Background The prognosis of out-of-hospital cardiac arrest (OHCA) is very poor. While several prehospital factors are known to be associated with improved survival, the impact of prehospital factors on different age groups is unclear. The objective of the study was to access the impact of prehospital factors and pre-existing comorbidities on OHCA outcomes in different age groups. Methods A retrospective observational analysis was conducted using the emergency medical service (EMS) database from January 2015 to December 2019. We collected information on prehospital factors, underlying diseases, and outcome of OHCAs in different age groups. Kaplan-Meier type survival curves and multivariable logistic regression were used to analyze the association between modifiable pre-hospital factors and outcomes. Results A total of 4188 witnessed adult OHCAs were analyzed. For the age group 1 (age ≦75 years old), after adjustment for confounding factors, EMS response time (odds ratio [OR] = 0.860, 95% confidence interval [CI]: 0.811–0.909, p < 0.001), public location (OR = 1.843, 95% CI: 1.179–1.761, p < 0.001), bystander CPR (OR = 1.329, 95% CI: 1.007–1.750, p = 0.045), attendance by an EMT-Paramedic (OR = 1.666, 95% CI: 1.277–2.168, p < 0.001), and prehospital defibrillation by automated external defibrillator (AED)(OR = 1.666, 95% CI: 1.277–2.168, p < 0.001) were prognostic factors for survival to hospital discharge in OHCA patients. For the age group 2 (age > 75 years old), age (OR = 0.924, CI:0.880–0.966, p = 0.001), EMS response time (OR = 0.833, 95% CI: 0.742–0.928, p = 0.001), public location (OR = 4.290, 95% CI: 2.450–7.343, p < 0.001), and attendance by an EMT-Paramedic (OR = 2.702, 95% CI: 1.704–4.279, p < 0.001) were independent prognostic factors for survival to hospital discharge in OHCA patients. Conclusions There were variations between younger and older OHCA patients. We found that bystander CPR and prehospital defibrillation by AED were independent prognostic factors for younger OHCA patients but not for the older group.

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Focal cortical dysplasia (FCD) is a congenital malformation of cortical development where the cortical neurons located in the brain area fail to migrate in the proper formation. Epilepsy, particularly medically refractory epilepsy, is the most common clinical presentation for all types of FCD. This study aimed to explore the expression change of circulating miRNAs in patients with FCD from serum exosomes. A total of nine patients with FCD and four healthy volunteers were enrolled in this study. The serum exosomes were isolated from the peripheral blood of the subjects. Transmission electron microscopy (TEM) was used to identify the exosomes. Both exosomal markers and neuronal markers were detected by Western blotting analysis to prove that we could obtain central nervous system-derived exosomes from the circulation. The expression profiles of circulating exosomal miRNAs were assessed using next-generation sequencing analysis (NGS). We obtained a total of 107 miRNAs with dominant fold change (>2-fold) from both the annotated 5p-arm and 3p-arm of 2780 mature miRNAs. Based on the integrated platform of HMDD v3.2, miRway DB and DIANA-miRPath v3.0 online tools, and confirmed by MiRBase analysis, four potentially predicted miRNAs from serum exosomes in patients with FCD were identified, including miR194-2-5p, miR15a-5p, miR-132-3p, and miR-145-5p. All four miRNAs presented upregulated expression in patients with FCD compared with controls. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and pathway category of four target miRNAs, we found eight possible signaling pathways that may be related to FCD. Among them, we suggest that the mTOR signaling pathway, PI3K-Akt signaling pathway, p53 signaling pathway, and cell cycle regulation and TGF-beta signaling pathway are high-risk pathways that play a crucial role in the pathogenesis of FCD and refractory epilepsy. Our results suggest that the circulating miRNAs from exosomes may provide a potential biomarker for diagnostic, prognostic, and therapeutic adjuncts in patients with FCD and refractory epilepsy.

Background. The survival rates of in-hospital cardiac arrests (IHCAs) are reportedly low at night, but the difference between the survival rates of cardiac origin and noncardiac origin IHCAs occurring at night remains unclear. Methods. Outcomes of IHCAs during different shifts (night, day, and evening) were compared and stratified according to the etiology (cardiac and noncardiac origin). Result. The rate of return of spontaneous circulation (ROSC) was 24.7% lower for cardiac origin IHCA and 19.4% lower for noncardiac origin IHCA in the night shift than in the other shifts. The survival rate was 8.4% lower for cardiac origin IHCA occurring during the night shift, but there was no difference for noncardiac origin IHCA. After adjusting the potential confounders, chances of ROSC (aOR: 0.3, CI: 0.15–0.63) and survival to discharge (aOR: 0.1; CI: 0.01–0.90) related to cardiac origin IHCA were lower during night shifts. Regarding noncardiac origin IHCA, chances of ROSC (aOR: 0.5, CI: 0.30–0.78) were lower in the night shift, but chances of survival to discharge (aOR: 1.3, CI: 0.43–3.69) were similar in these two groups. Conclusion. IHCA occurring at night increases mortality, and this is more apparent for cardiac origin IHCAs than for noncardiac origin IHCA.

Status epilepticus may cause molecular and cellular events, leading to hippocampal neuronal cell death. Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) is an important regulator of vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2), also known as fetal liver kinase receptor 1 (Flk-1). Resveratrol is an activator of PGC-1α. It has been suggested to provide neuroprotective effects in epilepsy, stroke, and neurodegenerative diseases. In the present study, we used microinjection of kainic acid into the left hippocampal CA3 region in Sprague Dawley rats to induce bilateral prolonged seizure activity. Upregulating the PGC-1α pathway will increase VEGF/VEGFR2 (Flk-1) signaling and further activate some survival signaling that includes the mitogen activated protein kinase kinase (MEK)/mitogen activated protein kinase (ERK) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways and offer neuroprotection as a consequence of apoptosis in the hippocampal neurons following status epilepticus. Otherwise, downregulation of PGC-1α by siRNA against pgc-1α will inhibit VEGF/VEGFR2 (Flk-1) signaling and suppress pro-survival PI3K/AKT and MEK/ERK pathways that are also accompanied by hippocampal CA3 neuronal cell apoptosis. These results may indicate that the PGC-1α induced VEGF/VEGFR2 pathway may trigger the neuronal survival signaling, and the PI3K/AKT and MEK/ERK signaling pathways. Thus, the axis of PGC-1α/VEGF/VEGFR2 (Flk-1) and the triggering of downstream PI3K/AKT and MEK/ERK signaling could be considered an endogenous neuroprotective effect against apoptosis in the hippocampus following status epilepticus.

Background Elevated serum lactate is associated with higher mortality in sepsis, whereas liver dysfunction is associated with higher serum lactate levels. We assessed the predictive ability of serum lactate in patients with liver cirrhosis and sepsis. Methods This retrospective study included 12 281 cases of suspected infection with initial serum blood lactate drawn during January 2007–December 2013. Results Using one-to-two propensity score matching analysis, 1053 and 2106 septic patients with and without underlying liver cirrhosis, respectively, were successfully matched. Lactate levels of survivors and nonsurvivors were 2.58 and 5.93 mmol/L, respectively, in patients without liver cirrhosis (WLC), 2.96 and 7.29 mmol/L, respectively, in patients with nondecompensated liver cirrhosis (NDLC), and 4.08 and 7.16 mmol/L, respectively, in patients with decompensated liver cirrhosis (DLC). In receiver operating characteristic curve analysis, the sensitivity and specificity for predicting mortality were 0.81 and 0.55, respectively, in the WLC group, 0.85 and 0.45, respectively, in the NDLC group, and 0.86 and 0.33, respectively, in the DLC group, using serum lactate levels >2.0 mmol/L. Conclusions The serum lactate level can be used to predict the severity of sepsis in patients with liver cirrhosis; however, its specificity would be lower at a cutoff of 2.0 mmol/L.

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Stroke is a neurological emergency, where the mechanism of the blood supply to the brain is impaired, resulting in brain cell ischemia and death. Neuroinflammation is a key component in the ischemic cascade that results in cell damage and death after cerebral ischemia. The triggering receptor expressed on myeloid cells-1 (TREM-1) modulates neuroinflammation after acute ischemic stroke. In the present study, 60 patients with acute ischemic stroke, who had been subjected to neurological examinations and National Institutes of Health Stroke Scale (NIHSS) and brain magnetic resonance imaging studies, were enrolled in the emergency room of Kaohsiung Chang Gung Memorial Hospital. Twenty-four healthy volunteers were recruited as controls. The serum levels of soluble TREM-1 (sTREM-1), human S100 calcium-binding protein B (S100B), and proinflammatory cytokines and chemokines, including tumor necrosis α (TNF-α), interleukin 1β, interleukin 6 (IL-6), interleukin 8, and interferon-γ were measured immediately after acute ischemic stroke. The serum levels of sTREM-1, TNFα, IL-6, and S100B were correlated with the stroke volume and NIHSS, after acute ischemic stroke. Additionally, the serum levels of sTREM-1 were significantly positively correlated with S100B. The functional outcomes were evaluated 6 months after ischemic stroke by the Barthel index, which was correlated with the age and levels of sTREM-1 and S100B. We suggest that acute ischemic stroke induces neuroinflammation by the activation of the TREM-1 signaling pathway and the downstream inflammatory machinery that modulates the inflammatory response and ischemic neuronal cell death. From a translational perspective, our results may allow for the development of a new therapeutic strategy for acute ischemic stroke by targeting the TREM-1 signaling pathway.