Relevant bibliographies by topics / Cell-to-cell spreading

Academic literature on the topic 'Cell-to-cell spreading'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Cell-to-cell spreading"

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Mothes, Walther, Nathan M. Sherer, Jing Jin, and Peng Zhong. "Virus Cell-to-Cell Transmission." Journal of Virology 84, no. 17 (April 7, 2010): 8360–68. http://dx.doi.org/10.1128/jvi.00443-10.

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ABSTRACT Viral infections spread based on the ability of viruses to overcome multiple barriers and move from cell to cell, tissue to tissue, and person to person and even across species. While there are fundamental differences between these types of transmissions, it has emerged that the ability of viruses to utilize and manipulate cell-cell contact contributes to the success of viral infections. Central to the excitement in the field of virus cell-to-cell transmission is the idea that cell-to-cell spread is more than the sum of the processes of virus release and entry. This implies that virus release and entry are efficiently coordinated to sites of cell-cell contact, resulting in a process that is distinct from its individual components. In this review, we will present support for this model, illustrate the ability of viruses to utilize and manipulate cell adhesion molecules, and discuss the mechanism and driving forces of directional spreading. An understanding of viral cell-to-cell spreading will enhance our ability to intervene in the efficient spreading of viral infections.
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Salsmann, Alexandre, Elisabeth Schaffner-Reckinger, and Nelly Kieffer. "RGD, the Rho’d to cell spreading." European Journal of Cell Biology 85, no. 3-4 (April 2006): 249–54. http://dx.doi.org/10.1016/j.ejcb.2005.08.003.

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McGrath, James L. "Cell Spreading: The Power to Simplify." Current Biology 17, no. 10 (May 2007): R357—R358. http://dx.doi.org/10.1016/j.cub.2007.03.057.

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Vilette, Didier, Josquin Courte, Jean Michel Peyrin, Laurent Coudert, Laurent Schaeffer, Olivier Andréoletti, and Pascal Leblanc. "Cellular mechanisms responsible for cell-to-cell spreading of prions." Cellular and Molecular Life Sciences 75, no. 14 (May 14, 2018): 2557–74. http://dx.doi.org/10.1007/s00018-018-2823-y.

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Vilette, Didier, Josquin Courte, Jean Michel Peyrin, Laurent Coudert, Laurent Schaeffer, Olivier Andréoletti, and Pascal Leblanc. "Correction to: Cellular mechanisms responsible for cell-to-cell spreading of prions." Cellular and Molecular Life Sciences 75, no. 14 (June 11, 2018): 2575. http://dx.doi.org/10.1007/s00018-018-2853-5.

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Colin, Morvane, Meryem Tardivel, Séverine Bégard, Luc Bousset, Simon Dujardin, Kevin Richetin, Nicole Deglon, Ronald Melki, and Luc Buee. "TAU SPREADING: HOW ARE TAU ASSEMBLIES TRANSFERRED FROM CELL TO CELL?" Alzheimer's & Dementia 13, no. 7 (July 2017): P906. http://dx.doi.org/10.1016/j.jalz.2017.07.320.

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McInnes, C., P. Knox, and D. J. Winterbourne. "Cell spreading on serum is not identical to spreading on fibronectin." Journal of Cell Science 88, no. 5 (December 1, 1987): 623–29. http://dx.doi.org/10.1242/jcs.88.5.623.

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Adhesion and spreading of cell lines on dishes coated with serum-derived proteins were studied after removal of cell-surface proteoglycans. A mixture of glycosaminoglycans lyases from heparin-induced Flavobacterium heparinum removed 80% of the [35S]sulphate-labelled glycosaminoglycans from the surface of attached cells within 30 min, but this had little effect on cell morphology. The rate of cell attachment to dishes coated with serum was unaffected by prior treatment of cells with this mixture of glycosaminoglycan lyases. While a heparan sulphate lyase preparation abolished cell spreading in response to fibronectin there was no effect of the enzyme on the spreading mediated by vitronectin. These results suggest that, although heparan sulphate is required for spreading on purified fibronectin, the spreading stimulated by serum under routine culture conditions requires neither cellular heparan sulphate nor serum-derived fibronectin.
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Mohamed, Nguyen-Vi, Thibaut Herrou, Vanessa Plouffe, Nicolas Piperno, and Nicole Leclerc. "Spreading of tau pathology in Alzheimer's disease by cell-to-cell transmission." European Journal of Neuroscience 37, no. 12 (June 2013): 1939–48. http://dx.doi.org/10.1111/ejn.12229.

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Kerkeni, W., Y. Ayari, L. Charfi, A. Bouzouita, H. Ayed, M. Cherif, M. R. Ben Slama, K. Mrad, A. Derouiche, and M. Chebil. "Transitional Bladder Cell Carcinoma Spreading to the Skin." Urology Case Reports 11 (February 2017): 17–18. http://dx.doi.org/10.1016/j.eucr.2016.11.028.

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Nisenholz, Noam, Aishwarya Paknikar, Sarah Köster, and Assaf Zemel. "Contribution of myosin II activity to cell spreading dynamics." Soft Matter 12, no. 2 (2016): 500–507. http://dx.doi.org/10.1039/c5sm01733e.

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Dissertations / Theses on the topic "Cell-to-cell spreading"

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Treloar, Katrina K. "Mathematical models for collective cell spreading." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/86960/1/Katrina_Treloar_Thesis.pdf.

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Collective cell spreading is frequently observed in development, tissue repair and disease progression. Mathematical modelling used in conjunction with experimental investigation can provide key insights into the mechanisms driving the spread of cell populations. In this study, we investigated how experimental and modelling frameworks can be used to identify several key features underlying collective cell spreading. In particular, we were able to independently quantify the roles of cell motility and cell proliferation in a spreading cell population, and investigate how these roles are influenced by factors such as the initial cell density, type of cell population and the assay geometry.
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Vo, Brenda. "Novel likelihood-free Bayesian parameter estimation methods for stochastic models of collective cell spreading." Thesis, Queensland University of Technology, 2016. https://eprints.qut.edu.au/99588/1/Brenda_Vo_Thesis.pdf.

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Biological processes underlying skin cancer growth and wound healing are governed by various collective cell spreading mechanisms. This thesis develops new statistical methods to provide key insights into the mechanisms driving the spread of cell populations such as motility, proliferation and cell-to-cell adhesion, using experimental data. The new methods allow us to precisely estimate the parameters of such mechanisms, quantify the associated uncertainty and investigate how these mechanisms are influenced by various factors. The thesis provides a useful tool to measure the efficacy of medical treatments that aim to influence the spread of cell populations.
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Sandmann, Rabea [Verfasser], Sarah [Akademischer Betreuer] Köster, and Florian [Akademischer Betreuer] Rehfeldt. "Blood Platelet Behavior on Structured Substrates : From Spreading Dynamics to Cell Morphology / Rabea Sandmann. Betreuer: Sarah Köster. Gutachter: Sarah Köster ; Florian Rehfeldt." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1078420084/34.

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Wilson, Cameron. "Mediation of Osteoblast Responses to Titanium Roughness by Adsorbed Proteins." Queensland University of Technology, 2005. http://eprints.qut.edu.au/16096/.

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Stable fixation of implants such as artificial teeth depends on the direct apposition of bone to the implanted material. While endosseous implants were traditionally allowed to "osseointegrate" over several months without carrying load, clinical and experimental data show that prostheses with roughened surfaces allow successful integration when subject to earlier loading and more challenging implant sites. However, to design implant surfaces for an optimal biological response requires an understanding of the mechanism by which roughened surfaces promote osseointegration. Research into this mechanism has, to date, focussed primarily on the response of osteoblastic cells to surface topography in vitro. While these have demonstrated some consistent trends in cell behaviour, the fundamental means by which cells sense and respond to roughness remain unclear. It has been suggested that cell responses to changes in topography may relate to differences in the proteins adsorbed from serum (in vitro). While experimental evidence indirectly suggests that physical features can affect protein adsorption, few studies have examined this with respect to surface roughness, particularly as a mediator of cell responses. To address this issue, cell culture and protein adsorption experiments were conducted on a limited range of surface textures. Titanium samples were ground to produce morphologically similar surfaces with three grades of roughness. A duplicate set of specimens were heated at 600°C for one hour, with the aim of masking potential variations in physicochemical properties with differing degrees of grinding. Osteoblast attachment and proliferation studies were conducted over a short time-frame of 48 hours or less, to highlight the effects of proteins adsorbed from serum rather than secreted by adherent cells. Gel electrophoresis provided a profile of the proteins adsorbed to each surface after 15 minutes, corresponding to the time by which the cells had settled onto the surface. Finally, confocal microscopy was used to examine cell morphology on each surface, and to visualize specific interactions between cellular structures and adsorbed adhesion-mediating proteins. Although the effects were inconsistent, attachment assays showed some indications that fewer cells attached in the first 90 minutes as roughness increased. This inverse cell number-roughness trend was significant at 48 hours; however, the variability in attachment assays prevented reliable separation of attachment and proliferation rate effects. While the reduction in cell number with increasing roughness is consistent with previous reports, it is typically observed at later time points, and thus may be increasingly confounded by contact inhibition and differentiation. Thermal oxidation of the titanium did not impact on osteoblast responses to roughness, although it significantly slowed cell proliferation. The latter result was unexpected on the basis of previous reports. One-dimensional gel electrophoresis revealed no significant differences in the composition of adsorbed layers with variations in roughness. However, as expected on account of wettability changes, the heat-treatment did correspond to significant changes in the adsorption profile. While this was not a highly sensitive analysis, it suggests that the cell responses to roughness changes were not governed by broadscale differences in the proteins initially available to adhering cells. In addition to the composition of the adsorbed layer, the distribution of proteins may also vary with topography. The immunofluorescence methods were not sufficiently sensitive to reveal the distribution of adsorbed adhesion proteins (vitronectin and fibronectin). However, the lack of clear labelling does suggest an absence of large accumulations due to specific topographic features. Further work is required to address this issue conclusively. Observations of cell morphology were consistent with widely-reported contact guidance phenomena on grooved surfaces, with elongation and alignment (with topography) increasing with groove depth. Cell elongation was also enhanced on the more hydrophilic, heat-treated titanium, but this effect diminished over time. Although increased elongation at 90 minutes corresponded to lower cell numbers at 48 hours, no causal relationship has yet been established.
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Wilson, Cameron John. "Mediation of Osteoblast Responses to Titanium Roughness by Adsorbed Proteins." Thesis, Queensland University of Technology, 2005. https://eprints.qut.edu.au/16096/1/Cameron_Wilson_Thesis.pdf.

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Stable fixation of implants such as artificial teeth depends on the direct apposition of bone to the implanted material. While endosseous implants were traditionally allowed to "osseointegrate" over several months without carrying load, clinical and experimental data show that prostheses with roughened surfaces allow successful integration when subject to earlier loading and more challenging implant sites. However, to design implant surfaces for an optimal biological response requires an understanding of the mechanism by which roughened surfaces promote osseointegration. Research into this mechanism has, to date, focussed primarily on the response of osteoblastic cells to surface topography in vitro. While these have demonstrated some consistent trends in cell behaviour, the fundamental means by which cells sense and respond to roughness remain unclear. It has been suggested that cell responses to changes in topography may relate to differences in the proteins adsorbed from serum (in vitro). While experimental evidence indirectly suggests that physical features can affect protein adsorption, few studies have examined this with respect to surface roughness, particularly as a mediator of cell responses. To address this issue, cell culture and protein adsorption experiments were conducted on a limited range of surface textures. Titanium samples were ground to produce morphologically similar surfaces with three grades of roughness. A duplicate set of specimens were heated at 600°C for one hour, with the aim of masking potential variations in physicochemical properties with differing degrees of grinding. Osteoblast attachment and proliferation studies were conducted over a short time-frame of 48 hours or less, to highlight the effects of proteins adsorbed from serum rather than secreted by adherent cells. Gel electrophoresis provided a profile of the proteins adsorbed to each surface after 15 minutes, corresponding to the time by which the cells had settled onto the surface. Finally, confocal microscopy was used to examine cell morphology on each surface, and to visualize specific interactions between cellular structures and adsorbed adhesion-mediating proteins. Although the effects were inconsistent, attachment assays showed some indications that fewer cells attached in the first 90 minutes as roughness increased. This inverse cell number-roughness trend was significant at 48 hours; however, the variability in attachment assays prevented reliable separation of attachment and proliferation rate effects. While the reduction in cell number with increasing roughness is consistent with previous reports, it is typically observed at later time points, and thus may be increasingly confounded by contact inhibition and differentiation. Thermal oxidation of the titanium did not impact on osteoblast responses to roughness, although it significantly slowed cell proliferation. The latter result was unexpected on the basis of previous reports. One-dimensional gel electrophoresis revealed no significant differences in the composition of adsorbed layers with variations in roughness. However, as expected on account of wettability changes, the heat-treatment did correspond to significant changes in the adsorption profile. While this was not a highly sensitive analysis, it suggests that the cell responses to roughness changes were not governed by broadscale differences in the proteins initially available to adhering cells. In addition to the composition of the adsorbed layer, the distribution of proteins may also vary with topography. The immunofluorescence methods were not sufficiently sensitive to reveal the distribution of adsorbed adhesion proteins (vitronectin and fibronectin). However, the lack of clear labelling does suggest an absence of large accumulations due to specific topographic features. Further work is required to address this issue conclusively. Observations of cell morphology were consistent with widely-reported contact guidance phenomena on grooved surfaces, with elongation and alignment (with topography) increasing with groove depth. Cell elongation was also enhanced on the more hydrophilic, heat-treated titanium, but this effect diminished over time. Although increased elongation at 90 minutes corresponded to lower cell numbers at 48 hours, no causal relationship has yet been established.
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Nguyen, Beth P. "Integrin alpha 6 beta 4 ligation to laminin 5 and phosphoinositide 3-OH kinase define differences in alpha 3 beta 1-laminin 5 and alpha 2 beta 1-collagen spreading : implications for epidermal wound repair /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/9286.

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Wong, Nelson Kwan Yin. "CD44 signaling in T cells leading to cell spreading and its regulation by CD45." Thesis, 2006. http://hdl.handle.net/2429/18417.

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CD44 is a widely expressed adhesion molecule that has been implicated in mediating cellular signaling. In this dissertation, the signaling pathway initiated by CD44 that leads to actin rearrangement and cell spreading in T cells was studied. The results indicate that engagement of CD44 leads to actin-dependent clustering of this adhesion molecule. CD44 clustering then initiates the recruitment of signaling proteins, including the Src-family kinases (SFK) Lck and Fyn, phosphatidylinositol-3 kinase (PI3K), and non-receptor related focal adhesion kinase Pyk2. The outcome of actin rearrangement and cell spreading resultant of CD44 signaling was determined by CD45, a transmembrane tyrosine phosphatase. In the absence of CD45, elongated cell spreading and F-actin polymerization along the longitudinal axis of the cells were observed. This was accompanied by the accumulation of tyrosine phosphorylation at CD44 microclusters. Moreover, Pyk2 phosphorylation was also associated with the CD44- induced elongated cell spreading. The CD44-induced signaling pathway that leads to Pyk2 phosphorylation and elongated cell spreading involves the activities of SFK, phospholipase C (PLC), and phosphatidylinositode-3-kinase (PI3K), as well as actin polymerization and calcium mobilization. These signaling components identified are also involved in T-cell receptor (TCR)/CD3 signaling, which is initiated during T cell activation; however, the CD44 pathway was distinct. This was supported by the observations that LAT (linker for activation of T cells) phosphorylation and ERK activation were not involved in CD44 signaling, while these events are observed in TCR/CD3 signaling. In the presence of CD45, BW5147 T cells formed F-actin rings and spread round on immobilized CD44 antibody. The formation of F-actin structures in CD45+ BW5147 T cells also required Src family kinase activity. Results from confocal microscopy studies suggest that CD45 was recruited to CD44 microclusters and this was associated with the prevention of sustained Lck activation. Overall, this work shows that CD44 mediates signals that result in actin reorganization and cell spreading in T cells; however, the outcome of these events is regulated by CD45. This is likely due to the negative regulatory effect of CD45 on SFK during CD44 signaling.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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Lum, Mabel Yuen Teng. "Identification of host cell proteins involved in Shigella flexneri pathogenesis." Thesis, 2014. http://hdl.handle.net/2440/87369.

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Shigella flexneri is the etiological agent of bacillary dysentery (shigellosis). It is transmitted via the faecal-oral route and is a significant human pathogen due to the high morbidity among children <5 years in developing countries. The key pathogenic features of Shigella include cell death induction in myeloid immune cells and circumventing cell death in colonic epithelial cells, the site of bacterial infection. Shigella also interact with host proteins to initiate de novo actin synthesis to facilitate its intra- and intercellular spread to disseminate in the host. In this thesis, the role of three host proteins: myosin IIA, dynamin II, and dynamin-related protein 1 (Drp1) during Shigella cell-to-cell spreading was examined. The myosin IIA specific kinase, myosin like chain kinase (MLCK), was previously shown to be important for Shigella plaque formation. Myosin IIA and MLCK have also been implicated in septin caging of non-motile Shigella which are targeted for degradation. Chemical inhibition and siRNA knockdown of myosin IIA reduced Shigella plaque formation. Curiously HeLa cells infected with Shigella mutants defective in cell-to-cell spreading have significantly reduced myosin IIA levels when quantified by immunofluorescence microscopy. Dynamin II and Drp1 are members of the dynamin superfamily. Both proteins have self-assembly driven GTPase activation. Dynamin II is important for clathrin-mediated endocytosis and pinches the budding clathrin-coated vesicle, and Drp1 is essential for mitochondrial fission. It was hypothesized that Shigella protrusion formation into adjacent host cells resembles endocytic and exocytic processes, and components of these processes may facilitate Shigella dissemination. When dynamin II GTPase was inhibited with dynasore and dynamin II was knocked down with siRNA, Shigella cell-to-cell spreading was significantly reduced. The in vivo efficacy of dynasore was tested in a murine Sereny model. No significant reduction in inflammation was observed but mice were protected against weight loss during infection. Further experimentation suggested dynasore protected mice against cytotoxic effects from the three secretion system (TTSS) effectors expressed by Shigella during infection. Drp1 was investigated in this thesis as dynasore also inhibits the GTPase of this mitochondrial fission protein. Mitochondrial fission is important in maintaining mitochondrial dynamics and also in events downstream of intrinsic apoptosis and programmed necrosis pathways activation. Loss of mitochondrial function in Shigella-induced epithelial cell death has been reported previously. Hence the role of Drp1 in Shigella plaque formation and HeLa death was examined with the Drp1-specific inhibitor, Mdivi-1, and siRNA knockdown. HeLa cell death was significantly reduced; suggesting loss of mitochondrial function observed previously may now be attributed to Drp1 and subsequent Drp1-mediated mitochondrial fission. The impairment in Shigella cell-to-cell spreading in the absence of Drp1 suggests maintaining an intact mitochondrial network is essential for Shigella lateral spread since loss of Drp1 function would result in excessive mitochondrial fusion, leading to formation of netlike or perinuclear structures. The outcomes of this thesis highlight the importance of host proteins during different stages of Shigella infection. By improving our understanding on the host and bacteria interaction, future work on novel approaches to prevent Shigella dissemination can be developed.
Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2014
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Klehmet, Juliane. "T-cell epitope spreading to myelin oligodendrocyte glycoprotein in HLA-DR4 transgenic mice experimental autoimmune encephalomyelitis /." 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014792446&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Books on the topic "Cell-to-cell spreading"

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Al-Anazi, KA, WK Al-Anazi, and AM Al-Jasser. Update on COVID-19 Infections and the Promising Role of Mesenchymal Stem Cell Therapies in their Management. Heighten Science Publications Inc., 2020. http://dx.doi.org/10.29328/ebook1002.

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The pandemic of COVID-19 has adversely affected almost every aspect of our lives but the world health and economic sectors suffer most of the repercussions of this disease. The search for a cure for this rapidly spreading virus which is causing massive life losses around the globe requires clear understanding of the immunopathogenesis of this virus as well as the mechanisms of actions of the various therapeutic modalities that are employed in the treatment of this life-threatening viral infection. Mesenchymal stem cells have antimicrobials effects in addition to their anti-inflammatory and immunomodulatory properties. They have been utilized in the treatment of various infections and their complications both in animal models and in human clinical trials. Mesenchymal stem cells derived from certain sources and their secretory products are particularly effective in the treatment of pneumonia, sepsis, acute lung injury, and acute respiratory distress syndrome which are common complications of COVID-19 infections. The review will discuss the various aspects of COVID-19 and it will highlight the promising role of mesenchymal stem cells in treating the complications of COVID-19 infections.
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Book chapters on the topic "Cell-to-cell spreading"

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Schmid, V., A. Bally, K. Beck, M. Haller, W. K. Schlage, and Ch Weber. "The extracellular matrix (mesoglea) of hydrozoan jellyfish and its ability to support cell adhesion and spreading." In Coelenterate Biology: Recent Research on Cnidaria and Ctenophora, 3–10. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3240-4_1.

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Weng, Nikki Jo-Hao, Rattapol Phandthong, and Prue Talbot. "A Video Bioinformatics Method to Quantify Cell Spreading and Its Application to Cells Treated with Rho-Associated Protein Kinase and Blebbistatin." In Computational Biology, 151–66. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-23724-4_8.

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Zimmermann, Miriam, Xu Qian, Andreas M. Kaufmann, and Andreas E. Albers. "The Role of Cancer Stem(–Like) Cells and Epithelial-to-Mesenchymal Transition in Spreading Head and Neck Squamous Cell Carcinoma." In Stem Cells and Cancer Stem Cells, Volume 11, 67–74. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7329-5_6.

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Scheer, U. "Contributions of Electron Microscopic Spreading Preparations (“Miller Spreads”) to the Analysis of Chromosome Structure." In Results and Problems in Cell Differentiation, 147–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-540-47783-9_10.

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Golz, Julia Carolin, and Kerstin Stingl. "Natural Competence and Horizontal Gene Transfer in Campylobacter." In Current Topics in Microbiology and Immunology, 265–92. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65481-8_10.

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AbstractThermophilic Campylobacter, in particular Campylobacter jejuni, C. coli and C. lari are the main relevant Campylobacter species for human infections. Due to their high capacity of genetic exchange by horizontal gene transfer (HGT), rapid adaptation to changing environmental and host conditions contribute to successful spreading and persistence of these foodborne pathogens. However, extensive HGT can exert dangerous side effects for the bacterium, such as the incorporation of gene fragments leading to disturbed gene functions. Here we discuss mechanisms of HGT, notably natural transformation, conjugation and bacteriophage transduction and limiting regulatory strategies of gene transfer. In particular, we summarize the current knowledge on how the DNA macromolecule is exchanged between single cells. Mechanisms to stimulate and to limit HGT obviously coevolved and maintained an optimal balance. Chromosomal rearrangements and incorporation of harmful mutations are risk factors for survival and can result in drastic loss of fitness. In Campylobacter, the restricted recognition and preferential uptake of free DNA from relatives are mediated by a short methylated DNA pattern and not by a classical DNA uptake sequence as found in other bacteria. A class two CRISPR-Cas system is present but also other DNases and restriction–modification systems appear to be important for Campylobacter genome integrity. Several lytic and integrated bacteriophages have been identified, which contribute to genome diversity. Furthermore, we focus on the impact of gene transfer on the spread of antibiotic resistance genes (resistome) and persistence factors. We discuss remaining open questions in the HGT field, supposed to be answered in the future by current technologies like whole-genome sequencing and single-cell approaches.
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Bey, E. M. "Spreading, growth and function of cells attached to a plasma clot interphase between agarose and the atmosphere." In Modern Approaches to Animal Cell Technology, 280–93. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-408-02732-8.50025-0.

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Saltzman, W. Mark. "Cell Adhesion." In Tissue Engineering. Oxford University Press, 2004. http://dx.doi.org/10.1093/oso/9780195141306.003.0011.

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The external surface of the cell consists of a phospholipid bilayer which carries a carbohydrate-rich coat called the glycocalyx; ionizable groups within the glycocalyx, such as sialic acid (N-acetyl neuraminate), contribute a net negative charge to the cell surface. Many of the carbohydrates that form the glycocalyx are bound to membrane-associated proteins. Each of these components— phospholipid bilayer, carbohydrate-rich coat, membrane-associated protein—has distinct physicochemical characteristics and is abundant. Plasma membranes contain ∼50% protein, ∼45% lipid, and ∼5% carbohydrate by weight. Therefore, each component influences cell interactions with the external environment in important ways. Cells can become attached to surfaces. The surface of interest may be geometrically complex (for example, the surface of another cell, a virus, a fiber, or an irregular object), but this chapter will focus on adhesion between a cell and a planar surface. The consequences of cell–cell adhesion are considered further in Chapter 8 (Cell Aggregation and Tissue Equivalents) and Chapter 9 (Tissue Barriers to Molecular and Cellular Transport). The consequences of cell–substrate adhesion are considered further in Chapter 7 (Cell Migration) and Chapter 12 (Cell Interactions with Polymers). Since the growth and function of many tissue-derived cells required attachment and spreading on a solid substrate, the events surrounding cell adhesion are fundamentally important. In addition, the strength of cell adhesion is an important determinant of the rate of cell migration, the kinetics of cell–cell aggregation, and the magnitude of tissue barriers to cell and molecule transport. Cell adhesion is therefore a major consideration in the development of methods and materials for cell delivery, tissue engineering, and tissue regeneration. The most stable and versatile mechanism for cell adhesion involves the specific association of cell surface glycoproteins, called receptors, and complementary molecules in the extracellular space, called ligands. Ligands may exist freely in the extracellular space, they may be associated with the extracellular matrix, or they may be attached to the surface of another cell. Cell–cell adhesion can occur by homophilic binding of identical receptors on different cells, by heterophilic binding of a receptor to a ligand expressed on the surface of a different cell, or by association of two receptors with an intermediate linker. Cell–matrix adhesion usually occurs by heterophilic binding of a receptor to a ligand attached to an insoluble element of the extracellular matrix.
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Saltzman, W. Mark. "Cell Interactions With Polymers." In Tissue Engineering. Oxford University Press, 2004. http://dx.doi.org/10.1093/oso/9780195141306.003.0018.

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Synthetic and natural polymers are an important element in new strategies for producing engineered tissue. Polymers are currently used in a wide range of biomedical applications, including applications in which the polymer remains in intimate contact with cells and tissues for prolonged periods. As discussed in Chapter 1, several classes of polymers have proven to be most useful in biomedical applications and, therefore, might be appropriate for tissue engineering applications. To produce tissue-engineered materials composed of polymers and cells, however, it is first necessary to understand the influence of these polymeric materials on cell viability, growth, and function. Cell interactions with polymers are usually studied using cell culture techniques. While in vitro studies do not reproduce the wide range of cellular responses observed following implantation of materials, the culture environment provides a level of control and quantification that cannot usually be obtained in vivo. Cells in culture are generally plated over a polymer surface and the extent of cell adhesion and spreading on the surface can be measured. By maintaining the culture for longer periods the influence of the substrate on cell viability, function, and motility can also be determined. Since investigators use different techniques to assess cell interactions with polymers, and because the differences between techniques are critically important for interpretation of interactions, some of the most frequently used in vitro methods are reviewed in this section. Before any measurement of cell interaction with a polymer substrate can be attempted, the polymeric material and the cells must come into contact. Preferably, this contact should be controlled (or at least understood) by the experimentalist. This is a critical, and often overlooked, aspect of all of these measurements. Some materials are easily fabricated in a format suitable for study; polystyrene films, for example, are transparent, durable, and strong. Other materials must be coated onto a rigid substrate (such as a glass coverslip) prior to study. Cell function is sensitive to chemical, morphological, and mechanical properties of the surface; therefore, almost every aspect of material preparation can introduce variables that are known to influence cell interactions.
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Sriram, Anitha, Yojana Bhor, Srushti Mahajan, Rahul Kumar, Saurabh Srivastava, Dharmendra Kumar Khatri, Shashi Bala Singh, and Pankaj Kumar Singh. "SARS-COV-2 Ingress - Triggering COVID-19 Infection." In An Update on SARS-CoV-2: Damage-response Framework, Potential Therapeutic Avenues and the Impact of Nanotechnology on COVID-19 Therapy Volume 1, 43–66. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815039863122010006.

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An important keynote that should be kept in mind is that to curb the spreading of the SARS-CoV-2 virus, one should understand how it enters host cells. This review provides deep insights into mechanistic intervention approaches of 2019- nCoV that target its host cell entry mechanisms. Majorly, there are three entryways for 2019-nCoV to target and infect the host cell, which is highly expressed with ACE2. The ‘S’- priming of TMPRSS2 associated cleavage is the primary entryway for a virus to access the targeted host cell via mediating the fusion process. The second way for virus entry is through the endocytosis phenomenon. The third way for virus entry is S pre-priming or S pre-cleaving of furin mediated fusion. Recent studies have proved that S1/S2' is a proteolytic cleavage site responsible for mediating viral entry. Hence, several protease inhibitors could be the potential targets to block proteolytic cleavage of the spike protein. This review describes the different entryways of 2019-nCoV and the impactful role of TMPRSS2 and furin host enzymes for a virus to get access into the targeted host cell; pre-fusion and post-fusion conformational states of 2019-nCoV spike protein; the role of viral suppressors of RNA in host immune evasion and the role of SPs, NSPs, and Orfs of 2019-nCoV in host immune evasion (host IFN response). Mutations of 2019-nCoVand its variants are reviewed in this article.
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A., Kodieswari. "Early Detection of Cancer Using Smartphones." In Advances in Medical Technologies and Clinical Practice, 25–31. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-5225-6067-8.ch003.

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Cancer disease is the second largest disease in the world with high death mortality. Cancer is an abnormal growth of a normal cell. There are more than 100 types of cancer like blood cancer, brain cancer, small intestine cancer, lung cancer, liver cancer, etc. The type of cancer can be classified by the type of cell which is initially affected. When cancer grows it does not show any symptom. The symptom will appear when the cancer cell grows in mass and the symptom of cancer depends on the type of cancer. The cause of cancers is environmental pollutants, food habits, inherited genetics, tobacco, stress, etc., but in practice, it is not possible to prove the cause of cancer since various cancers do not have specific fingerprints. After the heart attack, cancer is a second killer disease in India. The death mortality is high in cancer because in most of the cases it is identified at the final stage which causes more death. According to ICMR, among 1.27 billion Indian populations, the incidence of cancer is 70-90 per 100,000 populations and 70% of cancer is identified in the last stage accounting for high morality. There are many types of treatment to treat cancer and they are surgery, radiation therapy, chemotherapy, targeted therapy, hormone therapy, stem cell transplant, etc. All cancer treatments will have side effects and the treatments will help only if the cancer cells are identified at the early stage. So time factor is important in diagnosing of cancer cells; hence, early detection of cancer will reduce the mortality rate. This chapter proposed the early detection of cancer cells using image processing techniques by the structure of circulating tumor cell. Early detection of cancer cells is very difficult because the concentration of cancer cells are extremely small and about one million malignant cell is encountered per billion of healthy cells. The circulating tumor cells, CTC, are shed into the bloodstream as a tumor grows, and it is believed these cells initiate the spread of cancer. CTC are rare, existing as only a few per one billion blood cells, and a highly efficient technology like chip-based biosensor platforms is required to capture the CTC, which in turn helps to detect cancer cell at an early stage before spreading. In proposed method, the circulating tumor cell has used a marker to detect cancer at early stage.
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Conference papers on the topic "Cell-to-cell spreading"

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Hu, Jia, and Yaling Liu. "Cell Adhesion on a Wavy Surface." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14059.

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The ability to control the position of cells in an organized pattern on a substrate has become increasingly important for biosensing and tissue engineering applications [1–3]. With the advent of nanofabrication techniques, a number of researchers have studied the effects of nano-scale grooves on cell spreading, migration, morphology, signaling and orientation [4–6]. Recent studies have shown that cell adhesion/spreading can be influenced by a nanostructured surface [7]. In most current studies, the pattern dimensions are much smaller than the size of a cell. In this paper, we focus on studying cell response to micro scale patterns instead of nano-scale patterns.
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Weafer, Paul, Maarten H. van Es, Suzanne P. Jarvis, and Patrick J. McGarry. "Compression Force Measurement During Cell Spreading Using a Modified Atomic Force Microscope." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53741.

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Mechanical forces play a critical role in the regulation of cell spreading and cytoskeletal organization. It has been demonstrated that the force required to compress a spread cell is significantly higher than that required to compress a cell with a rounded morphology [1]. This increase in force can not be attributed to morphological changes alone [2], highlighting the importance of cytoskeletal remodeling during cell spreading in the resistance of cells to compressive forces.
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Vernerey, Franck J. "Biophysical Model of the Coupled Mechanisms of Cell Adhesion, Contraction and Spreading." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80309.

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Recent research has shown that cell spreading is highly dependent on the contractility of its cytoskeleton and the mechanical properties of its surrounding environment. This extended abstract introduces a mathematical formulation of cell spreading and contraction that couples the processes of stress fiber formation, protrusion growth through actin polymerization at the cell edge and dynamics of cross-membrane protein (integrins) enabling cell-substrate attachment. The evolving cell’s cytoskeleton is modeled as a mixture of fluid, proteins and filaments that can exchange mass and generate contraction. In particular, besides self-assembling into stress fibers, actin monomers are able to polymerize into an actin meshwork at the cell’s boundary in order to push the membrane forward and generate protrusion. These processes are possible via the development of cell-substrate attachment complexes that arise from the mechano-sensitive equilibrium of membrane proteins, known as integrins. Numerical simulations show that the proposed model is able to capture the dependency of cell spreading and contraction on substrate stiffness and chemistry. The very good agreement between model predictions and experimental observations suggests that mechanics plays a strong role into the coupled mechanisms of contraction, adhesion and spreading of adherent cells.
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Zhang, Feng-Yuan, Xiao-Guang Yang, and Chao-Yang Wang. "Visualization of Flooding in Operating Fuel Cell." In ASME 2005 Power Conference. ASMEDC, 2005. http://dx.doi.org/10.1115/pwr2005-50206.

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Flooding has been considered one of the important issues for the limitation of performance and durability of fuel cell. The flooding in fuel cell is investigated by developing visualization system with high spatial resolution, which is designed to give close images and movies of emergence, coalesce and removal of droplets in fuel cell. It has been shown that capillary force plays dominant role in liquid removal at low flow velocity, which is a typical operating condition in fuel cell. Increasing the hydrophilic properties of side walls and front wall of flow channel will result in higher liquid spreading and removal rates; while larger contact angle on GDL surface is preferred. The spreading time on front surface could be greatly reduced by decreasing the width of the flow channel. To get a stable performance of fuel cell, the water accumulation rate should be designed to be smaller that the ability of water removal.
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Li, Jianrong, Tianle Cheng, and Martin Y. M. Chiang. "Finite Element Modelling of Cell Adhesion Mediated by Receptor-Ligand Binding." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206297.

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The process of cell adhesion and spreading on the extracellular matrix (ECM) protein layer is mediated by the interaction of cell receptors and ECM ligands [1]. Receptors diffuse along the cell membrane surface and interact with ligands in ECM to form bonds. Cells spread and the adhesion zone grows as bond formation at the adhesion front increases to a critical level. This process involves coupling of reaction-diffusion and mechanical contact between cells and ECM. In this study, a novel numerical algorithm is developed to implement this coupling into the finite element method for modeling the process of cell adhesion and spreading. By taking the mass diffusion and the user-defined gap conductance features provided in a commercial FEM code, Abaqus [2], the process has been solved in an integrated and fully coupled manner. Preliminary results have been obtained from the simulation of cell spreading on a rigid substrate. The influence of glycocalyx layer (present at cell surface) on the adhesion development has also been incorporated into the modeling.
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Shi, X., S. Wu, Y. Liu, Q. Cui, and Z. Liang. "266 Intra-epithelial spreading of cervical squamous cell carcinoma to the upper genital tract." In IGCS 2020 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2020. http://dx.doi.org/10.1136/ijgc-2020-igcs.228.

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Gallant, Nathan D., and Kranthi Kumar Elineni. "Regulation of Adhesion Strength by Focal Adhesion Position and Cell Shape." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80832.

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Cell adhesion to extracellular matrices is critical to numerous cellular functions and is primarily mediated by integrin receptors. Binding and aggregation of integrins leads to the formation of focal adhesions (FA) which connect the cytoskeleton to the extracellular matrix in order to reinforce adhesion and transmit signals [1]. Preliminary observations indicated preferential recruitment of FAs to the periphery of the cell spreading area on both uniformly coated and micropatterned fibronectin surfaces (Fig. 1). The current study investigates the biophysical regulation of cell adhesion strength based on the size and position of FA with the central hypothesis that peripheral FAs stabilize adhesion strength. The hypothesis was tested by delineating the cell spreading area from the total cell adhesive area by employing microcontact printing to pattern substrates with a series of circular and annular adhesive islands which control cell shape (Fig. 2). A well characterized hydrodynamic shear assay known as the spinning disk device was used to quantify the adhesion strength of cells adhered to the micropatterns [2].
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Dejana, E., L. R. Languino, S. Colella, E. Plow, M. Ginsberg, and P. C. Marchisio. "THE LOCALIZATION OF PLATELET GpIIb-IIIa RELATED PROTEINS IN ENDOTHELIAL CELL ADHESION STRUCTURE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642814.

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Different laboratories bave reported that human endothelial cells (EC) synthesize and express surface proteins biochemically and immunologically related to platelet GpIIb-IIIa. However the functional role of this glycoprotein complex in EC has not yet been elucidated. In this study we investigated whether these molecules are involved in the process of EC adhesion to different substrata. Cultured human umbilical vein ECs ,seeded on purified fibrinogen(fg), or vitronectin(VN) coated coverslips, adhered ,underwent spreading, organization of thick microfilament bundles and formation of focal contacts as shown by immunofluorescence and interference reflection microscopy.Polyclonal antibodies raised against human platelet GpIIb-IIIa and cross reacting with the EC form, showed by immunofluorescence a discrete and well organized distribution at cell adhesion structures, Indeed they distributed at vinculin rich focal contacts at the membrane insertion of microfilament bundles of stress fiber type.They were also found at cell to cell contacts and in a diffuse pattern at the dorsal surface of EC.GpIIb-IIIa antibodies added to EC suspensions prior to plating inhibited EC adhesion and spreading in a concentration dependent way. This effect was present at different degrees when EC were seeded on fg or VN being clearly more evident on VN and somehow less apparent on fg.In addition when the antibodies were added to confluent EC monolayers for 24 h they disrupted cell to cell contacts and caused cell rounding and detachment Preimmune serum or control antibodies able to bind to EC external membrane but which did not recognized GpIIb-IIIa proteins were unable to inhibit EC attachment and spreading. These results indicate that EC GpIIb-IIIa complex is involved in the adhesion mechanism of these cells to extracellular matrix proteins.
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Ferrell, Nicholas, James Woodard, Daniel Gallego-Perez, Natalia Higuita-Castro, and Derek Hansford. "Polymer MEMS for Measuring Single Cell Forces." In ASME 2010 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/detc2010-29047.

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We have developed a polymer MEMS sensor for measuring mechanical forces generated by single adherent cells. Mechanical forces are known to play a role in cell regulation, and measuring these forces is an important step in understanding cellular mechanotransduction. The sensor consists of four polystyrene microcantilever beams with cell adhesion pads at each end. Finite element analysis was used to guide the design of a compound cantilever to allow measurement of forces in multiple directions. The device was evaluated by measuring forces generated by WS-1 human skin fibroblasts. A single cell was placed on the sensor using a custom micromanipulator. Forces were calculated by optically measuring the deflection of each probe during cell attachment and spreading. Measurements were performed on normal cells and those treated with cytochalasin D to disrupt the actin cytoskeleton. Cytochalasin D treated cells showed a significant decrease in force. This device can be used to evaluate the mechanical response of cells to a variety of chemical, mechanical, and other environmental stimuli.
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Shao, Yue, Jennifer M. Mann, and Jianping Fu. "Cell Shape Dictates Differential Sensitivity of Subcellular Contractile Forces in Response to Directional Substrate Stretch." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14225.

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In past decades, it has been well demonstrated that cellular contractile forces against the extracellular matrix (ECM) plays an important role in regulating cellular behaviors such as spreading, adhesion and differentiation [1]. Recent studies have found that focal adhesions (FAs) and subcellular contractile forces mediated by FAs have an intimate connection and form an important feedback loop to control cellular mechanotransduction in response to mechanical cues such as matrix rigidity, cell geometry and external forces [2]. Therefore, understanding how FA-mediated contractile forces are regulated by those factors is critical for our understanding of cellular mechanotransduction and mechano-responsiveness.
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Reports on the topic "Cell-to-cell spreading"

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Research, Gratis. The Mystery behind Bacterial Retrons. Gratis Research, December 2020. http://dx.doi.org/10.47496/gr.blog.05.

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Retron-mediated cell killing serves as a defensive strategy to prevent the spreading of phage infection in bacteria and the combined action of retron and CRISPR-based gene editing appear to be a potent gene-editing tool.
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