Relevant bibliographies by topics / Cells Motility

Contents

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

Academic literature on the topic 'Cells Motility'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 July 2024

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Journal articles on the topic "Cells Motility"

1

ULFENDAHL, M. "Motility in auditory sensory cells." Acta Physiologica Scandinavica 130, no. 3 (July 1987): 521–27. http://dx.doi.org/10.1111/j.1748-1716.1987.tb08171.x.

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Pate, Jack L. "Gliding motility in procaryotic cells." Canadian Journal of Microbiology 34, no. 4 (April 1, 1988): 459–65. http://dx.doi.org/10.1139/m88-079.

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Recho, Pierre, Thibaut Putelat, and Lev Truskinovsky. "Mechanics of motility initiation and motility arrest in crawling cells." Journal of the Mechanics and Physics of Solids 84 (November 2015): 469–505. http://dx.doi.org/10.1016/j.jmps.2015.08.006.

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Schwab, Albrecht, Peter Hanley, Anke Fabian, and Christian Stock. "Potassium Channels Keep Mobile Cells on the Go." Physiology 23, no. 4 (August 2008): 212–20. http://dx.doi.org/10.1152/physiol.00003.2008.

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Cell motility is a prerequisite for the creation of new life, and it is required for maintaining the integrity of an organism. Under pathological conditions, “too much” motility may cause premature death. Studies over the past few years have revealed that ion channels are essential for cell motility. This review highlights the importance of K+ channels in regulating cell motility.
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Sarna, Sushil K. "Are interstitial cells of Cajal plurifunction cells in the gut?" American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 2 (February 2008): G372—G390. http://dx.doi.org/10.1152/ajpgi.00344.2007.

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The proposed functions of the interstitial cells of Cajal (ICC) are to 1) pace the slow waves and regulate their propagation, 2) mediate enteric neuronal signals to smooth muscle cells, and 3) act as mechanosensors. In addition, impairments of ICC have been implicated in diverse motility disorders. This review critically examines the available evidence for these roles and offers alternate explanations. This review suggests the following: 1) The ICC may not pace the slow waves or help in their propagation. Instead, they may help in maintaining the gradient of resting membrane potential (RMP) through the thickness of the circular muscle layer, which stabilizes the slow waves and enhances their propagation. The impairment of ICC destabilizes the slow waves, resulting in attenuation of their amplitude and impaired propagation. 2) The one-way communication between the enteric neuronal varicosities and the smooth muscle cells occurs by volume transmission, rather than by wired transmission via the ICC. 3) There are fundamental limitations for the ICC to act as mechanosensors. 4) The ICC impair in numerous motility disorders. However, a cause-and-effect relationship between ICC impairment and motility dysfunction is not established. The ICC impair readily and transform to other cell types in response to alterations in their microenvironment, which have limited effects on motility function. Concurrent investigations of the alterations in slow-wave characteristics, excitation-contraction and excitation-inhibition couplings in smooth muscle cells, neurotransmitter synthesis and release in enteric neurons, and the impairment of the ICC are required to understand the etiologies of clinical motility disorders.
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Coelho Neto, José, and Oscar Nassif Mesquita. "Living cell motility." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 366, no. 1864 (August 2, 2007): 319–28. http://dx.doi.org/10.1098/rsta.2007.2091.

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The motility of living eukaryotic cells is a complex process driven mainly by polymerization and depolymerization of actin filaments underneath the plasmatic membrane (actin cytoskeleton). However, the exact mechanisms through which cells are able to control and employ ‘actin-generated’ mechanical forces, in order to change shape and move in a well-organized and coordinated way, are not quite established. Here, we summarize the experimental results obtained by our research group during recent years in studying the motion of living cells, such as macrophages and erythrocytes. By using our recently developed defocusing microscopy technique, which allows quantitative analysis of membrane surface dynamics of living cells using a simple bright-field optical microscope, we were able to analyse morphological and dynamical parameters of membrane ruffles and small membrane fluctuations, study the process of phagocytosis and also measure values for cell refractive index, membrane bending modulus and cell viscosity. Although many questions still remain unanswered, our data seem to corroborate some aspects of recent physical models of cell membranes and motility.
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Sharma, Pooja, Van K. Lam, Christopher B. Raub, and Byung Min Chung. "Tracking Single Cells Motility on Different Substrates." Methods and Protocols 3, no. 3 (August 4, 2020): 56. http://dx.doi.org/10.3390/mps3030056.

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Motility is a key property of a cell, required for several physiological processes, including embryonic development, axon guidance, tissue regeneration, gastrulation, immune response, and cancer metastasis. Therefore, the ability to examine cell motility, especially at a single cell level, is important for understanding various biological processes. Several different assays are currently available to examine cell motility. However, studying cell motility at a single cell level can be costly and/or challenging. Here, we describe a method of tracking random cell motility on different substrates such as glass, tissue-culture polystyrene, and type I collagen hydrogels, which can be modified to generate different collagen network microstructures. In this study we tracked MDA-MB-231 breast cancer cells using The CytoSMARTTM System (Lonza Group, Basel, Switzerland) for live cell imaging and assessed the average cell migration speed using ImageJ and wrMTrck plugin. Our cost-effective and easy-to-use method allows studying cell motility at a single cell level on different substrates with varying degrees of stiffness and varied compositions. This procedure can be successfully performed in a highly accessible manner with a simple setup.
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Melkonian, M. "Centrin-Mediated Motility: A Novel Cell Motility Mechanism in Eukaryotic Cells." Botanica Acta 102, no. 1 (February 1989): 3–4. http://dx.doi.org/10.1111/j.1438-8677.1989.tb00059.x.

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Xu, X., W. E. I. Li, G. Y. Huang, R. Meyer, T. Chen, Y. Luo, M. P. Thomas, G. L. Radice, and C. W. Lo. "Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions." Journal of Cell Biology 154, no. 1 (July 9, 2001): 217–30. http://dx.doi.org/10.1083/jcb.200105047.

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Connexin 43 (Cx43α1) gap junction has been shown to have an essential role in mediating functional coupling of neural crest cells and in modulating neural crest cell migration. Here, we showed that N-cadherin and wnt1 are required for efficient dye coupling but not for the expression of Cx43α1 gap junctions in neural crest cells. Cell motility was found to be altered in the N-cadherin–deficient neural crest cells, but the alterations were different from that elicited by Cx43α1 deficiency. In contrast, wnt1-deficient neural crest cells showed no discernible change in cell motility. These observations suggest that dye coupling may not be a good measure of gap junction communication relevant to motility. Alternatively, Cx43α1 may serve a novel function in motility. We observed that p120 catenin (p120ctn), an Armadillo protein known to modulate cell motility, is colocalized not only with N-cadherin but also with Cx43α1. Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43α1 deficiency. Based on these findings, we propose a model in which Cx43α1 and N-cadherin may modulate neural crest cell motility by engaging in a dynamic cross-talk with the cell's locomotory apparatus through p120ctn signaling.
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Shea, C., J. W. Nunley, and H. E. Smith-Somerville. "Variable expression of gliding and swimming motility in Deleya marina." Canadian Journal of Microbiology 37, no. 11 (November 1, 1991): 808–14. http://dx.doi.org/10.1139/m91-140.

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Surface-associated motility has been observed in the Deleya marina type strain ATCC 25374 (strain 219). Slime tracks and a complex growth pattern, characteristic of gliding motility, developed on semisolid marine-agar motility plates. Cell movement observed by light microscopy consisted of rapid glides and flips by single cells and groups of cells. Following the development of the gliding cell growth pattern, a subpopulation of swimming cells appeared. The variation in motility was random and reversible in subculture. Electron microscopic comparisons of cells of the two motility types showed that gliding cells had no obvious motility organelles, whereas swimming cells had polar flagella. Variable expression of gliding and swimming motility was also observed in D. marina strain 140 (ATCC 27129) and in two other species of the Deleya genus. Key words: gliding, morphological variation, Deleya, biofouling.
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Dissertations / Theses on the topic "Cells Motility"

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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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Bai, Limiao, and 白利苗. "In silico simulation of actin-based motility." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B46429116.

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Friedrich, Benjamin. "Chemotaxis of Sperm Cells." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2009. http://nbn-resolving.de/urn:nbn:de:bsz:14-ds-1235056439247-79608.

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Sperm cells are guided to the egg by chemoattractants in many species. Sperm cells are propelled in a liquid by the regular beat of their flagellum. In the presence of a concentration gradient of a chemoattractant, they can steer upwards the concentration gradient, a process called chemotaxis. Eggs release chemoattractants to guide the sperm cells to the egg. Sperm chemotaxis is best studied experimentally in the sea urchin. There, specific receptors in the flagellar membrane of the sperm cells are activated upon binding of chemoattractant molecules and trigger a signaling cascade which ultimately changes the activity of the molecular motors which drive the flagellar beat and result in a swimming response. Sea urchin sperm cells swim along circular and helical paths. Sperm cells of the sea urchin and several other species swim along helical paths far from boundary surfaces in the absence of chemoattractant. In a two-dimensional experimental geometry, sperm swimming paths are planar circles. The non-zero curvature of their swimming paths is a direct consequence of an asymmetry of their flagellar beat. In a concentration gradient of chemoattractant, sperm swimming path are drifting circles in two dimensions and bend helices in three dimensions. What is the working mechanism of sperm chemotaxis? In this thesis, we develop a theoretical description of sperm chemotaxis which can be subsumed as follows: While swimming along an approximately circular path in a concentration gradient a sperm cell traces a periodic concentration stimulus from the concentration field that has the frequency of circular swimming. The chemotactic signaling system processes this stimulus and causes a periodic modulation of the curvature of the swimming path which then gives rise to a swimming path which is a drifting circle. The relative direction of the drift with respect to the gradient direction is determined by the phase shift between the stimulus and the curvature oscillations. This picture is in perfect agreement with recent experimental findings. The mechanism is more general and also works in three dimensions for swimming along helical paths. Our results. Our theoretical description of sperm chemotaxis clarifies the concepts underlying sperm chemotaxis. In particular, we derive the role of internal timing of the chemotactic signaling system for sperm chemotaxis. We conclude that sampling a concentration field along circular and helical paths is a robust strategy for chemotaxis that does not require fine-tuning of parameters and which works reliable also in the presence of fluctuations. In a last chapter of this thesis, we discuss sperm chemotaxis in the more general context of an abstract search problem.
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Thurston, Gavin O. "Studies on the effect of radiation on 3T3 cell motility." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29441.

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The ability of mammalian cells to locomote is important in a variety of normal and pathological processes. Previous work has suggested that low doses of x-irradiation may perturb cell motility, a finding that may have important consequences in embryogenesis, cancer metastasis, and immune response. This thesis has sought to study in more detail the effect of radiation on mammalian cell motility. Work performed in other laboratories used the colloidal gold assay and time lapse cinemicroscopy to study x-irradiation induced changes to 3T3 fibroblast motility in tissue culture. These studies were repeated here, with qualitative results similar to those reported earlier. However, these methods were not amenable to a detailed quantitative analysis. For this, spatial and temporal information on the motility and dynamic morphology of a large number of cells is required. Such a task would be impossible to perform manually, thus an automated microscope system was developed that used a computer-driven precision stage and a solid state optical sensor to track individual cells in tissue culture. Information on motility and morphology was concurrently extracted from many cells. As part of the thesis, several techniques were developed to analyze and display these data, and to correlate motility and morphology observations. These techniques were directed at preserving the actual process of 3T3 cell motility, and parameters were measured to quantify the short term persistence of cell movement (on a time scale of 0.5 to 2 hours), and the long term persistence of cells in maintaining certain characteristic behaviour (on a time scale of 3 to 12 hours). The response of 3T3 fibroblasts to x-irradiation was characterized by a number of parameters. The population average cell speed was measured following treatment, and a dose response and time response was determined in the range of 1.5 Gy. Other motility parameters indicate that the normal process of cell motility, evidenced by a series of motile segments, was disrupted by x-rays. This was thought to reflect perturbation to the control mechanisms of cell motility. The morphology of 3T3 cells stained with Coomassie blue was examined in an effort to correlate the observed motility changes with changes in the fixed cell morphology. This stain is a general structural protein stain with higher affinity toward microfilaments. High doses of x-rays were required to produce significant perturbation to cell morphology, and in the dose regime of interest, the morphology of irradiated cells was not identifiably different from control. Of note is that it was the well spread, quiescent cells that seemed least perturbed by large doses of irradiation. In summary, x-rays apparently disrupt the normal process of cell motility. Several lines of evidence suggest that actively migrating cells are the most perturbed by irradiation. This work has developed techniques to quantify cell motility in a meaningful way, and to characterize the x-ray induced perturbations.
Science, Faculty of
Physics and Astronomy, Department of
Graduate
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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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Friedrich, Benjamin. "Chemotaxis of Sperm Cells." Doctoral thesis, Technische Universität Dresden, 2008. https://tud.qucosa.de/id/qucosa%3A23708.

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Sperm cells are guided to the egg by chemoattractants in many species. Sperm cells are propelled in a liquid by the regular beat of their flagellum. In the presence of a concentration gradient of a chemoattractant, they can steer upwards the concentration gradient, a process called chemotaxis. Eggs release chemoattractants to guide the sperm cells to the egg. Sperm chemotaxis is best studied experimentally in the sea urchin. There, specific receptors in the flagellar membrane of the sperm cells are activated upon binding of chemoattractant molecules and trigger a signaling cascade which ultimately changes the activity of the molecular motors which drive the flagellar beat and result in a swimming response. Sea urchin sperm cells swim along circular and helical paths. Sperm cells of the sea urchin and several other species swim along helical paths far from boundary surfaces in the absence of chemoattractant. In a two-dimensional experimental geometry, sperm swimming paths are planar circles. The non-zero curvature of their swimming paths is a direct consequence of an asymmetry of their flagellar beat. In a concentration gradient of chemoattractant, sperm swimming path are drifting circles in two dimensions and bend helices in three dimensions. What is the working mechanism of sperm chemotaxis? In this thesis, we develop a theoretical description of sperm chemotaxis which can be subsumed as follows: While swimming along an approximately circular path in a concentration gradient a sperm cell traces a periodic concentration stimulus from the concentration field that has the frequency of circular swimming. The chemotactic signaling system processes this stimulus and causes a periodic modulation of the curvature of the swimming path which then gives rise to a swimming path which is a drifting circle. The relative direction of the drift with respect to the gradient direction is determined by the phase shift between the stimulus and the curvature oscillations. This picture is in perfect agreement with recent experimental findings. The mechanism is more general and also works in three dimensions for swimming along helical paths. Our results. Our theoretical description of sperm chemotaxis clarifies the concepts underlying sperm chemotaxis. In particular, we derive the role of internal timing of the chemotactic signaling system for sperm chemotaxis. We conclude that sampling a concentration field along circular and helical paths is a robust strategy for chemotaxis that does not require fine-tuning of parameters and which works reliable also in the presence of fluctuations. In a last chapter of this thesis, we discuss sperm chemotaxis in the more general context of an abstract search problem.
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Garg, Ayush A. "Electromagnetic Fields Alter the Motility of Metastatic Breast Cancer Cells." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1563816767104018.

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Liu, Chenli, and 刘陈立. "Formation of novel biological patterns by controlling cell motility." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46541913.

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The Best PhD Thesis in the Faculties of Dentistry, Engineering, Medicine and Science (University of Hong Kong), Li Ka Shing Prize,2010-11
published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
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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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Ahmad, Omaima Farid. "The Role of Filamin A in Cell Motility, Adhesion and Invasion in Ovarian Cancer Cells." University of Toledo Honors Theses / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=uthonors1503407822068426.

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Books on the topic "Cells Motility"

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Bray, Dennis. Cell movements: From molecules to motility. 2nd ed. New York: Garland Pub., 2001.

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

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Preston, Terence M. The cytoskeleton and cell motility. Glasgow: Blackie, 1990.

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Preston, Terence M. The cytoskeleton and cell motility. Glasgow: Blackie, 1990.

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

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

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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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W, Alt, Deutsch Andreas 1960-, and Dunn Graham 1944-, eds. Dynamics of cell and tissue motion. Basel: Birkhauser, 1997.

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M, Sanger Jean, and Sanger Joseph W, eds. Cell motility and the cytoskeleton. [New York?]: Wiley-Liss, 1990.

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Book chapters on the topic "Cells Motility"

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Wozniak, Marcin J., and Victoria J. Allan. "Carrier Motility." In Trafficking Inside Cells, 233–53. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-93877-6_12.

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Preston, Terence M., Conrad A. King, and Jeremy S. Hyams. "Movement within Cells." In The Cytoskeleton and Cell Motility, 70–86. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0393-7_3.

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Preston, Terence M., Conrad A. King, and Jeremy S. Hyams. "Movement within Cells." In The Cytoskeleton and Cell Motility, 70–86. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-8010-2_3.

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Sanger, J. M., and J. W. Sanger. "Analysis of Cell Motility in Living Cells." In The Cytoskeleton, 127–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79482-7_14.

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Melkonian, Michael. "Centrin-Mediated Cell Motility in Eukariotic Cells." In Biological Motion, 117–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-51664-1_8.

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Carlsson, Anders E., and Alex Mogilner. "Mathematical and Physical Modeling of Actin Dynamics in Motile Cells." In Actin-based Motility, 381–412. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9301-1_16.

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Ogura, Atsuo, and Ryuzo Yanagimachi. "Microinsemination Using Spermatogenic Cells in Mammals." In Male Sterility and Motility Disorders, 189–202. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1522-6_17.

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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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Marceau, Normand, and Sabine H. H. Swierenga. "Cytoskeletal Events during Calcium- or EGF-Induced Initiation of DNA Synthesis in Cultured Cells." In Cell and Muscle Motility, 97–140. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-4723-2_5.

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Simon, Scott I., and Geert Schmid-Schoenbein. "Biophysical Analysis of Neutrophil Motility." In Biomechanics of Active Movement and Deformation of Cells, 429–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83631-2_13.

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Conference papers on the topic "Cells Motility"

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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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Abdulkadieva, M. M., V. V. Litvinenko, E. V. Vasilyeva, E. V. Sysolyatina, and S. A. Ermolaeva. "RELATIONSHIP OF L. MONOCYTOGENES MOTILITY CHARACTERISTICS WITH INVASION INTO HEP-2 CELLS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-162.

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The motility allows free-living microorganisms to spread and develop new habitats, and pathogenic ones to realize their virulence. The characteristics of the motility of bacterial cells include trajectories, speeds and collective movement. It has been shown for E. coli strains, that these characteristics affect adhesion to abiotic and biotic surfaces [1]. The aim of the work is to investigate the contribution of L. mononcytogenes motility to HEp-2 cells to invasion.
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Yunardi, Riky Tri, Agung Budianto Achmad, and Qurrotul A'yun. "Imaging Motility Pattern Analyzer Based on Optical Flow on Mice Sperm Cells Motility." In 2020 10th Electrical Power, Electronics, Communications, Controls and Informatics Seminar (EECCIS). IEEE, 2020. http://dx.doi.org/10.1109/eeccis49483.2020.9263448.

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Liu, Zhuolin, Kazuhiro Kurokawa, Furu Zhang, and Donald T. Miller. "Characterizing motility dynamics in human RPE cells." In SPIE BiOS, edited by Fabrice Manns, Per G. Söderberg, and Arthur Ho. SPIE, 2017. http://dx.doi.org/10.1117/12.2256144.

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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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Burgett, Monica E., Russell S. Tipps, Justin D. Lathia, Shideng Bao, Jeremy N. Rich, and Candece L. Gladson. "Abstract 5288: Glioma stem cells stimulate the motility of brain endothelial cells: Identification of cell-adhesion molecules mediating motility and direct interaction." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5288.

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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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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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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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Reports on the topic "Cells Motility"

1

Segall, Jeffrey E. Molecular Analysis of Motility in Metastatic Mammary Adenocarcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1998. http://dx.doi.org/10.21236/ada361091.

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Segall, Jeffrey E. Molecular Analysis of Motility in Metastatic Mammary Adenocarcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada300010.

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Segall, Jeffrey E. Molecular Analysis of Motility in Metastatic Mammary Adenocarcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada343279.

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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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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Addendum. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada458421.

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Wang, Fang. Inhibition of Invasiveness and Motility of Human Breast Cancer Cells by Sphingosine-1-Phosphate. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359261.

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Wang, Fang. Inhibition of Invasiveness and Motility of Human Breast Cancer Cells by Sphingosine-1-Phosphate. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada382431.

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Stoyanova, Tihomira, Veselina Uzunova, Albena Momchilova, Rumiana Tzoneva, and Iva Ugrinova. The Treatment of Breast Cancer Cells with Erufosine Leads to Actin Cytoskeleton Reorganization, Inhibition of Cell Motility, Cell Cycle Arrest and Apoptosis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, January 2021. http://dx.doi.org/10.7546/crabs.2021.01.11.

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