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specificity, and correct classification rates especially in underweight patients.Objective To study whether resolvin D1 (RvD1), a metabolite of docosahexaenoic acid (DHA), prevents NA-STZ-induced type 2 diabetes mellitus (type 2 DM) in vivo and if so, what could be the mechanism of this action. Material and methods Single intra-peritoneal (i.p) injection of NA-STZ (175 mg/kg body weight of NA and 65 mg/kg of STZ) was injected simultaneously with RvD1 (60 ng/animal) (injected for 5 consecutive days) to Wistar rats. The effect of RvD1 on plasma glucose levels and apoptotic (Bcl2/Bax) and inflammatory (NF-κB/iNOS) protein expression, plasma lipoxin A4 and BDNF (brain-derived neurotrophic factor) were studied. Protein expressions of PI3k-Akt-mTOR pathway along with histopathological studies of brain were also evaluated. XMUMP1 Results NA-STZ-induced type 2 DM rats showed hyperglycemia, enhanced plasma IL-6/TNF-α (p ≤0.01), reduced plasma BDNF (p ≤0.01) and LXA4 (p ≤0.01) levels and low BDNF in pancreatic, hepatic and brain tissues (p less then 0.001), which were restored to near normal (p ≤0.01) in RvD1 treated group. RvD1 increased insulin sensitivity by suppressing inflammation (NF-κB/iNOS) (p ≤0.01) and decreasing apoptosis (Bcl2/Bax) and restoring BDNF and LXA4 levels to near normal. RvD1 treatment increased phosphorylation of Akt (Ser473), and subsequent activation (phosphorylation) of downstream signaling molecules of PI3K and mTOR indicating that RvD1 acts through PI3K/Akt/mTOR axis. Discussion RvD1 is effective in preventing NA-STZ-induced type 2 DM in vivo by suppressing oxidative damage, enhancing the production of anti-inflammatory LXA4 and enhancing neuronal cell survival by augmenting the production of BDNF. Thus, RvD1 may be of benefit not only in preventing diabetes mellitus but also diabetes associated Alzheimer's disease and memory loss.Purpose This study aimed to evaluate the relationship between admission time and in-hospital mortality in acute aortic dissection (AAD) patients. Methods The risk factors of in-hospital clinical outcomes were retrospectively evaluated in patients with AAD. All the patients were enrolled from January to December 2017 and were divided into two groups depending on the time of admission daytime admissions were conducted from 8 00 to 17 30 hours whereas, nighttime admissions were from 17 30 to 8 00 hours. The primary endpoints were in-hospital mortality. Univariate and multivariable cox analyses were used to test the association between admission time and in-hospital mortality. Results The average age of the 363 participants in the present study was 52.25 ± 11.77 years, of which 81.6% were male. A total of 183 (50.4%) of these patients were admitted during nighttime. In-hospital mortality rate was higher in the nighttime admission group than in the daytime admission group (HR=1.86; 95%CI, 1.13 to 3.06, P=0.015). After adjusting for age, sex, and other risk factors, nighttime admission suggested as an independent risk factor for in-hospital mortality (HR=2.67, 95%CI, 1.30 to 5.46; P=0.007). Further subgroup analysis showed that none of the variables had a significant effect on the association between nighttime admission and in-hospital mortality. Conclusion Nighttime admission for type A acute aortic dissection is associated with a higher risk of in-hospital mortality. Therefore, health care systems should focus on managing the increased risk of in-hospital mortality among patients admitted at night, regardless of the cause.Atrial fibrillation is a leading cause of ischemic stroke. Stroke risk can be reduced with oral anticoagulation. Current guidelines recommend that decisions regarding anticoagulation after ablation be based solely on preprocedural risk. Factors that favor stopping oral anticoagulationafter atrial fibrillation ablation include lower CHA2DS2-VASc score, lesser extent of atrial cardiopathy as defined by atrial size, and fibrosis and higher bleeding risk. More extensive monitoring with insertable cardiac monitors, smart devices, and frequent pulse checks provide greater sensitivity for recurrence. The authors' strategy for managing oral anticoagulation after atrial fibrillation ablation is provided.Catheter ablation of atrial fibrillation necessitates ablation on the posterior left atrium. The anterior esophagus touches the posterior left atrium, although its course is highly variable. The proximity of the left atrium to the esophagus confers risk of injury with radiofrequency and cryoablation owing to the heat transfer that occurs with thermal ablation. Early detection of esophageal temperature changes with probes may decrease the extent of damage to the esophagus, but evidence is mixed. Avoiding ablation on the esophagus with esophageal deviation and modifying ablation approaches may decrease the risk of injury.Fluoroscopy continues to be considered an indispensable part of atrial fibrillation (AF) ablation worldwide. Deleterious effects of radiation exposure to patients, physicians, and catheter laboratory personnel are gaining increased consideration. Safety and efficacy of a fluoroless approach for AF ablation is comparable with outcomes achieved with fluoroscopy use. This article focuses on AF ablation with zero fluoroscopy use as well as current evidence on efficacy and safety of this technique. In contrast, minimal fluoroscopy is an alternative. Relying on intracardiac echocardiography for transseptal access and electroanatomic mapping for catheter manipulation can help implement this approach on a wider scale.The optimal ablation strategy for non-paroxysmal atrial fibrillation remains controversial. Non-PV triggers have been shown to have a major arrhythmogenic role in these patients. Common sources of non-PV triggers are posterior wall, left atrial appendage, superior vena cava, coronary sinus, vein of Marshall, interatrial septum, crista terminalis/Eustachian ridge, and mitral and tricuspid valve annuli. These sites are targeted empirically in selected cases or if significant ectopy is noted (with or without a drug challenge), to improve outcomes in patients with non-paroxysmal atrial fibrillation. This article focuses on summarizing the current evidence and the approach to mapping and ablation of these frequent non-PV trigger sites.