A Target Coverage Scheduling Scheme Based on Genetic Algorithms in Directional Sensor Networks

As a promising tool for monitoring the physical world, directional sensor networks (DSNs) consisting of a large number of directional sensors are attracting increasing attention. As directional sensors in DSNs have limited battery power and restricted angles of sensing range, maximizing the network lifetime while monitoring all the targets in a given area remains a challenge. A major technique to conserve the energy of directional sensors is to use a node wake-up scheduling protocol by which some sensors remain active to provide sensing services, while the others are inactive to conserve their energy. In this paper, we first address a Maximum Set Covers for DSNs (MSCD) problem, which is known to be NP-complete, and present a greedy algorithm-based target coverage scheduling scheme that can solve this problem by heuristics. This scheme is used as a baseline for comparison. We then propose a target coverage scheduling scheme based on a genetic algorithm that can find the optimal cover sets to extend the network lifetime while monitoring all targets by the evolutionary global search technique. To verify and evaluate these schemes, we conducted simulations and showed that the schemes can contribute to extending the network lifetime. Simulation results indicated that the genetic algorithm-based scheduling scheme had better performance than the greedy algorithm-based scheme in terms of maximizing network lifetime

Copeptin with high-sensitivity troponin at presentation is not inferior to serial troponin measurements for ruling out acute myocardial infarction

Objective We aimed to compare the multi-marker strategy (copeptin and high-sensitivity cardiac troponin I [hs-cTnI]) with serial hs-cTnI measurements to rule out acute myocardial infarction (AMI) in patients with chest pain. Methods This prospective observational study was performed in a single emergency department. To test the non-inferiority margin of 4% in terms of negative predictive value (NPV) between the multi-marker strategy (0 hour) and serial hs-cTnI measurements (0 and 2 hours), 262 participants were required. Samples for copeptin and hs-cTnI assays were collected at presentation (0 hour) and after 2 hours. The measured biomarkers were considered abnormal when hs-cTnI was >26.2 ng/L and when copeptin was >10 pmol/L. Results AMI was diagnosed in 28 patients (10.7%). The NPV of the multi-marker strategy was 100% (160/160; 95% confidence interval [CI], 97.7% to 100%), which was not inferior to that of serial hs-cTnI measurements (201/201; 100%; 95% CI, 98.2% to 100%). The sensitivity, specificity, and positive predictive value of the multi-marker strategy were 100% (95% CI, 87.7% to 100%), 68.1% (95% CI, 61.7% to 74.0%), and 27.2% (95% CI, 18.9% to 36.8%), respectively. The sensitivity, specificity, and positive predictive value of serial hs-cTnI measurements were 100% (95% CI, 87.7% to 100%), 85.5% (95% CI, 80.4% to 89.8%), and 45.2% (95% CI, 32.5% to 58.3%), respectively. Conclusion The multi-marker strategy (copeptin and hs-cTnI measurement) was not inferior to serial hs-cTnI measurements in terms of NPV for AMI diagnosis, with a sensitivity and NPV of 100%. Copeptin may help in the early rule-out of AMI in patients with chest pain

Effect of Bee Venom Acupuncture on Oxaliplatin-Induced Cold Allodynia in Rats

Oxaliplatin, a chemotherapy drug, often leads to neuropathic cold allodynia after a single administration. Bee venom acupuncture (BVA) has been used in Korea to relieve various pain symptoms and is shown to have a potent antiallodynic effect in nerve-injured rats. We examined whether BVA relieves oxaliplatin-induced cold allodynia and which endogenous analgesic system is implicated. The cold allodynia induced by an oxaliplatin injection (6 mg/kg, i.p.) was evaluated by immersing the rat’s tail into cold water (4°C) and measuring the withdrawal latency. BVA (1.0 mg/kg, s.c.) at Yaoyangguan (GV3), Quchi (LI11), or Zusanli (ST36) acupoints significantly reduced cold allodynia with the longest effect being shown in the GV3 group. Conversely, a high dose of BVA (2.5 mg/kg) at GV3 did not show a significant antiallodynic effect. Phentolamine (α-adrenergic antagonist, 2 mg/kg, i.p.) partially blocked the relieving effect of BVA on allodynia, whereas naloxone (opioid antagonist, 2 mg/kg, i.p.) did not. We further confirmed that an intrathecal administration of idazoxan (α2-adrenergic antagonist, 50 μg) blocked the BVA-induced anti-allodynic effect. These results indicate that BVA alleviates oxaliplatin-induced cold allodynia in rats, at least partly, through activation of the noradrenergic system. Thus, BVA might be a potential therapeutic option in oxaliplatin-induced neuropathy

Admission levels of high-density lipoprotein and apolipoprotein A-1 are associated with the neurologic outcome in patients with out-of-hospital cardiac arrest

Objective To investigate whether serum levels of high-density lipoprotein (HDL) and apolipoprotein A-1 (ApoA1), after the return of spontaneous circulation, can predict the neurologic outcome in patients with out-of-hospital cardiac arrest (OHCA). Methods This was a retrospective observational study conducted in a single tertiary hospital intensive care unit. All adult OHCA survivors with admission lipid profiles were enrolled from March 2013 to December 2015. Good neurologic outcome was defined as discharge cerebral performance categories 1 and 2. Results Among 59 patients enrolled, 13 (22.0%) had a good neurologic outcome. Serum levels of HDL (56.7 vs. 40 mg/dL) and ApoA1 (117 vs. 91.6 mg/dL) were significantly higher in patients with a good outcome. Areas under the HDL and ApoA1 receiver operating curves to predict good outcomes were 0.799 and 0.759, respectively. The proportion of good outcome was significantly higher in patients in higher tertiles of HDL and ApoA1 (test for trend, both P=0.003). HDL (P=0.018) was an independent predictor in the multivariate logistic regression model. Conclusion Admission levels of HDL and ApoA1 are associated with neurologic outcome in patients with OHCA. Prognostic and potential therapeutic values of HDL and ApoA1 merit further evaluation in the post-cardiac arrest state, as in other systemic inflammatory conditions such as sepsis

Enhancement of paclitaxel-induced breast cancer cell death via the glycogen synthase kinase-3 beta-mediated B-cell lymphoma 2 regulation

Glycogen synthase kinase-3 beta (GSK-3 beta) is a serine/threonine protein kinase that is known to mediate cancer cell death. Here, we show that B-cell lymphoma 2 (Bcl-2), an anti-apoptotic protein, is regulated by GSK-3 beta and that GSK-3 beta-mediated regulation of Bcl-2 is crucial for mitochondrial-dependent cell death in paclitaxel-stimulated cells. We demonstrate that MCF7 GSK3 beta siRNA cells are more sensitive to cell death than MCF7 GFP control cells and that in the absence of GSK-3 beta, Bcl-2 levels are reduced, a result enhanced by paclitaxel. Paclitaxel-induced JNK (c-Jun N-terminal kinase) activation is critical for Bcl-2 modulation. In the absence of GSK-3 beta, Bcl-2 was unstable in an ubiquitination-dependent manner in both basal-and paclitaxel-treated cells. Furthermore, we demonstrate that GSK-3 beta-mediated regulation of Bcl-2 influences cytochrome C release and mitochondrial membrane potential. Taken together, our data suggest that GSK-3 beta-dependent regulation of Bcl-2 is crucial for mitochondria-dependent cell death in paclitaxel-mediated breast cancer therapy.clos

Association between the simultaneous decrease in the levels of soluble vascular cell adhesion molecule-1 and S100 protein and good neurological outcomes in cardiac arrest survivors

Objective This study aimed to determine whether simultaneous decreases in the serum levels of cell adhesion molecules (intracellular cell adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1], and E-selectin) and S100 proteins within the first 24 hours after the return of spontaneous circulation were associated with good neurological outcomes in cardiac arrest survivors. Methods This retrospective observational study was based on prospectively collected data from a single emergency intensive care unit (ICU). Twenty-nine out-of-hospital cardiac arrest survivors who were admitted to the ICU for post-resuscitation care were enrolled. Blood samples were collected at 0 and 24 hours after ICU admission. According to the 6-month cerebral performance category (CPC) scale, the patients were divided into good (CPC 1 and 2, n=12) and poor (CPC 3 to 5, n=17) outcome groups. Results No difference was observed between the two groups in terms of the serum levels of ICAM-1, VCAM-1, E-selectin, and S100 at 0 and 24 hours. A simultaneous decrease in the serum levels of VCAM-1 and S100 as well as E-selectin and S100 was associated with good neurological outcomes. When other variables were adjusted, a simultaneous decrease in the serum levels of VCAM-1 and S100 was independently associated with good neurological outcomes (odds ratio, 9.285; 95% confidence interval, 1.073 to 80.318; P=0.043). Conclusion A simultaneous decrease in the serum levels of soluble VCAM-1 and S100 within the first 24 hours after the return of spontaneous circulation was associated with a good neurological outcome in out-of-hospital cardiac arrest survivors

The Effect of Direct Communication between Emergency Physicians and Interventional Cardiologists on Door to Balloon Times in STEMI

We developed an institutional protocol mandating emergency physicians to contact the interventional cardiologist directly in all cases of ST-segment elevation myocardial infarction (STEMI) and hypothesized that this would reduce door-to-balloon-times (DTBT). From January 2004 to July 2006, 208 patients with STEMI were treated with primary percutaneous coronary intervention (PCI). A total of 144 patients were treated before implementing the new protocol ("before") and 64 patients were treated after the implementation ("after"). The DTBT was significantly reduced from 148±101 min to 108±56 min (p<0.05). While only 25% of the "before" patients received PCI within 90 min after arrival, 50% of the "after" patients received PCI within 90 min (p<0.05). There were no significant differences between two groups in other outcomes (postprocedural TIMI flow, mortality, subsequent stroke, heart failure, shock, reinfarction, length of stay in intensive care unit, and the total hospital length of stay). In conclusion, mandating emergency physicians to directly notify interventional cardiologists of all STEMI patients reduces DTBT

Combination therapy of vitamin C and thiamine for septic shock in a multicentre, double-blind, randomized, controlled study (ATESS): study protocol for a randomized controlled trial

Background Septic shock is a life-threatening condition with underlying circulatory and cellular/metabolic abnormalities. Vitamin C and thiamine are potential candidates for adjunctive therapy; they are expected to improve outcomes based on recent experimental and clinical research. The aim of the Ascorbic Acid and Thiamine Effect in Septic Shock (ATESS) trial is to evaluate the effects of early combination therapy with intravenous vitamin C and thiamine on recovery from organ failure in patients with septic shock. Methods This study is a randomized, double-blind, placebo-controlled, multicentre trial in adult patients with septic shock recruited from six emergency departments in South Korea. Patients will be randomly allocated into the treatment or control group (1:1 ratio), and we will recruit 116 septic shock patients (58 per group). For the treatment group, vitamin C (50 mg/kg) and thiamine (200 mg) will be mixed in 50 ml of 0.9% saline and administered intravenously every 12 h for a total of 48 h. For the placebo group, an identical volume of 0.9% saline will be administered in the same manner. The primary outcome is the delta Sequential Organ Failure Assessment (SOFA) score (ΔSOFA = initial SOFA at enrolment – follow-up SOFA after 72 h). Discussion This trial will provide valuable evidence about the effectiveness of vitamin C and thiamine therapy for septic shock. If effective, this therapy might improve survival and become one of the main therapeutic adjuncts for patients with septic shock. Trial registration ClinicalTrials.gov, NCT03756220. Registered on 5 December 2018.This work was supported by a National Research Foundation of Korea grant funded by the Korean government (No. 2018R1C1B6006821). The government did not have any role in the study design; collection, management, analysis, and interpretation of data; writing of the report; and the decision to submit the report for publication

A new strategy for enhancing imputation quality of rare variants from next-generation sequencing data via combining SNP and exome chip data

Background: Rare variants have gathered increasing attention as a possible alternative source of missing heritability. Since next generation sequencing technology is not yet cost-effective for large-scale genomic studies, a widely used alternative approach is imputation. However, the imputation approach may be limited by the low accuracy of the imputed rare variants. To improve imputation accuracy of rare variants, various approaches have been suggested, including increasing the sample size of the reference panel, using sequencing data from study-specific samples (i.e., specific populations), and using local reference panels by genotyping or sequencing a subset of study samples. While these approaches mainly utilize reference panels, imputation accuracy of rare variants can also be increased by using exome chips containing rare variants. The exome chip contains 250 K rare variants selected from the discovered variants of about 12,000 sequenced samples. If exome chip data are available for previously genotyped samples, the combined approach using a genotype panel of merged data, including exome chips and SNP chips, should increase the imputation accuracy of rare variants. Results: In this study, we describe a combined imputation which uses both exome chip and SNP chip data simultaneously as a genotype panel. The effectiveness and performance of the combined approach was demonstrated using a reference panel of 848 samples constructed using exome sequencing data from the T2D-GENES consortium and 5,349 sample genotype panels consisting of an exome chip and SNP chip. As a result, the combined approach increased imputation quality up to 11 %, and genomic coverage for rare variants up to 117.7 % (MAF < 1 %), compared to imputation using the SNP chip alone. Also, we investigated the systematic effect of reference panels on imputation quality using five reference panels and three genotype panels. The best performing approach was the combination of the study specific reference panel and the genotype panel of combined data. Conclusions: Our study demonstrates that combined datasets, including SNP chips and exome chips, enhances both the imputation quality and genomic coverage of rare variants

The genetic architecture of type 2 diabetes

The genetic architecture of common traits, including the number, frequency, and effect sizes of inherited variants that contribute to individual risk, has been long debated. Genome-wide association studies have identified scores of common variants associated with type 2 diabetes, but in aggregate, these explain only a fraction of heritability. To test the hypothesis that lower-frequency variants explain much of the remainder, the GoT2D and T2D-GENES consortia performed whole genome sequencing in 2,657 Europeans with and without diabetes, and exome sequencing in a total of 12,940 subjects from five ancestral groups. To increase statistical power, we expanded sample size via genotyping and imputation in a further 111,548 subjects. Variants associated with type 2 diabetes after sequencing were overwhelmingly common and most fell within regions previously identified by genome-wide association studies. Comprehensive enumeration of sequence variation is necessary to identify functional alleles that provide important clues to disease pathophysiology, but large-scale sequencing does not support a major role for lower-frequency variants in predisposition to type 2 diabetes