IMPORTANCE Neurologically intact survival after out-of-hospital cardiac arrest (OHCA) has been increasing in Japan. However, associations between increased prehospital care, including bystander interventions and increases in survival, have not been well estimated. OBJECTIVE To estimate the associations between bystander interventions and changes in neurologically intact survival among patients with OHCA in Japan. DESIGN, SETTING, AND PARTICIPANTS Retrospective descriptive study using data from Japan's nationwide OHCA registry, which started in January 2005. The registry includes all patients with OHCA transported to the hospital by emergency medical services (EMS) and recorded patients' characteristics, prehospital interventions, and outcomes. Participants were 167 912 patients with bystander-witnessed OHCA of presumed cardiac origin in the registry between January 2005 and December 2012. EXPOSURES Prehospital interventions by bystander, including defibrillation using public-access automated external defibrillators and chest compression. MAIN OUTCOMES AND MEASURES Neurologically intact survival was defined as Glasgow-Pittsburgh cerebral performance category score 1 or 2 and overall performance category scores 1 or 2 at 1 month or at discharge. The association between the interventions and neurologically intact survival was evaluated. RESULTS From 2005 to 2012, the number of bystander-witnessed OHCAs of presumed cardiac origin increased from 17 882 (14.0 per 100 000 persons [95% CI, 13.8-14.2]) to 23 797 (18.7 per 100 000 persons [95% CI, 18.4-18.9]), and neurologically intact survival increased from 587 cases (age-adjusted proportion, 3.3% [95% CI, 3.0%-3.5%]) to 1710 cases (8.2% [95% CI, 7.8%-8.6%]). The rates of bystander chest compression increased from 38.6% to 50.9%, bystander-only defibrillation increased from 0.1% to 2.3%, bystander defibrillation combined with EMS defibrillation increased from 0.1% to 1.4%, and EMS-only defibrillation decreased from 26.6% to 23.5%. Performance of bystander chest compression, compared with no bystander chest compression, was associated with increased neurologically intact survival (8.4% [6594 survivors/78 592 cases] vs 4.1% [3595 survivors/88 720 cases]; odds ratio [OR], 1.52 [95% CI, 1.45-1.60]). Compared with EMS-only defibrillation (15.0% [6445 survivors/42 916 cases]), bystander-only defibrillation (40.7% [931 survivors/2287 cases]) was associated with increased neurologically intact survival (OR, 2.24 [95% CI, 1.93-2.61]), as was combined bystander and EMS defibrillation (30.5% [444 survivors/1456 cases]; OR, 1.50 [95% CI, 1.31-1.71]), whereas no defibrillation (2.0% [2369 survivors/120 653 cases]) was associated with reduced survival (OR, 0.43 [95% CI, 0.39-0.48]). CONCLUSIONS AND RELEVANCEIn Japan, between 2005 and 2012, the rates of bystander chest compression and bystander defibrillation increased and were associated with increased odds of neurologically intact survival.

Objectives To evaluate the effectiveness of pre-hospital adrenaline (epinephrine) administered by emergency medical services to patients with out of hospital cardiac arrest.Design Controlled propensity matched retrospective cohort study, in which pairs of patients with or without (control) adrenaline were created with a sequential risk set matching based on time dependent propensity score.

The aims of this study were to clarify the mechanism of cell death by apoptosis in the spinal cord after traumatic injury, and to examine the role of the mitogen-activated protein kinase (MAPK) pathways in the transmission of apoptosis signals. The rat spinal cord, experimentally injured by extradural static weight-compression, was studied by hematoxylin and eosin staining, Nissl-staining, terminal deoxynucleotidyl transferase (TdT) mediated dUTP nick-end labeling (TUNEL) staining, and immunostaining using polyclonal antibodies against Apoptosis Signal-regulating Kinase 1 (ASK1), c-Jun N-terminal kinase (JNK), and p38 MAPK. TUNEL-positive cells were present at all stages studied until 7 days after injury, and percentage positivity for these cells was maximal at 3 days after injury. Electron microscopic analysis revealed the occurrence of apoptosis in both neuronal cells and glial cells. TUNEL-positive glial cells were stained by oligodendrocyte-specific maker. Expression of ASK1 was maximal at 24 h after injury in the gray matter and at 3 days after injury in the white matter. Following the expression of ASK1, activated forms of JNK and p38 were observed in apoptotic cells detected by the TUNEL method. Colocalization of ASK1 and activated JNK or activated p38 was observed in the same cell. These findings suggest the involvement of the stress-activated MAPK pathways including ASK1 in the transmission of apoptosis signals after spinal cord injury.

The post-migration detention of Afghan asylum seekers in Japan was independently related to their worsened mental health.

Object. The aims of this study were to clarify the histological and histochemical changes associated with cell death in the spinal cord after acute traumatic injury and to examine the role of excitatory amino acid release mediated by N-methyl-d- aspartate (NMDA) receptors. Methods. Following laminectomy, the spinal cord in 70 rats was injured at the T-9 level by applying extradural static weight—compression, in which a cylindrical compressor was used to induce complete and irreversible transverse spinal cord injury (SCI) with paralysis of the lower extremities. The injured rats were killed between 30 minutes and 14 days after injury, and the injured cord was removed en bloc. Rats that received NMDA receptor antagonist (MK-801) were killed at the same time points as those that received saline. The specimens were stained with hematoxylin and eosin, Nissl, and Klüver—Barrera Luxol fast blue and subjected to in situ nick-end labeling, a specific in situ method used to allow visualization of apoptosis. Thirty minutes post-SCI, a large hematoma was observed at the compressed segment. Six hours after injury, large numbers of dead cells that were not stained by in situ nick-end labeling were observed. Between 12 hours and 14 days postinjury, nuclei stained by using the in situ nick-end labeling technique were observed not only at the injury site but also in adjoining segments that had not undergone mechanical compression, suggesting that the delayed cell death was due to apoptosis. The number of cells stained by in situ nick-end labeling was maximum at 3 days postinjury. The results of electron microscopic examination were also consistent with apoptosis. In the MK-801—treated rats, the number of cells stained by in situ nick-end labeling was smaller than in nontreated rats at both 24 hours and 7 days after injury. Conclusions. These findings suggest that NMDA-receptor activation promotes delayed neuronal and glial cell death due to apoptosis.

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ACADEMIC EMERGENCY MEDICINE 2012; 19:782–792 © 2012 by the Society for Academic Emergency Medicine Abstract Objectives:  This study aimed to investigate whether early epinephrine administration in out‐of‐hospital cardiopulmonary arrest (OHCA) patients was associated with improved outcomes and to address the selection bias inherent in observational studies (more severe cases are more likely to receive epinephrine). Methods:  This was a retrospective analysis of prospectively collected population‐based data of adult bystander‐witnessed OHCA patients from a nationwide Japanese registry between January 2007 and December 2008. To address selection bias, those who attained early return of spontaneous circulation (ROSC) without epinephrine administration were excluded, leaving 49,165 patients in the analysis. The outcomes were intact neurologic survival, defined as survival with cerebral performance category score 1or 2, and any survival at 1 month or at discharge (whichever was earlier). The primary predictor was the time from the start of cardiopulmonary resuscitation (CPR) by emergency medical services (EMS) to first epinephrine administration, with early epinephrine defined as within 10 minutes. Results:  Multivariate logistic regression analysis showed that cardiac origin OHCA patients who received early epinephrine (≤10 minutes) had significantly higher rates of intact neurologic survival (odds ratio [OR] = 1.39, 95% confidence interval [CI] = 1.08 to 1.78) and any survival (OR = 1.73, 95% CI = 1.46 to 2.04) than those who did not receive early epinephrine, after adjusting for potential confounders. Results for noncardiac OHCA patients were similar. Conclusions:  Early epinephrine administration may be associated with higher rates of intact neurologic survival and any survival in adult bystander‐witnessed OHCA patients. This article provides a potential method to address the selection bias inherent in observational studies that examine the effects of drug administration in OHCA patients.