In patients with spontaneous intracerebral hemorrhage (ICH), pre-hospital markers of disease severity might be useful to potentially triage patients to undergo early interventions. Here, we tested whether loss of consciousness (LOC) at the onset of ICH is associated with intraventricular hemorrhage (IVH) on brain computed tomography (CT). Among 3000 ICH cases from ERICH (Ethnic/Racial Variations of Intracerebral Hemorrhage study, NS069763), we included patients with complete ICH/IVH volumetric CT measurements and excluded those with seizures at ICH onset. Trained investigators extracted data from medical charts. Mental status at symptom onset (categorized as alert/oriented, alert/confused, drowsy/somnolent, coma/unresponsive/posturing) and 3-month disability (modified Rankin score, mRS) were assessed through standardized interviews of participants or dedicated proxies. We used logistic regression and mediation analysis to assess relationships between LOC, IVH, and unfavorable outcome (mRS 4-6). Two tharker to identify patients at risk of having or developing IVH. To document two sources of validity evidence for simulation-based assessment in neurological emergencies. A critical aspect of education is development of evaluation techniques that assess learner's performance in settings that reflect actual clinical practice. Simulation-based evaluation affords the opportunity to standardize evaluations but requires validation. We identified topics from the Neurocritical Care Society's Emergency Neurological Life Support (ENLS) training, cross-referenced with the American Academy of Neurology's core clerkship curriculum. We used a modified Delphi method to develop simulations for assessment in neurocritical care. We constructed checklists of action items and communication skills, merging ENLS checklists with relevant clinical guidelines. We also utilized global rating scales, rated one (novice) through five (expert) for each case. Participants included neurology sub-interns, neurology residents, neurosurgery interns, non-neurology critical care fellows, neurocritical care fellows, and neurology attending physicians. Ten evaluative simulation cases were developed. To date, 64 participants have taken part in 274 evaluative simulation scenarios. The participants were very satisfied with the cases (Likert scale 1-7, not at all satisfied-very satisfied, median 7, interquartile range (IQR) 7-7), found them to be very realistic (Likert scale 1-7, not at all realistic-very realistic, median 6, IQR 6-7), and appropriately difficult (Likert scale 1-7, much too easy-much too difficult, median 4, IQR 4-5). Interrater reliability was acceptable for both checklist action items (kappa = 0.64) and global rating scales (Pearson correlation r = .70). We demonstrated two sources of validity in ten simulation cases for assessment in neurological emergencies.We demonstrated two sources of validity in ten simulation cases for assessment in neurological emergencies.Mitochondria can be released by astrocytes as part of a help-me signaling process in stroke. In this study, we investigated the molecular mechanisms that underlie mitochondria secretion, redox status, and functional regulation in the extracellular environment. Exposure of rat primary astrocytes to NAD or cADPR elicited an increase in mitochondrial calcium through ryanodine receptor (RyR) in the endoplasmic reticulum (ER). Importantly, CD38 stimulation with NAD accelerated ATP production along with increasing glutathione reductase (GR) and dipicolinic acid (DPA) in intracellular mitochondria. When RyR was blocked by Dantrolene, all effects were clearly diminished. click here Mitochondrial functional assay showed that these activated mitochondria appeared to be resistant to H2O2 exposure and sustained mitochondrial membrane potential, while inhibition of RyR resulted in disrupted membrane potential under oxidative stress. Finally, a gain- or loss-of-function assay demonstrated that treatment with DPA in control mitochondria preserved GR contents and increased mitochondrial membrane potential, whereas inhibiting GR with carmustine decreased membrane potentials in extracellular mitochondria released from astrocytes. Collectively, these data suggest that ER-mitochondrial interaction mediated by CD38 stimulation may support mitochondrial energy production and redox homeostasis during the mode of mitochondrial transfer from astrocytes.The rs9958947 single nucleotide polymorphism (SNP) resides in the promoter region of the lipase G (LIPG) gene. This newly discovered SNP increases the risk of stroke in some Asian populations, including Chinese and Korean populations. Stroke is one of the top 5 leading causes of death in Malaysia, so it is of interest to investigate whether this SNP is associated with stroke risk in the Malaysian population. Therefore, this study investigates this association through a case-control study on a Malaysian population along with a comprehensive meta-analysis. Genotyping of LIPG rs9958947 SNP was performed for 241 Malaysians using real-time polymerase chain reaction, and the odds ratios (OR) with 95% confidence intervals were calculated. The meta-analysis was conducted using the software Comprehensive Meta-Analysis ver. 2.2.064. A p value less than 0.05 was considered statistically significant. We observed that the mean age of Malaysian stroke patients was less than that of stroke patients from Korea and China. The meta-analysis showed that the LIPG rs9958947 SNP was significantly associated with an increased risk of ischemic stroke in Asian populations (dominant (CC vs. CT + TT) OR = 1.45, p  0.05) and blood lipid levels.Among the neuroadaptations underlying the expression of cocaine-induced behaviors are modifications in glutamate-mediated signaling and synaptic plasticity via activation of mitogen-activated protein kinases (MAPKs) within the nucleus accumbens (NAc). We hypothesized that exposure to cocaine leads to alterations in MAPK signaling in NAc neurons, which facilitates changes in the glutamatergic system and thus behavioral changes. We have previously shown that following withdrawal from cocaine-induced behavioral sensitization (BS), an increase in glutamate receptor expression and elevated MAPK signaling was evident. Here, we set out to determine the time course and behavioral consequences of inhibition of extracellular signal-regulated kinase (ERK) or NMDA receptors following withdrawal from BS. We found that inhibiting ERK by microinjection of U0126 into the NAc at 1 or 6 days following withdrawal from BS did not affect the expression of BS when challenged with cocaine at 14 days. However, inhibition of ERK 1 day before the cocaine challenge abolished the expression of BS.