Primary Damage Research Articles

Thermal fatigue behavior of the ZGH451 Ni-based superalloy fabricated by direct energy deposition in the temperature range of 900–1100 °C

In this study, a novel Ni-based superalloy, ZGH451, has been fabricated using direct energy deposition (DED). The thermal fatigue resistance of ZGH451 is systematically evaluated at 900, 1000, and 1100 °C, primarily focusing on the crack initiation and propagation behaviors. The results indicate that higher peak temperatures lead to earlier initiation and more rapid propagation of cracks. Cracks are initiated at the defects and grain boundaries in the vicinity of the notch, and different crack propagation mechanisms (γ' phase slip shearing, γ' phase distortion shearing, and γ' phase rafting shearing at 900, 1000, and 1100 °C, respectively) are the main reason for the different cracks propagation behaviors under the three temperatures. The main crack propagation paths are oriented at approximately 45° with respect to the build direction, suggesting activation of the {111}<110> slip system. Additionally, oxidation reduces the matrix strength and passivates the crack tips, leading to varying rates of crack propagation. At elevated temperatures, the synergistic effects of thermal stress and oxidative erosion are found to be the primary damage mechanisms of thermal fatigue. Overall, the proposed ZGH451 superalloy demonstrates exceptional thermal fatigue resistance, providing a crucial experimental reference for thermal fatigue in additively manufactured superalloys.

Spinal cord injury: pathogenetic principles of molecular and cellular therapy

Spinal cord injury is a prognostically unfavorable condition due to the subsequent development of primary and secondary damage to the nervous structures, leading to various disorders of motor and sensory capabilities, which is also accompanied by dysfunction of the autonomic nervous system. Considering the initial complexities of regeneration processes in the central nervous system, in order to select treatment tactics for patients with spinal cord injury, it is important for doctors to know the cellular basis of the pathophysiological processes occurring in the spinal cord in the acute and chronic phases after injury, including in order to adequately select cells-targets of pharmacological drugs. Existing methods of treating neurotrauma can still do little to help prevent the death of neurons and the formation of glial scars, which make it impossible for the migration of cells involved in the processes of post-traumatic remodeling of the spinal cord and become an obstacle to the sprouting of regenerating axons. Unfortunately, preventing the formation of a glial scar remains an unsolved problem in clinical practice. In addition, in the case of spinal cord injuries in the clinic, it is extremely important to provide humoral stimulation to maintain the viability of nerve structures, for example, using numerous growth factors that are well known today, which have a beneficial effect on the intracellular regeneration of neurons and other cells involved in these processes, but the methodology for their delivery into the central nervous system has only been tested in animal models. That is why there is an urgent need to develop fundamentally new approaches to the treatment of the consequences of spinal cord injury, including cellular technologies based on transplantation of stem or differentiated cells in order to restore nerve structures and secretion of growth factors, the use of genetic constructs carrying genes for neurotrophic factors that can minimize development of post-traumatic destructive processes in the central nervous system. This review is devoted to these issues.

Identifying sub-cascades from the primary damage state of collision cascades

The morphology of a collision cascade is an important aspect in understanding the formation of defects and their distribution. While the number of sub-cascades is an essential parameter to describe the cascade morphology, the methods to compute this parameter are limited. We present a method to compute the number of sub-cascades from the primary damage state of the collision cascade. Existing methods analyze peak damage state or the end of ballistic phase to compute the number of sub-cascades which is not always available in collision cascade databases. We use density based clustering algorithm from unsupervised machine learning domain to identify the sub-cascades from the primary damage state. To validate the results of our method we first carry out a parameter sensitivity study of the existing algorithms. The study shows that the results are sensitive to input parameters and the choice of the time-frame analyzed. On a database of 100 collision cascades in W, we show that the method we propose, which analyzes primary damage state to predict number of sub-cascades, is in good agreement with the existing method that works on the peak state. We also show that the number of sub-cascades found with different parameters can be used to classify and group together the cascades that have similar time-evolution and fragmentation. It is seen that the number of SIA and vacancies, % defects in clusters and volume of the cascade, decrease with increase in the number of sub-cascades.

Impact of indoor air pollution on DNA damage and chromosome stability: a systematic review.

Indoor air pollution is becoming a rising public health problem and is largely resulting from the burning of solid fuels and heating in households. Burning these fuels produces harmful compounds, such as particulate matter regarded as a major health risk, particularly affecting the onset and exacerbation of respiratory diseases. As exposure to polluted indoor air can cause DNA damage including DNA sd breaks as well as chromosomal damage, in this paper, we aim to provide an overview of the impact of indoor air pollution on DNA damage and genome stability by reviewing the scientific papers that have used the comet, micronucleus, and γ-H2AX assays. These methods are valuable tools in human biomonitoring and for studying the mechanisms of action of various pollutants, and are readily used for the assessment of primary DNA damage and genome instability induced by air pollutants by measuring different aspects of DNA and chromosomal damage. Based on our search, in selected studies (in vitro, animal models, and human biomonitoring), we found generally higher levels of DNA strand breaks and chromosomal damage due to indoor air pollutants compared to matched control or unexposed groups. In summary, our systematic review reveals the importance of the comet, micronucleus, and γ-H2AX assays as sensitive tools for the evaluation of DNA and genome damaging potential of different indoor air pollutants. Additionally, research in this particular direction is warranted since little is still known about the level of indoor air pollution in households or public buildings and its impact on genetic material. Future studies should focus on research investigating the possible impact of indoor air pollutants in complex mixtures on the genome and relate pollutants to possible health outcomes.

Cannabidiol and Aza-BODIPY Coencapsulation for Photodynamic Therapy Enhancement in Liver Cancer Cells.

Photodynamic therapy (PDT) and cannabidiol (CBD) have been explored for their potential in synergistic cancer treatment. In this study, we employed CBD oil as a lipid phase, encapsulated within AZB-I@Lec-T to create lipid-based nanoparticles. Here, CBD oil does two tasks: it acts as a pyroptosis agent to destroy liver cancer cells and as a lipid phase to dissolve the photosensitizer. It was expected that this system would offer synergistic therapy between CBD and PDT better than a single use of each treatment. With a series of in vitro experiments, the nanoparticles exhibited induced apoptosis in 68% of HepG2 cells treated with AZB-I@Lec-T@CBD and near-infrared (NIR)-light irradiation, reducing expression levels of antioxidant defense system genes. Furthermore, both components worked well in a submicromolar range when combined in our formulation. These results highlight the potential for amplifying primary cellular damage with the combination of PDT and CBD encapsulation, providing a promising therapeutic approach for liver cancer treatment guidelines.

Neuroprotective and neuroregenerative drugs after severe traumatic brain injury : Anarrative review from aclinical perspective.

Traumatic brain injuries cause enormous individual and socioeconomic burdens. Survivors frequently struggle with motor handicaps as well as impaired cognition and emotion. In addition to the primary mechanical brain damage, complex secondary mechanisms are the main drivers of functional impairment. Many of these pathophysiological mechanisms are now well known: excitotoxic amino acids, breakdown of the blood-brain barrier, neuroinflammation with subsequent damage to cell organelles and membranes, cerebral edema, and apoptotic processes triggering neuronal death; however, paracrine resilience factors may counteract these processes. Specific neuroprotective and neuroregenerative intensive care therapies are few. This review highlights medical approaches aimed at mitigating secondary damage and promoting neurotrophic processes in severe traumatic brain injury. Some pharmacologic attempts that appeared very promising in experimental settings have had disappointing clinical results (progesterone, cyclosporineA, ronopterin, erythropoietin, dexanabinol). Thus, the search for drugs that can effectively limit ongoing posttraumatic neurological damage is ongoing. Some medications appear to be beneficial: N‑methyl-D-aspartate receptor (NMDA) antagonists (esketamine, amantadine, Mg++) reduce excitotoxicity and statins and cerebrolysin are known to counteract neuroinflammation. By supporting the impaired mitochondrial energy supply, oxidative processes are inhibited and neuroregenerative processes, such as neurogenesis, angiogenesis and synaptogenesis are promoted by citicoline and cerebrolysin. First clinical evidence shows an improvement in cognitive and thymopsychic outcomes, underlined by own clinical experience combining different therapeutic approaches. Accordingly, adjuvant treatment with neuroprotective substances appears to be apromising option, although more randomized prospective studies are still needed.

Strategies in product engineering of mesenchymal stem cell-derived exosomes: unveiling the mechanisms underpinning the promotive effects of mesenchymal stem cell-derived exosomes.

Articular cartilage injuries present a significant global challenge, particularly in the aging population. These injuries not only restrict movement due to primary damage but also exacerbate elderly degenerative lesions, leading to secondary cartilage injury and osteoarthritis. Addressing osteoarthritis and cartilage damage involves overcoming several technical challenges in biological treatment. The use of induced mesenchymal stem cells (iMSCs) with functional gene modifications emerges as a solution, providing a more stable and controllable source of Mesenchymal Stem Cells (MSCs) with reduced heterogeneity. Furthermore, In addition, this review encompasses strategies aimed at enhancing exosome efficacy, comprising the cultivation of MSCs in three-dimensional matrices, augmentation of functional constituents within MSC-derived exosomes, and modification of their surface characteristics. Finally, we delve into the mechanisms through which MSC-exosomes, sourced from diverse tissues, thwart osteoarthritis (OA) progression and facilitate cartilage repair. This review lays a foundational framework for engineering iMSC-exosomes treatment of patients suffering from osteoarthritis and articular cartilage injuries, highlighting cutting-edge research and potential therapeutic pathways.

High-Throughput Screening Method Using Escherichia coli Keio Mutants for Assessing Primary Damage Mechanism of Antimicrobials.

The Escherichia coli Keio mutant collection has been a tool for assessing the role of specific genes and determining their role in E. coli physiology and uncovering novel functions. In this work, specific mutants in the DNA repair pathways and oxidative stress response were evaluated to identify the primary targets of silver nanoparticles (NPs) and their mechanism of action. The results presented in this work suggest that NPs mainly target DNA via double-strand breaks and base modifications since the recA, uvrC, mutL, and nfo mutants rendered the most susceptible phenotype, rather than involving the oxidative stress response. Concomitantly, during the establishment of the control conditions for each mutant, the katG and sodA mutants showed a hypersensitive phenotype to mitomycin C, an alkylating agent. Thus, we propose that KatG catalase plays a key role as a cellular chaperone, as reported previously for the filamentous fungus Neurospora crassa, a large subunit catalase. The Keio collection mutants may also be a key tool for assessing the resistance mechanism to metallic NPs by using their potential to identify novel pathways involved in the resistance to NPs.

Assessment of TGx-DDI genes for genotoxicity in a comprehensive panel of chemicals

Background The TGx-DDI biomarker identifies transcripts specifically induced by primary DNA damage. Profiling similarity of TGx-DDI signatures can allow clustering compounds by genotoxic mechanism. This transcriptomics-based approach complements conventional toxicology testing by enhancing mechanistic resolution. Methods Unsupervised hierarchical clustering and t-distributed stochastic neighbor embedding (tSNE) were utilized to assess similarity of publicly-available per- and polyfluoroalkyl substances (PFAS) and ToxCast chemicals based on TGx-DDI modulation. TempO-seq transcriptomic data after highest chemical concentrations were analyzed. Results Clustering discriminated between genotoxic and non-genotoxic compounds while drawing similarity among chemicals with shared mechanisms. PFAS largely clustered distinctly from classical mutagens. However, dynamic range across PFAS types and durations indicated variable potential for DNA damage. tSNE visualization reinforced phenotypic groupings, with genotoxins clustering separately from non-DNA damaging agents. Discussion Unsupervised learning approaches applied to TGx-DDI profiles effectively categorizes chemical genotoxicity potential, aiding elucidation of biological response pathways. This transcriptomics-based strategy gives further insight into the role and effect of individual TGx-DDI biomarker genes and complements existing assays by enhancing mechanistic resolution. Overall, TGx-DDI biomarker profiling holds promise for predictive safety screening.

Experimental investigation of thermomechanical fatigue behavior in directionally solidified Ni-based superalloy under in-phase and out-of-phase conditions

The fatigue behavior of a directionally solidified (DS) Ni-based superalloy was investigated under in-phase (IP) and out-of-phase (OP) thermomechanical fatigue (TMF) conditions. Specimens were tested under strain control with a temperature range of 450–850 °C. In some tests, an optional 5 min out-of-phase dwell (OPD) time was introduced. In the case of IP TMF, the primary damage manifestation was predominantly intergranular cracks, whereas in the OP tests, the damage was mainly transgranular cracks. The fatigue life of IP TMF was found to be significantly shorter than that of OP TMF. This indicated that the intergranular cracks propagated faster than the transgranular cracks. The dwell time did not influence the dominant damage form; however, it led to an increase in the density of the microcracks. This increase resulted in a reduced lifetime, leading to lower stress amplitudes and higher plastic strain amplitudes compared with the continuous cycle tests. In addition, cycle hardening became apparent during the initial stages of cyclic loading. The microstructures and damage evolution were examined to provide insights into the changes in fatigue life. A model for predicting the fatigue life of DS Ni-based superalloy under given test conditions has been assessed. The proposed fracture mechanics model, which outlines the failure mechanism of directionally solidified Ni-based superalloy under TMF conditions, has proven to be effective in predicting fatigue life.

Does the Symbiotic Relationship Between Hydra Viridissima and Photoautotrophic Alga Provide an Evolutionary Advantage in Protecting DNA against Damage by the Cytotoxic or Genotoxic Mode of Action of Environmental Stressors?

The aim of this paper was to evaluate whether symbiotic cooperation between green hydra (Hydra viridissima) and photoautotrophic alga gives higher resistance of the preservation of DNA integrity compared to brown hydra (Hydra oligactis). Norflurazon concentrations were 0.061 or 0.61mg/L and UV-B light 254nm, 0.023mWcm- 2 applied separately or simultaneously. By alkaline comet assay primary DNA damage was assessed and cytotoxicity by fluorescent staining. Norflurazon at 0.61 mg L- 1 significantly increased DNA damage in brown hydras compared to the control (6.17 ± 0.6μm, 5.2 ± 1.7% vs. 2.9 ± 0.2μm, 1.2 ± 0.2%). Cytotoxicity was significantly elevated, being higher in brown hydras (25.7 ± 3.5% vs. 8.2 ± 0.2%). UV-B irradiation induced significant DNA damage in brown hydras (13.5 ± 1.0μm, 4.1 ± 1.0%). Simultaneous exposure to UV-B and norflurazon led to a synergistic DNA damaging. The frequency of cytotoxicity and hedgehog nucleoids was more pronounced in brown (78.3 ± 9.4%; 56.4 ± 6.0%) than in green hydras (34.7 ± 2.5%; 24.2 ± 0.6%). Evolutionary established symbiotic cooperation proved to provide resistance against cyto/genotoxicity.

Anisotropic dynamic compression response of an ultra-high strength steel fabricated by laser hybrid additive manufacturing

Directed energy deposition (DED) is a technological innovation revolutionizing in-situ repair, hybrid manufacturing, and multi-material integration manufacturing, characterized by microstructural heterogeneity on a macro-scale. However, the overall performance of these DED-fabricated components under dynamic loading, particularly along different directions, remains uncharted. This work explores the anisotropic dynamic compression response of an ultra-high strength steel, namely 35CrMnSiA steel, fabricated using DED on a wrought substrate. The laser hybrid additive manufactured samples were subjected to split Hopkinson pressure bar testing along different directions. The results show the following: 1) hybrid manufactured 35CrMnSiA steel has an anisotropic dynamic compression response due to the mismatched properties of each subzone induced by microstructural heterogeneity, 2) low-strength DED part shows higher strain under compression along the build direction but behaves similarly to the wrought material when compressed along the transverse direction, 3) intergranular void/crack is the primary damage mechanism, cracks preferred formed in wrought substrate due to the martensite with poor plastic dissipation ability, 4) when the interface is subjected to parallel directional impact loads, the strain mismatch between the two side subzones leads to interface separation. This study provides comprehensive understanding of the dynamic behavior of DED-fabricated components with heterogenous microstructure, and new insight into demanding tailored strategies to ensure consistent and predictable behavior under various loading conditions.

A new interatomic potential of W-Ni-Fe systems for point defects and mechanical property studies

W-Ni-Fe tungsten heavy alloys (WHAs) are a kind of ductile phase toughened composites that are becoming increasingly interesting as promising alternatives to monolithic tungsten for fusion reactor plasma-facing materials, because of their outstanding combination of strength, ductility and toughness. Understanding the radiation-induced microstructural features of WHAs associated with their mechanical property changes is therefore a topic of active research. The theoretical study of radiation-induced collision cascades by means of atomistic simulations such as classical molecular dynamics (MD) is highly desirable to provide a detailed analysis for the atom-level primary damage production. Here, we develop a Finnis–Sinclair type interatomic potential for W-Ni-Fe ternary systems based on previously proposed unary W and Fe potentials, and use it to study the point defects and mechanical properties of WHAs. The developed potential yields the bulk and defect properties of pure Ni that are in good agreement with experimental data and density functional theory calculations. In addition, it is also capable of reproducing alloy properties with a satisfactory accuracy, especially regarding the solute migration energies, as well as the ground-state interstitial defect configurations. The constructed potential further shows reasonable transferability to other mechanically relevant properties that are not contained in the fitting database. The present potential here will enable large-scale MD simulations of cascade, deformation and fracture of WHAs.

TIMP2 protects against sepsis-associated acute kidney injury by cAMP/NLRP3 axis-mediated pyroptosis.

The tissue inhibitor of metalloproteinases 2 (TIMP2) has emerged as a promising biomarker for predicting the risk of sepsis-associated acute kidney injury (SA-AKI). However, its exact role in SA-AKI and the underlying mechanism remains unclear. In this study, we investigated the impact of kidney tubule-specific Timp2 knockout mice on kidney injury and inflammation. Our findings demonstrated that Timp2-knockout mice exhibited more severe kidney injury than wild-type mice, along with elevated levels of pyroptosis markers NOD-like receptor protein 3 (NLRP3), Caspase1, and gasdermin D (GSDMD) in the early stage of SA-AKI. Conversely, the expression of exogenous TIMP2 in TIMP2-knockout mice still protected against kidney damage and inflammation. In in vitro experiments, using recombinant TIMP2 protein, TIMP2 knockdown demonstrated that exogenous TIMP2 inhibited pyroptosis of renal tubular cells stimulated by lipopolysaccharide (LPS). Mechanistically, TIMP2 promoted the ubiquitination and autophagy-dependent degradation of NLRP3 by increasing intracellular cyclic adenosine monophosphate (cAMP), which mediated NLRP3 degradation through recruiting the E3 ligase MARCH7, attenuating downstream pyroptosis, and thus alleviating primary tubular cell damage. These results revealed the renoprotective role of extracellular TIMP2 in SA-AKI by attenuating tubular pyroptosis, and suggested that exogenous administration of TIMP2 could be a promising therapeutic intervention for SA-AKI treatment.NEW & NOTEWORTHY Tissue inhibitor of metalloproteinase 2 (TIMP-2) has been found to be the best biomarker for predicting the risk of sepsis-associated acute kidney injury (SA-AKI). However, its role and the underlying mechanism in SA-AKI remain elusive. The authors demonstrated in this study using kidney tubule-specific knockout mice model of SA-AKI and primary renal tubule cells stimulated with lipopolysaccharide (LPS) that extracellular TIMP-2 promoted NOD-like receptor protein 3 (NLRP3) ubiquitination and autophagy-dependent degradation by increasing intracellular cyclic adenosine monophosphate (cAMP), thus attenuated pyroptosis and alleviated renal damage.

Elastic Damage Healing Model Coupling Secondary Damage Variable for Self Healing Materials

A one-dimensional constitutive model, based on the principles of continuum damage mechanics, is developed for capturing healing in certain materials during unloading and rest periods. A secondary damage variable is defined to address the drawback of existing models for damage and healing in capturing the complete material failure. An energy-based damage evolution function is adopted for primary and secondary damage variables, and phenomenological healing evolution is defined. The proposed implicit elastic damage-healing model is implemented by the return-mapping technique, and the model response is demonstrated for different loading histories.

Air Pollution and Primary DNA Damage among Zagreb (Croatia) Residents: A Cross-Sectional Study.

More than eight million premature deaths annually can be attributed to air pollution, with 99% of the world's population residing in areas below recommended air quality standards. Hence, the present study aimed to examine the association between primary DNA damage and air pollution data among 123 participants enrolled between 2011 and 2015 in Zagreb, Croatia. While most measured air pollutants adhered to regulatory limits, benzo[a]pyrene concentrations bound to PM10 exceeded them. Factorial analysis narrowed down air pollution data to four exposure factors (particulate matter, two metal factors, and other pollutants). Despite the absence of significant positive associations between modeled air pollution exposure factors and comet assay descriptors (tail length, tail intensity, tail moment, and highly damaged nuclei), the critical health implications of air pollution warrant further investigations, particularly with biomarkers of exposure and different biomarkers of effect in populations facing air pollution exposure.

Progressive Irreversible Proprioceptive Piezo2 Channelopathy-Induced Lost Forced Peripheral Oscillatory Synchronization to the Hippocampal Oscillator May Explain the Onset of Amyotrophic Lateral Sclerosis Pathomechanism.

Amyotrophic lateral sclerosis (ALS) is a mysterious lethal multisystem neurodegenerative disease that gradually leads to the progressive loss of motor neurons. A recent non-contact dying-back injury mechanism theory for ALS proposed that the primary damage is an acquired irreversible intrafusal proprioceptive terminal Piezo2 channelopathy with underlying genetic and environmental risk factors. Underpinning this is the theory that excessively prolonged proprioceptive mechanotransduction under allostasis may induce dysfunctionality in mitochondria, leading to Piezo2 channelopathy. This microinjury is suggested to provide one gateway from physiology to pathophysiology. The chronic, but not irreversible, form of this Piezo2 channelopathy is implicated in many diseases with unknown etiology. Dry eye disease is one of them where replenishing synthetic proteoglycans promote nerve regeneration. Syndecans, especially syndecan-3, are proposed as the first critical link in this hierarchical ordered depletory pathomechanism as proton-collecting/distributing antennas; hence, they may play a role in ALS pathomechanism onset. Even more importantly, the shedding or charge-altering variants of Syndecan-3 may contribute to the Piezo2 channelopathy-induced disruption of the Piezo2-initiated proton-based ultrafast long-range signaling through VGLUT1 and VGLUT2. Thus, these alterations may not only cause disruption to ultrafast signaling to the hippocampus in conscious proprioception, but could disrupt the ultrafast proprioceptive signaling feedback to the motoneurons. Correspondingly, an inert Piezo2-initiated proton-based ultrafast signaled proprioceptive skeletal system is coming to light that is suggested to be progressively lost in ALS. In addition, the lost functional link of the MyoD family of inhibitor proteins, as auxiliary subunits of Piezo2, may not only contribute to the theorized acquired Piezo2 channelopathy, but may explain how these microinjured ion channels evolve to be principal transcription activators.

Comparing Mfd- and UvrD-dependent models of transcription coupled DNA repair in live Escherichia coli using single-molecule tracking

During transcription-coupled DNA repair (TCR) the detection of DNA damage and initiation of nucleotide excision repair (NER) is performed by translocating RNA polymerases (RNAP), which are arrested upon encountering bulky DNA lesions. Two opposing models of the subsequent steps of TCR in bacteria exist. In the first model, stalled RNAPs are removed from the damage site by recruitment of Mfd which dislodges RNAP by pushing it forwards before recruitment of UvrA and UvrB. In the second model, UvrD helicase backtracks RNAP from the lesion site. Recent studies have proposed that both UvrD and UvrA continuously associate with RNAP before damage occurs, which forms the primary damage sensor for NER. To test these two models of TCR in living E. coli, we applied super-resolution microscopy (PALM) combined with single particle tracking to directly measure the mobility and recruitment of Mfd, UvrD, UvrA, and UvrB to DNA during ultraviolet-induced DNA damage. The intracellular mobilities of NER proteins in the absence of DNA damage showed that most UvrA molecules could in principle be complexed with RNAP, however, this was not the case for UvrD. Upon DNA damage, Mfd recruitment to DNA was independent of the presence of UvrA, in agreement with its role upstream of this protein in the TCR pathway. In contrast, UvrD recruitment to DNA was strongly dependent on the presence of UvrA. Inhibiting transcription with rifampicin abolished Mfd DNA-recruitment following DNA damage, whereas significant UvrD, UvrA, and UvrB recruitment remained, consistent with a UvrD and UvrA performing their NER functions independently of transcribing RNAP. Together, although we find that up to ∼8 UvrD-RNAP-UvrA complexes per cell could potentially form in the absence of DNA damage, our live-cell data is not consistent with this complex being the primary DNA damage sensor for NER.

Multiscale coupling analysis of energy absorption in 3D printed continuous fiber reinforced thermoplastic orthogonal fabric composites

Generally, serious delamination and defect propagation are the primary damage modes observed in 3D printed continuous fiber reinforced thermoplastic composites (3D printed CFTP composites) under low-velocity impact. The study of fabric structure design and its impact resistance is crucial for the practical application of 3D printed composites, yet the existing research in this area is limited. In this paper, the preparation scheme of 3D printed continuous fiber reinforced thermoplastic orthogonal fabric composites (3D printed CFTPOF composites) with the improved impact resistance is proposed initially. Then, the analysis models for the molding process and mechanical properties of the 3D printed CFTPOF composites are established. To address the limitations of current analysis methods for 3D printed composites, a coupled multiscale method (3DP-MS method), is proposed for predicting mechanical properties. The transfer of mechanical parameters between multiscale models is also established and validated through experiments. Finally, the impact performance and the energy absorption of 3D printed CFTPOF composites under different fabric paths and yarn distributions are analyzed and discussed. This paper provides theoretical basis and simulation method for the structural design of impact-resistant 3D printed CFTP composites.

Analysis of physical and mechanical properties of granite under different cooling methods under high-temperatures thermal cycles

This study explores the impact of external pressure and high-temperature erosion on the physical and mechanical properties of granite, the geothermal well storage medium, during geothermal exploitation. Objectives include evaluating the effects of repeated heating and cooling cycles at different temperatures on porosity, permeability and mechanical performance, with a focus on confining pressure's influence on permeability. The results indicate that under water-cooling and ambient conditions, porosity and permeability increase with cycle repetition, whereas compressive strength and elastic modulus decrease. Notably, Group B's (water-cooled) mechanical performance surpasses that of Group A (room temperature cooling) when porosity is below 1.5%. However, with increasing porosity owing to thermal cycling, Group B's granite becomes inferior to that of Group A. Micro-computed tomography scans reveal a post-cycling granite pore structure dominated by horizontal cracks, with primary uniaxial compression damage in the vertical direction. Thermal cycling reduces crack paths and load-bearing capacity, diminishing granite's mechanical performance. This study offers insights into subtle interactions between cooling methods and porosity during geothermal energy exploitation. It provides valuable guidance for optimizing geothermal energy use and mitigating potential adverse impacts on rock integrity, laying a foundation for further research and practical applications in geothermal energy exploitation.