Journal articles: 'Damage mechanism'

1

Hahnel, Robin. "Wanted: A Pollution Damage Revealing Mechanism." Review of Radical Political Economics 49, no. 2 (October 14, 2015): 233–46. http://dx.doi.org/10.1177/0486613415608134.

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This article proposes a theoretical, incentive compatible, pollution damage revealing mechanism to induce people to reveal how much they are damaged by environmental degradation so polluters can be charged for the amount of damage caused. The mechanism is embedded in the participatory planning procedure that is part of a theoretical alternative to capitalism known as a “participatory economy.”

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Hull, Derek, and Yi Bing Shi. "Damage mechanism characterization in composite damage tolerance investigations." Composite Structures 23, no. 2 (January 1993): 99–120. http://dx.doi.org/10.1016/0263-8223(93)90015-i.

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Guo, Hongrui, Huan Liu, Hongbin Wu, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li, Xun Wang, and Ling Zhao. "Nickel Carcinogenesis Mechanism: DNA Damage." International Journal of Molecular Sciences 20, no. 19 (September 21, 2019): 4690. http://dx.doi.org/10.3390/ijms20194690.

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Nickel (Ni) is known to be a major carcinogenic heavy metal. Occupational and environmental exposure to Ni has been implicated in human lung and nasal cancers. Currently, the molecular mechanisms of Ni carcinogenicity remain unclear, but studies have shown that Ni-caused DNA damage is an important carcinogenic mechanism. Therefore, we conducted a literature search of DNA damage associated with Ni exposure and summarized known Ni-caused DNA damage effects. In vitro and vivo studies demonstrated that Ni can induce DNA damage through direct DNA binding and reactive oxygen species (ROS) stimulation. Ni can also repress the DNA damage repair systems, including direct reversal, nucleotide repair (NER), base excision repair (BER), mismatch repair (MMR), homologous-recombination repair (HR), and nonhomologous end-joining (NHEJ) repair pathways. The repression of DNA repair is through direct enzyme inhibition and the downregulation of DNA repair molecule expression. Up to now, the exact mechanisms of DNA damage caused by Ni and Ni compounds remain unclear. Revealing the mechanisms of DNA damage from Ni exposure may contribute to the development of preventive strategies in Ni carcinogenicity.

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Shirai, Takashi, and Isao Ikemoto. "MECHANISM OF ALCOHOLIC TESTICULAR DAMAGE." Japanese Journal of Urology 83, no. 3 (1992): 305–14. http://dx.doi.org/10.5980/jpnjurol1989.83.305.

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Pocheptsova, E. G., I. V. Kuznetsov, and O. E. Matuzok. "Heart trauma: blunt damage mechanism." Medicine of Ukraine, no. 8(244) (September 26, 2020): 44–46. http://dx.doi.org/10.37987/1997-9894.2020.8(244).215482.

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Bi, Xin. "Mechanism of DNA damage tolerance." World Journal of Biological Chemistry 6, no. 3 (2015): 48. http://dx.doi.org/10.4331/wjbc.v6.i3.48.

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Besterci, Michal, Jozef Ivan, Ladislav Pešek, Oksana Velgosová, and Pavol Hvizdoš. "Damage mechanism of Al–12Al4C3." Materials Letters 58, no. 6 (February 2004): 867–70. http://dx.doi.org/10.1016/j.matlet.2003.08.001.

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Chen, Y. L., and J. Israelachvili. "New Mechanism of Cavitation Damage." Science 252, no. 5009 (May 24, 1991): 1157–60. http://dx.doi.org/10.1126/science.252.5009.1157.

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Bartkowiak, Miriam, Ludwig Schoettl, Peter Elsner, and Kay André Weidenmann. "Combined In Situ X-Ray Computed Tomography and Acoustic Emission Analysis for Composite Characterization - A Feasibility Study." Key Engineering Materials 809 (June 2019): 604–9. http://dx.doi.org/10.4028/www.scientific.net/kem.809.604.

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Fiber reinforced plastics show a wide range of different damage mechanisms such as matrix cracking, fiber breakage and interface failure. These can be observed in damaged specimens by means of volumetric images acquired by computed tomography (CT). As each failure mechanism causes a characteristic acoustic emission (AE) signal, AE analysis is a promising tool to identify damage mechanisms and offers the advantage that a real-time observation of the damage evolution during the testing period is possible. For a correlation of damage mechanisms and AE events, AE analysis was combined with in- situ CT measurements. This combined approach was validated by means of a 3-point-bending test on a discontinuous glass fiber reinforced sheet molding compound (GF-SMC) in which AE signals were acquired during loading using two high frequency piezoelectric sensors. At times of increasing AE activity, the test was interrupted in order to carry out a CT-scan of the specimen under load. AE events could subsequently be linked with the damage mechanisms observed in the CT-scans at different stages of damage to identify signal features that are characteristic for a certain mechanism. The sources of the signals could be localized and were in line with the actual location of damage.

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Christ, H. J., A. Jung, H. J. Maier, and R. Teteruk. "Thermomechanical fatigue—damage mechanisms and mechanism-based life prediction methods." Sadhana 28, no. 1-2 (February 2003): 147–65. http://dx.doi.org/10.1007/bf02717131.

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Zhao, Yongqiang, Quansheng Li, Kai Zhang, Yingming Yang, Dongxiao Zhang, Weilong Zhang, and Xiaojun Ding. "Experimental Study on Mechanical Properties and Failure Mechanism of Damaged Sandstone." Sustainability 15, no. 1 (December 28, 2022): 555. http://dx.doi.org/10.3390/su15010555.

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Solid materials such as rocks can contain primary defects, and internal defects are activated in the event of mining disturbance, which causes rock damage and destruction. Therefore, it is of great significance for rock engineering to study the mechanical properties and failure mechanism of damaged rock. In this study, damaged prefabricated crack sandstone specimens were prepared with the cyclic loading-unloading test, and the uniaxial loading test was carried out with damaged specimens. The evolution law of peak strength, elastic modulus, and peak strain of specimens with different damage degrees was studied, the quantitative relationship between the P-wave velocity and the damage degree was obtained, and the acoustic emission (AE) count and energy evolution characteristics of specimens with different damage degrees were analyzed. The energy evolution law of damaged specimens was revealed, and with the increase in damage degree, the elastic energy stored in the specimens can be converted into crack propagation more quickly, and the dissipated energy density increases rapidly, resulting in complete rock failure. The research results can provide theoretical support for the stability analysis and control of underground engineering rock mass in the event of multiple disturbances.

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Zheng, Sheng Bao, Shu Ping Jiang, and Xiao Wen Wang. "Research on the Mechanism of Earthquake Damage of Tunnels." Advanced Materials Research 538-541 (June 2012): 705–8. http://dx.doi.org/10.4028/www.scientific.net/amr.538-541.705.

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Many tunnels were subjected earthquake. According to the damaged features of tunnels in earthquakes indoorsand outdoors, the macroscopic damage of tunnels are summarized. On the base of the damage manifestation, the failure mechanism of tunnel damage is preliminarily analyzed. Comparison with the failure mode on the shaking table model test has been made, and some suggestion of on the weak links at the tunnel entrance, faults and shallow buried section for designers has been put forward.

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Dong, Jiwei, and Ningfei Huo. "Progressive tensile damage simulation and strength analysis of three-dimensional braided composites based on three unit-cells models." Journal of Composite Materials 52, no. 15 (October 30, 2017): 2017–31. http://dx.doi.org/10.1177/0021998317737828.

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In order to explore the micro-failure mechanism and predict tensile strength of three-dimensional braided composites, the three unit-cells models, namely interior cell, surface cell and corner cell, are established to simulate progressive damage of these materials. Macro model is firstly created and divided into three kinds of unit cells by their periodical distributions. A criterion is approached to determine damage and its pattern of each element, and stiffness degradation is implemented for the damaged elements with geometric damage theory. Periodical boundary conditions are applied on the models to calculate micro-stress and damage propagation is simulated with the increase of load. Each type of damage and its percentage is obtained by simulation and micro-failure mechanism is analyzed. Furthermore, the tensile strengths are predicted from calculated stress–strain curves. From simulation, composites with large braiding angle have more complicated micro-failure mechanism than composites with small braiding angle. It is also observed that there are more damages in surface cell than in interior cell and the damage types in the surface cell are various. The predicted results on the three unit-cells models agree well with the experimental data and are more accurate than only using an interior-cell model.

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Petruseva, I. O., A. N. Evdokimov, and O. I. Lavrik. "Molecular Mechanism of Global Genome Nucleotide Excision Repair." Acta Naturae 6, no. 1 (March 15, 2014): 23–34. http://dx.doi.org/10.32607/20758251-2014-6-1-23-34.

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Nucleotide excision repair (NER) is a multistep process that recognizes and eliminates a wide spectrum of damage causing significant distortions in the DNA structure, such as UV-induced damage and bulky chemical adducts. The consequences of defective NER are apparent in the clinical symptoms of individuals affected by three disorders associated with reduced NER capacities: xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD). These disorders have in common increased sensitivity to UV irradiation, greatly elevated cancer incidence (XP), and multi-system immunological and neurological disorders. The eucaryotic NER system eliminates DNA damage by the excision of 24-32 nt single-strand oligonucleotides from a damaged strand, followed by restoration of an intact double helix by DNA repair synthesis and DNA ligation. About 30 core polypeptides are involved in the entire repair process. NER consists of two pathways distinct in initial damage sensor proteins: transcription-coupled repair (TC-NER) and global genome repair (GG-NER). The article reviews current knowledge on the molecular mechanisms underlying damage recognition and its elimination from mammalian DNA.

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15

You Lung Chen, Tonya Kuhl, and Jacob Israelachvili. "Mechanism of cavitation damage in thin liquid films: Collapse damage vs. inception damage." Wear 153, no. 1 (March 1992): 31–51. http://dx.doi.org/10.1016/0043-1648(92)90259-b.

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16

Liu, Jin Bao, Jian Rong Xue, and Wei Zhu. "Damage Mechanism and Fracture Process of Concrete Gravity Dam under Earthquake Action." Advanced Materials Research 430-432 (January 2012): 142–45. http://dx.doi.org/10.4028/www.scientific.net/amr.430-432.142.

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Based on plastic-damage constitutive model of concrete, the developing process of damage domains is simulated for the earthquake analysis of concrete dam by taking account of the change of strain speed and stiffness degradation effect caused by material damage. The plastic-damage constitutive model is applied and the dam-reservoir dynamic interaction resulting from the transverse component of ground motion is modeled using the developed and generalized Westergaard formula added mass technique. Numerical simulation results show that the damaged domains mainly distribute at the change in geometry of upper part of the dam and vertical construction joints. The damaged domains of dam are same as the maximum tensile stress because the tensile strength of concrete is less its compress strength.

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Fan Juping, 范菊平, 张玲 Zhang Ling, and 贾新章 Jia Xinzhang. "HPM damage mechanism on bipolar transistors." High Power Laser and Particle Beams 22, no. 6 (2010): 1319–22. http://dx.doi.org/10.3788/hplpb20102206.1319.

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18

KONDO, T., Y. OGAWA, S. SUGIYAMA, T. ITO, T. SATAKE, and T. OZAWA. "Mechanism of isoproterenol induced myocardial damage." Cardiovascular Research 21, no. 4 (April 1, 1987): 248–54. http://dx.doi.org/10.1093/cvr/21.4.248.

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19

Xiao, Yingchun. "A multi-mechanism damage coupling model." International Journal of Fatigue 26, no. 11 (November 2004): 1241–50. http://dx.doi.org/10.1016/j.ijfatigue.2004.02.004.

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20

Zhang, Hui, Ren Shu Yang, Ling Zhao, and Hui Cao. "Mechanism of High-strength Concrete Damage Evolution Based on CT Observation." Advanced Materials Research 168-170 (December 2010): 498–504. http://dx.doi.org/10.4028/www.scientific.net/amr.168-170.498.

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To study damage evolution of high-strength concrete under the frozen environment, based on the background of YunCheng auxiliary shaft engineering, this paper studies the damage pattern of C100 concrete under loading by applying the method of industry CT scanning. It aims at showing the evolution process of concrete damage by contrasting of the damage factor on standard curing and negative temperature curing condition, which analyzes the trend of damage modulus of elasticity of C100 high-strength concrete uniaxial compression conditioned from the micro level, combining change of fractal dimension of concrete. The results showed that the change of fractal dimension can reflect the evolution trend of inner damage of concrete, fractal dimension is related with the size of concrete when it damaged. Negative temperature frozen brings about the increase of inner hole of high-strength concrete and decrease of modulus of elasticity, and the ratio of damage energy release rate and strain energy release rate decrease, the energy needed by concrete damage is very low. Moreover, the nonlinear positive correlation between fractal dimension and damage factor of high-strength concrete has been gained.

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21

Dmitrieva, Natalia I., Dmitry V. Bulavin, and Maurice B. Burg. "High NaCl causes Mre11 to leave the nucleus, disrupting DNA damage signaling and repair." American Journal of Physiology-Renal Physiology 285, no. 2 (August 2003): F266—F274. http://dx.doi.org/10.1152/ajprenal.00060.2003.

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High NaCl causes DNA double-strand breaks and cell cycle arrest, but the mechanism of its genotoxicity has been unclear. In this study, we describe a novel mechanism that contributes to this genotoxicity. The Mre11 exonuclease complex is a central component of DNA damage response. This complex assembles at sites of DNA damage, where it processes DNA ends for subsequent activation of repair and initiates cell cycle checkpoints. However, this does not occur with DNA damage caused by high NaCl. Rather, following high NaCl, Mre11 exits from the nucleus, DNA double-strand breaks accumulate in the S and G2 phases of the cell cycle, and DNA repair is inhibited. Furthermore, the exclusion of Mre11 from the nucleus by high NaCl persists following UV or ionizing radiation, also preventing DNA repair in response to those stresses, as evidenced by absence of H2AX phosphorylation at places of DNA damage and by impaired repair of damaged reporter plasmids. Activation of chk1 by phosphorylation on Ser345 generally is required for DNA damage-induced cell cycle arrest. However, chk1 does not become phosphorylated during high NaCl-induced cell cycle arrest. Also, high NaCl prevents ionizing and UV radiation-induced phosphorylation of chk1, but cell cycle arrest still occurs, indicating the existence of alternative mechanisms for the S and G2/M delays. DNA breaks that occur normally during processes such as DNA replication and transcription, as well as damages to DNA induced by genotoxic stresses, ordinarily are rapidly repaired. We propose that inhibition of this repair by high NaCl results in accumulation of DNA damage, accounting for the genotoxicity of high NaCl, and that cell cycle delay induced by high NaCl slows accumulation of DNA damage until the DNA damage-response network can be reactivated.

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Koniushenko, Yana, Petro Pidyukov, Tetiana Ustymenko, Olha Khakhutsiak, and Mykhailo Gultai. "Damage compensation mechanism in the criminal process." Cuestiones Políticas 40, no. 72 (March 7, 2022): 48–68. http://dx.doi.org/10.46398/cuestpol.4072.03.

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It discusses the problematic issues of consideration and resolution in a criminal case of a civil claim for compensation for property damage or compensation for moral damage caused by a criminal offense. The essence and content of the "civil claim in the criminal process" is determined, the advantages are noted, and the problems of a civil lawsuit in the criminal process of Ukraine are discussed. The authors propose to consider the filing of a civil claim as a right of the victim, corresponding to the obligation of the criminal prosecutor's office and the court to take measures for the timely reparation of damages. Some reasons are revealed that complicate the implementation of the principle of inevitability of civil liability for a crime committed simultaneously with the procedure for convicting the perpetrator. As a conclsuion se proposes to develop new approaches to the institution of a civil lawsuit in the criminal process of Ukraine, contributing to the improvement of the activities of the criminal prosecution authorities and the court to restore the violated civil rights of victims of crime.

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Adams, James David. "Probable Causes of Alzheimer’s Disease." Sci 3, no. 1 (March 2, 2021): 16. http://dx.doi.org/10.3390/sci3010016.

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A three-part mechanism is proposed for the induction of Alzheimer’s disease: (1) decreased blood lactic acid; (2) increased blood ceramide and adipokines; (3) decreased blood folic acid. The age-related nature of these mechanisms comes from age-associated decreased muscle mass, increased visceral fat and changes in diet. This mechanism also explains why many people do not develop Alzheimer’s disease. Simple changes in lifestyle and diet can prevent Alzheimer’s disease. Alzheimer’s disease is caused by a cascade of events that culminates in damage to the blood–brain barrier and damage to neurons. The blood–brain barrier keeps toxic molecules out of the brain and retains essential molecules in the brain. Lactic acid is a nutrient to the brain and is produced by exercise. Damage to endothelial cells and pericytes by inadequate lactic acid leads to blood–brain barrier damage and brain damage. Inadequate folate intake and oxidative stress induced by activation of transient receptor potential cation channels and endothelial nitric oxide synthase damage the blood–brain barrier. NAD depletion due to inadequate intake of nicotinamide and alterations in the kynurenine pathway damages neurons. Changes in microRNA levels may be the terminal events that cause neuronal death leading to Alzheimer’s disease. A new mechanism of Alzheimer’s disease induction is presented involving lactic acid, ceramide, IL-1β, tumor necrosis factor α, folate, nicotinamide, kynurenine metabolites and microRNA.

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Yang, X. H., Y. Zhang, Y. T. Hu, and C. Y. Chen. "Continuum Damage Mechanics for Thermo-Piezoelectric Materials." Journal of Mechanics 22, no. 2 (June 2006): 93–98. http://dx.doi.org/10.1017/s172771910000438x.

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AbstractWith rapidly increasing use of piezoelectric materials in high-temperature environment, it is becoming increasingly important for reliable design of piezoelectric devices to study thermo-electroelastic damage and fracture mechanism. As the first step, a thermo-piezoelectric damage constitutive model is presented from continuum damage mechanics and effective properties of a damaged material are connected with both damages and the initial coefficients according to the theorem of energy equivalence in this paper. Then the finite element equations for a thermo-electroelastic damage problem are given by use of the virtual work principle. Finally, as a numerical illustration example, damage fields around a crack-tip in a three-point bending PZT-5H beam subjected to different thermal loads are calculated and analyzed. It is shown from both the damage curves and contours that influence of environmental temperature on the mechanical damage distribution is great but slight on the electrical damage.

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Cosic, Mladen, and Stanko Brcic. "The development of controlled damage mechanisms-based design method for nonlinear static pushover analysis." Facta universitatis - series: Architecture and Civil Engineering 12, no. 1 (2014): 25–40. http://dx.doi.org/10.2298/fuace1401025c.

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This paper presents the original method of controlled building damage mechanisms based on Nonlinear Static Pushover Analysis (NSPA-DMBD). The optimal building damage mechanism is determined based on the solution of the Capacity Design Method (CDM), and the response of the building is considered in incremental situations. The development of damage mechanism of a system in such incremental situations is being controlled on the strain level, examining the relationship of current and limit strains in concrete and reinforcement steel. Since the procedure of the system damage mechanism analysis according to the NSPA-DMBD method is being iteratively implemented and designing checked after the strain reaches the limit, for this analysis a term Iterative-Interactive Design (IID) has been introduced. By selecting, monitoring and controlling the optimal damage mechanism of the system and by developed NSPA-DMBD method, damage mechanism of the building is being controlled and the level of resistance to an early collapse is being increased.

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Liu, H. T., L. Z. Sun, and H. C. Wu. "Monte Carlo Simulation of Particle-Cracking Damage Evolution in Metal Matrix Composites." Journal of Engineering Materials and Technology 127, no. 3 (March 10, 2005): 318–24. http://dx.doi.org/10.1115/1.1925291.

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In the modeling of microstructural damage mechanisms of composites, damage evolution plays an important role and has significant effects on the overall nonlinear behavior of composites. In this study, a microstructural Monte Carlo simulation method is proposed to predict the volume fraction evolution of damaged particles due to particle-cracking for metal matrix composites with randomly distributed spheroidal particles. The performance function is constructed using a stress-based damage criterion. A micromechanics-based elastoplastic and damage model is applied to compute the local stress field and to estimate the overall nonlinear response of the composites with particle-cracking damage mechanism. The factors that affect the damage evolution are investigated and the effects of particle shape and damage strength on damage evolution are discussed in detail. Simulation results are compared with experiments and good agreement is obtained.

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Innokentev, Aleksei, and Tomotake Kanki. "Mitophagy in Yeast: Molecular Mechanism and Regulation." Cells 10, no. 12 (December 17, 2021): 3569. http://dx.doi.org/10.3390/cells10123569.

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Mitophagy is a type of autophagy that selectively degrades mitochondria. Mitochondria, known as the “powerhouse of the cell”, supply the majority of the energy required by cells. During energy production, mitochondria produce reactive oxygen species (ROS) as byproducts. The ROS damage mitochondria, and the damaged mitochondria further produce mitochondrial ROS. The increased mitochondrial ROS damage cellular components, including mitochondria themselves, and leads to diverse pathologies. Accordingly, it is crucial to eliminate excessive or damaged mitochondria to maintain mitochondrial homeostasis, in which mitophagy is believed to play a major role. Recently, the molecular mechanism and physiological role of mitophagy have been vigorously studied in yeast and mammalian cells. In yeast, Atg32 and Atg43, mitochondrial outer membrane proteins, were identified as mitophagy receptors in budding yeast and fission yeast, respectively. Here we summarize the molecular mechanisms of mitophagy in yeast, as revealed by the analysis of Atg32 and Atg43, and review recent progress in our understanding of mitophagy induction and regulation in yeast.

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Verma, Nagendra, Matteo Franchitto, Azzurra Zonfrilli, Samantha Cialfi, Rocco Palermo, and Claudio Talora. "DNA Damage Stress: Cui Prodest?" International Journal of Molecular Sciences 20, no. 5 (March 1, 2019): 1073. http://dx.doi.org/10.3390/ijms20051073.

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DNA is an entity shielded by mechanisms that maintain genomic stability and are essential for living cells; however, DNA is constantly subject to assaults from the environment throughout the cellular life span, making the genome susceptible to mutation and irreparable damage. Cells are prepared to mend such events through cell death as an extrema ratio to solve those threats from a multicellular perspective. However, in cells under various stress conditions, checkpoint mechanisms are activated to allow cells to have enough time to repair the damaged DNA. In yeast, entry into the cell cycle when damage is not completely repaired represents an adaptive mechanism to cope with stressful conditions. In multicellular organisms, entry into cell cycle with damaged DNA is strictly forbidden. However, in cancer development, individual cells undergo checkpoint adaptation, in which most cells die, but some survive acquiring advantageous mutations and selfishly evolve a conflictual behavior. In this review, we focus on how, in cancer development, cells rely on checkpoint adaptation to escape DNA stress and ultimately to cell death.

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Wei, Jie, Yu Hong Chen, and Liang Jiang. "Damage Mechanism of Short Carbon Fiber Reinforced SiC-Based Composite." Key Engineering Materials 492 (September 2011): 39–42. http://dx.doi.org/10.4028/www.scientific.net/kem.492.39.

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Short carbon fiber reinforced silicon carbide (SiC)composites were prepared with boron (B) and carbon (C) as sintering additives via pressureless sintering at 2150°C. The damage mechanism of fiber was investigated as following: (1) The carbon fiber was seriously physically damaged in the process of material mixing; (2) The chemical damage of the carbon fiber was happened in the reaction with matrix as the high sintering temperature; (3) Numerous cavities exist between the carbon fiber and the matrix leads to the weak interfacial strength.

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Sydney Rose Addorisio, Rebecca Shteynberg, Matheus Dasilva, Jacob Mixon, Kyla Mucciarone, Lily Vu, Kristina Arsenault, et al. "Oxidative Stress Response in Bacteria: A Review." Fine Focus 8, no. 1 (July 18, 2022): 36–46. http://dx.doi.org/10.33043/ff.8.1.36-46.

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Oxidative Stress Response (OSR) is a defense mechanism used to maintain cellular homeostasis after an increase in levels of Reactive Oxygen Species (ROS). Due to ROS, cell components are vulnerable to damage including the membrane and DNA - which can impact essential functions and lead to cellular death. Without repair, damages caused by ROS have the potential to disrupt cell function in an irreparable manner. Bacterial cells respond to ROS using both endogenous and exogenous pathways depending on their method of metabolism and evolutionary ability. Bacteria have developed regulatory mechanisms to contain damage and are also known to use antioxidants as defense. In this review we will cover the damage induced by ROS to different cellular structures, and mechanisms of OSR used by bacterial cells to promote survival.

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ter Keurs, Henk EDJ, Ying Ming Zhang, Allen W. Davidoff, Penelope A. Boyden, Yu-ji Wakayama, and Masahito Miura. "Damage induced arrhythmias: mechanisms and implications." Canadian Journal of Physiology and Pharmacology 79, no. 1 (January 1, 2001): 73–81. http://dx.doi.org/10.1139/y00-114.

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Little is known about the role played by non-uniform myocardial stress and strain distributions and by non-uniform excitation contraction coupling in mechanisms underlying the premature beats that initiate an arrhythmia. We will review the evidence in support of a mechanism in which both non-uniform contraction and increased Ca2+ load of cells adjacent to acutely damaged cells are essential in the "spontaneous" generation of Ca2+ transients during the relaxation phase of the electrically driven twitch. The putative mechanism of initiation of the propagating Ca2+ waves involves feedback of rapid length (or force) changes to dissociation of Ca2+ from the contractile filaments. A novel aspect of this concept is that these mechanically elicited Ca2+ transients induce propagating Ca2+ waves that travel into the adjacent normal myocardium and cause after-depolarizations, which, in turn, may cause premature action potentials. These premature action potentials will further load the cells with Ca2+, which promotes the subsequent generation of propagating Ca2+ transients and leads to triggered arrhythmias. The damage-induced premature beats may also initiate re-entry arrhythmias in non-uniform myocardium. These observations strongly support the concept that abnormal cellular Ca2+ transport plays a crucial role in the initiation of arrhythmias in damaged and non-uniform myocardium.Key words: cardiac muscle, excitation-contraction coupling, damage, Ca2+, and arrhythmias.

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Lu, Ling, and Yu Lin Yang. "Experimental Study of Failure Performances of 51306-Coated Bearings under Lubricant Interruption Condition." Advanced Materials Research 383-390 (November 2011): 3876–81. http://dx.doi.org/10.4028/www.scientific.net/amr.383-390.3876.

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Some terrible disasters of aircrafts were caused by inadequate lubrication or interruption of lubricant delivery of the gas turbine engine mainshaft bearings. This paper introduces the design of the test equipment, performs the experiments of failure performance for 51306 coated bearings to respond to oil interruption under the actual situation. The main failure performance of test coated bearings has been demonstrated to be the cage damage of the test coated bearing. The failure mechanism model of the damaged cage of test coated bearings under oil interruption condition is established for the failure analysis of damage cages. The failure mechanism of the damaged cages is revealed. The main reason for the damages of test coated bearing cages under lubricant interruption condition is that the perpendicular component force acted on the cage increases continually to go with the increase of the friction force between the balls and the cage due to inadequate lubrication until the cage is broken.

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Guo, Peiyan, Ning Ma, Jingbo Shan, Techang Chen, Yujie Zhang, Sa Zhou, and Wenjian Ma. "Exogenous damage causes cell DNA damage through mediated reactive oxygen levels." E3S Web of Conferences 131 (2019): 01018. http://dx.doi.org/10.1051/e3sconf/201913101018.

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Many anti-tumor drugs can induce tumor apoptosis by increasing intracellular ROS. In the present study, we build a model which did not directly cause DNA damage, but simulated damage products. The model of this injury was transferred into the cell so that the cell’s damage recognition mechanism mistakenly recognized that its own DNA was damaged, which in turn induced a response. Based on this model, the damaged plasmids (exogenous DNA damage) were transferred into the cells and the amount of reactive oxygen in the cells was improved, and DNA damage of the cells was increased. Therefore, exogenous DNA damage can affect the accumulation of damage in cells by affecting the level of reactive oxygen species, which provides a reference for DNA damage repair research.

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Wang, Shu Hong, Heek Wang Lee, Xing Dong Zhao, and Ahmad Bashir. "An Experimental Study of Excavation Damaged Zone in Anisotropic Rock." Key Engineering Materials 353-358 (September 2007): 905–8. http://dx.doi.org/10.4028/www.scientific.net/kem.353-358.905.

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When a tunnel or an underground structure is excavated in rock mass, rock disturbed or damaged zone (EDZ) is formed around the excavation due to the stress concentration resulting from stress redistribution. Recent studies on the rock EDZ revealed it’s important to structural stability around underground opening. In this study, the fracture and damage mechanisms of rock induced by the accumulation of microcracks were investigated by AE tests. The results of the experiments showed that tensile failure was the major microscopic failure mechanism of rock in excavation damaged and disturbed zone. The expression of the damage magnitudes in each AE source leads to accurate prediction of macroscopic failure mechanisms. In addition, the orientation of the macroscopic failure plane could be estimated by the orientational distribution of microcracks.

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Chen, Mingjun, Wenyu Ding, Jian Cheng, Hao Yang, and Qi Liu. "Recent Advances in Laser-Induced Surface Damage of KH2PO4 Crystal." Applied Sciences 10, no. 19 (September 23, 2020): 6642. http://dx.doi.org/10.3390/app10196642.

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As a hard and brittle material, KDP crystal is easily damaged by the irradiation of laser in a laser-driven inertial confinement fusion device due to various factors, which will also affect the quality of subsequent incident laser. Thus, the mechanism of laser-induced damage is essentially helpful for increasing the laser-induced damage threshold and the value of optical crystal elements. The intrinsic damage mechanism of crystal materials under laser irradiation of different pulse duration is reviewed in detail. The process from the initiation to finalization of laser-induced damage has been divided into three stages (i.e., energy deposition, damage initiation, and damage forming) to ensure the understanding of laser-induced damage mechanism. It is clear that defects have a great impact on damage under short-pulse laser irradiation. The burst damage accounts for the majority of whole damage morphology, while the melting pit are more likely to appear under high-fluence laser. The three stages of damage are complementary and the multi-physics coupling technology needs to be fully applied to ensure the intuitive prediction of damage thresholds for various initial forms of KDP crystals. The improved laser-induced damage threshold prediction can provide support for improving the resistance of materials to various types of laser-induced damage.

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Zhi, Xiang Cao, Jia Zhu Xue, and Xiu Li Cao. "The Research on Damage and Failture Mechanism of Drivepipe under Seismic Load." Advanced Materials Research 374-377 (October 2011): 2096–99. http://dx.doi.org/10.4028/www.scientific.net/amr.374-377.2096.

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Geological factors and engineering factors is a major factor to damage, the drivepipe deformation under pressure seismic load which used to establish mathematical model of the mechanical model can calculated the stress and strain analysis of the casing. The drivepipe damage to this article on the mechanism research on the mechanical model of drivepipe analysis under Seismic load, based on the drivepipe through the focus on the impact and stress damage to the mechanical method of drivepipe deformation studies, and the models of a drivepipe failure mechanism of the mechanical and mathematical are established, which will scientifically, accurately predict the damaged drivepipe.

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Furtado, André, Hugo Rodrigues, António Arêde, and Humberto Varum. "A Review of the Performance of Infilled RC Structures in Recent Earthquakes." Applied Sciences 11, no. 13 (June 24, 2021): 5889. http://dx.doi.org/10.3390/app11135889.

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The primary objective is to present the most representative types of damage observed in reinforced concrete (RC) structures due to earthquakes. Those damages are divided according to the ten most representative types. Examples and the main reasons that could trigger each failure mechanism are presented. The definition of these damage types is supported by post-earthquake damage reconnaissance missions in Sichuan (China) in 2008, L’Aquila (Italy) in 2009, Lorca (Spain) in 2011, Emilia-Romagna (Italy) in 2012, Gorkha (Nepal) in 2015, Muisne (Ecuador) in 2016 and Chiapas (Mexico) in 2017. An extensive discussion is presented concerning the infill walls’ seismic behaviour and their interaction with the RC structural elements. The presentation of the significant learnings and findings concerning the typical damage herein presented and discussed are compared with the common Southern European construction practice. The impact of the infill walls on the rehabilitation costs of damaged RC buildings is also studied. These costs are compared to those related to the structural damage and rehabilitation of the entire building structure to understand the impact of the infill walls. Finally, a case study is presented to study the effect of implementing simplified retrofitting strategies to prevent the soft-storey mechanism, one of the most common problems observed in past earthquake events.

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Zhang, R. H., Z. Z. Zhang, J. H. Liu, B. M. Zhao, and H. L. Zhao. "Study on impact damage mechanism of gun propellant based on bonding contact model." Journal of Physics: Conference Series 2478, no. 3 (June 1, 2023): 032083. http://dx.doi.org/10.1088/1742-6596/2478/3/032083.

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Abstract As the main launch energy of barrel weapon, the dynamic mechanical properties of gun propellant is very important to evaluate the launch safety. Through the transverse drop hammer impact damage test at room temperature and the initial dynamic vivacity ratio test of the propellant, the crack growth law and the fracture degree of the damaged propellant were obtained separately. Based on the Hertz-Mindlin bonding contact model, the discrete element mechanical model of the rosette 19-hole gun propellant was established, and the transverse drop hammer impact damage simulation was carried out. The damage mechanism of the bonding contact model and the fracture degree of the damaged propellant were acquired, which were also verified by tests. The results show that the bonding contact model can accurately describe the impact damage law of propellant. The research results of this paper can be used to predict the abnormal chamber pressure caused by fracture of propellant, provides a research means for mechanical property evaluation of 3D printing gun propellant, and lays a theoretical foundation for quantitative evaluation of launch safety.

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Murakami, Keisuke, Yoshiko Sakamoto, and Tetsuya Nonaka. "ANALYTICAL INVESTIGATION OF SLAB BRIDGE DAMAGES CAUSED BY TSUNAMI FLOW." Coastal Engineering Proceedings 1, no. 33 (October 25, 2012): 42. http://dx.doi.org/10.9753/icce.v33.structures.42.

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Tsunami caused by Tohoku earthquake in 2011 had brought fatal damages on many kinds of infrastructures such as ports, roads, bridges, lifelines and other important structures. Among those damages, we have found many bridges whose superstructure was flooded away by tsunami flow. This study proposes a composite simulation method in order to investigate the damage on bridges caused by tsunami action. The numerical method consists of a hydraulic analysis and a structural one. The proposed method is applied to the damaged bridge whose superstructure was flooded away by Tohoku earthquake tsunami. Based on the structural analysis, this study discusses the mechanism of damage caused by tsunami flow. Furthermore, this study confirms the validity of hydraulic analysis through physical experiment.

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Gong Shuili, 巩水利, 李晋炜 Li Jinwei, and 吴冰 Wu Bing. "Damage Behavior and Mechanism of Laser Welding." APPLIED LASER 31, no. 1 (2011): 39–44. http://dx.doi.org/10.3788/al20113101.0039.

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Lavella, M., and D. Botto. "Fretting wear damage mechanism of CoMoCrSi coatings." Wear 477 (July 2021): 203896. http://dx.doi.org/10.1016/j.wear.2021.203896.

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42

Hiraishi, H. "Reinforced Concrete Members with Damage Mitigation Mechanism." Concrete Journal 46, no. 3 (2008): 3–9. http://dx.doi.org/10.3151/coj1975.46.3_3.

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Mahmud, Khandakar Abu Hasan Al, Fuad Hasan, Md Ishak Khan, and Ashfaq Adnan. "Shock-Induced Damage Mechanism of Perineuronal Nets." Biomolecules 12, no. 1 (December 22, 2021): 10. http://dx.doi.org/10.3390/biom12010010.

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The perineuronal net (PNN) region of the brain’s extracellular matrix (ECM) surrounds the neural networks within the brain tissue. The PNN is a protective net-like structure regulating neuronal activity such as neurotransmission, charge balance, and action potential generation. Shock-induced damage of this essential component may lead to neuronal cell death and neurodegenerations. The shock generated during a vehicle accident, fall, or improvised device explosion may produce sufficient energy to damage the structure of the PNN. The goal is to investigate the mechanics of the PNN in reaction to shock loading and to understand the mechanical properties of different PNN components such as glycan, GAG, and protein. In this study, we evaluated the mechanical strength of PNN molecules and the interfacial strength between the PNN components. Afterward, we assessed the PNN molecules’ damage efficiency under various conditions such as shock speed, preexisting bubble, and boundary conditions. The secondary structure altercation of the protein molecules of the PNN was analyzed to evaluate damage intensity under varying shock speeds. At a higher shock speed, damage intensity is more elevated, and hyaluronan (glycan molecule) is most likely to break at the rigid junction. The primary structure of the protein molecules is least likely to fail. Instead, the molecules’ secondary bonds will be altered. Our study suggests that the number of hydrogen bonds during the shock wave propagation is reduced, which leads to the change in protein conformations and damage within the PNN structure. As such, we found a direct connection between shock wave intensity and PNN damage.

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44

Liu, Hankun, Xiaodan Ren, Shixue Liang, and Jie Li. "Physical Mechanism of Concrete Damage under Compression." Materials 12, no. 20 (October 11, 2019): 3295. http://dx.doi.org/10.3390/ma12203295.

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Although considerable effort has been taken regarding concrete damage, the physical mechanism of concrete damage under compression remains unknown. This paper presents, for the first time, the physical reality of the damage of concrete under compression in the view of statistical and probabilistic information (SPI) at the mesoscale. To investigate the mesoscale compressive fracture, the confined force chain buckling model is proposed; using which the mesoscale parameters concerned could be directly from nanoindentation by random field theory. Then, the mesoscale parameters could also be identified from macro-testing using the stochastic damage model. In addition, the link between these two mesoscale parameters could be established by the relative entropy. A good agreement between them from nano- and macro- testing when the constraint factor approaches around 33, indicates that the mesoscale parameters in the stochastic damage model could be verified through the present research. Our results suggest that concrete damage is strongly dependent on the mesoscale random failure, where meso-randomness originates from intrinsic meso-inhomogeneity and meso-fracture arises physically from the buckling of the confined force chain system. The mesoscale random buckling of the confined force chain system above tends to constitute the physical mechanism of concrete damage under compression.

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Horibe, Susumu, and Guen Choi. "Fatigue Damage of Ceramics and Its Mechanism." Materia Japan 35, no. 7 (1996): 763–67. http://dx.doi.org/10.2320/materia.35.763.

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Schembre, J. M., and A. R. Kovscek. "Mechanism of Formation Damage at Elevated Temperature." Journal of Energy Resources Technology 127, no. 3 (March 16, 2005): 171–80. http://dx.doi.org/10.1115/1.1924398.

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The pore and grain surface of reservoir rocks often has clay and other fine material attached onto pore walls. It has been long recognized that brine salinity and pH are key factors affecting the attractive forces between pore surfaces and fines. If mobilized particles are assembled in sufficient quantities, they obstruct pore throats and reduce the permeability of the formation. There is anecdotal evidence of substantial fines migration during steam injection enhanced oil recovery operations. As of yet, the mechanism of fines release with temperature is unexplained. The Derjaguin, Landau, Verwey, and Overbeek theory of colloidal stability is used in conjunction with laboratory, core-scale experiments to demonstrate that high temperature, alkaline pH, and low salinity (typical characteristics of steam condensate) are sufficient to induce fines mobilization. Temperature is a key variable in calculations of fines stability. Hot-water floods are performed in Berea sandstone at temperatures ranging from 20°C to 200°C. Permeability reduction is observed with temperature increase and fines mobilization occurs repeatably at a particular temperature that varies with solution pH and ionic strength. A scanning electron microscope is used to analyze composition of the effluent samples collected during experiments. It confirms the production of fine clay material. On the practical side, this study provides design criteria for steam injection operations so as to control fines production.

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Kiwerski, Jerzy. "Differentiation of spinal damage through compression mechanism." Spinal Cord 29, no. 6 (July 1991): 411–18. http://dx.doi.org/10.1038/sc.1991.56.

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Nagahama, Masahiro, Kei Michiue, Masakazu Mukai, Sadayuki Ochi, and Jun Sakùrai. "Mechanism of Membrane Damage byClostridium perfringensAlpha-Toxin." Microbiology and Immunology 42, no. 8 (August 1998): 533–38. http://dx.doi.org/10.1111/j.1348-0421.1998.tb02321.x.

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Bhakdi, S., J. Tranum-Jensen, and A. Sziegoleit. "Mechanism of membrane damage by streptolysin-O." Infection and Immunity 47, no. 1 (1985): 52–60. http://dx.doi.org/10.1128/iai.47.1.52-60.1985.

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KAWANISHI, SHOSUKE, and YUSUKE HIRAKU. "Mechanism of Metal-Mediated Oxidative DNA Damage." Eisei kagaku 41, no. 6 (1995): 399–410. http://dx.doi.org/10.1248/jhs1956.41.399.

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Journal articles on the topic 'Damage mechanism'

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