Relevant bibliographies by topics / Cell

Contents

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

Academic literature on the topic 'Cell'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 July 2024

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Journal articles on the topic "Cell"

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Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (October 31, 2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.
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Ahmed Elkammar, Hala. "Effect of human bone marrow derived mesenchymal stem cells on squamous cell carcinoma cell line." International Journal of Academic Research 6, no. 1 (January 30, 2014): 110–16. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.14.

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Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.
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Fujimoto, Naohiro, Bin Han, Masayoshi Nomura, and Tetsuro Matsumoto. "WS1-1-1 Nitrogen-Containing Bisphosphonates Inhibit the Growth of Renal Cell Carcinoma Cells(Renal Cell Cancer)." Japanese Journal of Urology 99, no. 2 (2008): 142. http://dx.doi.org/10.5980/jpnjurol.99.142_1.

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Ohshima, Kôichi, Junji Suzumiya, and Masahiro Kikuchi. "T cell rich B cell lymphoma." Journal of the Japan Society of the Reticuloendothelial System 36, no. 5-6 (1996): 391–93. http://dx.doi.org/10.3960/jslrt1961.36.391.

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Gaddikeri1, Kavitha, and Deepak D. Bhorgonde2. "Assessment of role of mast cells in oral squamous cell carcinoma." Asian Pacific Journal of Health Sciences 3, Supplimentary 2016 (December 31, 2016): 63–66. http://dx.doi.org/10.21276/apjhs.2016.3.4s.9.

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Abramova, V. A., A. Kali, N. Abdolla, O. Yu Yurikova, Yu V. Perfilyeva, Ye O. Ostapchuk, R. T. Tleulieva, S. K. Madenova, and N. N. Belyaev. "Influence of tumor cells on natural killer cell phenotype and cytotoxicity." International Journal of Biology and Chemistry 8, no. 1 (2015): 9–14. http://dx.doi.org/10.26577/2218-7979-2015-8-1-9-14.

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CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.
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YAMAMOTO, Takamitsu. "C207 DEVELOPMENT OF FUEL CELLS POWERED RAILWAY VEHICLE(Fuel Cell-1)." Proceedings of the International Conference on Power Engineering (ICOPE) 2009.2 (2009): _2–213_—_2–218_. http://dx.doi.org/10.1299/jsmeicope.2009.2._2-213_.

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Nagayama, Kazuaki. "OS18-1 Nuclear-cytoskeletal Interactions in Vascular Smooth Muscle Cells : Possible Roles in the Regulation of Cell Differentiation(Cell and Tissue mechanics 1,OS18 Cell and tissue mechanics,BIOMECHANICS)." Abstracts of ATEM : International Conference on Advanced Technology in Experimental Mechanics : Asian Conference on Experimental Mechanics 2015.14 (2015): 235. http://dx.doi.org/10.1299/jsmeatem.2015.14.235.

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Dissertations / Theses on the topic "Cell"

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Islam, Azharul. "Cell-walls of growing plant cells." Thesis, University of Westminster, 2013. https://westminsterresearch.westminster.ac.uk/item/8z033/cell-walls-of-growing-plant-cells.

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The plant primary cell wall is a three-dimensional interwoven network of cellulose microfibrils, cross-linked by xyloglucan and dispersed in a pectin matrix. It has been suggested that in the wall of growing plant cells, xyloglucan is bound to the rigid cellulose microfibrils by hydrogen bonds and holds the microfibrils together by forming molecular tethers, which is referred to as the ‘sticky network’ model. Plant growth occurs when these tethers are peeled from the microfibrils by expansins or broken by glycosidases or transglycosylases. A number of researchers have presented theoretical difficulties and observations inconsistent with this model and a new hypothesis has been proposed, claiming that the cellulose – xyloglucan cross-links may act as ‘scaffolds’ holding the microfibrils apart. Analogies with synthetic polymers suggests that the spacing between the cellulose microfibrils may be an important determinant of the mechanical properties of the cell wall and the results presented in this thesis support this hypothesis. Water contents of Acetobacter xylinus synthesized cellulose based cell wall analogues (as a mimic of primary cell wall) and sunflower hypocotyl cell walls were altered using high molecular weight polyethylene glycol (PEG) solution, and their extension under a constant load was measured using a creep extensiometer and showed that there were clear reduction (30-35%) in extensibility suggesting that water content of the wall and therefore the cell wall free volume directly influence wall extensibility. When hydration of A. xylinus cellulose composite pellicles was reduced using PEG 6000 solution and re-hydrated in buffer solution, followed by treatment with α-expansin or snail acetone powder extract, it was found that expansin and snail powder extracts caused a rapid rehydration of the composites and that the pellicles only returned to their original weights after these treatments, suggesting that expansin and snail powder can increase the free volume of the wall perhaps contributing to the increases in extensibility that they cause. Assays on cell wall fragments also indicated that expansin increased the cell wall free volume, demonstrated by changes of the turbidity of fragment suspensions. The role of pectic polysaccharide, RG-II, in cell wall biomechanics was also investigated using mechanical and biochemical testing of available Arabidopsis thaliana cell wall mutants and by incorporating RG-II (purified from red wine) with Acetobacter cellulose. It was demonstrated that RG-II significantly increased the hydration of cellulose composite; hydration rate was 15 -16% more than the composite without RG-II and thus increased the pellicle extensibility. From the results, it is evidenced that cell wall extension is not only the consequences of breaking hydrogen bonds between cellulose microfibrils and xyloglucan by expansins or glycosidases and transglycosylases, but also a wider range of factors are involved including cell wall water content, cell wall free volume and the pectic polymers, especially RG-II.
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Mittal, Nikhil 1979. "Cell-cell and cell-medium interactions in the growth of mouse embryonic stem cells." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/62602.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Physics, 2010.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (p. 100-108).
Embryonic stem cells serve as powerful models for the study of development and disease and hold enormous potential for future therapeutics. Due to the potential for embryonic stem cells (ESCs) to provide a variety of tissues for use in regenerative medicine, there has been great interest in the identification of factors that govern the differentiation of ESCs into specific lineages. Much of this research builds on previous studies of the role of intercellular signaling in the specification of various cell types in the developing embryo. However, relatively little work has been done on understanding the role of cell-cell communication in the self-renewal of ESCs. In the first part of this thesis I describe the development and testing of new devices for studying intercellular signaling - the nDEP microwell array and the Bio Flip Chip (BFC). We used the BFC to show that cell-cell interaction improves the colony-forming efficiency and the self-renewal of mouse ESCs. Further, we demonstrate that the interaction is at least partly diffusible. In the next part of the thesis I describe our use of more traditional assays to validate the results obtained using the BFC and to further explore the role of diffusible signaling in the survival of mouse ESCs. We demonstrate the existence of an optimal density for 2-day culture of mouse ESCs. Further, we demonstrate that the increase in growth with plating density (103-104 cells/cm2) is at least partly due to the existence of one or more survival-enhancing autocrine factor(s) in mouse ESC cultures, and that one of these factors is Cyclophilin A. Finally, we demonstrate that changes in the low molecular weight composition of the medium are likely responsible for the decrease in growth at high plating densities (>104 cells/cm2). We use a numerical model to show that competition between the positive effect (on growth) of autocrine survival factors and the negative effect of nutrient depletion can account for the observed optimal growth density. Our study provides new insight into the processes underlying, and optimization of, growth in cell types that lack contact inhibition such as cancer cells and stem cells.
by Nikhil V. Mittal.
Ph.D.
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Pat, Sze Wa. "Cell metabolism in cell death and cell growth." HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.

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Rabodzey, Aleksandr. "Flow-induced mechanotransduction in cell-cell junctions of endothelial cells." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/41586.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Biological Engineering Division, 2006.
Includes bibliographical references (leaves 86-92).
Endothelial cells show an unexpected behavior shortly after the onset of laminar flow: their crawling speed decreases ~40% within the first 30 min, but only in a confluent monolayer of endothelial cells, not in subconfluent cultures, where cell-cell interactions are limited. This led us to study early shear effects on cell-cell adherens junctions. We found a 30±6% increase in the number of VE-cadherin molecules in the junctions. The strength of interactions of endothelial cells with surfaces coated with recombinant VE-cadherin protein also increased after laminar flow. These observations suggest that endothelial cell junction proteins respond to flow onset. The process of clustering may induce diffusion of monomers to the junction area, resulting in an overall increase in VE-cadherins in the junctions. To directly confirm the role of adherens junctions in the decrease in cell crawling speed, we used siRNA-knockdown technique to produce cells lacking VE-cadherin. These cells showed no decline in crawling speed under flow. Our interpretation is consistent with previous data on junction disassembly 8 hr after flow onset. The speed of endothelial cell crawling returns to the original level by that time, and junctional disassembly may explain that phenomenon. In order to understand better the change in VE-cadherin distribution under flow and during junction formation and remodelling, we developed a mathematical model of VE-cadherin redistribution in endothelial cells. This model allowed us to develop a quantitative framework for analysis of VE-cadherin redistribution and estimate the amount of protein in the junctions and on the apical surface. In addition to that, the model explains rapid junction disassembly in the leukocyte transmigration and junction formation in subconfluent cells.
(cont.) These studies show that intercellular adhesion molecules are important in the force transmission and shear stress response. Their role, however, is not limited to flow mechanotransduction. Intercellular force transmission has an important application - organ development and, specifically, angiogenesis. We studied the role of VE-cadherin in vessel development in HUVECs and showed that VE-cadherin-null cells do not form vessels in the in vitro assay. This observation confirms the important role of intercellular force transmission in response to external force caused by flow or exerted by other cells.
by Aleksandr Rabodzey.
Ph.D.
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Sarvi, Sana. "Small cell lung cancer and cancer stem cell-like cells." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9542.

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Small cell lung cancer (SCLC) is a highly aggressive malignancy with extreme mortality and morbidity. Although initially chemo- and radio-sensitive, almost inevitable recurrence and resistance occurs. SCLC patients often present with metastases, making surgery not feasible. Current therapies, rationally designed on underlying pathogenesis, produce in vitro results, however, these have failed to translate into satisfactory clinical outcomes. Recently, research into cancer stem cells (CSCs) has gained momentum and form an attractive target for novel therapies. Based on this concept, CSCs are the cause of neoplastic tissue development that are inherently resistant to chemotherapy, explaining why conventional therapies can shrink the tumour but are unable to eliminate the tumour completely, leading to eventual recurrence. Here I demonstrate that SCLC H345 and H69 cell lines contain a subset of cells expressing CD133, a known CSC marker. CD133+ SCLC sub-population maintained their stem cell-like phenotype over a prolonged period of culture, differentiated in appropriate conditions and expressed the embryonic stem cell marker Oct-4 indicating their stem-like phenotype. Additionally, these cells displayed augmented clonogenic efficacy, were chemoresistant and tumorigenic in vivo, distinct from the CD133- cells. Thus, the SCLC CD133 expressing cells fulfil most criteria of CSClike definition. The molecular mechanisms associated with CD133+ SCLC chemoresistance and growth is unknown. Up-regulated Akt activity, a known promoter of resistance with survival advantage, was observed in CD133+ SCLC cells. Likewise, these cells demonstrated elevated expression of Bcl-2, an anti-apoptotic protein compared to their negative counterpart explaining CD133+ cell chemoresistance phenotype. Additionally, CD133+ cells revealed greater expression of neuropeptide receptors, gastrin releasing peptide (GRP) and V1A receptors compared to the CD133- cells. Addition of exogenous GRP and arginine vasopressin (AVP) to CD133+ SCLC cells promoted their clonogenic growth in semi-solid medium, illustrating for the first time neuropeptide dependent growth of these cells. A novel peptide (peptide-1) was designed based on the known structure of the substance P analogues that have shown benefit in animal models and in early clinical trials. This compound inhibited the growth of SCLC cells in in vitro with improved potency and stability compared to previous analogues and reduced tumorigenicity in vivo. Interestingly, peptide-1 was more effective in CD133+ cells due to increased expression of neuropeptide receptors on these cells. In conclusion, my results show that SCLC cells retain a sub-population of cells that demonstrate CSC-like phenotype. Preferential activation of Akt and Bcl-2 survival pathways and enhanced expression of neuropeptide receptors contribute to CD133+ SCLC chemoresistance and growth. Therefore, it can be proposed that CD133+ cells are the possible cause of SCLC development, treatment resistance and disease recurrence. Despite being chemoresistant, CD133+ cells demonstrated sensitivity to peptide-1. The identification of such new analogue that demonstrates efficacy towards resistant CD133+ SCLC cells is a very exciting step forward in the identification of a potential new therapy for resistant disease.
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Wong, Ching-hang. "Cell-cell interactions and cell junction dynamics in the mammalian testis." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31993084.

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Chowdhury, Azazul Islam. "Role of Cell-cell Interactions and Palmitate on β-cells Function." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230841.

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The islets of Langerhans secrets insulin in response to fluctuations of blood glucose level and efficient secretion requires extensive intra-islet communication. Secretory failure from islets is one of the hallmark in progression of type 2 diabetes.  Changes in islet structure and high levels of saturated free fatty acids may contribute to this failure. The aim of this thesis is to study the role of cell-cell interactions and palmitate on β-cells functions. To address the role of cell-cell interactions on β-cells functions MIN6 cells were cultured as monolayers and as pseudoislets. Glucose stimulated insulin secretion was higher in pseudoislets compared to monolayers. Transcript levels of mitochondrial metabolism as well glucose oxidation rate was higher in pseudoislets. Insulin receptor substrate-1 (IRS-1) phosphorylation was altered when cells were grown as pseudoislets. Proteins expression levels related to glycolysis, cellular connections and translational regulations were up-regulated in pseudoislets. We propose the superior capacity of pseudoislets compared to monolayers depend on metabolism, cell coupling, gene translation, protein turnover and differential IRS-1 phosphorylation. To address the role of palmitate on β-cells human islets were cultured in palmitate. Long term palmitate treatment decreased insulin secretion which is associated with up-regulation of suppressor of cytokine signaling-2 (SOCS2) and protein inhibitor of activated STAT-1 (PIAS1). Up-regulation of SOCS2 decreased phosphorylation of Akt at site T308, whereas PIAS1 decreased protein level of ATP- citrate lyase (ACLY) and ATP synthase subunit B (ATP5B). We propose long term palmitate treatment reduces phosphatidylinositol 3-kinase (PI3K) activity, attenuates formation of acetyl-CoA and decreases ATP synthesis which may aggravate β-cells dysfunction.
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Wang, Wei. "Modulation of immune cell responses by small cell lung cancer cells." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/modulation-of-immune-cell-responses-by-small-cell-lung-cancer-cells(7bdc85c2-acd8-4f13-9d2b-e2ce07d1567b).html.

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Small Cell Lung Cancer (SCLC) accounts for 15-20% of all lung cancers and kills at least one person every 2 hours in the UK. There is no effective treatment and overall 2-year survival is less than 5%. Patients with SCLC have poorly understood local and systemic immune defects. Previous studies have shown several important defects in cell-mediated immune responses in patients with SCLC. A better understanding of interactions between SCLC tumour cells and immune cells may lead to the development of novel therapeutic approaches. There is increasing recognition that immunological biomarkers may add to traditional histological analyses and can be exploited in the management of multiple epithelial malignancies. There are currently no such markers used in the management of SCLC. In my PhD project, I have shown that cell lines from different SCLC patients have differential immunosuppressive capabilities. These properties are mediated by the secretion of differing levels of soluble molecules that can suppress the mixed leukocyte reaction (MLR) and CD4+ T cell proliferation, induce IL-10 secretion and differentiation of functional CD4+CD25+CD127+FoxP3+Helios- regulatory T cells (Tregs) from naïve CD4+ T cells. IL-15 is secreted by SCLC cells in culture in proportion to their immunosuppressive capability. Its in vivo relevance is supported by its presence in tumour biopsy samples. The suppressive effect on CD4+ T cell proliferation and the induction of Treg cell population was not affected by blocking IL-10 or TGF-β signalling but was partially reversed by blocking IL-15 activity. Therefore, IL-15 is one, though not the only, soluble molecule produced by SCLC cells to mediate immune suppression by inducing increased population of Treg cells. This may represent a mechanism by which SCLC cells can suppress the immune response. In addition, SCLC cells supressed TNF-α release from monocytes in response to LPS stimulation, down-regulated expression of CD16 and CD86 and upregulated expression of CD163 and CD206 on monocyte-derived macrophages (MDMs) upon activation. This M2-like phenotype poralization was associated with decreased TNF-α and IL-6 production and increased IL-10 secretion. These effects were abrogated by blocking the signalling of bombesin-like peptides (BLPs) that are neuropeptides produced by SCLC cells using a GRP receptor (GRP-R) antagonist. Therefore, the polarization of macrophages to an M2-like phenotype by SCLC cell-derived BLPs may represent another mechanism by which SCLC tumours suppress the immune response. Finally, SCLC tumour biopsies were shown to be infiltrated with various mononuclear immune cells and Treg cells. CD45 and FoxP3 were used as paninflammatory cell and Treg cell markers respectively. An elevated CD45+ infiltrate was predictive of prolonged survival in SCLC independent of age, sex, stage or treatment strategy. An elevated FoxP3+/CD45+ ratio was predictive of a significantly worse prognosis. This study identifies potential mechanisms by which SCLC tumour cells may downregulate local and systemic immune response, and also identifies an independent prognostic marker to predict patient survival in SCLC. Further, IL- 15 and BLPs are potential novel therapeutic targets in SCLC.
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Wong, Ching-hang, and 黃政珩. "Cell-cell interactions and cell junction dynamics in the mammalian testis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31993084.

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Sampangi, Sandeep. "Autologous human kidney proximal tubule epithelial cells (PTEC) modulate dendritic cell (DC), T cell and B cell responses." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82033/1/Sandeep_Sampangi_Thesis.pdf.

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This is a comprehensive study of human kidney proximal tubular epithelial cells (PTEC) which are known to respond to and mediate the pathological process of a range of kidney diseases. It identifies various molecules expressed by PTEC and how these molecules participate in down-regulating the inflammatory process, thereby highlighting the clinical potential of these molecules to treat various kidney diseases. In the disease state, PTEC gain the ability to regulate the immune cell responses present within the interstitium. This down-regulation is a complex interaction of contact dependent/independent mechanisms involving various immuno-regulatory molecules including PD-L1, sHLA-G and IDO. The overall outcome of this down-regulation is suppressed DC maturation, decreased number of antibody producing B cells and low T cell responses. These manifestations within a clinical setting are expected to dampen the ongoing inflammation, preventing the damage caused to the kidney tissue.
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Books on the topic "Cell"

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Ltd, Addison-Wesley Longman, and Pearson Education Canada Inc, eds. Cells and cell systems. Toronto, Ont: Addison-Wesley, 2000.

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Cells and cell function. London: Wayland, 2009.

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Ballard, Carol. Cells and cell function. New York: Rosen Central, 2010.

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Cells and cell function. Chicago, Ill: Heinemann Library, 2005.

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P, Colgan Sean, ed. Cell-cell interactions: Methods and protocols. Totowa, N.J: Humana Press, 2006.

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Pierre, Bongrand, ed. Physical basis of cell-cell adhesion. Boca Raton, Fla: CRC Press, 1988.

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J, Nelson W., and Fuchs Elaine, eds. Cell-cell junctions. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2010.

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J, Nelson W., and Fuchs Elaine, eds. Cell-cell junctions. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2010.

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Baudino, Troy A., ed. Cell-Cell Interactions. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7.

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Baluska, Frantisek, Dieter Volkmann, and Peter W. Barlow. Cell-Cell Channels. New York, NY: Springer New York, 2006. http://dx.doi.org/10.1007/978-0-387-46957-7.

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Book chapters on the topic "Cell"

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Prabhu, S. R. "Cell Structure and Function, Cell Division and Cell Cycle, Cell Types and Stem Cells." In Textbook of General Pathology for Dental Students, 15–25. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-31244-1_4.

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van Lent, Jan W. M., and Corinne Schmitt-Keichinger. "Viral Movement Proteins Induce Tubule Formation in Plant and Insect Cells." In Cell-Cell Channels, 160–75. New York, NY: Springer New York, 2006. http://dx.doi.org/10.1007/978-0-387-46957-7_11.

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Garcia, Eduardo, and Vincent Piguet. "Virological Synapse for Cell-Cell Spread of Viruses." In Cell-Cell Channels, 288–97. New York, NY: Springer New York, 2006. http://dx.doi.org/10.1007/978-0-387-46957-7_22.

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van Bel, Aart J. E. "Sieve-Pore Plugging Mechanisms." In Cell-Cell Channels, 113–18. New York, NY: Springer New York, 2006. http://dx.doi.org/10.1007/978-0-387-46957-7_7.

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Jorgensen, Claus, and Alexei Poliakov. "Proteomics Analysis of Contact-Initiated Eph Receptor–Ephrin Signaling." In Cell-Cell Interactions, 1–16. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7_1.

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Moore, Keith, Adam Vandergriff, and Jay D. Potts. "Microencapsulation of Stem Cells to Study Cellular Interactions." In Cell-Cell Interactions, 113–20. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7_10.

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Feinstein, Timothy N. "Cell-Surface Protein–Protein Interaction Analysis with Time-Resolved FRET and Snap-Tag Technologies." In Cell-Cell Interactions, 121–29. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7_11.

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Lee, William T. "Single Cell Analysis of Lipid Rafts." In Cell-Cell Interactions, 131–45. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7_12.

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Zhang, Jian, Wei-hui Guo, Andrew Rape, and Yu-li Wang. "Micropatterning Cell Adhesion on Polyacrylamide Hydrogels." In Cell-Cell Interactions, 147–56. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7_13.

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Cohen, Daniel M., Mike T. Yang, and Christopher S. Chen. "Measuring Cell–Cell Tugging Forces Using Bowtie-Patterned mPADs (Microarray Post Detectors)." In Cell-Cell Interactions, 157–68. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7_14.

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Conference papers on the topic "Cell"

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Hensel, J. Peter, Randall S. Gemmen, Brian J. Hetzer, Jimmy D. Thornton, Jeffrey S. Vipperman, William W. Clark, and A. Fatih Ayhan. "Fuel Cell Performance Improvements Using Cell-to-Cell Flow Distribution Control." In ASME 2004 2nd International Conference on Fuel Cell Science, Engineering and Technology. ASMEDC, 2004. http://dx.doi.org/10.1115/fuelcell2004-2482.

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Balanced flow distribution to each cell in a fuel cell stack plays a significant role in the stack being able to operate at maximum capability and efficiency. This paper discusses the performance improvements in proton exchange membrane fuel cell stacks that can be obtained by using cell-to-cell flow distribution control. In a specially instrumented four-cell stack that employs needle valves to externally control the air and fuel flows to each cell, fuel to a single cell was reduced. The V-I curves collected under these conditions (unbalanced) are compared to curves collected when the fuel flow to each cell was equal (balanced). Reducing the fuel flow to a single cell by 30% decreased the V-I curve cutoff load by 8.5% — demonstrating the negative effect that unbalanced fuel flows can have on stack performance. Typical fuel cell stacks have no dynamic means to keep flows in the stack balanced between the cells, but this work indicates that flow balancing among cells can extend the V-I curve for a fuel cell to higher current values, allowing fuel cell stacks to operate reliably at higher loading and fuel utilizations. Plans to use novel, custom-built micro-valves to dynamically balance flow to individual cells in a fuel cell stack are being pursued as a result of this work, and the status of this development effort is provided.
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BATCHELOR, ERIC, MARICEL G. KANN, TERESA M. PRZYTYCKA, BENJAMIN J. RAPHAEL, and DAMIAN WOJTOWICZ. "MODELING CELL HETEROGENEITY: FROM SINGLE-CELL VARIATIONS TO MIXED CELLS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814447973_0043.

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Burt, A. C., I. B. Celik, R. S. Gemmen, A. V. Smirnov, and W. A. Rogers. "Cell-to-Cell Variations With Increasing SOFC Stack Size." In ASME 2004 2nd International Conference on Fuel Cell Science, Engineering and Technology. ASMEDC, 2004. http://dx.doi.org/10.1115/fuelcell2004-2448.

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This numerical study considers the influence of stack size on cell-to-cell performance variations within a stack of planar solid oxide fuel cells. In order to model large stacks (>10 cells) a pseudo 2-D scheme was implemented using the parallel technique of domain decomposition and was solved on a Beowulf cluster. Results were obtained for stacks of 5, 10, and 20 cells. The results indicate that although significant variations in temperature were observed the voltage variations were practically negligible for cases with uniform flow distribution. Non-uniform fuel flow distribution resulted in more significant cell voltage variations. With the assumption of adiabatic boundary conditions, increasing stack size resulted in slightly lower average cell temperatures but increased outlet temperature of the fuel and air channel in the top cell.
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Terao, Kyohei, Murat Gel, Atsuhito Okonogi, Takaaki Suzuki, Fumikazu Oohira, Masao Washizu, and Hidetoshi Kotera. "Single Cell Stimulation Assay: Microfluidic Substance Delivery to a Laterally Trapped Cell." In ASME-JSME-KSME 2011 Joint Fluids Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/ajk2011-36009.

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We propose a novel cell stimulation device for the analysis of cell responses to chemical stimuli. In order to deliver chemical substances to target single cells, we developed a microfluidic device having microchannels and apertures in the side wall to subject stimuli to laterally trapped cells. The channels were designed to allow simple flow control with single syringe pump. We demonstrated single cell trapping and culturing of pancreatic β cell with the device. To test its feasibility in cell stimulation assay, intracellular response of the cell to glucose stimulation was demonstrated.
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Prudnikov, Igor, Anton Smirnov, and Volodymyr Tsyvkin. "Apoptosomes and proteasomes from exosomes generated by human hematopoietic stem cells." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08924.

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Mat Nayan, Norazirah, Rosfaiizah Siran, Andrean Husin, and Siti Hamimah Sheikh Abd Kadir. "The Effects of Prenatal Bisphenol A exposure on Neural Signaling Activity in Male Rat Hippocampus and its Neurobehavioral Outcomes." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08928.

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Prudnikov, Igor, Anton Smirnov, and Volodymyr Tsyvkin. "The actin cytoskeleton is a key element of the apoptosome assembly in the developing brain." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08923.

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Murray, Taryn, Tyler Wenzel, and Andis Klegeris. "Cardiolipin regulates select functions of astrocytes dysregulated in chronic neuroinflammatory states." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08926.

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Popp, Henning D., Vanessa Kohl, Alice Fabarius, Oliver Drews, Miriam Bierbaum, Ahmed Jawhar, Ali Darwich, et al. "Genotoxic bystander signals from irradiated human mesenchymal stromal cells mainly localize in the 10 – 100 kDa fraction of conditioned medium." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08925.

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Medica, Davide, Vincenzo Cantaluppi, Rossana Franzin, Alessandra Stasi, Giuseppe Castellano, Massimiliano Migliori, Vincenzo Panichi, and Giovanni Camussi. "Extracellular Vesicles derived from Endothelial Progenitor Cells inhibit complement- and cytokine-mediated injury of renal glomerular endothelial cells and podocytes." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08932.

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Reports on the topic "Cell"

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Williams, Thomas. Cell Biology Board Game: Cell Survival (School Version). University of Dundee, 2022. http://dx.doi.org/10.20933/100001270.

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Cells are the smallest units of life. The environment around cells is always changing. Cells need to adapt to survive. This curriculum linked game and lesson plan introduces the world of cells to pupils 8-13. But can they keep their cells alive? This is a guide to how the cell survival resources can be used in a lesson and can be adapted as the teacher sees fit to do so. This lesson is aimed at 8-13 year olds, and fits into an hour long session. The Cell Survival Game has been adapted for both home use and for use in the classroom, and is accompanied by a series of videos. Learning Outcomes – Cells are the smallest unit of life – There are many different types of cells, and some examples of cell types – Cells experience many dangers, and some examples of dangers – How cells notice and defend themselves against dangers Links to the Curriculum – Health and Wellbeing: I am developing my understanding of the human body – Languages: I can find specific information in a straight forward text (book and instructions) to learn new things, I discover new words and phrases (relating to cells) – Mathematics: I am developing a sense of size and amount (by using the dice), I am exploring number processes (addition and subtraction) and understand they represent quantities (steps to finish line), I am learning about measurements (cell sizes) and am exploring patterns (of cell defences against dangers) – Science: I am learning about biodiversity (different types of microbes), body systems, cells and how they work. – Technology: I am learning about new technologies (used to understand how cells work).
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Williams, Thomas. Cell Biology Board Game: Cell Survival (Home Version). University of Dundee, 2022. http://dx.doi.org/10.20933/100001271.

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Williams, Thomas, Caroline Erolin, and Muireann McMahon. Cell Survival: Deluxe Edition. University of Dundee, May 2023. http://dx.doi.org/10.20933/100001283.

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Cells are the smallest units of life. The environment around cells is always changing and cells need to adapt to survive. Can you keep your cell alive in this special edition of Cell Survival? Great for 1 or more people age 3+, lasts around 15 mins per game.
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Williams, Thomas, Caroline Erolin, and Muireann McMahon. Cell Survival Deluxe: School Version. University of Dundee, July 2023. http://dx.doi.org/10.20933/100001284.

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Cells are the smallest units of life. The environment around cells is always changing. Cells need to adapt to survive. This curriculum linked game and lesson plan introduces the world of cells to pupils 8-13. But can they keep their cells alive? This is a guide to how the cell survival resources can be used in a lesson and can be adapted as the teacher sees fit to do so. This lesson is aimed at 8-13 year olds, and fits into an hour long session. This Cell Survival Game has been adapted for use in the classroom and contains new and improved artwork. Accompanying videos and activity sheets complete the learning experience. Learning Outcomes – Cells are the smallest unit of life – There are many different types of cells, and some examples of cell types – Cells experience many dangers, and some examples of dangers – How cells notice and defend themselves against dangers Links to the Curriculum – Health and Wellbeing: I am developing my understanding of the human body – Languages: I can find specific information in a straight forward text (book and instructions) to learn new things, I discover new words and phrases (relating to cells) – Mathematics: I am developing a sense of size and amount (by using the dice), I am exploring number processes (addition and subtraction) and understand they represent quantities (steps to finish line), I am learning about measurements (cell sizes) and am exploring patterns (of cell defences against dangers) – Science: I am learning about biodiversity (different types of microbes), body systems, cells and how they work. – Technology: I am learning about new technologies (used to understand how cells work). Accompanying videos and activity sheets (available at https://dx.doi.org/10.20933/100001270) complete the learning experience.
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Singh, Anjali. Ultimate Guide to Automated Cell Counter: Plus Purchasing Tips. ConductScience, June 2022. http://dx.doi.org/10.55157/cs20220614.

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An automated cell counter is a machine that uses either image analysis or electrical impedance principles to count cells automatically. The electrical impedance principle involves measuring changes in electrical resistance as cells pass through an aperture, while the light-scattering principle observes how cells scatter light when exposed to it. There are four main types of automated cell counting methods: Coulter Counter, Image Analysis Method, Flow Cytometry, and Stereological Cell Counting. Each method has its benefits and limitations, offering faster and more objective cell counting compared to manual methods, but also facing challenges like cost and potential counting inaccuracies. To use an automated cell counter, samples are prepared by pipetting cell suspension onto counting slide chambers, and the machine then provides a total cell count per ml.
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Williams, Thomas. Cell Biology Board Game: Cell Life Cycle Top Trumps. University of Dundee, January 2023. http://dx.doi.org/10.20933/100001277.

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All living things from whole people to single cells and even viruses have life cycles. Explore the weird and wonderful world of life cycles at the level of the cell in this top trumps inspired game. Print and cut out the cards, then play anywhere you want!
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Petitte, James, Hefzibah Eyal-Giladi, and Malka Ginsburg. The Study of Primordial Germ Cell Development as a Tool for Gene Transfer in Chickens. United States Department of Agriculture, October 1991. http://dx.doi.org/10.32747/1991.7561071.bard.

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The ability to introduce novel genetic material into the genome of commercial poultry has been impeded by a lack of kowledge regarding the origin in the early embryo of the target cell of interest, namely, the germ cell. Hence, this project investigated the emergence of primordial germ cells (PGCs) during the early development of the avian embryo to aid in efforts to produce transgenic poultry on a routine basis. The strategy was to introduce foreign DNA into the area of the unincubated embryo that is destined to give rise to the germ line. The objectives of this project were: 1) to identify and localize a subpopulation of cells in the early embryo which will give rise to PGCs, 2) to determine the best location and stage of development to transfer donor cells for efficient germline chimerism, and 3) to transfect donor cells to produce transgenic/germline chimeric embryos. We show that by using the monoclonal antibody SSEA-1 and by various cell culture techniques that germ cells appear to segregate from the somatic lineages at St. X., a process that is gradual and continues through St. XIV. Using microsurgical transplantation between quail and chick embryos, we demonstrated that the inner 1/3 of the area pellucida between states X-XII gives rise to about 2/3 of the germ cell population at the time of their residence in the germinal crescent. Because of the non-localized emergence of PGCs, attempts to introduce foreign DNA into clonal precursors of germ cells through liposome-mediated transfection yielded unacceptable levels of efficiency. However, through our investigation of germ cell origins, an in vitro model of germ cell differentiation was developed that could offer a means of determining the factors required for the long term culture of avian PGCs thereby providing a convenient means of manipulating the avian genome.
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Jones, Jonathan. Cell-Matrix Interactions in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada300395.

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Lopez, C. M., X. Yao, R. Samajdar, and K. Vajaria. Assembling coin cells in half cell format. National Physical Laboratory, April 2024. http://dx.doi.org/10.47120/npl.mgpg153.

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Sopori, Bhushan, and Daniel J. Friedman. Improving Silicon Solar Cell Efficiency Through Advanced Cell Processing, Highly Uniform Texturing, and Thinner Cells. Office of Scientific and Technical Information (OSTI), February 2019. http://dx.doi.org/10.2172/1496856.

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