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Cell proliferation assay – method optimisation for in vivo labeling of DNA in the rat forestomach

REFERENCES 1. Fukushima S, Hirose M, Wanibuchi H: Squamous cell carcinoma forestomach, Rat. In: Digestive System: Monographs on Pathology of Laboratory Animals. Berlin, Germany: Springer-Verlag; 1997, 354-358. 2. Frantz JD, Betton GR, Cartwright ME, Crissman JW, Macklin AW, Maronpot RR: Proliferative lesions of the non-glandular and glandular stomach in rats GI-3. In: Guides for Toxicologic Pathology. Washington DC, USA: STP/ARP/AFIP; 1991, 1-20. 3. Cantoreggi S, Dietrich DR, Lutz WK: Induction of cell proliferation in the forestomach of F344

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Analysis of expression of genes responsible for regulation of cellular proliferation and migration – microarray approach based on porcine oocyte model

happening during oocytes development and improve knowledge about relationships between oocyte and cumulus cells. The aim of the study was to examine the oocyte genes involved in two ontology groups, “regulation of cell migration” and “regulation of cell proliferation” discovered using microarray method. Our results could provide an information about the interactions within COCs and propose new markers for cellular migration and proliferation. Material and Methods Animals A total of 45 pubertal crossbred Landrace gilts bred on a local, commercial farm were used in

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p38 MAPK regulates the expression of ether à go-go potassium channel in human osteosarcoma cells

-induced oxidative stress and glucose uptake inhibition: implication for neurodegeneration. Biochem J 2010; 430: 439-51. 27. Ouadid-Ahidouch H, Le Bourhis X, Roudbaraki M, Toillon RA, Delcourt P, N Prevarskaya. Changes in the K+ current-density of MCF-7 cells during progression through the cell cycle: possible involvement of a h-ether.a-gogo K+ channel. Receptors Channels 2001; 7: 345-56. 28. Asher V, Warren A, Shaw R, Sowter H, Bali A, Khan R. The role of Eag and HERG channels in cell proliferation and apoptotic cell death in SK-OV-3

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Immunohistochemical detection of tumour cell proliferation and intratumoural microvessel density in canine malignant mammary tumours

microvessel density, Chalkley count, and computer image analysis. J Pathol 1995, 177, 275-283. 7. Gasparini G.: Prognostic value of vascular endothelial growth factor in breast cancer. Oncologist 2000, 5, 37-44. 8. Geraldes M., Gartner F., Schmitt F.: Immunohistochemical study of hormonal receptors and cell proliferation in normal canine mammary glands and spontaneous mammary tumours. Vet Rec 2000, 1, 403-406. 9. Goldschmidt M., Pena L., Rasotto R., Zappulli V.: Classification and grading of canine mammary tumours. Vet Pathol

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Comparison of Ethanol and Acetaldehyde Toxicity in Rat Astrocytes in Primary Culture

cell proliferation by ethanol. J Neurochem 1996;67:2236-45. Russo A, Palumbo M, Scifo C, Cardile V, Barcellona mL, Renis M. Ethanol-induced oxidative stress in rat astrocytes: role of hsp70. Cell Biol Toxicol 2001;17:153-68. Muscoli C, Fresta M, Cardile V, Palumbo M, Renis M, Puglisi G, Paolino D, Nisticò, S, Rotiroti D, Mollace V. Ethanol-induced injury in rat primary cortical astrocytes involves oxidative stress: effect of idebenone. Neurosci Lett 2002;329:21-4. Gonthier B

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Cytotoxicity of Polyphenolic/Flavonoid Compounds in a Leukaemia Cell Culture

M, Noble M. N-acetyl-L-cysteine is a pluripotent protector against cell death and enhancer of trohic factor - mediated cell survival in vitro. Proc Natl Acad Sci USA 1994;91:7496-500. Burdon R, Gill V. Cellular generated active oxygen species and HeLa cell proliferation. Free Radical Res Commun 1993;19: 203-213. Richter C, Park JW, Ames BN. Normal oxidative damage to mitochondrial and nuclear DNA is extensive. Proc Natl Acad Sci USA 1988;85:6465-7. Burton RH. Supeoxide and hydrogen

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The Transcription Factor Creb is Involved in Sorafenib-Inhibited Renal Cancer Cell Proliferation, Migration and Invasion

Abstract

Our previous reports showed that the cyclic-AMP-response element-binding protein (CREB) served as a proto-oncogene in the process of tumorigenesis and mediated the growth and metastatic activity of renal cancer cells. Our study, therefore, explored the role of CREB in sorafenib- -inhibited cell proliferation, migration and invasion. Renal cancer cells were cultured in medium containing sorafenib for 12, 24, 48 and 72 h. The MTT assay was used to study the cytotoxic effects of sorafenib. Cell invasion and migration were assayed in wound healing and transwell experiments, respectively. Protein expression levels were evaluated by western blotting. The results show that sorafenib treatment decreased cell viability in a dose- and time-dependent manner. Sorafenib inhibited cell migration and invasion and decreased the expression of MMP-2 and MMP-9. Moreover, addition of the recombinant plasmid pCI-neo/ CREB (PN) reversed the sorafenib-induced inhibition of cell proliferation, migration and invasion. These results show that CREB is associated with the sorafenib-induced inhibition of proliferation, migration and invasion.

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Disturbance of Cell Proliferation in Response to Mobile Phone Frequency Radiation

Disturbance of Cell Proliferation in Response to Mobile Phone Frequency Radiation

The aim of study was to determine the influence of mobile phone frequency radiation on the proliferation, cytoskeleton structure, and mitotic index of V79 cells after 1 h, 2 h, and 3 h of exposure. V79 cells were cultured in standard laboratory conditions and exposed to continuous-wave (CW) RF/MW radiation of 935 MHz, electric field strength of (8.2±0.3) V m-1, and specific absorption rate (SAR) of 0.12 W kg-1. To identify proliferation kinetics, the cells were counted for each hour of exposure 24 h, 48 h, 72 h, and 96 h after respective exposures. Microtubule proteins were determined using specific immunocytochemical methods. Cell smears were analysed under a fluorescent microscope. The study included negative and positive controls. Mitotic index was determined by estimating the number of dividing cells 24 h after exposure and dividing it with the total number of cells. In comparison to the controls, cell proliferation declined in cells exposed for three hours 72 h after irradiation (p<0.05). Microtubule structure was clearly altered immediately after three hours of irradiation (p<0.05). The mitotic index in RF/MW-exposed cells did not differ from negative controls. However, even if exposure did not affect the number of dividing cells, it may have slowed down cell division kinetics as a consequence of microtubule impairment immediately after exposure.

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Suppressive Effect of Fig (Ficus Carica) Latex on Esophageal Cancer Cell Proliferation

. Therapeutic Effects of Fig Tree Latex on Bovine Papillomatosis. J Vet Med B Infect Dis Vet Public Health 2003; 50(10): 473 -6. http://dx.doi.org/10.1046/j.1439-0450.2003.00702.x PMid:14720183 12. Serraclara A, Hawkins F, Perez C, Dominguez E, Campillo JE, Torres MD. Hypoglycemic action of an oral figleaf decoction in type-I diabetic patients. Diabetes Res Clin Pract 1998; 39(1): 19-22. http://dx.doi.org/10.1016/S0168-8227(97)00112-5 13. Rubnov S, Kashman Y, Rabinowitz R, Schlesinger M, Mechoulam R. Suppressors of cancer cell proliferation

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A mathematical model of HIV-1 infection including the saturation effect of healthy cell proliferation

-444. De Boer, R. J. and Perelson, A. S. (1995). Towards a general function describing T-cell proliferation, Journal of Theoretical Biology   175 (4): 567-576. De Leenheer, P. and Smith, H. L. (2003). Virus dynamics: A global analysis, SIAM Journal of Applied Mathematics   63 (4): 1313-1327. Diekmann, O., Heesterbeek, J. A. P. and Metz, J. (1990). On the definition and the computation of the basic reproduction ratio R 0 in models for infectious diseases in heterogeneous populations, Journal of Mathematical Biology

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