Relevant bibliographies by topics / Cellular Proliferation

Academic literature on the topic 'Cellular Proliferation'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Contents

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

Journal articles on the topic "Cellular Proliferation":

1

Yao, Guang. "Modelling mammalian cellular quiescence." Interface Focus 4, no. 3 (June 6, 2014): 20130074. http://dx.doi.org/10.1098/rsfs.2013.0074.

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Cellular quiescence is a reversible non-proliferating state. The reactivation of ‘sleep-like’ quiescent cells (e.g. fibroblasts, lymphocytes and stem cells) into proliferation is crucial for tissue repair and regeneration and a key to the growth, development and health of higher multicellular organisms, such as mammals. Quiescence has been a primarily phenotypic description (i.e. non-permanent cell cycle arrest) and poorly studied. However, contrary to the earlier thinking that quiescence is simply a passive and dormant state lacking proliferating activities, recent studies have revealed that cellular quiescence is actively maintained in the cell and that it corresponds to a collection of heterogeneous states. Recent modelling and experimental work have suggested that an Rb-E2F bistable switch plays a pivotal role in controlling the quiescence–proliferation balance and the heterogeneous quiescent states. Other quiescence regulatory activities may crosstalk with and impinge upon the Rb-E2F bistable switch, forming a gene network that controls the cells’ quiescent states and their dynamic transitions to proliferation in response to noisy environmental signals. Elucidating the dynamic control mechanisms underlying quiescence may lead to novel therapeutic strategies that re-establish normal quiescent states, in a variety of hyper- and hypo-proliferative diseases, including cancer and ageing.
2

Hatchell, D. L., T. McAdoo, S. Sheta, R. T. King, and J. V. Bartolome. "Quantification of Cellular Proliferation in Experimental Proliferative Vitreoretinopathy." Archives of Ophthalmology 106, no. 5 (May 1, 1988): 669–72. http://dx.doi.org/10.1001/archopht.1988.01060130731033.

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Zhang, Jian Chun, Howard E. Savage, Peter G. Sacks, Thomas Delohery, R. R. Alfano, A. Katz, and Stimson P. Schantz. "Innate cellular fluorescence reflects alterations in cellular proliferation." Lasers in Surgery and Medicine 20, no. 3 (1997): 319–31. http://dx.doi.org/10.1002/(sici)1096-9101(1997)20:3<319::aid-lsm11>3.0.co;2-8.

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CLARKE, CHRISTINE L., and ROBERT L. SUTHERLAND. "Progestin Regulation of Cellular Proliferation*." Endocrine Reviews 11, no. 2 (May 1990): 266–301. http://dx.doi.org/10.1210/edrv-11-2-266.

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Lenkala, Divya, Eric R. Gamazon, Bonnie LaCroix, Hae Kyung Im, and R. Stephanie Huang. "MicroRNA biogenesis and cellular proliferation." Translational Research 166, no. 2 (August 2015): 145–51. http://dx.doi.org/10.1016/j.trsl.2015.01.012.

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Mankoff, David A., Anthony F. Shields, and Kenneth A. Krohn. "PET imaging of cellular proliferation." Radiologic Clinics of North America 43, no. 1 (January 2005): 153–67. http://dx.doi.org/10.1016/j.rcl.2004.09.005.

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VINCENT, P. C. "Leukemic Cellular Proliferation: A Perspective." Annals of the New York Academy of Sciences 459, no. 1 Hematopoietic (December 1985): 308–27. http://dx.doi.org/10.1111/j.1749-6632.1985.tb20839.x.

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Zlotorynski, Eitan, and Reuven Agami. "A PASport to Cellular Proliferation." Cell 134, no. 2 (July 2008): 208–10. http://dx.doi.org/10.1016/j.cell.2008.07.003.

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Verdoorn, Cornelis. "Cellular Migration, Proliferation, and Contraction." Archives of Ophthalmology 104, no. 8 (August 1, 1986): 1216. http://dx.doi.org/10.1001/archopht.1986.01050200122064.

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Abrisqueta, Pau, Neus Villamor, Ana Muntañola, Carles Codony, Mireia Camós, Eva Calpe, Maria Joao Baptista, et al. "Biological Analysis and Prognostic Significance of Proliferative Cellular Compartment in Chronic Lymphocytic Leukemia (CLL)." Blood 114, no. 22 (November 20, 2009): 667. http://dx.doi.org/10.1182/blood.v114.22.667.667.

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Abstract Abstract 667 Historically CLL has been considered a non-proliferative disease characterized by accumulation of leukemic cells. However, recent clinical and biological observations are questioning this concept. From the clinical standpoint, although some patients have lymphocyte counts stable during the course of the disease, others exhibit a short lymphocyte doubling time, suggesting the existence of a significant cell proliferation. Some specific anatomic locations (bone marrow (BM) and lymph nodes) seem to be more prone to proliferation than peripheral blood (PB). The amount of cell proliferation and its prognostic significance has not been properly analyzed. Against this background, gene expression profiling of proliferation genes and the amount of cell proliferation in different tissue compartments (BM and PB) were examined in patients with CLL. In isolated CD19/CD5+ tumoral cells from 20 paired PB and BM samples, expression of genes (n=93) involved in the initiation and development of the cell cycle was analyzed by low-density TaqMan® arrays. The amount of proliferative (Ki67 positive) CLL cells was measured by flow cytometry in 50 paired samples. In addition, coexpression of molecules associated with cellular activation (CD38, CD71, CD69), adhesion (CD49d), chemokine receptors (CXCR4, CXCR3, CCR7), interaction between T and B cells (CD86), signaling (ZAP-70), and Toll-like receptors (TLR9) was compared between Ki67+ and Ki67- CLL subpopulations. Finally, the degree of proliferation was correlated with the main clinical and biological characteristics. As assessed by gene expression profile, the great majority of genes involved in the initiation and development of cell cycle were more expressed in BM than in PB. Of note, Ki67+ CLL cells were significantly higher in BM than in PB (mean: 1.13% vs 0.88%; p= 0.004). This difference on Ki67+ expression between BM and PB was particularly significant (mean: 1.6% vs 1.1%; p=0.01) in patients who progressed of their disease at any particularly time (n=20), whereas it was not observed in patients with stable disease. Proliferating (Ki67+) CLL cells had significantly increased expression of ZAP-70 (mean fluorescence intensity (MFI): 162 vs 94, p<0.001), CD38 (MFI: 75 vs 27, p<0.001), CD86 (MFI: 31 vs 11, p=0.002), CD71 (MFI: 73 vs 24, p<0.001), and TLR9 (MFI: 49 vs 25, p<0.001) in comparison to non-proliferating Ki67- cells; CXCR4 was significantly decreased in proliferating cells (MFI: 212 vs 340, p=0.006). No differences were observed in CD49d, CD69, CCR7, and CXCR3 expression between Ki67+ and Ki67- CLL cells. When Ki67 expression was analyzed at diagnosis (n=41 paired samples, median follow-up of 4.2 years), patients with Ki67+ CLL cells ≥ 1% in BM had a shorter time to progression than those with Ki67 <1% (progression at 4 years: 47% vs 12%, respectively; p=0.008) (figure). In addition, patients with lymphocyte doubling time < 12 months, ZAP-70 expression ≥ 20%, or CD38 expression ≥ 30%, but not with increased CD49d expression, exhibit a higher percentage of Ki67+ CLL cells in both BM and PB (Table). In conclusion, in CLL expression of genes related to proliferation was significantly increased in BM compared to PB. Moreover, the number of proliferating CLL cells was also increased in BM, particularly in those patients with an aggressive disease, and presented different immunophenotype characteristics in comparison to non-proliferating CLL cells. Finally, the amount of Ki67+ CLL cells correlated with a shorter time to progression. These results challenge the concept of CLL as disease more accumulative than proliferative. These new insights on the proliferation pathways in CLL not only may provide a better understanding of the pathogenesis of this disease, but also would be of prognostic relevance and can support the use of new treatments aimed at inhibiting proliferation in CLL. Lymphocyte doubling timeZAP-70CD38CD49d<12 months (n=10)>12 months (n=37)≥20% (n=15)<20% (n=35)≥30% (n=19)<30% (n=31)≥30% (n=17)<30% (n=32)Mean% Ki67+ CLL cells in PB1.20.7P=0.021.40.6P<0.0011.10.7P=0.0151.10.8P=0.08Mean% Ki67+ CLL cells in BM1.60.8P=0.03220.8P=0.0011.31P=0.191.50.9P=0.053 Disclosures: No relevant conflicts of interest to declare.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Cellular Proliferation":

1

Gan, Lisha. "Corneal cellular proliferation and wound healing /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4505-5/.

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Kranc, Kamil. "The role of Cited2 in cellular proliferation." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398233.

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Sangfelt, Olle. "Effects of interferon on cellular proliferation and apoptosis /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19981014sang.

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Stacy, Andrew Jared. "Regulation of ΔNp63α by TIP60 promotes cellular proliferation." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1596151919161674.

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Chakravarthy, Usha. "The effect of gamma radiation on intraocular cellular proliferation." Thesis, Queen's University Belfast, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317046.

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Maiti, Baidehi. "E2F and survivin - key players in cellular proliferation and transformation." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1173801044.

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Khav, Eddie. "Visualizing an RB-E2F Cellular Switch that Controls Cell Proliferation." Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/297627.

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Mammalian cell proliferation is regulated by an Rb-E2F gene network. The input node of this network, Cyclin D, receives graded growth signals; the output node, E2F, generates an all-or-none response. That is, the Rb-E2F gene network functions as a cellular switch, converting analog growth signals into digital E2F activities. The On or Off of this Rb-E2F switch determines the On or Off of cell proliferation. To help better understand the analog/digital conversion mechanism, we constructed a reporter cell line to visualize the dynamic expression of Cyclin D and E2F genes by red and green fluorescence in individual cells, respectively.
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Simmons, Ambrosia. "The Role of Polarity Complex Proteins in Neural Progenitor Proliferation." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/552083.

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Biomedical Sciences
Ph.D.
Cortical malformations arise from defects in any stage of brain development and often result in life-long disability ranging from epilepsy to developmental delay and even perinatal lethality. The neuroepithelium of the emergent cortex lays the foundation on which the future cortex will develop, and as such, neuroepithelial tissue and the neural progenitor cells (NPCs) which comprise it are critical to the proper growth and development of the cortex. Here I demonstrate the significance of neuroepithelial cell polarity determinants in cortical development and how they affect both junctional integrity and the regulation of NPC proliferation leading to a variety of cortical malformations. Until now, the role of basal polarity complex protein Lgl1 in cortical development remained elusive due to perinatal lethality in animal models. To bypass this, we developed a novel conditional knockout mouse model of Lgl1 in the neuroepithelium and show that Lgl1 is essential to the maintenance of neuroepithelial integrity and regulation of NPC proliferation. Loss of Lgl1 results in a displaced ventricular zone with widespread ectopic proliferation resulting in severe periventricular nodular heterotopia (PNH). Furthermore, Lgl1 loss reduces the cell cycle length resulting in hyperproliferation leading to neuronal overproduction. Together, this work identifies a novel genetic cause of PNH. Next, I aimed to characterize the interaction of Lgl1 with other polarity proteins and downstream signaling pathways in cortical development. Apical and basal polarity proteins have demonstrated mutual antagonism in the establishment/maintenance of epithelial polarity; however, little is known about the role of this antagonism on cortical size and structure or the signaling pathways through which it acts. To address these questions we generated multiple genetic mouse models to investigate the opposing roles of basal protein, Lgl1, and either apical proteins Pals1 or Crb2. Concurrent loss of Pals1 and Lgl1 was able to prevent heterotopic nodules and increase proliferation compared to loss of Pals1 alone. However, cortical size was severely diminished due to overriding effects of Pals1 on cell survival that was unmitigated by Lgl1 loss. Remarkably, loss of both Crb2 and Lgl1 restored the cortex and hippocampus to near normal morphology with a profound rescue of cortical size, suggesting their essential antagonism in both cortical and hippocampal development. Importantly, genetic manipulation through reduction of YAP/TAZ expression in the Lgl1 CKO eliminates periventricular nodules and restores cortical thickness to that of WT cortices. This important finding implicates Lgl1 in the regulation of YAP/TAZ in cortical development. Finally, we investigated a possible downstream target of Pals1 in cell survival, BubR1. My work demonstrates that loss of Pals1 reduces BubR1 expression, which is an essential regulator of the mitotic checkpoint and causative gene of the human disorder Mosaic Variegated Aneuploidy. I show that loss of BubR1 results in significant apoptosis across all cell types in the cortex leading to microcephaly. These data provide the first link between cell polarity determinants and mitotic regulation in the cortex and suggests that BubR1 reduction likely contributes to the decreased cell survival following Pals1 loss. Overall these findings implicate impaired polarity complex function in a wide variety of NPC defects resulting in multiple cortical malformations. My work shows that polarity proteins regulate every stage of the NPCs life cycle from cell division and proliferation to cell survival through regulation of mitosis and YAP/TAZ signaling.
Temple University--Theses
9

Reed, Jennifer. "Interferon-gamma increases CD4+ T cell survival and proliferation." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432655.

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Anderson, Elizabeth. "Co-ordinate regulation of cellular proliferation and apoptosis in rodent liver." Thesis, University of Surrey, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441719.

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Books on the topic "Cellular Proliferation":

1

Guest, Simon Sean. Strathmin is an intracellular regulator of cellular proliferation. Birmingham: University of Birmingham, 1996.

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Renato, Baserga, ed. Biological regulation of cell proliferation. New York: Raven Press, 1986.

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Jones, Neil Austin. The role of a major cytosolic protein in cellular proliferation. Birmingham: University of Birmingham, 1992.

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L, Boynton Alton, and Leffert H. L, eds. Control of animal cell proliferation. Orlando: Academic Press, 1985.

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M, Veneziale Carlo, ed. Control of cell growth and proliferation. New York, N.Y: Van Nostrand Reinhold, 1985.

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riazi, Sheila. Pathophysiological links between impaired elastogenesis and increased cellular proliferation in development of cardiovascular disorders. Ottawa: National Library of Canada, 2002.

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Burton, Jean. A study of cellular proliferation rates in squamous cell carcinomas of the lung, with relation to p53 status. [S.l: The Author], 1994.

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Meridith, Alan T. Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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International Conference on Gene Regulation, Oncogenesis, and AIDS (1st 1989 Loutráki, Greece). Oncogenesis: Oncogenes in signal transduction and cell proliferation : papers delivered at the First International Conference on Gene Regulation, Oncogenesis, and AIDS, Loutraki, Greece, September 15-21, 1989. Edited by Papas Takis S. Woodlands, Tex: Portfolio Pub. Co., 1990.

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Wei, Dai, ed. Checkpoint responses in cancer therapy. Totowa, NJ: Humana Press, 2008.

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Book chapters on the topic "Cellular Proliferation":

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Brockhoff, Gero. "DNA and Proliferation Analysis by Flow Cytometry." In Cellular Diagnostics, 390–425. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000209173.

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Matatall, Katie A., Claudine S. Kadmon, and Katherine Y. King. "Detecting Hematopoietic Stem Cell Proliferation Using BrdU Incorporation." In Cellular Quiescence, 91–103. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_7.

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Jalbert, Emilie, and Eric M. Pietras. "Analysis of Murine Hematopoietic Stem Cell Proliferation During Inflammation." In Cellular Quiescence, 183–200. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_14.

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Mierke, Claudia Tanja. "Cell Proliferation, Survival, Necrosis and Apoptosis." In Cellular Mechanics and Biophysics, 743–824. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58532-7_16.

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Dover, R. "Basic Methods for Assessing Cellular Proliferation." In Assessment of Cell Proliferation in Clinical Practice, 63–81. Tokyo: Springer Japan, 1992. http://dx.doi.org/10.1007/978-4-431-68287-5_4.

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Dover, R. "Basic Methods for Assessing Cellular Proliferation." In Assessment of Cell Proliferation in Clinical Practice, 63–81. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3190-8_4.

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Horan, Paul Karl, Sue E. Slezak, and Bruce D. Jensen. "Cellular Proliferation History by Fluorescent Analysis." In Flow Cytometry, 133–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84616-8_8.

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Guerrieri, Ferruccio. "The F0F1-ATP Synthase in Cell Proliferation and Aging." In Frontiers of Cellular Bioenergetics, 677–92. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_27.

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Herbig, A. Katherine, Sameh Girgis, and Patrick J. Stover. "Effects of Cellular Glycine on Cell Proliferation." In Chemistry and Biology of Pteridines and Folates, 491–94. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0945-5_83.

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Macieira-Coelho, Alvaro. "Slowing Down of the Cell Cycle During Fibroblast Proliferation." In Cellular Ageing and Replicative Senescence, 29–47. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26239-0_3.

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Conference papers on the topic "Cellular Proliferation":

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Qian, Xu, He Hujun, Yang Guangtao, and Yang Xu. "Effect of Formaldehyde on Cellular Proliferation of HEK293 Cells." In 2007 1st International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/icbbe.2007.122.

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Dho, So Hee, Ji Young Kim, Chang-Jin Kim, William M. Nauseef, So-Young Choi, Kwang-Pyo Lee, and Ki-Sun Kwon. "Abstract 2916: NOXX: Friend or foe for cellular proliferation." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2916.

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Blahna, Matthew T., Matthew R. Jones, Lee J. Quinton, and Joseph P. Mizgerd. "Zcchc11 Enhances Cellular Proliferation Independent Of Its Uridyltransferase Activity." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2124.

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"The Effect of Hydroalcoholic Extract of Junipers communis on Proliferation BHK Cells." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916411.

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Savage, Howard E., Venkateswara Kolli, Jian C. Zhang, Robert R. Alfano, Peter G. Sacks, and Stimson P. Schantz. "Tissue autofluorescence spectroscopy: in-vivo alterations may reflect cellular proliferation." In OE/LASE '94, edited by Robert R. Alfano. SPIE, 1994. http://dx.doi.org/10.1117/12.175991.

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Chung, Eunna, and M. N. Rylander. "Thermal Preconditioning Protocols for Cartilage Tissue Engineering." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193107.

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Successful creation of cartilaginous engineered tissues is often limited by insufficient cellular proliferation and formation of extracellular matrix. Stress conditioning protocols using heat have been shown to induce up-regulation of molecular chaperones called heat shock proteins (HSP) [1]. These proteins have been linked to enhanced cell proliferation and collagen synthesis which is critical for formation of the extracellular matrix. Therefore, identification of effective thermal stress preconditioning protocols that enhance HSP expression could substantially advance development of replacement tissues for cartilaginous tissues [2]. Our project focused on identifying thermal preconditioning protocols that enhance HSP70 expression while minimizing cellular injury for ultimate use in improving cell proliferation and extracellular matrix formation for cartilage.
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Solarte, Efrain, Hernan Urrea, William Criollo, and Oscar Gutierrez. "LED illumination effects on proliferation and survival of meningioma cellular cultures." In BiOS, edited by Valery V. Tuchin, Donald D. Duncan, and Kirill V. Larin. SPIE, 2010. http://dx.doi.org/10.1117/12.843060.

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Blahna, Matthew T., Matthew R. Jones, Lee J. Quinton, and Joseph P. Mizgerd. "The Uridyl-Transferase Enzyme Zcchc11 Prevents Senescence And Promotes Cellular Proliferation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4926.

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Shi, Caleb, Robert Chang, and Donna Leonardi. "The Effects of Mechanical Vibration on Cellular Health in Differentiated Neuroblastoma Cells." In ASME 2018 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/detc2018-86280.

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The effects of mechanical impact forces on neurological health is a critical concern, likely due to issues of traumatic brain injury (TBI) in sports and brain damage stemming from the potential of “sonic terrorism.” The quantitative analysis and evaluation of such forces on brain tissue function is very difficult. To address this issue, this research proposes a novel approach of using a cellular model subjected to mechanical vibration for analysis. Here, neuron-like differentiated neuroblastoma cells were subjected to vibration at frequencies of 20, 200, 2000, and 20000 Hz for a period of 24 hours at constant amplitude. Cell proliferation and inflammatory cytokine production, including IL-6, IL-1β, and TGF-β1, was measured as response of the cells and indicators of cellular health after vibrational treatment. Cell proliferation was found to increase after 20, 200, and 20000 Hz treatments; p<0.05) and decrease after 2000 Hz treatment (p<0.05). IL-6 production was found to decrease after 200 and 20000 Hz treatments (p<0.01) and increase after 20 and 2000 Hz treatments (p<0.01). IL-1β protein production was found to decrease after 20 Hz and increase after 200 Hz treatments (p<0.001), while TGF-β1 was found to decrease after 200 Hz treatment (p<0.001). The results suggest that cell proliferation and cytokine production serve as a sensitive measure to external impact forces applied to the cells. In addition, it is suggested that inflammatory mechanisms exhibit inhibitory “cross-talk” between IL-6 and IL-1β signaling pathways at 20 and 200 Hz. Inflammatory cytokine data suggest frequency-specific responses, which can be used not only to better understand the mechanism of vibration induced cellular damage, but also to unveil the cellular signaling processes.
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Neish, Andrew Scott. "Abstract PL01-02: Influence of the microbiota on cellular proliferation and survival." In Abstracts: Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; September 27 - October 1, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1940-6215.prev-14-pl01-02.

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Reports on the topic "Cellular Proliferation":

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Sun, Lina, Yanan Han, Hua Wang, Huanyu Liu, Shan Liu, Hongbin Yang, Xiaoxia Ren, and Ying Fang. MicroRNAs as Potential Biomarkers for the Diagnosis of Inflammatory Bowel Disease: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0027.

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Review question / Objective: The purpose of this systematic review was to systematically review the clinical studies regarding miRNAs as diagnostic biomarkers for inflammatory bowel disease and assess the overall diagnostic accuracy of miRNAs. Condition being studied: The symptoms of inflammatory bowel disease (IBD) are highly variable. The diagnosis of IBD must be made through medical history, physical, laboratory, radiologic, endoscopic, and histological examinations. However, these diagnostic techniques are not specific and sometimes even equivocal. Therefore, reliable biomarkers are urgently needed in the diagnosis of IBD. Several clinical and preclinical researches have shown that dysregulated microRNAs (miRNAs) play a crucial role in IBD development. miRNAs, as single-stranded noncoding RNAs that contain 22-24 nucleotides, can post-transcriptionally regulate gene expression by blocking mRNA translation or degrading target mRNAs. miRNAs are widely involved in physiological and pathological cellular processes, such as differentiation, proliferation and apoptosis. Besides, they are stable, noninvasive, and resistant to degradation by ribonucleases, making them valuable targets in the diagnosis, monitoring, prognosis, and treatment of diseases. To date, inconsistent results have been found about miRNA expression profiling in the patients with IBD. Moreover, the diagnostic accuracy of miRNAs for IBD has not been reported in any meta-analysis.
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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
3

Zhou, Ting, Roni Shapira, Peter Pauls, Nachman Paster, and Mark Pines. Biological Detoxification of the Mycotoxin Deoxynivalenol (DON) to Improve Safety of Animal Feed and Food. United States Department of Agriculture, July 2010. http://dx.doi.org/10.32747/2010.7613885.bard.

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The trichothecene deoxynivalenol (DON, vomitoxin), one of the most common mycotoxin contaminants of grains, is produced by members of the Fusarium genus. DON poses a health risk to consumers and impairs livestock performance because it causes feed refusal, nausea, vomiting, diarrhea, hemolytic effects and cellular injury. The occurrence of trichothecenes contamination is global and they are very resistant to physical or chemical detoxification techniques. Trichothecenes are absorbed in the small intestine into the blood stream. The overall objective of this project was to develop a protecting system using probiotic bacteria that will express trichothecene 3-O-acetyltransferase (Tri101) that convert T-2 to a less toxic intermediate to reduce ingested levels in-situ. The major obstacle that we had faced during the project is the absence of stable and efficient expression vectors in probiotics. Most of the project period was invested to screen and isolate strong promoter to express high amounts of the detoxify enzyme on one hand and to stabilize the expression vector on the other hand. In order to estimate the detoxification capacity of the isolated promoters we had developed two very sensitive bioassays.The first system was based on Saccharomyces cerevisiae cells expressing the green fluorescent protein (GFP). Human liver cells proliferation was used as the second bioassay system.Using both systems we were able to prove actual detoxification on living cells by probiotic bacteria expressing Tri101. The first step was the isolation of already discovered strong promoters from lactic acid bacteria, cloning them downstream the Tri101 gene and transformed vectors to E. coli, a lactic acid bacteria strain Lactococcuslactis MG1363, and a probiotic strain of Lactobacillus casei. All plasmid constructs transformed to L. casei were unstable. The promoter designated lacA found to be the most efficient in reducing T-2 from the growth media of E. coli and L. lactis. A prompter library was generated from L. casei in order to isolate authentic probiotic promoters. Seven promoters were isolated, cloned downstream Tri101, transformed to bacteria and their detoxification capability was compared. One of those prompters, designated P201 showed a relatively high efficiency in detoxification. Sequence analysis of the promoter region of P201 and another promoter, P41, revealed the consensus region recognized by the sigma factor. We further attempted to isolate an inducible, strong promoter by comparing the protein profiles of L. casei grown in the presence of 0.3% bile salt (mimicking intestine conditions). Six spots that were consistently overexpressed in the presence of bile salts were isolated and identified. Their promoter reigns are now under investigation and characterization.

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