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Until the Mw 6.6 Luding earthquake ruptured the Moxi section of the Xianshuihe fault (XSHF) on 5 September 2022, the region had not experienced an Mw >6 earthquake since instrumental records began. We used Global Positioning System (GPS) and Sentinel-1 interferometric synthetic aperture radar (InSAR) observations to image the coseismic deformation and constrain the location and geometry of the seismogenic fault using a Bayesian method We then present a distributed slip model of the 2022 Mw6.6 Luding earthquake, a left-lateral strike-slip earthquake that occurred on the Moxi section of the Xianshuihe fault in the southwest Sichuan basin, China. Two tracks (T26 and T135) of the InSAR data captured a part of the coseismic surface deformation with the line-of-sight displacements range from ∼−0.16 m to ~0.14 m in the ascending track and from ~−0.12 m to ~0.10 m in the descending track. The inverted best-fitting fault model shows a pure sinistral strike-slip motion on a west-dipping fault plane with a strike of 164.3°. We adopt a variational Bayesian approach and account for the uncertainties in the fault geometry to retrieve the distributed slip model. The inverted result shows that the maximum slip of ~1.82 m occurred at a depth of 5.3 km, with the major slip concentrated within depths ranging from 0.9–11 km. The InSAR-determined moment is 1.3 × 1019 Nm, with a shear modulus of 30 GPa, equivalent to Mw 6.7. The published coseismic slip models of the 2022 Luding earthquake show apparent differences despite the use of similar geodetic or seismic observations. These variations underscore the uncertainty associated with routinely performed source inversions and their interpretations for the underlying fault model. [ABSTRACT FROM AUTHOR]

This work established a finite element analysis (FEA) model of an inserted tooth-type slip assembly under bear setting load and axial load, calculated the differences between the inserted teeth of the sidetracking packer slip-formed furrow shapes on the casing face, and analyzed the setting reliability of the inserted tooth slip sidetracking packer. The orthogonal optimization analysis of the structural parameters of the sidetracking packer was carried out on the basis of the furrow effect. Finally, the setting experiment was conducted with the inserted tooth slip sidetracking packer developed to verify correctness of the FEA model and the simulation results. The results show that in the FEA and calculation of the setting process of the inserted tooth-type slip, it is not only necessary to consider the furrow friction coefficient, but also the effect of the ridge on the furrow friction coefficient. The corresponding furrow friction coefficient varies according to the different furrow effects occurring on the casing surface caused by the various types of teeth inserted on the packer slips. The furrow effect is related to the sharpness of the tooth tips of the slips. The sharper the tooth tips, the more obvious the furrow effect is. Under the dual effects of the furrow effect and the adhesion effect, the carbide teeth of the slip feed into the casing wall to produce a uniform and distinct indentation on the premise of meeting the inserted tooth strength to ensure a reliable setting and hanging the inserted tooth slip sidetracking packer. The optimal combination of slip parameters was obtained by taking the optimal bite depth uniformity as the objective function: slip tooth installation spacing L = 10 mm, slip tooth installation angle α = 80°, slip tooth diameter d = 10 mm, and slip wedge angle β = 6°. The standard deviation of bite depth uniformity of the optimized slip teeth is 74.45% lower than that before optimization. The research results of this paper basically meet the requirements of engineering applications. [ABSTRACT FROM AUTHOR]

Tripterygium glycoside tablet (TGT), as a common clinical drug, can easily cause liver damage due to the narrow therapeutic window. Glycyrrhizic acid (GA) has a hepatoprotective effect, but the characteristics and mechanism of GA's impact on TGT-induced acute liver injury by regulating oxidative stress remain unelucidated. In this study, TGT-induced acute liver injury models were established in vitro and in vivo. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (AKP), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), catalase (CAT), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were quantified. The anti-apoptotic effect of GA was tested using flow cytometry. Potential target proteins of GA were profiled via activity-based protein profiling (ABPP) using a cysteine-specific (IAA-yne) probe. The results demonstrate that GA markedly decreased the concentrations of ALT, AST, AKP, MDA, LDH, TNF-α, IL-1β and IL-6, whereas those of SOD, GSH and CAT increased. GA could inhibit TGT-induced apoptosis in BRL-3A cells. GA bound directly to the cysteine residue of PKM2. The CETSA and enzyme activity results validate the specific targets identified. GA could mitigate TGT-induced acute liver injury by mediating PKM2, reducing oxidative stress and inflammation and reducing hepatocyte apoptosis. [ABSTRACT FROM AUTHOR]

In the civil aviation industry, security risk management has shifted from post-accident investigations and analyses to pre-accident warnings in an attempt to reduce flight risks by identifying currently untracked flight events and their trends and effectively preventing risks before they occur. The use of flight monitoring data for flight anomaly detection is effective in discovering unknown and potential flight incidents. In this paper, we propose a time-feature attention mechanism and construct a deep hybrid model for flight anomaly detection. The hybrid model combines a time-feature attention-based convolutional autoencoder with the HDBSCAN clustering algorithm, where the autoencoder is constructed and trained to extract flight features while the HDBSCAN works as an anomaly detector. Quick access record (QAR) flight data containing information of aircraft landing at Kunming Changshui International and Chengdu Shuangliu International airports are used as the experimental data, and the results show that (1) the time-feature-based convolutional autoencoder proposed in this paper can better extract the flight features and further discover the different landing patterns; (2) in the representation space of the flights, anomalous flight objects are better separated from normal objects to provide a quality database for subsequent anomaly detection; and (3) the discovered flight patterns are consistent with those at the airports, resulting in anomalies that could be interpreted with the corresponding pattern. Moreover, several examples of anomalous flights at each airport are presented to analyze the characteristics of anomalies. [ABSTRACT FROM AUTHOR]

Mitochondrial quality control is sustained by Miro1 (Rhot1), a calcium-binding membrane-anchored GTPase during mitophagy. The exact mechanism that operates the interaction of Miro1 with mitophagy machinery and their role in cigarette smoke (CS)-induced mitochondrial dysfunction that often results in lung inflammation is unclear. We hypothesized that Miro1 plays an important role in regulating mitophagy machinery and the resulting lung inflammation by CS exposure to mice. The lung epithelial Rhot1fl/fl (WT) and Rhot1CreCC10 mice were exposed to mainstream CS for 3 days (acute) and 4 months (chronic). Acute CS exposure showed a notable increase in the total inflammatory cells, macrophages, and neutrophils that are associated with inflammatory mediators. Chronic exposure showed increased infiltration of neutrophils versus air controls. The effects of acute and chronic CS exposure were augmented in the Rhot1CreCC10 group, indicating that epithelial Miro1 ablation led to the augmentation of inflammatory cell infiltration with alteration in the inflammatory mediators. Thus, Rhot1/Miro1 plays an important role in regulating CS-induced lung inflammatory responses with implications in mitochondrial quality control. [ABSTRACT FROM AUTHOR]

We propose and numerically demonstrate an 800 Gbps silicon photonic transmitter with sub-decibel surface-normal optical interfaces. The silicon photonic transmitter is composed of eight silicon Mach–Zehnder optical modulators and an interleaved AMMI WDM device. This WDM device comprises two 1 × 4 angled MMI and a Mach–Zehnder interferometer (MZI) optical interleaver with an apodized bidirectional grating which has about −0.5 dB coupling loss. Both the Mach–Zehnder electro-optical modulators and MZI optical interleaver regard the bidirectional grating coupler as vertical optical coupler and 3-dB power splitter/combiner. By importing the S-parameter matrices of all the components which have been carefully designed in simulation software, the circuit-level model of the optical transmitter can be built up. On this basis, the static and dynamic performance characterization were carried out numerically. For NRZ modulation, the optical transmitter exhibits the overall optical loss of 4.86–6.72 dB for eight wavelength channels. For PAM4 modulation, the optical loss is about 0.5 dB larger than that of NRZ modulation, which varies between 5.38–7.27 dB. From the eye diagram test results, the WDM silicon photonic transmitter can achieve single channel data transmission at 100 Gb/s NRZ data or 50 GBaud/s PAM4 symbol rate with acceptable bit error rate. [ABSTRACT FROM AUTHOR]

Multi-walled carbon nanotubes are engineered nanomaterials (ENMs) that have a fiber-like structure which may be a concern for the development of cellular senescence. Premature senescence, a state of irreversible cell cycle arrest, is implicated in the pathogenesis of chronic lung diseases such as pulmonary fibrosis (PF). However, the crosstalk between downstream pathways mediating fibrotic and senescent responses of MWCNTs is not well-defined. Here, we exposed human bronchial epithelial cells (BEAS-2B) to MWCNTs for up to 72 h and demonstrate that MWCNTs increase reactive oxygen species (ROS) production accompanied by inhibition of cell proliferation. In addition, MWCNT exposure resulted in the increase of p21 protein abundance and senescence associated β-galactosidase (SA β-gal) activity. We also determined that co-exposure with the cytokine, transforming growth factor-β (TGF-β) exacerbated cellular senescence indicated by increased protein levels of p21, p16, and γH2A.X. Furthermore, the production of fibronectin and plasminogen activator inhibitor (PAI-1) was significantly elevated with the co-exposure compared to MWCNT or TGF-β alone. Together, our study suggests that the cellular senescence potential of MWCNTs may be enhanced by pro-fibrotic mediators, such as TGF-β in the surrounding microenvironment. [ABSTRACT FROM AUTHOR]

Metabolites are essential intermediate products in metabolism, and metabolism dysregulation indicates different types of diseases. Previous studies have shown that cigarette smoke dysregulated metabolites; however, limited information is available with electronic cigarette (e-cig) vaping. We hypothesized that e-cig vaping and cigarette smoking alters systemic metabolites, and we propose to understand the specific metabolic signature between e-cig users and cigarette smokers. Plasma from non-smoker controls, cigarette smokers, and e-cig users was collected, and metabolites were identified by UPLC-MS (ultra-performance liquid chromatography mass spectrometer). Nicotine degradation was activated by e-cig vaping and cigarette smoking with increased concentrations of cotinine, cotinine N-oxide, (S)-nicotine, and (R)-6-hydroxynicotine. Additionally, we found significantly decreased concentrations in metabolites associated with tricarboxylic acid (TCA) cycle pathways in e-cig users versus cigarette smokers, such as d-glucose, (2R,3S)-2,3-dimethylmalate, (R)-2-hydroxyglutarate, O-phosphoethanolamine, malathion, d-threo-isocitrate, malic acid, and 4-acetamidobutanoic acid. Cigarette smoking significant upregulated sphingolipid metabolites, such as d-sphingosine, ceramide, N-(octadecanoyl)-sphing-4-enine, N-(9Z-octadecenoyl)-sphing-4-enine, and N-[(13Z)-docosenoyl]-sphingosine, versus e-cig vaping. Overall, e-cig vaping dysregulated TCA cycle-related metabolites while cigarette smoking altered sphingolipid metabolites. Both e-cig and cigarette smoke increased nicotinic metabolites. Therefore, specific metabolic signatures altered by e-cig vaping and cigarette smoking could serve as potential systemic biomarkers for early pathogenesis of cardiopulmonary diseases. [ABSTRACT FROM AUTHOR]

Recently, there has been an outbreak of a condition named e-cigarette or vaping products-associated lung injury (EVALI). The primary components of vaping products include tetrahydrocannabinol (THC), vitamin E acetate (VEA) and medium-chain triglycerides (MCT), may be responsible for acute lung toxicity. Currently, little information is available on the physiological and biological effects of exposure to these products. We hypothesized that these CBD/counterfeit vape cartridges and their constituents (VEA and MCT) induce pulmonary toxicity, mediated by oxidative damage and inflammatory responses, leading to acute lung injury. We studied the potential mechanisms of CBD/counterfeit vape cartridge aerosol induced inflammatory response by evaluating the generation of reactive oxygen species by MCT, VEA, and cartridges and their effects on the inflammatory state of pulmonary epithelium and immune cells both in vitro and in vivo. Cells exposed to these aerosols generated reactive oxygen species, caused cytotoxicity, induced epithelial barrier dysfunction, and elicited an inflammatory response. Using a murine model, the parameters of acute toxicity to aerosol inhalation were assessed. Infiltration of neutrophils and lymphocytes was accompanied by significant increases in IL-6, eotaxin, and G-CSF in the bronchoalveolar lavage fluid (BALF). In mouse BALF, eicosanoid inflammatory mediators, leukotrienes, were significantly increased. Plasma from e-cig users also showed increased levels of hydroxyeicosatetraenoic acid (HETEs) and various eicosanoids. Exposure to CBD/counterfeit vape cartridge aerosols showed the most significant effects and toxicity compared to MCT and VEA. In addition, we determined SARS-CoV-2 related proteins and found no impact associated with aerosol exposures from these tested cartridges. Overall, this study demonstrates acute exposure to specific CBD/counterfeit vape cartridges induces in vitro cytotoxicity, barrier dysfunction, and inflammation and in vivo mouse exposure induces acute inflammation with elevated proinflammatory markers in the pathogenesis of EVALI. [ABSTRACT FROM AUTHOR]