Computational optimization of the dual-mode dual-fuel concept through genetic algorithm at different engine loads

[EN] The diesel/gasoline dual-mode dual-fuel (DMDF) combustion concept was optimized in a compression-ignition engine by combining the computational fluid dynamics (CFD) simulations with the genetic algorithm. Seven operating parameters with remarkable influences on the engine performance were chosen as the variables to be optimized for simultaneously minimizing the fuel efficiency, nitrogen oxides (NOx), and soot emissions. Moreover, the potential of the further improvement of the DMDF combustion concept was discussed, and the rationality of this strategy was demonstrated. The results indicate that, at low load, simultaneous improvement of the fuel economy and emissions can be realized by strengthening the homogeneous combustion. At mid load, the fuel economy can be improved by reducing the heat transfer losses, while the NOx emissions are sacrificed to some extent. At high load, improved fuel economy can be realized by transferring a part of diffusion combustion to premixed reactivity-controlled compression ignition (RCCI) combustion. Concerning the operating parameters, lower intake temperature is beneficial to decrease the transfer losses, and the control of intake temperature is crucial for the stable operation of DMDF combustion under wide load conditions. Overall, gross indicated thermal efficiency above 45% is achieved, and the NOx and soot emission can be maintained under the Euro 6 standard for the test load range.This work was partially supported by the National Natural Science Foundation of China (Grant Nos. 51961135105 and 91641117) and China Postdoctoral Science Foundation (Grant No. 2019M661094). The experimental results used in this investigation were obtained in a project funded by VOLVO Group Trucks Technology. The authors also acknowledge FEDER and Spanish Ministerio de Economia y Competitividad for partially supporting this research through TRANCO project (TRA2017-87694-R) and the Universitat Politecnica de Valencia for partially supporting this research through Convocatoria de ayudas a Primeros Proyectos de Investigacion (PAID-06-18).Xu, G.; Monsalve-Serrano, J.; Jia, M.; García Martínez, A. (2020). Computational optimization of the dual-mode dual-fuel concept through genetic algorithm at different engine loads. Energy Conversion and Management. 208:1-13. https://doi.org/10.1016/j.enconman.2020.112577S113208Johnson TV. Diesel emission control in review. SAE Technical Paper. 2009; no. 2009-01-0121.Reitz, R. D., & Duraisamy, G. (2015). Review of high efficiency and clean reactivity controlled compression ignition (RCCI) combustion in internal combustion engines. Progress in Energy and Combustion Science, 46, 12-71. doi:10.1016/j.pecs.2014.05.003Lim, J. H., & Reitz, R. D. (2014). 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K6PC-5 Activates SphK1-Nrf2 Signaling to Protect Neuronal Cells from Oxygen Glucose Deprivation/Re-Oxygenation

Background/Aims: New strategies are required to combat neuronal ischemia-reperfusion injuries. K6PC-5 is a novel sphingosine kinase 1 (SphK1) activator whose potential activity in neuronal cells has not yet been tested. Methods: Cell survival and necrosis were assessed with a Cell Counting Kit-8 assay and lactate dehydrogenase release assay, respectively. Mitochondrial depolarization was tested by a JC-1 dye assay. Expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling components were examined by quantitative real-timePCR and western blotting. Results: K6PC-5 protected SH-SY5Y neuronal cells and primary murine hippocampal neurons from oxygen glucose deprivation/re-oxygenation (OGDR). K6PC-5 activated SphK1, and SphK1 knockdown by targeted short hairpin RNA (shRNA) almost completely abolished K6PC-5-induced neuronal cell protection. Further work showed that K6PC-5 inhibited OGDR-induced programmed necrosis in neuronal cells. Importantly, K6PC-5 activated Nrf2 signaling, which is downstream of SphK1. Silencing of Nrf2 by targeted shRNA almost completely nullified K6PC-5-mediated neuronal cell protection against OGDR. Conclusion: K6PC-5 activates SphK1-Nrf2 signaling to protect neuronal cells from OGDR. K6PC-5 might be a promising neuroprotective strategy for ischemia-reperfusion injuries

Allelopathic interactions of linoleic acid and nitric oxide increase the competitive ability of Microcystis aeruginosa

The frequency and intensity of cyanobacterial blooms are increasing worldwide with major societal and economic costs. Interactions between toxic cyanobacteria and eukaryotic algal competitors can affect toxic bloom formation, but the exact mechanisms of interspecies interactions remain unknown. Using metabolomic and proteomic profiling of co-cultures of the toxic cyanobacterium Microcystis aeruginosa with a green alga as well as of microorganisms collected in a Microcystis spp. bloom in Lake Taihu (China), we disentangle novel interspecies allelopathic interactions. We describe an interspecies molecular network in which M. aeruginosa inhibits growth of Chlorella vulgaris, a model green algal competitor, via the release of linoleic acid. In addition, we demonstrate how M. aeruginosa takes advantage of the cell signaling compound nitric oxide produced by C. vulgaris, which stimulates a positive feedback mechanism of linoleic acid release by M. aeruginosa and its toxicity. Our high-throughput system-biology approach highlights the importance of previously unrecognized allelopathic interactions between a broadly distributed toxic cyanobacterial bloom former and one of its algal competitors

Sequence variations in DNA repair gene XPC is associated with lung cancer risk in a Chinese population: a case-control study

<p>Abstract</p> <p>Background</p> <p>The nucleotide excision repair (NER) protein, xeroderma pigmentosum C (XPC), participates in recognizing DNA lesions and initiating DNA repair in response to DNA damage. Because mutations in <it>XPC </it>cause a high risk of cancer in XP patients, we hypothesized that inherited sequence variations in <it>XPC </it>may alter DNA repair and thus susceptibility to cancer.</p> <p>Methods</p> <p>In this hospital-based case-control study, we investigated five <it>XPC </it>tagging, common single nucleotide polymorphisms (tagging SNPs) in 1,010 patients with newly diagnosed lung cancer and 1,011 matched cancer free controls in a Chinese population.</p> <p>Results</p> <p>In individual tagging SNP analysis, we found that rs3731055<it>AG+AA </it>variant genotypes were associated with a significantly decreased risk of lung adenocarcinoma [adjusted odds ratio (OR), 0.71; 95% confidence interval (CI), 0.56–0.90] but an increased risk of small cell carcinomas [adjusted OR, 1.79; 95% CI, 1.05–3.07]. Furthermore, we found that haplotype <it>ACCCA </it>was associated with a decreased risk of lung adenocarcinoma [OR, 0.78; 95% CI, 0.62–0.97] but an increased risk of small cell carcinomas [OR, 1.68; 95% CI, 1.04–2.71], which reflected the presence of rs3731055<it>A </it>allele in this haplotype. Further stratified analysis revealed that the protective effect of rs3731055<it>AG+AA </it>on risk of lung adenocarcinoma was more evident among young subjects (age ≤ 60) and never smokers.</p> <p>Conclusion</p> <p>These results suggest that inherited sequence variations in <it>XPC </it>may modulate risk of lung cancer, especially lung adenocarcinoma, in Chinese populations. However, these findings need to be verified in larger confirmatory studies with more comprehensively selected tagging SNPs.</p

The 5p15.33 Locus Is Associated with Risk of Lung Adenocarcinoma in Never-Smoking Females in Asia

Genome-wide association studies of lung cancer reported in populations of European background have identified three regions on chromosomes 5p15.33, 6p21.33, and 15q25 that have achieved genome-wide significance with p-values of 10−7 or lower. These studies have been performed primarily in cigarette smokers, raising the possibility that the observed associations could be related to tobacco use, lung carcinogenesis, or both. Since most women in Asia do not smoke, we conducted a genome-wide association study of lung adenocarcinoma in never-smoking females (584 cases, 585 controls) among Han Chinese in Taiwan and found that the most significant association was for rs2736100 on chromosome 5p15.33 (p = 1.30×10−11). This finding was independently replicated in seven studies from East Asia totaling 1,164 lung adenocarcinomas and 1,736 controls (p = 5.38×10−11). A pooled analysis achieved genome-wide significance for rs2736100. This SNP marker localizes to the CLPTM1L-TERT locus on chromosome 5p15.33 (p = 2.60×10−20, allelic risk = 1.54, 95% Confidence Interval (CI) 1.41–1.68). Risks for heterozygote and homozygote carriers of the minor allele were 1.62 (95% CI; 1.40–1.87), and 2.35 (95% CI: 1.95–2.83), respectively. In summary, our results show that genetic variation in the CLPTM1L-TERT locus of chromosome 5p15.33 is directly associated with the risk of lung cancer, most notably adenocarcinoma