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This study examines psychopathology and personality correlates of non-suicidal self-injury (NSSI) and suicide-related behavior (SRB) in an understudied sample of adolescents who have exhibited behaviors (e.g., delinquent acts, premature high school termination) that place them at-risk for poor psychosocial outcomes. Participants included a predominantly White male sample of 182 adolescents (M = 16.82 years). In addition to information about NSSI and SRB histories, participants self-reported various facets of personality and psychopathology on the Personality Assessment Inventory-Adolescent (PAI-A). Logistic regression analyses indicated that the Suicidal Ideation (SUI) scale on the PAI-A was the strongest predictor of both NSSI and SRB history, as it outperformed other relevant PAI-A scales and the Suicide Potential Index (SPI), an aggregate scale that was designed to assess for suicide risk using the PAI for adults. Receiver operating characteristic (ROC) curve analyses were also conducted to determine optimal cutoff scores for significant PAI-A predictors. Findings from the current study can be used to identify NSSI and SRB risk and target these life-threatening behaviors when working with at-risk adolescents. Highlights PAI-A SUI outperformed other PAI-A variables in predicting NSSI and SRB risk. PAI SPI did not perform as well in adolescents compared to adult samples. Cutoff scores in the current sample were well below those in the PAI-A manual. Findings from the current study can be used to identify NSSI and SRB risk and target these life-threatening behaviors when working with at-risk adolescents. Highlights PAI-A SUI outperformed other PAI-A variables in predicting NSSI and SRB risk. PAI SPI did not perform as well in adolescents compared to adult samples. Cutoff scores in the current sample were well below those in the PAI-A manual.The role of the human microbiome in the brain and behavioral development is an area of increasing attention. https://www.selleckchem.com/products/pnd-1186-vs-4718.html Recent investigations have found that diverse mechanisms and signals including the immune, endocrine and neural associations are responsible for the communication between gut microbiota and the brain. The studies have suggested that alteration of intestinal microbiota using probiotic formulations may offer a significant role in the maturation and organization of the brain and can shape the brain and behavior as well as mood and cognition in human subjects. The understanding of the possible impact of gut microflora on neurological function is a promising phenomenon that can surely transform the neurosciences and may decipher the novel etiologies for neurodegenerative and psychiatric disorders.A single bout of aerobic exercise improves executive function; however, the mechanism for the improvement remains unclear. One proposal asserts that an exercise-mediated increase in cerebral blood flow (CBF) enhances the efficiency of executive-related cortical structures. To examine this, participants completed separate 10-min sessions of moderate- to heavy-intensity aerobic exercise, a hypercapnic environment (i.e., 5% CO2), and a nonexercise and nonhypercapnic control condition. The hypercapnic condition was included because it produces an increase in CBF independent of metabolic demands. An estimate of CBF was achieved via transcranial Doppler ultrasound and near-infrared spectroscopy that provided measures of middle cerebral artery blood velocity (BV) and deoxygenated hemoglobin (HHb), respectively. Exercise intensity was adjusted to match participant-specific changes in BV and HHb associated with the hypercapnic condition. Executive function was assessed before and after each session via antisaccades (i min of aerobic exercise and 10 min of inhaling a hypercapnic gas, a manipulation known to increase CBF independently of metabolic demands. Both exercise and hypercapnic conditions improved executive function for at least 20 min. Accordingly, an increase in CBF is a candidate mechanism for the postexercise improvement in executive function.Data from studies of elbow-flexor (EF) or knee-extensor (KE) muscles suggest that a fatigue-related decrease in motoneuron excitability only occurs in EF. It is unknown how motoneuron excitability changes after sustained fatiguing maximal voluntary isometric contractions (MVICs) in EF and KE in the same participants. In two sessions, eight healthy men performed a 2-min MVIC of EF or KE to induce fatigue with brief MVICs before and six times after the 2-min MVIC. Electromyographic responses elicited by corticospinal tract stimulation at the transmastoid [cervicomedullary motor-evoked potential (CMEP)] or thoracic [thoracic motor-evoked potential (TMEP)] level were recorded from EF and KE, respectively. To account for muscle excitability, CMEPs and TMEPs were normalized to maximal M-wave (Mmax) elicited by peripheral nerve stimulation during each brief MVIC. Immediately after the 2-min MVIC, biceps brachii and brachioradialis CMEP/Mmax were 88% (SD 11%) (P = 0.026) and 87% (SD 12%) (P = 0.029) of pre-MVIC (PRE)ected by fatigue. This finding can help to increase understanding of the effect of a fatigue and subsequent recovery on neural processes.Sarin is a highly toxic nerve agent that was developed for chemical warfare during World War II and is used in present conflicts. Immediate effects of acute sarin exposure are established; however, whether effects persist after initial signs have subsided is debated. The National Toxicology Program (NTP) conducted a systematic review to evaluate the evidence for long-term neurological effects following acute ( less then 24 hour) exposure to sarin. The literature search and screening process identified 32 data sets within the 34 human studies and 47 data sets within the 51 animal studies (from 6837 potentially relevant references) that met the objective and the inclusion criteria. Four main health effect categories of neurological response were identified as having sufficient data to reach hazard conclusions (1) cholinesterase levels; (2) visual and ocular effects; (3) effects on learning, memory, and intelligence; and (4) morphology and histopathology in nervous system tissues. NTP concluded that acute sarin exposure is known to be a neurological hazard to humans in the period following exposure up to 7 days and suspected to be a hazard week to years after exposure, given a lower level of evidence in later time periods.
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