Does Posture Influence the Stroop Effect ?

Rosenbaum, Mama, and Algom (2017, Psychological Science, 28, 1864-1867) reported that participants completing the Stroop task (i.e., name the hue of a colour word when the hue and word meaning are congruent or incongruent), showed a smaller Stroop effect (i.e., the difference in response times (RT) between congruent and incongruent trials) when they completed the task standing than when sitting. Here, we report two attempted replications of Rosenbaum et al.’s findings. In Experiment 1 we replicated Rosenbaum et al.’s methodology while also including neutral trials to evaluate whether posture affected Stroop interference (by comparing incongruent and neutral trials) and/or Stroop facilitation (by comparing congruent and neutral trials). In Experiment 2 participants completed only congruent and incongruent trials but were also instructed to keep their feet flat on the floor approximately hip-width apart and avoid leaning on the desk. Because Rosenbaum et al. proposed that standing is attentionally demanding and consumes resources needed for the Stroop task, we hoped that having participants focus on their posture in Experiments 2 might, if anything, increase our chances of replicating Rosenbaum et al.’s findings. Results from both experiments yielded the standard Stroop effect (i.e., slower RTs on incongruent vs. congruent trials (and neutral trials in Experiment 1)), but we failed to detect any influence of posture (sitting vs. standing) on the magnitude of the Stroop effect. Taken together, the results suggest that posture does not influence the magnitude of the Stroop effect to the extent that was previously suggested

Paleolithic Protection in a Western World: A Look Into Preagricultural Nutrition as a Remedy for the Diseases of Civilization

The aim of this investigation is to discover the associations of the Western diet to noncommunicable diseases and to determine if a reversion to a Paleolithic diet will provide treatment and prevention of these diseases. Noncommunicable diseases, otherwise known as “Diseases of Civilization”, are lifestyle influenced diseases and encompass obesity, diabetes mellitus, cardiovascular disease, and associated cancers. Incidences of these diseases have skyrocketed in the past century and show no signs of decline. Since 1900, the death rates due to heart disease and cancer have risen to account for 47% of total deaths in the United States in 2010. (Tippett, 2014) This investigation provides a look into the influence of processed foods, fast foods, and the biochemical processes of the human body to discover the effects of diet on disease. Based on the results of this investigation, the Paleolithic diet serves as an ideal diet to follow in order to prevent contraction of noncommunicable diseases. However, execution of this diet is very difficult. Therefore, small steps towards the dietary habits of Paleolithic people such as purchasing seasonal, locally grown food, avoiding processed foods and fast foods, and spending more time cooking and learning about healthy foods could begin to change the effects of this epidemic

A Translational Metabonomic Assessment of Aristolochic Acid- Induced Nephropathies

Aristolochic acid nephropathy (AAN) is a global term including any form of toxic interstitial nephropathy that is caused either by the ingestion of plants containing aristolochic acids (AA) as part of traditional phytotherapies or by the environmental contaminants in food. Originally, AAN was reported in Belgium in individuals having ingested slimming pills containing powdered root extracts of a Chinese herb, Aristolochia fangchi. However, it is estimated that exposure to AA affects thousands of people all over the world, particularly in the Balkans, Taiwan and China. Despite warnings from the Regulatory Agencies regarding the safety of products containing AA, many AAN cases remain frequently described worldwide. This chapter aims at giving a global picture of AAN through the descriptions of clinical cases and animal models, which were developed to better understand the mode of action of AA when inducing acute/chronic kidney diseases. Major advances in the translational research on biomarkers of AAN are reviewed, with an intended emphasis on the “omics” assessment of this nephrotoxicity

Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury

This work explores the distribution of various markers expressed by interstitial cells in rat kidneys after ischemic injury (35 minutes) during regeneration of S3 tubules of outer stripe of outer medulla (OSOM). Groups of experimental animals (n = 4) were sacrificed every two hours during the first 24 hours post-ischemia as well as 2, 3, 7, 14 days post-ischemia. The occurrence of lineage markers was analyzed on kidney sections by immunohistochemistry and morphometry during the process of tubular regeneration. In postischemic kidneys, interstitial cell proliferation, assessed by 5-bromo-2′-deoxyuridine (BrdU) and Proliferating Cell Nuclear Antigen (PCNA) labeling, was prominent in outer medulla and reach a maximum between 24 and 72 hours after reperfusion. This population was characterized by the coexpression of vimentin and nestin. The density of -Neural Cell Adhesion Molecule (NCAM) positive interstitial cells increased transiently (18–72 hours) in the vicinity of altered tubules. We have also localized a small population of α-Smooth Muscle Actin (SMA)-positive cells confined to chronically altered areas and characterized by a small proliferative index. In conclusion, we observed in the postischemic kidney a marked proliferation of interstitial cells that underwent transient phenotypical modifications. These interstitial cells could be implicated in processes leading to renal fibrosis

Delayed exercise training improves obesity-induced chronic kidney disease by activating ampk pathway in high-fat diet-fed mice

Exercise training is now recognized as an interesting therapeutic strategy in managing obesity and its related disorders. However, there is still a lack of knowledge about its impact on obesity-induced chronic kidney disease (CKD). Here, we investigated the effects of a delayed protocol of endurance exercise training (EET) as well as the underlying mechanism in obese mice presenting CKD. Mice fed a high-fat diet (HFD) or a low-fat diet (LFD) for 12 weeks were subsequently submitted to an 8-weeks EET protocol. Delayed treatment with EET in obese mice prevented body weight gain associated with a reduced calorie intake. EET intervention counteracted obesity-related disorders including glucose intolerance, insulin resistance, dyslipidaemia and hepatic steatosis. Moreover, our data demonstrated for the first time the beneficial effects of EET on obesity-induced CKD as evidenced by an improvement of obesity-related glomerulopathy, tubulo-interstitial fibrosis, inflammation and oxidative stress. EET also prevented renal lipid depositions in the proximal tubule. These results were associated with an improvement of the AMPK pathway by EET in renal tissue. AMPK-mediated phosphorylation of ACC and ULK-1 were particularly enhanced leading to increased fatty acid oxidation and autophagy improvement with EET in obese mice

Overexpression of Wild-Type Human Alpha-Synuclein Causes Metabolism Abnormalities in Thy1-aSYN Transgenic Mice

Parkinson’s disease is a progressive neurodegenerative disorder characterized by loss of dopaminergic neurons, pathological accumulation of alpha-synuclein and motor symptoms, but also by non-motor symptoms. Metabolic abnormalities including body weight loss have been reported in patients and could precede by several years the emergence of classical motor manifestations. However, our understanding of the pathophysiological mechanisms underlying body weight loss in PD is limited. The present study investigated the links between alpha-synuclein accumulation and energy metabolism in transgenic mice overexpressing Human wild-type (WT) alpha-synuclein under the Thy1 promoter (Thy1-aSYN mice). Results showed that Thy1-aSYN mice gained less body weight throughout life than WT mice, with significant difference observed from 3 months of age. Body composition analysis of 6-month-old transgenic animals showed that body mass loss was due to lower adiposity. Thy1-aSYN mice displayed lower food consumption, increased spontaneous activity, as well as a reduced energy expenditure compared to control mice. While no significant change in glucose or insulin responses were observed, Thy1-aSYN mice had significantly lower plasmatic levels of insulin and leptin than control animals. Moreover, the pathological accumulation of alpha-synuclein in the hypothalamus of 6-month-old Thy1-aSYN mice was associated with a down-regulation of the phosphorylated active form of the signal transducer and activator of transcription 3 (STAT3) and of Rictor (the mTORC2 signaling pathway), known to couple hormonal signals with the maintenance of metabolic and energy homeostasis. Collectively, our results suggest that (i) metabolic alterations are an important phenotype of alpha-synuclein overexpression in mice and that (ii) impaired STAT3 activation and mTORC2 levels in the hypothalamus may underlie the disruption of feeding regulation and energy metabolism in Thy1-aSYN mice

Functional abdominal pain disorders and patient- and parent- reported outcomes in children with inflammatory bowel disease in remission

BACKGROUND: Chronic abdominal pain occurs frequently in pediatric patients with inflammatory bowel disease (IBD) in remission. AIMS: To assess the prevalence and factors associated with Functional Abdominal Pain Disorders among IBD children in remission (IBD-FAPD). METHODS: Patients with IBD for > 1 year, in clinical remission for ≥ 3 months were recruited from a National IBD network. IBD-FAPDs were assessed using the Rome III questionnaire criteria. Patient- or parent- reported outcomes were assessed. RESULTS: Among 102 included patients, 57 (56%) were boys, mean age (DS) was 15.0 (± 2.0) years and 75 (74%) had Crohn's disease. Twenty-two patients (22%) had at least one Functional Gastrointestinal Disorder among which 17 had at least one IBD-FAPD. Past severity of disease or treatments received and level of remission were not significantly associated with IBD-FAPD. Patients with IBD-FAPD reported more fatigue (peds-FACIT-F: 35.9 ± 9.8 vs. 43.0 ± 6.9, p = 0.01) and a lower HR-QoL (IMPACT III: 76.5 ± 9.6 vs. 81.6 ± 9.2, p = 0.04) than patients without FAPD, and their parents had higher levels of State and Trait anxiety than the other parents. CONCLUSIONS: Prevalence of IBD-FAPD was 17%. IBD-FAPD was not associated with past severity of disease, but with fatigue and lower HR-QoL