Relevant bibliographies by topics / Damage function

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Damage function'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Damage function"

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Windartik, Emyk, Ima Rahmawati, Ita Ainun Jariyah, Raras Merbawani, Indah Lestari, Ifa Ro’ifah, and Arief Andriyanto. "The Degree of Diabetic Wounds Affects Kidney Function Damage." Nurse Media Journal of Nursing 9, no. 2 (December 27, 2019): 159–66. http://dx.doi.org/10.14710/nmjn.v9i2.24210.

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Background: The peripheral neuropathy is the cause of hospitalization for patients with diabetes mellitus (DM) and damages kidney function due to the circulatory system with high sugar levels. High sugar levels in DM patients with diabetic wounds can trigger glomerular damage resulting in the decrease of kidney function.Purpose: This study aims to analyze the relationship between the degree of diabetic wounds and kidney functions in patients with DM.Methods: A cross-sectional study was conducted on 723 DM patients who experienced diabetic wounds in a hospital in Mojokerto, East Java, Indonesia. A purposive sampling technique was used to recruit the samples. The data of this study were medical records of diabetic patients. A simple linear regression test was employed to analyze the data.Results: The result showed that the degree of diabetic wound was significantly related to kidney function damage (p=0.000). The relationship between the degree of diabetic wounds and the decline in kidney function was shown by an R-squared value of 0.768, meaning that the degree of diabetic wound affected the decline of kidney function by 76.8%, while the 23.2% was affected by other factors.Conclusion:The degree of diabetic injury affects the decline of kidney function in DM patients by 76.8%. Nurses should do health promotion about controlling blood sugar levels in DM patients with the prevention of four pillars of diabetes, including education, nutrition, physical activity, and stress.
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Kim, Moon-Jeong, and Hee-Chang Eun. "Identification of damage-expected members of truss structures using frequency response function." Advances in Mechanical Engineering 9, no. 1 (January 2017): 168781401668791. http://dx.doi.org/10.1177/1687814016687911.

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A damaged member in a truss structure leads to a variation in the initial responses of its adjacent members. A flexibility-based approach extracting from the modal data should be implemented as one of the structural damage detection methods. The frequency response function data as dynamic measurements provide more information on the system characteristics compared with modal data. Proper orthogonal modes from the frequency response functions extracted in the given frequency ranges and their modified forms can be utilized as damage indices to detect damages. This study considers damage detection of a truss structure using a frequency response function–based approach transformed to the proper orthogonal modes and a flexibility-based approach using the first few modal data for undamaged and damaged states. The utilization of these two methods is compared through numerical experiments on truss structures. The methods can rarely detect the damaged member accurately, but a group of damage-expected members is detected despite the existence of external noise. It is shown that the frequency response function–based approach can be utilized more explicitly than the flexibility-based approach.
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Yang, Tian-qun, Yuichi Majima, Yongqing Guo, Teruhiko Harada, Takeshi Shimizu, and Kazuhiko Takeuchi. "Mucociliary Transport Function and Damage of Ciliated Epithelium." American Journal of Rhinology 16, no. 4 (July 2002): 215–19. http://dx.doi.org/10.1177/194589240201600407.

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The influence of epithelial damage on mucociliary transport was studied in relation to the amount of mucus. The mucosal epithelium of mucus-depleted frog palate was dissected and mounted on a plastic plate. Mechanical damages were created on the frog mucosa by pressing a different thickness of boards (2, 3, 5, and 8 mm). Two different amounts of frog mucus (7.9 L [small amount of mucus {S-mucus}]) and 51.0 L [large amount of mucus {L-mucus}])were applied on the frog mucosa with and without mucosal damage. There was no difference in mucociliary transport rate (MTR) on undamaged frog mucosa between S-mucus and L-mucus. However, on the damaged mucosa, MTR of S-mucus was significantly decreased compared with that of L-mucus. Moreover, capability of mucus transportation across the mucosal damage was significantly lower in S-mucus than in L-mucus. Results indicate that the larger the mucus amount becomes, the more the mucus travels the damaged epithelium. Moreover, MTR of L-mucus was decreased with increasing the degree of epithelial damage. This study indicates that the degree of loss of cilia is an important factor of mucociliary deceleration. (American Journal of Rhinology 16, 215–219, 2002)
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Zhang, Wei, Limin Sun, and Liye Zhang. "Local damage identification method using finite element model updating based on a new wavelet damage function." Advances in Structural Engineering 21, no. 10 (December 27, 2017): 1482–94. http://dx.doi.org/10.1177/1369433217746837.

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As the number of unknown parameters in a finite element model updating problem increases, the challenges in finding reliable and meaningful updating result surges. Although traditional damage functions have illustrated an excellent ability in reducing unknown parameters, they are imprecise for identifying local damages. To solve this problem, a new type of damage function termed the wavelet damage function, which specializes in local damage identification, is proposed in this article. It utilizes the properties of the Haar wavelet and wavelet multi-resolution analysis. During the wavelet damage function–based finite element model updating procedure, unknown parameters in finite element models are not directly adjusted. Instead, wavelet coefficients of the parameters are estimated stepwise and then the final updating results are reconstructed through the inverse discrete wavelet transform. Numerical simulations and experimental verifications are conducted, and the corresponding results show that wavelet damage function can offer better accuracy as well as higher computational efficiency in the identification of local damages than the traditional damage functions.
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Boettle, M., J. P. Kropp, L. Reiber, O. Roithmeier, D. Rybski, and C. Walther. "About the influence of elevation model quality and small-scale damage functions on flood damage estimation." Natural Hazards and Earth System Sciences 11, no. 12 (December 19, 2011): 3327–34. http://dx.doi.org/10.5194/nhess-11-3327-2011.

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Abstract. The assessment of coastal flood risks in a particular region requires the estimation of typical damages caused by storm surges of certain characteristics and annualities. Although the damage depends on a multitude of factors, including flow velocity, duration of flood, precaution, etc., the relationship between flood events and the corresponding average damages is usually described by a stage-damage function, which considers the maximum water level as the only damage influencing factor. Starting with different (microscale) building damage functions we elaborate a macroscopic damage function for the entire case study area Kalundborg (Denmark) on the basis of multiple coarse-graining methods and assumptions of the hydrological connectivity. We find that for small events, the macroscopic damage function mostly depends on the properties of the elevation model, while for large events it strongly depends on the assumed building damage function. In general, the damage in the case study increases exponentially up to a certain level and then less steep.
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Matsuoka, Masashi, and Miguel Estrada. "Development of Earthquake-Induced Building Damage Estimation Model Based on ALOS/PALSAR Observing the 2007 Peru Earthquake." Journal of Disaster Research 8, no. 2 (March 1, 2013): 346–55. http://dx.doi.org/10.20965/jdr.2013.p0346.

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With the aim of developing a model for estimating building damage from synthetic aperture radar (SAR) data in the L-band, which is appropriate for Peru, we propose a regression discriminant function based on field survey data in Pisco, which was seriously damaged in the 2007 Peru earthquake. The proposed function discriminates among damage ranks corresponding to the severe damage ratio of buildings using ALOS/PALSAR imagery of the disaster area before and after the earthquake. By calculating differences in and correlations of backscattering coefficients, which were explanatory variables of the regression discriminant function, we determined an optimum window size capable of estimating the degree of damage more accurately. A normalized likelihood function for the severe damage ratio was developed based on discriminant scores of the regression discriminant function. The distribution of the severe damage ratio was accurately estimated, furthermore, from PALSAR imagery using data integration of the likelihood function with fragility functions in terms of the seismic intensity of the earthquake.
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Ruilope, Luis M. "Arterial Function and Cardiorenal Damage." Journal of Clinical Hypertension 16, no. 6 (April 25, 2014): 398. http://dx.doi.org/10.1111/jch.12318.

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NINIC, D., and H. STARK. "A multiaxial fatigue damage function." International Journal of Fatigue 29, no. 3 (March 2007): 533–48. http://dx.doi.org/10.1016/j.ijfatigue.2006.04.003.

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Dackermann, Ulrike, Wade A. Smith, Mehrisadat Makki Alamdari, Jianchun Li, and Robert B. Randall. "Cepstrum-based damage identification in structures with progressive damage." Structural Health Monitoring 18, no. 1 (October 16, 2018): 87–102. http://dx.doi.org/10.1177/1475921718804730.

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This article aims at developing a new framework to identify and assess progressive structural damage. The method relies solely on output measurements to establish the frequency response functions of a structure using cepstrum-based operational modal analysis. Two different damage indicative features are constructed using the established frequency response functions. The first damage feature takes the residual frequency response function, defined as the difference in frequency response function between evolving states of the structure, and then reduces its dimension using principle component analysis; while in the second damage indicator, a new feature based on the area under the residual frequency response function curve is proposed. The rationale behind this feature lies in the fact that damage often affects a number of modes of the system, that is, it affects the frequency response function over a wide range of frequencies; as a result, this quantity has higher sensitivity to any structural change by combining all contributions from different frequencies. The obtained feature vectors serve as inputs to a novel multi-stage neural network ensemble designed to assess the severity of damage in the structure. The proposed method is validated using extensive experimental data from a laboratory four-girder timber bridge structure subjected to gradually progressing damage at various locations with different severities. In total, 13 different states of the structure are considered, and it is demonstrated that the new damage feature outperforms the conventional principle component analysis–based feature. The contribution of the work is threefold: first, the application of cepstrum-based operational modal analysis in structural health monitoring is further validated, which has potential for real-life applications where only limited knowledge of the input is available; second, a new damage feature is proposed and its superior performance is demonstrated; and finally, the comprehensive test framework including extensive progressive damage cases validates the proposed technique.
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Zhao, Jie, Hans DeSmidt, and Meng Peng. "Harmonic Transfer Function Based Damage Identification of Breathing Cracked Jeffcott Rotor." Shock and Vibration 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/4056236.

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This paper proposes a vibration-based damage identification method based on 6-dof Jeffcott rotor system, which is based on harmonic balance and Newton-Raphson methods. First, the equations of motion are derived by using energy method and Lagrange principle. The crack model is based on strain energy release rate (SERR) in fracture mechanics and modified to accommodate 6-dof Jeffcott rotor model. Then, Gear’s method is used to solve the vibration responses of nominal and damaged rotor systems. By processing vibration responses, the transfer function shifts between nominal and damaged systems are taken as the input of damage identification algorithm. Finally, damage severity can be correlated with the damage parameter estimated via developed damage identification model. Numerical examples are shown to demonstrate the effectiveness in identifying the breathing crack in the rotor system.
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Dissertations / Theses on the topic "Damage function"

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Byrne, Christopher. "Muscle function after exercise-induced muscle damage." Thesis, Bangor University, 2001. https://research.bangor.ac.uk/portal/en/theses/muscle-function-after-exerciseinduced-muscle-damage(2bbf5fe1-f35b-4b7b-9790-ff3a04b86875).html.

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Muscle function after exercise-induced muscle damage has traditionally been evaluated by measures of isometric strength at a single joint angle or muscle length. The thesis investigates the effect of muscle damage on other muscle function parameters such as, isometric strength as a function of muscle length, concentric strength as a function of angular velocity, strength across muscle actions, the stretch-shortening cycle, power output, and fatigability. Study 1 The first part of this study aimed to determine how the muscle length at which strength is measured affects reductions in isometric strength following eccentric exercise-induced muscle damage. The damaging exercise protocol consisted of 100 maximal voluntary eccentric actions of the knee extensors, performed in the prone position through a range of motion from 40° to 140° (0° = full extension) at an angular velocity of 90 deg's-1. Isometric strength of the knee extensors was measured at short muscle length (10° knee flexion) and optimal length (80°). A significantly greater relative loss of strength was observed at short versus optimal muscle length (76.3 ± 2.5% vs. 82.1 ± 2.7% of pre-exercise values, P<0.05) over the seven day testing period following eccentric exercise. The second part of the study investigated isometric strength at optimal length and concentric strength at slow (30 deg's 1) and fast (180 deg's 1) angular velocities of movement. No differences were apparent in the magnitude and rate of recovery of strength across isometric (82.1 ± 2.7%) and slow (86.6 ± 2.0%) and fast (84.3 ± 1.5%) concentric muscle actions. Both the popping sarcomere hypothesis of 2 muscle damage and a failure in excitation-contraction coupling are possible explanations for the reduction in strength being affected by the muscle length at which it is measured. Both would be expected to affect strength to a greater extent at short versus optimal muscle lengths. Study 2 The second study investigated knee extensor muscle strength during isometric, concentric and eccentric muscle actions and vertical jump performance under conditions of squat jump (SJ), countermovement jump (CMJ) and drop jump (DJ). These measures were taken before, 1 hour after, and on days 1,2,3,4 and 7 following a damaging exercise protocol consisting of 100 barbell squats (10 sets x 10 reps @ 70% body mass load). Strength was significantly reduced for four days, however, no differences were observed in the magnitude or rate of recovery of isometric strength at 80° knee flexion and concentric and eccentric strength at 90 deg's'. Vertical jump performance was significantly reduced for three days and was dependent on the type of jump being performed. The relative decline in SJ performance was significantly greater than that in CMJ performance (91.6 ± 1.1% vs. 95.2 ± 1.3% of pre-exercise values, P<0.05) and the relative decline in SJ was significantly greater than that in DJ performance (91.6 ± 1.1% vs. 95.2 ± 1.4%, P<0.05). No differences were observed in the relative decline in CMJ and DJ performance (95.2 ± 1.3% vs. 95.2 ± 1.4%, P> 0.05). The stretch-shortening cycle (SSC) of muscle function is utilised in CMJ and DJ but not in SJ. The SSC has a clear purpose: to allow the final phase (concentric action) to take place with greater force or power output, as compared to the condition where the movement is initiated by a concentric action alone. 3 Utilisation of the SSC in performance seems to attenuate the detrimental performance effects of exercise-induced muscle damage. Study 3 The third and final study investigated the effects of exercise-induced muscle damage on maximal power output and knee extensor fatigability under isometric and dynamic conditions. Under isometric conditions, strength was assessed at 40° and 80° knee flexion and fatigability was assessed by a sustained 60s maximum voluntary contraction (MVC) at each joint angle. For dynamic conditions, maximum power output and fatigue were assessed during a maximal 30s cycle ergometer test. These measures were taken before, 1 hour after, and on days 1,2,3, and 7 following a damaging exercise protocol consisting of 100 eccentric squats (10 sets x 10 reps @ 80% concentric 1 RM). Isometric strength was significantly reduced (P < 0.05) for seven days but no significant differences were observed in the magnitude of strength loss and the pattern of recovery between the two joint angles. Fatigability was quantified as the slope (b) of a linear regression line fitted to the torque and power decay during the 60s MVC and the 30s cycle test, respectively. Prior to muscle damage, subjects were significantly less fatigable (P < 0.05) at 40° (b = -2.39 ± 0.26) versus 80° (b = -5.50 ± 0.72). After muscle damage, subjects became significantly less fatigable at both 40° and 80° with recovery taking three days at 401 and seven days at 80°. Before damaging exercise, a greater rate of fatigue was observed under dynamic (b = -12.75 ± 2.3) versus isometric (80°) conditions (b = -5.50 ± 0.72). Isometric and dynamic fatigue 4 followed a similar temporal pattern after damaging exercise. When the effects of muscle damage on strength at 801 and maximal power output were compared, differences in the extent of performance loss and the time course of recovery were observed. At 1 hour post-exercise, strength was affected to a greater extent (30% reduction) than power (13% reduction) and whereas strength followed a linear recovery pattern, power suffered further decrements at day 1 (18%) and day 2 (16%) before starting to recover. The results indicate that under conditions of voluntary activation muscle becomes weaker but less fatigable under isometric and dynamic conditions following exercise-induced muscle damage. The lower starting torque / power output and the slower rate of decline in torque / power output observed in post-damage fatigue curves may be a phenomenon of selective type II fibre damage. Evidence suggests that type II fibres are selectively damaged during eccentric exercise and therefore post-damage fatigue curves may be missing their contribution to performance. The different recovery patterns observed for isometric and dynamic performance may indicate an inability to maintain central motor drive during complex dynamic tasks when damage is present.
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Ohtsuki, Akimichi. "Organic Chemical Approaches to DNA Function and Damage." 京都大学 (Kyoto University), 2011. http://hdl.handle.net/2433/142392.

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Li, Xiaoling. "Investigation of tissue transglutaminase function in apoptosis." Thesis, Nottingham Trent University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251281.

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Karras, Georgios Ioannis. "Mechanism and function of RAD6-mediated DNA damage tolerance." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-129233.

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Nafria, Javier Garcia. "Structure-function studies on proteins involved in DNA damage prevention." Thesis, University of York, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.547327.

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Burrage, Joseph. "Analysis of the function of LSH in DNA damage repair." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/9416.

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DNA damage from both normal metabolic activities and environmental factors such as UV and radiation can cause as many as 1 million individual lesions to the DNA per cell per day (Lodish et al 2004). Cells respond to this continuous damage by employing many, highly efficient DNA repair mechanisms and undergo apoptosis when normal DNA repair fails. Of the many types of DNA damage that can occur, double strand breaks (DSBs) are the most toxic (Featherstone & Jackson 1999). A single unrepaired DSB is enough to induce cellular apoptosis and several mechanisms have developed to repair DSBs. The recognition, signalling and repair of DSBs involve large multi-­‐subunit complexes that bind to both the DNA and modified histone tails, which require modification of the chromatin in order to access their bind sites and function effectively (Allard et al 2004). Consequently several chromatin-­‐remodelling proteins have been implicated in DSB repair (van Attikum et al 2004, Chai et al 2005). LSH (Lymphoid specific helicase) is a putative chromatin-­‐remodelling enzyme that interacts with DNA methyltransferases and has been connected to DNA methylation (Myant & Stancheva, 2008). Knockouts of LSH or its homologues in A. thaliana and M. musculus show a reduction in DNA methylation of 60-­‐70% (Jeddeloh et al 1999, Dennis et al 2001). However in addition to this phenotype, knockout A. thaliana also have an increased sensitivity to DNA damage (Shaked et al 2006). A homologue of LSH has also been identified in S. cerevisiae, which interacts with known repair proteins (Collins et al 2007) and may be involved in DSB repair. Although the majority of Lsh-­‐/-­‐ mice die shortly after birth, 40% of the line produced by Sun et al survive and show unexplained premature aging (Sun et al 2004). As premature aging is a hallmark of increased acquisition of DNA damage there is the possibility of a conserved role for LSH in mammalian DNA damage repair. Here I show that LSH depleted mammalian cells have an increased sensitivity specifically to DSB inducing agents and show increased levels of apoptosis. Further analysis shows that cells lacking LSH repair DSBs slower, indicating a novel role for LSH in mammalian repair of DSB. I performed an in depth analysis of the DSB defects in LSH depleted cells in an attempt to elucidate the function of LSH in DSB repair. I found that LSH depleted cells can correctly recognise DSBs but recruit downstream signalling and repair factors, such as γH2AX, less efficiently. I show that reduced recruitment of downstream DSB repair factors is not accompanied by extended cell cycle checkpoint signalling. This suggests that LSH depleted cells continue through the mitosis with unrepaired DSBs, which most likely leads to apoptosis and the increased sensitivity to DSB inducing agents. These experiments also showed that recruitment of DSB signalling and repair factors is not impaired equally at all breaks, and I present a model system created to quantitatively compare individually breaks between WT and LSH depleted cells to identify DSB that require LSH for efficient repair. I also preformed an analysis of Lsh-­/-­ MEFs containing WT or catalytic null mutant LSH rescue constructs and I show that WT but not catalytic null LSH can restore efficient DSB repair. These studies identify a novel role for LSH in mammalian DSB repair and demonstrate the importance of its catalytic activity.
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Maisse, Carine. "Regulation and function of the DeltaNp73 isoforms after DNA damage." Paris 6, 2004. http://www.theses.fr/2004PA066598.

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Les cellules d’un organisme subissent chaque jour des stress dus à l’environnement (rayons UV, agents chimiques, métaux lourds) pouvant conduire à des lésions du patrimoine génétique ou à un déséquilibre de l’état RedOx. De nombreux systèmes cellulaires permettent tout d’abord d’identifier le dommage puis d’induire éventuellement la réparation de l’ADN ou la mort de la cellule si le dommage subi est irréversible. Une cellule cancéreuse est le résultat d’échecs cumulés des systèmes de contrôle intra et extra-cellulaires et de mort programmée. Identifiée en 1979, la protéine p53 est un facteur de transcription muté dans 50% des cancers. Elle joue un rôle central dans la régulation de la prolifération cellulaire, de la réparation de l’ADN et de l’apoptose après stress, génotoxique ou non. Etonnamment, p53 semblait jouer seule ce rôle prépondérant qui lui a valu la dénomination de "gardienne du génome", et, pendant 20 ans, toutes tentatives pour caractériser d'éventuels homologues sont restées vaines. En 1997, p73, un homologue de p53, fut identifiée dans la bande p36 du chromosome 1, une région dont la délétion est souvent associée à de nombreux neuroblastomes. La caractérisation de p73 fut accueillie avec enthousiasme et sa grande homologie avec p53 semblait pouvoir expliquer les 50% de cancers présentant une p53 non mutée. L'année suivante, un deuxième homologue fut identifié et caractérisé: p63. Les trois membres de la famille p53 présentent une grande homologie, notamment dans le domaine de liaison à l'ADN : p73 et p63 sont en effet capables d'activer l'expression de nombreux gènes cibles de p53 et d'induire l'apoptose ou de bloquer le cycle cellulaire. Toutefois, 6 ans après leur découverte, p73 et p63 semblent de plus en plus différents de leur "parente" p53. La génération et l'étude de souris déficientes pour les membres de la famille illustrent ces différences : si les souris manquant p53 atteignent normalement l'âge adulte et développent spontanément des tumeurs, les souris manquant p73 ou p63 présentent de graves troubles du développement embryonnaire, indiquant un rôle majeur dans la différenciation cellulaire. Si p73 et p63 présentent une structure globale comparable à p53 (un domaine de transactivation, un domaine de liaison à l’ADN et un domaine d’oligomérisation, impliqué dans la tétramérisation de la protéine nécessaire à son activité transcriptionnelle), elles possèdent en effet un prolongement du domaine C-terminal, absent de la séquence de p53, et qui semble impliqué dans leurs propriétés propres. La maturation des transcrits de p73 et p63 donne lieu à différents splicing variants (6 pour p73 et au moins 3 pour p63) en C-terminal, dont les fonctions transcriptionnelles et le pattern d'expression sont différents. De plus, les formes les plus longues des deux protéines présentent un domaine SAM (Sterile Alpha Motif), commun à de nombreuses protéines impliquées dans le développement. Ce domaine est souvent muté dans des syndromes humains impliquant p63, ce qui laisse présager un rôle important dans la régulation de l'activité de p63 et p73. Par ailleurs, des formes tronquées en N-terminal ont été décrites dans la souris : ces formes sont nommées ΔΝ, elles ne possèdent pas le domaine de transactivation, au contraire des formes longues (TA). Ainsi, ΔΝp73 et ΔΝp63 agissent dans la souris comme dominants négatifs des fonctions pro-apoptotiques de TAp73 et TAp63. Il a été établi par la suite que ΔΝp73 et ΔΝp63 sont transcrites à partir d'un second promoteur, localisé dans le troisième intron de la forme longue. L'étude présentée ici décrit la première caractérisation de la forme ΔΝp73 humaine, la régulation de son expression et de son activité. De même que ΔΝp73 murine, la forme humaine inhibe les fonctions pro-apoptotiques de TAp73 et p53, via interactions protéines/protéines ou compétition pour les sites de liaison sur les promoteurs cibles. De plus, la présence d’un élément de réponse à p53 situé dans le promoteur de ΔΝp73 caractérise une boucle de régulation négative qui s’ajoute à la boucle de régulation MDM2/p53. ΔΝp73 agissant comme un oncogène, il semble donc que le ratio ΔΝ/TA ou ΔΝ/p53 soit fondamental à l’équilibre cellulaire et que sa dérégulation puisse être impliquée dans la formation tumorale, ce ratio pouvant être contrôlé au niveau transcriptionnel ou post-traductionel de la protéine ΔΝp73. L’étude du promoteur de ΔΝp73 a mis en évidence de nombreux éléments de réponse à différents facteurs de transcription. De récents travaux ayant associé une augmentation de ΔΝp73 à certains types de neuroblastomes, nous nous sommes particulièrement intéressés à N-Myc, facteur de transcription également amplifié dans certains neuroblastomes. Nous n’avons pu toutefois mettre en évidence une activation transcriptionnelle directe de ΔΝp73 de la part de N-Myc, mais d’autres éléments de réponse restent encore à caractériser, notamment NFκB et p300, tous deux impliqués dans la régulation de l’apoptose. Par ailleurs, l’étude de modifications post-traductionnelles de ΔΝp73 a mis en évidence une rapide dégradation de la protéine après dommages à l’ADN induits par rayons Ultra-Violets ou traitement par drogues, libérant ainsi p53 et TAp73 de son inhibition et permettant ainsi l’apoptose ou l’arrêt du cycle cellulaire. De plus, notre étude a mis en évidence une très brève hémie-vie de la forme ΔΝ par rapport aux formes contenant le domaine de transactivation. Ainsi, le ratio ΔΝ/formes longues pourrait également dépendre d’une fine régulation de la dégradation des deux protéines<br>In our search for the underlying causes of cancer, TP53 is the most intensively studied gene. P53 plays a central role for balancing the antagonistic processes of proliferation and apoptosis. As a sequence-specific transcription factor, p53 regulates the expression of genes involved in cell cycle arrest and apoptosis in response to genotoxic damage or cellular stress. Failure of p53 function consequently leads to uncontrolled cell growth, a defining feature of cancer cells. Given the importance of p53 as a tumor suppressor, it is therefore no wonder that p53 is the most frequent site of genetic alterations found in human cancers. The recent discovery of two TP53-related genes, TP73 and TP63 with striking sequence homology, was therefore a big surprise, raising the possibility that other tumor suppressors exist which share the power of p53 in preventing cancer formation. The three members of the p53 family share significant homology both at the genomic and at the protein level. The highest level of identity is reached in the DBD (DNA-Binding Domain), suggesting that they can bind to the same DNA sequence and transactivate the same promoters. In fact, p73 and p63 are able to activate some p53 targets and to induce apoptosis, but they appear more and more different from their relative. The study of the respective knock-out mice gives a good illustration of these differences : while p53-null mice develop normally but present spontaneous tumors, the p73 and p63-null mice present severe developmental troubles but no spontaneous tumors, indicating that they may have more complex functions. Conversely to p53, p73 and p63 contain additional C-terminal extensions. In both proteins, these extensions show alternative splicing, which results in at least six C-terminal variants for p73 and three for p63. These isoforms have different transcription and biological properties, and their expression patterns change among normal tissues. Moreover, the α variants of p73 and p63 have close to their C terminus a SAM (Sterile Alpha Motif) domain, which is thought to be responsible for regulating p53-like functions, and is implicated in various human syndromes where p63 is mutated. In addition to the C-terminal variants aminoterminous truncated variants of p73 and p63 exist : ΔNp73 and ΔΝp63. These N-terminally truncated isoforms lack the transactivation domain (TA), which is coded by the first 3 exons, and derive from the use of an alternative promoter (P2) located in intron 3 and an additional exon (exon 3'). While TAp73 isoforms work as transcription factors and can induce irreversible cell cycle arrest and apoptosis like p53, the ΔNp73 isoforms that lack the transactivation domain are incapable of directly inducing gene expression and do not induce growth arrest or cell death. However, the ΔNp73 forms have a very important regulatory role, since they exert a dominant negative effect on p53 and TAp73 by blocking their transactivation activity, and hence their ability to induce apoptosis. The relative levels of expression of the ΔNp73 isoforms can therefore determine the function of both TAp73 and p53. It is most interesting that the ΔNp73 promoter (P2) contains a very efficient p53/p73 responsive element and consequently, p53 and TAp73 efficiently induce ΔNp73 expression. Moreover, upon strong DNA damage, induced by UV irradiation or drug treatment, ΔNp73 is rapidly degraded, releasing the block exerted on p53 and TAp73 and thus allowing cell cycle arrest and apoptosis to proceed. Hence, ΔNp73 is part of a dominant negative feedback loop that regulates the function of both p53 and TAp73 and this regulation can be overcome in case of strong DNA damage
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De, Moura Miguez Araujo Sofia Jorge. "Interactions and function of nucleotide excision repair protein complexes." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322320.

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Zhang, Muyu [Verfasser], Bernd [Akademischer Betreuer] Markert, and Rüdiger [Akademischer Betreuer] Schmidt. "Auto-correlation-function-based damage index for damage detection and system identification / Muyu Zhang ; Bernd Markert, Rüdiger Schmidt." Aachen : Universitätsbibliothek der RWTH Aachen, 2016. http://d-nb.info/1130327329/34.

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Chapman, J. R. "Molecular analysis of mediator-protein function in the DNA damage response." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597474.

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I report the identification of phosphorylation sites in MDC1 that are phosphorylated by ATM in response to ionizing radiation (IR), and demonstrates that these motifs are required for the efficient recruitment of BRCA1 and 53BP1 into IRIF. We identified the E3 Ubiquitin ligase RNF8 as critical for this process, and show that upon phosphorylation, these MDC1 sites are bound directly by the FHA domain of RNF8, directing it to generate ubiquitinated proteins at DSB sites. We demonstrate that it is the formation of these ubiquitin conjugates at DSB sites that facilitate BRCA1 and 53BP1 recruitment into IRIF. I report a novel interaction-surface in MDC1 that is phosphorylated constitutively by the protein kinase CK2. These phosphorylation sites in MDC1 are bound directly by NBS1, in a manner dependent on its FHA and tandem BRCT domains. I demonstrate that this interaction surface on MDC1 is essential for promoting MDC1-NBS1 interactions and NBS1 retention on chromatin flanking DSB sites. We have elucidated the structure of the FHA-tandem-BRCT domains of Schizosaccharomyes pombe Nbs1 by X-ray crystallography. Phosphorylated MDC1 Ser-Asp-Thr-Asp (pSDpTD)-like motifs are evolutionarily conserved NBS1 binding motifs <i>In vitro</i>. I identified similar CK2-consensus sites conserved in the fission yeast DNA repair protein Ctp1 (CtIP). Nbs1 FHA domain-mediated binding of these Ctp1 sites is crucial for MRN-dependent functions in yeast. These findings suggest that the unique and specialist domain architecture of NBS1<i> </i>underpins an evolutionary conserved adaptor-function mode for MRN-dependent responses to DNA damage.
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Books on the topic "Damage function"

1

Schwartz, Marvin. Recovery of inferior alveolar nerve function following nerve damage. [Toronto: Faculty of Dentistry, University of Toronto], 1990.

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Kysela, Boris. Ionizing radiation-induced DNA damage and repair in relation to biological function. Uxbridge: Brunel University, 1994.

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Spence, John W. Theoretical damage function for the effects of acid deposition on galvanized steel structures. Research Triangle Park, NC: U.S. Environmental Protection Agency, Atmospheric Sciences Research Laboratory, 1988.

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Spence, John W. Theoretical damage function for the effects of acid deposition on galvanized steel structures. Research Triangle Park, NC: U.S. Environmental Protection Agency, Atmospheric Sciences Research Laboratory, 1988.

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The healing power of neurofeedback: The revolutionary LENS technique for restoring optimal brain function. Rochester, Vt: Healing Arts Press, 2006.

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Brain injury survival kit: 365 tips, tools & tricks to deals with cognitive function loss. New York: Demos Medical Pub., 2009.

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Söderback, Ingrid. Intellectual function training and intellectual housework training in patients with acquired brain damage: A study of occupational therapy methods. Stockholm: Folksam, 1988.

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Schutz, Larry E. Head injury recovery in real life. San Diego: Plural Pub., 2010.

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Brain repair after stroke. Cambridge: Cambridge University Press, 2010.

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Abraham, Kenneth S. The forms and functions of tort law. 2nd ed. New York, N.Y: Foundation Press, 2002.

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Book chapters on the topic "Damage function"

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Dickerson, J. W. T. "Recovery of Function: Nutritional Factors." In Recovery from Brain Damage, 23–33. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3420-4_2.

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Mitchell, David, and Rita Ghosh. "Oxidative Damage and Promoter Function." In Oxidative Damage to Nucleic Acids, 91–99. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72974-9_7.

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Rose, F. D., Ian Q. Whishaw, and M. W. van Hof. "Hemidecortication and Recovery of Function: Animal Studies." In Recovery from Brain Damage, 115–35. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3420-4_7.

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Symon, Lindsay. "Recovery of Brain Function Following Ischemia." In Mechanisms of Secondary Brain Damage, 102–9. Vienna: Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-9266-5_15.

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Sinden, John D., Kathryn M. Marsden, and Helen Hodges. "Neural Transplantation and Recovery of Function: Animal Studies." In Recovery from Brain Damage, 35–65. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3420-4_3.

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Hitchcock, Edward. "Neural Implants and Recovery of Function: Human Work." In Recovery from Brain Damage, 67–78. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3420-4_4.

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Doménech, Mónica, Cristina Sierra, and Antonio Coca. "Questionnaires for Cognitive Function Evaluation." In Assessment of Preclinical Organ Damage in Hypertension, 191–96. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15603-3_18.

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Hayakawa, Mika, Satoru Sugiyama, Kazuki Hattori, Masaaki Takasawa, and Takayuki Ozawa. "Age-Associated Damage in Mitochondrial DNA in Human Hearts." In Cellular Function and Metabolism, 95–103. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3078-7_14.

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Winkler, C., and D. Kirik. "Parkinson’s Disease II: Replacement of Dopamine and Restoration of Striatal Function." In Brain Damage and Repair, 549–61. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/1-4020-2541-6_36.

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Manson, Graeme, S. G. Pierce, Keith Worden, and Daley Chetwynd. "Classification Using Radial Basis Function Networks with Uncertain Weights." In Damage Assessment of Structures VI, 135–42. Stafa: Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-976-8.135.

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Conference papers on the topic "Damage function"

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BRUNS, MARLENE, BENEDIKT HOFMEISTER, CLEMENS HÜBLER, and RAIMUND ROLFES. "Damage Localization Via Model Updating Using a Damage Distribution Function." In Structural Health Monitoring 2019. Lancaster, PA: DEStech Publications, Inc., 2019. http://dx.doi.org/10.12783/shm2019/32202.

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Marchesin, Dan, Gustavo Hime, Pavel Bedrikovetsky, and Amaury Alvarez. "Robust Fast Recovery Of The Filtration Function For Flow Of Water With Particles In Porous Media." In European Formation Damage Conference. Society of Petroleum Engineers, 2007. http://dx.doi.org/10.2118/107770-ms.

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Lew, Jiann-Shiun, and Jiann-Shiun Lew. "Transfer function parameter changes due to structural damage." In 38th Structures, Structural Dynamics, and Materials Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1997. http://dx.doi.org/10.2514/6.1997-1317.

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Schulz, Mark, P. Pai, Sunil Thyagarajan, and Jaycee Chung. "Structural damage diagnosis by frequency response function optimization." In Dynamics Specialists Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1996. http://dx.doi.org/10.2514/6.1996-1223.

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Beni, S. A., R. Hammamian, and M. R. Haghifam. "Estimation of customers damage function by questionnaire method." In 22nd International Conference and Exhibition on Electricity Distribution (CIRED 2013). Institution of Engineering and Technology, 2013. http://dx.doi.org/10.1049/cp.2013.1078.

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Dudding, Ashley T. "Bogie Spring Fatigue Damage - A Function of Static Displacement." In International Truck & Bus Meeting & Exposition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 1992. http://dx.doi.org/10.4271/922432.

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Cuomo, Stefano, Gian Piero M. Fierro, and Michele Meo. "Damage localization on composite structures: radial basis function application." In Nondestructive Characterization and Monitoring of Advanced Materials, Aerospace, Civil Infrastructure, and Transportation XIV, edited by Peter J. Shull, Tzu-Yang Yu, Andrew L. Gyekenyesi, and H. Felix Wu. SPIE, 2020. http://dx.doi.org/10.1117/12.2559213.

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Tanner, Roger I., Fuzhong Qi, and Shaocong Dai. "Bread dough rheology: Computing with a damage function model." In PROCEEDINGS OF THE INTERNATIONAL CONFERENCE OF COMPUTATIONAL METHODS IN SCIENCES AND ENGINEERING 2010 (ICCMSE-2010). AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4906672.

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Lew, Jiann-Shiun, Carlo Hyde, and Montanez Wade. "Damage Detection of Flexible Beams Using Transfer Function Correlation." In ASME 1999 Design Engineering Technical Conferences. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/detc99/vib-8373.

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Abstract In this paper, we use the change of the identified transfer function parameters of structural dynamics for damage detection of a flexible beam system. The technique used for damage detection is based on the correlation between the identified parameter change and the change of the analytical model, such as a finite element model, due to damage. A least-squares technique is developed to identify the transfer function parameters from the experimental data. In the damage detection process, first the location of damage is identified, then the intensity of damage is estimated. Applying the presented approach to a flexible beam, only one sensor is needed to successfully locate the damage position and accurately estimate the intensity of damage.
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Du, Detao, Xinbing Liu, Jeffrey A. Squier, and Gerard A. Mourou. "Laser-induced breakdown as a function of pulse duration: from 7 ns to 150 fs." In Laser-Induced Damage in Optical Materials: 1994, edited by Harold E. Bennett, Arthur H. Guenther, Mark R. Kozlowski, Brian E. Newnam, and M. J. Soileau. SPIE, 1995. http://dx.doi.org/10.1117/12.213723.

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Reports on the topic "Damage function"

1

Hong, Harrison, Jeffrey Kubik, Neng Wang, Xiao Xu, and Jinqiang Yang. Pandemics, Vaccines and an Earnings Damage Function. Cambridge, MA: National Bureau of Economic Research, September 2020. http://dx.doi.org/10.3386/w27829.

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Sirbu, Bianca. Function of ZFAND3 in the DNA Damage Response. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada566216.

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Adams, B. Microstructural dependence of the cavitation damage function in FCC materials. Office of Scientific and Technical Information (OSTI), January 1990. http://dx.doi.org/10.2172/6986490.

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Boyer, Thomas G. Regulation of BRCA1 Function by DNA Damage-Induced Site-Specific Phosphorylation. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada439207.

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Griffin, Patrick J. Detailed Description of the Derivation of the Silicon Damage Response Function. Office of Scientific and Technical Information (OSTI), March 2016. http://dx.doi.org/10.2172/1561023.

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Giraldez, J., S. Booth, K. Anderson, and K. Massey. Valuing Energy Security: Customer Damage Function Methodology and Case Studies at DoD Installations. Office of Scientific and Technical Information (OSTI), October 2012. http://dx.doi.org/10.2172/1055367.

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Depriest, Kendall. Silicon Damage Response Function Derivation and Verification: Assessment of Impact on ASTM Standard E722. Office of Scientific and Technical Information (OSTI), June 2016. http://dx.doi.org/10.2172/1259547.

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Taylor, Jimmy D., Greg K. Yarrow, and James E. Miller. Beavers. U.S. Department of Agriculture, Animal and Plant Health Inspection Service, March 2017. http://dx.doi.org/10.32747/2017.7207729.ws.

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The American beaver (Castor canadensis) is known as an “ecosystem engineer” because of the benefits their dams provide to biological diversity and ecosystem function. It also is considered a “keystone species” because of its ability to transform its environment, creating new habitats upon which other species depend. Despite the many positive benefits beavers provide through foraging and dam building, beavers also create conflict with people when their activities cause damage. The focus of this publication is to provide basic information on beaver ecology, damage, and management.
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Rahmani, Mehran, and Manan Naik. Structural Identification and Damage Detection in Bridges using Wave Method and Uniform Shear Beam Models: A Feasibility Study. Mineta Transportation Institute, February 2021. http://dx.doi.org/10.31979/mti.2021.1934.

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This report presents a wave method to be used for the structural identification and damage detection of structural components in bridges, e.g., bridge piers. This method has proven to be promising when applied to real structures and large amplitude responses in buildings (e.g., mid-rise and high-rise buildings). This study is the first application of the method to damaged bridge structures. The bridge identification was performed using wave propagation in a simple uniform shear beam model. The method identifies a wave velocity for the structure by fitting an equivalent uniform shear beam model to the impulse response functions of the recorded earthquake response. The structural damage is detected by measuring changes in the identified velocities from one damaging event to another. The method uses the acceleration response recorded in the structure to detect damage. In this study, the acceleration response from a shake-table four-span bridge tested to failure was used. Pairs of sensors were identified to represent a specific wave passage in the bridge. Wave velocities were identified for several sensor pairs and various shaking intensities are reported; further, actual observed damage in the bridge was compared with the detected reductions in the identified velocities. The results show that the identified shear wave velocities presented a decreasing trend as the shaking intensity was increased, and the average percentage reduction in the velocities was consistent with the overall observed damage in the bridge. However, there was no clear correlation between a specific wave passage and the observed reduction in the velocities. This indicates that the uniform shear beam model was too simple to localize the damage in the bridge. Instead, it provides a proxy for the overall extent of change in the response due to damage.
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Viksna, Ludmila, Oksana Kolesova, Aleksandrs Kolesovs, Ieva Vanaga, and Seda Arutjunana. Clinical characteristics of COVID-19 patients (Latvia, Spring 2020). Rīga Stradiņš University, December 2020. http://dx.doi.org/10.25143/fk2/hnmlhh.

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Data include following variables: Demographics, epidemiological history, comorbidities, diagnosis, complications, and symptoms on admission to the hospital. Also, body’s temperature and SpO2. Blood cells: white cells count (WBC), neutrophils (Neu), lymphocytes (Ly), eosinophils (Eo) and monocytes (Mo), percentages of segmented and banded neutrophils, erythrocytes (RBC), platelet count (PLT), hemoglobin (Hb), and hematocrit (HCT); Inflammatory indicators: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); Tissue damage indicators: alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and troponin T (TnT); Electrolytes: potassium and sodium concentration; Renal function indicators: creatinine and glomerular filtration rate (GFR); Coagulation tests: D-dimer, prothrombin time, and prothrombin index on admission to the hospital.
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