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In this work, a surface acoustic wave (SAW) temperature sensor based on a quartz substrate was designed and investigated. Employing the Coupling-of-Modes (COM) model, a detailed analysis was conducted on the effects of the number of interdigital transducers (IDTs), the number of reflectors, and their spacing on the performance of the SAW device. The impact of the transversal mode of quartz SAWs on the device was subsequently examined using the finite element method (FEM). The simulation results indicate that optimizing these structural parameters significantly enhances the sensor’s sensitivity and frequency stability. SAW devices with optimal structural parameters were fabricated, and their resonant frequencies were tested across a temperature range of 25–150 °C. Experimental results demonstrate that the SAW temperature sensor maintains high performance stability and data reliability throughout the entire temperature range, achieving a Bode-Q of 7700. Furthermore, the sensor exhibits excellent linearity and repeatability. An analysis of the sensor’s response under varying temperature conditions reveals a significant temperature dependency on its Temperature Coefficient of Frequency (TCF). This feature suggests that the sensor possesses potential advantages for applications in industrial process control and environmental monitoring.

Arachidonyl and adrenoyl PE phospholipids generated by ACSL4, an acyl-CoA synthase, are doubly or triply oxidized by lipoxygenases and other iron-containing sources of oxidation to promote ferroptotic cell death. Enigmatic lipid peroxidation products have been claimed as the proximate executioners of ferroptosis—a specialized death program triggered by insufficiency of glutathione peroxidase 4 (GPX4). Using quantitative redox lipidomics, reverse genetics, bioinformatics and systems biology, we discovered that ferroptosis involves a highly organized oxygenation center, wherein oxidation in endoplasmic-reticulum-associated compartments occurs on only one class of phospholipids (phosphatidylethanolamines (PEs)) and is specific toward two fatty acyls—arachidonoyl (AA) and adrenoyl (AdA). Suppression of AA or AdA esterification into PE by genetic or pharmacological inhibition of acyl-CoA synthase 4 (ACSL4) acts as a specific antiferroptotic rescue pathway. Lipoxygenase (LOX) generates doubly and triply-oxygenated (15-hydroperoxy)-diacylated PE species, which act as death signals, and tocopherols and tocotrienols (vitamin E) suppress LOX and protect against ferroptosis, suggesting a homeostatic physiological role for vitamin E. This oxidative PE death pathway may also represent a target for drug discovery.

Much attention is being paid to using high-performance convolutional neural networks (CNNs) in the area of ship detection in optical remoting sensing (ORS) images. However, the problem of false negatives (FNs) caused by side-by-side ships cannot be solved, and the number of false positives (FPs) remains high. This paper uses a DLA-34 network with deformable convolution layers as the backbone. The network has two priority branches: a recall-priority branch for reducing the number of FNs, and a precision-priority branch for reducing the number of FPs. In our single-shot detection method, the recall-priority branch is based on an anchor-free module without non-maximum suppression (NMS), while the precision-priority branch utilizes an anchor-based module with NMS. We perform recall-priority branch functions based on the output part of the CenterNet object detector to precisely predict center points of bounding boxes. The Bidirectional Feature Pyramid Network (BiFPN), combined with the inference part of YOLOv3, is used to improve the precision of precision-priority branch. Finally, the boxes from two branches merge, and we propose priority-based selection (PBS) for choosing the accurate ones. Results show that our proposed method sharply improves the recall rate of side-by-side ships and significantly reduces the number of false alarms. Our method also achieves the best trade-off on our improved version of HRSC2016 dataset, with 95.57% AP at 56 frames per second on an Nvidia RTX-2080 Ti GPU. Compared with the HRSC2016 dataset, not only are our annotations more accurate, but our dataset also contains more images and samples. Our evaluation metrics also included tests on small ships and incomplete forms of ships.

Recent studies on myogenic satellite cells (SCs) in Duchenne muscular dystrophy (DMD) documented altered division capacities and impaired regeneration potential of SCs in DMD patients and animal models. It remains unknown, however, if SC-intrinsic effects trigger these deficiencies at pre-contractile stages of myogenesis rather than resulting from the pathologic environment. In this study, we isolated SCs from a porcine DMD model and age-matched wild-type (WT) piglets for comprehensive analysis. Using immunofluorescence, differentiation assays, traction force microscopy (TFM), RNA-seq, and label-free proteomic measurements, SCs behavior was characterized, and molecular changes were investigated. TFM revealed significantly higher average traction forces in DMD than WT SCs (90.4 ± 10.5 Pa vs. 66.9 ± 8.9 Pa; p = 0.0018). We identified 1390 differentially expressed genes and 1261 proteins with altered abundance in DMD vs. WT SCs. Dysregulated pathways uncovered by gene ontology (GO) enrichment analysis included sarcomere organization, focal adhesion, and response to hypoxia. Multi-omics factor analysis (MOFA) integrating transcriptomic and proteomic data, identified five factors accounting for the observed variance with an overall higher contribution of the transcriptomic data. Our findings suggest that SC impairments result from their inherent genetic abnormality rather than from environmental influences. The observed biological changes are intrinsic and not reactive to the pathological surrounding of DMD muscle.

Programmed death (apoptosis) is turned on in damaged or unwanted cells to secure their clean and safe self-elimination. The initial apoptotic events are coordinated in mitochondria, whereby several proapoptotic factors, including cytochrome c , are released into the cytosol to trigger caspase cascades. The release mechanisms include interactions of B-cell/lymphoma 2 family proteins with a mitochondria-specific phospholipid, cardiolipin, to cause permeabilization of the outer mitochondrial membrane. Using oxidative lipidomics, we showed that cardiolipin is the only phospholipid in mitochondria that undergoes early oxidation during apoptosis. The oxidation is catalyzed by a cardiolipin-specific peroxidase activity of cardiolipin-bound cytochrome c . In a previously undescribed step in apoptosis, we showed that oxidized cardiolipin is required for the release of proapoptotic factors. These results provide insight into the role of reactive oxygen species in triggering the cell-death pathway and describe an early role for cytochrome c before caspase activation.

The risk of radionuclide release in terrorist acts or exposure of healthy tissue during radiotherapy demand potent radioprotectants/radiomitigators. Ionizing radiation induces cell death by initiating the selective peroxidation of cardiolipin in mitochondria by the peroxidase activity of its complex with cytochrome c leading to release of haemoprotein into the cytosol and commitment to the apoptotic program. Here we design and synthesize mitochondria-targeted triphenylphosphonium-conjugated imidazole-substituted oleic and stearic acids that blocked peroxidase activity of cytochrome c /cardiolipin complex by specifically binding to its haem-iron. We show that both compounds inhibit pro-apoptotic oxidative events, suppress cyt c release, prevent cell death, and protect mice against lethal doses of irradiation. Significant radioprotective/radiomitigative effects of imidazole-substituted oleic acid are observed after pretreatment of mice from 1 h before through 24 h after the irradiation. Radiomitigating compounds could be used to protect against ionizing radiation. In this study, mitochondria-targeted oleic and stearic acid derivatives are shown to inhibit pro-apoptotic oxidative events, prevent cell death, and protect mice against lethal doses of radiation.

Jiang, J., Stoyanovsky, D. A., Belikova, N. A., Tyurina, Y. Y., Zhao, Q., Tungekar, M. A., Kapralova, V., Huang, Z., Mintz, A. H., Greenberger, J. S. and Kagan, V. E. A Mitochondria-Targeted Triphenylphosphonium-Conjugated Nitroxide Functions as a Radioprotector/Mitigator. Removal of excessive mitochondrial reactive oxygen species by electron scavengers and antioxidants is a promising therapeutic strategy to reduce the detrimental effects of radiation exposure. Here we exploited triphenylphosphonium (TPP) cation as a means to target nitroxide radicals to mitochondria. We synthesized a library of TPP-conjugated nitroxides and tested their radioprotective effects in γ-irradiated mouse embryo cells and human epithelial BEAS-2B cells. Cells were incubated with conjugates either before or after irradiation. We found that [2-(1-oxyl-2,2,6,6-tetramethyl-piperidin-4-ylimino)-ethyl]-triphenyl-phosphonium (TPEY-Tempo) significantly blocked radiation-induced apoptosis as revealed by externalization of phosphatidylserine on the cell surface and inhibition of cytochrome c release from mitochondria. Using electron paramagnetic resonance, we showed that TPEY-Tempo was integrated into cells and mitochondria, where it underwent one-electron reduction to hydroxylamine. TPEY-Tempo acted as an electron scavenger that prevented superoxide generation and cardiolipin oxidation in mitochondria. Finally, TPEY-Tempo increased the clonogenic survival rate of irradiated cells. The cellular integration efficiencies of nonradioprotective TPP conjugates, including Mito-Tempo (Alexis, San Diego, CA), were markedly lower, although these homologues were integrated into isolated succinate-energized mitochondria to a similar extent as TPEY-Tempo. We conclude that mitochondrial targeting of TPP-conjugated nitroxides represents a promising approach for the development of novel radioprotectors.

Inflammatory bowel disease (IBD) is a heterogeneous group of chronic inflammatory gastrointestinal conditions with variable disease courses often requiring significant healthcare expenditures. We aimed to identify disease trajectory patterns based on longitudinal financial expenditures and to assess the association of classic disease activity parameters with financial charges. This was an analysis of a consented, prospective, natural history IBD registry (2009-2013) from a tertiary IBD center of 2,203 patients and their associated medical charges excluding pharmacy expenses. We applied group-based trajectory modeling to longitudinal healthcare financial charges to determine patterns of charges. We assessed the association between charge patterns and disease activity, quality of life, healthcare utilization, and medication requirement. The final model included 1,600 IBD patients with 5-year charges. We identified six distinct trajectories over the study period. Consistently High charges were associated with Crohn's disease (66.0% Consistently High patients, P<0.01), perianal involvement (22.6%, P<0.01), ulcerative colitis extent (89.7% extensive, P=0.01), prior IBD surgery (52.5%, P<0.01), and depression/anxiety (36.2%, P<0.01). Compared with other trajectories, Consistently High charges had higher 5-year disease activity indices (Harvey-Bradshaw P<0.01; ulcerative colitis activity index P<0.01), elevated C-reactive protein rates (72.3%, P<0.01), IBD surgery (64.5%, P<0.01), hospitalization (97.2%, P<0.01), corticosteroid (70.9%, P<0.01) and antitumor necrosis factor requirement (50.4%, P<0.01), and worse quality of life (P<0.01). Annual trends in parameters were reflected in temporal changes in financial charges. The majority of financial burden stemmed from inpatient care. Healthcare financial charges represent a novel phenotype in IBD that reflect trends in classic disease activity parameters and allow for subgroup identification of temporal disease trajectories.

The thermal compression experiments of TB17 titanium alloy under different thermal deformation process parameters were carried out using a thermal simulation compressor. The high-temperature plastic flow behaviour of the alloy was studied. It was found that with the decrease of the deforming temperature and the increase of the strain rate, the flow stress increased, and the discontinuous yield phenomenon occurred in hot deformation. The larger the strain rate, the more obvious the discontinuous yield phenomenon. The thermal activation energy Q decreased with the increase of strain, and the average value of activation energy Q is 209.54 KJ / mol. The constitutive equation of high-temperature plastic flow of TB17 titanium alloy was established. The predicted values of this equation are in good agreement with the experimental values. The average error is 3.987 %, and the correlation coefficient is 0.9972, which has high accuracy. Based on the Prasad criterion, the hot processing map of TB17 titanium alloy was constructed. It was found that the flow instability zone was mainly concentrated in the high strain rate region. The flow instability zone was determined to be 795 °C ~ 895 °C, 0.046s -1 ~ 1s -1 , and the stable deformation zone was mainly located in the region with high temperature and low strain rate. The optimum processing parameter range is 860 °C ~ 895 °C, 0.001 s -1 ~ 0.025 s -1 .

We propose a nonvolatile terahertz (THz) switch which is able to perform the switching with transient stimulus. The device utilizes graphene as its floating-gate layer, which changes the transmissivity of THz signal by trapping the tunneling charges. The conventional top-down electrode configuration is replaced by a left-right electrode configuration, so THz signals could transmit through this device with the transmissivity being controlled by voltage pulses. The two electrodes are made of metals with different work functions. The resultant asymmetrical energy band structure ensures that both electrical programming and erasing are viable. With the aid of localized surface plasmon resonances in graphene ribbon arrays, the modulation depth is 89% provided that the Femi level of graphene is tuned between 0 and 0.2 eV by proper voltage pulses.