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Relevant bibliographies by topics / Marophase Colony Stimulating Factors

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Academic literature on the topic 'Marophase Colony Stimulating Factors'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "Marophase Colony Stimulating Factors"

1

&NA;. "Granulocyte colony-stimulating factors/granulocyte-macrophage colony-stimulating factors." Reactions Weekly &NA;, no. 1166 (August 2007): 13. http://dx.doi.org/10.2165/00128415-200711660-00041.

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&NA;. "Granulocyte colony-stimulating factors/granulocyte-macrophage colony-stimulating factors." Reactions Weekly &NA;, no. 523 (October 1994): 7. http://dx.doi.org/10.2165/00128415-199405230-00027.

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Fox, R. M. "Colony-Stimulating Factors." PharmacoEconomics 6, Supplement 2 (1994): 1–8. http://dx.doi.org/10.2165/00019053-199400062-00003.

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Gordon, Michael S., and Janice L. Gabrilove. "Colony-stimulating factors." Current Opinion in ONCOLOGY 2, no. 6 (December 1990): 1152–58. http://dx.doi.org/10.1097/00001622-199012000-00021.

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&NA;. "Colony-stimulating factors." Reactions Weekly &NA;, no. 532 (December 1994): 7. http://dx.doi.org/10.2165/00128415-199405320-00022.

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Field, Max. "Colony-Stimulating Factors." Clinical Immunotherapeutics 3, no. 4 (April 1995): 255–61. http://dx.doi.org/10.1007/bf03259277.

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Hamblin, Professor T. J. "Colony-stimulating factors." Leukemia Research 15, no. 4 (January 1991): 279. http://dx.doi.org/10.1016/0145-2126(91)90134-f.

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McGuire, William L., Janice Gabrilove, Malcolm A. S. Moore, and John Rinehart. "Colony-stimulating factors." Breast Cancer Research and Treatment 14, no. 2 (November 1989): 193–200. http://dx.doi.org/10.1007/bf01810735.

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Metcalf, Donald. "Colony-stimulating factors." Cell 61, no. 5 (June 1990): 756–57. http://dx.doi.org/10.1016/0092-8674(90)90184-g.

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Wakefield, Philip E., William D. James, Curt P. Samlaska, and Monte S. Meltzer. "Colony-stimulating factors." Journal of the American Academy of Dermatology 23, no. 5 (November 1990): 903–12. http://dx.doi.org/10.1016/0190-9622(90)70313-7.

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Dissertations / Theses on the topic "Marophase Colony Stimulating Factors"

1

Mohamad, Anuar Nur Najmi. "Regulation of vascular cells function by colony stimulating factors." Thesis, University of Bristol, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.702911.

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Ku, Chun-Ying. "Colony-Stimulating Factor from Umbilical Cord Endothelial Cells." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc935638/.

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Conditioned media prepared from umbilical cord (UC) segments or endothelial cells (EC) contain colony stimulating activity, Both UCCM and ECCM were partially purified by DEAE-Sepharose and ACA44 gel filtration chromatography. The molecular weights were estimated as 25,000 and 31,000 for UC-CSF and EC-CSF, respectively. UC-CSF was further fractionated by Con A Sepharose, IEF and HPLC on a hydrophobic phenyl column. The highly purified CSF stimulates human macrophage and granulocyte colony formation, indicating it is GM-CSF in nature. Characterization studies have revealed that both CSFs are heat stable at 60°C for 30 min. They are sensitive to digestion by protease and to periodate oxidation but are stable to treatment with sulfhydryl reagents. The synthesis of CSF in endothelial cells is inhibited by actinomycin D, cycloheximide and puromycin, indicating that protein and RNA synthesis are required for CSF production. Among the mitogens tested, only LPS exhibited stimulatory activity on the production of CSF. Metabolic modulators such as dibutyryl cAMP, isobutylmethylxanthine, PGE2 and lactoferrin inhibit CSF production, while PGF2 enhances CSF production.

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Ku, Chun-Ying. "Regulation of Colony-Stimulating Factor-1 Biosynthesis." Thesis, University of North Texas, 1990. https://digital.library.unt.edu/ark:/67531/metadc332103/.

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Recent studies suggest that synthesis of the Colony-stimulating factor (CSF) is a well regulated process. However, the molecular mechanisms of the signal transduction of the various inducers of CSF such as monokines and lymphokines are not well understood. Using Interleukin 1 (IL-1) stimulation of CSF-1 in the MIA PaCa-2 cell line as a model system, the involvement of G-protein has been studied. The IL-1 induction of CSF-1 synthesis can be inhibited by both Pertussis toxin and Cholera toxin, which are known to modify the Gᵢ and Gₛ proteins respectively, thus activating adenylate cyclase to release more cAMP. The toxin inactivation can be prevented by inhibitors of the ADP-ribosylation such as, benzamide and MBAMG. Addition of dibutyryl-cAMP inhibits the IL-1 induced CSF production. Both Theophylline and Forskolin which increase cAMP by inhibiting phosphodiesterase and stimulating adenylate cyclase respectively, also inhibit CSF-1 production. Results from these studies have shown that cAMP level inversely regulates the biosynthesis of CSF-1. Preincubation of MIA PaCa-2 cells with IL-1 and 5'- guanylylimidodiphosphate (GppNHp) prevents the inhibitory effect of pertussis toxin on CSF-1 production. These data are consistent with the hypothesis that IL-1 binds to its receptor and couples to Gᵢ∝ resulting in the inhibition of adenylate cyclase and reducing cAMP level. Lowering of the' cAMP level leads to the activation of CSF-1 gene expression. The activity of another inducer of CSF-1 production in this system, 12-0-tetradecanoylphorbol-13-acetate (TPA), can be abolished by 1- (5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), which is a specific inhibitor of protein kinase C. However, H-7 failed to inhibit IL-1 stimulated CSF-1 production. Other known activators of protein kinase C namely, Ca²⁺ and L-α-l-oleoyl-2-acetoyl-sn- 3-glycerol (OAG), also increase CSF production. On the other hand, Indomethacin which is known to inhibit prostaglandin E (PGE), stimulates CSF-1 production in MIA PaCa-2 cells. These data suggest that different mechanisms for stimulation of CSF-1 synthesis exist in MIA PaCa-2 cells depending on the inducer. The IL-1 stimulated pathway which does not require PKC activity and appears to be associated with adenylyl cyclase regulation whereas phorbol ester induced pathway involves protein kinase C in the signaling process as expected.

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Liu, Mu-ya. "Induced CSF-1 Production and its Effects on C-FMS Transfected Monoblastic U937 Cells." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc798317/.

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This study examined how the monoblast-like human histiocytic lymphoma cell line U937 can be induced by phorbol 12-myristrate 13-acetate (PMA) to undergo differentiation. In order to study the mechanism of action of CSF-1, a CSF-1 receptor gene (c-fms) was transfected into U937 cells. Exogenous CSF-1 treatment induced an autocrine response in this CSF-1 was determined and all events were shown to be time dependent. CSF-1 stimulation also enhanced proto-oncogene c-jun and c-myc gene expression. Complementary DNA coding for Jun or Fos was introduced into U937 cells by transfection. The transfection did not generate a high level of CSF-1 gene expression which suggests that Fos and Jun alone are insufficient to induce CSF-1 synthesis.

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Tazi, Abdellatif. "Les colony-stimulating factors dans les réponses immunitaires et inflammatoires pulmonaires." Paris 5, 1993. http://www.theses.fr/1993PA05CD02.

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Hormis leurs actions sur les cellules hématopoïétiques médullaires, les colony-stimulating factors (C S F) jouent un rôle important dans les réponses immunitaires et inflammatoires. Dans ce travail, nous avons étudié la production du granulocyte-C S F (G-CSF) et du granulocyte-macrophage-CSF (GM-CSF) par les cellules inflammatoires/immunitaires et parenchymateuses pulmonaires, dans des situations physiologiques et pathologiques. Après avoir mis au point une méthode de dosage biologique spécifique du G-CSF, nous avons montré que les macrophages alvéolaires humains normaux produisent des quantités importantes de ce facteur en réponse à l'endotoxine in vitro. De plus, les cellules alvéolaires recueillies par lavage, provenant de sujets ayant une pneumopathie bactérienne secrètent spontanément du G-CSF en quantité notable, vraisemblablement du fait de leur exposition à l'endotoxine in vivo. Ces données suggèrent que ce facteur joue un rôle dans la régulation du nombre et de la fonction des polynucléaires neutrophiles dans le poumon au cours de processus infectieux. D'autre part, nous avons exploré le rôle du GM-CSF dans la distribution et l'état de différenciation de cellules essentielles à l'initiation des réponses immunitaires : les cellules dendritiques (CD) et les cellules de Langerhans (CL). A l'aide de techniques d'immunohistochimie et d'hybridation in situ, nous avons montré que le GM-CSF est produit par l'épithélium bronchiolaire normal, qui représente le seul site où l'on retrouve des CL. Dans les situations pathologiques qui s'accompagnent de l'accumulation d'un nombre important de CL dans le poumon (hyperplasie épithéliale alvéolaire, cancers bronchopulmonaires et histiocytose X pulmonaire), nous avons retrouvé une corrélation étroite entre la production de GM-CSF au sein de ces lésions et la présence ainsi que le nombre de CL infiltrant ces sites. L'ensemble de ces résultats suggère fortement que la synthèse locale de GM-CSF par certaines cellules pulmonaires normales ou pathologiques joue un rôle important dans la distribution et la différenciation des CD/CL dans le poumon humain.

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Hercus, Timothy Robert. "Structure-junction studies on human granulocyte-macrophage colony-stimulating factor /." Title page, table of contents and summary only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phh539.pdf.

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Shieh, Jae-Hung. "Purification, Characterization and Receptor Binding of Human Colony-Stimulating Factor-1." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc331991/.

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Human colony-stimulating factor-1 (CSF-1) was purified from the serum-free conditioned medium of a human pancreatic carcinoma cell line. The four-step procedure included chromatography on DEAE Sepharose, Con A Sepharose and HPLC on phenyl column and reverse-phase C-3 column. The purity of human CSF-1 was demonstrated by sodium dodecyl sulfatepolyacrylamide gel electrophoresis (SDS—PAGE) as a single diffuse band with a molecular weight (Mr) of 42,000-50,000 and was further confirmed by a single amino-terminal amino acid residue of glutamate. Under reducing conditions, purified CSF-1 appeared on SDS-PAGE as a single protein band with a Mr of 21,000-25,000 and concurrently lost its biological activity, indicating that human CSF-1 consists of two similar subunits and that the intact quaternary structure is essential for biological activity. When treated with neuraminidase and endo-8~D~N—acetylglucosaminidase D, the Mr of CSF-1 was reduced to 36,000-40,000 and to a Mr of 18,000-20,000 in the presence of mercaptoethanol.

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8

Towers, Terri L. "Vitamin D3-mediated transcriptional repression : of the granulocyte-macrophage colony stimulating factor gene /." Access full-text from WCMC, 1998. http://proquest.umi.com/pqdweb?did=733066141&sid=3&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Olivares, Fontt Elizabeth. "Rôle du granolocyte-macrophage colony-stimulating factors lors de l'infection expérimentale à Trypanosoma cruzi." Doctoral thesis, Universite Libre de Bruxelles, 1995. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212546.

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Elliott, Michael J. H. "The interactions of interleukin-3 and granulocyte-macrophage colony-stimulating factor with human monocytes /." Title page, table of contents and abstract only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09phe464.pdf.

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Books on the topic "Marophase Colony Stimulating Factors"

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K�rholz, Dieter, and Wieland Kiess. Cytokines and Colony Stimulating Factors. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593453.

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1945-, Dexter T. Michael, Garland John M. 1942-, and Testa Nydia G. 1938-, eds. Colony-stimulating factors: Molecular and cellular biology. New York: M. Dekker, 1990.

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1942-, Garland John M., Quesenberry Peter J, and Hilton Douglas J. 1964-, eds. Colony-stimulating factors: Molecular and cellular biology. 2nd ed. New York: M. Dekker, 1997.

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1950-, Nicola Nicos, ed. The hemopoietic colony-stimulating factors: From biology to clinical applications. Cambridge: Cambridge University Press, 1995.

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Dieter, Körholz, and Kiess W, eds. Cytokines and colony stimulating factors: Methods and protocols. Totowa, N.J: Humana Press, 2003.

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The molecular control of blood cells. Cambridge, Mass: Harvard University Press, 1988.

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Imperial Cancer Research Fund (Great Britain). Haemopoietic growth factors: Their role in the treatment of cancer. Edited by Dexter T. Michael 1945-. Oxford, U.K: Published for the Imperial Cancer Research Fund by Oxford University Press, 1990.

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Summon up the blood: In dogged pursuit of the blood cell regulators. Miamisburg, Ohio: AlphaMed Press, 2001.

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A, Buskard Noel, and Maroun Jean A, eds. Colony-stimulating factors in clinical practice: Proceedings of a joint Symposium of the Canadian Association of Medical Oncologists and the Canadian Hematology Society,in Association with the Royal College of Physicians and Surgeons of Canada, sponsored by an educational grant from Sandoz Canada Inc. and Schering Canada Inc., held in Quebec city, 21 September, 1991. London: Royal Society of Medicine Services, 1992.

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Roland, Mertelsmann, and Herrmann Friedhelm 1949-, eds. Hematopoietic growth factors in clinical applications. New York: Dekker, 1990.

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Book chapters on the topic "Marophase Colony Stimulating Factors"

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Shankar, Ananth. "Colony-stimulating factors." In Evidence-Based Pediatric Oncology, 207–29. Oxford: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118625309.ch24.

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Baccarini, M., and E. R. Stanley. "Colony Stimulating Factor-1." In Growth Factors, Differentiation Factors, and Cytokines, 188–200. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74856-1_14.

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Welte, K., and E. Platzer. "Granulocyte Colony-Stimulating Factor." In Growth Factors, Differentiation Factors, and Cytokines, 201–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74856-1_15.

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Molineux, Graham. "Granulocyte Colony-Stimulating Factors." In Hematopoietic Growth Factors in Oncology, 33–53. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7073-2_3.

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Sherr, C. J., and E. R. Stanley. "Colony-Stimulating Factor 1 (Macrophage Colony-Stimulating-Factor)." In Peptide Growth Factors and Their Receptors I, 667–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-49295-2_15.

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Sherr, C. J., and E. R. Stanley. "Colony-Stimulating Factor 1 (Macrophage Colony-Stimulating-Factor)." In Peptide Growth Factors and Their Receptors I, 667–98. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3210-0_15.

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Molineux, Graham. "Granulocyte Colony-Stimulating Factor." In Hematopoietic Growth Factors in Oncology, 83–95. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_5.

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Nagata, S. "Granulocyte Colony-Stimulating Factor." In Peptide Growth Factors and Their Receptors I, 699–722. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-49295-2_16.

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Nagata, S. "Granulocyte Colony-Stimulating Factor." In Peptide Growth Factors and Their Receptors I, 699–722. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3210-0_16.

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Bonilla, Mary Ann, and Ann Jakubowski. "Colony-Stimulating Factors in Leukopoiesis." In Humoral Factors in the Regulation of Tissue Growth, 71–93. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9272-9_4.

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Conference papers on the topic "Marophase Colony Stimulating Factors"

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Tilman, Jessica, Peter Barnes, and Louise Donnelly. "Colony stimulating factors cannot correct defective phagocytosis in COPD lung tissue macrophages." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3974.

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Younis, T., D. Rayson, and C. Skedgel. "Abstract P6-07-07: Febrile neutropenia primary prophylaxis with granulocyte-colony stimulating factors (G-CSF) in breast cancer." In Abstracts: Thirty-Sixth Annual CTRC-AACR San Antonio Breast Cancer Symposium - Dec 10-14, 2013; San Antonio, TX. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/0008-5472.sabcs13-p6-07-07.

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Ben Abdallah, SS, N. Letarte, C. Messier, D. Charpentier, L. Yelle, R. Younan, and A. Bestawros. "Abstract P3-15-09: Impact of granulocyte colony-stimulating factors on febrile neutropenia risk during early-stage breast cancer treatment." In Abstracts: Thirty-Sixth Annual CTRC-AACR San Antonio Breast Cancer Symposium - Dec 10-14, 2013; San Antonio, TX. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/0008-5472.sabcs13-p3-15-09.

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Zhao, Jingyi, Yingjian He, Zhaoqing Fan, Jinfeng Li, Xinguang Wang, Yang Yang, Xue Chen, and Tao Ouyang. "Abstract P3-11-22: Efficacy of two kinds of granulocyte colony-stimulating factors to support neoadjuvant dose-dense chemotherapy in primary breast cancer." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p3-11-22.

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Moran, Kellyn M., Zhaoju Wu, Sruthi Adimadhyam, Todd A. Lee, Brian C. Chiu, and Gregory S. Calip. "Abstract 4225: Myelodysplastic syndrome and acute myeloid leukemia following use of chemo-immunotherapy and granulocyte colony-stimulating factors among elderly non-Hodgkin lymphoma patients." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4225.

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Krendyukov, A., E. Botteri, and G. Curigliano. "Abstract P3-14-05: Safety of granulocyte colony-stimulating factors and their biosimilars: A meta-analysis of randomized clinical trials in breast cancer patients receiving cytotoxic chemotherapy." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p3-14-05.

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Adeboyeje, G., A. Agiro, A. Goodwin, A. DeVries, and J. Malin. "Abstract P5-08-06: Impact of a decision-support tool on the utilization of colony-stimulating factors and incidence of febrile neutropenia among patients with breast cancer." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p5-08-06.

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Reports on the topic "Marophase Colony Stimulating Factors"

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Hansen, Peter J., and Zvi Roth. Use of Oocyte and Embryo Survival Factors to Enhance Fertility of Heat-stressed Dairy Cattle. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697105.bard.

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The overall goal was to identify survival factors that can improve pregnancy success following insemination or embryo transfer in lactating dairy cows exposed to heat stress. First, we demonstrated that oocytes are actually damaged by elevated temperature in the summer. Then we tested two thermoprotective molecules for their effect on oocyte damage caused by heat shock. One molecule, ceramide was not thermoprptective. Another, insulin-like growth factor-1 (IGF) reduced the effects of heat shock on oocyte apoptosis and oocyte cleavage when added during maturation. We also used lactating cows exposed to heat stress to determine whether bovine somatotropin (bST), which increases IGF1 levels in vivo, would improve fertility in summer. Cows treated with bST received a single injection at 3 days before insemination. Controls received no additional treatment. Treatment with bST did not significantly increase the proportion of inseminated cows diagnosed pregnant although it was numerically greater for the bST group (24.2% vs 17.8%, 124–132 cows per group). There was a tendency (p =0.10) for a smaller percent of control cows to have high plasma progesterone concentrations (≥ 1 ng/ml) at Day 7 after insemination than for bST-treated cows (72.6 vs 81.1%). When only cows that were successfully synchronized were considered, the magnitude of the absolute difference in the percentage of inseminated cows that were diagnosed pregnant between bST and control cows was reduced (24.8 vs 22.4% pregnant for bST and control). Results failed to indicate a beneficial effect of bST treatment on fertility of lactating dairy cows. In another experiment, we found a tendency for addition of IGF1 to embryo culture medium to improve embryonic survival after embryo transfer when the experiment was done during heat stress but not when the experiment was done in the absence of heat stress. Another molecule tested, granulocyte-macrophage colony-stimulating factor (GM-CSF; also called colony-stimulating factor-2), improved embryonic survival in the absence of heat stress. We also examined whether heat shock affects the sperm cell. There was no effect of heat shock on sperm apoptosis (programmed cell death) or on sperm fertilizing ability. Therefore, effects of heat shock on sperm function after ejaculation if minimal. However, there were seasonal changes in sperm characteristics that indicates that some of the decrease in dairy cow fertility during the summer in Israel is due to using semen of inferior quality. Semen was collected from five representative bulls throughout the summer (August and September) and winter (December and January). There were seasonal differences in ion concentration in seminal plasma and in the mRNA for various ion channels known to be involved in acrosome reactions. Furthermore, the proportion of sperm cells with damaged acrosomes was higher in post-thaw semen collected in the summer than in its counterpart collected in winter (54.2 ± 3.5% vs. 51.4 ± 1.9%, respectively; P < 0.08Further examination is required to determine whether such alterations are involved in the low summer fertility of dairy cows.

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