Driver performance under simulated and actual driving conditions: validity and orthogonality

This study contrasted the performance of drivers under actual and simulated driving conditions, in order to assess the validity of the simulators and test the hypothesis that driving is composed of largely orthogonal sub-tasks. Thirty experienced drivers completed an on-road driving test and drove two different simulators, each simulator drive comprising seven difficulty-moderated driving scenarios. Between-simulator contrasts revealed largely absolute validity, the anticipated effects of increased difficulty within driving scenarios, but weak relationships between performance of different driving scenarios. On-road driving was reliably assessed by a nationally-recognised expert driving assessor, as reflected by standard statistical measures of reliability and consistency. However, on-road driving revealed relatively little cross-category correlation of on-road driving errors, or between on-road and simulator driving. Thus, despite the compelling evidence of absolute and relative validity within and between simulators, there is little evidence of criterion validity (i.e. relationship to on road driving, as assessed by the expert assessor). Moreover, the study provides strong evidence for orthogonality in the driving task- driving comprises large numbers of relatively separate tasks

Diet and general cognitive ability in the UK Biobank dataset

Accumulating evidence suggests that dietary interventions might have potential to be used as a strategy to protect against age-related cognitive decline and neurodegeneration, as there are associations between some nutrients, food groups, dietary patterns, and some domains of cognition. In this study, we aimed to conduct the largest investigation of diet and cognition to date, through systematically examining the UK Biobank (UKB) data to find out whether dietary quality and food groups play a role on general cognitive ability. This cross-sectional population-based study involved 48,749 participants. UKB data on food frequency questionnaire and cognitive function were used. Also, healthy diet, partial fibre intake, and milk intake scores were calculated. Adjusted models included age, sex, and BMI. We observed associations between better general cognitive ability and higher intakes of fish, and unprocessed red meat; and moderate intakes of fibre, and milk. Surprisingly, we found that diet quality, vegetable intake, high and low fibre and milk intake were inversely associated with general cognitive ability. Our results suggest that fish and unprocessed red meat and/or nutrients that are found in fish and unprocessed red meat might be beneficial for general cognitive ability. However, results should be interpreted in caution as the same food groups may affect other domains of cognition or mental health differently. These discrepancies in the current state of evidence invites further research to examine domain-specific effects of dietary patterns/food groups on a wide range of cognitive and affective outcomes with a special focus on potential covariates that may have an impact on diet and cognition relationship

Bifidobacterium longum 1714 improves sleep quality and aspects of well-being in healthy adults: a randomized, double-blind, placebo-controlled clinical trial

Stress and sleep are linked with overall well-being. Bifidobacterium longum 1714 has been shown to influence stress responses and modulate neural responses during social stress, and influence sleep quality during examination stress in healthy adults. Here, we explored the ability of this strain to alter sleep quality in adults using subjective and objective measures. Eighty-nine adults (18-45y) with impaired sleep quality assessed with the Pittsburgh Sleep Quality Index (PSQI) and with a global score ≥ 5 were randomized to receive B. longum 1714 or placebo daily for eight weeks. Assessing the effect of the strain on PSQI global score was the primary objective. Secondary objectives assessed sleep quality and well-being subjectively and sleep parameters using actigraphy objectively. While PSQI global score improved in both groups, B. longum 1714 significantly improved the PSQI component of sleep quality (p < 0.05) and daytime dysfunction due to sleepiness (p < 0.05) after 4 weeks and social functioning (p < 0.05) and energy/vitality (p < 0.05) after 8 weeks, compared to placebo. No significant effect on actigraphy measures were observed. The 1714 strain had a mild effect on sleep, demonstrated by a faster improvement in sleep quality at week 4 compared to placebo, although overall improvements after 8 weeks were similar in both groups. B. longum 1714 improved social functioning and increased energy/vitality in line with previous work that showed the strain modulated neural activity which correlated with enhanced vitality/reduced mental fatigue (ClinicalTrials.gov: NCT04167475). Recent work has highlighted the gut microbiota as a key contributor to healthy brain development, function, and emotional well-being throughout life 1 possibly through the regulation of our immune, metabolic, and nervous system 2-4. Changes in the gut microbiota composition between healthy people and those with mental health disorders such as anxiety 5-7 and depression 8-11 have pinpointed the gut microbiota as a potential significant target to influence mental health. More recently, the role of 'psychobiotics' has demonstrated considerable impact on the stress response 12-17 and symptoms of depression 18-20 and anxiety 21 via the microbiota-gut-brain-axis in a strain specific manner. Such 'psychobiotics' may alleviate symptoms of excessive stress, anxiety, and depression by affecting physiological outputs and processes in the host such as immune function 22 , tryptophan metabolism 23 , corticosterone/cortisol 17,24 , neurotransmitters 25-27 , microbial metabolites 28 , and brain-derived neurotrophic factor (BDNF) 29. Indeed, given the role of the gut microbiota as a key factor contributing to mood and mental health, it is reasonable to consider the gut as a window to mental well-being. Sleep is complex and multifactorial, therefore multiple physiologic processes can influence its quality 30,31. More recently, a growing body of evidence points to the consequences of poor sleep on immune function 32 and the microbiota-gut-brain axis as a potential regulator of sleep health 33-35. Adding to this evidence, changes in the gut microbiota composition have been described following sleep deprivation 36-38 and accompanying sleep disorders 39-41 , with improvements in sleep efficiency and sleep duration contributing to enhanced gut OPE

Systems and technologies for objective evaluation of technical skills in laparoscopic surgery

Minimally invasive surgery is a highly demanding surgical approach regarding technical requirements for the surgeon, who must be trained in order to perform a safe surgical intervention. Traditional surgical education in minimally invasive surgery is commonly based on subjective criteria to quantify and evaluate surgical abilities, which could be potentially unsafe for the patient. Authors, surgeons and associations are increasingly demanding the development of more objective assessment tools that can accredit surgeons as technically competent. This paper describes the state of the art in objective assessment methods of surgical skills. It gives an overview on assessment systems based on structured checklists and rating scales, surgical simulators, and instrument motion analysis. As a future work, an objective and automatic assessment method of surgical skills should be standardized as a means towards proficiency-based curricula for training in laparoscopic surgery and its certification

Catechol-O-Methyltransferase Val158Met Polymorphism Associates with Individual Differences in Sleep Physiologic Responses to Chronic Sleep Loss

Val158Met polymorphism was a novel marker in healthy adults of differential vulnerability to chronic partial sleep deprivation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily and persistent basis. allelic frequencies were higher in whites than African Americans.-related treatment responses and risk factors for symptom exacerbation

Deficiency of Vasodilator-Stimulated Phosphoprotein (VASP) Increases Blood-Brain-Barrier Damage and Edema Formation after Ischemic Stroke in Mice

Background: Stroke-induced brain edema formation is a frequent cause of secondary infarct growth and deterioration of neurological function. The molecular mechanisms underlying edema formation after stroke are largely unknown. Vasodilator-stimulated phosphoprotein (VASP) is an important regulator of actin dynamics and stabilizes endothelial barriers through interaction with cell-cell contacts and focal adhesion sites. Hypoxia has been shown to foster vascular leakage by downregulation of VASP in vitro but the significance of VASP for regulating vascular permeability in the hypoxic brain in vivo awaits clarification. Methodology/Principal Findings: Focal cerebral ischemia was induced in Vasp2/2 mice and wild-type (WT) littermates by transient middle cerebral artery occlusion (tMCAO). Evan’s Blue tracer was applied to visualize the extent of blood-brainbarrier (BBB) damage. Brain edema formation and infarct volumes were calculated from 2,3,5-triphenyltetrazolium chloride (TTC)-stained brain slices. Both mouse groups were carefully controlled for anatomical and physiological parameters relevant for edema formation and stroke outcome. BBB damage (p,0.05) and edema volumes (1.7 mm360.5 mm3 versus 0.8 mm360.4 mm3; p,0.0001) were significantly enhanced in Vasp2/2 mice compared to controls on day 1 after tMCAO. This was accompanied by a significant increase in infarct size (56.1 mm3617.3 mm3 versus 39.3 mm3610.7 mm3, respectively; p,0.01) and a non significant trend (p.0.05) towards worse neurological outcomes. Conclusion: Our study identifies VASP as critical regulator of BBB maintenance during acute ischemic stroke. Therapeutic modulation of VASP or VASP-dependent signalling pathways could become a novel strategy to combat excessive edema formation in ischemic brain damage

Shift Work in Nurses: Contribution of Phenotypes and Genotypes to Adaptation

Daily cycles of sleep/wake, hormones, and physiological processes are often misaligned with behavioral patterns during shift work, leading to an increased risk of developing cardiovascular/metabolic/gastrointestinal disorders, some types of cancer, and mental disorders including depression and anxiety. It is unclear how sleep timing, chronotype, and circadian clock gene variation contribute to adaptation to shift work.Newly defined sleep strategies, chronotype, and genotype for polymorphisms in circadian clock genes were assessed in 388 hospital day- and night-shift nurses.Night-shift nurses who used sleep deprivation as a means to switch to and from diurnal sleep on work days (∼25%) were the most poorly adapted to their work schedule. Chronotype also influenced efficacy of adaptation. In addition, polymorphisms in CLOCK, NPAS2, PER2, and PER3 were significantly associated with outcomes such as alcohol/caffeine consumption and sleepiness, as well as sleep phase, inertia and duration in both single- and multi-locus models. Many of these results were specific to shift type suggesting an interaction between genotype and environment (in this case, shift work).Sleep strategy, chronotype, and genotype contribute to the adaptation of the circadian system to an environment that switches frequently and/or irregularly between different schedules of the light-dark cycle and social/workplace time. This study of shift work nurses illustrates how an environmental "stress" to the temporal organization of physiology and metabolism can have behavioral and health-related consequences. Because nurses are a key component of health care, these findings could have important implications for health-care policy

Intermittent Hypoxia-Induced Cognitive Deficits Are Mediated by NADPH Oxidase Activity in a Murine Model of Sleep Apnea

Background: In rodents, exposure to intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), is associated with neurobehavioral impairments, increased apoptosis in the hippocampus and cortex, as well as increased oxidant stress and inflammation. Excessive NADPH oxidase activity may play a role in IH-induced CNS dysfunction. Methods and Findings: The effect of IH during light period on two forms of spatial learning in the water maze and well as markers of oxidative stress was assessed in mice lacking NADPH oxidase activity (gp91phox _/Y) and wild-type littermates. On a standard place training task, gp91phox _/Y displayed normal learning, and were protected from the spatial learning deficits observed in wild-type littermates exposed to IH. Moreover, anxiety levels were increased in wild-type mice exposed to IH as compared to room air (RA) controls, while no changes emerged in gp91phox _/Y mice. Additionally, wild-type mice, but not gp91phox _/Y mice had significantly elevated levels of NADPH oxidase expression and activity, as well as MDA and 8-OHDG in cortical and hippocampal lysates following IH exposures. Conclusions: The oxidative stress responses and neurobehavioral impairments induced by IH during sleep are mediated, at least in part, by excessive NADPH oxidase activity, and thus pharmacological agents targeting NADPH oxidase may provid

The NOX toolbox: validating the role of NADPH oxidases in physiology and disease

Reactive oxygen species (ROS) are cellular signals but also disease triggers; their relative excess (oxidative stress) or shortage (reductive stress) compared to reducing equivalents are potentially deleterious. This may explain why antioxidants fail to combat diseases that correlate with oxidative stress. Instead, targeting of disease-relevant enzymatic ROS sources that leaves physiological ROS signaling unaffected may be more beneficial. NADPH oxidases are the only known enzyme family with the sole function to produce ROS. Of the catalytic NADPH oxidase subunits (NOX), NOX4 is the most widely distributed isoform. We provide here a critical review of the currently available experimental tools to assess the role of NOX and especially NOX4, i.e. knock-out mice, siRNAs, antibodies, and pharmacological inhibitors. We then focus on the characterization of the small molecule NADPH oxidase inhibitor, VAS2870, in vitro and in vivo, its specificity, selectivity, and possible mechanism of action. Finally, we discuss the validation of NOX4 as a potential therapeutic target for indications including stroke, heart failure, and fibrosis