Knock detection in spark ignition engines based on complementary ensemble improved intrinsic time-scale decomposition (CEIITD) and Bi-spectrum

Engine knock limits the thermal efficiency improvement of spark-ignition (SI) engines. Thus, the extract research of the knock characteristics has a great significance for the development of gasoline engines. The research proposes a novel knock detection and diagnosis method in SI engines using the CEIITD (Complementary Ensemble Improved Intrinsic time-scale decomposition) and Bi-spectrum algorithm. The CEIITD algorithm is used to extract the knock characteristics. The results show that the CEIITD algorithm can effectively and clearly extract the knock shock characteristics (including light knock) through the vibration signals. A Bi-spectrum analysis can further distinguish between the light knock signal and normal combustion signal. The Bi-spectrum results also show that knock characteristic has a strong non-Gaussian property. At last, the Band pass filter and Improved ITD method were employed to identify the knock characteristics from these cylinder block vibration signals. The comparison result shows that the CEIITD method proposed in this paper is more suitable to detect the knock characteristic

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Optimized Fuzzy Skyhook Control for Semi-Active Vehicle Suspension with New Inverse Model of Magnetorheological Fluid Damper

To improve the performance of vehicle suspension, this paper proposes a semi-active vehicle suspension with a magnetorheological fluid (MRF) damper. We designed an optimized fuzzy skyhook controller with grey wolf optimizer (GWO) algorithm base on a new neuro-inverse model of the MRF damper. Because the inverse model of the MRF damper is difficult to establish directly, the Elman neural network was applied. The novelty of this study is the application of the new inverse model for semi-active vibration control and optimization of the semi-active suspension control method. The calculation results showed that the new inverse model can accurately calculate the required control current. The fuzzy skyhook control method optimized by the grey wolf optimizer (GWO) algorithm was established based on the inverse model to control the suspension vibration. The simulation results showed that the optimized fuzzy skyhook control method can simultaneously reduce the amplitude of vertical acceleration, suspension deflection, and tire dynamic load

Addition of Nano CaF2@SiO2 and SiC Whiskers in Ceramic Tools for Wear Reduction and Improved Machinability

The addition of CaF2@SiO2 and SiC whiskers to ceramic tools can improve their flexural strength and fracture toughness, reduce surface damage, and improve their cutting performance. The cutting experiments showed that under the same cutting conditions, the surface roughness of the workpiece processed with the Al2O3/TiC/SiC/CaF2@SiO2 (ATSC10) tool was significantly lower than that of the workpiece processed with the Al2O3/TiC/ SiC (ATS) tool. Additionally, the main cutting force and cutting temperature when cutting with the ATSC10 tool were lower by 30 and 31.7%, respectively. These results were attributed to the precipitation of CaF2 from the nanocoated particles during cutting and the formation of a uniform and continuous lubricating film on the surface of the tool. The wear on the front surface of the ATS tool was mainly adhesive, and that on the back tool surface was mainly abrasive. For ATSC10, the main forms of wear on the tool front surface were adhesive and abrasive, whereas the main form of wear on the tool back surface was abrasive with slight adhesive wear. The addition of nano-coated particles and whiskers improved the mechanical properties of the cutting tool while maintaining good cutting performance

Deoxycholic Acid-Mediated Sphingosine-1-Phosphate Receptor 2 Signaling Exacerbates DSS-Induced Colitis through Promoting Cathepsin B Release

We recently have proved that excessive fecal DCA caused by high-fat diet may serve as an endogenous danger-associated molecular pattern to activate NLRP3 inflammasome and thus contributes to the development of inflammatory bowel disease (IBD). Moreover, the effect of DCA on inflammasome activation is mainly mediated through bile acid receptor sphingosine-1-phosphate receptor 2 (S1PR2); however, the intermediate process remains unclear. Here, we sought to explore the detailed molecular mechanism involved and examine the effect of S1PR2 blockage in a colitis mouse model. In this study, we found that DCA could dose dependently upregulate S1PR2 expression. Meanwhile, DCA-induced NLRP3 inflammasome activation is at least partially achieved through stimulating extracellular regulated protein kinases (ERK) signaling pathway downstream of S1PR2 followed by promoting of lysosomal cathepsin B release. DCA enema significantly aggravated DSS-induced colitis in mice and S1PR2 inhibitor as well as inflammasome inhibition by cathepsin B antagonist substantially reducing the mature IL-1β production and alleviated colonic inflammation superimposed by DCA. Therefore, our findings suggest that S1PR2/ERK1/2/cathepsin B signaling plays a critical role in triggering inflammasome activation by DCA and S1PR2 may represent a new potential therapeutic target for the management of intestinal inflammation in individuals on a high-fat diet

Deoxycholic acid triggers NLRP3 inflammasome activation and aggravates DSS-induced colitis in mice

A westernized high-fat diet (HFD) is associated with the development of inflammatory bowel disease (IBD). High level fecal deoxycholic acid (DCA) caused by HFD contributes to the colonic inflammatory injury of IBD, however, the mechanism concerning the initiation of inflammatory response by DCA remains unclear. In this study, we sought to investigate the role and mechanism of DCA in the induction of inflammation via promoting NLRP3 inflammasome activation. Here we for the first time showed that DCA dose-dependently induced NLRP3 inflammasome activation and highly pro-inflammatory cytokine-IL-1β production in macrophages. Mechanistically, DCA triggered NLRP3 inflammasome activation by promoting cathepsin B release at least partially through sphingosine-1-phosphate receptor 2 (S1PR2). Colorectal instillation of DCA significantly increased mature IL-1β level in colonic tissue and exacerbated DSS-induced colitis, while in vivo blockage of NLRP3 inflammasome or macrophage depletion dramatically reduced the mature IL-1β production and ameliorated the aggravated inflammatory injury imposed by DCA. Thus, our findings show that high level fecal DCA may serve as an endogenous danger signal to activate NLRP3 inflammasome and contributes to HFD-related colonic inflammation. NLRP3 inflammasome may represent a new potential therapeutical target for treatment of IBD

Gut microbial metabolite deoxycholic acid facilitates Th17 differentiation through modulating cholesterol biosynthesis and participates in high-fat diet-associated colonic inflammation

Abstract Background High-fat diet (HFD) is closely associated with the increased prevalence of inflammatory bowel disease (IBD). Excessive gut microbial metabolite deoxycholic acid (DCA) caused by HFD plays significant roles in eliciting intestinal inflammation, however, the mechanism underlining the induction of inflammatory response by DCA has not been fully elucidated. The purpose of this study was to investigate the role of DCA in the triggering of inflammation via affecting CD4+ T cell differentiation. Results Murine CD4+T cells were cultured under Th1, Th2 or Th17-polarizing conditions treated with or without different dosage of DCA, and flowcytometry was conducted to detect the effect of DCA on CD4+ T cell differentiation. Alteration of gene expression in CD4+ T cells upon DCA treatment was determined by RNA-sequencing and qRT-PCR. Bioinformatic analysis, cholesterol metabolic profiling, ChIP assay and immuno-fluorescent staining were further applied to explore the DCA-regulated pathway that involved in CD4+T cell differentiation. The results showed that DCA could dose-dependently promote the differentiation of CD4+ T cell into Th17 linage with pathogenic signature. Mechanistically, DCA stimulated the expression of cholesterol biosynthetic enzymes CYP51 and led to the increased generation of endogenous RORγt agonists, including zymosterol and desmosterol, therefore facilitating Th17 differentiation. Up-regulation of CYP51 by DCA was largely mediated via targeting transcription factor SREBP2 and at least partially through bile acid receptor TGR5. In addition, DCA-supplemented diet significantly increased intestinal Th17 cell infiltration and exacerbated TNBS-induced colitis. Administration of cholestyramine to eliminate fecal bile acid obviously alleviated colonic inflammation accompanied by decreased Th17 cells in HFD-fed mice. Conclusions Our data establish a link between DCA-induced cholesterol biosynthesis in immune cells and gut inflammation. Modulation of bile acid level or targeting cholesterol metabolic pathway may be potential therapeutic measurements for HFD-related colitis

Amplitude analysis and branching fraction measurement of D+s→K−K+π+π0

Relative fractions and phases of the intermediate decays are determined. With the detection efficiency estimated by the results of the amplitude analysis, the branching fraction of Dþ s → K−Kþπþπ0 decay is measured to be ð5.42 0.10stat 0.17systÞ%