Executive function in schizophrenia and autism in adults shares common components separating high and low performance groups.

The profile of executive function (EF) in adults with Schizophrenia (SCZ) and autism spectrum disorder (ASD) remains unclear. This study aims to ascertain if distinct EF patterns can be identified between each clinical condition by comparing the neuropsychological profile of adults with SCZ and ASD, for whom the differential diagnosis is still highly challenging. Forty-five individuals (15 SCZ, 15 ASD, 15 controls) matched for age, sex, education level, and handedness underwent intelligence evaluation and neuropsychological testing for working memory, inhibition, planning and set-shifting, and verbal fluency subdomains. Principal component analysis (2D-PCA) using variables representing 4 domains was employed to identify patterns in neuropsychological profiles. The ASD group had lower scores on the Digits Forward subtest compared to the SCZ group (7.2 ± 2.1 vs. 9.3 ± 1.9, p = 0.003; Cohen's d: 1.05). ASD also performed significantly worse on the Stroop Word Test compared to the control group (77.7± 17.9 vs. 98.0 ± 12.7, p = 0.009; Cohen's d: 1.31). No significant differences were observed between ASD and SCZ on other EF measures. The larger contributors for the dimensions in 2D-PCA were the Digits Forward subtest and Stroop Word Test. Still, there was substantial overlap between the clinical groups. This study suggests a high degree of similarity of EF between SCZ and ASD. Through four EF measures, the discrimination of low and high-functioning EF groups spanning both diagnostic categories may help to identify the individuals who could better benefit from cognitive rehabilitation strategies.

Exposure to DEP Modifies the Human Umbilical Artery Vascular Resistance Contributing to Hypertension in Pregnancy.

Hypertensive disorders in pregnancy (HDP) are the most prevalent diseases during pregnancy. In addition to the already identified risk factors, exposure to environmental contaminants has been also considered a new one. Phthalates, which are classified as priority environmental pollutants due to their ubiquitousness and endocrine disrupting properties, have been implicated in HDP in some epidemiological studies. Nevertheless, phthalates' vascular impacts still need to be clarified. Thus, we aimed to understand the connection between phthalates exposure and the occurrence of gestational hypertension, as well as the pathway involved in the pathological vascular effects. We investigated diethyl phthalate's (DEP) effect on the vascular reactivity of the human umbilical arteries (HUAs) from normotensive and hypertensive pregnant women. Both DEP's nongenomic (within minutes effect) and genomic (24 h exposure to DEP) actions were evaluated, as well as the contribution of cyclic guanosine monophosphate and Ca2+ channel pathways. The results show that short-term exposure to DEP interferes with serotonin and histamine receptors, while after prolonged exposure, DEP seems to share the same vasorelaxant mechanism as estrogens, through the NO/sGC/cGMP/PKG signaling pathway, and to interfere with the L-type Ca2+ channels. Thus, the vascular effect induced by DEP is similar to that observed in HUA from hypertensive pregnancies, demonstrating that the development of HDP may be a consequence of DEP exposure.

Neurofeedback training of executive function in autism spectrum disorder: distinct effects on brain activity levels and compensatory connectivity changes.

BACKGROUND: Deficits in executive function (EF) are consistently reported in autism spectrum disorders (ASD). Tailored cognitive training tools, such as neurofeedback, focused on executive function enhancement might have a significant impact on the daily life functioning of individuals with ASD. We report the first real-time fMRI neurofeedback (rt-fMRI NF) study targeting the left dorsolateral prefrontal cortex (DLPFC) in ASD. METHODS: Thirteen individuals with autism without intellectual disability and seventeen neurotypical individuals completed a rt-fMRI working memory NF paradigm, consisting of subvocal backward recitation of self-generated numeric sequences. We performed a region-of-interest analysis of the DLPFC, whole-brain comparisons between groups and, DLPFC-based functional connectivity. RESULTS: The ASD and control groups were able to modulate DLPFC activity in 84% and 98% of the runs. Activity in the target region was persistently lower in the ASD group, particularly in runs without neurofeedback. Moreover, the ASD group showed lower activity in premotor/motor areas during pre-neurofeedback run than controls, but not in transfer runs, where it was seemingly balanced by higher connectivity between the DLPFC and the motor cortex. Group comparison in the transfer run also showed significant differences in DLPFC-based connectivity between groups, including higher connectivity with areas integrated into the multidemand network (MDN) and the visual cortex. CONCLUSIONS: Neurofeedback seems to induce a higher between-group similarity of the whole-brain activity levels (including the target ROI) which might be promoted by changes in connectivity between the DLPFC and both high and low-level areas, including motor, visual and MDN regions.

Polyphenols: immunonutrients tipping the balance of immunometabolism in chronic diseases.

Mounting evidence progressively appreciates the vital interplay between immunity and metabolism in a wide array of immunometabolic chronic disorders, both autoimmune and non-autoimmune mediated. The immune system regulates the functioning of cellular metabolism within organs like the brain, pancreas and/or adipose tissue by sensing and adapting to fluctuations in the microenvironment's nutrients, thereby reshaping metabolic pathways that greatly impact a pro- or anti-inflammatory immunophenotype. While it is agreed that the immune system relies on an adequate nutritional status to function properly, we are only just starting to understand how the supply of single or combined nutrients, all of them termed immunonutrients, can steer immune cells towards a less inflamed, tolerogenic immunophenotype. Polyphenols, a class of secondary metabolites abundant in Mediterranean foods, are pharmacologically active natural products with outstanding immunomodulatory actions. Upon binding to a range of receptors highly expressed in immune cells (e.g. AhR, RAR, RLR), they act in immunometabolic pathways through a mitochondria-centered multi-modal approach. First, polyphenols activate nutrient sensing via stress-response pathways, essential for immune responses. Second, they regulate mammalian target of rapamycin (mTOR)/AMP-activated protein kinase (AMPK) balance in immune cells and are well-tolerated caloric restriction mimetics. Third, polyphenols interfere with the assembly of NLR family pyrin domain containing 3 (NLRP3) in endoplasmic reticulum-mitochondria contact sites, inhibiting its activation while improving mitochondrial biogenesis and autophagosome-lysosome fusion. Finally, polyphenols impact chromatin remodeling and coordinates both epigenetic and metabolic reprogramming. This work moves beyond the well-documented antioxidant properties of polyphenols, offering new insights into the multifaceted nature of these compounds. It proposes a mechanistical appraisal on the regulatory pathways through which polyphenols modulate the immune response, thereby alleviating chronic low-grade inflammation. Furthermore, it draws parallels between pharmacological interventions and polyphenol-based immunonutrition in their modes of immunomodulation across a wide spectrum of socioeconomically impactful immunometabolic diseases such as Multiple Sclerosis, Diabetes (type 1 and 2) or even Alzheimer's disease. Lastly, it discusses the existing challenges that thwart the translation of polyphenols-based immunonutritional interventions into long-term clinical studies. Overcoming these limitations will undoubtedly pave the way for improving precision nutrition protocols and provide personalized guidance on tailored polyphenol-based immunonutrition plans.

Portuguese observational cross-sectional clinical imaging study protocol to investigate central dopaminergic mechanisms of successful weight loss through bariatric surgery.

INTRODUCTION: Bariatric surgery (BS) is the treatment of choice for refractory obesity. Although weight loss (WL) reduces the prevalence of obesity-related comorbidities, not all patients maintain it. It has been suggested that central mechanisms involving dopamine receptors may play a role in successful WL. This protocol describes an observational cross-sectional study to test if the binding of central dopamine receptors is similar in individuals who responded successfully to BS and age- and gender-matched normal-weight healthy individuals (controls). As secondary goals, the protocol will investigate if this binding correlates with key parameters such as age, hormonal status, anthropometric metrics and neurobehavioural scores. Finally, as exploratory goals, we will include a cohort of individuals with obesity before and after BS to explore whether obesity and type of BS (sleeve gastrectomy and Roux-en-Y gastric bypass) yield distinct binding values and track central dopaminergic changes resulting from BS. METHODS AND ANALYSIS: To address the major research question of this observational study, positron emission tomography (PET) with [11C]raclopride will be used to map brain dopamine type 2 and 3 receptors (D2/3R) non-displaceable binding potential (BPND) of individuals who have successfully responded to BS. Mean regional D2/3R BPND values will be compared with control individuals by two one-sided test approaches. The sample size (23 per group) was estimated to demonstrate the equivalence between two independent group means. In addition, these binding values will be correlated with key parameters to address secondary goals. Finally, for exploratory analysis, these values will be compared within the same individuals (before and after BS) and between individuals with obesity and controls and types of BS. ETHICS AND DISSEMINATION: The project and informed consent received ethical approval from the Faculty of Medicine and the Coimbra University Hospital ethics committees. Results will be disseminated in international peer-reviewed journals and conferences.

Functional and structural connectivity success predictors of real-time fMRI neurofeedback targeting DLPFC: Contributions from central executive, salience, and default mode networks.

Real-time functional magnetic resonance imaging (rt-fMRI) neurofeedback (NF), a training method for the self-regulation of brain activity, has shown promising results as a neurorehabilitation tool, depending on the ability of the patient to succeed in neuromodulation. This study explores connectivity-based structural and functional success predictors in an NF n-back working memory paradigm targeting the dorsolateral prefrontal cortex (DLPFC). We established as the NF success metric the linear trend on the ability to modulate the target region during NF runs and performed a linear regression model considering structural and functional connectivity (intrinsic and seed-based) metrics. We found a positive correlation between NF success and the default mode network (DMN) intrinsic functional connectivity and a negative correlation with the DLPFC-precuneus connectivity during the 2-back condition, indicating that success is associated with larger uncoupling between DMN and the executive network. Regarding structural connectivity, the salience network emerges as the main contributor to success. Both functional and structural classification models showed good performance with 77% and 86% accuracy, respectively. Dynamic switching between DMN, salience network and central executive network seems to be the key for neurofeedback success, independently indicated by functional connectivity on the localizer run and structural connectivity data.

Improved Chemical and Radiochemical Synthesis of Neuropeptide Y Y2 Receptor Antagonist N-Methyl-JNJ-31020028 and Preclinical Positron Emission Tomography Studies.

Neuropeptide Y (NPY) is one of the most abundant peptides in the central nervous system of mammals and is involved in several physiological processes through NPY Y1, Y2, Y4 and Y5 receptors. Of those, the Y2 receptor has particular relevance for its autoreceptor role in inhibiting the release of NPY and other neurotransmitters and for its involvement in relevant mechanisms such as feeding behaviour, cognitive processes, emotion regulation, circadian rhythms and disorders such as epilepsy and cancer. PET imaging of the Y2 receptor can provide a valuable platform to understand this receptor's functional role and evaluate its potential as a therapeutic target. In this work, we set out to refine the chemical and radiochemical synthesis of the Y2 receptor antagonist N-[11C]Me-JNJ31020028 for in vivo PET imaging studies. The non-radioactive reference compound, N-Me-JNJ-31020028, was synthesised through batch synthesis and continuous flow methodology, with 43% and 92% yields, respectively. N-[11C]Me-JNJ-31020028 was obtained with a radiochemical purity > 99%, RCY of 31% and molar activity of 156 GBq/µmol. PET imaging clearly showed the tracer's biodistribution in several areas of the mouse brain and gut where Y2 receptors are known to be expressed.

Irreversible atrophy in memory brain regions over 7 years is predicted by glycemic control in type 2 diabetes without mild cognitive impairment.

Memory-related impairments in type 2 diabetes may be mediated by insulin resistance and hyperglycemia. Previous cross-sectional studies have controversially suggested a relationship between metabolic control and a decrease in hippocampal volumes, but only longitudinal studies can test this hypothesis directly. We performed a longitudinal morphometric study to provide a direct test of a possible role of higher levels of glycated hemoglobin with long term brain structural integrity in key regions of the memory system - hippocampus, parahippocampal gyrus and fusiform gyrus. Grey matter volume was measured at two different times - baseline and after ~7 years. We found an association between higher initial levels of HbA1C and grey matter volume loss in all three core memory regions, even in the absence of mild cognitive impairment. Importantly, these neural effects persisted in spite of the fact that patients had significantly improved their glycemic control. This suggests that early high levels of HbA1c might be irreversibly associated with subsequent long-term atrophy in the medial temporal cortex and that early intensive management is critical.

Functional reorganization of memory processing in the hippocampus is associated with neuroprotector GLP-1 levels in type 2 diabetes.

Type 2 diabetes (T2D) often impairs memory functions, suggesting specific vulnerability of the hippocampus. In vivo neuroimaging studies relating encoding and retrieval of memory information with endogenous neuroprotection are lacking. The neuroprotector glucagon-like peptide (GLP-1) has a high receptor density in anterior/ventral hippocampus, as shown by animal models. Using an innovative event-related fMRI design in 34 participants we investigated patterns of hippocampal activity in T2D (n = 17) without mild cognitive impairment (MCI) versus healthy controls (n = 17) during an episodic memory task. We directly measured neurovascular coupling by estimating the hemodynamic response function using event-related analysis related to encoding and retrieval of episodic information in the hippocampus. We applied a mixed-effects general linear model analysis and a two-factor ANOVA to test for group differences. Significant between-group differences were found for memory encoding, showing evidence for functional reorganization: T2D patients showed an augmented activation in the posterior hippocampus while anterior activation was reduced. The latter was negatively correlated with both GLP-1 pre- and post-breakfast levels, in the absence of grey matter changes. These results suggest that patients with T2D without MCI have pre-symptomatic functional reorganization in brain regions underlying episodic memory, as a function of the concentration of the neuroprotective neuropeptide GLP-1.

Neuroanatomical predictors of transcranial direct current stimulation (tDCS)-induced modifications in neurocognitive task performance in typically developing individuals.

Transcranial direct current stimulation (tDCS) is a non-invasive neuromodulation technique gaining more attention in neurodevelopmental disorders (NDDs). Due to the phenotypic heterogeneity of NDDs, tDCS is unlikely to be equally effective in all individuals. The present study aimed to establish neuroanatomical markers in typical developing (TD) individuals that may be used for the prediction of individual responses to tDCS. 57 TD male and female children received 2mA anodal and sham tDCS, targeting the left dorsolateral prefrontal cortex (DLPFCleft), right inferior frontal gyrus, and bilateral temporo-parietal junction. Response to tDCS was assessed based on task performance differences between anodal and sham tDCS in different neurocognitive tasks (N-back, Flanker, Mooney Faces Detection, Attentional Emotional Recognition task). Measures of cortical thickness (CT) and surface area (SA) were derived from 3-Tesla structural MRI scans. Associations between neuroanatomy and task performance were assessed using a general linear model. Machine learning (ML) algorithms were employed to predict responses to tDCS. Overall, vertex-wise estimates of SA were more closely linked to differences in task performance than measures of CT. Across ML algorithms, highest accuracies were observed for the prediction of N-back task performance differences following stimulation of the DLPFCleft, where 65% of behavioural variance was explained by variability in SA. Lower accuracies were observed for all other tasks and stimulated regions. This suggests that it may be possible to predict individual responses to tDCS for some behavioural measures and target regions. In the future, these models might be extended to predict treatment outcome in individuals with NDDs.Significance statement Transcranial direct current stimulation (tDCS) is a non-invasive neuromodulation technique that has recently gained more attention in neurodevelopmental disorders (NDDs), such as autism and attention-deficit/hyperactivity disorder. However, due to the phenotypic heterogeneity of NDDs, tDCS is unlikely to be equally effective in all individuals. The present study aimed to establish neuroanatomical biomarkers in typical developing individuals that may be used for the prediction of individual responses to tDCS. Our findings suggest that it may be possible to accurately predict individual responses to tDCS for some behavioural measures using measures of neuroanatomy. In the future, our models might be extended to predict treatment outcome in individuals with clinical diagnoses, and may allow for more individualized, person-centred interventions.

Standard Doses of Cholecalciferol Reduce Glucose and Increase Glutamine in Obesity-Related Hypertension: Results of a Randomized Trial.

In arterial hypertension, the dysregulation of several metabolic pathways is closely associated with chronic immune imbalance and inflammation progression. With time, these disturbances lead to the development of progressive disease and end-organ involvement. However, the influence of cholecalciferol on metabolic pathways as a possible mechanism of its immunomodulatory activity in obesity-related hypertension is not known. In a phase 2, randomized, single-center, 24-week trial, we evaluated, as a secondary outcome, the serum metabolome of 36 age- and gender-matched adults with obesity-related hypertension and vitamin D deficiency, before and after supplementation with cholecalciferol therapy along with routine medication. The defined endpoint was the assessment of circulating metabolites using a nuclear magnetic resonance-based metabolomics approach. Univariate and multivariate analyses were used to evaluate the systemic metabolic alterations caused by cholecalciferol. In comparison with normotensive controls, hypertensive patients presented overall decreased expression of several amino acids (p < 0.05), including amino acids with ketogenic and glucogenic properties as well as aromatic amino acids. Following cholecalciferol supplementation, increases were observed in glutamine (p < 0.001) and histidine levels (p < 0.05), with several other amino acids remaining unaffected. Glucose (p < 0.05) and acetate (p < 0.05) decreased after 24 weeks in the group taking the supplement, and changes in the saturation of fatty acids (p < 0.05) were also observed, suggesting a role of liposoluble vitamin D in lipid metabolism. Long-term cholecalciferol supplementation in chronically obese and overweight hypertensives induced changes in the blood serum metabolome, which reflected systemic metabolism and may have fostered a new microenvironment for cell proliferation and biology. Of note, the increased availability of glutamine may be relevant for the proliferation of different T-cell subsets.

Neural inhibition as implemented by an actor-critic model involves the human dorsal striatum and ventral tegmental area.

Inhibition is implicated across virtually all human experiences. As a trade-off of being very efficient, this executive function is also prone to many errors. Rodent and computational studies show that midbrain regions play crucial roles during errors by sending dopaminergic learning signals to the basal ganglia for behavioural adjustment. However, the parallels between animal and human neural anatomy and function are not determined. We scanned human adults while they performed an fMRI inhibitory task requiring trial-and-error learning. Guided by an actor-critic model, our results implicate the dorsal striatum and the ventral tegmental area as the actor and the critic, respectively. Using a multilevel and dimensional approach, we also demonstrate a link between midbrain and striatum circuit activity, inhibitory performance, and self-reported autistic and obsessive-compulsive subclinical traits.

Rosuvastatin effect on atherosclerotic plaque metabolism: A subclinical atherosclerosis imaging study with 18F-NaF PET-CT.

BACKGROUND AND AIMS: Atherosclerotic plaque fluorine-18 sodium fluoride (18F-NaF) uptake on positron emission tomography with computed tomography (PET-CT) identifies active microcalcification and has been shown to correlate with clinical instability in patients with cardiovascular (CV) disease. Statin therapy promotes coronary macrocalcification over time. Our aim was to investigate rosuvastatin effect on atheroma 18F-NaF uptake. METHODS: Subjects with high CV risk but without CV events underwent 18F-NaF-PET-CT in a single-centre. Those with subclinical atherosclerosis and significant 18F-NaF plaque uptake were included in a single-arm clinical trial, treated with rosuvastatin 20 mg/daily for six months, and re-evaluated by 18F-NaF-PET-CT. Primary endpoint was reduction in maximum atheroma 18F-NaF uptake in the coronary, aortic or carotid arteries, assessed by the tissue-to-background ratio (TBR). The secondary endpoint was corrected uptake per lesion (CUL) variation. RESULTS: Forty individuals were enrolled and 38 included in the pharmacological trial; mean age was 64 years, two-thirds were male and most were diabetic. The 10-year expected CV risk was 9.5% (6.0-15.3) for SCORE2 and 31.7 ± 18.7% for ASCVD systems. After six months of rosuvastatin treatment (n = 34), low-density lipoprotein cholesterol lowered from 133.6 ± 33.8 to 58.8 ± 20.7 mg dL-1 (60% relative reduction, p < 0.01). There was a significant 19% reduction in maximum plaque 18F-NaF uptake after treatment, from 1.96 (1.78-2.22) to 1.53 (1.40-2.10), p < 0.001 (primary endpoint analysis). The secondary endpoint CUL was reduced by 23% (p = 0.003). CONCLUSION: In a single-centre non-randomized clinical trial of high CV risk individuals with subclinical atherosclerosis, the maximum atherosclerotic plaque 18F-NaF uptake was significantly reduced after six months of high-intensity statin.

EEG as a potential ground truth for the assessment of cognitive state in software development activities: A multimodal imaging study.

Cognitive human error and recent cognitive taxonomy on human error causes of software defects support the intuitive idea that, for instance, mental overload, attention slips, and working memory overload are important human causes for software bugs. In this paper, we approach the EEG as a reliable surrogate to MRI-based reference of the programmer's cognitive state to be used in situations where heavy imaging techniques are infeasible. The idea is to use EEG biomarkers to validate other less intrusive physiological measures, that can be easily recorded by wearable devices and useful in the assessment of the developer's cognitive state during software development tasks. Herein, our EEG study, with the support of fMRI, presents an extensive and systematic analysis by inspecting metrics and extracting relevant information about the most robust features, best EEG channels and the best hemodynamic time delay in the context of software development tasks. From the EEG-fMRI similarity analysis performed, we found significant correlations between a subset of EEG features and the Insula region of the brain, which has been reported as a region highly related to high cognitive tasks, such as software development tasks. We concluded that despite a clear inter-subject variability of the best EEG features and hemodynamic time delay used, the most robust and predominant EEG features, across all the subjects, are related to the Hjorth parameter Activity and Total Power features, from the EEG channels F4, FC4 and C4, and considering in most of the cases a hemodynamic time delay of 4 seconds used on the hemodynamic response function. These findings should be taken into account in future EEG-fMRI studies in the context of software debugging.

White matter diffusion estimates in obsessive-compulsive disorder across 1653 individuals: machine learning findings from the ENIGMA OCD Working Group.

White matter pathways, typically studied with diffusion tensor imaging (DTI), have been implicated in the neurobiology of obsessive-compulsive disorder (OCD). However, due to limited sample sizes and the predominance of single-site studies, the generalizability of OCD classification based on diffusion white matter estimates remains unclear. Here, we tested classification accuracy using the largest OCD DTI dataset to date, involving 1336 adult participants (690 OCD patients and 646 healthy controls) and 317 pediatric participants (175 OCD patients and 142 healthy controls) from 18 international sites within the ENIGMA OCD Working Group. We used an automatic machine learning pipeline (with feature engineering and selection, and model optimization) and examined the cross-site generalizability of the OCD classification models using leave-one-site-out cross-validation. Our models showed low-to-moderate accuracy in classifying (1) "OCD vs. healthy controls" (Adults, receiver operator characteristic-area under the curve = 57.19 ± 3.47 in the replication set; Children, 59.8 ± 7.39), (2) "unmedicated OCD vs. healthy controls" (Adults, 62.67 ± 3.84; Children, 48.51 ± 10.14), and (3) "medicated OCD vs. unmedicated OCD" (Adults, 76.72 ± 3.97; Children, 72.45 ± 8.87). There was significant site variability in model performance (cross-validated ROC AUC ranges 51.6-79.1 in adults; 35.9-63.2 in children). Machine learning interpretation showed that diffusivity measures of the corpus callosum, internal capsule, and posterior thalamic radiation contributed to the classification of OCD from HC. The classification performance appeared greater than the model trained on grey matter morphometry in the prior ENIGMA OCD study (our study includes subsamples from the morphometry study). Taken together, this study points to the meaningful multivariate patterns of white matter features relevant to the neurobiology of OCD, but with low-to-moderate classification accuracy. The OCD classification performance may be constrained by site variability and medication effects on the white matter integrity, indicating room for improvement for future research.

Burnout and attachment in oncology and palliative care healthcare professionals.

OBJECTIVES: Examine the prevalence of burn-out in health professionals working in a hospital dedicated to patients with cancer. Explore the relationship between attachment style and burn-out in healthcare professionals working in Oncology and Palliative Care. METHODS: Cross-sectional descriptive and correlational study with a sample of 337 health professionals working in a tertiary hospital dedicated to oncology care. The evaluation protocol included a sociodemographic questionnaire, two burn-out (Copenhagen Burnout Inventory (CBI) and Maslach Burnout Inventory) and attachment (Adult Attachment Scale) scales. Statistical analysis was performed by IBM SPSS Statistics V.25. The tests were performed at a significance level of 5%. RESULTS: In the sample, there is a predominance of professionals working in oncology services (76,8%). Comparing professionals who work in oncology services and palliative care, it appears that just over half have high levels of personal burn-out, however the groups do not differ significantly (53.5% vs 56.8%, p=0.619); the same is observed in work-related (p=0.626) and patient-related burn-out (p=0.672). The number of hours per week in which one has the perception that is exposed to suffering is positively correlated with personal, work-related burn-out and exhaustion (p<0.05). Correlating the two burn-out scales in the sample, it is observed that higher levels of personal, work-related and patient-related burn-out are associated with higher levels of emotional exhaustion and depersonalisation, as well as lower levels of personal accomplishment (p<0.001). Considering the correlation between the burn-out dimensions and attachment scale, it appears that high levels of exhaustion, depersonalisation, personal, work-related and patient-related burn-out were associated with higher levels of anxiety (p<0.001). Similar results were found in the palliative care professionals sample. CONCLUSIONS: The constant exposure to the suffering of others places high emotional demands on oncology and palliative care professionals, making them vulnerable to burn-out. Burn-out is a multifactorial process, that involves individual characteristics with environmental effects. There are no significant differences between Oncology and Palliative Care professionals. Higher levels of personal, work-related and patient-related burn-out are associated with higher levels of anxiety. These results suggest that an anxious attachment style increases the risk of burn-out . In the sample, the most important predictor of burn-out was the number of hours per week exposed to suffering. In order to prevent burn-out, there is a growing evidence that suggests mindfulness, exercise, high-quality sleep and pursuit of happiness can improve burn-out in healthcare professionals. This work brings the advantage of using two burn-out assessment scales (particularly CBI scale), in addition to trying to correlate the level of burn-out and attachment in professionals exposed to suffering.

Neurochemical differences in core regions of the autistic brain: a multivoxel 1H-MRS study in children.

Autism spectrum disorder (ASD) is a neurodevelopmental condition which compromises various cognitive and behavioural domains. The understanding of the pathophysiology and molecular neurobiology of ASD is still an open critical research question. Here, we aimed to address ASD neurochemistry in the same time point at key regions that have been associated with its pathophysiology: the insula, hippocampus, putamen and thalamus. We conducted a multivoxel proton magnetic resonance spectroscopy (1H-MRS) study to non-invasively estimate the concentrations of total choline (GPC + PCh, tCho), total N-acetyl-aspartate (NAA + NAAG, tNAA) and Glx (Glu + Gln), presenting the results as ratios to total creatine while investigating replication for ratios to total choline as a secondary analysis. Twenty-two male children aged between 10 and 18 years diagnosed with ASD (none with intellectual disability, in spite of the expected lower IQ) and 22 age- and gender-matched typically developing (TD) controls were included. Aspartate ratios were significantly lower in the insula (tNAA/tCr: p = 0.010; tNAA/tCho: p = 0.012) and putamen (tNAA/tCr: p = 0.015) of ASD individuals in comparison with TD controls. The Glx ratios were significantly higher in the hippocampus of the ASD group (Glx/tCr: p = 0.027; Glx/tCho: p = 0.011). Differences in tNAA and Glx indices suggest that these metabolites might be neurochemical markers of region-specific atypical metabolism in ASD children, with a potential contribution for future advances in clinical monitoring and treatment.

A human cortical adaptive mutual inhibition circuit underlying competition for perceptual decision and repetition suppression reversal.

A model based on inhibitory coupling has been proposed to explain perceptual oscillations. This 'adapting reciprocal inhibition' model postulates that it is the strength of inhibitory coupling that determines the fate of competition between percepts. Here, we used an fMRI-based adaptation technique to reveal the influence of neighboring neuronal populations, such as reciprocal inhibition, in motion-selective hMT+/V5. If reciprocal inhibition exists in this region, the following predictions should hold: 1. stimulus-driven response would not simply decrease, as predicted by simple repetition-suppression of neuronal populations, but instead, increase due to the activity from adjacent populations; 2. perceptual decision involving competing representations, should reflect decreased reciprocal inhibition by adaptation; 3. neural activity for the competing percept should also later on increase upon adaptation. Our results confirm these three predictions, showing that a model of perceptual decision based on adapting reciprocal inhibition holds true. Finally, they also show that the net effect of the well-known repetition suppression phenomenon can be reversed by this mechanism.

Trust-based health decision-making recruits the neural interoceptive saliency network which relates to temporal trajectories of Hemoglobin A1C in Diabetes Type 1.

Experimental approaches in neuroeconomics generally involve monetary utility. Utility in the health domain is relevant in diabetes because constant daily life decisions are critical for self-consequential long-term outcomes. We used fMRI to investigate self-consequent decision-making in the health and economic domains in Type 1 Diabetes Mellitus and controls (N = 50). We focused on two critical phases of decision-making: Investment and Feedback (Positive or Negative). Patients showed larger BOLD activation of limbic, and reward/dopaminergic regions in particular in the health trust game. Importantly, the worse the trajectory of metabolic control (increasing HbA1C), the higher the BOLD activity in regions of the interoceptive saliency network. This was manifested by positive correlations between brain activity during investment in anterior cingulate cortex and insula and HbA1c blood level progression. We conclude that the neural correlates of health-consequent decision-making domain involve limbic and reward related dopaminergic regions in Type 1 Diabetes Mellitus. Furthermore, the temporal trajectory of HbA1C blood levels is correlated with neural risk processing in the saliency network. Evidence for differential risk processing in the health versus the neuroeconomic context, and the discovery of a role for the saliency interoceptive network in metabolic control trajectories suggests a new perspective on the development of personalized interventions.