the avian community within the interiors of large high‐severity patches.
Main conclusions
As fire activity increases due to accumulating forest fuels and accelerating climate change, high‐severity patches and their resulting early‐seral habitats are becoming more extensive with less edge and more interior area. Such changes are likely to decrease avian diversity locally and shift community composition away from forest‐associated species. Management actions that promote the full range of fire effects but limit high‐severity patch size may best conserve bird diversity within fire‐adapted ecosystems.
Ageing is associated with declines in both perception and cognition. We review evidence for an interaction between perceptual and cognitive decline in old age. Impoverished perceptual input can ...increase the cognitive difficulty of tasks, while changes to cognitive strategies can compensate, to some extent, for impaired perception. While there is strong evidence from cross-sectional studies for a link between sensory acuity and cognitive performance in old age, there is not yet compelling evidence from longitudinal studies to suggest that poor perception causes cognitive decline, nor to demonstrate that correcting sensory impairment can improve cognition in the longer term. Most studies have focused on relatively simple measures of sensory (visual and auditory) acuity, but more complex measures of suprathreshold perceptual processes, such as temporal processing, can show a stronger link with cognition. The reviewed evidence underlines the importance of fully accounting for perceptual deficits when investigating cognitive decline in old age.
To determine the hormonal effects of reducing sleep duration under controlled feeding conditions.
Randomized, crossover study.
Inpatient.
Twenty-seven normal weight, 30- to 45-yr-old men and women ...habitually sleeping 7-9 hr/night.
PARTICIPANTS WERE STUDIED UNDER TWO SLEEP CONDITIONS: short (4 hr in bed) or habitual (9 hr in bed) sleep. A controlled diet was provided for each 4-day study period.
Fasting blood samples were obtained daily and frequent blood samples were obtained throughout day 4. The main outcomes measures included glucose, insulin, leptin, ghrelin, adiponectin, total glucagon-like peptide 1 (GLP-1) and peptide YY(3-36) (PYY(3-36)) concentrations. Body weights were reduced by 2.2 ± 0.4 lb and 1.7 ± 0.4 lb during the habitual and short sleep phases, respectively (both P < 0.0001). There was no effect of sleep duration on glucose, insulin, and leptin profiles (all P > 0.05). Ghrelin and GLP-1 responses differed by sex. Short sleep increased fasting (P = 0.054) and morning (08:00-12:00) (P = 0.042) total ghrelin in men but not women. The reverse was observed for GLP-1: afternoon levels (12:30-19:00) were lower (P = 0.016) after short sleep compared with habitual sleep in women but not men.
These data suggest that, in the context of negative energy balance, short sleep does not lead to a state of increased insulin resistance, but may predispose to overeating via separate mechanisms in men and women.
Trial registration on http://www.clinicaltrials.gov. #NCT00935402.
Inflammasomes are protein complexes assembled upon recognition of infection or cell damage signals, and serve as platforms for clustering and activation of procaspase-1. Oligomerisation of initiating ...proteins such as AIM2 (absent in melanoma-2) and NLRP3 (NOD-like receptor family, pyrin domain-containing-3) recruits procaspase-1 via the inflammasome adapter molecule ASC (apoptosis-associated speck-like protein containing a CARD). Active caspase-1 is responsible for rapid lytic cell death termed pyroptosis. Here we show that AIM2 and NLRP3 inflammasomes activate caspase-8 and -1, leading to both apoptotic and pyroptotic cell death. The AIM2 inflammasome is activated by cytosolic DNA. The balance between pyroptosis and apoptosis depended upon the amount of DNA, with apoptosis seen at lower transfected DNA concentrations. Pyroptosis had a higher threshold for activation, and dominated at high DNA concentrations because it happens more rapidly. Gene knockdown showed caspase-8 to be the apical caspase in the AIM2- and NLRP3-dependent apoptotic pathways, with little or no requirement for caspase-9. Procaspase-8 localised to ASC inflammasome 'specks' in cells, and bound directly to the pyrin domain of ASC. Thus caspase-8 is an integral part of the inflammasome, and this extends the relevance of the inflammasome to cell types that do not express caspase-1.
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