Relevant bibliographies by topics / Granulocyte colony stimulating factor (G-CSF)

Academic literature on the topic 'Granulocyte colony stimulating factor (G-CSF)'

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Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Granulocyte colony stimulating factor (G-CSF)"

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Lieschke, Graham J. "Granulocyte colony stimulating factor (G-CSF)." Australian Prescriber 17, no. 4 (October 1, 1994): 96–99. http://dx.doi.org/10.18773/austprescr.1994.100.

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Schaafsma, MR, JH Falkenburg, N. Duinkerken, J. Van Damme, BW Altrock, R. Willemze, and WE Fibbe. "Interleukin-1 synergizes with granulocyte-macrophage colony-stimulating factor on granulocytic colony formation by intermediate production of granulocyte colony-stimulating factor." Blood 74, no. 7 (November 15, 1989): 2398–404. http://dx.doi.org/10.1182/blood.v74.7.2398.2398.

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Abstract Interleukin-1 (IL-1) was found to act synergistically with granulocyte- macrophage colony-stimulating factor (GM-CSF) on granulocytic colony growth of normal human bone marrow cells, depleted of mononuclear phagocytes and T lymphocytes. Using CD34/HLA-DR-enriched bone marrow cells we demonstrated that this activity of IL-1 was not a direct action on hematopoietic progenitor cells, but an effect of an intermediate factor produced by residual accessory cells in response to IL-1. Neutralization experiments using an anti-IL-6 antiserum showed that IL-1-induced IL-6 did not contribute to the observed synergy. Furthermore, IL-6 by itself had neither a direct stimulatory effect on CFU-GM colony growth, nor did it act synergistically with GM-CSF on granulocytic or monocytic colony formation. Neutralization experiments with an anti-G-CSF monoclonal antibody showed that IL-1-induced G-CSF production was responsible for the synergy with GM-CSF. Using combinations of G-CSF and GM-CSF this synergistic activity could be detected at concentrations of G-CSF as low as 0.1 ng/mL (10 U/mL). Our results indicate that IL-1, but not IL-6, stimulates the GM-CSF- dependent proliferation of relatively mature myeloid progenitor cells in the presence of small numbers of accessory cells.
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Schaafsma, MR, JH Falkenburg, N. Duinkerken, J. Van Damme, BW Altrock, R. Willemze, and WE Fibbe. "Interleukin-1 synergizes with granulocyte-macrophage colony-stimulating factor on granulocytic colony formation by intermediate production of granulocyte colony-stimulating factor." Blood 74, no. 7 (November 15, 1989): 2398–404. http://dx.doi.org/10.1182/blood.v74.7.2398.bloodjournal7472398.

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Interleukin-1 (IL-1) was found to act synergistically with granulocyte- macrophage colony-stimulating factor (GM-CSF) on granulocytic colony growth of normal human bone marrow cells, depleted of mononuclear phagocytes and T lymphocytes. Using CD34/HLA-DR-enriched bone marrow cells we demonstrated that this activity of IL-1 was not a direct action on hematopoietic progenitor cells, but an effect of an intermediate factor produced by residual accessory cells in response to IL-1. Neutralization experiments using an anti-IL-6 antiserum showed that IL-1-induced IL-6 did not contribute to the observed synergy. Furthermore, IL-6 by itself had neither a direct stimulatory effect on CFU-GM colony growth, nor did it act synergistically with GM-CSF on granulocytic or monocytic colony formation. Neutralization experiments with an anti-G-CSF monoclonal antibody showed that IL-1-induced G-CSF production was responsible for the synergy with GM-CSF. Using combinations of G-CSF and GM-CSF this synergistic activity could be detected at concentrations of G-CSF as low as 0.1 ng/mL (10 U/mL). Our results indicate that IL-1, but not IL-6, stimulates the GM-CSF- dependent proliferation of relatively mature myeloid progenitor cells in the presence of small numbers of accessory cells.
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Collins, Steven J., Jon Ulmer, Louise E. Purton, and Gretchen Darlington. "Multipotent hematopoietic cell lines derived from C/EBPα(−/−) knockout mice display granulocyte macrophage–colony-stimulating factor, granulocyte– colony-stimulating factor, and retinoic acid–induced granulocytic differentiation." Blood 98, no. 8 (October 15, 2001): 2382–88. http://dx.doi.org/10.1182/blood.v98.8.2382.

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Abstract The transcription factor C/EBPα is an important mediator of granulocyte differentiation and regulates the expression of multiple granulocyte-specific genes including the granulocyte–colony-stimulating factor (G-CSF) receptor, neutrophil elastase, and myeloperoxidase. Indeed C/EBPα knockout mice display a profound block in granulocyte differentiation. To study this block in granulocytic differentiation in more detail, retroviral vector-mediated transduction of a dominant-negative retinoic acid receptor was used to establish hematopoietic growth factor–dependent, lympho-myeloid progenitor cell lines from the fetal livers of both the C/EBPα knockout animals (C/EBPα(−/−)) and their heterozygous littermates (C/EBPα(+/−)). Surprisingly, the C/EBPα(−/−) cell lines displayed significant spontaneous granulocytic differentiation, and this differentiation was markedly enhanced when the cells were stimulated with granulocyte macrophage (GM)–CSF. This GM-CSF–mediated differentiation was associated with the up-regulation of G-CSF receptor mRNA, and the combination of GM-CSF and G-CSF generated more than 95% mature neutrophils in the C/EBPα(−/−) cultures. The addition of all-transretinoic acid also enhanced this granulocytic differentiation of the cultured C/EBPα(−/−) cells, indicating that the activated retinoic acid receptors can enhance granulocytic differentiation through a molecular pathway that is independent of C/EBPα. These studies clearly indicate that terminal granulocytic differentiation associated with the up-regulation of C/EBPα-responsive genes can occur in the absence of C/EBPα, and they indicate the existence of multiple independent molecular pathways potentially used by primitive hematopoietic precursors that can lead to the development of mature granulocytes.
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Cetean, Sînziana, Călin Căinap, Anne-Marie Constantin, Simona Căinap, Alexandra Gherman, Luminița Oprean, Adriana Hangan, and Radu Oprean. "The importance of the granulocyte-colony stimulating factor in oncology." Medicine and Pharmacy Reports 88, no. 4 (September 20, 2015): 468–72. http://dx.doi.org/10.15386/cjmed-531.

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Granulocyte-colony stimulating factor (G-CSF) is a glycoprotein, the second CSF, sharing some common effects with granulocyte macrophage-colony stimulating factor (GM-CSF), interleukin-3 (IL-3) and interleukin-5 (IL-5). G-CSF is mainly produced by fibroblasts and endothelial cells from bone marrow stroma and by immunocompetent cells (monocytes, macrophages). The receptor for G-CSF (G-CSFR) is part of the cytokine and hematopoietin receptor superfamily and G-CSFR mutations cause severe congenital neutropenia.The main action of G-CSF - G-CSFR linkage is stimulation of the production, mobilization, survival and chemotaxis of neutrophils, but there are many other G-CSF effects: growth and migration of endothelial cells, decrease of norepinephrine reuptake, increase in osteoclastic activity and decrease in osteoblast activity.In oncology, G-CSF is utilized especially for the primary prophylaxis of chemotherapy-induced neutropenia, but it can be used for hematopoietic stem cell transplantation, it can produce monocytic differentiation of some myeloid leukemias and it can increase some drug resistance.The therapeutic indications of G-CSF are becoming more and more numerous: non neutropenic patients infections, reproductive medicine, neurological disturbances, regeneration therapy after acute myocardial infarction and of skeletal muscle, and hepatitis C therapy.
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Brown, TJ, J. Liu, C. Brashem-Stein, and M. Shoyab. "Regulation of granulocyte colony-stimulating factor and granulocyte- macrophage colony-stimulating factor expression by oncostatin M." Blood 82, no. 1 (July 1, 1993): 33–37. http://dx.doi.org/10.1182/blood.v82.1.33.bloodjournal82133.

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Oncostatin M (OM) is structurally and functionally related to a subclass of hematopoietic cytokines including leukemia-inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), granulocyte colony- stimulating factor (G-CSF), and interleukin-6 (IL-6). Using human endothelial cells (HEC) as a model for cytokine regulation of hematopoietic growth factor expression, we tested OM as an inducer of colony-stimulating activity. Colony-forming cell assays supplemented with culture supernatants from OM-treated HEC contained a threefold increase in colony-forming unit granulocyte-macrophage colonies. Specific immunoassay (enzyme-linked immunosorbent assay) of culture supernatants indicated that OM treatment of HEC resulted in a dose- and time-dependent increase in the accumulation of G-CSF and granulocyte- macrophage CSF (GM-CSF) (> 28-fold). The ED50 for OM induction of G-CSF and GM-CSF protein expression was 17 and 7 pmol/L, respectively. Increased protein expression was associated with a similar increase in steady-state expression of G-CSF and GM-CSF mRNA. Furthermore, a period of 12 to 24 hours elapsed before there were measurable increases in CSF expression, suggesting that OM may stimulate CSF production through a mechanism requiring the synthesis or activation of a secondary mediating factor or pathway. These findings provide the first evidence that OM may regulate myelopoiesis by inducing the cellular expression of hematopoietic growth factors.
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Morinaga, Ryota, Takashi Kawahara, Shinnosuke Kuroda, Yoshiaki Inayama, and Hiroji Uemura. "Granulocyte Colony-Stimulating Factor-Producing Bladder Cancer." Case Reports in Oncology 12, no. 2 (August 6, 2019): 603–7. http://dx.doi.org/10.1159/000502174.

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Granulocyte colony-stimulating factor (G-CSF)-producing bladder cancer is rare, with only 75 cases reported in Japan. A 67-year-old woman was referred to our institution for the further examination of gross hematuria. Cystoscopy revealed a 7-cm bladder tumor. The initial white blood cell count was 17,100/μL, and a transurethral resected specimen showed G-CSF expression. CT revealed that the tumor had invaded the colon. As the patient had uncontrollable schizophrenia, radical cystectomy was abandoned. We herein report a case of G-CSF-producing bladder tumor.
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Paszko-Patej, G., D. Sienkiewicz, B. Okurowska-Zawada, and W. Kułak. "Granulocyte colony-stimulating factor potential use in the treatment of children with cerebral palsy." Progress in Health Sciences 7, no. 1 (May 19, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.1882.

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Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates the bone marrow to produce granulocytes and stem cells and release them into the blood. Recent studies demonstrated the presence of CSF-receptor (G-CSFR) system in the brain and spinal cord, and their roles in neuroprotection and neural tissue repair, as well as improvement in functional recovery. G-CSF exerts neuroprotective actions through the inhibition of apoptosis and inflammation, and the stimulation of neurogenesis. This review highlights recent studies on the potential use of G-CSF in cerebral palsy.
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Chakraborty, Arup, Eric R. Hentzen, Scott M. Seo, and C. Wayne Smith. "Granulocyte colony-stimulating factor promotes adhesion of neutrophils." American Journal of Physiology-Cell Physiology 284, no. 1 (January 1, 2003): C103—C110. http://dx.doi.org/10.1152/ajpcell.00165.2002.

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Granulocyte colony stimulating factor (G-CSF) is well known for its ability to drive the maturation and mobilization of neutrophils. G-CSF also appears to have the potential to activate functions of mature neutrophils, influencing recruitment at sites of inflammation and tissue injury. We investigated the ability of G-CSF to stimulate adhesion of isolated blood neutrophils. G-CSF induced significant adherence to intercellular adhesion molecule (ICAM)-1 that was both macrophage antigen-1 (Mac-1) and leukocyte function-associated antigen-1 dependent. The kinetics of G-CSF-stimulated adhesion to ICAM-1 peaked at 11 min without detectable surface upregulation of Mac-1. This was in marked contrast to chemokines, in which peak activation of adhesion is seen within 1 min of stimulation. In contrast to chemokine-induced adhesion, G-CSF stimulation was not inhibited by pertussis toxin. G-CSF also augmented the attachment of neutrophils to activated human umbilical vein endothelial cells (HUVEC) through specific effects on neutrophils, because HUVEC appear to lack functional G-CSF receptors.
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Kitching, A. Richard, Xiao Ru Huang, Amanda L. Turner, Peter G. Tipping, Ashley R. Dunn, and Stephen R. Holdsworth. "The Requirement for Granulocyte-Macrophage Colony-Stimulating Factor and Granulocyte Colony-Stimulating Factor in Leukocyte-Mediated Immune Glomerular Injury." Journal of the American Society of Nephrology 13, no. 2 (February 2002): 350–58. http://dx.doi.org/10.1681/asn.v132350.

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ABSTRACT. Proliferative glomerulonephritis in humans is characterized by the presence of leukocytes in glomeruli. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) can potentially stimulate or affect T cell, macrophage, and neutrophil function. To define the roles of GM-CSF and G-CSF in leukocyte-mediated glomerulonephritis, glomerular injury was studied in mice genetically deficient in either GM-CSF (GM-CSF −/− mice) or G-CSF (G-CSF −/− mice). Two models of glomerulonephritis were studied: neutrophil-mediated heterologous-phase anti-glomerular basement membrane (GBM) glomerulonephritis and T cell/macrophage-mediated crescentic autologous-phase anti-GBM glomerulonephritis. Both GM-CSF −/− and G-CSF −/− mice were protected from heterologous-phase anti-GBM glomerulonephritis compared with genetically normal (CSF WT) mice, with reduced proteinuria and glomerular neutrophil numbers. However, only GM-CSF −/− mice were protected from crescentic glomerular injury in the autologous phase, whereas G-CSF −/− mice were not protected and in fact had increased numbers of T cells in glomeruli. Humoral responses to the nephritogenic antigen were unaltered by deficiency of either GM-CSF or G-CSF, but glomerular T cell and macrophage numbers, as well as dermal delayed-type hypersensitivity to the nephritogenic antigen, were reduced in GM-CSF −/− mice. These studies demonstrate that endogenous GM-CSF plays a role in experimental glomerulonephritis in both the autologous and heterologous phases of injury.
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Dissertations / Theses on the topic "Granulocyte colony stimulating factor (G-CSF)"

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Jasper, Melinda Jane. "Paracrine regulation of ovarian function by granulocyte-macrophage colony-stimulating factor (GM-CSF) & colony-stimulating factor-1 (CSF-1) /." Title page and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phj39.pdf.

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Schmidt-Mende, Jan Georg. "Apoptosis in the myelodysplastic syndromes : protective effect of G-CSF/." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-471-6/.

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Azoulay, Elie. "Approche expérimentale des circonstances de toxicité pulmonaire aigue͏̈ ou chronique du Granulocyte-Colony-Stimulating-Factor (G-CSF)." Paris 12, 2002. http://www.theses.fr/2002PA120005.

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INTRODUCTION : Le Granulocyte Colony Stimulating Factor (G-CSF) est largement prescrit chez les patients d'hématocancérologie pour raccourcir les durées de neutropénie après chimiothérapie. Le G-CSF est aussi évalué chez des patients non neutropéniques ayant des altérations fonctionnelles des polynucléaires neutrophiles (PN). Plusieurs observations de pneumopathies médicamenteuses au G-CSF ont été rapportées: il s'agit le plus souvent de patients âgés de plus de 65 ans, ayant reçu plus de trois cures de chimiothérapie pour lymphome non hodgkinien, présentant une pneumopathie interstitielle diffuse non infectieuse pendant ou après la sortie d'aplasie. Néanmoins, cette entité reste discutée du fait: (1) de sa rareté, (2) de l'évident bénéfice à prescrire du G-CSF contre un risque incertain de pneumopathie, (3) que les études randomisées comparant G-CSF à placebo n'ont pas démontré de surcroît de pneumopathies, (4) de l'innocuité du G-CSF chez les patients non neutropéniques. QUESTION POSEE : Quelles sont les situations à risque de toxicité pulmonaire du G-CSF? INTERVENTION: Le G-CSF (25 microg/kg/j) a été administré dans plusieurs situations d'agressions pulmonaires, à des rats non neutropéniques, neutropéniques ou en sortie d'aplasie. Les explorations ont comporté une quantification de l'oedème pulmonaire, des concentrations de protéines dans le lavage bronchoalvéolaire, du recrutement alvéolaire, de la séquestration pulmonaire en PN (myéloperoxydase), des concentrations sériques et pulmonaires en TNF-alpha et IL1-beta, de la pression artérielle pulmonaire (cathétérisme droit) de la compliance pulmonaire statique, des constatations anatomopathologiques (muscularisation, fibrose). Les rôles respectifs du PN et du macrophage ont été approchés par des expériences associant la lidocaine, les anticorps anti-TNF-alpha et te cyclophosphamide. . .
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Xiong, Yu. "Impact du G-CSF sur le phénotype et les fonctions des cellules NK dans le cadre d’une immunothérapie post-allogreffe de cellules souches hématopoïétiques." Thesis, Université de Lorraine, 2016. http://www.theses.fr/2016LORR0106/document.

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Les cellules Natural Killer (NK) sont capables de lyser les cellules tumorales sans la nécessité de reconnaitre un antigène tumoral spécifique. Cette propriété leur confère un avantage par rapport aux lymphocytes T et les rend intéressantes à utiliser en tant que cellules effectrices pour l’immunothérapie adoptive. A ce jour, le potentiel thérapeutique des cellules NK n’a pas été complétement exploré notamment dans le contexte du traitement de la rechute post-allogreffe de cellules souches hématopoïétiques. Actuellement, les patients en rechute post-greffe sont traités avec des injections de lymphocytes du donneur (DLI) parfois issues de petites fractions du greffon de cellules souches hématopoïétiques congelées. Les cellules souches périphériques étant fréquemment utilisées comme source de cellules souches et parfois utilisées comme DLI, nous avons souhaité évaluer l’impact du G-CSF sur le phénotype et les fonctions des cellules NK présentes dans ces fractions. Dans cet objectif, nous avons comparé différentes sources de cellules NK isolées à partir de sang de donneurs sains, de sang mobilisé de donneurs sains ou de patients et observé l’évolution des différentes sous-populations de cellules NK issues de ces prélèvements au décours d’une expansion en présence d’IL-15. Nos résultats ont montré que l’administration de G-CSF diminuait la proportion de cellules NK CD56brightCD16+ au profit d’une population CD16-, diminuait la prolifération des cellules NK lors de l’expansion en culture, et modifiait les propriétés fonctionnelles des cellules NK
The ability of natural killer (NK) cells to kill tumor cells without the need to recognize a tumor-specific antigen provides advantages over T cells and makes them appealing for a use as effectors for adoptive immunotherapy. However, the full therapeutic potential of NK cell-based immunotherapy has not been fully investigated in the context of leukemic relapse after hematopoietic stem cell transplantation. Today, patients relapsing after hematopoietic stem cell transplantation are often treated with donor lymphocyte infusion (DLI) based on small cell fractions frozen at the time of the stem cell transplantation. Since peripheral blood stem cells are increasingly used as stem cell source and as source of cells for DLI, we aimed to evaluate the impact of G-SCF mobilization on NK cell phenotype and functions. Therefore, we compared the expansion capacity, the phenotype and the function of NK cells from blood for healthy donors, from allogeneic HSCT healthy donors or from autologous HSCT from patients. We also determine the impact of G-CSF on NK cell subset repartition before and after expansion in presence of IL-15. Our results showed that G-CSF administration to patients decreases CD56brightCD16+ NK cell population, proliferation and function. Overcoming this impairment in lymphoid capacity may be important to facilitate post-transplant immunotherapy
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Haenel, Claude. "Neutropenie cyclique et traitement par rg-csf : a propos d'une observation." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR1M217.

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Held, Thomas. "Evaluation von Granulozyten Kolonie-stimulierendem Faktor (G-CSF) und einem monoklonalen Antikörper gegen Kapselpolysaccharid zur Therapie der experimentellen Klebsiella pneumoniae-Pneumonie." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/13759.

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G-CSF besitzt direkte Effekte auf die Aktivierung bakterizider Eigenschaften neutrophiler Granulozyten und verbessert das Überleben bakteriell infizierter Tiere. Daher wurde in der hier vorliegenden Arbeit der Effekt einer prophylaktischen oder therapeutischen Gabe von G-CSF bei experimenteller Pneumonie durch Klebsiella pneumoniae in Mäusen untersucht. Unerwarteterweise verschlechterte aber eine prophylaktische G-CSF-Gabe das Überleben und führte dosisabhängig zu einer Steigerung der bakteriellen Dissemination von der Lunge in Leber und Milz. Im Gegensatz dazu konnte ein spezifisch gegen K2-Kapselpolysaccharid (K2-KPS) von K. pneumoniae gerichteter monoklonaler Antikörper signifikant die Vermehrung der Bakterien in Lunge, Leber und Milz reduzieren. Die Blockierung von TNF?? durch Pentoxifyllin hingegen verzögerte die Letalität nach Induktion der Pneumonie, verhinderte sie jedoch nicht. In vitro konnte hier nachgewiesen werden, daß G-CSF spezifisch an K. pneumoniae bindet und daß diese Bindung an mehrere Proteine mit einem Molekulargewicht von 41, 25 und 21 kDa erfolgt. Die Bindung von G-CSF an K. pneumoniae führte zu einer signifikant erhöhten Produktion des wichtigsten Virulenzfaktors, K2-KPS. Dies verminderte in vitro signifikant eine Phagozytose der Bakterien durch neutrophile Granulozyten. Damit gelang es zum ersten Mal, die Bindung von G-CSF an ein gram-negatives Bakterium, K. pneumoniae, nachzuweisen und zu zeigen, daß diese Bindung in vitro zu einer erhöhten Produktion des wichtigsten Virulenzfaktors und in vivo zur Verschlechterung einer experimentellen Pneumonie durch erhöhte bakterielle Disseminierung bei prophylaktischer Gabe von G-CSF vor Infektion führt. Die weitere Untersuchung dieser Phänomene hinsichtlich einer möglichen Bindung von G-CSF auch an andere Bakterien könnte zu einer differenzierten supportiven Therapie bakterieller Infektionen mit G-CSF in nicht neutropenischen Patienten führen.
Besides its well-established effects on granulocytopoiesis, granulocyte colony-stimulating factor (G-CSF) has been shown to have direct effects on the recruitment and bactericidal ability of neutrophils, resulting in improved survival of experimentally infected animals. The effect of G-CSF on the course of experimental pneumonia induced by Klebsiella pneumoniae was studied. Using a highly reproducible murine model, the paradoxical finding that mortality from infection was significantly increased when animals received G-CSF before induction of pneumonia could be demonstrated. Administration of G-CSF promoted replication of bacteria in the liver and spleen, thus indicating an impairment rather than an enhancement of antibacterial mechanisms. By contrast, a monoclonal antibody against Klebsiella K2 capsule significantly reduced bacterial multiplication in the lung, liver, and spleen, and abrogated the increased mortality caused by G-CSF. Blocking of TNF-? with pentoxifylline, however, could not prevent increased mortality caused by G-CSF. In vitro studies showed a direct effect of G-CSF on K pneumoniae resulting in inreased capsular polysaccharide (CPS) production. When bacteria were coincubated with therapeutically achievable concentrations of G-CSF, phagocytic uptake and killing by neutrophils was impaired. Western blot analysis showed three binding sites of G-CSF to K pneumoniae. Thus, in this model, the direct effect of G-CSF on a bacterial virulence factor, CPS production, outweighed any beneficial effect of G-CSF on recruitment and stimulation of leukocytes. Further investigations of possible binding of G-CSF to other bacteria might influence a differentiated supportive therapy of bacterial infections in non-neutropenic patients with this growth factor.
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Liu, Hebin. "RUNX1/AML1 functions and mechanisms regulating granulocyte-macrophage colony-stimulating factor transcription." Doctoral thesis, Umeå : Department of Molecular Biology, Umeå University, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-486.

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Robertson, Sarah A. "Granulocyte-macrophage colony stimulating factor (GM-CSF) : a paracrine regulator in the pre-implantation mouse uterus." Title page, abstract and contents only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phr6515.pdf.

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McCormack, Matthew Paul. "The biological effects of constitutively active mutants of the common [beta] subunit of the human IL-3, IL-5 and GM-CSF receptors /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phm1305.pdf.

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Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1999?
Amendments to thesis in pocket on back cover. Copy of author's previously published article in pocket on back cover. Bibliography: leaves 124-172.
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Braunstein, Kirsten Daniela. "Untersuchungen zur Regulation von Interleukin-1ß (IL-1ß), Granulocyte Colony Stimulating Factor (G-CSF) und Vascular Endothelial Growth Factor (VEGF) in humanem Endometrium." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-65676.

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Books on the topic "Granulocyte colony stimulating factor (G-CSF)"

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

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Foote, MaryAnn, G. Molineux, and Tara Arvedson. Twenty years of G-CSF: Clinical and nonclinical discoveries. Basel: Springer, 2012.

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1950-, Morstyn George, Dexter T. Michael 1945-, and Foote MaryAnn, eds. Filgrastim (r-metHuG-CSF) in clinical practice. 2nd ed. New York: Dekker, 1998.

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J, Quesenberry Peter, Asano Shigetaka 1943-, and Saito Kazuhisa 1922-, eds. Hematopoietic growth factors: Molecular biology to clinical applications of rG-CSF : proceedings of a satellite symposium of the Sixth International Congress of Mucosal Immunology, Tokyo, July 22, 1990. Amsterdam: Excerpta Medica, 1991.

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

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Foote, MaryAnn, Tara Arvedson, and Graham Molineux. Twenty Years of G-CSF: Clinical and Nonclinical Discoveries. Springer, 2012.

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Foote, MaryAnn, Tara Arvedson, and Graham Molineux. Twenty Years of G-CSF: Clinical and Nonclinical Discoveries. Springer, 2014.

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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 "Granulocyte colony stimulating factor (G-CSF)"

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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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Hirsch, Bradford R., and Gary H. Lyman. "Economics of the Recombinant Human Granulocyte Colony-Stimulating Factors." In Twenty Years of G-CSF, 409–20. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0218-5_22.

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Jakubowski, Ann. "Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF):Biology and Clinical Status." In Principles of Cancer Biotherapy, 432–46. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-009-0029-5_20.

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Zhao, Li-Ru, Suning Ping, and Fei Hao. "The Combination of Stem Cell Factor (SCF) and Granulocyte-Colony Stimulating Factor (G-CSF) in Repairing the Brain Post-acute Stroke." In Cellular and Molecular Approaches to Regeneration and Repair, 197–215. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66679-2_10.

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Link, H., M. Freund, H. Kirchner, M. Stoll, H. Schmid, P. Bucsky, J. Seidel, et al. "Enhancement of Autologous Bone Marrow Transplantation with Recombinant Human Granulocyte-Macrophage Colony-Stimulating Factor (rhGM-CSF)." In Cancer Therapy, 96–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73721-3_12.

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Hosoi, Shinji, Kazunari Murozumi, Katsutoshi Sasaki, Mitsuo Satoh, Tatsuya Tamaoki, and Seiji Sato. "Optimization of cell culture conditions for G-CSF (granulocyte colony-stimulating factor) production by genetically engineered Namalwa KJM-1 cells." In Animal Cell Culture and Production of Biologicals, 299–306. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3550-4_35.

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Scheibenbogen, C., G. Zenke, B. Faggs, K. Motoyoshi, L. Kanz, H. Sawert, W. Brugger, and R. Andreesen. "Secretion of Colony-Stimulating Factor for Macrophages (M-CSF) and Granulocyte/Macrophages (GM-CSF) is Developmentally Regulated in Human Macrophages." In Cytokines in Hemopoiesis, Oncology, and AIDS, 45–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75510-1_6.

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Geigert, John, and Barbara F. D. Ghrist. "Development and Shelf-Life Determination of Recombinant Human Granulocyte-Macrophage Colony-Stimulating Factor (LEUKINE®, GM-CSF)." In Pharmaceutical Biotechnology, 329–42. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47452-2_8.

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Ottmann, O. G., K. Welte, L. M. Souza, and M. A. S. Moore. "Proliferative Effects of a Recombinant Human Granulocyte Colony-Stimulating Factor (rG-CSF) on Highly Enriched Hematopoietic Progenitor Cells." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 244–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72624-8_50.

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Moore, M. A. S., K. Welte, J. Gabrilove, and L. M. Souza. "Biological Activities of Recombinant Human Granulocyte Colony Stimulating Factor (rhG-CSF) and Tumor Necrosis Factor: In Vivo and In Vitro Analysis." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 210–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72624-8_45.

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Conference papers on the topic "Granulocyte colony stimulating factor (G-CSF)"

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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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Kuroda, Hiromasa. "Abstract 1416: Granulocyte-colony stimulating factor (G-CSF) enhances stemness by inducing myeloid-derived suppressor cell (MDSC) in cervical cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1416.

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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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Nayak, V. H., P. A. Nourani, H. H. Gutierrez, H. Batra, J. K. Thachuthara-George, and K. B. Turner. "Hereditary Pulmonary Alveolar Proteinosis Secondary to Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) Alpha-Receptor Mutation." 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.a1985.

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Blaes, AH, V. Chia, C. Solid, J. Page, RL Barron, MR Choi, and TJ Arneson. "Abstract P1-15-01: Patterns of granulocyte colony stimulating factor (G-CSF) use in elderly breast cancer (BC) patients receiving myelosuppressive chemotherapy." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p1-15-01.

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Uchida, K., M. Muroya, BC Trapnell, K. Yamada, K. Mori, Y. Seto, and Y. Yamada. "Reduced Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) Bioactivity with Surgical Stress Associated with Early Postoperative Complications." 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.a4722.

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Engelmann, Cornelius, Adam Herber, Tony Ildh, Ingolf Schiefke, Alexander Zipprich, Anett Schmiedeknecht, Stefan Zeuzem, et al. "O10 Granulocyte-Colony Stimulating Factor (G-CSF) to treat acute-on-chronic liver failure; results of the first multicenter randomized trial (GRAFT study)." In Abstracts of the British Association for the Study of the Liver Annual Meeting, 22–24 November 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-basl.10.

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PARK, SUN-HWA, and AREE MOON. "Abstract 5196: Granulocyte-colony stimulating factor (G-CSF) plays a causative role for H-Ras-mediated invasion and migration of human breast epithelial cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5196.

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Nakata, Koh, Takahito Nei, Shinya Urano, Natsuki Motoi, and Ryushi Tazawa. "Isotype Switch Of Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) Autoantibody Is Promoted In Autoimmune Pulmonary Alveolar Proteinosis." 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.a2345.

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Tazawa, Ryushi, Toru Arai, Toshinori Takada, Yasunori Kasahara, Yoshiko Tsuchihashi, Takahito Nei, Masayuki Hojo, et al. "Pulmonary Alveolar Proteinosis (PAP) And Inhaled Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) Therapy--Clinical Features Predicting Recurrence." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5794.

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Reports on the topic "Granulocyte colony stimulating factor (G-CSF)"

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Hou, Zhijin, Fangjie Jiang, Jie Yang, Liu Yang, Zha Hao, Xiaoling Yang, Bie Jia, and Yushi Meng. What is the impact of granulocyte colony-stimulating factor (G-CSF) in subcutaneous injection or intrauterine infusion and during both the fresh and frozen embryo transfer cycles on recurrent implantation failure: A systematic review and meta-analysis? INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0040.

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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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