Improved walking energy efficiency might persist in presence of simulated full weight regain after multidisciplinary weight loss in adolescents with obesity: the POWELL study.

AIM: Weight loss leads to a reduction of the energy cost of walking but the respective implications of the metabolic and mechanic changes remain unknown. The present study compares the post-weight loss energy cost of walking (Cw) with and without a total reload of the induced weight reduction in adolescents with obesity. METHODS: Energy cost of walking and substrate use were evaluated during a graded walking exercise (4×6-min at 0.75, 1, 1.25, 1.5 m.s-1) before (V1) and after a 12-week intervention in 21 adolescents with obesity (11 girls; 13.8 ± 1.4 y). After weight loss, the walking exercise was randomly repeated once without weight reload (V2) and once with a loading corresponding to the total induced weight loss during the program (V2L). Body composition was assessed before and after the intervention. RESULTS: Body weight and fat mass decreased in response to the 12-week intervention (p < 0.001), while FFM did not change. The absolute gross Cw (ml.m-1) was higher on V1 compared with V2 at every speed. The absolute net Cw (ml.m-1) was higher on V1 compared to V2L at 0.75 m.s-1 (p = 0.04) and 1 m.s-1 (p = 0.02) and higher on V2L compared with V2 at 1.5 m.s-1 (p = 0.03). Net Cw (ml.m-1.kg-1) on V1 being higher than V2 (p < 0.001), and V2L higher than V2 (p = 0.006). The absolute CHO oxidation (mg.min-1) did not show any condition effect (p = 0.12) while fat utilization was higher on V1 compared to V2 and V2L (p < 0.001). Relative to body weight CHO oxidation was lower on V1 compared to V2 (p = 0.04) and V2L (p = 0.004) while relative to body weight fat oxidation was higher on V1 than V2 (p = 0.002). CONCLUSION: Adolescents with obesity might not show an entire rise back to pre-weight loss values of their metabolic cost of walking when weight gain is simulated. These new findings suggest metabolic and physiological adaptations to weight loss of the energy metabolism that remain to be clarified.

The relationship between learning slopes and Alzheimer's Disease biomarkers in cognitively unimpaired participants with and without subjective memory concerns.

OBJECTIVE: Learning slopes represent serial acquisition of information during list-learning tasks. Although several calculations for learning slopes exist, the Learning Ratio (LR) has recently demonstrated the highest sensitivity toward changes in cognition and Alzheimer's disease (AD) biomarkers. However, investigation of learning slopes in cognitively unimpaired individuals with subjective memory concerns (SMC) has been limited. The current study examines the association of learning slopes to SMC, and the role of SMC in the relationship between learning slopes and AD biomarkers in cognitively unimpaired individuals. METHOD: Data from 950 cognitively unimpaired participants from the Alzheimer's Disease Neuroimaging Initiative (aged 55 to 89) were used to calculate learning slope metrics. Learning slopes among those with and without SMC were compared with demographic correction, and the relationships of learning slopes with AD biomarkers of bilateral hippocampal volume and ß-amyloid pathology were determined. RESULTS: Learning slopes were consistently predictive of hippocampal atrophy and ß-amyloid deposition. Results were heightened for LR relative to the other learning slopes. Additionally, interaction analyses revealed different associations between learning slopes and hippocampal volume as a function of SMC status. CONCLUSIONS: Learning slopes appear to be sensitive to SMC and AD biomarkers, with SMC status influencing the relationship in cognitively unimpaired participants. These findings advance our knowledge of SMC, and suggest that LR - in particular - can be an important tool for the detection of AD pathology in both SMC and in AD clinical trials.

Clinical Utility of Routine Postprocedural Computed Tomography of the Head Following Elective Neuroendovascular Interventions.

BACKGROUND: Little evidence supports acquisition of routine head imaging after uncomplicated elective neurosurgical procedures for patients with unchanged neurological examinations; however, imaging is still performed by some neurointerventionalists. We assessed the clinical utility of routine computed tomography of the head (CTH) following elective neuroendovascular interventions, including aneurysm coiling, aneurysm stent-assisted coiling, aneurysm flow diversion, arteriovenous malformation/fistula embolization, middle meningeal artery embolization for subdural hematoma, extracranial carotid artery stenting, and venous sinus stenting. METHODS: Retrospective chart review identified patients undergoing neuroendovascular intervention from 2011 to 2021 at our institution. Demographic, clinical, and radiographic variables, including presenting signs and symptoms, antiplatelets and/or anticoagulant medications, intraprocedural complications, postprocedural CTH findings, and postprocedural neurological examinations, were recorded. Association of clinical variables with an abnormal postprocedural CTH was assessed with univariate analysis. Patients with ruptured vascular pathology, preoperative embolizations, and missing postprocedural CTH images and/or reports were excluded. RESULTS: Of 509 procedures identified, 354 were eligible for analysis; 4.8% of patients (17/354) had abnormal findings on postprocedural CTH. Nine patients had intraprocedural complications or new postprocedural neurological deficits that would have prompted imaging regardless of institutional practice. None of the remaining 8 (2.3%) patients required additional procedures. New postprocedural neurological deficit was the only significant predictor of abnormal postprocedural CTH (odds ratio = 6.79; 95% confidence interval, 2.01-20.32; P = 0.0009). CONCLUSIONS: In a large cohort of patients undergoing elective neuroendovascular intervention, no patients were identified for whom routine postprocedural CTH alone meaningfully altered their clinical care. Routine CTH is not necessary after uncomplicated elective neuroendovascular interventions performed with careful postprocedural neurological assessment.

A new strategy for the decellularization of whole organs by hydrostatic pressure.

Tissue engineering has been able to develop novel decellularization-recellularization techniques, which facilitates the research for the generation of functional organs. This is based in the initial obtention of the organ's extracellular matrix (ECM). Therefore, any improvement in the decellularization process would have a positive impact in the results of the recellularization process. Nevertheless, commonly the methods and equipment employed for this process are expensive and thus limit the access of this technique to various research groups globally. To develop a decellularization technique with the exclusive use of hydrostatic pressure of detergent solutions, to have an easily accessible and low-cost technique that meets the basic requirements of acellularity and functionality of the ECM. This experimental study was performed in 10 male Wistar rats, obtaining the liver to carry out serial washes, with 1%, 2%, and 3% Triton X-100 solutions and 0.1% SDS. The washes were performed by using a gravity perfusion system (GPS), which assured us a continuous hydrostatic pressure of 7.5 mmHg. The obtained ECM was processed using stains and immunostaining to determine the residual cell content and preservation of its components. The staining showed a removal of cellular and nuclear components of approximately 97% of the acellular ECM, with an adequate three-dimensional pattern of collagen and proteoglycans. Furthermore, the acellular ECM allowed the viability of a primary hepatocyte culture. The use of the GPS decellularization technique allowed us to obtain an acellular and functional ECM, drastically reducing experimentation costs.

SIRT1 mediates hypoxic postconditioning- and resveratrol-induced protection against functional connectivity deficits after subarachnoid hemorrhage.

Functional connectivity (FC) is a sensitive metric that provides a readout of whole cortex coordinate neural activity in a mouse model. We examine the impact of experimental SAH modeled through endovascular perforation, and the effectiveness of subsequent treatment on FC, through three key questions: 1) Does the endovascular perforation model of SAH induce deficits in FC; 2) Does exposure to hypoxic conditioning provide protection against these FC deficits and, if so, is this neurovascular protection SIRT1-mediated; and 3) does treatment with the SIRT1 activator resveratrol alone provide protection against these FC deficits? Cranial windows were adhered on skull-intact mice that were then subjected to either sham or SAH surgery and either left untreated or treated with hypoxic post-conditioning (with or without EX527) or resveratrol for 3 days. Mice were imaged 3 days post-SAH/sham surgery, temporally aligned with the onset of major SAH sequela in mice. Here we show that the endovascular perforation model of SAH induces global and network-specific deficits in FC by day 3, corresponding with the time frame of DCI in mice. Hypoxic conditioning provides SIRT1-mediated protection against these network-specific FC deficits post-SAH, as does treatment with resveratrol. Conditioning-based strategies provide multifaceted neurovascular protection in experimental SAH.

Diazaborines oxidize slowly with H2O2 but rapidly with peroxynitrite in aqueous buffer.

Reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) and peroxynitrite (ONOO-) oxidize arylboronic acids to their corresponding phenols. When used in molecular imaging probes and in ROS-responsive molecules, however, simple arylboronic acids struggle to discriminate between H2O2 and ONOO- because of their fast rate of reaction with both ROS. Here, we show that diazaborines (DABs) react slowly with H2O2 but rapidly with peroxynitrite in an aqueous buffer. In addition to their slow reaction with H2O2, the immediate product of DAB oxidation with H2O2 and ONOO- can yield a kinetically trapped CN Z-isomer that slowly equilibrates with its E-isomer. Taken together, our work shows that diazaborines exhibit enhanced kinetic discrimination between H2O2 and ONOO- compared to arylboronic acids, opening up new opportunities for diazaborine-based tools in chemical biology.

Two rTMS sessions per week: a practical approach for treating major depressive disorder.

INTRODUCTION: Depression is one of the leading causes of disability in the world, and a disease that contributes greatly to the global burden of disease. Repetitive transcranial magnetic stimulation (rTMS) has proven to be a well-tolerated, effective treatment for depression. The present study was designed to evaluate the efficacy of an rTMS treatment scheme with a fewer number of sessions per week. METHODS: In total 91 adult university students with major depressive disorder (MDD). This was a double-blind, randomized clinical trial in which 15 sessions of rTMS were given to each one of two treatment groups made up of adults with active MDD. One treatment group received two sessions per week, the other received five. The study protocol included their respective sham rTMS groups. The patients who received active rTMS also participated in a follow-up procedure that consisted of two sessions of active rTMS per month for three more months. RESULTS: Measurements by the Hamilton Rating Scale for Depression (HAMD) showed that the groups which received active rTMS had higher percentages of antidepressant response at 96 and 95.5% for five and two sessions/week, respectively, compared to the sham rTMS groups: 27.3 and 4.5% for five and two sessions/week, respectively. Observations at the end of the 3-month follow-up phase showed that the improvements in HAMD scores were maintained in both groups. CONCLUSION: This study contributes to demonstrating that rTMS with a more practical schedule of two sessions/week is an effective antidepressant treatment that could be considered the first choice for managing symptoms of depression.

Erratum: Vitamin D sufficiency enhances differentiation of patient-derived prostate epithelial organoids.

[This corrects the article DOI: 10.1016/j.isci.2020.101974.].

Does sex influence the effects of experimental sleep curtailment and circadian misalignment on regulation of appetite?

Sleep curtailment and circadian misalignment disrupt energy sensing and eating behaviors, which can contribute to weight gain and obesity-related comorbidities. Herein, we review the effects of experimental manipulations of sleep duration and circadian alignment on circulating concentrations of appetite hormones, specifically leptin and ghrelin. Further, we focus on sex differences in hormonal and behavioral responses related to food intake. The studies reviewed suggest potential sex-specific effects of sleep curtailment on key hormones involved in the gut-brain axis, presumably leading to downstream effects on neural processes involved in food seeking and consumption behaviors. However, there is insufficient evidence to declare any sex-specific effects of circadian misalignment on appetite regulation. More research is needed to elucidate the complex sex-specific relationships between sleep, circadian rhythms, energy homeostasis, and appetite regulating mechanisms. Greater knowledge of these mechanisms would aid in the development of targeted methods to mitigate risk for obesity and related metabolic diseases.

Diet- but not exercise-induced iso-energetic deficit induces compensatory appetitive responses.

Although physical exercise and dietary restriction can be both used to induce energy deficits, they have been suggested to favor different compensatory appetitive responses. While dietary restriction might favor increased subsequent energy intake and appetite sensations, such compensatory responses have not been observed after a similar deficit by exercise. The present work provides a first overview of the actual evidences discussing the effects of iso-energetic deficits induced by exercise versus dietary restriction on subsequent energy intake, appetite sensations, and on the potentially involved hedonic and physiological mechanisms.

Automated Quantification of Reduced Sulcal Volume Identifies Early Brain Injury After Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND AND PURPOSE: Early brain injury may be a more significant contributor to poor outcome after aneurysmal subarachnoid hemorrhage (aSAH) than vasospasm and delayed cerebral ischemia. However, studying this process has been hampered by lack of a means of quantifying the spectrum of injury. Global cerebral edema (GCE) is the most widely accepted manifestation of early brain injury but is currently assessed only through subjective, qualitative or semi-quantitative means. Selective sulcal volume (SSV), the CSF volume above the lateral ventricles, has been proposed as a quantitative biomarker of GCE, but is time-consuming to measure manually. Here we implement an automated algorithm to extract SSV and evaluate the age-dependent relationship of reduced SSV on early outcomes after aSAH. METHODS: We selected all adults with aSAH admitted to a single institution with imaging within 72 hours of ictus. Scans were assessed for qualitative presence of GCE. SSV was automatically segmented from serial CTs using a deep learning-based approach. Early SSV was the lowest SSV from all early scans. Modified Rankin Scale score of 4 to 6 at hospital discharge was classified as a poor outcome. RESULTS: Two hundred forty-four patients with aSAH were included. Sixty-five (27%) had GCE on admission while 24 developed it subsequently within 72 hours. Median SSV on admission was 10.7 mL but frequently decreased, with minimum early SSV being 3.0 mL (interquartile range, 0.3-11.9). Early SSV below 5 mL was highly predictive of qualitative GCE (area under receiver-operating-characteristic curve, 0.90). Reduced early SSV was an independent predictor of poor outcome, with a stronger effect in younger patients. CONCLUSIONS: Automated assessment of SSV provides an objective biomarker of GCE that can be leveraged to quantify early brain injury and dissect its impact on outcomes after aSAH. Such quantitative analysis suggests that GCE may be more impactful to younger patients with SAH.

Improvement in borderline personality disorder symptomatology after repetitive transcranial magnetic stimulation of the dorsomedial prefrontal cortex: preliminary results

Objective: Current treatment for borderline personality disorder (BPD) involves psychological and pharmacological interventions. However, neuromodulation techniques such as repetitive transcranial magnetic stimulation (rTMS) may positively affect BPD symptomatology. The objective of this study was to evaluate the clinical and neuropsychological effects of rTMS on the dorsomedial prefrontal cortex (DMPFC) in BPD patients. Methods: Fourteen patients with BPD were randomized into two groups (active vs. sham) for 15 sessions of rTMS on the DMPFC. Clinical effects were measured using the Borderline Symptoms List (BSL), Clinical Global Impression Scale for BPD (CGI-BPD), Borderline Evaluation of Severity over Time (BEST), Hamilton Depression Rating Scale (HDRS), Hamilton Anxiety Rating Scale (HARS), and Barratt's Impulsiveness Scale (BIS). Neuropsychological effects were determined by a Stop-Signal Task (SST), the Wisconsin Card-Sorting Test (WCST), and the Iowa Gambling Test (IGT). Results: Within-group comparison showed significant differences (p < 0.05) in CGI-BPD (total score and six of nine psychopathologic domains), BEST, HDRS, HARS, and IGT scores for active modality. Conclusion: The 5 Hz-DMPFC rTMS technique was well tolerated and lessened the severity of BPD symptomatology, especially abandonment, affective issues, interpersonal relationships, suicidal behavior, anger, and paranoid ideation. Cognitive improvement was seen in decision-making. Additional studies are needed to fully evaluate the effects of rTMS on BPD symptomatology. Clinical Trial Registration: NCT03832777.

Vitamin D sufficiency enhances differentiation of patient-derived prostate epithelial organoids.

Vitamin D is an essential steroid hormone that regulates systemic calcium homeostasis and cell fate decisions. The prostate gland is hormonally regulated, requiring steroids for proliferation and differentiation of secretory luminal cells. Vitamin D deficiency is associated with an increased risk of lethal prostate cancer, which exhibits a dedifferentiated pathology, linking vitamin D sufficiency to epithelial differentiation. To determine vitamin D regulation of prostatic epithelial differentiation, patient-derived benign prostate epithelial organoids were grown in vitamin D-deficient or -sufficient conditions. Organoids were assessed by phenotype and single-cell RNA sequencing. Mechanistic validation demonstrated that vitamin D sufficiency promoted organoid growth and accelerated differentiation by inhibiting canonical Wnt activity and suppressing Wnt family member DKK3. Wnt and DKK3 were also reduced by vitamin D in prostate tissue explants by spatial transcriptomics. Wnt dysregulation is a known contributor to aggressive prostate cancer, thus findings further link vitamin D deficiency to lethal disease.

Spontaneous resolution of exuberant localized sporotrichosis after childbirth.

Sporotrichosis is caused by the thermodimorphic fungi of the genus Sporothrix. It is the most common cutaneous mycosis in Latin America, but it is considered uncommon in pregnancy. We report a pregnant woman with with an exuberant ulcerated plaque that proved to be localized sporotrichosis. Therapy choice is a difficult decision in this group of patients. In this case, there was complete resolution of the infection after delivery, without any therapeutic intervention.

SIRT1 mediates hypoxic preconditioning induced attenuation of neurovascular dysfunction following subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Vasospasm and delayed cerebral ischemia (DCI) contribute significantly to the morbidity/mortality associated with aneurysmal subarachnoid hemorrhage (SAH). While considerable research effort has focused on preventing or reversing vasospasm, SAH-induced brain injury occurs in response to a multitude of concomitantly acting pathophysiologic mechanisms. In this regard, the pleiotropic epigenetic responses to conditioning-based therapeutics may provide an ideal SAH therapeutic strategy. We previously documented the ability of hypoxic preconditioning (PC) to attenuate vasospasm and neurological deficits after SAH, in a manner that depends on the activity of endothelial nitric oxide synthase. The present study was undertaken to elucidate whether the NAD-dependent protein deacetylase sirtuin isoform SIRT1 is an upstream mediator of hypoxic PC-induced protection, and to assess the efficacy of the SIRT1-activating polyphenol Resveratrol as a pharmacologic preconditioning therapy. METHODS: Wild-type C57BL/6J mice were utilized in the study and subjected to normoxia or hypoxic PC. Surgical procedures included induction of SAH via endovascular perforation or sham surgery. Multiple endpoints were assessed including cerebral vasospasm, neurobehavioral deficits, SIRT1 expression via quantitative real-time PCR for mRNA, and western blot for protein quantification. Pharmacological agents utilized in the study include EX-527 (SIRT1 inhibitor), and Resveratrol (SIRT1 activator). RESULTS: Hypoxic PC leads to rapid and sustained increase in cerebral SIRT1 mRNA and protein expression. SIRT1 inhibition blocks the protective effects of hypoxic PC on vasospasm and neurological deficits. Resveratrol pretreatment dose-dependently abrogates vasospasm and attenuates neurological deficits following SAH - beneficial effects that were similarly blocked by pharmacologic inhibition of SIRT1. CONCLUSION: SIRT1 mediates hypoxic preconditioning-induced protection against neurovascular dysfunction after SAH. Resveratrol mimics this neurovascular protection, at least in part, via SIRT1. Activation of SIRT1 is a promising, novel, pleiotropic therapeutic strategy to combat DCI after SAH.

Improvement in borderline personality disorder symptomatology after repetitive transcranial magnetic stimulation of the dorsomedial prefrontal cortex: preliminary results.

OBJECTIVE: Current treatment for borderline personality disorder (BPD) involves psychological and pharmacological interventions. However, neuromodulation techniques such as repetitive transcranial magnetic stimulation (rTMS) may positively affect BPD symptomatology. The objective of this study was to evaluate the clinical and neuropsychological effects of rTMS on the dorsomedial prefrontal cortex (DMPFC) in BPD patients. METHODS: Fourteen patients with BPD were randomized into two groups (active vs. sham) for 15 sessions of rTMS on the DMPFC. Clinical effects were measured using the Borderline Symptoms List (BSL), Clinical Global Impression Scale for BPD (CGI-BPD), Borderline Evaluation of Severity over Time (BEST), Hamilton Depression Rating Scale (HDRS), Hamilton Anxiety Rating Scale (HARS), and Barratt's Impulsiveness Scale (BIS). Neuropsychological effects were determined by a Stop-Signal Task (SST), the Wisconsin Card-Sorting Test (WCST), and the Iowa Gambling Test (IGT). RESULTS: Within-group comparison showed significant differences (p < 0.05) in CGI-BPD (total score and six of nine psychopathologic domains), BEST, HDRS, HARS, and IGT scores for active modality. CONCLUSION: The 5 Hz-DMPFC rTMS technique was well tolerated and lessened the severity of BPD symptomatology, especially abandonment, affective issues, interpersonal relationships, suicidal behavior, anger, and paranoid ideation. Cognitive improvement was seen in decision-making. Additional studies are needed to fully evaluate the effects of rTMS on BPD symptomatology. CLINICAL TRIAL REGISTRATION: NCT03832777.

Microvascular platelet aggregation and thrombosis after subarachnoid hemorrhage: A review and synthesis.

Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) has been associated with numerous pathophysiological sequelae, including large artery vasospasm and microvascular thrombosis. The focus of this review is to provide an overview of experimental animal model studies and human autopsy studies that explore the temporal-spatial characterization and mechanism of microvascular platelet aggregation and thrombosis following SAH, as well as to critically assess experimental studies and clinical trials highlighting preventative therapeutic options against this highly morbid pathophysiological process. Upon review of the literature, we discovered that microvascular platelet aggregation and thrombosis occur after experimental SAH across multiple species and SAH induction techniques in a similar time frame to other components of DCI, occurring in the cerebral cortex and hippocampus across both hemispheres. We discuss the relationship of these findings to human autopsy studies. In the final section of this review, we highlight the important therapeutic options for targeting microvascular platelet aggregation and thrombosis, and emphasize why therapeutic targeting of this neurovascular pathology may improve patient care. We encourage ongoing research into the pathophysiology of SAH and DCI, especially in regard to microvascular platelet aggregation and thrombosis and the translation to randomized clinical trials.

Intranasal deferoxamine can improve memory in healthy C57 mice, suggesting a partially non-disease-specific pathway of functional neurologic improvement.

INTRODUCTION: Intranasal deferoxamine (IN DFO) has been shown to decrease memory loss and have beneficial impacts across several models of neurologic disease and injury, including rodent models of Alzheimer's and Parkinson's disease. METHODS: In order to assess the mechanism of DFO, determine its ability to improve memory from baseline in the absence of a diseased state, and assess targeting ability of intranasal delivery, we treated healthy mice with IN DFO (2.4 mg) or intraperitoneal (IP) DFO and compared behavioral and biochemical changes with saline-treated controls. Mice were treated 5 days/week for 4 weeks and subjected to behavioral tests 30 min after dosing. RESULTS: We found that IN DFO, but not IP DFO, significantly enhanced working memory in the radial arm water maze, suggesting that IN administration is more efficacious as a targeted delivery route to the brain. Moreover, the ability of DFO to improve memory from baseline in healthy mice suggests a non-disease-specific mechanism of memory improvement. IN DFO treatment was accompanied by decreased GSK-3ß activity and increased HIF-1α activity. CONCLUSIONS: These pathways are suspected in DFO's ability to improve memory and perhaps represent a component of the common mechanism through which DFO enacts beneficial change in models of neurologic disease and injury.

El consumo de riesgo de alcohol y el riesgo de dependencia al alcohol presentan correlatos neurofisiológicos diferentes / Hazardous alcohol consumption and risk of alcohol dependence present different neurophysiological correlates

Introducción. El consumo de riesgo de alcohol (CRA) es un patrón de consumo que puede resultar dañino para el usuario o para los demás. Investigaciones previas sugieren que el CRA y la dependencia al alcohol comparten algunas características neurofisiológicas, pero difieren en otras. Objetivo. Determinar si el CRA y la dependencia al alcohol presentan correlatos neurofisiológicos diferentes. Sujetos y métodos. Doscientos sujetos realizaron la prueba de detección de CRA y riesgo de dependencia al alcohol (DEP). Se realizó un estudio de electroencefalografía cuantitativa para determinar la potencia absoluta, la potencia relativa y la frecuencia media de las bandas delta, theta, alfa y beta en sujetos con CRA, con DEP y controles. Resultados. Un total de 114 sujetos cumplió los criterios de inclusión. El grupo con CRA presentó mayor potencia absoluta, mayor potencia relativa y menor frecuencia media de la banda beta en comparación con los controles, mientras que el grupo con DEP presentó menor potencia absoluta de la banda delta que los controles. Conclusiones. El DEP y el CRA presentan diferentes correlatos neurofisiológicos. Hay un efecto importante de la gravedad de la dependencia al alcohol sobre sus correlatos neurofisiológicos. Nuestros resultados apoyan la existencia de dos tipos distintos de desinhibición conductual

Introduction. Hazardous alcohol consumption (HAC) is a pattern of alcohol use that may result in harm for the user and/or for those around them. Prior research has suggested that HAC and alcohol dependence share some neurophysiological features but differ in others. Aim. To determine whether HAC and alcohol dependence presented different neurophysiological correlates. Subjects and methods. Two hundred subjects were screened for HAC or alcohol dependence. A quantitative electroencephalographic analysis of delta, theta, alpha and beta absolute power, relative power and mean frequency in subjects with HAC but not alcohol dependence, subjects with risk of alcohol dependence and controls was performed. Results. One hundred and fourteen subjects met inclusion criteria. The HAC group presented with higher beta absolute power and relative power, as well as a lower beta mean frequency than the control group, while the group with risk of alcohol dependence presented lower delta absolute power than controls. Conclusions. HAC and risk of alcohol dependence present different neurophysiological correlates. There is an important effect of the severity of alcohol dependence on neurophysiological correlates of this condition. Our results support the existence of two different types of behavioral disinhibition