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Articoli di riviste sul tema "Instability mechanisms"

Autore: Grafiati

Pubblicato: 7 settembre 2024

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1

Baird, D. M. "Mechanisms of telomeric instability." Cytogenetic and Genome Research 122, no. 3-4 (2008): 308–14. http://dx.doi.org/10.1159/000167817.

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2

Thompson, Sarah L., Samuel F. Bakhoum, and Duane A. Compton. "Mechanisms of Chromosomal Instability." Current Biology 20, no. 6 (2010): R285—R295. http://dx.doi.org/10.1016/j.cub.2010.01.034.

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3

He Bai and M. Arcak. "Instability Mechanisms in Cooperative Control." IEEE Transactions on Automatic Control 55, no. 1 (2010): 258–63. http://dx.doi.org/10.1109/tac.2009.2036301.

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4

Sharma, G., R. V. Ramanujan, and G. P. Tiwari. "Instability mechanisms in lamellar microstructures." Acta Materialia 48, no. 4 (2000): 875–89. http://dx.doi.org/10.1016/s1359-6454(99)00378-x.

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5

Venkatesan, Shriram, Adayapalam T. Natarajan, and M. Prakash Hande. "Chromosomal instability—mechanisms and consequences." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 793 (November 2015): 176–84. http://dx.doi.org/10.1016/j.mrgentox.2015.08.008.

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6

Gollin, Susanne M. "Mechanisms leading to chromosomal instability." Seminars in Cancer Biology 15, no. 1 (2005): 33–42. http://dx.doi.org/10.1016/j.semcancer.2004.09.004.

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7

Shah, Prediman K. "Molecular mechanisms of plaque instability." Current Opinion in Lipidology 18, no. 5 (2007): 492–99. http://dx.doi.org/10.1097/mol.0b013e3282efa326.

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8

Sirignano, William A. "Driving Mechanisms for Combustion Instability." Combustion Science and Technology 187, no. 1-2 (2014): 162–205. http://dx.doi.org/10.1080/00102202.2014.973801.

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9

Gallaire, F., and J. M. Chomaz. "Instability mechanisms in swirling flows." Physics of Fluids 15, no. 9 (2003): 2622–39. http://dx.doi.org/10.1063/1.1589011.

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10

Huang, Jinhua, Jinping Liang, Lijia Huang, and Tingting Li. "Mechanisms of Atherosclerotic Plaque Instability." International Journal of Biology and Life Sciences 5, no. 1 (2024): 9–12. http://dx.doi.org/10.54097/83r6jq74.

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Abstract (sommario):

Cardiovascular disease (CVD) is the leading cause of mortality in humans worldwide. The main cause of CVD is the formation of thrombi due to by unstable atherosclerotic plaque rupture on the arterial wall. Long-term accumulation of thrombi results in vascular remodeling, and subsequent-stenosis of the lumen obstructs the blood flow, thereby leading to myocardial tissue ischemia and hypoxia. Sustained ischemia and hypoxia lead to myocyte necrosis, resulting in irreversible myocardial injury. Many molecular and cellular mechanisms are associated with atherosclerotic plaque instability (API). For example, macrophages can produce various inflammatory factors, adhesion factors, chemokines and matrix metalloproteinases (MMPs), which play important roles in the pathophysiological mechanisms of API and in maintaining plaque stability. These molecules may help predict unstable atherosclerotic plaques. If the plaque is stable, it will not be prone to rupture or thrombosis. Accordingly, in this review, we will discuss the different pathophysiological mechanisms of API and the related roles of macrophages in the mechanisms of API mainly in animal models and humans. We believe this review will provide a theoretical basis for the development of treatments and diagnostic approaches for the management of API.

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11

Hadadi, Mohammad, Ismaeil Ebrahimi, Mohammad Ebrahim Mousavi, Gholamreza Aminian, Ali Esteki, and Mehdi Rahgozar. "The effect of combined mechanism ankle support on postural control of patients with chronic ankle instability." Prosthetics and Orthotics International 41, no. 1 (2016): 58–64. http://dx.doi.org/10.1177/0309364615596068.

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Background:Chronic ankle instability is associated with neuromechanical changes and poor postural stability. Despite variety of mechanisms of foot and ankle orthoses, almost none apply comprehensive mechanisms to improve postural control in all subgroups of chronic ankle instability patients.Objectives:The purpose of this study was to investigate the effect of an ankle support implementing combined mechanisms to improve postural control in chronic ankle instability patients.Study design:Cross-sectional study.Methods:An ankle support with combined mechanism was designed based on most effective action mechanisms of foot and ankle orthoses. The effect of this orthosis on postural control was evaluated in 20 participants with chronic ankle instability and 20 matched healthy participants. The single-limb stance balance test was measured in both groups with and without the new orthosis using a force platform.Results:The results showed that application of combined mechanism ankle support significantly improved all postural sway parameters in chronic ankle instability patients. There were no differences in means of investigated parameters with and without the orthosis in the healthy group. No statistically significant differences were found in postural sway between chronic ankle instability patients and healthy participants after applying the combined mechanism ankle support.Conclusion:The combined mechanism ankle support is effective in improving static postural control of chronic ankle instability patients to close to the postural sway of healthy individual. the orthosis had no adverse effects on balance performance of healthy individuals.Clinical relevanceApplication of the combined mechanism ankle support for patients with chronic ankle instability is effective in improving static balance. This may be helpful in reduction of recurrence of ankle sprain although further research about dynamic conditions is needed.

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12

Eyler, Daniel E., Kylie A. Burnham, Thomas E. Wilson, and Patrick J. O’Brien. "Mechanisms of glycosylase induced genomic instability." PLOS ONE 12, no. 3 (2017): e0174041. http://dx.doi.org/10.1371/journal.pone.0174041.

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13

Pearson, Christopher E., Kerrie Nichol Edamura, and John D. Cleary. "Repeat instability: mechanisms of dynamic mutations." Nature Reviews Genetics 6, no. 10 (2005): 729–42. http://dx.doi.org/10.1038/nrg1689.

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14

Kim, Seoyoung, Shaun E. Peterson, Maria Jasin, and Scott Keeney. "Mechanisms of germ line genome instability." Seminars in Cell & Developmental Biology 54 (June 2016): 177–87. http://dx.doi.org/10.1016/j.semcdb.2016.02.019.

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15

Filipič, Metka. "Mechanisms of cadmium induced genomic instability." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 733, no. 1-2 (2012): 69–77. http://dx.doi.org/10.1016/j.mrfmmm.2011.09.002.

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16

Jefford, Charles Edward, and Irmgard Irminger-Finger. "Mechanisms of chromosome instability in cancers." Critical Reviews in Oncology/Hematology 59, no. 1 (2006): 1–14. http://dx.doi.org/10.1016/j.critrevonc.2006.02.005.

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17

Bayly, B. J., S. A. Orszag, and T. Herbert. "Instability Mechanisms in Shear-Flow Transition." Annual Review of Fluid Mechanics 20, no. 1 (1988): 359–91. http://dx.doi.org/10.1146/annurev.fl.20.010188.002043.

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18

Libby, Peter. "Mechanisms Underlying Instability of Atherosclerotic Plaques." Journal of Vascular and Interventional Radiology 7, no. 1 (1996): 26–27. http://dx.doi.org/10.1016/s1051-0443(96)70018-0.

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19

Glover, Thomas W., Martin F. Arlt, Anne M. Casper, and Sandra G. Durkin. "Mechanisms of common fragile site instability." Human Molecular Genetics 14, suppl_2 (2005): R197—R205. http://dx.doi.org/10.1093/hmg/ddi265.

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20

Dreher, T. M., and G. W. Stevens. "Instability Mechanisms of Supported Liquid Membranes." Separation Science and Technology 33, no. 6 (1998): 835–53. http://dx.doi.org/10.1080/01496399808544879.

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21

Graziano, Simona, and Susana Gonzalo. "Mechanisms of oncogene-induced genomic instability." Biophysical Chemistry 225 (June 2017): 49–57. http://dx.doi.org/10.1016/j.bpc.2016.11.008.

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22

Kaufmann, William K., Craig C. Carson, Bernard Omolo, et al. "Mechanisms of chromosomal instability in melanoma." Environmental and Molecular Mutagenesis 55, no. 6 (2014): 457–71. http://dx.doi.org/10.1002/em.21859.

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23

JIANG, HAN, MING-WEN CHEN, and ZI-DONG WANG. "EFFECT OF ANISOTROPIC SURFACE TENSION ON THE MORPHOLOGICAL STABILITY OF DEEP CELLULAR CRYSTAL GROWTH IN DIRECTIONAL SOLIDIFICATION." Surface Review and Letters 26, no. 06 (2019): 1850210. http://dx.doi.org/10.1142/s0218625x18502104.

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Abstract (sommario):

This paper studies the effect of anisotropic surface tension on the morphological stability of deep cellular crystal in directional solidification by using the matched asymptotic expansion method and multiple variable expansion method. We find that the morphological stability of deep cellular crystal growth with anisotropic surface tension shows the same mechanism as that with isotropic surface tension. The deep cellular crystal growth contains two types of global instability mechanisms: the global oscillatory instability, whose neutral modes yield strong oscillatory dendritic structures, and the low-frequency instability, whose neutral modes yield weakly oscillatory cellular structures. Anisotropic surface tension has the significant effect on the two global instability mechanisms. As the anisotropic surface tension increases, the unstable domain of global oscillatory instability decreases, whereas the unstable domain of the global low-frequency instability increases.

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24

Cox, John P. "Theory of Cepheid Pulsation: Excitation Mechanisms." International Astronomical Union Colloquium 82 (1985): 126–46. http://dx.doi.org/10.1017/s0252921100109248.

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AbstractThe various excitation mechanisms (eight in all) that have been proposed to account for the vibrational instability of variable stars, are surveyed. The most widely applied one is perhaps the “envelope ionization mechanism.” This can account for most of the essential characteristics of the “instability strip.” A simple explanation of the period-luminosity relation of classical Cepheids is given. A few outstanding problems in pulsation theory are also listed.

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25

Pavalavanni, Pradeep Kumar, Min-Seon Jo, Jae-Eun Kim, and Jeong-Yeol Choi. "Numerical Study of Unstable Shock-Induced Combustion with Different Chemical Kinetics and Investigation of the Instability Using Modal Decomposition Technique." Aerospace 10, no. 3 (2023): 292. http://dx.doi.org/10.3390/aerospace10030292.

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An unstable shock-induced combustion (SIC) case around a hemispherical projectile has been numerically studied which experimentally produced a regular oscillation. Comparison of detailed H2/O2 reaction mechanisms is made for the numerical simulation of SIC with higher-order numerical schemes intended for the use of the code for the hypersonic propulsion and supersonic combustion applications. The simulations show that specific reaction mechanisms are grid-sensitive and produce spurious reactions in the high-temperature region, which trigger artificial instability in the oscillating flow field. The simulations also show that specific reaction mechanisms develop such spurious oscillations only at very fine grid resolutions. The instability mechanism is investigated using the dynamic mode decomposition (DMD) technique and the spatial structure of the decomposed modes are further analyzed. It is found that the instability triggered by the high-temperature reactions strengthens the reflecting compression wave and pushes the shock wave further and disrupts the regularly oscillating mechanism. The spatial coherent structure from the DMD analysis shows the effect of this instability in different regions in the regularly oscillating flow field.

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26

Bernier, D., F. Lacas, and S. Candel. "Instability Mechanisms in a Premixed Prevaporized Combustor." Journal of Propulsion and Power 20, no. 4 (2004): 648–56. http://dx.doi.org/10.2514/1.11461.

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27

Wright, E. G. "Radiation-induced genomic instability: manifestations and mechanisms." International Journal of Low Radiation 1, no. 2 (2004): 231. http://dx.doi.org/10.1504/ijlr.2004.003875.

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28

Smith, Marc K. "Instability mechanisms in dynamic thermocapillary liquid layers." Physics of Fluids 29, no. 10 (1986): 3182. http://dx.doi.org/10.1063/1.865836.

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29

Wanschura, M., V. M. Shevtsova, H. C. Kuhlmann, and H. J. Rath. "Convective instability mechanisms in thermocapillary liquid bridges." Physics of Fluids 7, no. 5 (1995): 912–25. http://dx.doi.org/10.1063/1.868567.

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30

Shtern, Vladimir. "Mechanisms of jet instability: role of deceleration." Fluid Dynamics Research 50, no. 5 (2018): 051408. http://dx.doi.org/10.1088/1873-7005/aab0fc.

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31

Jotkar, Mamta, José Miguel Pérez, Vassilis Theofilis, and Rama Govindarajan. "Instability Mechanisms in Straight-Diverging-Straight Channels." Procedia IUTAM 14 (2015): 236–45. http://dx.doi.org/10.1016/j.piutam.2015.03.046.

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32

Bichara, M., J. Wagner, and I. B. Lambert. "Mechanisms of tandem repeat instability in bacteria." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 598, no. 1-2 (2006): 144–63. http://dx.doi.org/10.1016/j.mrfmmm.2006.01.020.

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33

Duijf, Pascal H. G., Devathri Nanayakkara, Katia Nones, Sriganesh Srihari, Murugan Kalimutho, and Kum Kum Khanna. "Mechanisms of Genomic Instability in Breast Cancer." Trends in Molecular Medicine 25, no. 7 (2019): 595–611. http://dx.doi.org/10.1016/j.molmed.2019.04.004.

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34

KOMAROVA, NATALIA L., and SUZANNE J. M. H. HULSCHER. "Linear instability mechanisms for sand wave formation." Journal of Fluid Mechanics 413 (June 25, 2000): 219–46. http://dx.doi.org/10.1017/s0022112000008429.

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A height- and flow-dependent model for turbulent viscosity is employed to explain the generation of sand waves in tidal seas. This new model resolves the problem of excitation of very long waves in sand wave formation, because it leads to damping of the long waves and gives a finite separation between the most excited mode and the zero mode. For parameters within their physically realistic ranges, a linear analysis of the resulting system yields a first excited mode whose wavelength is similar to the characteristic wavelength of sand waves observed in nature. The physical mechanism of sand wave formation as predicted by the new model is explained in detail. The dispersion relation obtained can be the starting point for a weakly nonlinear analysis of the system.

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35

Luongo, A., and G. Piccardo. "Linear instability mechanisms for coupled translational galloping." Journal of Sound and Vibration 288, no. 4-5 (2005): 1027–47. http://dx.doi.org/10.1016/j.jsv.2005.01.056.

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36

Riyopoulos, Spilios. "Instability mechanisms in storage-ring FEL oscillators." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 296, no. 1-3 (1990): 485–98. http://dx.doi.org/10.1016/0168-9002(90)91255-a.

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37

de Cárcer, Guillermo, Pablo Huertas, and Andres J. López-Contreras. "Chromosome instability: From molecular mechanisms to disease." DNA Repair 66-67 (June 2018): 72–75. http://dx.doi.org/10.1016/j.dnarep.2018.04.006.

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38

Tsetseris, L., X. J. Zhou, D. M. Fleetwood, R. D. Schrimpf, and S. T. Pantelides. "Physical mechanisms of negative-bias temperature instability." Applied Physics Letters 86, no. 14 (2005): 142103. http://dx.doi.org/10.1063/1.1897075.

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39

Hasson, Alam S., and Rhon E. Manor. "Steady-state instability in tropospheric chemical mechanisms." Atmospheric Environment 37, no. 34 (2003): 4735–45. http://dx.doi.org/10.1016/j.atmosenv.2003.08.018.

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40

Debatisse, Michelle, Benoît Le Tallec, Anne Letessier, Bernard Dutrillaux, and Olivier Brison. "Common fragile sites: mechanisms of instability revisited." Trends in Genetics 28, no. 1 (2012): 22–32. http://dx.doi.org/10.1016/j.tig.2011.10.003.

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41

Zheng, S. J., J. Wang, J. S. Carpenter, et al. "Plastic instability mechanisms in bimetallic nanolayered composites." Acta Materialia 79 (October 2014): 282–91. http://dx.doi.org/10.1016/j.actamat.2014.07.017.

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42

Schoisswohl, U., and H. C. Kuhlmann. "Instability mechanisms in buoyant-thermocapillary liquid pools." PAMM 7, no. 1 (2007): 4100031–32. http://dx.doi.org/10.1002/pamm.200700696.

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43

Beale, David, and Shyr Wen Lee. "Nonlinear equation instability boundaries in flexible mechanisms." Mechanism and Machine Theory 31, no. 2 (1996): 215–27. http://dx.doi.org/10.1016/0094-114x(95)00063-5.

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44

Blalock, Darryl, Andrew Miller, Michael Tilley, and Jinxi Wang. "Joint Instability and Osteoarthritis." Clinical Medicine Insights: Arthritis and Musculoskeletal Disorders 8 (January 2015): CMAMD.S22147. http://dx.doi.org/10.4137/cmamd.s22147.

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Abstract (sommario):

Joint instability creates a clinical and economic burden in the health care system. Injuries and disorders that directly damage the joint structure or lead to joint instability are highly associated with osteoarthritis (OA). Thus, understanding the physiology of joint stability and the mechanisms of joint instability-induced OA is of clinical significance. The first section of this review discusses the structure and function of major joint tissues, including periarticular muscles, which play a significant role in joint stability. Because the knee, ankle, and shoulder joints demonstrate a high incidence of ligament injury and joint instability, the second section summarizes the mechanisms of ligament injury-associated joint instability of these joints. The final section highlights the recent advances in the understanding of the mechanical and biological mechanisms of joint instability-induced OA. These advances may lead to new opportunities for clinical intervention in the prevention and early treatment of OA.

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45

Hackett, Jennifer A., and Carol W. Greider. "End Resection Initiates Genomic Instability in the Absence of Telomerase." Molecular and Cellular Biology 23, no. 23 (2003): 8450–61. http://dx.doi.org/10.1128/mcb.23.23.8450-8461.2003.

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ABSTRACT Telomere dysfunction causes genomic instability. However, the mechanism that initiates this instability when telomeres become short is unclear. We measured the mutation rate and loss of heterozygosity along a chromosome arm in diploid yeast that lacked telomerase to distinguish between mechanisms for the initiation of instability. Sequence loss was localized near chromosome ends in the absence of telomerase but not after breakage of a dicentric chromosome. In the absence of telomerase, the increase in mutation rate is dependent on the exonuclease Exo1p. Thus, exonucleolytic end resection, rather than chromosome fusion and breakage, is the primary mechanism that initiates genomic instability when telomeres become short.

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46

Appenzeller, I. "Instability in Massive Stars: An Overview." Symposium - International Astronomical Union 116 (1986): 139–49. http://dx.doi.org/10.1017/s0074180900148831.

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Dynamical, vibrational, and thermal instabilities of massive blue stars are discussed as possible mechanisms for the observed brightness variations of such objects. Relaxation oscillations (on local thermal time scales) due to dynamical instabilities of the stellar wind flows appear to be the most likely mechanism, at least for the S Dor variables. Very massive main-sequence stars with M > 103 M⊙ should be violently vibrationally unstable and therefore should differ significantly from stable main-sequence stars of lower mass.

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47

Lam, Michael-Angelo Y. H., Linda J. Cummings, and Lou Kondic. "Stability of thin fluid films characterised by a complex form of effective disjoining pressure." Journal of Fluid Mechanics 841 (March 1, 2018): 925–61. http://dx.doi.org/10.1017/jfm.2017.919.

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We discuss instabilities of fluid films of nanoscale thickness, with a particular focus on films where the destabilising mechanism allows for linear instability, metastability, and absolute stability, depending on the mean film thickness. Our study is motivated by nematic liquid crystal films; however, we note that similar instability mechanisms, and forms of the effective disjoining pressure, appear in other contexts, such as the well-studied problem of polymeric films on two-layered substrates. The analysis is carried out within the framework of the long-wave approximation, which leads to a fourth-order nonlinear partial differential equation for the film thickness. Within the considered formulation, the nematic character of the film leads to an additional contribution to the disjoining pressure, changing its functional form. This effective disjoining pressure is characterised by the presence of a local maximum for non-vanishing film thickness. Such a form leads to complicated instability evolution that we study by analytical means, including the application of marginal stability criteria, and by extensive numerical simulations that help us develop a better understanding of instability evolution in the nonlinear regime. This combination of analytical and computational techniques allows us to reach novel understanding of relevant instability mechanisms, and of their influence on transient and fully developed fluid film morphologies. In particular, we discuss in detail the patterns of drops that form as a result of instability, and how the properties of these patterns are related to the instability mechanisms.

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48

Cuceu, Corina, Bruno Colicchio, Eric Jeandidier, et al. "Independent Mechanisms Lead to Genomic Instability in Hodgkin Lymphoma: Microsatellite or Chromosomal Instability." Cancers 10, no. 7 (2018): 233. http://dx.doi.org/10.3390/cancers10070233.

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Background: Microsatellite and chromosomal instability have been investigated in Hodgkin lymphoma (HL). Materials and Methods: We studied seven HL cell lines (five Nodular Sclerosis (NS) and two Mixed Cellularity (MC)) and patient peripheral blood lymphocytes (100 NS-HL and 23 MC-HL). Microsatellite instability (MSI) was assessed by PCR. Chromosomal instability and telomere dysfunction were investigated by FISH. DNA repair mechanisms were studied by transcriptomic and molecular approaches. Results: In the cell lines, we observed high MSI in L428 (4/5), KMH2, and HDLM2 (3/5), low MSI in L540, L591, and SUP-HD1, and none in L1236. NS-HL cell lines showed telomere shortening, associated with alterations of nuclear shape. Small cells were characterized by telomere loss and deletion, leading to chromosomal fusion, large nucleoplasmic bridges, and breakage/fusion/bridge (B/F/B) cycles, leading to chromosomal instability. The MC-HL cell lines showed substantial heterogeneity of telomere length. Intrachromosmal double strand breaks induced dicentric chromosome formation, high levels of micronucleus formation, and small nucleoplasmic bridges. B/F/B cycles induced complex chromosomal rearrangements. We observed a similar pattern in circulating lymphocytes of NS-HL and MC-HL patients. Transcriptome analysis confirmed the differences in the DNA repair pathways between the NS and MC cell lines. In addition, the NS-HL cell lines were radiosensitive and the MC-cell lines resistant to apoptosis after radiation exposure. Conclusions: In mononuclear NS-HL cells, loss of telomere integrity may present the first step in the ongoing process of chromosomal instability. Here, we identified, MSI as an additional mechanism for genomic instability in HL.

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49

Embacher, Martin, and H. F. Fasel. "Direct numerical simulations of laminar separation bubbles: investigation of absolute instability and active flow control of transition to turbulence." Journal of Fluid Mechanics 747 (April 14, 2014): 141–85. http://dx.doi.org/10.1017/jfm.2014.123.

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AbstractLaminar separation bubbles generated on a flat plate by an adverse pressure gradient are investigated using direct numerical simulations (DNSs). Two-dimensional periodic forcing is applied at a blowing/suction slot upstream of separation. Control of separation through forcing with various frequencies and amplitudes is examined. For the investigation of absolute instability mechanisms, baseflows provided by two-dimensional Navier–Stokes calculations are analysed by introducing pulse disturbances and computing the three-dimensional flow response using DNS. The primary instability of the time-averaged flow is investigated with a local linear stability analysis. Employing a steady flow solution as baseflow, the nonlinear and non-parallel effects on the self-sustained disturbance development are illustrated, and a feedback mechanism facilitated by the upstream flow deformation is identified. Secondary instability is investigated locally using spatially periodic baseflows. The flow response to pulsed forcing indicates the existence of an absolute secondary instability mechanism, and the results indicate that this mechanism is dependent on the periodic forcing. Results from three-dimensional DNS provide insight into the global instability mechanisms of separation bubbles and complement the local analysis. A forcing strategy was devised that suppresses the temporal growth of three-dimensional disturbances, and as a consequence, breakdown to turbulence does not occur. Even for a separation bubble that has transitioned to turbulence, the flow relaminarizes when applying two-dimensional periodic forcing with proper frequencies and amplitudes.

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50

Czechowski, L., and J. M. Floryan. "Marangoni Instability in a Finite Container-Transition Between Short and Long Wavelengths Modes." Journal of Heat Transfer 123, no. 1 (2000): 96–104. http://dx.doi.org/10.1115/1.1339005.

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Marangoni instability in a finite container with a deformable interface in the absence of gravity has been investigated. It is shown that the critical Marangoni number Macr is a non-monotonic function of the length of the container. Two different physical mechanisms driving convection are indicated. The advection of heat is essential for the first, advective (“classical”) mechanism that gives rise to short wavelength modes. The interface deformation is essential for the second mechanism that gives rise to long wavelength modes. If the container is sufficiently long, the second mechanism leads to an unconditional instability. The available results suggest that the unconditional instability leads to segmentation of the interface.

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