Damage Accumulation Research Articles

Hollow cerium nanoparticles synthesized by one-step method for multienzyme activity to reduce colitis in mice

BACKGROUND Inflammatory bowel disease (IBD) is a common chronic intestinal inflammatory disease. High oxidative stress is a treatment target for IBD. Cerium oxide (CeO2) nanomaterials as nanozymes with antioxidant activity are potential drugs for the treatment of colitis. AIM To synthesize hollow cerium (H-CeO2) nanoparticles by one-step method and to validate the therapeutic efficacy of H-CeO2 in IBD. METHODS H-CeO2 was synthesized by one-step method and examined its characterization and nanoenzymatic activity. Subsequently, we constructed dextran sulfate sodium (DSS)-induced colitis in mice to observe the effects of H-CeO2 on colonic inflammation. The effects of H-CeO2 on colon inflammation and reactive oxygen species (ROS) levels in IBD mice were detected by hematoxylin and eosin staining and dichlorofluorescein diacetate staining, respectively. Finally, the biological safety of H-CeO2 on mice was evaluated by hematoxylin and eosin staining, blood routine, and blood biochemistry. RESULTS H-CeO2 nanoparticles prepared by the one-step method were uniform, monodisperse and hollow. H-CeO2 had a good ability to scavenge ROS, ∙OH and ∙OOH. H-CeO2 reduced DSS-induced decreases in body weight and colon length, colonic epithelial damage, inflammatory infiltration, and ROS accumulation. H-CeO2 administration reduced the disease activity index of DSS-induced animals from about 8 to 5. H-CeO2 had no significant effect on body weight, total platelet count, hemoglobin, white blood cell, and red blood cell counts in healthy mice. No significant damage to major organs was observed in healthy mice following H-CeO2 administration. CONCLUSION The one-step synthesis of H-CeO2 nanomaterials had good antioxidant activity, biosafety, and inhibited development of DSS-induced IBD in mice by scavenging ROS.

Thymoquinone-Loaded Chitosan Nanoparticles Combat Testicular Aging and Oxidative Stress Through SIRT1/FOXO3a Activation: An In Vivo and In Vitro Study

Background: Aging is a complex biological process characterized by the accumulation of molecular and cellular damage over time, often driven by oxidative stress. This oxidative stress is particularly detrimental to the testes, where it causes degeneration, reduced testosterone levels, and compromised fertility. D-galactose (D-gal) is commonly used to model aging as it induces oxidative stress, mimicking age-related cellular and molecular damage. Testicular aging is of significant concern due to its implications for reproductive health and hormonal balance. This research examines the protection by thymoquinone (TQ) or thymoquinone-loaded chitosan nanoparticles (NCPs) against D-galactose (D-gal)-induced aging in rat testes, focusing on biochemical, histological, and molecular changes. Aging, which is driven largely by oxidative stress, leads to significant testicular degeneration, reducing fertility. D-gal is widely used to model aging due to its ability to induce oxidative stress and mimic age-related damage. TQ, a bioactive ingredient of Nigella sativa, has earned a reputation for its anti-inflammatory, anti-apoptotic, and antioxidant characteristics, but its therapeutic application is limited by its poor bioavailability. Methods: Thymoquinone was loaded into chitosan nanoparticles (NCPs) to enhance its efficacy, and this was hypothesized to improve its stability and bioavailability. Four groups of male Wistar rats participated in the study: one for the control, one for D-gal, one for D-gal + TQ, and the last one for D-gal + NCP. Results: The results exhibited that D-gal substantially increased oxidative injury, reduced testosterone levels, and caused testicular damage. Treatment with TQ and NCPs significantly reduced oxidative stress, improved antioxidant enzyme levels, and restored testosterone levels, with NCPs showing a stronger protective effect than TQ alone. A histological analysis confirmed that NCPs better preserved testicular structure and function. Additionally, the NCP treatment upregulated the expression of key genes of oxidative stress resistance, mitochondrial function, and reproductive health, including SIRT1, FOXO3a, and TERT. Conclusions: The findings suggest that NCPs offer enhanced protection against aging-related testicular damage compared with TQ alone, which is likely due to the improved bioavailability and stability provided by the nanoparticle delivery system. This research emphasizes the potential of NCPs as a more effective therapeutic strategy for mitigating oxidative stress and age-related reproductive dysfunction. Future research should further explore the mechanisms underlying these protective effects.

Numerical Simulation of Fatigue Damage in Cross-Ply CFRP Laminates: Exploring Frequency Dependence and Internal Heat Generation Effects

A numerical simulation investigating the frequency dependence of fatigue damage progression in carbon fiber-reinforced plastics (CFRPs) is conducted in this study. The initiation and propagation of transverse cracks under varying fatigue test frequencies are successfully simulated, consistent with experiments, using an enhanced degradable Hashin failure model that was originally developed by the authors in 2022. The results obtained from the numerical simulation in the present study, which employs adjusted numerical values for the purpose of damage acceleration, indicate that the number of cycles required for the formation of three transverse cracks was 174 cycles at 0.1 Hz, 209 cycles at 1 Hz, and 165 cycles at 10 Hz. Based on these results, it is demonstrated that under high-frequency cyclic loading, internal heat generation caused by dissipated energy from mechanical deformation, attributed to the viscoelastic and/or plastic behavior of the material, exceeds thermal dissipation to the environment, leading to an increase in specimen temperature. Consequently, damage progression accelerates under high-frequency fatigue. In contrast, under low-frequency fatigue, viscoelastic dissipation becomes more pronounced, reducing the number of cycles required to reach a similar damage state. The rate of damage accumulation initially increases with test frequency but subsequently decreases. This observation underscores the importance of incorporating these findings into discussions on the fatigue damage of real structural components.

U2AF1 mutation causes an oxidative stress and DNA repair defect in hematopoietic and leukemic cells.

U2AF1 is a core component of spliceosome and controls cell-fate specific alternative splicing. U2AF1 mutations have been frequently identified in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) patients, and mutations in U2AF1 are associated with poor prognosis in hematopoietic malignant diseases. Here, by forced expression of mutant U2AF1 (U2AF1 S34F) in hematopoietic and leukemic cell lines, we find that U2AF1 S34F causes increased reactive oxygen species (ROS) production. In hematopoietic cell line, a defect in mitochondrial function and DNA damage response deficiency are found in U2AF1 S34F expressing 32D cells. In leukemic cell line Molm13 cells, U2AF1 mutation leads to resistance to DNA damaging agents. Accumulation of DNA damage is also found in U2AF1 S34F expressing leukemic cells when treated with DNA damage agent. Finally, in our established hematopoietic-specific U2af1 S34F knock-in mice model, U2AF1 mutation leads to the development of myelodysplastic/myeloproliferative neoplasm (MDS/MPN) and causes DNA damage accumulation in hematopoietic cells. Our study provides evidence that U2AF1 mutation causes DNA damage response deficiency and DNA damage accumulation in hematopoietic cells, and suggests that mutant U2AF1 induced higher ROS production, resistance to DNA damaging agents and increased genomic instability may contribute to poor prognosis of AML patients with U2AF1 mutations.

The potential impact of glycine supplementation on the process of aging

Aging is a multifactorial process characterized by the progressive loss of cellular integrity, metabolic flexibility, mitochondrial function, and the gradual accumulation of oxidative and inflammatory damage. These changes increase vulnerability to age-related disorders, including cardiovascular disease, neurodegenerative conditions, metabolic syndrome, and frailty. Glycine, the simplest amino acid, has recently gained attention as a potential nutritional and therapeutic intervention to modulate various pathways implicated in aging. Beyond its structural role in collagen and other proteins, glycine is a critical precursor for glutathione- an essential intracellular antioxidant- plays a role in neurotransmission, and is involved in the synthesis of heme, creatine, and bile acids. Emerging studies suggest that glycine supplementation may alleviate oxidative stress, dampen chronic low-grade inflammation, improve insulin sensitivity, enhance mitochondrial function, and even mimic aspects of methionine restriction- a dietary approach known to extend lifespan in animal models. These combined effects may help preserve physiological function, slow the onset of age-associated diseases, and promote healthspan. Nevertheless, the evidence base is still evolving; most current data derive from animal models, in vitro experiments, and limited human trials. Rigorous, long-term, randomized controlled studies are needed to identify optimal dosing, determine long-term safety, and clarify whether glycine can be strategically leveraged as an anti-aging nutrient. If confirmed, glycine’s safety, affordability, and accessibility may make it a compelling option for improving the quality of aging worldwide.

The role of the hypothalamus-gut microbiota in the pathogenesis of periparturient fatty liver disease in dairy cows.

During the periparturient period, dairy cows experience negative energy balance due to reduced feed intake, leading to adipose tissue breakdown, liver damage, and fat accumulation. This study examined the gut-liver-brain axis to explore the link between fatty liver disease, changes in hypothalamic appetite-related neurons, and microbiome shifts in dairy cows. Thirty cows were monitored, with daily DMI recordings and blood sampling. Postpartum brain, liver, and ileal contents were collected from 10 selected cows, divided into two groups: H-DMI (slight DMI decrease) and L-DMI (severe DMI decrease). The L-DMI group of cows exhibited higher plasma NEFA, BHBA, ALT, and AST levels, along with severe hepatic steatosis and lipid accumulation. Transcriptome sequencing of the hypothalamic arcuate nucleus (ARC) revealed decreased expression of Hypocretin Neuropeptide Precursor (HCRT), orexin-A (OX-A), Orexin Receptor Type 1 (OX1R), and Cannabinoid Receptor 1 (CB1) in the L-DMI group, while Pro-opiomelanocortin (POMC) and Melanocortin 4 Receptor (MC4R) expression increased. Metagenomic analysis of ileal contents showed reduced abundance of Ruminococcus spp. in the L-DMI group, which may be associated with fatty liver disease (FL). Integrated omics analysis showed that increased MC4R expression was correlated with the elevated abundance of bacteria such as Akkermansia glycaniphila, and reduced abundance of species such as Methanobrevubacter thaueri and Ruminococcus spp. Decreased HCRT expression was also linked to Akkermansia glycaniphila. In conclusion, these changes may affect DMI through the OX-A/POMC pathway, with neurological and gut microbiome alterations potentially leading to appetite suppression, negative energy balance, and the development of fatty liver disease.

Selenoproteome depletion enhances oxidative stress and alters neutrophil functions in Citrobacter rodentium infection leading to gastrointestinal inflammation.

Reactive oxygen species (ROS) play a critical role in modulating a range of proinflammatory functions in neutrophils, as well as regulating neutrophil apoptosis and facilitating the resolution of an inflammatory response. Selenoproteins with the 21st amino acid, selenocysteine (Sec), regulate the immune mechanisms through the modulation of the redox homeostasis aiding in the efficient resolution of inflammation, while their role in neutrophil functions during diseases remains unclear. To study the role of selenoproteins in neutrophils during infection, we challenged the granulocyte-specific tRNASec (Trsp) knockout mice (TrspN) with Citrobacter rodentium (C. rodentium), a murine pathogenic bacterium. Reduced bacterial shedding during the disease-clearing phase and increased tissue damage and neutrophil accumulation in the colon of the TrspN mice were observed following infection. TrspN neutrophils showed increased intracellular ROS accumulation during ex vivo C. rodentium stimulation and upregulated fMLP-induced chemotaxis. We also observed delayed neutrophil apoptosis, reduced efferocytosis of TrspN neutrophils, and increased abundance of apoptotic cells in the colon of TrspN mice. Together, these studies indicate that selenoprotein depletion results in increased neutrophil migration to the gut accompanied by ROS accumulation, while downregulating neutrophil apoptosis and subsequent efferocytosis by macrophages. Such an increase in inflammation followed by impaired resolution culminates in decreased bacterial load but with exacerbated host tissue damage.

Application of EPR spectroscopy method for comparative analysis of structural damage accumulation kinetics in two-phase lithium-containing ceramics

Application of EPR spectroscopy method for comparative analysis of structural damage accumulation kinetics in two-phase lithium-containing ceramics

Fatigue damage accumulation model of a High-Pressure oil pipe based on fatigue probability under Multi-Level cyclic loading

Fatigue damage accumulation model of a High-Pressure oil pipe based on fatigue probability under Multi-Level cyclic loading

Assessment of dwell-fatigue properties of nickel-based superalloy coated with a multi-layered thermal and environmental barrier coating

A three-layered experimental thermal and environmental barrier coating (TEBC) was deposited using air plasma spraying technology on cylindrical specimens of nickel-based superalloy MAR-M247. TEBC consists of mullite (Al6Si2O13) and hexacelsian (BaAl2Si2O8) upper layer, Y2O3 stabilised ZrO2 interlayer and CoNiCrAlY bond coat deposited on the grit-blasted surface of MAR-M247. The cyclic plastic response and damage mechanisms in uncoated and TEBC-coated MAR-M247 have been studied in isothermal dwell-fatigue tests conducted under strain control with constant strain amplitude at 900 °C. In each cycle, 5-minute dwells were introduced in both tensile and compression peaks of the hysteresis loop. Fatigue hardening/softening curves, stress relaxation curves, cyclic stress-strain curves and fatigue life curves are reported. Ceaseless mild softening has been found in both uncoated and TEBC-coated MAR-M247. TEBC-coated MAR-M247 showed an improved lifetime in the whole range of tested strain amplitudes. Data obtained from stress relaxation curves were used to assess the fraction of creep damage. The generalised damage accumulation rule was used to evaluate damage due to fatigue-creep-environment interaction. A study of the surface relief and internal microstructure using SEM and TEM helped to interpret the specifics of fatigue behaviour of uncoated and TEBC-coated material. The effectiveness of this newly developed TEBC, together with the dwell sensitivity of MAR-M247, were discussed from the perspective relevant to dwell-fatigue cyclic straining.

Genomic 8-oxoguanine modulates gene transcription independent of its repair by DNA glycosylases OGG1 and MUTYH.

8-oxo-7,8-dihydroguanine (OG) is one of the most abundant oxidative lesions in the genome and is associated with genome instability. Its mutagenic potential is counteracted by a concerted action of 8-oxoguanine DNA glycosylase (OGG1) and mutY homolog DNA glycosylase (MUTYH). It has been suggested that OG and its repair has epigenetic-like properties and mediates transcription, but genome-wide evidence of this interdependence is lacking. Here, we applied an improved OG-sequencing approach reducing artificial background oxidation and RNA-sequencing to correlate genome-wide distribution of OG with gene transcription in OGG1 and/or MUTYH-deficient cells. Our data identified moderate enrichment of OG in the genome that is mainly dependent on the genomic context and not affected by DNA glycosylase-initiated repair. Interestingly, no association was found between genomic OG deposition and gene expression changes upon loss of OGG1 and MUTYH. Regardless of DNA glycosylase activity, OG in promoter regions correlated with expression of genes related to metabolic processes and damage response pathways indicating that OG functions as a cellular stress sensor to regulate transcription. Our work provides novel insights into the mechanism underlying transcriptional regulation by OG and DNA glycosylases OGG1 and MUTYH and suggests that oxidative DNA damage accumulation and its repair utilize different pathways.

Reduced organ damage accumulation in adult patients with SLE on anifrolumab plus standard of care compared to real-world external controls.

Anifrolumab is approved for the treatment of systemic lupus erythematosus (SLE). We aimed to determine if anifrolumab plus standard of care (SOC) was associated with reduced organ damage accumulation in adult patients with moderately to severely active SLE compared to real-world (RW) external controls from the University of Toronto Lupus Clinic (UTLC) cohort who received SOC only. Patients who initiated 300 mg anifrolumab in the TULIP (Treatment of Uncontrolled Lupus via the Interferon Pathway) trials were included in the anifrolumab arm; key eligibility criteria were applied to the UTLC to create the RW SOC arm. Propensity score and censoring weighting were used to account for baseline confounding and loss to follow-up. The primary endpoint was change in Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI) score from baseline to week 208, and the secondary endpoint was time to first SDI score increase. 354 patients were included in the anifrolumab arm, and 561 patients were included in the RW SOC arm. Following weighting, mean change in SDI was 0.416 points lower (95% CI: -0.582, -0.249; P < .001) in the anifrolumab arm than in the RW SOC arm. Patients in the anifrolumab arm were 59.9% less likely (hazard ratio: 0.401; 95% CI: 0.213, 0.753, P = .005) to experience an increase in SDI within 208 weeks. Patients who received anifrolumab accumulated significantly less organ damage after 208 weeks than patients who received RW SOC. The addition of anifrolumab to SOC is effective at preventing and/or delaying organ damage in patients with moderately to severely active SLE.

Effect of acute performance fatigue on tibial bone strain during basketball maneuvers.

The tibia is one of the most common sites for bone stress injury (BSI) in active individuals. BSIs are thought to occur in response to damage accumulation from repetitive loading below the tissue's yield limit. The effect of fatigue on musculoskeletal biomechanics and tibial bone strain during athletic movements remains unclear. In this study, participant-specific finite element (FE) and musculoskeletal models in 10 collegiate-basketball players were used to analyze the effect of acute performance fatigue on joint kinematics and torques, ground reaction forces (GRFs), and the magnitude and distribution of tibial bone strains during select basketball maneuvers. Participants were fatigued by performing repeated exercises wearing a weighted vest until their vertical jump height decreased by 20 %. Fatigue reduced the vertical GRF during midstance of a jump task, and lowered hip and knee peak extension torques and ankle plantarflexion. However, fatigue had limited impact on tibial bone strain magnitude and distribution during jumping. In contrast, there was a shift in peak strain timing following fatigue during a lateral cut task and reduced strain at various times of stance during sprinting. The results suggest that fatigue was induced and, if anything, reduced tibial bone strain. As increased bone strain is thought to be associated with increased BSI risk, the reduced strain observed in the current study suggests that fatigue may actually be partly protective, possibly as a result of reduced muscle activation and force production.

Molecular Dynamics Simulation of Low-Cycle Fatigue Behavior of Single/Polycrystalline Iron

The fatigue plastic mechanism and dislocation characteristics of engineering materials are the key to studying fatigue damage. In this study, the molecular dynamics (MD) method was employed to investigate the microstructural characteristics and fatigue mechanical properties of both single-crystalline and polycrystalline iron under varying strain amplitudes associated with cyclic hardening, cyclic softening, and cyclic saturation. The occurrence, accumulation, and formation process of the local plastic fatigue damage of monocrystalline/polycrystalline iron under fatigue load are discussed. The local plastic initiation and accumulation of single-crystal iron occur at the intersection of slip planes, which is the dislocation source. The 1/2&lt;111&gt; dislocation plays an important role in the fatigue plastic accumulation of single-crystal iron. Polycrystalline iron undergoes grain rotation and coalescence during cyclic loading. The grain size responsible for plastic deformation gradually increases. The initiation and accumulation of local plasticity occurs at the grain boundary, which eventually leads to fatigue damage at the grain boundary.

Research on the Accumulative Damage of Flywheels Due to In-Space Charging Effects

High-speed rotating flywheel bearings, designed for space applications, generate a high-resistance hydrodynamic lubrication film, which isolates the rotor, transforming it into a conductor. This phenomenon introduces a novel failure mode—flywheel bearing electrical damage caused by space charging effects. This paper first reviews the sources of common shaft voltages in flywheels and the mechanisms of electrical damage and improves the principle of deep charge causing shaft voltages in flywheel bearings, proposing that surface charge is another source of shaft voltages. The quantified analysis model of flywheel bearing electrical damage in relation to rotational speed and high-energy electron flux is derived, indicating that the damage caused by space charge–discharge to the bearing is of small magnitude and only becomes apparent after long-term accumulation, thus being easily overlooked. Based on the causal chain of electrical damage, a correlation analysis model consistent with physical principles is constructed, and the correlation between on-orbit anomalies of the flywheel and high-energy electron flux is confirmed through the use of big data. Preliminary experiments are conducted to validate all of the research results. Finally, suggestions are given for the reliable design, application, and testing of flywheels.

Prevalence of metabolically associated steatotic liver disease in the elderly: analysis and perspectives

Metabolically associated steatotic liver disease (MASLD) is becoming a major public health problem, especially among the elderly. The recent change in nomenclature from “nonalcoholic fatty liver disease” to “MASLD” reflects a more accurate understanding of the pathogenesis of the disease, linking it to metabolic disorders such as insulin resistance, obesity, and metabolic syndrome. This new terminology emphasizes the importance of a comprehensive approach to the diagnosis and treatment of the disease, given its close association with metabolic disorders and cardiovascular risk. Current estimates suggest that 24 % of the adult population, i. e. one billion people worldwide, suffer from the disease. Interestingly, the prevalence of fatty liver disease peaks between the ages of 40–50 years in men and 60–69 years in women, and then declines slightly in older age groups (over 70 years). The prevalence of MASLD is increasing worldwide, reflecting the increasing incidence of obesity, type 2 diabetes mellitus, and metabolic syndrome. The elderly are particularly susceptible to MASLD due to age-related metabolic changes, comorbidities. Aging is associated with changes in lipid metabolism, insulin resistance, and increased fat mass, which predispose the elderly to hepatic lipid accumulation and subsequent liver damage. In addition, age-related decline in the liver»s regenerative capacity may exacerbate the progression of hepatic steatosis to advanced stages such as steatohepatitis and hepatic fibrosis. However, MASLD in the elderly remains under-recognized and under-diagnosed, posing challenges for timely intervention and treatment. Prospects for addressing MASLD in the elderly emphasize the importance of comprehensive geriatric assessment, including evaluation of metabolic health and liver function.

Global transcriptome profiling of ST09 treated breast cancer cells identifies miR-197-5p/GPX3 antioxidant axis as a regulator of tumorigenesis.

ROS (Reactive Oxygen Species) has a dual role in tumorigenesis. Some cancers have high ROS conditions, and others have low ROS. TNBC thrives on high ROS compared to other Breast Cancer subtypes. Several antioxidant enzymes catalyze the detoxification of reactive oxygen species and prevent free radicals from damaging DNA and accumulation of mutation. Curcumin, a polyphenol dietary supplement, acts as a potent antioxidant, is known to reduce inflammation, and has anticancer properties. Here, we aim to understand alterations in the transcriptome (miRNA and mRNA expression) induced by ST09 in breast cancer cell lines. We identified an antioxidant system that is upregulated in breast cancer cell lines. Among the antioxidant enzymes regulated by miRNA was GPX3. A novel miRNA-mRNA antioxidant axis, miR-197-5p/GPX3, was observed in the TNBC cell line. We further validated the regulation of GPX3 by miRNA using luciferase assay. GPX3 overexpression, knockdown, and activity assay indicated the anti-tumorigenic role of GPX3 in the TNBC cell line. Further, treatment of TNBC xenograft with ST09 showed tumor reduction in vivo. ST09 potentiates the effect of standard-of-care (SOC) drug Cisplatin in vivo. ST09 can be exploited as a single chemotherapeutic agent or in combination treatment modalities, reducing the dosage of potent drugs.

The spectral analysis of the state parameters of technical systems in the regular and damaged states

It is noted that reaction of bearing elements of structures and engineering components to service loadings, impacts of physical fields and corrosive environments is initiation not only fields of stresses and strains, but also fields of damages. At the same time depending on conditions of a loading and environment various mechanisms of accumulation of damages and fracture which indicators are essential changes in spectra of a response of technical systems to different impacts are realized. The analysis of parameters of a state of such systems by registration of spectral characteristics of service processes allows to carry out estimations of levels of their damage in rather full degree. On the basis of results of research of service states of technical systems on spectral diagnostic parameters approaches to the analysis of amplitude-frequency characteristicses of their actual states both in the regular allowed states, and upon transition to dangerous states owing to accumulation in them of dangerous service damages are offered. At the same time criteria of transition of technical systems from regular in emergency and catastrophic states at accumulation of critical limits of damage are formulated. Examples of the dispersed initiation of microcracks in material of structures parts at a cyclic deformation with their propagation in the main fractures, and also examples of the analysis of dynamic states on vibration spectra of a response of simple and compound technical systems with the crack which arose in them and with existence of defects are given. At the same time the possibility of obtaining initial computation and experimental information on parameters of a stress-strain state and damage of installation with use of methods of the spectral analysis of a response of a compound structure to vibration impact as a result of initiation of damage of its separate parts is shown. Results of such spectral analysis can be used for diagnostics and monitoring of conditions of regular service of high-loaded installations of a technosphere and transition of their states to limit emergency and catastrophic in relation to objects of power engineerings, space-rocket and aircraft equipment.

The Time-Domain Design Stress Method for Fatigue Analysis of the Reactor Pressure Vessel in Floating Nuclear Power Plants

Nuclear power technology has rapidly advanced with the growing global demand for clean energy. As one of the core components of nuclear power plants (NPPs), the design and lifespan evaluation of reactor pressure vessels (RPVs) are critically important. However, while fatigue analysis methods for RPVs in land-based NPPs are relatively well established, the application of these methods to floating nuclear power plants (FNPPs) faces great challenges. Existing analysis methods are difficult to directly apply, and no widely accepted fatigue analysis approach currently exists for this context due to the complex working conditions in marine environments. A time-domain design stress (TDDS) method is developed in this study for the fatigue analysis of RPVs in FNPPs. This method systematically analyzes the impacts of wave loads, internal pressure, and thermal effects on the fatigue life of RPVs by simplifying the wave environment into a time-domain model of roll and pitch motions and adopting the regular wave superposition techniques. This method further adjusts the initial phases of regular waves considering the uncertainty of various load combinations, and superimposes the stress components caused by regular waves with different initial phases, thermal loads, and pressure loads. Subsequently, stress history curves are analyzed using the rainflow counting method, and combined with the damage accumulation theory, the upper and lower limits of fatigue damage are obtained. The results demonstrate that compared to traditional methods in time-domain analysis, the proposed TDDS method provides greater accuracy in evaluating the fatigue life of RPVs in FNPPs, with the average error in fatigue damage values being only 0.033%. Furthermore, the TDDS method reduces analysis time by approximately 70%, which significantly improves computational performance. These findings underscore the reliability and effectiveness of this method in practical applications.

Mechanical Response of Mudstone Based on Acoustic Emission Fractal Features

In this study, the effect of the stress amplitude on the mechanical behavior of mudstone was systematically investigated by cyclic loading and unloading experiments and acoustic emission (AE) monitoring. The results show that at low-stress amplitudes, mudstone specimens show better elastic recovery ability, lower damage accumulation and higher structural stability. At high-stress amplitudes, the irreversible damage of the mudstone increases significantly, the internal fractures gradually expand and penetrate through, and the risk of instability increases significantly. This is manifested by the gradual increase in cumulative irreversible strain of mudstone at different stress amplitudes, up to 0.144%. In addition, different stress amplitudes have significant effects on energy evolution characteristics, with low-stress amplitudes mainly showing elastic deformation and a high percentage of recoverable energy, while high-stress amplitudes show a high percentage of dissipated energy. Under the condition of high-stress amplitude, such as the mudstone specimen #4, the percentage of tensile failure is 81.15%. Tensile failure dominates at all stress amplitudes, where the failure mechanism within mudstone is mainly characterized by the extension of tensile-type fractures. Through the multifractal analysis of AE signals, this study reveals the effect of the stress amplitude on the fracture extension mode and failure mechanism of mudstone. As the stress amplitude increases, Δα and Δf show an increasing trend. This indicates that the fracture extension process transforms from a relatively homogeneous and simple mode to a more inhomogeneous and complex mode. This transformation reflects the nonlinear and multiscale fracture characteristics of mudstone under high-stress conditions. The results of this study help to understand the mechanical behavior of mudstone under cyclic loading during coal mining and provide theoretical support for safe coal production.