Relevant bibliographies by topics / Instability-induced

Academic literature on the topic 'Instability-induced'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Instability-induced"

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Alexandre, Jean, Vincenzo Branchina, and Janos Polonyi. "Instability induced renormalization." Physics Letters B 445, no. 3-4 (January 1999): 351–56. http://dx.doi.org/10.1016/s0370-2693(98)01491-9.

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Bloch, Anthony M., Michael I. Weinstein, and Patrick Hagerty. "Radiation Induced Instability." SIAM Journal on Applied Mathematics 64, no. 2 (January 2004): 484–524. http://dx.doi.org/10.1137/s0036139902418717.

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Chen, Zhong-Ying. "Noise-induced instability." Physical Review A 42, no. 10 (November 1, 1990): 5837–43. http://dx.doi.org/10.1103/physreva.42.5837.

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Markenscoff, Xanthippi. "Diffusion induced instability." Quarterly of Applied Mathematics 59, no. 1 (March 1, 2001): 147–51. http://dx.doi.org/10.1090/qam/1811099.

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Naugolnykh, Konstantin A. "Sound induced plume instability." Journal of the Acoustical Society of America 137, no. 4 (April 2015): 2372. http://dx.doi.org/10.1121/1.4920621.

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Morgan, William F. "RADIATION-INDUCED GENOMIC INSTABILITY." Health Physics 100, no. 3 (March 2011): 280–81. http://dx.doi.org/10.1097/hp.0b013e3182082f12.

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Khurram, Tariq, Liu Yuzhou, Jiwani Faiz, and Rana Fauzia. "Scurvy Induced Hemodynamic Instability." British Journal of Medicine and Medical Research 10, no. 10 (January 10, 2015): 1–5. http://dx.doi.org/10.9734/bjmmr/2015/18066.

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Ujhelyi, Michael R., Gerald E. Halula, and Kenneth A. Skau. "EXOGENOUSADENOSINEREVERSESTHEOPHYLLINE INDUCED HEMODYNAMIC INSTABILITY." Critical Care Medicine 21, Supplement (April 1993): S262. http://dx.doi.org/10.1097/00003246-199304001-00257.

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Rajasingh, Charlotte Mary, Thomas G. Weiser, Lisa M. Knowlton, Lakshika Tennakoon, David A. Spain, and Kristan L. Staudenmayer. "Trauma-induced insurance instability." Journal of Trauma and Acute Care Surgery 84, no. 6 (June 2018): 876–84. http://dx.doi.org/10.1097/ta.0000000000001832.

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Kronenberg, A. "Radiation-induced Genomic Instability." International Journal of Radiation Biology 66, no. 5 (January 1994): 603–9. http://dx.doi.org/10.1080/09553009414551691.

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Dissertations / Theses on the topic "Instability-induced"

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Santos, Tapia Celia. "Understanding chromosomal instability-induced senescence." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/671915.

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Aneuploidy, defined as a chromosome number that deviates from a multiple of the haploid set, is a common feature in human cancer, and around 70% of human solid tumours are aneuploid. The resulting metabolic imbalance is proposed to play a fundamental role in the compromised fitness of these cells and lead to malignant transformation by causing proteotoxic stress and affecting cell cycle proliferation and growth. However, most of the molecular pathways and cellular behaviours underlying aneuploid-induced tumorigenesis remain uncharacterized. Drosophila larval epidermal primordia have proved useful model systems to demonstrate the contribution of aneuploidy-induced metabolic stress to tumour growth. By depleting different Spindle Assembly Checkpoint (SAC) genes in the epithelial cells, we induce chromosomal instability and generate aneuploidy. When prevented from undergoing programmed cell death (PCD), these cells give rise to a neoplasic overgrowth. Here we propose that CIN-induced aneuploidy in epithelial cells activates low levels of the c-Jun N-terminal kinase (JNK) and the DNA damage response (DDR). This induces a G1 stall that prevents the accumulation of damage. However, when due to CIN these cells become highly aneuploid, they delaminate from the epithelium and acquire a senescent behaviour. This senescent behaviour is dependent on high levels of JNK and DDR signalling, and induce the secretion of wide variety of factors - also known as the senescence-associated secretory phenotype (SASP) -, and a permanent G2 arrest, among other senescent features. In addition, we have identified two target effectors, Fizzy-related and String, that are miss-regulated and could act downstream JNK and the DDR to induce the G2 arrest. Finally, we were able to explore two different ways to target CIN-aneuploid cells based on their basal levels of replicative stress: genetic (CycE/Dap overexpression) and chemical (Hydroxyurea), which significantly affect tissue growth and impair tumour progression.
La aneuploidía, que se define como un número de cromosomas diferente al haploide, es una característica muy común en cáncer ya que se encuentra en alrededor de 68% de los tumores sólidos. Esta resulta en un desequilibrio metabólico que compromete la función celular induciendo estrés proteotóxico y afectando el crecimiento celular, dando lugar a así a una transformación maligna de estas células. Sin embargo, muchos de los mecanismos moleculares detrás de esta transformación generada por la aneuploidía son aún desconocidos. En este trabajo, usamos el epitelio del ala de Drosophila como tejido modelo para demostrar la contribución de la aneuploidía al crecimiento tumoral. Mediante la inhibición de genes del checkpoint del huso mitótico, inducimos inestabilidad cromosómica y aneuploidía que, tras bloquear la muerte celular, da lugar a un sobrecrecimiento tumoral. Cuando las células no tienen aún altos niveles de aneuploidía, activan bajos niveles de la quinasa c-Jun N-terminal (JNK) y activan la respuesta a daño en el DNA (DDR). Esto induce un arresto temporal en G1 que previene la acumulación de más daño. Sin embargo, debido a la inestabilidad cromosómica, estas células continúan proliferando y acumulan altos niveles de aneuploidía, delaminan del epitelio y adquieren un comportamiento senescente. Este depende de la activación de altos niveles de JNK y la DDR y tiene como consecuencia la secreción de distintos factores (SASP) y un arresto permanente en G2, entre otras características senescentes. Además, hemos podido identificar dos factores involucrados en el arresto, Tribbles and String, que podrían actuar en respuesta a JNK y a la DDR para hacer efectivo el arresto en G2. Finalmente, exploramos dos maneras distintas de afectar los tumores CIN aprovechando que sufren daño en el DNA: genéticamente (mediante la sobre-expresión de CycE/Dap) y químicamente (mediante el tratamiento con hidroxiurea), afectando ambas el crecimiento del tejido e inhibiendo la progresión tumoral.
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Papadopoulou, Charikleia. "Replication stress-induced epigenetic instability." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708935.

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Li, Maoxin. "Seepage induced instability in widely graded soils." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/862.

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Internal instability of a widely graded cohesionless soil refers to a phenomenon in which its finer particles migrate within the void network of its coarser particles, as a result of seepage flow. Onset of internal instability of a soil is governed by a combination of geometric and hydromechanical constraints. Much concern exists for embankment dams and levees built using soils with a potential for internal instability. Migration of finer particles to a boundary where they can exit, by washing out, may cause erosion or piping failure and, occasionally, induce collapse of these soil structures. There is a need, in professional practice, to better understand the phenomenon and to develop improved methods to evaluate the susceptibility of a soil. A series of permeameter tests was performed on six widely-graded cohesionless materials. The objectives are to assess the geometric indices proposed for evaluation of susceptibility, and examine hydromechanical factors influence the onset of internal instability. A modified slurry mixing technique, with discrete deposition, was found satisfactory for reconstitution of the homogeneous saturated test specimens. The onset of internal instability was founded to be triggered by a combination of effective stress and hydraulic gradient. The finding yields a hydromechanical envelope, unique for a particular gradation shape, at which internal instability initiated. Three commonly used geometric criteria were comprehensively evaluated with reference to these experimental data and also a database compiled from the literature. The relative conservatism of each criterion was examined and a modified semi-empirical geometric rule then proposed based on the capillary tube model. A theoretical framework for plotting the hydromechanical envelope was established based on an extension of the α concept of Skempton and Brogan, and subsequently verified by test data. Finally, a novel unified approach was proposed to assess the onset of internal instability, based on combining geometric and hydromechanical indices of a soil.
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Krivets, V. V., K. J. Ferguson, and J. W. Jacobs. "Turbulent mixing induced by Richtmyer-Meshkov instability." AMER INST PHYSICS, 2017. http://hdl.handle.net/10150/625211.

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Richtmyer-Meshkov instability is studied in shock tube experiments with an Atwood number of 0.7. The interface is formed in a vertical shock tube using opposed gas flows, and three-dimensional random initial interface perturbations are generated by the vertical oscillation of gas column producing Faraday waves. Planar Laser Mie scattering is used for flow visualization and for measurements of the mixing process. Experimental image sequences are recorded at 6 kHz frequency and processed to obtain the time dependent variation of the integral mixing layer width. Measurements of the mixing layer width are compared with Mikaelian's [1] model in order to extract the growth exponent. where a fairly wide range of values is found varying from theta approximate to 0.2 to 0.6.
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Pornprompanya, Methasit. "Instability of excitation waves induced by electrical fields." [S.l. : s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975449834.

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Ivanochko, Danton. "ATRX Protects Cells Against Replication-Induced Genomic Instability." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35123.

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Expansive proliferation of neural progenitor cells (NPCs) is a prerequisite to the temporal waves of neuronal differentiation that generate the six-layered cerebral cortex. NPC expansion places a heavy burden on proteins that regulate chromatin packaging and genome integrity, which is further reflected by the growing number of developmental disorders caused by mutations in chromatin regulators. Accordingly, mutations in ATRX, a chromatin remodelling protein required for heterochromatin maintenance at telomeres and simple repeats, cause the ATR-X syndrome. Here, we demonstrate that proliferating ATRX-null cells accumulate DNA damage, while also exhibiting sensitivity to hydroxyurea-induced replication fork stalling. Specifically, PARP1 hyperactivation and replication-dependent double strand DNA breakage indicated replication fork protection defects, while DNA fiber assays confirmed that ATRX was required to protect replication forks from degradation. Interestingly, inhibition of the exonuclease MRE11 by the small molecule mirin could prevent degradation. Thus, ATRX is required to limit replication stress during NPC expansion.
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Hosseini, Seyed M., Ardeshir Hanifi, and Dan Henningson. "Effect of freestream turbulence on roughness-induced crossflow instability." KTH, Stabilitet, Transition, Kontroll, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-123192.

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The effect of freestream turbulence on generation of crossflow disturbances over swept wings is investigated through direct numerical simulations.  The set up follows  the  experiments  performed  by Downs  et  al.  in their  TAMU  experi- ment.  In this experiment the authors use ASU(67)-0315 wing geometry which promotes  growth  of crossflow  disturbances.   Distributed  roughness  elements are locally placed near the leading edge with a span-wise wavenumber, to ex- cite the corresponding crossflow vortices.  The response of boundary layer to external disturbances such as roughness heights, span-wise wavenumbers, Rey- nolds numbers and freestream turbulence characteristics are studied.  It must be noted that the experiments were conducted at a very low level of freestream turbulence  intensity  (T u).   In this  study,  we fully  reproduce the  freestream isotropic homogenous turbulence through a DNS code using detailed freestream spectrum data provided by the experiment. The generated freestream fields are then applied as the inflow boundary condition for direct numerical simulation of the wing. The geometrical set up is the same as the experiment along with application of distributed roughness elements near the leading edge to precipi- tate stationary crossflow disturbances.  The effects of the generated freestream turbulence are then studied on the initial amplitudes and growth of the bound- ary layer perturbations.  It appears that the freestream turbulence damps out the dominant stationary crossflow vortices.

QC 20130604

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Al-Mayah, Ammar Hassan Jasim. "Radiation-induced genomic instability and cellular communication : mechanistic investigations." Thesis, Oxford Brookes University, 2012. https://radar.brookes.ac.uk/radar/items/573581b4-6468-4c41-8fab-17bfdcf489d6/1/.

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Communication between irradiated and un-irradiated (bystander) cells can cause damage in cells that are not directly targeted by ionizing radiation (IR); a process known as the bystander effect (BE). BE can also lead to genomic instability GI) within the progeny of bystander cells, similar to the progeny of directly irradiated cells. The molecular factors that mediate this cellular communication can be transferred between cells via gap junctions or be released into the extracellular media/microenvironment of cells and tissue following irradiation. Although GI is thought to be a critical step in the onset and progression of cancer, BE response contributions in such processes are still not clear. Therefore, this study was designed to investigate the risks or benefits associated with the induction of non-targeted effects especially BE following exposure to low LET X-ray radiation using two different cell types. Additionally, the project aims to achieve an increased understanding of the mechanisms of non-targeted effects of ionizing radiation by examining the molecular signalling via exosomes within the irradiated, bystander and progeny of irradiated and bystander cell population. Different cell combinations were established between tumour (MCF7) and nontumour (HMT-3522S1) human breast epithelial cells using a 6-well plate co-culture system. The cells were irradiated with two doses of X-ray; 0.1 Gy (a diagnostic procedure relevant dose) and 2 Gy (therapeutic dose) and a sham-irradiation dose of 0 Gy (for control groups of experiment). The co-culturing time was 4 hours for all cell combination, whereupon a media transfer approach as used to induce BE within the cells in the exosome part of this study. The early and late cellular damage responses were evaluated by the following biological endpoints: cytogenetic/chromosomal analysis, apoptotic analysis, telomere length and telomerase activity measurements. In addition to these biological endpoints, the comet assay was utilised to estimate the initial and delayed DNA damage within the cells that had been treated with exosomes, previously extracted from the irradiated, bystander and control cell media. The results showed that 2 Gy direct irradated MCF7 and HMT cells were both able to induce early and late chromosomal damage in the bystander MCF7 and HMT cells. Furthermore, these bystander cells exhibited early and delayed telomeric instability, which could prompt further GI at later time-points. In comparison, 0.1 Gy direct irradiated MCF7 cells were only able to induce initial and delayed chromosomal damage within the bystander MCF7, which also demonstrated a high level of telomeric instability at early and late time-points. While, bystander HMT cells did not show chromosomal damage after 1, 12 and 24 generations/population doublings following co-culture with 0.1 Gy direct irradiated MCF7 or HMT cells. 0.1 Gy bystander HMT cells did reveal a high level of apoptosis at early and late time points, which might be due the removal of cells with a high level of chromosomal damage. Interestingly, the 0.1 Gy bystander HMT cells exhibited significant levels of telomeric instability at early and late time points, which could contribute to chromosomal instability at later time-points. The investigation in to the mechanisms of molecular signalling via exosomes showed that the exosomes of irradiated cell conditioned media (ICCM) from MCF7 cells had the ability to induce BE within MCF7 and HMT cells similar to the effects of ICCM following 2 Gy X-ray. The exosomes that were isolated from the MCF7 bystander cell media had a similar effect as the ICCM on the MCF7 and HMT bystander cells. These exosome-bystander cells also showed GI within their progeny after 24 generations and retained the ability to induce cellular damage to fresh un-irradiated MCF7 cells, demonstrating an underlying mechanism for propagating the delayed damage responses. The inhibition of the exosome’s cargo molecules by RNase treatment and protein denaturating (boiling of exosmes) significantly abrogated BE and GI in both MCF7 and HMT bystander cells following 2 Gy X-ray. Thus data demonstrated crucial roles for exosome RNA and protein molecules in the non-targeted effects of IR induction. In summary, our investigations demonstrate that BE has detrimental consequences within the tumour and non-tumour breast epithelial cells (MCF7 and HMT3522S1) following low and high doses of X-ray irradiation, and these detrimental consequences are frequently mediated by exosomes that contain RNA and protein molecules. Inhibition of these molecules can abrogate BE and GI following a radiotherapy dose, which can potentially have an application in clinical radiotherapy.
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Bright, Scott James. "The role of lysosomes in radiation induced genomic instability." Thesis, Oxford Brookes University, 2013. https://radar.brookes.ac.uk/radar/items/a72f01e0-a29b-41a8-ad4c-e54ae04ed7ee/1/.

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Our understanding of ionizing radiation and its associated biological effects has recently under- gone a paradigm shift from a DNA-centric model to one inclusive of non-targeted effects (NTE), so called for the lack of direct radiation interaction with DNA. Two effects encompassed within the NTE paradigm are termed genomic instability (GI) and bystander effects (BE). GI can be described as an increase in rate of genetic alterations many cell generations after the initial radi- ation exposure. BE can be defined as the manifestation of radiation like effects in un-irradiated cells that have communicated with cells that have been irradiated either through inter-signalling utilising gap junctions or the secretion of a soluble diffusion signalling factor. The exact mechanisms that underlie these processes are still under investigation but a wealth of evidence suggests that a number of mechanisms are involved. These include; cytokine signalling, oxidative stress, inflammation and sub-cellular alterations, in addition to factors such as genetic background and radiation quality/dose. This study was designed to investigate lysosomal involvement in radiation induced NTE, whether it be downstream of one of the above mentioned mechanisms, or independent of their involve- ment. To this end the primary human fibroblast cell line, HF19, was exposed to X-rays at therapeutic and diagnostic doses of 2 and 0.1 Gy respectively. Bystander groups were also established by media transfer techniques. Cells were analysed over the first 24 hours and then at 1 and 20 population doublings, initially for detection of GI and BE and thus confirm the suitability of the system. The lysosomes were then analysed for permeability and their distri- bution within the cell. Oxidative stress was also measured in a bid to correlate this event with lysosomal perturbations. Finally lysosomal contents, in particular DNaseIIα, were analysed for their cellular location along with analysis of nuclear membrane permeability which we surmised would facilitate the redistribution of lysosomal enzymes. The results demonstrated that HF19 cells were susceptible to the induction of GI and BE. The latter was noted within the first hour following irradiation in both 0.1 and 2 Gy bystander groups. High levels of chromosomal instability were also induced in both 0.1 and 2 Gy directly irradiated groups, 1 population doubling after exposure. Chromosomal instability was still noted at 20 population doublings mainly in the 2 Gy although the 0.1 Gy group did show elevated levels. A similar pattern was observed in the bystander group. However we were unable to detect sustained production of the bystander signal at 20 population doublings. Lysosomal properties were also characterised and measured at corresponding time points; large alterations were observed in the first 24 hours following irradiation, furthermore, the lysosomes appeared more permeable at 20 population doublings especially in bystander groups, however, these changes did not correlate with increases in oxidative stress. As a result we further exam- ined cells for changes in the distribution of lysosomal enzymes, in particular DNaseIIα, however no significant changes were observed. Nuclear permeability was additionally investigated as to whether increased permeability facilitated enzyme redistribution; however permeability ap- peared reduced rather than increased. In summary, our investigations have demonstrated and confirmed that HF19 cells are susceptible to the induction of GI and BE following low LET X-ray exposure. The results suggest that the mechanism of radiation induced GI and BE responses can be correlated with alterations in lysosomal membrane permeability which appears independent of oxidative stress. We also demonstrated that if lysosomes are involved in NTE it is unlikely to be through direct action of DNaseIIα but rather from enzymes such as acid sphingomylinase. To conclude, radiation was able to alter lysosomes and nuclear permeability at delayed time points which was correlated with GI , however it appears DNaseIIα is not involved. It also appears that an early effect of the bystander signal may have antioxidant property.
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Kim, Hyun-Min. "Genome instability induced by triplex forming mirror repeats in S.cerevisiae." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/33874.

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The main goal of this research is to understand molecular mechanisms of GAA/TTC-associated genetic instability in a model eukaryotic organism, S. cerevisiae. We demonstrate that expanded GAA/TTC repeats represent a threat to eukaryotic genome integrity by triggering double-strand breaks and gross chromosomal rearrangements. The fragility potential strongly depends on the length of the tracts and orientation of the repeats relative to the replication origin and to block replication fork progression. MutSbeta complex and endonuclease activity of MutLalpha play an important role in facilitation of fragility. In addition to GAA/TTC triplex forming repeats, non-GAA polypurine polypyrimidine mirror repeats that are prone to the formation of similar structures were found to be hotspots for rearrangements in humans and other model organisms. These include H-DNA forming sequences located in the major breakpoint cluster region at BCL2, intron 21 of PKD1, and promoter region of C-MYC. Lastly, we have investigated the effect of the triplex-binding small molecules, azacyanines, on GAA-mediated fragility using the chromosomal arm loss assay. We have found that in vivo, azacyanines stimulate (GAA/TTC)-mediated arm loss in a dose dependent manner in actively dividing cells. Azacyanines treatment enhances the GAA-induced replication arrest. We discovered that also, azacyanines at concentrations that induce fragility also inhibit cell growth. Over 60% of yeast cells are arrested at G2/M stage of the cell cycle. This implies an activation of DNA-damage checkpoint response.
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Books on the topic "Instability-induced"

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Li, Jia. Effect of geomagnetically induced current (GIC) on second harmonic instability of HVDC converter. Ottawa: National Library of Canada, 1993.

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Hofmeister, R. Jon. Earthquake-induced slope instability: Methodology of relative hazard mapping, Salem Hills and Eola Hills, Marion and Polk counties, Oregon. Portland, Or: State of Oregon, Dept. of Geology and Mineral Industries, 2000.

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Hofmeister, R. Jon. Earthquake-induced slope instability: Methodology of relative hazard mapping, Salem Hills and Eola Hills, Marion and Polk counties, Oregon. [Portland, Or.]: Dept. of Geology and Mineral Industries, 2000.

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Hofmeister, R. Jon. Earthquake-induced slope instability: Methodology of relative hazard mapping, Salem Hills and Eola Hills, Marion and Polk counties, Oregon. [Portland, Or.]: Dept. of Geology and Mineral Industries, 2000.

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Crespellani, Teresa, ed. Terremoto e ricerca. Florence: Firenze University Press, 2008. http://dx.doi.org/10.36253/978-88-8453-819-2.

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The profound cultural transformation that has taken place in Italian seismic studies in the last ten years is distinguished by the growing interest in the problem of assessing the effects of earthquakes linked to local conditions, and in the related issue of a precise definition of the properties of the soil in the sphere of the dynamic and cyclical stresses induced by seismic actions. Despite the profound awareness of the extent to which the nature of the soil contributes to the destructive effects of earthquakes, we are still a long way from the possibility of a realistic forecast of the seismic behaviour of the Italian soils. This is because the identification of the dynamic properties calls for experimental equipment that is technologically complex and costly as well as lengthy observation and qualified personnel. The rare experimental data that have been acquired to date hence represent a fundamental element for scientific reflection. This book has been conceived with a view to setting at the disposal of a broader public the results of the tests conducted on site and in the laboratory on the soil of certain significant seismic areas using the dynamic-type apparatus of the Geotechnical Laboratory of the Department of Civil and Environmental Engineering (DICeA) of the University of Florence. It presents a selection of the works of the Geotechnical section of the DICeA that have been published in various specialist international and national ambits. These studies were largely launched following the seismic sequence in Umbria and the Marches, in collaboration with several Regional Authorities and Research Institutes for the reduction of the seismic risk in Italy (GNDT, IRRS, INGV). In addition to the experimental techniques and the results obtained, the models and the geotechnical procedures adopted for assessing the effects of site and soil instability in certain specific deposits of the Italian territory are also expounded.
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Krishnan, Radhakrishnan, and Lewis Research Center. Institute for Computational Mechanics in Propulsion., eds. A fully implicit time accurate method for hypersonic combustion: Application to shock-induced combustion instability. Cleveland, Ohio: National Aeronautics and Space Administration, Lewis Research Center, Ohio Aerospace Institute, Institute for Computational Mechanics in Propulsion, 1994.

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Barzilai, Ori, Mark H. Bilsky, and Ilya Laufer. Spine Metastases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0028.

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A decision-making framework called NOMS (neurologic, oncologic, mechanical, and systemic) facilitates and guides therapeutic decisions for patients with spinal metastases. Patients should be evaluated for signs of myelopathy or cauda equina. The Epidural Spinal Cord Compression scale facilitates reporting of the degree of radiographic spinal cord compression. A determination of the expected histology-specific tumor response to conventionally fractionated external beam radiation and systemic therapy should be made. Radiation therapy effectively treats biologic pain and radiosensitive tumors such as multiple myeloma. Patients should undergo a careful evaluation of movement-associated pain as tumor-induced spinal instability is an independent indication for surgery. Determination of tumor-associated mechanical instability can be facilitated by the Spinal Instability Neoplastic Score. Herein, the authors present a case of spinal multiple myeloma managed using the NOMS framework and in consideration of current evidence and treatment paradigms.
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Sabato, Stefano. Neuroblastoma Resection. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0038.

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Neuroblastoma is the most common extracranial solid tumor of childhood. Staging of neuroblastoma has both prognostic value and guides therapy and interventions. Surgical resection and chemotherapy remain the main modes of therapy, and chemotherapeutic agents have both immediate and long-term implications for the anesthetic management of these patients. Though less common, some patients may have catecholamine-induced hemodynamic instability. Thorough perioperative planning and adequate vascular access are required for these procedures. This chapter will prepare the reader to know how to assess and optimize a child with neuroblastoma for surgery, appreciate some of the difficulties of anesthesia for the child with cancer, and understand the principles of management of major blood loss during pediatric surgery.
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Tanaka, H. Phase separation in soft matter: the concept of dynamic asymmetry. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198789352.003.0015.

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In this article, we review the basic physics of viscoelastic phase separation including fracture phase separation. We show that with an increase in the ratio of the deformation rate of phase separation to the slowest mechanical relaxation rate the type of phase separation changes from fluid phase separation, to viscoelastic phase separation, to fracture phase separation. We point out that there is a physical analogy of this to the transition of the mechanical fracture behaviour of materials under shear from liquid-type, to ductile, to brittle fracture. This allows us to discuss phase separation and shear-induced instability of disordered materials including soft matter, on the same physical ground. Finally it should be noted that what we are going to describe in this article has not necessarily been firmly established and there still remain many open problems to be studied in the future.
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van Houselt, Arie, and Harold J. W. Zandvliet. Self-organizing atom chains. Edited by A. V. Narlikar and Y. Y. Fu. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199533046.013.9.

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This article examines the intriguing physical properties of nanowires, with particular emphasis on self-organizing atom chains. It begins with an overview of the one-dimensional free electron model and some interesting phenomena of one-dimensional electron systems. It derives an expression for the 1D density of states, which exhibits a singularity at the bottom of the band and extends the free-electron model, taking into consideration a weak periodic potential that is induced by the lattice. It also describes the electrostatic interactions between the electrons and goes on to discuss two interesting features of 1D systems: the quantization of conductance and Peierls instability. Finally, the article presents the experimental results of a nearly ideal one-dimensional system, namely self-organizing platinum atom chains on a Ge(001) surface, focusing on their formation, quantum confinement between the Pt chains and the occurrence of a Peierls transition within the chains.
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Book chapters on the topic "Instability-induced"

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Eslami, Reza, Richard B. Hetnarski, Jozef Ignaczak, Naotake Noda, Naobumi Sumi, and Yoshinobu Tanigawa. "Thermally Induced Instability." In Theory of Elasticity and Thermal Stresses, 535–69. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6356-2_21.

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Vahid-Araghi, Orang, and Farid Golnaraghi. "Friction-Induced Instability." In Friction-Induced Vibration in Lead Screw Drives, 31–66. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1752-2_4.

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Wang, Jiunn-Ming. "Coherent-instability-induced radiation." In Lecture Notes in Physics, 255–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/3540565884_14.

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Jeng, Dong-Sheng. "Wave-Induced Seabed Instability." In Porous Models for Wave-seabed Interactions, 79–108. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-33593-8_4.

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Yue, Ning J., Kent Lambert, Jay E. Reiff, Anthony E. Dragun, Ning J. Yue, Jay E. Reiff, Jean St. Germain, et al. "Radiation-Induced Genomic Instability." In Encyclopedia of Radiation Oncology, 718–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_290.

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Wang, Jiunn-Ming. "Coherent-Instability-Induced Radiation." In Frontiers of Particle Beams: Factories with e+ e- Rings, 255–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-13972-1_14.

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Verhulst, Ferdinand. "Quenching Damping-Induced Instability." In Springer Proceedings in Physics, 543–47. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2069-5_73.

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Vinogradov, A. M. "Nonlinear Instability Induced by Creep." In Creep in Structures, 659–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84455-3_76.

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Yu, Huan, and Miroslav Krstic. "Control Under Routing-Induced Instability." In Systems & Control: Foundations & Applications, 277–89. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-19346-0_12.

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Scanlon, Susan E., and Peter M. Glazer. "Genetic Instability Induced by Hypoxic Stress." In Stress-Induced Mutagenesis, 151–81. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6280-4_8.

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Conference papers on the topic "Instability-induced"

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Matsuo, A. "Instability of projectile-induced combustion." In 40th AIAA Aerospace Sciences Meeting & Exhibit. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2002. http://dx.doi.org/10.2514/6.2002-775.

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Creek, Jefferson Louis, Jianxin Wang, and Jill S. Buckley. "Asphaltene Instability Induced by Light Hydrocarbons." In Offshore Technology Conference. Offshore Technology Conference, 2008. http://dx.doi.org/10.4043/19690-ms.

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Hiraki, Koju, Harald Kleine, Hirotaka Maruyama, Tetsuya Hayashida, Kazuya Kitamura, Jun Yonai, Takashi Nakajima, and Goji Etoh. "Flow instability induced by spiked bodies." In 28th International Congress on High-Speed Imaging and Photonics, edited by Harald Kleine and Martha Patricia Butron Guillen. SPIE, 2008. http://dx.doi.org/10.1117/12.823751.

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Sherif, Hany A. "Geometric Induced Instability in Drum Brakes." In Annual Colloquium On Brakes & Engineering Display. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 1993. http://dx.doi.org/10.4271/933072.

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Wada, Yukari, and Kazunori Kuwana. "Flame Fractal Dimension Induced by Hydrodynamic Instability." In ASME/JSME 2011 8th Thermal Engineering Joint Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/ajtec2011-44222.

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Premixed flames self-turbulized due to hydrodynamic instability have self-similar, fractal-like structures as evidenced by the acceleration of spherically-propagating flames. The fractal dimension of a self-turbulized premixed flame needs to be known if its apparent flame speed is to be estimated. CFD simulations of outwardly-propagating flames have been conducted to predict their fractal dimensions. There are, however, difficulties in accurately determining fractal dimension based on the flame-propagation behavior of such an outwardly-propagating flame. This paper demonstrates a newly proposed method to determine the fractal dimension based on the CFD simulation of a planar flame. The fractal dimension is computed from the dependency of apparent flame speed on the computational domain size. The computed fractal dimension well agrees with the experimental value. The box-counting method is also applied to calculate the flame’s fractal dimension. The fractal dimensions obtained by these two methods agree well, confirming the fractal nature of the self-turbulized flame.
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Jeng, Dong-Sheng. "Wave-Induced Seabed Instability around a Breakwater." In Coastal Structures and Solutions to Coastal Disasters Joint Conference 2015. Reston, VA: American Society of Civil Engineers, 2017. http://dx.doi.org/10.1061/9780784480304.083.

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Krivets, V. V., K. J. Ferguson, and J. W. Jacobs. "Turbulent mixing induced by Richtmyer-Meshkov instability." In SHOCK COMPRESSION OF CONDENSED MATTER - 2015: Proceedings of the Conference of the American Physical Society Topical Group on Shock Compression of Condensed Matter. Author(s), 2017. http://dx.doi.org/10.1063/1.4971732.

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Murphy, J. B., and J. M. Wang. "A study on microwave instability induced radiation." In Proceedings of the 1999 Particle Accelerator Conference (Cat. No.99CH36366). IEEE, 1999. http://dx.doi.org/10.1109/pac.1999.795463.

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Pourazarm, Pariya, Yahya Modarres-Sadeghi, and Matthew A. Lackner. "Flow-induced instability of wind turbine blades." In 32nd ASME Wind Energy Symposium. Reston, Virginia: American Institute of Aeronautics and Astronautics, 2014. http://dx.doi.org/10.2514/6.2014-1219.

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Zaza, Osmanov, Felix A. Aharonian, Werner Hofmann, and Frank Rieger. "Centrifugally induced curvature drift instability in AGN." In HIGH ENERGY GAMMA-RAY ASTRONOMY: Proceedings of the 4th International Meeting on High Energy Gamma-Ray Astronomy. AIP, 2008. http://dx.doi.org/10.1063/1.3076708.

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Reports on the topic "Instability-induced"

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Evans, Helen, David Sedwick, and Martina Veigl. Genomic Instability Induced by Low Dose Irradiation. Office of Scientific and Technical Information (OSTI), July 2006. http://dx.doi.org/10.2172/890743.

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Murphy, Charles H. A Symptom of Payload-Induced Flight Instability. Fort Belvoir, VA: Defense Technical Information Center, September 1990. http://dx.doi.org/10.21236/ada227515.

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Caponi, E. A., H. C. Yuen, F. A. Milinazzo, and P. G. Saffman. Water Wave Instability Induced by a Drift Layer. Fort Belvoir, VA: Defense Technical Information Center, November 1989. http://dx.doi.org/10.21236/ada215530.

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Berk, H., D. Ryutov, and Yu Tsidulko. Temperature-gradient instability induced by conducting end walls. Office of Scientific and Technical Information (OSTI), April 1990. http://dx.doi.org/10.2172/6745675.

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Boslough, Mark, and George Backus. Agent Model Development for Assessing Climate-Induced Geopolitical Instability. Office of Scientific and Technical Information (OSTI), December 2005. http://dx.doi.org/10.2172/1141843.

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Hahm, T. S. Flow shear induced Compton scattering of electron drift instability. Office of Scientific and Technical Information (OSTI), February 1992. http://dx.doi.org/10.2172/5746326.

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Hahm, T. S. Flow shear induced Compton scattering of electron drift instability. Office of Scientific and Technical Information (OSTI), February 1992. http://dx.doi.org/10.2172/10125128.

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Howard L. Liber and Jeffrey L. Schwartz. Molecular Mechanisms of Radiation-Induced Genomic Instability in Human Cells. Office of Scientific and Technical Information (OSTI), October 2005. http://dx.doi.org/10.2172/887495.

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Liber, Howard L. Molecular mechanisms of radiation-induced genomic instability in human cells. Office of Scientific and Technical Information (OSTI), February 2003. http://dx.doi.org/10.2172/811204.

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Chawla, Ambika. Climate-Induced Migration and Instability: The Role of City Governments. One Earth Future Foundation, June 2017. http://dx.doi.org/10.18289/oef.2017.016.

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