Failure Model Research Articles

DHODH Alleviates Heart Failure via the Modulation of CoQ-Related Ferroptotic Inhibition.

Heart failure (HF) is a clinical syndrome that seriously endangers human health and quality of life as the terminal stage of cardiovascular diseases. Ferroptosis as a new iron-dependent programmed cell death mode that is closely related to the occurrence and development of cardiovascular diseases. Dihydroorotate dehydrogenase (DHODH) has been found to play a crucial role in inhibiting ferroptosis and improving mitochondrial function, and its expression can be upregulated by estradiol (E2). Recent studies have found that DHODH can inhibit ferroptosis by reducing coenzyme Q (CoQ) to CoQH2. Therefore, this study aims to explore the effect of up-regulation of DHODH on the pathological hypertrophy and fibrosis of heart failure and its mechanisms. The mouse heart failure model was established by transverse aortic constriction (TAC), surgery in mice. Two days after the operation, a subcutaneous injection of E2 or the same volume of sesame oil was given for 8 weeks. Then, the left ventricular systolic function related indicators of mice were measured by echocardiography, and the degree of myocardial fibrosis of mice was detected by histological analysis; the expression levels of heart failure markers were detected by quantitative polymerase chain reaction (q-PCR) and western blot (WB) analysis; the morphological changes of mitochondria in cardiac cells of mice were observed by transmission electron microscopy. Cell model were established by stimulating with phenylephrine for 96 hours. Ferroptosis markers were detected by kits and WB analysis. Mitochondrial function was verified by a JC-1 fluorescent probe, and 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) staining. The knockdown results were detected by WB analysis after transfection of small interfering RNA (siRNA) of CoQ. Fer-1 was added as a positive control to verify the ferroptosis-related changes of myocardial cells. In the animal model, we found that E2 treatment alleviates TAC-induced cardiac hypertrophy and fibrosis and suppresses cardiomyocyte ferroptosis by promotes DHODH upregulation in murine cardiomyocytes. In the cell model, DHODH upregulation protects against phenylephrine-induced cardiomyocytes with failure. However, the effect on up-regulating DHODH was inhibited by transfection to down-regulate CoQ expression. The up-regulation of DHODH could effectively ameliorate the manifestations of heart failure such as myocardial hypertrophy and fibrosis in mice after TAC surgery, inhibit ferroptosis of cardiac myocytes, and ameliorate mitochondrial function. The mechanism involves CoQ-related biological processes.

Path-Dependent Progressive Failure Analysis for 3D-Printed Continuous Carbon Fibre Reinforced Composites

In order to predict the damage behaviours of 3D-printed continuous carbon fibre (CCF) reinforced composites, when additional short carbon fibre (SCF) composite components are employed for continuous printing or special functionality, a novel path-dependent progressive failure (PDPF) numerical approach is developed. First, a progressive failure model using Hashin failure criteria with continuum damage mechanics to account for the damage initiation and evaluation of 3D-printed CCF reinforced polyamide (PA) composites is developed, based on actual fibre placement trajectories with physical measurements of 3D-printed CCF/PA constituents. Meanwhile, an elastic-plastic model is employed to predict the plastic damage behaviours of SCF/PA parts. Then, the accuracy of the PDPF model was validated so as to study 3D-printed CCF/PA composites with either negative Poisson’s ratio or high stiffness. The results demonstrate that the proposed PDPF model can achieve higher prediction accuracies in mechanical properties of these 3D-printed CCF/PA composites. Mechanism analyses show that the stress distribution is generally aggregated in the CCF areas along the fibre placement paths, and the shear damage and matrix tensile/compressive damage are the key damage modes. This study provides a new approach with valuable information for characterising complex 3D-printed continuous fibre-matrix composites with variable mechanical properties and multiple constituents.

Xionggui Decoction alleviates heart failure in mice with myocardial infarction by inhibiting oxidative stress-induced cardiomyocyte apoptosis

To explore the protective effect of Xionggui Decoction against cardiac myopathy in a mouse model of heart failure following myocardial infarction (MI) and explore the underlying mechanism. We searched TCMSP, GeneCards, and CTD databases for the targets of active ingredients Xionggui Decoction and heart failure, and the intersecting targets were analyzed with GO and KEGG pathway enrichment analysis using DAVID database. In a mouse model of heart failure following acute MI induced by coronary artery ligation, the cardiac protective effects of 3 g/kg Xionggui Decoction were evaluated by assessing cardiac function, cardiac myopathy and ventricular remodeling of the mice using HE staining, Masson staining, RT-qPCR, and immunohistochemistry. We also tested the effect of Xionggui Decoction at 50 and 100 μg/mL on tertbutylhydrogen peroxide (TBHP)-induced apoptosis of H9C2 cells using CCK8 assay, detection kits for ROS, MDA, SOD, JC-1 and Hoechst 33342/PI staining. Network pharmacological analysis identified 62 potential targets of Xionggui Decoction for treatment of heart failure, and the core targets included PTGS2, ESR1, caspase-3, PPARG, HSP90AA1, BCL2, JUN, and GSK3B, which were involved in cell apoptosis and the AGE-RAGE, P53, PI3K-Akt, and VEGF signaling pathways. In the mouse models of heart failure, treatment with Xionggui Decoction significantly alleviated cardiac myopathy and ventricular remodeling, obviously improved heart function of the mice, lowered myocardial expressions of caspase-3 and BAX, and enhanced the expression of BCL2. In H9C2 cells, Xionggui Decoction significantly alleviated TBHP-induced cell apoptosis by inhibiting oxidative stress in the cells. Xionggui Decoction can alleviate myocardial injury and improve cardiac function in mice with heart failure following acute MI possibly by inhibiting cardiomyocyte apoptosis induced by oxidative stress.

Transverse aortic constriction multi-omics analysis uncovers pathophysiological cardiac molecular mechanisms.

Time-course multi-omics data of a murine model of progressive heart failure (HF) induced by transverse aortic constriction (TAC) provide insights into the molecular mechanisms that are causatively involved in contractile failure and structural cardiac remodelling. We employ Illumina-based transcriptomics, Nanopore sequencing and mass spectrometry-based proteomics on samples from the left ventricle (LV) and right ventricle (RV, RNA only) of the heart at 1, 7, 21 and 56 days following TAC and Sham surgery. Here, we present Transverse Aortic COnstriction Multi-omics Analysis (TACOMA), as an interactive web application that integrates and visualizes transcriptomics and proteomics data collected in a TAC time-course experiment. TACOMA enables users to visualize the expression profile of known and novel genes and protein products thereof. Importantly, we capture alternative splicing events by assessing differential transcript and exon usage as well. Co-expression-based clustering algorithms and functional enrichment analysis revealed overrepresented annotations of biological processes and molecular functions at the protein and gene levels. To enhance data integration, TACOMA synchronizes transcriptomics and proteomics profiles, enabling cross-omics comparisons. With TACOMA (https://shiny.dieterichlab.org/app/tacoma), we offer a rich web-based resource to uncover molecular events and biological processes implicated in contractile failure and cardiac hypertrophy. For example, we highlight: (i) changes in metabolic genes and proteins in the time course of hypertrophic growth and contractile impairment; (ii) identification of RNA splicing changes in the expression of Tpm2 isoforms between RV and LV; and (iii) novel transcripts and genes likely contributing to the pathogenesis of HF. We plan to extend these data with additional environmental and genetic models of HF to decipher common and distinct molecular changes in heart diseases of different aetiologies. Database URL: https://shiny.dieterichlab.org/app/tacoma.

Ginsenoside Rb1 ameliorates heart failure through DUSP-1-TMBIM-6-mediated mitochondrial quality control and gut flora interactions

BackgroundThere is currently no specific therapeutic drug available for heart failure in clinical practice. Numerous studies have validated the efficacy of Ginsenoside Rb1, an active component found in various herbal remedies used for heart failure treatment, in effectively ameliorating myocardial ischemia. However, the precise mechanism of action and molecular targets of Ginsenoside Rb1 remain unclear. PurposeThis study aims to explore the molecular mechanisms through which Ginsenoside Rb1 synergistically modulates the gut flora and mitochondrial quality control network in heart failure by targeting the DUSP-1-TMBIM-6-VDAC1 axis. Study designThis study utilized DUSP-1/VDAC1 knockout (DUSP-1-/-/VDAC1-/-) and DUSP-1/VDAC1 transgenic (DUSP-1+/+/VDAC1+/+) mouse models of heart failure, established through Transverse Aortic Constriction (TAC) surgery and genetic modification techniques. The mice were subsequently subjected to treatment with Ginsenoside Rb1. MethodsA series of follow-up multi-omics analyses were conducted, including assessments of intestinal flora, gene transcription sequencing, single-cell databases, and molecular biology assays of primary cardiomyocytes, to investigate the mechanism of action of Ginsenoside Rb1. ResultsGinsenoside Rb1 was found to have multiple regulatory mechanisms on mitochondria. Notably, DUSP-1 was discovered to be a crucial molecular target of Ginsenoside Rb1, controlling both intestinal flora and mitochondrial function. The regulatory effects of DUSP-1 on inflammation and mitochondrial quality control were mediated by changes in TMBIM-6 and VDAC1. Furthermore, NLRP3-mediated inflammatory responses were found to interact with mitochondrial quality control, exacerbating myocardial injury under stress conditions. Ginsenoside Rb1 modulated the DUSP-1-TMBIM-6-VDAC1 axis, inhibited the release of pro-inflammatory factors, altered the structural composition of the gut flora, and protected impaired heart function. These effects indirectly influenced the crosstalk between inflammation, mitochondria, and gut flora. ConclusionThe DUSP-1-TMBIM-6-VDAC1 axis, an upstream pathway regulated by Ginsenoside Rb1, is a profound mechanism through which Ginsenoside Rb1 improves cardiac function in heart failure by modulating inflammation, mitochondria, and gut flora.

NAD+ precursors prolong survival and improve cardiac phenotypes in a mouse model of Friedreich's Ataxia.

Friedreich's ataxia (FRDA) is a progressive disorder caused by insufficient expression of frataxin, which plays a critical role in assembly of iron-sulfur centers in mitochondria. Individuals are cognitively normal but display a loss of motor coordination and cardiac abnormalities. Many ultimately develop heart failure. Administration of nicotinamide adenine dinucleotide-positive (NAD+) precursors has shown promise in human mitochondrial myopathy and rodent models of heart failure, including mice lacking frataxin in cardiomyocytes. We studied mice with systemic knockdown of frataxin (shFxn), which display motor deficits and early mortality with cardiac hypertrophy. Hearts in these mice do not "fail" per se but become hyperdynamic with small chamber sizes. Data from an ongoing natural history study indicate that hyperdynamic hearts are observed in young individuals with FRDA, suggesting that the mouse model could reflect early pathology. Administering nicotinamide mononucleotide or riboside to shFxn mice increases survival, modestly improves cardiac hypertrophy, and limits increases in ejection fraction. Mechanistically, most of the transcriptional and metabolic changes induced by frataxin knockdown are insensitive to NAD+ precursor administration, but glutathione levels are increased, suggesting improved antioxidant capacity. Overall, our findings indicate that NAD+ precursors are modestly cardioprotective in this model of FRDA and warrant further investigation.

Vasohibin inhibition improves myocardial relaxation in a rat model of heart failure with preserved ejection fraction.

Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome associated with increased myocardial stiffness and cardiac filling abnormalities. Prior studies implicated increased α-tubulin detyrosination, which is catalyzed by the vasohibin enzymes, as a contributor to increased stabilization of the cardiomyocyte microtubule network (MTN) and stiffness in failing human hearts. We explored whether increased MTN detyrosination contributed to impaired diastolic function in the ZSF1 obese rat model of HFpEF and designed a small-molecule vasohibin inhibitor to ablate MTN detyrosination in vivo. Compared with ZSF1 lean and Wistar Kyoto rats, obese rats exhibited increased tubulin detyrosination concomitant with diastolic dysfunction, left atrial enlargement, and cardiac hypertrophy with a preserved left ventricle ejection fraction, consistent with an HFpEF phenotype. Ex vivo myocardial phenotyping assessed cardiomyocyte mechanics and contractility. Vasohibin inhibitor treatment of isolated cardiomyocytes from obese rats resulted in reduced stiffness and faster relaxation. Acute in vivo treatment with vasohibin inhibitor improved diastolic relaxation in ZSF1 obese rats compared with ZSF1 lean and Wistar Kyoto rats. Vasohibin inhibition also improved relaxation in isolated human cardiomyocytes from both failing and nonfailing hearts. Our data suggest the therapeutic potential for vasohibin inhibition to reduce myocardial stiffness and improve relaxation in HFpEF.

Short failure localization in advanced package using optoelectronic sampling terahertz time domain reflectometry and deconvolution method

Failure localization in advanced packaging is a challenging task. Optoelectronic sampling Terahertz time-domain reflectometry (OES THz TDR) employs ultrafast lasers to generate high-frequency THz pulse. The THz pulse is coupled into advanced package trace using radio frequency probe. When there is an open or short failure in the circuit, TDR signal could be captured. Deconvolution processing method was introduced to remove noise from multiple reflections of the remaining circuit. A short failure model with remaining circuit was studied. After deconvolution, the TDR localization accuracy improves from 573 μm to 12 μm, and the correlation coefficient improved from 99.612 % to 99.955 %. Advanced package sample including substrate, C4 bump, interposer, and micro bump was analyzed. By comparing the TDR waveform of short failure sample and references, the short failure is localized inside of the die. By destroying the failure sample and measuring the current-voltage curve, the short failure location is verified.

Deformation and failure behavior of 2024-T42 sheet under impact loading

The deformation and failure behavior of 2024-T42 aluminum alloy sheet was investigated through a combined experimental-numerical method. Nine types of specimens were designed to cover a wide range of stress triaxialities and strain rates. Quasi-static and dynamic tests were carried out by electronic testing machine and split Hopkinson tensile bar respectively, and digital image correlation (DIC) method was introduced to measure the deformation. The phenomenological damage model GISSMO (generalized incremental stress state dependent damage model) and Johnson-Cook model were adopted to simulate all of the above tests and the load-displacement curves through numerical simulation were derived. An optimization method was developed to obtain all the model parameters by matching the load-displacement curves from simulation with those from tests by LS-OPT. Finally, drop weight tests and tensile tests of the central-hole plate were conducted. The applicability and accuracy of the damage models were verified by comparing the simulation results with the experiments, which indicates that GISSMO model predicts better the tests than the Johnson-Cook failure model.

An EGF technique to infer the source parameters of a circular crack growing at a variable rupture velocity

Circular crack models with a constant rupture velocity struggle to effectively model both the amplitude and duration of first P-wave pulses generated by small magnitude seismic events. Assuming a constant rupture velocity is unphysical, necessitating a deceleration phase in the rupture velocity to uphold the causality of the healing process. Moreover, a comprehensive failure model might encompass an initial nucleation phase, typically characterized by an increase of the initial rupture velocity. Studies have demonstrated that quasi-dynamic circular crack models featuring variable rupture velocities can accurately model the shape of the observed first P-wave pulse. Based on these principles, an Empirical Green’s function (EGF) approach was previously formulated to estimate the source parameters of small magnitude earthquakes, called MAIN. In addition to determine the source radius and stress drop, this method also enables the inference of the temporal evolution of rupture velocity. However, this method encounters difficulties when the noise-to-signal ratio in the recordings of smaller earthquakes used as EGF exceeds 5%, a common situation when employing regional-scale recordings of small-magnitude earthquakes as EGF. Through synthetic tests, we demonstrated that, in such instances, the problem of this technique is that the alignment between the onset of P waves of EGF and MAIN is not rightly recovered after the initial inversion step. Consequently, a novel inversion method has been developed to address this issue, enabling the identification of the optimal alignment of P-wave arrivals in EGF and MAIN across all stations. A Bayesian statistical approach is proposed to meticulously investigate the solutions of model parameters and their correlations. Using the new technique on a small magnitude earthquake (ML = 3.3) occurred in Central Italy enabled us to identify the most likely rupture models and examine the issue of correlation among model parameters. Application of Occam’s Razor Principle suggests that, for the investigated event, a circular crack model should be favored over a heterogeneous rupture model.

Enhancing flood wave modelling of reservoir failure: a comparative study of structure-from-motion based 2D and 3D methodologies

Predicting flood wave propagation from reservoir failures is critical to practical flood hazard assessment and risk management. Flood waves are sensitive to topography, channel geometry, structures, and natural features along floodplain paths. Thus, the accuracy of flood wave modelling depends on how precisely those features are represented. This study introduces an enhancing approach to flood wave modelling by accurately representing three-dimensional objects in floodplains using the structure-from-motion (SfM). This method uses an unmanned aerial vehicle to capture topographic complexities and account for ground objects that impact flood propagation. Using the three-dimensional volume of fluid numerical approach significantly improves an enhanced representation of turbulent flow dynamics and computational efficiency, especially in handling large topography datasets. Reproductions from this enhanced three-dimensional approach were validated against recent reservoir failure observations and contrasted with traditional two-dimensional models. The results revealed that the suggested three-dimensional methodology achieved a significant 84.4% reproducibility when juxtaposed with actual inundation traces. It was 35.5%p more accurate than the two-dimensional diffusion wave equation (DWE) and 17.1%p more than the shallow water equation (SWE) methods in predicting flood waves. This suggests that the reproducibility of the DWE and SWE decreases compared to the three-dimensional approach when considering more complex floodplains. These results demonstrate that three-dimensional flood wave analysis with the SfM methodology is optimal for effectively minimising topographic and flood wave reproduction errors across extensive areas. This dual reduction in errors significantly enhances the reliability of flood hazard assessments and improves risk management by providing more precise and realistic predictions of flood waves.

Travel Characteristics and Vulnerability Analysis of Road Resource Utilization Based on Taxi GPS Data

Residents’ travel and logistics are greatly affected by urban transportation networks, which are one of the most important supports for urban socio-economic activities. Urban transportation systems tend to cripple when faced with challenges such as natural hazards and social unrest. This paper proposes a framework for a vulnerability analysis of urban road networks (URNs) based on real traffic flows with GPS data. An improved K-shell critical node identification method is proposed based on structural and traffic characteristics. Then, a cascade failure model is proposed to analyze the structural and functional vulnerability of the URN by combining the load capacity model and the vulnerability model. This paper takes the Harbin main city URN as an example and first analyzes the passenger travel distribution and the relationship between travel orders, population and POI. Four deliberate attack methods are proposed to analyze the vulnerability of the URN under deliberate attack on commute days and rest days. The experimental results show that URNs exhibit intense vulnerability, with the fastest cascading failure occurring based on improved K-shell node failure. Furthermore, URNs are more vulnerable on rest days compared to commuter days. These findings could be used to inform a vulnerability-based spatiotemporal design of UBNs and provide theoretical support for managing traffic congestion on different days.

Shear buckling behaviour of sinusoidal corrugated web girders with stiffened circular openings

The mechanical properties and failure behaviours of three different specimens of sinusoidal corrugated web girders with stiffened circular openings were investigated experimentally and numerically. The experimental outcomes showed similarities in the mechanical properties and failure model of the specimens, despite differences in the geometric dimensions. The numerical simulations further confirmed the buckling as well as post-buckling behaviours of the experimental results. The influence of initial geometric imperfections on the shear buckling load of the corrugated web girders was quantified and neglecting geometric imperfections led to an overestimation of the actual shear load capacity, emphasizing the importance of considering imperfections in the design of structural components. The investigation results showed that the shear load capacities of the girders were significantly affected by the thickness of the opening stiffeners, and that the presence of openings reduced the load carrying capacity and the overall stiffness of the beams, whereas the existence of opening stiffeners increased both the ultimate load bearing capacity and the global stiffness. However, the strengthening effect of the opening stiffener becomes less pronounced beyond a specific thickness. Besides, a comparison between hand calculations and numerical simulations show that the recently developed calculation method provided a more reliable prediction of the shear buckling resistance of corrugated web with stiffened openings. This investigation provides valuable guidance on the shear buckling behaviour of sinusoidal corrugated web girders with circular opening stiffeners, thus benefiting the design and analysis of steel structural components with sinusoidal corrugated web.

Extracts from Artemisia annua Alleviates Myocardial Remodeling through TGF-β1/Smad2/3 Pathway and NLRP3 Inflammasome

Artemisinin and its derivatives, the well-known anti-malarial drugs extracted from traditional Chinese medicine, Artemisia annua, have been implicated in treating fibrotic diseases. However, whether artemisinin affects cardiac fibrosis in the pathogenesis of heart failure is still unknown. This study aimed to evaluate the possible effects of artemisinin on cardiac function and myocardial fibrosis in the heart failure model and to explore the underlying mechanisms. Isoproterenol was injected subcutaneously for induction of the cardiac fibrosis model. Proteomic analysis was performed after 4 four weeks of artemisinin treatment. Echocardiography was used to evaluate cardiac function and structure. Hematoxylin and eosin (H&E) staining, as well as Masson trichrome staining, were performed for histopathology. The α-SMA, collagen I, and III expression in the myocardium was detected by immunohistochemical staining. The ratio of heart weight to body weight (HW/BW, mg/kg) and the ratio of heart weight to tibia length (HW/TL, mg/mm) were calculated as indicators for cardiac remodeling. Brain natriuretic peptide (BNP) levels were quantified in rat plasma using enzymelinked immunosorbent assay (ELISA). In contrast, the protein levels of TGF-β1, p-Smad2/3, and Smad2/3 were assessed in the myocardium and fibroblasts via western blot analysis. RT-qPCR was performed to analysis the expression of Col-I, Col-III, α-SMA, NLRP3, Caspase-1, IL-1β, and IL-18. Proteomic analysis identified 227 differentially expressed proteins (DEPs), including 119 upregulated and 108 downregulated proteins. These proteins were identified as the core proteins targeted by artemisinin for improving myocardial remodeling. GO annotation of the DEPs indicated that the DEPs were mainly associated with biological processes such as inflammation regulation. In the in vivo study of an isoproterenol-induced rat cardiac remodeling model, we found that artemisinin administration significantly ameliorated cardiac dysfunction and reduced collagen production by suppressing TGFβ-1/Smads signaling and inhibiting NLRP3 inflammasome activation. As manifested by downregulating the expression of α-SMA, Col-I, and Col-III, NLRP3, IL-1β, IL-18, Caspase-1 mRNA, and TGF-β1, p-SMAD 2/3 protein in the myocardium. Similar beneficial effects of artemisinin were consistently observed in TGF-β1 treated primary cardiac fibroblasts. Extracts from Artemisia annua relieves myocardial remodeling through TGF-β1/Smad2/3 pathway and NLRP3 inflammasome

Physics-based natural gradient boosting probabilistic prediction model for seismic failure modes of reinforced concrete columns

A novel physics-based natural gradient boosting (PNGB) probabilistic prediction model for flexure failure (FF), flexure-shear failure (FSF) and shear failure (SF) of reinforced concrete (RC) columns under strong earthquakes has been developed to address the limitations of empirical and machine learning (ML) models, which often fail to learn physical laws, insufficiently consider uncertainties, and exhibit poor generalization performance. Firstly, an improved natural gradient boosting (NGB) probabilistic model of seismic failure modes was created by using natural gradient boosting and gradient boosting regressor algorithms. Then a new hyperparameter optimization method for the improved NGB probabilistic model was proposed based on the ML algorithms and the physical laws. Finally, the predictive performance and engineering practicability of the PNGB probabilistic model were verified compared to empirical and ML models. According to the analysis results, the PNGB model can effectively improve the predictive recall of FF, FSF and SF by about 19–65 %, 20–67 % and 20–56 % respectively compared with empirical models, and by about 1–7 %, 7–43 % and 6–32 % respectively compared with ML models. Moreover, the PNGB model exhibits satisfactory generalization performance and minimal dispersion, which can be used to calibrate the ML models based on the confidence intervals. Furthermore, the result predicted by the PNGB model satisfies the physical laws relating to the seismic failure modes and design parameters, which can further represent the competitive relationships of various seismic failure modes.

Failure analysis and formability improvement of GLARE laminates in warm active hydroforming technology: Experimental and numerical approach

Warm hydroforming shows considerable promise as a forming technology for Fiber Metal Laminates (FMLs) parts due to its capacity to enhance the formability of materials. However, a detailed investigation into the failure behavior during hydroforming is still lacking. In this paper, a systematic experiment was performed to analyze the possible failure modes for GLARE in warm active hydroforming. Five main defect modes have been identified, including fiber crack, combined Al & fiber crack, wrinkle, low resin, and voids defects. The related formation mechanisms have been analyzed based on both experiments and numerical methods. Additionally, the effects of critical process parameters, including the blank holder force (BHF), liquid pressure rate (PR), and temperature (T) on failure behavior are thoroughly investigated and quantified. The use of step-loading BHF was recommended to enhance formability, which caused a nearly 36% decrease in the prepreg tensile damage criteria coefficient. Conversely, decreasing PR or increasing T significantly improved the formability of GLARE but resulted in low resin content and significant void defects. Consequently, a feasibility map that quantified the BHF and liquid pressure effects on various defects was developed, leading to optimized parameters for manufacturing a box-shaped part. This study not only explores the failure model of FMLs but also offers valuable insights for process parameter improvement and how to optimize key parameters in engineering processes.

Simulation of Rock Crack Propagation and Failure Behavior Based on a Mixed Failure Model with SPH

Simulation of Rock Crack Propagation and Failure Behavior Based on a Mixed Failure Model with SPH

Cascading Failure in Cyber-Physical Systems: A Review on Failure Modeling and Vulnerability Analysis.

Cascading failures pose a significant security threat to networked systems, with recent global incidents underscoring their destructive potential. The security threat of cascading failures has always existed, but the evolution of cyber-physical systems (CPSs) has introduced novel dimensions to cascading failures, intensifying their threats owing to the intricate fusion of cyber and physical domains. Addressing these threats requires a nuanced understanding achieved through failure modeling and vulnerability analysis. By analyzing the historical failures in different CPSs, the cascading failure in CPSs is comprehensively defined as a complicated propagation process in coupled cyber and physical systems, initialized by natural accidents or human interference, which exhibits a progressive evolution within the networked structure and ultimately results in unexpected large-scale systemic failures. Subsequently, this study advances the development of instructions for modeling cascading failures and conducting vulnerability analyses within CPSs. The examination also delves into the core challenges inherent in these methodologies. Moreover, a comprehensive survey and classification of extant research methodologies and solutions are undertaken, accompanied by a concise evaluation of their advancements and limitations. To validate the performance of these methodologies, numerical experiments are conducted to ascertain their distinct features. In conclusion, this article advocates for future research initiatives, particularly emphasizing the exploration of uncertainty analysis, defense strategies, and verification platforms. By addressing these areas, the resilience of CPSs against cascading failures can be significantly enhanced.

Behavior of reinforced CHS T-joints by welding collar plates under load

The paper presents a comprehensive test program on collar plate reinforced CHS T-joints under different preload conditions, in order to investigate the effect of preload and welding thermal on reinforced joints. A total of four specimens, including specimens with and without preload when the collar plates were welded, were tested under brace axial loading. The test results, including welding temperature field, development of strain as well as welding residual deformation during the welding process are measured and presented in this paper. Furthermore, the failure model and compressive strength of the collar plate reinforced T-joints were determined. The test results demonstrated that the localized high temperature and rapid attenuation are the characteristics of the welding temperature field, which instantaneous peak temperature rose to 1808 °C at the local area and attenuated to 600 °C in an elliptic range of about 3.1 cm × 1.7 cm. The failure modes of collar plate reinforced CHS T-joints do not change with preload on the chord and welding thermal. Furthermore, preload on the chord reduces the compressive strength of reinforced joints. The strain distribution and residual deformation are affected by the thermal expansion and cold shrinkage, while the development of the welding temperature field is not affected by the preload. Finally, for compressive strength of CHS T-joints reinforced with collar plate by welding, the applicability of the reduction coefficient due to preload calculated by existing codes was assessed by comparing design values with experimental results. A finite element model by ANSYS, considering the welding heat, was established. Key parameters affecting the strength of the T-joint at the reinforced collar plate under load were identified through parametric study with finite element models. Construction recommendations of welded CHS T-joints are proposed.

Towards accurate prediction of the dynamic behavior and failure mechanisms of three-dimensional braided composites: A multiscale analysis scheme

In this paper, a dynamic multiscale model is proposed for three-dimensional four-directional (3D4D) braided composites, considering the effects of strain rate and shear enhanced failure mechanism. The strain rate-dependent constitutive models are established for both resin and yarns. The accuracy of the yarn model is validated by comparing the simulated stress-strain curves with the experimental results obtained from the Split Hopkinson Pressure Bar (SHPB) tests with various strain rates. The shear enhancement coefficient of the yarn is determined from the failure envelopes with a discussion of crack propagation angles. The results show that, based on the calculated microscale properties, the mesoscale model accurately predicts both the longitudinal and transverse compressive strain-stress behavior of 3D4D braided composites at different strain rates. A comparative analysis reveals that the shear-enhanced failure model achieves a better prediction compared with other counterparts, such as Hashin-Rotem and Tsai-Wu Models. The proposed dynamic multiscale scheme for 3D braided composites is an efficient and accurate tool to characterize their multiscale features and strain rate-dependent behavior.