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A thermal protection system is critical for ensuring the safe take-off and return of various aircraft. A key heat-resistant material within this system is the ceramic fiber insulation tile (CFIT), which is a porous three-dimensional network material with density ranges from 0.3 to 0.4 g/cm that exhibits complex mechanical behaviors. Due to the complexity of the service environment, experimental methods cannot accurately capture the mechanical behavior of a CFIT. Although simulation-based methods can provide insights, an accurate constitutive model for CFITs has yet to be established. To predict its complex mechanical behavior, an elastic-plastic damage constitutive model was established for CFITs. Based on the Hashin criteria and four fundamental assumptions, a yield rule was modified by introducing a damage factor in the TTT direction. The model was encoded into a user-material subroutine (UAMT) integrated within ABAQUS to capture the mechanical responses under four typical working conditions. The change trend of the simulation curve closely aligned with that of the experiment curve, better characterizing the stress-strain relationship of the CFIT under different working conditions such as compression, tension, and shear and the error was less than 18%. The proposed approach was validated by designing a millimeter-level indentation experiment. The results in this paper demonstrate that the maximum loading depths of the simulation and experiment were consistent, and the relative errors were within 12%, respectively. The research provides a reliable elastic-plastic damage constitutive model to predict the mechanical behavior of CFITs under complex working conditions.
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http://dx.doi.org/10.3390/ma17246094 | DOI Listing |
Neurobiol Dis
September 2025
University of Nebraska Medical Center, College of Medicine, Department of Neurological Sciences, Omaha, NE, USA. Electronic address:
Amongst the major histopathological hallmarks in Alzheimer's disease are intracellular neurofibrillary tangles consisting of hyperphosphorylated and aggregated Tau, synaptic dysfunction, and synapse loss. We have previously shown evidence of synaptic mitochondrial dysfunction in a mouse model of Tauopathy that overexpresses human Tau (hTau). Here, we questioned whether the levels or activity of Parkin, an E3 ubiquitin ligase involved in mitophagy, can influence Tau-induced synaptic mitochondrial dysfunction.
View Article and Find Full Text PDFDev Cell
June 2025
Terry Fox Laboratory, BC Cancer Research Institute, Vancouver, BC V5Z1L3, Canada; Cell and Developmental Biology, Faculty of Medicine, University of British Columbia, Vancouver, BC V6T1Z4, Canada; Department of Medical Genetics, University of British Columbia, Vancouver, BC V6T1Z4, Canada; School of
By mapping histone modifications in a human stem cell model of hepatic differentiation, we identified an enhancer landscape that is dynamic and stage specific, with many primed at the definitive endoderm stage. While hepatic enhancers gained active histone modifications, non-hepatic enhancers lost H3K4me1 after hepatic specification. T-box transcription factor 3 (TBX3) was found to bind to hepatic enhancers and promoters.
View Article and Find Full Text PDFJ Control Release
September 2025
State Key Laboratory of Bioreactor Engineering, Newworld Institute of Biotechnology, East China University of Science and Technology, Shanghai 200237, PR China. Electronic address:
Live bacterial therapeutics (LBT) represent a transformative modality for managing refractory chronic diseases. However, the absence of optimized microbial chassis systems is a significant barrier to clinical translation. To bridge this gap, we engineered Escherichia coli Nissle 1917 (EcN) into a versatile platform that meets the requirements for strain development and clinical application.
View Article and Find Full Text PDFFront Mol Neurosci
August 2025
Department of Neuroscience, Tufts University School of Medicine, Boston, MA, United States.
Introduction: The potassium chloride co-transporter 2 (KCC2) is the principal Cl extrusion mechanism employed by mature neurons in the central nervous system (CNS) and plays a critical role in determining the efficacy of fast synaptic inhibition mediated by type A -aminobutyric acid receptors (GABARs) to protect against epileptogenesis. It has previously been demonstrated that epileptic seizures down-regulate KCC2 and induce neuronal apoptosis through the extrinsic apoptotic pathway. However, the mechanism by which neuronal death is induced by KCC2 loss remains unknown.
View Article and Find Full Text PDFBiophys J
September 2025
Department of Molecular Physiology and Biophysics, University of Vermont Larner College of Medicine, Burlington, VT 05405. Electronic address:
Intracellular vesicular transport by kinesin-1 motors through numerous 3-dimensional (3D) microtubule (MT) intersections must be regulated to support proper vesicle delivery. Knowing kinesin-1 can be regulated via autoinhibition, does kinesin-1 exhibit autoinhibition on cargo, and could this regulate vesicular transport through 3D MT intersections in vitro? To answer this question, we compared liposome transport by ∼10 nearly full-length kinesin-1 motors with KLC bound (KinΔC) versus constitutively active control (K543). In 3D MT intersections, KinΔC-liposomes terminate (48%), go straight (43%), but rarely turn (9%), starkly contrasting K543-liposomes which go straight (57%), turn (31%), but rarely terminate (12%).
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