Relevant bibliographies by topics / Cell motilty

Academic literature on the topic 'Cell motilty'

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Published: 14 March 2023

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Journal articles on the topic "Cell motilty"

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Schmidt-Tanguy, Aline, Annette Romanski, Mathilde Hunault-Berger, and Oliver G. Ottmann. "Different Roles of Two Autotaxin Isoforms in Proliferation, Migration and Adhesion in the Non-Mutational Tyrosine Kinase Inhibitor Resistant Acute Lymphoblastic Leukemia Cell Line SupB15." Blood 112, no. 11 (November 16, 2008): 1915. http://dx.doi.org/10.1182/blood.v112.11.1915.1915.

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Abstract The Bcr-Abl oncogene is present in 30–40% of adult patients with acute lymphoblastic leukemia (ALL). The Abl kinase inhibitor imatinib-based therapy has become standard for this subset ALL. Acquired resistance to imatinib occurs frequently and is associated with mutations in the tyrosine kinase domain (TKD) approximately in about 80% of patients. In contrast, TKD mutations are uncommon in primary imatinib resistance which appears to be multifactorial, although the underlying mechanisms have been incompletely elucidated. We have established a Ph+ cell line for the analysis of non-mutational resistance mechanisms of imatinib resistance: SupB15RT, a Bcr-Abl expressing lymphoblastic cell line derived from SupB15WT cell line by gradually increasing the exposure to imatinib. SupB15RT shows cross-resistance to the second generation Abl kinase inhibitors Nilotinib and Dasatinib. We have shown that several commonly implicated mechanisms of imatinib resistance do not play a role in conferring the imatinib resistance in SupB15RT cells. By comparative gene expression analysis of SupB15WT vs. SupB15RT cells using Affymetrix- Microarrays, we identified 29 differentially regulated genes. Autotaxin (ATX) is one of the most highly up-regulated genes in imatinib resistant SupB15RT cells, and suggested a contribution to imatinib resistance. ATX is an exo-enzyme (pyrophosphophatase/phosphodiesterase). It plays a role in tumor progression and migration as a tumor cell autocrine motilty factor in various solid tumor cell types. ATX is involved in the synthesis of the signaling molecule, lysophosphatidic acid (LPA) which promotes survival and motility. It was the aim of this study to determine whereas ATX plays a functional role for imatinib resistance in Ph+ ALL. Using RT-PCR we demonstrated that 2 isoforms of ATX are expressed in SupB15RT cells: ATXshort and ATXlong. ATXlong (863 aa) contains highly basic insertion in the catalytic domain (52 residues). We retroviraly transfected BaF3 cells with p185 and/or ATXshort or ATXlong to analyze its influence on growth, adhesion and migration in mouse cell model. In comparison to wild type BaF3 cells the proliferation of BaF3 cells expressing ATXshort is enhanced (1,5-fold), whereas ATXlong expressing BaF3 cells showed no difference in proliferation in comparison to Mock infected cells. The proliferation of p185 expressing BaF3 cells co-expressing ATXshort or ATXlong is not inhibited by the treatment with 1μM imatinib after 3 days in contrast to p185 expressing BaF3 cells. In adhesion experiments, BaF3 cells expressing ATXshort showed a higher attachment independent of p185 expression. We also performed migration experiments using transwell assays. These assays showed more migration with cells co-expressing p185 and ATXlong compared to p185 alone. This is in agreement with our results for SupB15RT vs. SupB15WT with a 3-fold migration increase of SupB15RT. Application of 10% fetal calf serum (FCS) in migration experiments resulted in a 1,5-fold higher migration of the ATXlong expressing BaF3 cells compared to culture without FCS. One explanation for this finding may be that FCS contains lysophosphatidic choline (LPC) which is converted to LPA by ATX. Although expression of both 2 isoforms of ATX is important for the increased proliferation, it seems that the 2 isoforms have different cellular functions in Ph+ lymphoblastic cells. ATXshort seems to enhance adhesion whereas ATXlong plays an important role in motility. Taken together our results indicate a role for ATX in TK- inhibitor resistant SupB15RT cells through LPA signaling via LPA receptors. The ratio between ATXshort and ATXlong probably is important for the intracellular signaling and has to be explored.
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An, Xingyue, Gabrielle Romain, Melisa Martinez-Paniagua, Irfan N. Bandey, Jay R. T. Adolacion, Mohsen Fathi, Ivan Liadi, et al. "CAR+ T cell anti-tumor efficacy revealed by multi-dimensional single-cell profiling." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 134.2. http://dx.doi.org/10.4049/jimmunol.202.supp.134.2.

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Abstract T cells engineered to express chimeric antigen receptor (CAR) targeting CD19 have shown promising clinical responses in patients with certain hematologic malignancies, however, it is desirable to be able to enrich cells with enhanced anti-tumor efficacy prior to infusion. We utilized a suite of high-throughput technologies with single-cell resolution, including Timelapse Imaging Microscopy In Nanowell Grids (TIMING) that integrates cytokine profiling to reveal that persistent motility of CD19- specific CAR T cells is correlated to desirable polyfunctionality (elimination of tumor cells and cytokine secretion), contributing to anti-tumor effects. We implemented a marker-free Boyden chamber-based method to enrich CAR+ T cells with persistent motility (motile cell). Integration of transcriptomic profiling, immune phenotyping and metabolism demonstrated that motile cells are more naïve-like with higher oxidative metabolism and spare respiratory capacity. Our result also revealed that the master metabolic regulator AMP kinase (AMPK) is required for CAR+ T cells with high motility. We used a xenograft leukemia mouse model (CD19+ NALM-6) and validated that the motile cells have enhanced persistence and superior anti-cancer effect in vivo compared to the parental un-sorted population. Collectively, our multi-dimensional results demonstrated that persistent motility is a selectable biomarker of expanded CAR+ T cell bioactivity.
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Cramer, Louise P., Timothy J. Mitchison, and Julie A. Theriot. "Actin-dependent motile forces and cell motility." Current Opinion in Cell Biology 6, no. 1 (February 1994): 82–86. http://dx.doi.org/10.1016/0955-0674(94)90120-1.

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Murakami, Shinya, Yo Otsuka, Manabu Sugimoto, and Toshiyuki Mitsui. "3H1010 Controlled cell migration with ultrasound(Cell Biology III:Cytoskeleton & Motility,Oral Presentation)." Seibutsu Butsuri 52, supplement (2012): S70. http://dx.doi.org/10.2142/biophys.52.s70_4.

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Kolobov, A. V., A. A. Polezhaev, and G. I. Solyanik. "The Role of Cell Motility in Metastatic Cell Dominance Phenomenon: Analysis by a Mathematical Model." Journal of Theoretical Medicine 3, no. 1 (2000): 63–77. http://dx.doi.org/10.1080/10273660008833065.

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Metastasis is the outcome of several selective sequential steps where one of the first and necessary steps is the progressive overgrowth or dominance of a small number of metastatic cells in a tumour. In spite of numerous experimental investigations concerning the growth advantage of metastatic cells, the mechanisms resulting in their dominance are still unknown. Metastatic cell overgrowth occurs even if doubling time of the metastatic subpopulation is shorter than that of all others subpopulations in a heterogeneous tumour. In order to examine the hypothesis that under conditions of competition of cell subpopulations for common substrata cell motility of the slow-growing subpopulation can result in its dominance in a heterogeneous tumour, a mathematical model of heterogeneous tumour growth is suggested. The model describes two cell subpopulations which can grow with different rates and transform into the resting state depending on the concentration of the substrate consumed by both subpopulations. The slow-growing subpopulation is assumed to be motile. In numerical simulations it is shown that this subpopulation is able to overgrow the other one. The dominance phenomenon (resulting from random cell motion) depends on the motility coefficient in a threshold manner: in a heterogeneous tumour the slow-dividing motile subpopulation is able to overgrow its non-motile counterparts if its motility coefficient exceeds a certain threshold value. Computations demonstrate independence of the motile cells overgrowth from the initial tumour composition.
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Rezvan, Ali, Gabrielle Romain, Mohsen Fathi, Darren Heeke, Melisa Martinez-Paniagua, Xingyue An, Irfan N. Bandey, et al. "Multiomic dynamic single-cell profiling of CAR T cell populations associated with efficacy." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 54.18. http://dx.doi.org/10.4049/jimmunol.208.supp.54.18.

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Abstract T-cell therapy with specificity redirected through chimeric antigen receptors (CARs) has shown efficacy for the treatment of hematologic malignancies. Although treatment with CAR T cell can result in high response rates, the properties of the cells that comprise the cellular infusion product, associated with clinical benefit are incompletely understood. We utilized a suite of high-throughput single-cell assays including single-cell RNA-sequencing (scRNA-seq); confocal microscopy; and Timelapse Imaging Microscopy In Nanowell Grids (TIMING). TIMING profiling of a cohort of 16 patients showed that persistent motility of T cells in the presence of tumor cells was associated with both serial killing capacity and polyfunctionality. Confocal microscopy on these same T cells revealed that persistent motility is linearly correlated with both mitochondrial volume and lysosomal number. ScRNA-seq demonstrated that T cells from responders were enriched in pathways related to T-cell proliferative capacity; interferon responses; and a distinct cluster of pathways related to actin cytoskeleton and migration. We employed a marker-free sorting strategy for enriching T cells with persistent motility. RNA-seq on sorted motile T cells showed an enrichment of the core motility signature. These motile T cells also demonstrated superior in vivo anti-leukemia efficacy in comparison to unsorted T cells. Lastly, we also confirmed the association with increased persistent motility and killing of CAR T cells across diverse CARs. In aggregate, our data identified that independent of CAR design or biomanufacturing, persistent motility serves as a selectable cell-intrinsic biomarker, desired in the bioactivity of expanded CAR+ T cells.
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Marth, W., S. Praetorius, and A. Voigt. "A mechanism for cell motility by active polar gels." Journal of The Royal Society Interface 12, no. 107 (June 2015): 20150161. http://dx.doi.org/10.1098/rsif.2015.0161.

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We analyse a generic motility model, with the motility mechanism arising by contractile stress due to the interaction of myosin and actin. A hydrodynamic active polar gel theory is used to model the cytoplasm of a cell and is combined with a Helfrich-type model to account for membrane properties. The overall model allows consideration of the motility without the necessity for local adhesion. Besides a detailed numerical approach together with convergence studies for the highly nonlinear free boundary problem, we also compare the induced flow field of the motile cell with that of classical squirmer models and identify the motile cell as a puller or pusher, depending on the strength of the myosin–actin interactions.
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Breier, Rebekka E., Cristian C. Lalescu, Devin Waas, Michael Wilczek, and Marco G. Mazza. "Emergence of phytoplankton patchiness at small scales in mild turbulence." Proceedings of the National Academy of Sciences 115, no. 48 (November 8, 2018): 12112–17. http://dx.doi.org/10.1073/pnas.1808711115.

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Phytoplankton often encounter turbulence in their habitat. As most toxic phytoplankton species are motile, resolving the interplay of motility and turbulence has fundamental repercussions on our understanding of their own ecology and of the entire ecosystems they inhabit. The spatial distribution of motile phytoplankton cells exhibits patchiness at distances of decimeter to millimeter scales for numerous species with different motility strategies. The explanation of this general phenomenon remains challenging. Furthermore, hydrodynamic cell–cell interactions, which grow more relevant as the density in the patches increases, have been so far ignored. Here, we combine particle simulations and continuum theory to study the emergence of patchiness in motile microorganisms in three dimensions. By addressing the combined effects of motility, cell–cell interaction, and turbulent flow conditions, we uncover a general mechanism: The coupling of cell–cell interactions to the turbulent dynamics favors the formation of dense patches. Identification of the important length and time scales, independent from the motility mode, allows us to elucidate a general physical mechanism underpinning the emergence of patchiness. Our results shed light on the dynamical characteristics necessary for the formation of patchiness and complement current efforts to unravel planktonic ecological interactions.
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Alexandre, Gladys. "Chemotaxis Control of Transient Cell Aggregation." Journal of Bacteriology 197, no. 20 (July 27, 2015): 3230–37. http://dx.doi.org/10.1128/jb.00121-15.

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Chemotaxis affords motile cells the ability to rapidly respond to environmental challenges by navigating cells to niches favoring growth. Such a property results from the activities of dedicated signal transduction systems on the motility apparatus, such as flagella, type IV pili, and gliding machineries. Once cells have reached a niche with favorable conditions, they often stop moving and aggregate into complex communities termed biofilms. An intermediate and reversible stage that precedes commitment to permanent adhesion often includes transient cell-cell contacts between motile cells. Chemotaxis signaling has been implicated in modulating the transient aggregation of motile cells. Evidence further indicates that chemotaxis-dependent transient cell aggregation events are behavioral responses to changes in metabolic cues that temporarily prohibit permanent attachment by maintaining motility and chemotaxis. This minireview discusses a few examples illustrating the role of chemotaxis signaling in the initiation of cell-cell contacts in bacteria moving via flagella, pili, or gliding.
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Cozzolino, Mauro, Venturina Stagni, Laura Spinardi, Nadia Campioni, Carla Fiorentini, Erica Salvati, Stefano Alemà, and Anna Maria Salvatore. "p120 Catenin Is Required for Growth Factor–dependent Cell Motility and Scattering in Epithelial Cells." Molecular Biology of the Cell 14, no. 5 (May 2003): 1964–77. http://dx.doi.org/10.1091/mbc.e02-08-0469.

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Cadherin-mediated cell–cell adhesion is dynamically modulated during epithelial–mesenchymal transition triggered by activation of receptor tyrosine kinases (RTK) in epithelial cells. Several cadherin-binding proteins have been identified that control cell–cell adhesion. However, the mechanisms by which intercellular adhesion and cell motility are coregulated are still unknown. Here, we delineate a hitherto uncharted cooperation between RTKs, RhoA GTPase, and p120 catenin in instructing a motile behavior to epithelial cells. We found that expression of an N-terminus–deleted p120 catenin in a variety of epithelial cell types, including primary keratinocytes, effectively competes for endogenous p120 at cadherin binding sites and abrogates EGF-stimulated cell motility as well as HGF-induced cell scattering. The deleted mutant also inhibits the PI3K-dependent RhoA activation ensuing receptor activation. Conversely, we also show that the ectopic expression of full-length p120 in epithelial cells promotes cytoskeletal changes, stimulates cell motility, and activates RhoA. Both motogenic response to p120 and RhoA activation require coactivation of signaling downstream of RTKs as they are suppressed by ablation of the Ras/PI3K pathway. These studies demonstrate that p120 catenin is a necessary target of RTKs in regulating cell motility and help define a novel pathway leading to RhoA activation, which may contribute to the early steps of metastatic invasion.
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Dissertations / Theses on the topic "Cell motilty"

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Sayyad, Wasim Amin. "Role of Myosin II and Arp 2/3 in the motility and force generation of Neuronal Growth Cones." Doctoral thesis, SISSA, 2015. http://hdl.handle.net/20.500.11767/3890.

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Differentiating neurons have to find chemical cues to form the correct synaptic connections with the other neurons so that they can create a functional neuronal network. During their development differentiating neurons project neurites, at the distal part of which there is a growth cone (GCs). The growth cone has highly motile structures, referred as lamellipodia and filopodia. Lamellipodia and filopodia sense the environment and process the mechanical and chemical stimulus and also exert forces. During my work for the completion of my PhD thesis, I used Optical Tweezers, video imaging and immunocytochemistry to quantify the motility and the force exerted by lamellipodia and filopodia from Dorsal Ganglion (DRG) neurons. I have also precisely quantified the role of some proteins and signaling pathways which regulate the motility of the DRG GCs. The first part of my results entitled, “The role of myosin-II in force generation of DRG filopodia and lamellipodia”, characterizes the role of Myosin II in growth cone dynamics. Myosin II has been shown to control the retrograde flow of actin polymers, to be involved in the orchestration of actin and microtubules (MTs) dynamics and to possess contractile activity. GCs advance due to combined effects of the adhesion of lamellipodia and filopodia on the substrate and the contractile activity of Myosin II. Therefore, I probed the functional role of Myosin II on GCs dynamics by using its specific inhibitor, Blebbistatin. I show that the force exerted by lamellipodia decreased but surprisingly the force exerted by filopodia increased upon treatment with Blebbistatin. Moreover I show that the well organized and distributed structures of lamellipodia and filopodia of the GCs depend on the activity of Myosin II and confirmed the coupling between actin and microtubule dynamics. The next chapter, “The role of Rac1 in force generation of DRG neurons”, describes the function of Rac1 and its downstream effector Arp2/3 in lamellipodia and filopodia formation and dynamics. It is well known that Rac1 Rho-GTPase acts as a switch between GTP bound active state and GDP bound inactive state. I observed that GCs retract following partial inhibition of Arp2/3 but recover their usual motility within 5-10 minutes. I found that this recovery is caused by the activation of Rac1. This indicates that Rac1 acts as switch and activates upon Arp2/3 inhibition, possibly through integrin pathways. I also confirmed that the activity of Arp2/3 not only regulates the formation of lamellipodia but also controls the dynamics and formation of filopodia.
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Choi, Mi-Yon. "P53 mediated cell motility in H1299 lung cancer cells." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.

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Studies have shown that gain-of- function mutant p53, AKT, and NFκB promote invasion and metastasis in tumor cells. Signals transduced by AKT and p53 are integrated via negative feedback between the two pathways. Tumor derived p53 was also indicated to induce NFκB gene expression. Due to the close relationship between p53/AKT and p53/NFκB, we hypothesized that AKT and NFκB can enhance motility in cells expressing mutant p53. Effects on cell motility were determined by scratch assays. CXCL5- chemokine is also known to induce cell motility. We hypothesized that enhanced cell motility by AKT and NFκB is mediated, in part, by CXCL5. CXCL5 expression levels in the presence and absence of inhibitors were determined by qRT-PCR. We also hypothesized that gain-of-function mutant p53 contributes to the activation of AKT. The effect of mutant p53 on AKT phosphorylation was investigated with a Ponasterone A- inducible mutant cell line (H1299/R175H) and vector control. These results indicated that AKT and NFκB enhance motility in cells expressing mutant p53 and this enhanced motility is, in part, mediated by CXCL5. However, AKT phosphorylation was independent of mutant p53.
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Yang, Lingyan. "The role of reduced-on random-motile (ROM) in the regulation of lung cancer cell migration and vesicle trafficking." Thesis, The University of Sydney, 2010. https://hdl.handle.net/2123/28847.

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Cancer is a complex disease, with over 100 different types and subtypes. Based on clinical features and biological properties, lung cancers can be separated into two major categories: non-small cell lung cancer and small cell lung cancer. In this study, we explore the function of the Reduced On-random Motile (ROM) protein in the regulation of non-small cell lung cancer cell migration and vesicle trafficking.
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Biondini, Marco. "RALlying through cell motility and invasion." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T042.

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La formation des métastases est un processus en plusieurs étapes à travers lequel les cellules néoplasiques se détachent de la tumeur primaire pour constituer des tumeurs secondaires à distance. Les capacités à migrer et à envahir, des cellules tumorales sont cruciales dans la cascade métastatique. Selon le type cellulaire et les stimuli présents dans le microenvironnement tumoral, les cellules peuvent se déplacer collectivement ou individuellement selon un programme de migration mésenchymateuse ou amiboïde. Différentes voies de signalisation sont liées à la régulation de la motilité cellulaire. Les GTPases Rho (Rac1, Cdc42 et RhoA) contrôlent la migration en régulant la dynamique du cytosquelette d’actine, la contraction acto-myosine et les microtubules. Rac1 régule la motilité mésenchymateuse en favorisant la formation des lamellipodes via un complexe multiprotéique, le « Wave Regulatory Complex (WRC) » et RhoA contrôle la motilité amiboïde en favorisant la contraction du cytosquelette d'acto-myosine. Les protéines Ral (RalA et RalB) appartenant à une autre famille de petites G, ont été récemment impliquées dans la régulation de la migration cellulaire. RalB, à travers le complexe « Exocyst » joue un rôle essentiel dans la motilité. Dans ce travail de thèse, nous avons étudié les mécanismes moléculaires par lesquels la voie RalB/Exocyste contrôle la motilité et l'invasion cellulaire. La première partie de ce travail démontre que l’Exocyste interagit avec SH3BP1, une protéine GAP (GTPase Activating Protein) (projet 1). Nous montrons que l’interaction entre SH3BP1 et Rac1 est nécessaire à l’activité de Rac1 au front de migration. Dans le projet 2, nous montrons que l’Exocyste interagit directement avec WRC, ce qui est un élément clé de la polymérisation de l'actine. Cette interaction est nécessaire à la localisation du complexe WRC au front de migration où il contrôle la formation de protrusions membranaires. Dans de nombreux carcinomes, la transition épithélio-mésenchymateuse (EMT) joue un rôle important dans la promotion de la migration, l’invasion et la formation des métastases. Le projet 3 a permis de mieux caractériser la plasticité de migration et l’invasion des cellules cancéreuses post-EMT et d’étudier la contribution de Ral dans l'invasion des cellules post-EMT. Nous montrons qu’après l’EMT les cellules envahissent la matrice individuellement ? en utilisant la contraction du cytosquelette d'acto-myosine. Nous montrons que RalB est nécessaire à l’invasion des cellules post-EMT, et à la contractilité cellulaire. Nous proposons que le rôle de RalB dans l'invasion passe par GEF-H1 qui est une protéine GEF (Guanine Nucleotide Exchange Factor) de Rho associée à l’Exocyste. Dans la dernière partie de ce manuscrit, nous présentons le logiciel « AVeMap » que nous avons développé afin d’automatiser la quantification des paramètres de la migration cellulaire.En résumé, dans ce travail de thèse nous montrons que la voie Ral/Exocyste est un organisateur moléculaire nécessaire à l’exécution à la fois de la motilité cellulaire contrôlée par Rac1 et à la motilité contrôlée par Rho
Metastasis is a multistep process by which cancer cells migrate away from the primary neoplastic mass to give rise to secondary tumors at distant sites. Thus, the acquisition of motility and invasive traits by tumor cells is a crucial step for metastasis to occur. Depending on the cell type and the environment, cells can move collectively keeping stable cell-cell contacts or as individual cells, which translocate by exploiting either mesenchymal or amoeboid motility programs.Different molecules and pathways have been linked to the regulation of cell motility. Rho small GTPases (Rac1, Cdc42 and RhoA) control cell migration through their actions on actin assembly, actomyosin contractility and microtubules. Rac1 drives mesenchymal-type motility by promoting lamellipodia formation via the Wave Regulator Complex (WRC). On the contrary, amoeboid motility is governed by RhoA which promotes cell movement via the generation of actomyosin contractile force. Another family of small GTPases, the Ral proteins, was recently involved in the regulation of cell migration. RalB, through the mobilization of its main effector the Exocyst complex, was shown to play an essential role in cell motility. In this work of thesis we investigated the molecular mechanisms through which RalB/Exocyst pathway controls cell motility and invasion.In the first part of this manuscript we show that Exocyst interacts with the RacGAP SH3BP1 (project 1). In mesenchymal moving cells Exocyst/SH3BP1 interaction is required to organize membrane protrusion formation by spatially regulating the activity of Rac1 at the cellular front. In addition, in project 2, we show that the Exocyst binds to the wave regulator complex (WRC), a key promoter of actin polymerization. We provide evidences for Exocyst to be involved in driving the WRC to the leading edge of motile cells, where it can stimulate actin polymerization and membrane protrusions. Reactivation of a developmental program termed epithelial-mesenchymal transition (EMT) was recently shown to promote motility, invasion and metastasis of neoplastic cells. Tumor cells undergoing EMT loose cell-cell contacts acquire a fibroblastoid phenotype and invade the surrounding tissues as individual cells. In project 3 we characterized the invasion plasticity of cancer cells after EMT and we investigated the molecular contribution of Ral to post-EMT invasion. We showed that upon EMT cells disseminate individually in a Rho-driven fashion exploiting the generation of actomyosin force to deform the extracellular matrix. We document that RalB silencing severely impairs actomyosin contractility and dissemination of post-EMT cells. We hypothesize that RalB regulates invasion by controlling the dynamics of the Rho pathway via the Exocyst-associated RhoGEF GEF-H1 in post-EMT cells. Finally, in the last part of this thesis manuscript, we present the PIV-based “AVeMap” software which has been developed to quantify in a fully automated way cell migration and its parameters (Project 4).Taken together the results presented in this thesis manuscript point out the Ral/Exocyst pathway as a key molecular organizer of the execution of both Rac1- and Rho-driven motility programs
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Dean, Seema. "Does the cytoskeleton manipulate the auxin-induced changes in structure and motility of the endoplasmic reticulum?" Thesis, University of Canterbury. School of Biological Sciences, 2004. http://hdl.handle.net/10092/5036.

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The variations in ER structure and motility under different stages of cell development remain largely unexplored. Here, I observe ER structure and the changes that take place in this structure over time in growing and non-growing live epidermal cells of the pea tendril. The ER was labelled by green fluorescent protein, fused to the KDEL-ER retention signal and confocal scanning laser microscopy was used to localize the fluorescent signal. I found both the structure and motility of growing cells to be different to non-growing cells. The growing cells had a more open arrangement of the cortical ER, fewer lamellae and showed greater tubular dynamics, while the non-growing cells had a denser arrangement of the cortical ER network, with more lamellae and less tubular dynamics. Furthermore, these differences in the cortical ER structure and dynamics were due to growth as, the ER in non-growing cells showed characteristics similar to those seen in growing cells when these cells were induced to grow by the exogenous application of auxin. These changes in ER structure and dynamics were dependant on both the microtubules and actin cytoskeleton networks.
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Tozluoglu, M. "Multiscale modelling of cancer cell motility." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1383588/.

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Cell motility is required for many biological processes, including cancer metastasis. The molecular requirements for migration and, the morphology of migrating cells, can vary considerably depending on matrix geometry. Therefore, predicting the optimal migration strategy or the effect of experimental perturbation is difficult. This thesis presents a computational model of single cell motility that encompasses flexible cell morphology, actin polymerisation based protrusions, cell cortex asymmetry, plasma membrane blebbing, local cortex heterogeneity at the protein level, cell–extracellular matrix adhesion, and varying extracellular matrix geometries. This computational model is used to explore the theoretical requirements for rapid migration in different matrix geometries. The analysis reveals that confinement of the cell within the extracellular matrix brings profound changes in the relationship between cortical contractility and cell velocity. In confined environments with discontinuity, the relationship between adhesion and cell velocity is fundamentally altered: adhesion becomes dispensable for a large range of gap sizes in between the extracellular matrix filaments. The utility of the model is shown by predicting cancer cell behaviour in vivo, in terms of both cell velocity and the morphology of the motile cell. Furthermore, the model is challenged to predict the effects of selected biochemical perturbations that alter i) cortical contractility, ii) cell-ECM adhesion, and iii) signalling between the cell-ECM adhesion sites and intracellular regulators of cell motility machinery. Multiphoton intravital imaging is used to verify bleb driven migration of melanoma, breast cancer cells, and, surprisingly, endothelial cells at tumour margins. Intravital imaging of melanoma verified model predictions on cell velocity, cell morphology, nucleus behaviour, and effects of anti-invasive interventions. The model succesfully predicted melanoma velocities in vitro and in vivo. Moreover, it successfully predicted the effects of anti-invasive interventions, showing all perturbations will result in significant reduction in cell velocity in vitro, whereas only perturbation of cortical contractility will affect cell velocity in vivo. The model also successfully predicted the interactions of the cell nucleus with the cell cortex and the cell morphology upon intervensions. Overall, from measure ment of rather simple variables in vitro, the model has been able to predict the in vivo response of three very different putative anti-invasive interventions.
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Rucka, Marta. "Metabolic regulation of tumour cell motility." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/380962/.

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Di, Kaijun. "The role of Id-1 on the proliferation, motility and mitotic regulation of prostate epithelial cells." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38588985.

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Hadjisavas, Michael. "Induction of mitogenesis and cell-cell adhesion by porcine seminal plasma." Title page, contents and abstract only, 1992. http://web4.library.adelaide.edu.au/theses/09PH/09phh1293.pdf.

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Includes list of publications by the author. Includes bibliographical references (leaves 103-123) Evaluates the nature of the interactions occurring between semen and cells of the uterus that occur following mating in pigs. Describes a novel ability of porcine seminal plasma to induce dose dependent cell-cell adhesion and mitogenesis amongst peripheral blood lymphocytes in vitro.
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Stakaitytė, Gabrielė. "Merkel cell polyomavirus small T antigen’s role in cell motility." Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/15538/.

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Merkel cell carcinoma (MCC) is an aggressive skin cancer of neuroendocrine origin with a high likelihood of recurrence and metastasis. In 2008, Merkel cell polyomavirus (MCPyV) was discovered monoclonally integrated within the host genome of at least 80% of MCC tumours. MCPyV transforms and maintains MCC tumours via the expression of the large and small tumour (LT and ST) antigens. Specifically, ST is thought to be the major transforming factor in the tumourigenesis of MCC. Since the discovery of MCPyV, a number of mechanisms have been suggested to account for replication and tu- mour formation, but to date, little is known about potential links between MCPyV T antigen expression and the highly metastatic nature of MCC. In this thesis, the link between MCPyV and MCC metastasis is explored by focusing on the role of MCPyV ST in promoting cell motility. Cell motility and migration is a complex, multi-step, and multi-component process, intrinsic in cancer progression and metastasis. Previous work in the Whitehouse laboratory has implicated the microtubule network in MCPyV ST-induced cell motility. This thesis builds upon those findings to show that MCPyV ST-induced cell motility is dependent on multiple factors, including the activity of integrin receptors, Rho-family GTPases and the actin cytoskeleton, and intracellular chloride channels. This thesis also further explores the MCPyV ST-PP4C interaction in MCPyV ST-induced cell motility and proposes a mechanism by which this interaction activates integrin receptors to promote cell motility, thereby contributing to the metastatic nature of MCC. Furthermore, the relocalisation of intracellular chloride channels CLIC1 and CLIC4 to the cell surface is shown to be important in MCPyV ST-induced cell motility. Overall, results presented herein describe a novel mechanism by which a tumour virus induces cell motility, ultimately leading to cancer metastasis. Therefore, there may be implications for the potential future therapeutic targets for disseminated MCC.
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Books on the topic "Cell motilty"

1

Ridley, Anne, Michelle Peckham, and Peter Clark, eds. Cell Motility. Chichester, UK: John Wiley & Sons, Ltd, 2004. http://dx.doi.org/10.1002/0470011742.

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1948-, Goldberg I. D., Rosen E. M, Long Island Jewish Medical Center., National Cancer Institute (U.S.). Laboratory of Pathology., and International Conference on Cytokines and Cell Motility (1990 : New York, N.Y.), eds. Cell motility factors. Basel: Birkhäuser Verlag, 1991.

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1935-, Ishikawa Harunori, Hatano Sadashi 1929-, Satō Hidemi 1926-, and Yamada Conference (10th : 1984 : Nagoya-shi, Japan), eds. Cell motility: Mechanism and regulation. New York: A.R. Liss, 1986.

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Cell movement and cell behaviour. London: Allen & Unwin, 1986.

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Lackie, J. M. Cell movement and cell behaviour. London: Allen & Unwin, 1986.

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Bray, Dennis. Cell movements. New York: Garland Pub., 1992.

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Melkonian, Michael, ed. Algal Cell Motility. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-9683-7.

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Goldberg, I. D., ed. Cell Motility Factors. Basel: Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7494-6.

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Verma, Navin Kumar, ed. T-Cell Motility. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9036-8.

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1948-, Melkonian Michael, ed. Algal cell motility. New York: Chapman and Hall, 1992.

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Book chapters on the topic "Cell motilty"

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Wada, Masamitsu, and Noriyuki Suetsugu. "Chloroplast Motility." In Cell Biology, 1–16. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7881-2_10-3.

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Thiriet, Marc. "Cell Motility." In Control of Cell Fate in the Circulatory and Ventilatory Systems, 357–417. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0329-6_6.

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Méndez, Vicenç, Daniel Campos, and Frederic Bartumeus. "Cell Motility." In Springer Series in Synergetics, 209–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-39010-4_7.

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Häder, Donat-P., and Egbert Hoiczyk. "Gliding Motility." In Algal Cell Motility, 1–38. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-9683-7_1.

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Annuario, Emily, Kristal Ng, and Alessio Vagnoni. "High-Resolution Imaging of Mitochondria and Mitochondrial Nucleoids in Differentiated SH-SY5Y Cells." In Methods in Molecular Biology, 291–310. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_15.

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AbstractMitochondria are highly dynamic organelles which form intricate networks with complex dynamics. Mitochondrial transport and distribution are essential to ensure proper cell function, especially in cells with an extremely polarised morphology such as neurons. A layer of complexity is added when considering mitochondria have their own genome, packaged into nucleoids. Major mitochondrial morphological transitions, for example mitochondrial division, often occur in conjunction with mitochondrial DNA (mtDNA) replication and changes in the dynamic behaviour of the nucleoids. However, the relationship between mtDNA dynamics and mitochondrial motility in the processes of neurons has been largely overlooked. In this chapter, we describe a method for live imaging of mitochondria and nucleoids in differentiated SH-SY5Y cells by instant structured illumination microscopy (iSIM). We also include a detailed protocol for the differentiation of SH-SY5Y cells into cells with a pronounced neuronal-like morphology and show examples of coordinated mitochondrial and nucleoid motility in the long processes of these cells.
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Wagner, Gottfried, and Franz Grolig. "Algal Chloroplast Movements." In Algal Cell Motility, 39–72. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-9683-7_2.

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Williamson, Richard E. "Cytoplasmic Streaming in Characean Algae: Mechanism, Regulation by Ca2+, and Organization." In Algal Cell Motility, 73–98. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-9683-7_3.

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Goldstein, Stuart F. "Flagellar Beat Patterns in Algae." In Algal Cell Motility, 99–153. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-9683-7_4.

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Kamiya, Ritsu. "Molecular Mechanism of Flagellar Movement." In Algal Cell Motility, 155–78. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-9683-7_5.

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Melkonian, Michael, Peter L. Beech, Christos Katsaros, and Dorothee Schulze. "Centrin-Mediated Cell Motility in Algae." In Algal Cell Motility, 179–221. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-9683-7_6.

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Conference papers on the topic "Cell motilty"

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Du, Huijing, Zhiliang Xu, Morgen Anyan, Oleg Kim, W. Matthew Leevy, Joshua D. Shrout, and Mark Alber. "Pseudomonas Aeruginosa Cells Alter Environment to Efficiently Colonize Surfaces Using Fluid Dynamics." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80316.

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Many bacteria use motility described as swarming to colonize surfaces and form biofilm. Swarming motility has been shown important to biofilm formation [1], where cells act not as individuals but as coordinated groups to move across surfaces, often within a thin-liquid film [2]. Production of a surfactant during swarm improves bacterial motility by lowering surface tension of the liquid film [2]. The mechanism of cell motion during swarming are currently best described for Escherichia coli and Paenibacillus spp., which spread as monolayers of motile cells [3,4]. For Pseudomonas aeruginosa (P. aeruginosa), which does not swarm as a monolayer, the cell and fluid patterns are difficult to discern using current experimental methods. It is not yet known if swarming P. aeruginosa cells behave solely as swimming cells [5] or if twitching, sliding, or walking motility [6] are also important to swarming.
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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Chasiotis, I., D. C. Street, H. L. Fillmore, and G. T. Gillies. "AFM Studies of Tumor Cell Invasion." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43293.

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Our recent investigations on human brain tumor (glioma) cell micro and nanodynamics via AFM methodologies have shown that brain tumor invadopodia (malignant cytostructural cell extensions with sensory, motility, and invasive characteristics extended by tumor cells into their environment) can assume specific geometries based on cell plating density and the location/distance of neighboring cells indicating strong cell sensing and signaling mechanisms between malignant cells and their surroundings. In certain occasions, cancer cell processes (extensions) have been found to be highly directional measuring more than 80 μm while invading neighboring cells by following a connecting straight path. Moreover, strong chemical gradients are suggested to influence the growth and motility of cell processes allowing for gradual adjustments of the direction of the invasive tumor extension. In response to external signals, tumor cell invadopodia develop micron-sized side-ligaments that follow the chemical gradients in their neighborhood and assist the reorientation of their main intrusive elements.
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Thangawng, Abel L., Rodney S. Ruoff, Jonathan C. Jones, and Matthew R. Glucksberg. "Substrate Stiffness Affects Laminin-332 Matrix Deposition in Cultured Keretinocytes." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176292.

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It has been reported that the mechanical properties of a substrate influence cell motility, morphology, and adhesion [1–3]. This work is an attempt to move a step further beyond cells’ sensing the mechanical properties of their environment, by determining whether the secretion and assembly of laminin extracellular matrix is regulated by the mechanical environment in which the cell is placed. We hypothesize that this matrix then influences the behavior of the cell, particularly with regard to its motility.
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Milutinovic´, Dejan, and Devendra P. Garg. "Parameters and Driving Force Estimation of Cell Motility via Expectation-Maximization (EM) Approach." In ASME 2010 Dynamic Systems and Control Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/dscc2010-4152.

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Motility is an important property of immune system cells. To describe cell motility, we use a continuous stochastic process and estimate its parameters and driving force based on a maximum likelihood approach. In order to improve the convergence of the maximization procedure, we use expectation-maximization (EM) iterations. The iterations include numerical maximization and the Kalman filter. To illustrate the method, we use cell tracks obtained from the intravital video microscopy of a zebrafish embryo.
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Samadi, Zahra, Malihe Mehdizadeh Allaf, Thomas Vourc'h, Christopher T. DeGroot, and Hassan Peerhossaini. "Are Active Fluids Age-Dependent?" In ASME 2022 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/fedsm2022-87914.

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Abstract Active fluids are often is known as the aqueous suspensions of self-propelled elements such as bacteria, algae, or sperm cells, which their properties fundamentally differ from conventional fluids. Active fluids exhibit remarkable physical manifestations over a wide range of scales, from time-dependent microscopic diffusion to the large-scale colonization of aqueous spaces. Properties of active fluids depend on the behavior of microbial suspensions, among which motility plays a crucial role. In this work, we focus on the effect of microbial growth and aging on microorganism motility. Hence, the motility behavior of cyanobacterium Synechocystis sp. CPCC 534, and its relationship with aging were investigated in a closed microfluidic chip. The growth of Synechocystis cultures was followed from the lag phase, through exponential and linear growth up to the stationary phase. Culture samples were periodically examined; cell populations were measured by spectroscopy technique and cell trajectories were tracked by video-microscopy. Cell trajectory length and average cell motility were extracted from the video recordings and were correlated with the age and growth phase of the bacterium.
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Parker, Kevin Kit, and Donald E. Ingber. "Cell Motility in Microfabricated Models of the Tissue Microenvironment." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23075.

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Abstract We conducted studies using micropatterned substrates to elucidate how cell shape and geometric confinement regulates the inter- and intracellular signaling pathways required for cell motility. When cells were cultured on individual cell-sized square adhesive islands coated with ECM, they extend to the edge of the island and assume a square shape. When these cells were stimulated with growth factors, they preferentially extended lamellipodia from the corners versus the sides. This process was mediated by myosin-generated isometric tension that induced tight spatial localization of Rac in the corners. When two or three capillary endothelial cells are constrained to a fibronectin (FN) island, coordinated cell migration results in stable rotation of the entire system about its center. Thus, the emergent pattern is due to the coordinated migration behavior of the cells. These observations suggest that ECM-induced mechanotransduction potentiates compartmentalized signaling pathways and the multicellular organization required of tissue morphogenesis.
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Šuráňová, Markéta, Daniel Zicha, Pavel Veselý, Jan Brábek, Veronika Jůzová, and Radim Chmelík. "In Vitro Screening with Holographic Incoherent Quantitative Phase Imaging Focuses on Finding Medicaments for Repurposing as Anti-Metastatic Agents Designated as Migrastatics." In European Conference on Biomedical Optics. Washington, D.C.: Optica Publishing Group, 2021. http://dx.doi.org/10.1364/ecbo.2021.em1a.38.

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Live lung cancer cells in vitro were exposed to selected medicaments with putative anti- metastatic potential and examined by time-lapse hiQPI, providing simultaneous measurements of the effect on cell growth and motility with unprecedented accuracy.
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Sitaula, Ranjan, and Sankha Bhowmick. "Modeling of Osmotic Injury in Bovine Sperm During Desiccation." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19325.

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Although desiccation preservation offers promise as an alternative method for the preservation of mammalian cells, there has been limited success in achieving survival at very low water content [1]. Osmotic injury is one of the major damage factors during cellular dehydration. During the drying process, cells experience increased extracellular hypertonic environment as a result of evaporation of water. This factor coupled with the limited permeability of cell membranes leads to irreversible cellular damage. In the current study, we have studied the effect of hypertonic osmolality and exposure time on bovine sperm motility. The goal was to develop a theoretical osmotic damage model to predict motility loss during dehydration. Modeling was performed by using a first order rate equation. Motility data from the hypertonic exposure experiments were used to determine the first order reaction parameters and the cumulative osmotic damage (COD), which provided a measure of the extent of osmotic damage. The parameters were then used to predict motility of natural convection desiccation process. Experimental drying data was compared to the predicted data to determine the extent of osmotic damage.
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Masuda, Michiaka, and Keigi Fujiwara. "Three Distinct Types of Morphological Responses of Cultured Vascular Endothelial Cells to Physiological Levels of Fluid Shear Stress." In ASME 2003 1st International Conference on Microchannels and Minichannels. ASMEDC, 2003. http://dx.doi.org/10.1115/icmm2003-1124.

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Vascular endothelial cells are known to respond to fluid shear stress. To gain insights into the mechanism of flow response by these cells, various types of in vitro devices in which endothelial cells can be cultured under flowing culture medium have been designed. Using such a device, one can apply known levels of (usually laminar) fluid shear stress to cultured endothelial cells. We have made two types of devices: a viscometer-based cone-and-plate flow apparatus and a parallel plate chamber. The cone-and-plate apparatus is used to do biochemical analyses of flow effects on cells while the parallel plate chamber is used to observe dynamic behavior of endothelial cells under flow. We were able to maintain confluent endothelial cell cultures under flow for over a week in the parallel plate flow apparatus. Using this chamber and high resolution time-lapse video microscopy, we studied morphological changes of endothelial cells exposed to different levels of fluid shear stress. We found that endothelial cells in a confluent monolayer exhibited three types of fluid shear stress level-dependent morphological and motile responses within a narrow fluid shear stress range between 0.1–10 dyn/cm2. Endothelial cells cultured under no flow exhibited variable shapes and no preferred orientation of their long cell axes and showed a jiggling motion. When exposed to fluid shear stress levels of below 0.5 dyn/cm2, endothelial cell morphology and motility were not affected. However, when fluid shear stress levels were increased to 2–4 dyn/cm2, they became polygonal and showed increased random-walk activity. Fluid shear stress over 6 dyn/cm2 caused endothelial cells to initially become polygonal and increase their random-walk activity, but they soon became elongated and aligned in the direction of flow. As the cells elongated and aligned, they migrated in the direction of flow. The average velocity of this directed cell migration was less than that of cells moving randomly under the same flow condition at earlier times. These observations indicate that endothelial cells are able to detect and respond to a surprisingly small change in fluid shear stress. It is possible that endothelial cell physiology in vivo is also regulated by small changes in fluid shear stress and that a fluid shear stress change of a few dynes per cm2 within a certain region of an artery could trigger atherogenesis in that particular location.
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Reports on the topic "Cell motilty"

1

Wells, Alan, Douglas A. Lauffenburger, and Timothy Turner. Cell Motility in Tumor Invasion. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada428576.

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Wells, Alan, Douglas A. Lauffenburger, and Timothy Turner. Cell Motility in Tumor Invasion. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada410314.

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Wells, Alan, Douglas A. Lauffenburger, and Timothy Turner. Cell Motility in Tumor Invasion. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada417877.

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Bodt, B. A., and R. J. Young. Hyperactivated Rabbit Sperm Cell Motility Parameters. Fort Belvoir, VA: Defense Technical Information Center, March 1995. http://dx.doi.org/10.21236/ada294502.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada439284.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurotibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada411714.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada422403.

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Brackanbury, Robert W. Control of Carcinoma Cell Motility by E-Cadherin. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada403381.

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Brackenbury, Robert W. Control of Carcinoma Cell Motility by E-Cadherin. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada409404.

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Brackenbury, Robert. Control of Carcinoma Cell Motility by E-Cadherin. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada390725.

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