Psychopathic traits were assessed using the Hare Psychopathy Checklist Youth Version (PCLYV). Consistent with hypotheses, interpersonal and affective traits (i.e., PCLYV Factor 1 and Facet 1 scores) were associated with reduced FA in the right UF. Additionally, lifestyle traits (i.e., PCLYV Facet 3 scores) were associated with increased FA in the left UF. Results are consistent with previously published studies reporting reduced FA in the right UF in adult psychopathic offenders and increased left UF FA in youth meeting criteria for certain externalizing disorders. OBJECTIVE Perinatal thalamic injury is associated with epilepsy with electrical status epilepticus in sleep (ESES). The aim of this study was to prospectively quantify the risk of ESES and to assess neuroimaging predictors of neurodevelopment. METHODS We included patients with perinatal thalamic injury. MRI scans were obtained in the neonatal period, around three months of age and during childhood. Thalamic and total brain volumes were obtained from the three months MRI. Diffusion characteristics were assessed. Sleep EEGs distinguished patients into ESES (spike-wave index (SWI) >85%), ESES-spectrum (SWI 50-85%) or no ESES (SWI  less then  50%). Serial Intelligence Quotient (IQ)/Developmental Quotient (DQ) scores were obtained during follow-up. Imaging and EEG findings were correlated to neurodevelopmental outcome. RESULTS Thirty patients were included. Mean thalamic volume at three months was 8.11 (±1.67) ml and mean total brain volume 526.45 (±88.99) ml. In the prospective cohort (n = 23) 19 patients (83%) developed ESES (-spectrum) abnormalities after a mean follow-up of 96 months. In the univariate analysis, larger thalamic volume, larger total brain volume and lower SWI correlated with higher mean IQ/DQ after 2 years (Pearson's r = 0.74, p = 0.001; Pearson's r = 0.64, p = 0.005; and Spearman's rho -0.44, p = 0.03). In a multivariable mixed model analysis, thalamic volume was a significant predictor of IQ/DQ (coefficient 9.60 [p  less then  0.001], i.e., corrected for total brain volume and SWI and accounting for repeated measures within patients, a 1 ml higher thalamic volume was associated with a 9.6 points higher IQ). Diffusion characteristics during childhood correlated with IQ/DQ after 2 years. SIGNIFICANCE Perinatal thalamic injury is followed by electrical status epilepticus in sleep in the majority of patients. Thalamic volume and diffusion characteristics correlate to neurodevelopmental outcome. Current theories of psychosis highlight the role of abnormal learning signals, i.e., prediction errors (PEs) and uncertainty, in the formation of delusional beliefs. We employed computational analyses of behaviour and functional magnetic resonance imaging (fMRI) to examine whether such abnormalities are evident in clinical high risk (CHR) individuals. Non-medicated CHR individuals (n = 13) and control participants (n = 13) performed a probabilistic learning paradigm during fMRI data acquisition. We used a hierarchical Bayesian model to infer subject-specific computations from behaviour - with a focus on PEs and uncertainty (or its inverse, precision) at different levels, including environmental 'volatility' - and used these computational quantities for analyses of fMRI data. Computational modelling of CHR individuals' behaviour indicated volatility estimates converged to significantly higher levels than in controls. Model-based fMRI demonstrated increased activity in prefrontal and insular regions of CHR individuals in response to precision-weighted low-level outcome PEs, while activations of prefrontal, orbitofrontal and anterior insula cortex by higher-level PEs (that serve to update volatility estimates) were reduced. Additionally, prefrontal cortical activity in response to outcome PEs in CHR was negatively associated with clinical measures of global functioning. Our results suggest a multi-faceted learning abnormality in CHR individuals under conditions of environmental uncertainty, comprising higher levels of volatility estimates combined with reduced cortical activation, and abnormally high activations in prefrontal and insular areas by precision-weighted outcome PEs. This atypical representation of high- and low-level learning signals might reflect a predisposition to delusion formation. Nitroxyl (HNO), one-electron reduced and protonated sibling of nitric oxide (NO), is a potential regulator of cardiovascular functions. It produces positive inotropic, lusitropic, myocardial anti-hypertrophic and vasodilator properties. Despite of these favorable actions, the significance and the possible mechanisms of HNO in diabetic hearts have yet to be fully elucidated. H9c2 cells or primary neonatal mouse cardiomyocytes were incubated with normal glucose (NG) or high glucose (HG). Male C57BL/6 mice received intraperitoneal injection of streptozotocin (STZ) to induce diabetes. Here, we demonstrated that the baseline fluorescence signals of HNO in H9c2 cells were reinforced by both HNO donor Angeli's salt (AS), and the mixture of hydrogen sulfide (H2S) donor sodium hydrogen sulfide (NaHS) and NO donor sodium nitroprusside (SNP), but decreased by HG. Pretreatment with AS significantly reduced HG-induced cell vitality injury, apoptosis, reactive oxygen species (ROS) generation, and hypertrophy in H9c2 cells. This effect was mediated by induction of caveolin-3 (Cav-3)/endothelial nitric oxide (NO) synthase (eNOS) complex. Disruption of Cav-3/eNOS by pharmacological manipulation or small interfering RNA (siRNA) abolished the protective effects of AS in HG-incubated H9c2 cells. In STZ-induced diabetic mice, administration of AS ameliorated the development of diabetic cardiomyopathy, as evidenced by improved cardiac function and reduced cardiac hypertrophy, apoptosis, oxidative stress and myocardial fibrosis without affecting hyperglycemia. This study shed light on how interaction of NO and H2S regulates cardiac pathology and provide new route to treat diabetic cardiomyopathy with HNO. Renal ischemia/reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), a potentially fatal syndrome characterized by a rapid decline in kidney function. Excess production of superoxide contributes to the injury.  https://www.selleckchem.com/products/gdc6036.html  We hypothesized that oral administration of a high dose of vitamin B12 (B12 - cyanocobalamin), which possesses a superoxide scavenging function, would protect kidneys against IRI and provide a safe means of treatment. Following unilateral renal IR surgery, C57BL/6J wild type (WT) mice were administered B12 via drinking water at a dose of 50 mg/L. After 5 days of the treatment, plasma B12 levels increased by 1.2-1.5x, and kidney B12 levels increased by 7-8x. IRI mice treated with B12 showed near normal renal function and morphology. Further, IRI-induced changes in RNA and protein markers of inflammation, fibrosis, apoptosis, and DNA damage response (DDR) were significantly attenuated by at least 50% compared to those in untreated mice. Moreover, the presence of B12 at 0.3 μM in the culture medium of mouse proximal tubular cells subjected to 3 hr of hypoxia followed by 1 hr of reperfusion in vitro showed similar protective effects, including increased cell viability and decreased reactive oxygen species (ROS) level.