Relevant bibliographies by topics / GM-CSF

Academic literature on the topic 'GM-CSF'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 September 2023

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Journal articles on the topic "GM-CSF"

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Sands, Bruce E. "GM-CSF." Inflammatory Bowel Diseases 12 (April 2006): S12. http://dx.doi.org/10.1097/00054725-200604002-00024.

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Ratto, Alessandra, Claudio Petterino, Tullio Florio, and Federica Barbieri. "Goat anti-human GM-CSF recognizes canine GM-CSF." Veterinary Clinical Pathology 41, no. 1 (March 2012): 3–4. http://dx.doi.org/10.1111/j.1939-165x.2012.00407.x.

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&NA;. "DT388-GM-CSF." Inpharma Weekly &NA;, no. 1152 (August 1998): 7. http://dx.doi.org/10.2165/00128413-199811520-00012.

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Senzer, N., C. Bedell, and J. Nemunaitis. "OncoVEX(GM-CSF)." Drugs of the Future 35, no. 6 (2010): 449. http://dx.doi.org/10.1358/dof.2010.035.06.1500437.

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Senzer, N., C. Bedell, and J. Nemunaitis. "OncoVEX(GM-CSF)." Drugs of the Future 35, no. 6 (2010): 449. http://dx.doi.org/10.1358/dof.2010.35.6.1500437.

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Tazawa, Ryushi, and Koh Nakata. "GM-CSF Therapy for Pulmonary Alveolar Proteinosis." Nihon Naika Gakkai Zasshi 99, no. 7 (2010): 1623–27. http://dx.doi.org/10.2169/naika.99.1623.

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Reed, Jacquelyn A., Machiko Ikegami, Eli R. Cianciolo, Wei Lu, Patricia S. Cho, William Hull, Alan H. Jobe, and Jeffrey A. Whitsett. "Aerosolized GM-CSF ameliorates pulmonary alveolar proteinosis in GM-CSF-deficient mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 4 (April 1, 1999): L556—L563. http://dx.doi.org/10.1152/ajplung.1999.276.4.l556.

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Surfactant proteins and phospholipids accumulate in the alveolar spaces and lung tissues of mice deficient in granulocyte-macrophage colony-stimulating factor (GM-CSF), with pathological findings resembling the histology seen in the human disease pulmonary alveolar proteinosis (PAP). Previous metabolic studies in GM-CSF-deficient [GM(−/−)] mice indicated that defects in surfactant clearance cause the surfactant accumulation in PAP. In the present study, GM(−/−) mice were treated daily or weekly with recombinant mouse GM-CSF by aerosol inhalation or intraperitoneal injection for 4–5 wk. Lung histology, alveolar macrophage differentiation, and surfactant protein B immunostaining returned toward normal levels in the GM-CSF aerosol-treated mice. Alveolar and lung tissue saturated phosphatidylcholine and surfactant protein B concentrations were significantly decreased after treatment with aerosolized GM-CSF. Cessation of aerosolized GM-CSF for 5 wk resulted in increased saturated phosphatidylcholine pool sizes that returned to pretreatment levels. In contrast, PAP did not improve in GM(−/−) mice treated daily for 5 wk with larger doses of systemic GM-CSF. Aerosolized GM-CSF improved PAP in the GM(−/−) mice, demonstrating that surfactant homeostasis can be influenced by local administration of GM-CSF to the respiratory tract.
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McNiece, I., R. Andrews, M. Stewart, S. Clark, T. Boone, and P. Quesenberry. "Action of interleukin-3, G-CSF, and GM-CSF on highly enriched human hematopoietic progenitor cells: synergistic interaction of GM-CSF plus G-CSF." Blood 74, no. 1 (July 1, 1989): 110–14. http://dx.doi.org/10.1182/blood.v74.1.110.110.

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Abstract Purified preparations of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), and interleukin 3 (IL-3 or multi-CSF) alone and in combination, have been compared for their stimulatory effects on human granulocyte-macrophage colony forming cells (GM-CFC). In cultures of unseparated normal human bone marrow, the combinations of G-CSF plus IL-3 and GM-CSF plus IL-3 stimulated additive numbers of GM colonies, while GM-CSF plus G-CSF stimulated greater than additive numbers of GM colonies, compared with the sum of the colony formation obtained with each factor alone. Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. In order to address the possibility of secondary factor involvement in the synergistic interaction of GM-CSF and G-CSF, CD33+/CD34+ colony forming cells were separated from normal and post FU marrow by two color fluorescence activated cell sorting. In cultures of CD33+/CD34+ cells the combination of GM-CSF plus G-CSF stimulated a synergistic increase in GM colonies while GM-CSF plus IL-3 stimulated additive numbers of colonies. These results suggest that GM-CSF, G-CSF, and IL-3 stimulate distinct populations of GM-CFC. Furthermore GM-CSF and G-CSF interact synergistically and this action is a direct effect on progenitor cells not stimulated by GM-CSF or G-CSF alone.
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McNiece, I., R. Andrews, M. Stewart, S. Clark, T. Boone, and P. Quesenberry. "Action of interleukin-3, G-CSF, and GM-CSF on highly enriched human hematopoietic progenitor cells: synergistic interaction of GM-CSF plus G-CSF." Blood 74, no. 1 (July 1, 1989): 110–14. http://dx.doi.org/10.1182/blood.v74.1.110.bloodjournal741110.

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Purified preparations of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), and interleukin 3 (IL-3 or multi-CSF) alone and in combination, have been compared for their stimulatory effects on human granulocyte-macrophage colony forming cells (GM-CFC). In cultures of unseparated normal human bone marrow, the combinations of G-CSF plus IL-3 and GM-CSF plus IL-3 stimulated additive numbers of GM colonies, while GM-CSF plus G-CSF stimulated greater than additive numbers of GM colonies, compared with the sum of the colony formation obtained with each factor alone. Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. In order to address the possibility of secondary factor involvement in the synergistic interaction of GM-CSF and G-CSF, CD33+/CD34+ colony forming cells were separated from normal and post FU marrow by two color fluorescence activated cell sorting. In cultures of CD33+/CD34+ cells the combination of GM-CSF plus G-CSF stimulated a synergistic increase in GM colonies while GM-CSF plus IL-3 stimulated additive numbers of colonies. These results suggest that GM-CSF, G-CSF, and IL-3 stimulate distinct populations of GM-CFC. Furthermore GM-CSF and G-CSF interact synergistically and this action is a direct effect on progenitor cells not stimulated by GM-CSF or G-CSF alone.
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Khanjari, F. "GM-CSF and proteinosis." Thorax 58, no. 7 (July 1, 2003): 645. http://dx.doi.org/10.1136/thorax.58.7.645.

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Dissertations / Theses on the topic "GM-CSF"

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Bailie, Karen Elizabeth Margaret. "G-CSF and GM-CSF : effects on neonatal neutrophils." Thesis, Queen's University Belfast, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.482043.

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Chevalier, Anne Sophie. "Utilisation thérapeutique du G-CSF et du GM-CSF en hématologie." Paris 5, 1993. http://www.theses.fr/1993PA05P248.

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Hallsworth, Matthew Pearce. "GM-CSF and eosinophil survival in asthma." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341883.

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Bernstone, Laura. "Characterisation of HIV-1 infection and M-CSF and GM-CSF macrophages." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572833.

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Macrophages are a natural target cell for HIV-1 infection, and they contribute to the development of disease as they are important for transmission, dissemination and persistence of the virus in an infected patient. Macrophages are less well-studied than T cells and cell lines in relation to HIV-1 infection, yet macrophages are highly specialised and key aspects of the HIV-1 life cycle in these cells are already known to differ compared to other cell types. HIV-1 entry into macrophages has been suggested to occur by macropinocytosis, however the entry route in these cells has not been fully characterised. In this thesis I have tested a panel of pharmacological inhibitors of cellular proteins and uptake pathways, in order to delineate the requirements for HIV-1 entry into macrophages and to determine the nature of the entry route. My findings suggest that the following host factors are important for entry; membrane cholesterol, actin rearrangements, dynamin, sodium-hydrogen exchange, Pak1, and Rac. Other factors including clathrin, PI-3 kinase, Rho kinase and some isoforms of PKC were found to be dispensable for infection or to inhibit infection. Macrophages are a heterogeneous group of cells, and tissue macrophages from different parts of the body differ in their morphology, phenotype and function. I have used the growth factors M-CSF and GM-CSF to direct monocytes to differentiate into distinct types of macrophage. This allowed me to determine that different macrophages differ in their susceptibility to infection and in their ability to support replication. This is likely to be due to variation in HIV-1 receptor expression and the levels of key HIV-1 transcription factors, respectively. Overall this thesis contributes to existing knowledge regarding HIV-1 infection of macrophages. These findings may assist with the design of entry inhibitors, and with therapies designed to eradicate HIV-1 from infected individuals.
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Lin, Tony Wei Ting. "The role of GM-CSF/G-CSF & BKLF in the development of atherosclerosis." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10407.

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The studies described in this thesis are aimed to investigate the role of the pro-inflammatory cytokine GM-CSF/G-CSF, transcriptional factor KLF3 and psychological stress in KLF3 deficiency mice on neointimal formation, a common feature of atherosclerosis with the aid of perivascular collar model on murine model. The present study supports an important role for GM/CSF-G/CSF and KLF in atherosclerosis. There is now overwhelming evidence that the monocyte/macrophage has a crucial role in the initiation and progression of atherosclerotic plaque and this has led to the view that the recruitment and activity of these cells may represent important therapeutic targets. Atherosclerosis is multi-factorial and well-established risk factor include: hypertension, hypercholesterolemia, diabetes, smoking and aging (Altman 2003), increasing evidence suggest an important role for psychological factor (stress) in the development of CHD. Furthermore, accumulating evidence suggests that GM-CSF/G-CSF and KLF3 has protective effect against atherosclerosis. The studies described in this thesis investigated on the effect of the pro-inflammatory cytokine (the role of GM-CSF/G-CSF and KLF3) and the psychological factor (stress and the role KLF3) factors on neointimal formation, a common feature of atherosclerosis. The experimental models of neointimal formation play an important role in understanding the pathogenesis of atherosclerosis (White, 1989), which could contribute to the development of therapeutic modalities and examining the effectiveness of potential interventions that target neointimal proliferative disease. Several mouse models of atherosclerosis have been employed experimentally worldwide. In this thesis murine perivascular collar placement around the femoral artery injury model was investigated for the neointimal formation. Chapter 3 describes the role of the pro-inflammatory cytokine GM-CSF/G-CSF in the pathophysiology of atherosclerosis. GM-CSF/G-CSF exhibits many biological functions including; mediation of inflammatory responses effects (Kleemann, Zadelaar et al. 2008). The role of GM-CSF/G-CSF in injury-mediated neointimal formation is complex. Moreover, the effect of atherosclerotic state on the role of GM-CSF/G-CSF in the acute injury model has not been previously explored. Our study demonstrated that GM-CSF/G-CSF deficiency resulted in delayed neointimal formation at an earlier examined time-point (2 weeks). Thus, it suggested that GM-CSF/G-CSF displayed a net pro-atherogenic effect in this model of perivascular collar endothelial injury. This information could be used for improved early detection, prevention and treatment of atherosclerosis. Chapter 4 describes the role of KLF3 on neointimal formation. KLF3 had profound effects on using in vitro and in vivo either in animal models or in human subject (Cao, Sun et al. 2010). KLF3 have potent effects in stimulating proliferation (Dang, Pevsner et al. 2000; McConnell and Yang 2010), maturation, and function of hematopoietic cells cytokines (Turner and Crossley 1999; Cao, Sun et al. 2010). KLF3 exhibits a myeloproliferative disorder suggests that KLF3 regulates important process involved in haematopoietic differentiation (Turner and Crossley 1999). The studies discussed here reveal that KLF3 deficiency can have profound effects on cell differentiation, and function in vitro and in vivo. In addition, correlating and contrasting KLF3 structure-function relationships in vascular biology may enable an improved understanding of their physiologic and pathologic functions. Our study demonstrated that KLF3 deficiency resulted in delayed neointimal formation at an earlier examined time-point (2 weeks), suggesting that KLF3 deficiency may showed a net pro-atherogenic effect in this model of perivascular collar endothelial injury. This knowledge might be used for improved early detection, prevention and treatment of atherosclerosis. Future investigations are required to further clarify the underlying mechanisms, and the potential therapeutic benefit on KLF3 deficiency treatment in vascular proliferative disorders. Chapter 5 describes the role of stress and KLF3 deficiency on neointimal formation. Accumulating evidence suggests an important role for psychosocial factors such as stress in the development of CHD (Rozanski, Blumenthal et al. 1999); however the role of psychological stress in early responses in injury-induced neointimal formation remains debate. KLF3 deficiency mice exhibit reduced detrimental effects of chronic stress by induces vascular inflammation (Liu, Wen et al. 2010; Lu, Haldar et al. 2010), and therefore provide a unique genetic animal model to gain insight into the effect of stress on the aetiology of atherogenesis. This study evaluated the effect of acute psychological stress mediated by physical restraint on neointimal formation, and these effects were further explored in the absence of KLF3 deficiency. Although KLF3 deficiency showed minor effects (reduced inflammation and vessel proliferation), it was not found to be protective against stress-mediated increase in neointimal formation. This study suggested that acute psychological stress contributes to the pathogenesis of vessel neointimal proliferative disorders. Precise underlying mechanisms involving stress and KLF3 deficiency in neointimal formation require further clarification. However, these findings have provided some valuable insight on the role of stress and KLF3 deficiency in vessel proliferative responses. Therefore, the role of KLF3 deficiency in stress and neointimal formation appears complex at early stage. Future studies on the effect of stress on hemodynamic responses and their role on neointimal formation can be further investigated with the perivascular collar endothelial collar model as well as their potential pharmacological modulation.
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Mirabella, Fabio. "Regulation of the human IL-3/GM-CSF locus." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487744.

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The human Interleukin-3 (IL-3) and Granulocyte-Macrophage Colony-Stimulating-Factor (GM-CSF) genes are two closely linked cytokine genes that are located within a conserved cytokine gene cluster. They are expressed in an inducible tissue-specific manner in a variety of haemopoietic cell types, and they contribute to the regulation of inflammatory responses arid haemopoiesis. For this reason their expression is strictly regulated. The experiments in this thesis describe an investigation into the factors and DNA elements involved in the control and regulation of these genes during T cell development. They focus in particular on the roles that DNase I hypersensitive sites (DHSs) and the nuclear proteins CTCF and RAD21 play within the GM-CSF/IL-3 gene locus.
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Grant, Olivia M. "GM-CSF Stress-Induced Priming of the Dendritic Cell." Ohio Dominican University Honors Theses / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=oduhonors1449522036.

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Adkins, Karissa Kathleen 1971. "Glucocorticoid regulation of GM-CSF in bronchial epithelial cells." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282844.

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Inflammation plays a central role in the pathogenesis of asthma. Glucocorticoids are first line antiinflammatory therapy in the treatment of asthma and are effective inhibitors of inflammatory cytokines. Clinical data demonstrate that granulocyte-macrophage colony-stimulating factor (GM-CSF) production by airway epithelial cells may be an important target of inhaled glucocorticoid therapy. In this study, the regulatory mechanisms of GM-CSF expression by interleukin-1β (IL-1β) and the synthetic glucocorticoid dexamethasone (DEX) were examined in the BEAS-2B human bronchial epithelial cell line. It is hypothesized that glucocorticoids inhibit GM-CSF production in these cells through transcriptional mechanisms involving induction of the NF-κB inhibitory protein, IκB-α. Treatment of the BEAS-2B cells with IL-1β induced GM-CSF protein and mRNA levels, and further investigation showed this induction was mediated through transcriptional mechanisms. DEX treatment of BEAS-2B cells inhibited IL-1β-induced GM-CSF protein and mRNA production. GM-CSF mRNA was rapidly degraded in these cells, and DEX treatment did not significantly affect this decay rate. These data suggest that dexamethasone repression of GM-CSF expression is mediated predominantly through transcriptional mechanisms. This study then examined expression of IκB-α in the BEAS-2B cells as a possible mechanism of glucocorticoid repression of GM-CSF. IκB-α RNA levels were minimally induced by DEX in these cells, but this did not result in concurrent induction of IκB-α protein. Additional analysis showed that DEX treatment of BEAS-2B cells did not prevent nuclear translocation of the NF-κB subunit p65, or IL-1β-induced degradation of IκB-α protein. From these data, this study concludes that induction of IκB-α is not a significant mechanism of glucocorticoid-mediated repression of GM-CSF in the BEAS-2B cells.
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Aziz, Khalil Abdul. "Influence of GM-CSF and G-CSF on the mutual interactions between platelets and neutrophils." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241473.

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Osborne, Cameron Stuart. "Transcriptional regulation of the GM-CSF gene in T lymphocytes /." Title page, contents and summary only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09pho81.pdf.

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Books on the topic "GM-CSF"

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M, Marty, ed. Manual of GM-CSF. Oxford: Blackwell Science, 1996.

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Howard, Scarffe J., Royal Society of Medicine Services (Great Britain), Sandoz Pharmaceuticals, and Schering-Plough Corporation, eds. Breakthrough in cytokine therapy: An overview of GM-CSF. London: Royal Society of Medicine Services, 1991.

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The Role of GM-CSF/IL-3/IL-5 Receptor Common β Subunit (CBS) in Hematopoietic Stem and Progenitor Cell (HSPC) Expansion, Monocytosis and Atherosclerosis. [New York, N.Y.?]: [publisher not identified], 2013.

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van, Furth Ralph, ed. Hemopoietic growth factors and mononuclear phagocytes. Basel: New York, 1993.

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Gregory, Bock, and Goode Jamie, eds. The molecular basis of cellular defence mechanisms. Chichester: Wiley, 1997.

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Gorin, N. C. Molgramostim Gm-csf: Possibilities And Perspectives (International Congress & Symposium). Royal Society of Medicine Press Ltd, 1992.

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Venet, Fabienne, and Alain Lepape. Immunoparesis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0313.

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In parallel with an exaggerated pro-inflammatory response, critically-ill patients develop an immunosuppressive phase, termed immunoparesis/immunoparalysis or immune reprogramming. Innate and adaptive immune responses are affected. In particular, impaired neutrophil recruitment to injury sites and abnormal accumulation in remote sites; monocyte deactivation with preferential anti-inflammatory cytokine production and altered antigen presentation capacity; and a dramatic lymphopenia associated with major induction of apoptosis, functional, and phenotypic alterations have been described. The intensity and duration of this injury-induced immune dysfunction have been associated with an increased risk of death and secondary nosocomial infections. Innovative therapeutic strategies aiming at restoring immunological functions are currently being tested. GM-CSF appears to be an interesting candidate while IFN-γ‎ and IL-7 represent novel future therapeutic approaches. There is thus an urgent need for further clinical trials of such immunoadjuvant therapies that should include large cohorts of critically-ill patients stratified by relevant markers of immune dysfunction.
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Symposium, CIBA Foundation. The Molecular Basis of Cellular Defence Mechanisms - Symposium No. 204. John Wiley & Sons, 1997.

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Book chapters on the topic "GM-CSF"

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Baum, H. "GM-CSF." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1306-1.

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Baum, H. "GM-CSF." In Springer Reference Medizin, 1010. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1306.

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Williams, William V. "GM-CSF Antagonists." In New Drugs for Asthma, Allergy and COPD, 251–55. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062175.

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Dranoff, Glenn, and Kenneth F. May. "GM-CSF and Whole Cells." In Cancer Therapeutic Targets, 251–59. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_37.

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Dranoff, Glenn, and Kenneth F. May. "GM-CSF and Whole Cells." In Cancer Therapeutic Targets, 1–9. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_37-2.

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Hartung, Thomas, Sonja von Aulock, and Albrecht Wendel. "Growth Factors G-CSF and GM-CSF: Clinical Options." In Multiple Organ Failure, 621–29. New York, NY: Springer New York, 2000. http://dx.doi.org/10.1007/978-1-4612-1222-5_64.

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Link, H. "Therapie mit den hämatopoetischen Wachstumsfaktoren G-CSF und GM-CSF." In Kompendium Internistische Onkologie, 2025–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-31303-6_124.

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Würfel, Wolfgang. "G-CSF and GM-CSF: Clinical Applications in Reproductive Medicine." In In Vitro Fertilization, 751–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-43011-9_62.

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Vellenga, E. "The Expression and Regulation of G-CSF and GM-CSF." In Acute Leukemias V, 131–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-78907-6_20.

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Salajegheh, Ali. "Granulocyte-Macrophage and Granulocyte Colony Stimulating Factor (GM-CSF and G-CSF)." In Angiogenesis in Health, Disease and Malignancy, 127–32. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_20.

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Conference papers on the topic "GM-CSF"

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Zimlich, William C., Francesca Mariani, Bernhard Muellinger, Zamir Kadija, Juliane Gleske, Philipp Kroneberg, Manuel Frey, Ilaria Campo, Ernesto Pozzi, and Maurizio Luisetti. "Aerosol Characterization of Nebulized GM-CSF." 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.a5987.

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Tazawa, R., T. Ueda, M. Abe, K. Tatsumi, R. Eda, S. Kondoh, K. Morimoto, et al. "Antibody Against Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) and Inhaled GM-CSF for Pulmonary Alveolar Proteinosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3067.

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Nakata, K., K. Ohashi, R. Tazawa, Y. Inoue, BC Trapnell, M. Terada, H. Nakayama, and T. Takada. "GM-CSF Inhalation Promotes the Clearance of GM-CSF Autoantibody in the Lung of Autoimmune Pulmonary Alveolar Proteinosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3033.

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Debeuf, N., C. Bosteels, K. F. A. Van Damme, E. De Leeuw, J. Declercq, B. Maes, V. Bosteels, et al. "Loss of GM-CSF-dependent instruction of alveolar macrophages in COVID-19 provides a rationale for inhaled GM-CSF treatment." In ERS Lung Science Conference 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.lsc-2023.137.

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Tazawa, R., Y. Inoue, T. Takada, T. Arai, Y. Nasuhara, N. Hizawa, Y. Kasahara, et al. "Aerosolized GM-CSF Therapy of Pulmonary Alveolar Proteinosis (PAP)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3031.

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Wu, H., T. Suzuki, BC Trapnell, and FX McCormack. "Alveolar Macrophage Activation in KGF Treated Mice Is Associated with Early Release of GM-CSF, Followed by GM-CSF Dependent STAT5 Phosphorylation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3238.

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Chan, Jamie S., Ross Vlahos, David Haylock, Sussie Nilsson, Ivan Bertoncello, and Gary P. Anderson. "Macrophage Progenitor Recruitment And Functional Specification Is Controlled By A M-CSF/ GM-CSF/ Osteopontin Axis." 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.a3781.

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Khasawneh, M., D. C. Patel, and A. Ataya. "Persistent Eosinophilia Due to Subcutaneous GM-CSF Therapy in aPAP." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4949.

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Suzuki, Takuji, Takuro Sakagami, J. C. van der Loo, Brenna Carey, Claudia Chalk, and Bruce Trapnell. "A Novel Cell Line (mAM-hGM-R) For Measuring The Bioactivity Of GM-CSF And Neutralizing Capacity Of GM-CSF Autoantibodies In Human Serum." 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.a2983.

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Suzuki, T., T. Sakagami, B. Rubin, R. Wood, B. Carey, JA Whitsett, and BC Trapnell. "Pulmonary Alveolar Proteinosis (PAP) Caused by GM-CSF Receptor α Defects." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3023.

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Reports on the topic "GM-CSF"

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Emens, Leisha A., and Elizabeth M. Jaffee. Enhancement of an Allogeneic GM-CSF-Secreting Breast Cancer Vaccine by Immunomodulatory Doses of Cyclophosphamide and Doxorubicin. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417167.

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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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Abstract:
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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