Evaluation of executive functions, cognitive control and a neurocognitive profile of college binge drinkers, An

2014 Summer.Introduction: Binge drinking is a detrimental behavior which presents with consumption of large amounts of alcohol however, does not present with symptoms of dependence. The college population is a unique group to investigate due to the neuroplasticity and development those in this cohort are undergoing. Specifically, this age group is experiencing a natural period of neural immaturity specific to the prefrontal cortex. In addition to being identified by the personal, physical, and academic detriments caused by binge drinking, it was hypothesized this population of binge drinkers could be categorized with a neurocognitive profile which varies from their non-drinking peers. Participants: One hundred and ninety seven Colorado State University students were recruited and categorized in to different levels of binge alcohol consumption on non-drinkers based on two self-report measures. Method: Alcohol consumption was evaluated through a sex based questionnaire and the Alcohol Use Disorder Identification Test. Neurocognitive performance was assessed through six tasks: Wisconsin Card Sorting Test, Delay Discounting Task, One Touch Stockings of Cambridge, Trail Making Task (A and B), the Behavioral Rating Inventory of Executive Function, and the Dysexecutive Questionnaire. Results: An initial MANOVA was used to assess differences between non-drinkers and binge drinkers, showing no significance, F (12, 19) = 1.96, p = 0.09. A secondary MANOVA was used to evaluate differences across different categories of binge drinkers and non-drinkers, where significance was noted, F (36, 92.32) = 1.56, p = 0.045. The post hoc tests suggest the significance of this relationship was due to poorer performance on the WCST by binge drinkers, F (3, 42) = 3.27; p = 0.03. Conclusions: Though the deficits were not as vast as hypothesized, the inability for binge drinkers to complete an equal number of categories in the WCST as their non-drinking peers holds interesting conclusions. Those which are discussed relate to binge drinkers' inefficient self-reporting of executive functioning performance, as well as allowing us to possibly understand why we see differences in binge drinkers' perception of alcohol outcomes and their personal self-efficacy with alcohol consumption

Event-related potentials in college-aged binge drinkers and non drinkers

2010 Summer.Includes bibliographic references (pages 27-29).Covers not scanned.Print version deaccessioned 2022.Recent research has begun investigating whether there are neurophysiological differences in individuals who drink heavily compared to those who do not drink. Research has shown significantly reduced P3 amplitudes in response to neutral but not alcohol-related stimuli in alcoholics and their children. The purpose of this study was to further investigate this phenomenon comparing event-related potentials (ERP) of high drinkers to non drinkers when presented positive, negative and alcohol related images. Participants were categorized as a drinker or non drinker based on the Alcohol Use Disorders Identification Test (AUDIT), a self report measure of alcohol use. Group comparisons were made based on differences in amplitude and latency of the P2 and the late positive potential (LPP), a component believed to be more evaluative in nature. This data indicated significant difference in the amplitude of the P2, meaning initial attention is greater in the binge drinkers compared to the non-drinking group. No differences were found in LPP amplitudes between drinkers and non-drinkers. These results suggest that there may be neurophysiological indices for binge drinking which may be useful for identifying individuals who are either at risk or currently abusing alcohol

Evaluation of penalty functions for semi-global matching cost aggregation

The stereo matching method semi-global matching (SGM) relies on consistency constraints during the cost aggregation which are enforced by so-called penalty terms. This paper proposes new and evaluates four penalty functions for SGM. Due to mutual dependencies, two types of matching cost calculation, census and rank transform, are considered. Performance is measured using original and degenerated images exhibiting radiometric changes and noise from the Middlebury benchmark. The two best performing penalty functions are inversely proportional and negatively linear to the intensity gradient and perform equally with 6.05 % and 5.91 % average error, respectively. The experiments also show that adaptive penalty terms are mandatory when dealing with difficult imaging conditions. Consequently, for highest algorithmic performance in real-world systems, selection of a suitable penalty function and thorough parametrization with respect to the expected image quality is essential.Stifterverband für die deutsche Wissenschaf

TREM-1 links dyslipidemia to inflammation and lipid deposition in atherosclerosis.

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune responses, but its significance in non-infectious diseases remains unclear. Here, we demonstrate that TREM-1 promotes cardiovascular disease by exacerbating atherosclerosis. TREM-1 is expressed in advanced human atheromas and is highly upregulated under dyslipidemic conditions on circulating and on lesion-infiltrating myeloid cells in the Apoe(-/-) mouse model. TREM-1 strongly contributes to high-fat, high-cholesterol diet (HFCD)-induced monocytosis and synergizes with HFCD serum-derived factors to promote pro-inflammatory cytokine responses and foam cell formation of human monocyte/macrophages. Trem1(-/-)Apoe(-/-) mice exhibit substantially attenuated diet-induced atherogenesis. In particular, our results identify skewed monocyte differentiation and enhanced lipid accumulation as novel mechanisms through which TREM-1 can promote atherosclerosis. Collectively, our findings illustrate that dyslipidemia induces TREM-1 surface expression on myeloid cells and subsequently synergizes with TREM-1 to enhance monopoiesis, pro-atherogenic cytokine production and foam cell formation

Attenuation of myocardial reperfusion injury in pigs by Mirococept, a membrane-targeted complement inhibitor derived from human CR1

Objectives Membrane-targeted application of complement inhibitors may ameliorate ischemia/reperfusion (I/R) injury by directly targeting damaged cells. We investigated whether Mirococept, a membrane-targeted, myristoylated peptidyl construct derived from complement receptor 1 (CR1) could attenuate I/R injury following acute myocardial infarction in pigs. Methods In a closed-chest pig model of acute myocardial infarction, Mirococept, the non-tailed derivative APT154, or vehicle was administered intracoronarily into the area at risk 5 min pre-reperfusion. Infarct size, cardiac function and inflammatory status were evaluated. Results Mirococept targeted damaged vasculature and myocardium, significantly decreasing infarct size compared to vehicle, whereas APT154 had no effect. Cardioprotection correlated with reduced serum troponin I and was paralleled by attenuated local myocardial complement deposition and tissue factor expression. Myocardial apoptosis (TUNEL-positivity) was also reduced with the use of Mirococept. Local modulation of the pro-inflammatory and pro-coagulant phenotype translated to improved left ventricular end-diastolic pressure, ejection fraction and regional wall motion post-reperfusion. Conclusions Local modification of a pro-inflammatory and pro-coagulant environment after regional I/R injury by site-specific application of a membrane-targeted complement regulatory protein may offer novel possibilities and insights into potential treatment strategies of reperfusion-induced injur

Locally targeted cytoprotection with dextran sulfate attenuates experimental porcine myocardial ischaemia/reperfusion injury

Aims Intravascular inflammatory events during ischaemia/reperfusion injury following coronary angioplasty alter and denudate the endothelium of its natural anticoagulant heparan sulfate proteoglycan (HSPG) layer, contributing to myocardial tissue damage. We propose that locally targeted cytoprotection of ischaemic myocardium with the glycosaminoglycan analogue dextran sulfate (DXS, MW 5000) may protect damaged tissue from reperfusion injury by functional restoration of HSPG. Methods and results In a closed chest porcine model of acute myocardial ischaemia/reperfusion injury (60 min ischaemia, 120 min reperfusion), DXS was administered intracoronarily into the area at risk 5 min prior to reperfusion. Despite similar areas at risk in both groups (39±8% and 42±9% of left ventricular mass), DXS significantly decreased myocardial infarct size from 61±12% of the area at risk for vehicle controls to 39±14%. Cardioprotection correlated with reduced cardiac enzyme release creatine kinase (CK-MB, troponin-I). DXS abrogated myocardial complement deposition and substantially decreased vascular expression of pro-coagulant tissue factor in ischaemic myocardium. DXS binding, detected using fluorescein-labelled agent, localized to ischaemically damaged blood vessels/myocardium and correlated with reduced vascular staining of HSPG. Conclusion The significant cardioprotection obtained through targeted cytoprotection of ischaemic tissue prior to reperfusion in this model of acute myocardial infarction suggests a possible role for the local modulation of vascular inflammation by glycosaminoglycan analogues as a novel therapy to reduce reperfusion injur

Evolution of humoral immune response to SARS-CoV-2 mRNA vaccine in liver transplant recipients - a longitudinal study.

BACKGROUND AND AIM Liver transplant recipients show suboptimal vaccine-elicited immune responses to severe acute respiratory coronavirus 2 (SARS-CoV-2) vaccination. This study aimed to assess real-world data on SARS-CoV-2 antibodies after the second and third SARS-CoV-2 vaccination in liver transplant recipients in Switzerland. METHODS We enrolled liver transplant recipients who attended regular follow-up visits between 01/07/2021 and 30/04/2022 at the outpatient clinic of the Department of Visceral Surgery and Medicine at Bern University Hospital, Switzerland. Following the Swiss Federal Office of Public Health recommendations, we measured SARS-CoV-2 anti-spike IgG antibodies in 117 liver transplant recipients ≥4 weeks after the second SARS-CoV-2 mRNA vaccination from 07/2021-04/2022. In case of antibody levels of 100 AU/ml were defined as "responders", those with 12-100 AU/ml as "partial responders" and those with <12 AU/ml as "non-responders". RESULTS After two vaccinations, 36/117 (31%) were responders, 42/117 (36%) were partial responders and 39/117 (33%) were non-responders. The humoral immune response improved significantly after the third vaccination, resulting in 31/55 (56%) responders among the previous partial or non-responders. A total of 26 patients developed COVID-19, of whom two had a moderate or severe course (both non-responders after three doses). DISCUSSION One third of liver transplant recipients showed an optimal response following two vaccinations; a third dose achieved a complete antibody response in more than half of partial and non-responders. We observed only one severe course of COVID-19 and no deaths from COVID-19 in the vaccinated liver transplant recipients

Online Assessment of Human-Robot Interaction for Hybrid Control of Walking

Restoration of walking ability of Spinal Cord Injury subjects can be achieved by different approaches, as the use of robotic exoskeletons or electrical stimulation of the user’s muscles. The combined (hybrid) approach has the potential to provide a solution to the drawback of each approach. Specific challenges must be addressed with specific sensory systems and control strategies. In this paper we present a system and a procedure to estimate muscle fatigue from online physical interaction assessment to provide hybrid control of walking, regarding the performances of the muscles under stimulation

LRR-protein RNH1 dampens the inflammasome activation and is associated with COVID-19 severity.

Inflammasomes are cytosolic innate immune sensors of pathogen infection and cellular damage that induce caspase-1-mediated inflammation upon activation. Although inflammation is protective, uncontrolled excessive inflammation can cause inflammatory diseases and can be detrimental, such as in coronavirus disease (COVID-19). However, the underlying mechanisms that control inflammasome activation are incompletely understood. Here we report that the leucine-rich repeat (LRR) protein ribonuclease inhibitor (RNH1), which shares homology with LRRs of NLRP (nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain containing) proteins, attenuates inflammasome activation. Deletion of RNH1 in macrophages increases interleukin (IL)-1β production and caspase-1 activation in response to inflammasome stimulation. Mechanistically, RNH1 decreases pro-IL-1β expression and induces proteasome-mediated caspase-1 degradation. Corroborating this, mouse models of monosodium urate (MSU)-induced peritonitis and lipopolysaccharide (LPS)-induced endotoxemia, which are dependent on caspase-1, respectively, show increased neutrophil infiltration and lethality in Rnh1 &lt;sup&gt;-/-&lt;/sup&gt; mice compared with wild-type mice. Furthermore, RNH1 protein levels were negatively related with disease severity and inflammation in hospitalized COVID-19 patients. We propose that RNH1 is a new inflammasome regulator with relevance to COVID-19 severity