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Trauma-Induced Coagulopathy is a severe condition that rapidly manifests following traumatic injury and is characterized by shock, hypoperfusion, and vascular damage. This study employed bioinformatics methods to identify crucial hub genes and pathways associated with TIC. Microarray datasets (accession number GSE223245) were obtained from the Gene Expression Omnibus (GEO) database. The data were subjected analyses to identify the Differentially Expressed Genes (DEGs), which were further subjected to GO and KEGG pathway analyses. Subsequently, a Protein-Protein Interaction (PPI) network was constructed and hub DEGs closely linked to TIC were identified using CytoHubba, MCODE, and CTD scores. The diagnostic value of these hub genes was evaluated using Receiver Operating Characteristic (ROC) analysis. Among the analyzed genes, 269 were identified as DEGs, comprising 103 upregulated and 739 downregulated genes. Notably, several significant hub genes were associated with the development of TIC, as revealed by bioinformatic analyses. This study highlights the critical impact of newly discovered genes on the development and progression of TIC. Further validation through experimental research and clinical trials is required to confirm these findings.

Vibration signal and its derivative have shown some promise in structural damage detection in previous research. However, the theoretical and practical difficulties of multi-damage detection in plate structures based on dynamic responses remain. In this paper, an efficient damage localization index based on frequency response function (FRF) is presented. The imaginary part of FRF (IFRF) is extracted to derive the new localization index due to its relation to modal flexibility. For avoiding the finite element model error, two-dimensional gapped smoothing method (GSM) is employed without the need for baseline data from a presumably undamaged structure. Experimental studies on a steel plate with two localized defects in different boundary conditions are performed. The results are compared with some typical damage indices in the literature, such as mode shapes, uniform load surface and IFRF. In order to mitigate the inherent disadvantages of GSM in anti-noise ability, a simple statistical treatment based on Thompson outlier analysis is finally used for noise suppression. The effect of damage level and boundary condition on the detection results is also investigated.

Room temperature creep (RTC) at a crack tip and its influence on the fatigue crack growth behavior of a 304 stainless steel have been studied at room temperature. A time-dependent deformation has been observed at the crack tips under various stress intensity factors. The deformation increases with increasing stress intensity factor. Either acceleration or retardation of fatigue crack growth rate is found after holding at KRTC, which depends on the load pattern. A demarcation line is observed on the fracture surface following the holding period. This implies that the crack propagation root or mode changed after the hold time.

Aim： SKF83959 （3-methyl-6-chloro-7,8-hydroxy-1-（3-methylphenyl）-2,3,4,5-tetrahydro-1H-3-benzazepine） is an atypical dopamine receptor-1 （D1 receptor） agonist, which exhibits many D1 receptor-independent effects. In the present work, we examined the effects of SKF83959 on monoaminergic transporters in vitro and its anti-depressant activity in vivo. Methods： Human serotonin transporter （SERT）, norepinephrine transporters （NET） or dopamine transporters （DAT） were stably expressed in CHO cells. The uptake kinetics of SERT, NET, and DAT were examined using [3H]-serotonin, [3H]-norepinephrine or [3H]-dopamine, respectively. A triple reuptake inhibitor DOV21947 was used as the positive control. Tail suspension test and forced swimming test were conducted in mice. SKF83959 or DOV21947 （2-8 mg/kg） were intraperitoneally injected 30 min before the tests. Results： SKF83959 was a competitive inhibitor of SERT （Ki=1.43±0.45 μmol/L）, but a noncompetitive inhibitor of NET （Ki=0.60±0.07 μmol/L） and DAT （Ki=9.01±0.80 μmol/L）. In contrast, DOV21947 was a competitive inhibitor of SERT （Ki=0.89±0.24 μmol/L） and DAT （Ki=1.47±0.31 μmol/L） and a noncompetitive inhibitor of NET （Ki=0.18±0.04 μmol/L）. In mice, both SKF83959 and DOV21947 elicited anti-depressant activity in a dose-dependent manner. Conclusion： SKF83959 functions as a novel triple reuptake inhibitor in vitro and exerts anti-depressant effects in vivo.

We present an extended model for identifying structural boundary condition parameters, considering the coupling terms (stiffness and damping) between translation and rotation which are commonly ignored in general cases. Two objective functions are established based on impulse response functions (IRFs). Frequency parameterization, which considers the minimum distance to be minimized, is employed. The inverse problem of boundary identification is then solved using Newton-Raphson method. The results of numerical simulation and experimental study assessed the performance of the proposed method.

Lock-in infrared thermography method was gradually being used in fatigue studies because of its advantages such as real-time, quick-reaction, non-contact, non-destructive and so on. In this paper, non-destructive testing was applied to fatigue specimen with defects, based on lock-in infrared thermography. In parallel, the result was analyzed by using lock-in infrared thermography system developed by Cedip in French. The results show that more information of internal detects can be found from phase image than that from amplitude image. The experiment procedure indicated that a proper testing frequency was the key to the non-destructive testing. The data revealed that deeper depth and larger area of defect led to a precise testing result.

The fatigue parameters of welded joints made of FV520B were obtained considering the real operating situations. The fatigue fracture types were divided into two groups. The scanning electron microscope (SEM) was applied to carefully study the fatigue fracture surfaces so as to investigate the fatigue failure mechanisms. The microstructures of the base metal and the weld seam were studied by the metallographic microscope (MM), SEM and TEM in support of the dissimilar mechanical property analysis. The present paper concluded that the fatigue microcracks mainly initiated from the surface near the weld toe and inclusions in the weld seam, the heat-affected zone (HAZ) disappeared due to the postweld heat-treatment processes, and that the fatigue resistance of the base metal was better than the weld seam.

Peptide-mediated cell-to-cell signaling has crucial roles in coordination and definition of cellular functions in plants. Peptide-receptor matching is important for understanding the mechanisms underlying peptide-mediated sig- naling. Here we report the structure-guided identification of root meristem growth factor （RGF） receptors important for plant development. An assay based on a signature ligand recognition motif （Arg-x-Arg） conserved in a subfamily of leucine-rich repeat receptor kinases CLRR-RKs） identified the functionally uncharacterized LRR-RK At4926540 as a receptor of RGF1 （RGFR1）. We further solved the crystal structure of RGF1 in complex with the LRR domain of RGFR1 at a resolution of 2.6 A, which reveals that the Arg-x-Gly-Gly （RxGG） motif is responsible for specific rec- ognition of the sulfate group of RGF1 by RGFR1. Based on the RxGG motif, we identified additional four RGFRs. Participation of the five RGFRs in RGF-induced signaling is supported by biochemical and genetic data. We also of- fer evidence showing that SERKs function as co-receptors for RGFs. Taken together, our study identifies RGF receptors and co-receptors that can link RGF signals with their downstream components and provides a proof of principle for structure-based matching of LRR-RKs with their peptide ligands.

The tumor suppressor Merlin/NF2 functions upstream of the core Hippo pathway kinases Latsl/2 and Mst1/2, as well as the nuclear E3 ubiquitin ligase CRL4DcAF1. Numerous mutations of Merlin have been identified in Neurofibromatosis type 2 and other cancer patients. Despite more than two decades of research, the upstream regulator of Merlin in the Hippo pathway remains unknown. Here we show by high-resolution crystal structures that the Latsl/2-binding site on the Merlin FERM domain is physically blocked by Merlin＇s auto-inhibitory tail. Angiomotin binding releases the auto-inhibition and promotes Merlin＇s binding to Latsl/2. Phosphorylation of Ser518 outside the Merlin＇s auto-inhibitory tail does not obviously alter Merlin＇s conformation, but instead prevents angiomotin from binding and thus inhibits Hippo pathway kinase activation. Cancer-causing mutations clustered in the angiomotin- binding domain impair angiomotin-mediated Merlin activation. Our findings reveal that angiomotin and Merlin respectively interface cortical actin filaments and core kinases in Hippo signaling, and allow construction of a complete Hippo signaling pathway.

In this study, we successfully constructed a composite of bone marrow mesenchymal stem cells and a chitosan-collagen scaffold in vitro, transplanted either the composite or bone marrow mesenchymal stem cells alone into the ischemic area in animal models, and compared their effects. At 14 days after co-transplantation of bone marrow mesenchymal stem cells and the hi- tosan-collagen scaffold, neurological function recovered noticeably. Vascular endothelial growth factor expression and nestin-labeled neural precursor cells were detected in the iscbemic area, surrounding tissue, hippocampal dentate gyrus and subventricular zone. Simultaneously, a high level of expression of glial fibrillary acidic protein and a low level of expression of neuron-spe- cific enolase were visible in BrdU-labeled bone marrow mesenchymal stem cells. These findings suggest that transplantation of a composite of bone marrow mesenchymal stem cells and a chi- tosan-collagen scaffold has a neuroprotective effect following ischemic stroke.