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Dissertations / Theses on the topic 'Granulocyte-colony stimulating factor'

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Published: 4 June 2021

Last updated: 1 March 2023

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1

Somerville, Linda Elizabeth. "Granulocyte colony-stimulating factor : structure-function studies." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287428.

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2

Werner, Jorn Martin. "NMR studies of human granulocyte colony-stimulating factor." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242044.

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3

Devereux, Stephen. "Isoforms of the granulocyte : macrophage colony stimulating factor receptor." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402143.

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4

Vecchione, Anna. "Characterisation of recombinant equine granulocyte-macrophage colony stimulating factor." Thesis, Royal Veterinary College (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416369.

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5

Ghaban, Hadel. "Development of a long-acting granulocyte colony stimulating factor." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/20674/.

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6

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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7

Freeburn, Robin William. "Studies of the granulocyte-macrophage colony stimulating factor in leukaemia." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267717.

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8

Smith, Philip John. "Transcriptional regulation of granulocyte-macrophage colony-stimulating factor by glucocorticoids." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326062.

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9

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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10

Kojima, Seiji. "Use of granulocyte colony-stimulating factor for treatment of aplastic anemia." Nagoya University School of Medicine, 1999. http://hdl.handle.net/2237/5344.

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11

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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12

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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13

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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14

Chan, Chu-fung. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B40687284.

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15

Foley, Catherine. "Mathematical modeling for designing new treatment strategies with Granulocyte-Colony Stimulating Factor." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21947.

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Mathematical modeling can help providing better understanding of the nature and characteristics of regulatory processes in hematology. We first review different mathematical approaches used for modeling so-called dynamical hematological diseases, which are characterized by oscillations in one or more blood cell lines. Then, we present two delay differential equation (DDE) models of the hematopoietic system designed for the study of the effects of Granulocyte-Colony Stimulating Factor (G-CSF) administration. G-CSF is used clinically for treating subjects presenting low numbers of white blood cells, a condition referred to as neutropenia that can result from different causes. However, even though G-CSF is widely used in clinical practice, it is not clear whether the standard G-CSF administration schedule is optimal. The aim of this work is to study alternative treatment regimens that would optimize the use of G-CSF using a mathematical modeling approach. The first model we propose is a comprehensive model that considers G-CSF administration for cyclical neutropenia, a dynamical disorder characterized by oscillations in the circulating neutrophil count. The second model focuses on the effects of two recombinant forms of G-CSF (filgrastim and pegfilgrastim) for the treatment of chemotherapy-induced neutropenia. For each model, we use a combination of mathematical analysis and numerical simulations to study alternative G-CSF treatment regimens that would be efficient while reducing the amount of drug. We found that the dynamical properties of the model could be exploited for designing better G-CSF treatment strategies.
La modélisation mathématique est un outil qui permet d'obtenir une meilleure compréhension des différents processus de régulation en hématologie. Dans un premier temps, nous révisons différentes approches qui sont utilisées pour modéliser les maladies hématologiques dites dynamiques. Celles-ci sont caractérisées par la présence d'oscillations dans le niveau d'un ou de plusieurs types de cellules sanguines. Ensuite, nous présentons deux nouveaux modèles d'équations différentielles à délais (EED) du système hématopoïétique, qui sont dédiés à l'étude des effets de l'administration du granulocyte-colony stimulating factor (G-CSF). Le G-CSF est utilisé en pratique pour traiter les patients dont le niveau de globules blancs est faible, une condition appelée neutropénie, qui peut survenir dans plusieurs contextes. Cependant, même si le G-CSF est largement utilisé dans le milieu médical, il n'est pas clair que le protocole d'administration standard soit optimal. L'objectif de cette thèse est d'étudier des protocoles de traitement alternatifs qui optimiseraient l'utilisation du G-CSF en utilisant une approche de modélisation mathématique. Le premier modèle que nous proposons est un modèle qui inclut tous les types de cellules sanguines et qui considère l'administration du G-CSF dans le cas de la neutropénie cyclique, une maladie caractérisée par la présence d'oscillations dans le nombre de globules blancs, de plaquettes et de globules rouges. Dans le second modèle, nous nous intéressons aux effets de deux formes de G-CSF (filgrastim et pegfilgrastim) qui sont utilisés pour traiter la neutropénie qui survient fréquemment suite à la chimiothérapie. Pour chacun des modèles, nous utilisons une combinaison d'analyse mathématique et de simulations numériques pour étudier des traitements alternatifs de G-CSF qui seraient efficaces tout en réduisant la quantité de médicament utilisée. Nos résultats suggèrent que les pr

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16

McCracken, Sharon. "Granulocyte colony stimulating factor and its receptor at the maternal fetal interface." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298604.

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17

Chan, Chu-fung, and 陳柱峰. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40687284.

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18

Jeffery, Grahame Mark. "Immunological and receptor studies with recombinant human granulocyte-macrophage colony stimulating factor." Thesis, University of Southampton, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316432.

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19

Dwivedi, Pankaj. "Phosphoproteomics analysis of normal and malignant granulocyte-colony stimulating factor receptor signaling." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1530270360628733.

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20

Oishi, Akio. "Granulocyte colony stimulating factor protects retinal photoreceptor cells against light-induced damage." Kyoto University, 2009. http://hdl.handle.net/2433/124314.

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21

Freeley, Simon. "The role of complement and granulocyte colony stimulating factor in ANCA associated vasculitis." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-complement-and-granulocyte-colony-stimulating-factor-in-anca-associated-vasculitis(997a1669-beac-4225-8a9a-51afc5004276).html.

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Hieutrophil cytoplasmic antibody (ANCA) associated vasculitis is a systemic disease i affects the kidneys, lungs, and other tissues. ANCA were first described in patients i focal necrotising glomerulonephritis in 1982, with myeloperoxidase )) and proteinase 3 (PR3) subsequently shown to be the antigenic targets responsible rthe perinuclear and cytoplasmic staining patterns, respectively. Infection is thought to erbate disease partially through the production of the proinflammatory cytokine TNFot i primes neutrophils for respiratory burst. In this thesis, the role of another cytokine, Milocyte-colony stimulation factor (GCSF) is examined both in vitro and in vivo. Previous i have implicated the complement system in ANCA vasculitis. Furthermore, TNFot •d neutrophils which have been activated with ANCA in vitro are known to release a >r into the supernatant which causes complement activation in normal serum. This w has yet to be identified, although many candidates such as the alternative pathway aonent properdin have been suggested. In this work it is shown that GCSF antrations are elevated in patients with acute ANCA vasculitis and that GCSF can prime ted neutrophils for anti-MPO induced respiratory burst. A passive antibody transfer i model of anti-MPO vasculitis was established and GCSF administration was shown to te disease. Experiments also explored other models of anti-MPO vasculitis based •PO-deficient mice. The mouse model was also used to investigate the effect of icy of either properdin or MASP2 in disease. Using the passive anti-MPO passive Sr model, properdin deficiency was shown to have no effect on the extent of disease ! MASP2-deficiency exacerbated disease by a mechanism which has yet to be identified. iwork has established GCSF as a key cytokine and possible therapeutic target, and I novel observations on complement in ANCA vasculitis.

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22

Tremellen, Kelton Paul. "The immunoregulatory role of seminal plasma in early murine and human pregnancy /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09pht789.pdf.

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23

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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24

Prevost, Jay Michael. "Identification of the soluble granulocyte-macrophage colony stimulating factor receptor protein in vivo and development of a soluble model of the high-affinity cell surface receptor for granulocyte-macrophage colony stimulating factor." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0015/MQ52093.pdf.

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25

Chopra, Rajesh. "The expression and regulation of the granulocyte macrophage colony- stimulating factor receptor (GM-CSFR)." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362585.

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26

Bedford, Russell Alison Ruth. "The role of granulocyte colony-stimulating factor in augmenting human neonatal neutrophil host defence." Thesis, University of London, 2009. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518115.

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27

Hiraumi, Yoshimi. "Granulocyte colony-stimulating factor protects cardiac mitochondria in the early phase of cardiac injury." Kyoto University, 2009. http://hdl.handle.net/2433/126456.

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28

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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29

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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30

Chiou, Chuang-Jiun. "Expression of Granulocyte-Macrophage Colony-Stimulating Factor Gene in Insect Cells by a Baculovirus Vector." Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc798471/.

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The focus of this research is to describe the production and characterization of the human granulocyte-macrophage colony-stimulating factor (hGM-CSF) in insect cells, using Autographa californica buclear polyhedrosis virus (AcNPV) as an expression vector. All three forms of biological activity of hGM-CSF. Following N-glycanase treatment, the two glycosylated hGM-CSF proteins (15.5 and 16.5 KDa) which bound to Concanavalin A affinity column ran as a 14.5-15.5 KDa band on SDS-PAGE. Western blot analysis of expression in Sf9 cells treated with tunicamycin revealed only the presence of the 14.5 KDa species. The N-terminal amino acid sequence of the recombinant hGM-CSF was identical to that of natural hGM-CSF deduced from cDNA. These results demonstrate that baculovirus-produced hGM-CSF could be N-glycosylated in Sf9 cells, the signal peptide of recombinant hGM-CSF could be recognized and cleaved by infected insect cells and the resultant molecule secreted into the medium.

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31

Henriques, Alexandre. "Viral delivery of granulocyte-colony stimulating factor in a mouse model of amyotrophic lateral sclerosis." Strasbourg, 2010. http://www.theses.fr/2010STRA6261.

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La sclérose latérale amyotrophique (SLA) est une maladie neurodégénérative causée par la dégénérescence des neurones moteurs de la moelle épinière et du cortex moteur. Les causes de la pathologie restent mal connues et le seul traitement efficace connu ne prolonge la survie des patients que de quelques mois. Le G-CSF est un facteur de croissance avec des effets neuroprotecteurs et neurorégénérateurs, qui a un potentiel thérapeutique pour la SLA. L’administration chronique de facteurs de croissance vers le système nerveux central présente certaines difficultés en terme de biodistribution. La thérapie génique à base de vecteurs viraux, tels que les adeno-associated virus, permet de contourner ces difficultés. Pour étudier les potentiel thérapeutique du G-CSF dans la SLA, nous avons administré le G-CSF par thérapie génique dans un modèle murin de cette maladie, les souris SOD-1G93A. Nous avons montré que l’administration de vecteurs viraux codant pour le G-CSF a présenté de multiples bénéfices pour les souris SOD-1G93A. En effet, nous avons pu déterminer que ce traitement permet d’améliorer les capacités motrices des souris, de retarder la progression des symptômes, notamment les plus sévères comme la paralysie, mais surtout d’augmenter la survie des souris de 10%. Ces bénéfices sur les symptômes et la survie sont associé à un plus grand nombre de motoneurones après traitement (+50% de neurones moteurs en comparaison avec les souris contrôles). Nous avons également montré que ces effets étaient directement neuroprotecteur in vivo sur les neurones moteurs et montré que cet effet était vraisemblablement lié à une protection des jonctions neuromusculaires
Amyotrophic Lateral Sclerosis is a fatal disease characterized by muscular weakness, progressive atrophy and paralysis, caused by degeneration of motoneurons. The origin of the disease remains unknown and therapeutic options are limited for ALS patients. G-CSF is a growth factor with neuroprotective and regenerative properties in the CNS. Viral delivery of growth factors is a promising approach for chronic neurodegenerative diseases. The adeno-associated virus (AAV) allows a long-term and constant delivery of therapeutic proteins after a single injection. To determine whether G-CSF is a good drug candidate for ALS, we investigated its effects on a mouse model of ALS, the SOD-1G93A mouse. We injected the AAV vector coding for G-CSF in the spinal cord of SOD-1G93A mice. This injection leads to CNS-specific delivery of G-CSF, improves motor functions, and increases life expectancy by 10% for the SOD-1G93A mice. At a cellular level, G-CSF was able to reduce motoneuron degeneration in the spinal cord (+50% survival compared to the control group). We have also shown that the neuroprotective effects of G-CSF are direct on the motoneurons and that G-CSF preserves the neuromuscular junctions. Thus, AAV vector are a highly attractive delivery route for ALS patients and G-CSF is a promising candidate drug for a clinical trial in ALS

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32

Hunter, Melissa Piper. "Characterization of positive and negative signaling pathways activated by the granulocyte colony-stimulating factor receptor /." The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488195633518091.

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33

Schirmer, Stephan Henrik. "Circulating cells and cytokines in arteriogenesis." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2008. http://dare.uva.nl/document/115099.

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34

Eischen, Alice. "Differenciation des monocytes humains en macrophages." Strasbourg 1, 1995. http://www.theses.fr/1995STR1M402.

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35

Alli, Zaman. "Expression of biologically active human granulocyte macrophage colony stimulating factor in the seeds of transgenic tobacco." Thesis, University of Ottawa (Canada), 2001. http://hdl.handle.net/10393/9046.

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The feasibility of producing recombinant (rt) and biologically active granulocyte-macrophage colony stimulating factor (GM-CSF) in the seeds of transgenic tobacco plants was investigated. The rice seed-specific glutelin promoter (Gt1) was used to direct the expression of the human (h) GM-CSF coding sequence in tobacco seeds. Transgenic tobacco plants producing rthGM-CSF were compared in biological assays with tobacco plants expressing a glutelin/rthGM-CSF fusion protein, driven by the Gt3 promoter. The T7 Sequencing kit from Pharmacia was used to sequence and confirm the authenticity of the Gt1 expression construct. The glutelin-1 signal sequence was fused in the correct orientation to the hGM-CSF cDNA. The rthGM-CSF expression cassette (2.5 kb) was subcloned in a plant binary vector pRD400, which contained a kanamycin resistance gene. The pRD400 vector containing the 2.5 kb construct was used to transform Agrobacterium tumefaciens cells. Tobacco (Nicotiana tabacum cv. Xanthi) leaf sections were transformed by A. tumefaciens carrying the complete 2.5 kb construct. (Abstract shortened by UMI.)

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36

Rahmati, Mona. "Granulocyte-Colony Stimulating Factor and Embryo Implantation Process : Effects on Human Endometrium and on Murine Abortion Prone Model CBA/J x DBA/2." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T048/document.

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L’immunologie de la reproduction englobe les principes de l’immunologie générale et les aspects spécifiques de la reproduction et du développement. Les Colony Stimulating Factors (CSFs) sont une illustration de l'application médicale de ce domaine. Dans la famille des CSFs, le Granulocyte-Colony Stimulating Factor (G-CSF) apparaît aujourd'hui comme une thérapie innovante dans divers cas d'échec de la reproduction, bien que ses cibles et ses effets ne soient pas encore clairement établis. Dans ce travail, à travers une revue sur les CSFs dans la reproduction, une étude consacrée aux gènes cibles du G-CSF dans l'endomètre humain, et une étude consacrée aux effets de la supplémentation systémique en G-CSF sur l’implantation embryonnaire murine, nous avons essayé d'approcher certains mécanismes d'action possibles pour cette cytokine. Dans les modèles murins fertiles et pro-abortifs, la supplémentation systémique en G-CSF, ciblant spécifiquement l’endomètre préimplantatoire, modifie les taux d’implantation embryonnaire. Dans l’endomètre humain, certaines dérégulations préimplantatoires de gènes cibles du G-CSF ont également été observées chez les patients infertiles. L'influence du G-CSF sur ces gènes cibles a été également illustrée dans un modèle ex-vivo de culture endométriale. Ces cibles dont l’expression est influencée par le G-CSF sont décrites comme des molécules clés dans le processus implantatoire, intervenant sur l’adhésion embryonnaire, la migration cellulaire, le remodelage des tissus et l'angiogenèse locale. Ces données suggèrent des possibilités de diagnostic préventif et pré-conceptionnel de certains échecs de reproduction, considérés jusqu’à maintenant comme idiopathiques, et de thérapies innovantes orientées, afin d’optimiser la réceptivité du biosenseur endométrial afin de permettre une implantation embryonnaire harmonieuse et une grossesse évolutive
Reproductive Immunology involves general immunology principles and special aspects of reproduction and development. Colony Stimulating Factors (CSFs) are an illustration of the medical application of this domain. In the CSF family, Granulocyte-Colony Stimulating Factor (G-CSF) appears today as a promising therapy in various cases of reproductive failure although its targets and effects are not clearly established. In this work, through a review on CSFs in reproduction, a study dedicated to human endometrial targets of G-CSF, and a study dedicated to systemic G-CSF supplementation effects on murine embryo implantation, we tried to approach some possible mechanisms of action of this cytokine. In the considered non-abortive and abortion-prone murine models, the timed systemic G-CSF supplementation, targeting specifically the pre implantation endometrium, influenced the embryo implantation process. Some pre conceptual human endometrial dysregulations of G-CSF target genes were also observed in infertile patients. The endometrial influence of G-CSF on these target genes was also illustrated in an ex-vivo model. These molecules under G-CSF influence are described as critically involved in embryo implantation process, by influencing embryo adhesion, cell migration, tissue remodelling and angiogenesis. These data suggest possible pre-conceptual preventive diagnosis of such reproductive failures and future orientated therapies to optimise the endometrial biosensor and the further embryo implantation and ongoing pregnancy

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37

Warby, Tammra. "Interactions between granulocyte-macrophage colony-stimulating factor and human monocyte-derived macrophages following infection with HIV-1 /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19318.pdf.

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38

Eapen, Abey. "Recombinant human granulocyte colony stimulating factor for unexplained recurrent miscarriage : a randomised placebo controlled multi-centre study." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8297/.

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Immune mediated mechanisms are thought to contribute to recurrent pregnancy losses. A number of treatment options with limited evidence are being used in clinical practice to treat women with recurrent miscarriages. The objectives of this thesis was a. To summarise the available evidence for granulocyte colony stimulating factor (G-CSF) in reproductive medicine. b. To perform a randomised controlled study (RCT) to evaluate the efficacy and safety of recombinant human granulocyte colony stimulating factor (rhG-CSF) in women with unexplained recurrent miscarriages. The main conclusions from this thesis are: a. The systematic narrative review found that available evidence is of poor quality, but suggestive of benefit with granulocyte colony stimulating factor in women with recurrent miscarriages. b. The RCT concluded that administration of rhG-CSF does not improve pregnancy outcomes among women with a history of unexplained recurrent miscarriages. RhG-CSF appears to be safe for both mothers and their offspring/s.

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39

Jacobi, Stella Nadine [Verfasser]. "Der Einsatz von Granulocyte-Colony Stimulating Factor zur Behandlung der diastolischen Funktionsstörung im Mausmodell / Stella Nadine Jacobi." Gießen : Universitätsbibliothek, 2021. http://d-nb.info/1230476180/34.

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40

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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41

Aram, Jehan Jalal. "Granulocyte-macrophage colony-stimulating factor : expression and regulation in human immune responses with relevance to multiple sclerosis." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/48853/.

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Background: Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) is a haematopoietic growth factor and a pro-inflammatory cytokine produced by T cells and other immune cells. Recent evidence suggests that GM-CSF plays an important role in multiple sclerosis (MS) pathogenesis. Few recent studies have detected GM-CSF expression by immune cells in MS. In this thesis, the expression of GM-CSF and its receptor by different subtypes of peripheral blood mononuclear cells (PBMCs) in MS was investigated. In addition, GM-CSF regulation was studied in the above-mentioned cells in MS. Finally, GM-CSF neutralization was performed in a phase Ib clinical trial, and some immune-related effects were investigated. Aims: To evaluate the expression of GM-CSF and its receptor by PBMC subsets in MS; to determine the key factors regulating their expression by PBMC subsets in MS; to detect the differentiation of helper T cells producing GM-CSF (Th-GM) in MS patients, and to detect the frequency of immune cells after GM-CSF neutralization in MS in vivo. Subjects and Methods: Patients were mainly untreated relapsing-remitting MS (RRMS) during remission stage, and some were MS patients during a relapse. Healthy controls were also enrolled. All subjects consented to participation in the study before donating peripheral blood. PBMCs were isolated using Ficoll density gradient centrifugation. Flow cytometry and q-PCR were used to detect the expression of GM-CSF and its receptor. Multiplex bead assay was used to quantify GM-CSF with other pro-inflammatory and anti-inflammatory cytokines. Results: The frequency of stimulated GM-CSF-expressing cells (helper T (Th), cytotoxic T (Tc), monocytes, NK cells, and B cells) is significantly higher in the mixed PBMC population of untreated RRMS patients when compared to healthy volunteers. The frequency of Th1 cells expressing GM-CSF was higher in MS patients than healthy controls. The expression of GM-CSF by isolated and stimulated NK cells was not different in MS patients and controls. PBMC culture supernatants were shown to contain significantly higher concentrations of IL-2, IL-12, IL-1β, and GM-CSF in MS patients than controls. Blocking IL-2 and IL-12 significantly reduced GM-CSF expression by Tc, NK, and B cells in MS patients, but not in healthy controls. MS patients during relapse had significantly higher frequency of Th-GM (CD3+CD8-IL-17-IFN-γ-IL-3+GM-CSF+) cells than healthy controls. EBV infected B cells expressed GM-CSF receptor in less frequency than non-infected B cells. In vivo GM-CSF neutralization in MS patients resulted in significant reduction in the frequency of CD8+ T cells and CD4+CD45RA+CD25++ (naïve) Tregs and an increase in CD4+CD35+foxp3 (total) Tregs. Conclusions: Th1 (and Th in general), Tc, monocytes, NK and B cells are all high producers of GM-CSF in MS. IL-2 and IL-12 are the main regulators of GM-CSF expression by Tc, NK, and B cells in MS patients. GM-CSF and its receptor may not be major survival or proliferation factors for EBV infected B cells. The newly identified Th-GM cells were detected in higher frequency in MS patients during relapse, which may suggest a new source for GM-CSF production in MS. The recent safety, tolerability, and immune-related results of GM-CSF neutralization in MS are encouraging. Therefore, GM-CSF is a potential therapeutic target in MS.

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LICARI, VERONIQUE. "Maladie de kaposi localisee chez un sujet hiv negatif : action antitumorale du gm-csf." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20131.

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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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Wiik, H. (Heikki). "Inflammatory response following abdominal surgery and its modulation by recombinant human granulocyte colony-stimulating factor (rhG-CSF, filgrastim)." Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514268474.

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Abstract The effects of perioperative filgrastim (rhG-CSF) and surgery per se on the postoperative acute phase reaction were studied by assessing leukocyte functions, cytokine levels and tenascin-C (Tn-C) and procollagen propeptide (PINP, PIIINP) concentrations in different body fluid compartments in patients undergoing gastrointestinal surgery. Thirty consecutive patients were randomized to receive either filgrastim or placebo for five days, starting 12 hours before colorectal surgery. Filgrastim treatment led to marked neutrophilia with decreased neutrophil migration in peripheral blood but not in peritoneal fluid 48 hours postoperatively. Neutrophil phagocytosis and bacterial killing did not differ between the groups. Filgrastim caused increased postoperative expression of neutrophil CD11b/CD18 in blood but not in peritoneal fluid or wound fluid. CD11b/CD18 expression was higher in both wound fluid and peritoneal fluid than in blood in the placebo group. The expression of neutrophil CD62L was higher in blood than in peritoneal fluid or wound fluid in both groups. The serum concentration of interleukin (IL)-8 was lower in the filgrastim group 5 hours postoperatively. The concentrations of IL-1β, IL-6, transforming growth factor (TGF)-β and IL-10 did not differ between the groups. The cytokine levels were markedly higher locally in the wound and in the peritoneal cavity compared to circulating blood. No adverse events attributable to filgrastim were seen. Leukocyte counts, neutrophil and monocyte functions and the levels of IL-6, IL-8 and granulocyte colony-stimulating factor (G-CSF) were measured from 18 patients before and after colorectal surgery. Surgery caused an increase in neutrophil and monocyte counts along with lymphocytopenia. Neutrophil phagocytosis was decreased 4 and 24 hours postoperatively, but normalized after that. A distinct systemic cytokine response was seen postoperatively. In a study with 24 patients, Tn-C concentration increased in wound fluid during the first postoperative week after abdominal surgery. The Tn-C level was markedly higher in wound fluid than in serum.

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Krieger, Markus [Verfasser], and Stephan [Akademischer Betreuer] Frings. "THE HEMATOPOIETIC CYTOKINE GRANULOCYTE-MACROPHAGE COLONY STIMULATING FACTOR IS INVOLVED IN COGNITIVE PROCESSING / Markus Krieger ; Betreuer: Stephan Frings." Heidelberg : Universitätsbibliothek Heidelberg, 2011. http://d-nb.info/1179782526/34.

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46

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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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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Farrell, Lindi. "Use of Recombinant Human Granulocyte Colony Stimulating Factor as an Adjunct in Antifungal Chemotherapy in Various Animal Model Systems." DigitalCommons@USU, 1995. https://digitalcommons.usu.edu/etd/3914.

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The growing neutropenic patient population provides an ideal target for opportunistic fungal infections. Several effective antifungal drugs are toxic at high doses and contraindicated for long-term treatment. Recombinant human granulocyte colony stimulating factor (rhG-CSF) has been shown to increase neutrophilic numbers and functions, thus providing enhanced host defense. Improved efficacy by using rhG-CSF in conjunction with various antifungal agents was the primary focus of these studies. Use of rhG-CSF in a murine model of vaginal candidiasis did not reduce vaginal colony counts, or improve vaginal histophathology scores. Administration of rhG-CSF in a murine model of pulmonary aspergillosis improved survival, clinical signs, and gross pathology and histophathology scores of the lungs, and increased weight gain. The rhG-CSF was not shown to be an effective therapeutic treatment in this model of vaginal candidiasis. The rhG-CSF was, however, an effective prophylactic treatment in this model of pulmonary aspergillosis.

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Al-Shami, Amin. "Granulocyte-macrophage colony-stimulating factor-activated signaling pathways in human neutrophils, the mechanism of activation of phosphatidylinositol 3-kinase." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ36223.pdf.

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Williams, Marc Adrian. "A study of granulocyte-macrophage colony stimulating factor and the immunological function of the monocyte against malignancy and infection." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367835.

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