Relevant bibliographies by topics / Degranulation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Degranulation'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 June 2025

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Journal articles on the topic "Degranulation"

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Dvorak, A. M., R. A. Monahan-Earley, H. F. Dvorak, and S. J. Galli. "Ultrastructural cytochemical and autoradiographic demonstration of nonspecific esterase(s) in guinea pig basophils." Journal of Histochemistry & Cytochemistry 35, no. 3 (1987): 351–60. http://dx.doi.org/10.1177/35.3.3819377.

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We used ultrastructural autoradiographic and cytochemical methods to localize esterase activities in unstimulated guinea pig basophils and in basophils undergoing degranulation or recovery from degranulation. We used tritium-labeled diisopropylfluorophosphate (DFP) as a probe for serine enzymes and localized this probe by ultrastructural autoradiography to cytoplasmic granules of immature or mature unstimulated basophils, as well as to granules released by degranulating basophils. Ultrastructural cytochemistry using alpha naphthyl acetate (ANA) as substrate localized nonspecific esterase activity to extruded granules, either within the interiors of degranulation sacs or within granules completely separated from degranulating basophils. Extruded granules retained their esterase activity for as long as 24 hr after antigen-induced degranulation. The plasma membranes of unstimulated or degranulating basophils, as well as of basophils recovering from degranulation, displayed prominent cell surface ANA esterase ectoenzyme activity. Lipid bodies, organelles present in the cytoplasm of both control and recovering basophils, were also alpha naphthyl acetate esterase (ANAE)-positive. Thus, cytochemical and autoradiographic techniques localized esterase and/or [3H]-DFP-binding activities to cytoplasmic granules, lipid bodies, and cell surface of basophils, and these enzyme activities persisted during both degranulation and recovery from degranulation.
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Gan, Xiaoliang, Dandan Xing, Guangjie Su, et al. "Propofol Attenuates Small Intestinal Ischemia Reperfusion Injury through Inhibiting NADPH Oxidase Mediated Mast Cell Activation." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/167014.

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Both oxidative stress and mast cell (MC) degranulation participate in the process of small intestinal ischemia reperfusion (IIR) injury, and oxidative stress induces MC degranulation. Propofol, an anesthetic with antioxidant property, can attenuate IIR injury. We postulated that propofol can protect against IIR injury by inhibiting oxidative stress subsequent from NADPH oxidase mediated MC activation. Cultured RBL-2H3 cells were pretreated with antioxidant N-acetylcysteine (NAC) or propofol and subjected to hydrogen peroxide (H2O2) stimulation without or with MC degranulator compound 48/80 (CP). H2O2significantly increased cells degranulation, which was abolished by NAC or propofol. MC degranulation by CP further aggravated H2O2induced cell degranulation of small intestinal epithelial cell, IEC-6 cells, stimulated by tryptase. Rats subjected to IIR showed significant increases in cellular injury and elevations of NADPH oxidase subunits p47phoxand gp91phoxprotein expression, increases of the specific lipid peroxidation product 15-F2t-Isoprostane and interleukin-6, and reductions in superoxide dismutase activity with concomitant enhancements in tryptase andβ-hexosaminidase. MC degranulation by CP further aggravated IIR injury. And all these changes were attenuated by NAC or propofol pretreatment, which also abrogated CP-mediated exacerbation of IIR injury. It is concluded that pretreatment of propofol confers protection against IIR injury by suppressing NADPH oxidase mediated MC activation.
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Li, Wen-Wu, Tian-Zhi Guo, De-yong Liang, Yuan Sun, Wade S. Kingery, and J. David Clark. "Substance P Signaling Controls Mast Cell Activation, Degranulation, and Nociceptive Sensitization in a Rat Fracture Model of Complex Regional Pain Syndrome." Anesthesiology 116, no. 4 (2012): 882–95. http://dx.doi.org/10.1097/aln.0b013e31824bb303.

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Background Patients with complex regional pain syndrome have increased tryptase in the skin of the affected extremity indicating mast cell (MC) accumulation and degranulation, processes known to be mediated by substance P (SP). The dysregulation of SP release from primary afferent neurons is characteristic of complex regional pain syndrome. The authors hypothesized that SP acting through the neurokinin-1 receptor results in mast cell accumulation, degranulation, and nociceptive sensitization in a rat model of complex regional pain syndrome. Methods Groups of 6-10 rats underwent tibia fracture and hind limb casting for 4 weeks, and the hind paw skin was harvested for histologic and immunohistochemical analysis. The effects of a selective neurokinin-1 receptor antagonist (LY303870) and of direct SP intraplantar injection were measured. Dermal MC degranulation induced by sciatic nerve stimulation and the effects of LY303870 on this process were investigated. Finally, the antinociceptive effects of acute and chronic treatment with a MC degranulator (48/80) were tested. Results The authors observed that fracture caused MC accumulation, activation, and degranulation, which were inhibited by LY303870; the percentage of MCs in close proximity to peptidergic nerve fibers increased after fracture; electrical stimulation caused MC activation and degranulation, which was blocked by LY303870; intraplantar SP-induced MC degranulation and acute administration of 48/80 caused MC degranulation and enhanced postfracture nociception, but MC-depleted animals showed less sensitization. Conclusions These results indicate that facilitated peptidergic neuron-MC signaling after fracture can cause MC accumulation, activation, and degranulation in the injured limb, resulting in nociceptive sensitization.
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Marshall, J. S., R. H. Stead, C. McSharry, L. Nielsen, and J. Bienenstock. "The role of mast cell degranulation products in mast cell hyperplasia. I. Mechanism of action of nerve growth factor." Journal of Immunology 144, no. 5 (1990): 1886–92. http://dx.doi.org/10.4049/jimmunol.144.5.1886.

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Abstract A variety of mast cell degranulating agents have previously been shown to induce mast cell hyperplasia in adult rats. In neonates 2.5 S nerve growth factor (NGF) induces a hyperplasia of both mucosal and connective tissue mast cells (MMC and CTMC). We have examined the role of the potent mast cell degranulating properties of NGF on its ability to induce mast cell hyperplasia. Administration of NGF in combination with the mast cell stabilizing agent disodium cromoglycate was found to abrogate the CTMC hyperplasia induced by NGF alone. Treatment of neonatal rats with the alternate degranulating agent compound 48/80 was found to induce a limited CTMC but not a MMC hyperplasia. A supernatant obtained by degranulating purified adult rat peritoneal mast cells with anti-IgE was found to induce hyperplasia of the CTMC population similar to that observed with NGF administration. However, this degranulation product supernatant only induced a limited MMC hyperplasia as judged by RMCP II content of the tissues. These results suggest that NGF has dual action inducing mast cell hyperplasia; CTMC hyperplasia being dependent on the ability of NGF to degranulate mast cells. MMC hyperplasia induced by NGF is independent of CTMC degranulation. Degranulation products from peritoneal mast cells act to increase both MMC and CTMC populations in the neonate. These data suggest that the CTMC population may be regulated by an autocrine positive feedback mechanism in vivo.
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Bhakta, Suhani B., Stefan M. Lundgren, Bethany N. Sesti, et al. "Neutrophil-like cells derived from the HL-60 cell-line as a genetically-tractable model for neutrophil degranulation." PLOS ONE 19, no. 2 (2024): e0297758. http://dx.doi.org/10.1371/journal.pone.0297758.

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Research on neutrophil biology has been limited by the short life span and limited genetic manipulability of these cells, driving the need for representative and efficient model cell lines. The promyelocytic cell line HL-60 and its subline PLB-985 can be differentiated into neutrophil-like cells (NLCs) and have been used to study neutrophil functions including chemotaxis, phagocytosis, endocytosis, and degranulation. Compared to neutrophils derived from hematopoietic stem cells, NLCs serve as a cost-effective neutrophil model. NLCs derived from both HL-60 and PLB-985 cells have been shown to perform degranulation, an important neutrophil function. However, no study has directly compared the two lines as models for degranulation including their release of different types of mobilizable organelles. Furthermore, Nutridoma, a commercially available supplement, has recently been shown to improve the chemotaxis, phagocytosis, and oxidative burst abilities of NLCs derived from promyelocytic cells, however it is unknown whether this reagent also improves the degranulation ability of NLCs. Here, we show that NLCs derived from both HL-60 and PLB-985 cells are capable of degranulating, with each showing markers for the release of multiple types of secretory organelles, including primary granules. We also show that differentiating HL-60 cells using Nutridoma does not enhance their degranulation activity over NLCs differentiated using Dimethyl Sulfoxide (DMSO) plus Granulocyte-colony stimulating factor (G-CSF). Finally, we show that promyelocytic cells can be genetically engineered and differentiated using these methods, to yield NLCs with a defect in degranulation. Our results indicate that both cell lines serve as effective models for investigating the mechanisms of neutrophil degranulation, which can advance our understanding of the roles of neutrophils in inflammation and immunity.
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Kilinc, E., Y. Dagistan, B. Kotan, and A. Cetinkaya. "Effects of Nigella sativa seeds and certain species of fungi extracts on number and activation of dural mast cells in rats." Physiology International 104, no. 1 (2017): 15–24. http://dx.doi.org/10.1556/2060.104.2017.1.8.

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In this study, we aimed to investigate the effects of Nigella sativa seeds and certain species of fungi extracts on the number and degranulation states of dural mast cells in rats. Rats were fed ad libitum with normal tap water or tap water with extract of N. sativa seed, Ramaria condensata, Lactarius salmonicolor, Lactarius piperatus, and Tricholoma terreum for 3 days. Mast cells in dura mater were counted and evaluated in terms of granulation and degranulation states. Compound 48/80, a mast cell degranulating agent, and T. terreum significantly increased the percent of degranulated mast cells in dura mater, respectively (p < 0.01 and p < 0.05). Moreover, T. terreum causes a significant increase in the total number of mast cells (p < 0.05). N. sativa significantly inhibited mast cell degranulation induced by both the compound 48/80 and T. terreum (p < 0.05), and significantly decreased the mast cell numbers increased by T. terreum (p < 0.05). Our results suggested that T. terreum following ingestion can contribute to headaches like migraine via dural mast cell degranulation and N. sativa may be able to exert analgesic and anti-inflammatory effects by stabilizing dural mast cells. However, investigation is needed to determine the ingredients of N. sativa that may be responsible for these beneficial effects.
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Baehner, Robert L., and Morris J. Karnovsky. "Degranulation deconstructed." Journal of Clinical Investigation 122, no. 5 (2012): 1596–97. http://dx.doi.org/10.1172/jci62990.

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Solomkin, Joseph S. "Degranulation Inhibition." Archives of Surgery 121, no. 1 (1986): 77. http://dx.doi.org/10.1001/archsurg.1986.01400010083011.

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Bansal, Geetanjali, Zhihui Xie, and Kirk Druey. "Rgs13 inhibits IgE-mediated allergic responses (37.5)." Journal of Immunology 178, no. 1_Supplement (2007): S19. http://dx.doi.org/10.4049/jimmunol.178.supp.37.5.

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Abstract Mast cells (MCs) evoke immediate hypersensitivity by degranulating in response to antigen (Ag) exposure and releasing preformed mediators such as histamine and leukotreines. Classically, the high affinity immune receptor for immunoglobulin E (FcεRI) mediates MC degranulation and anaphylaxis in response to antigen. In addition, various G protein coupled receptors (GPCRs) on MCs such as those for adenosine and sphingosine-1-phosphate (S1P) may also activate MCs. Since GPCR signaling is inhibited by Regulator of G protein Signaling (RGS) proteins, we studied the potential regulation of MC activation by RGS proteins. We identified Rgs1, 8, 13 and 18 in murine bone marrow-derived MCs (BMMCs). Rgs13−/− (KO) mice with LacZ knock-in were generated. Surprisingly, G protein-mediated degranulation induced by either adenosine or S1P was similar in WT and KO mice. In contrast, IgE/Ag -dependent degranulation and intracellular Ca++ flux as well as in vivo passive cutaneous anaphylaxis responses were significantly higher in KO BMMCs suggesting that Rgs13 affects IgE/Ag dependent pathway rather that GPCR-mediated pathway leading to MC activation. Reconstitution of KO BMMCs with WT Rgs13 inhibited degranulation to IgE/Ag. Analysis of effectors downstream of FcεRI revealed that Rgs13 interacts with PI3K and inhibits its activation in response to IgE/Ag. Thus, Rgs13 could represent a new therapeutic target for MC-dependent allergic responses. Work was funded by DIR, NIAID/NIH.
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Kaur, Gunjanpreet, Nirmal Singh, and Amteshwar Singh Jaggi. "Mast cells in neuropathic pain: an increasing spectrum of their involvement in pathophysiology." Reviews in the Neurosciences 28, no. 7 (2017): 759–66. http://dx.doi.org/10.1515/revneuro-2017-0007.

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AbstractMast cells are immunological cells that are diversely distributed in different parts of the body. Their role in various pathological conditions such as hypersensitivity, atherosclerosis, pulmonary hypertension, and male infertility has been reported by different scientists. Apart from these, a number of studies have shown their important role in pathogenesis of neuropathic pain of diverse aetiology. They have been found to release active mediators, primarily histamine and serotonin on degranulation in response to different stimuli including chemical, nerve damage, toxin or disease-related conditions. The mast cells stabilizer has shown pain attenuating effects by preventing degranulation of mast cells. Similarly, compound 48/80 (first dose 200 μg/100 g and after 6-h interval, second dose of 500 μg/100 g) caused the degranulation of the accumulated endoneurial histamine and 5-HT antagonists have shown pain relieving effects by attenuating the effects of histamine and serotonin, respectively. On the other hand, the mast cell degranulator compound 48/80 has shown dual action depending on its time of administration. The present review discusses the critical role of mast cells in the generation and maintenance of neuropathic pain in experimental models.
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Dissertations / Theses on the topic "Degranulation"

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Hoenderdos, Kim. "Modulation of neutrophil degranulation by hypoxia." Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/247459.

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Neutrophils are key effector cells of the innate immune system. They employ a number of powerful ‘weapons’ to eliminate pathogens, including an array of destructive proteins packaged into distinctive granule subsets. In addition to their microbicidal activity, these granule proteins are capable of causing substantial tissue damage if inappropriately deployed. To mitigate against this possibility, most physiological stimuli induce minimal extracellular degranulation. Sites of inflammation and infection are usually hypoxic, and it has been shown that oxygen depletion compromises neutrophil function by impairing the generation of reactive oxygen species and hence bacterial killing. The key finding reported in this thesis is that hypoxia substantially increases the release of all neutrophil granule subsets, as measured by the release of (active) hallmark proteins (elastase, myeloperoxidase, lactoferrin and matrix metalloproteinase-9). In consequence, supernatants from hypoxic neutrophils induced substantially more damage to lung epithelial cell layers than supernatants from neutrophils cultured under normoxic conditions; this damage was protein- and protease-dependent. This pattern of damage was seen consistently across lung adenocarcinoma-derived epithelial cells, primary immortalised lung epithelial cells, and primary human bronchial epithelial cells grown in physiological air-liquid interface culture. Surprisingly, the mechanism of hypoxia-augmented degranulation was found to be independent of protein synthesis and specifically, of the transcription factor HIF-1α (the ‘master-regulator’ of hypoxic responses); thus, hypoxia did not affect mRNA transcript or protein abundance of the major granule components, and hypoxia mimetics failed to recapitulate the phenotype. Inhibition of the key pathways known to be involved in neutrophil degranulation, including, phosphatidylinositol 3-kinase and phospholipase C, but not calcium flux prevented augmented granule release under hypoxia In conclusion, hypoxia induces a destructive neutrophil phenotype, with increased release of multiple histotoxic proteases. This may contribute to tissue injury and disease pathogenesis in a range of clinically important conditions.
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Admiraal, Claudia Johanna. "Eosinophil degranulation as an allergy activation marker." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/59048.

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Dexter, Emily Jane. "The role of adenosine in mast cell degranulation." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314292.

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Swindle, Emily Jane. "Mast cells as a source and target for nitric oxide and reactive oxygen species." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269602.

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Zankl, Claudia. "Stereoselektive Synthese von Sphingolipiden zur Inhibierung der Degranulation von Mastzellen." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2009. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-23408.

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Die Degranulation von Mastzellen soll durch Glycosphingolipide, welche mit der Zellmembran wechselwirken inhibiert werden. Der Sphingosingrundkörper wurde in zehn-stufigen Synthese ausgehend von N-Boc-Serin, aufgebaut. Die anschließende Glycosylierung erfolgte nach der Trichloracetimidatmethode in sehr guten Ausbeuten und stellte den Schlüsselschritt dar. Durch die Variation von unter Anderem der Amidseitenkette, der Glycosylkopfgruppe und des Sphingosingrundkörpers wurde eine Vielzahl an Derivaten für das Screening im Degranulationsassay bereitgestellt<br>The present dissertation covers the synthesis of glycosphingolipids which interact with the cell membrane in order to inhibit the degranulation of mast cells. The sphingosin body was synthesized in ten steps starting from N-Boc-Serin. The key step, the glycosylation was achieved using the trichloracetimidat method. The variation of the amid sidechain, the gylcosyl headgroup and the sphingosin body created a number of derivatives that were tested in the degranulation assay
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Foweraker, J. E. "A study of eosinophil granule proteins and in vitro degranulation." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377204.

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Sinniah, Ajantha. "Annexin A1 as an endogenous regulator of mast cell degranulation." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/9089.

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Annexin A1 (Anx-A1) is a 37kDa protein that is secreted by some cells in response to glucocorticoids (GCs) and which mediates several of their acute anti-inflammatory effects. In addition to GCs, ‘mast cell stabilising’ cromones such as nedocromil also mobilise Anx-A1 by promoting its phosphorylation by protein kinase C (PKC) and hence its secretion, which explains their acute efficacy as anti-allergic agents. This thesis addresses a fundamental aspect of Anx-A1 in the actions of anti-allergic drugs. In this study, anti-allergic drugs such as H1 antagonists, mast cell stabilisers and ‘dual action’ drugs were first tested for their ability to enhance Anx-A1 phosphorylation in a model system using U937 cells. Biochemical and immuno-fluorescent techniques were used to study the mechanisms by which these drugs suppress mediator release from cord blood derived mast cells (CDMCs) and murine bone-marrow derived mast cells (BMDMCs) from wild type and Anx-A1 null-mice. This thesis suggest that PKC activation is crucial for Anx-A1 export in mast cells and nedocromil in the presence of dexamethasone, prolongs the duration of PKC activation and subsequently phosphorylation, externalisation and release of Anx-A1 from CDMCs. The ability of nedocromil to inhibit β-hexosaminidase, tryptase, histamine and PGD2 release are dependent on Anx-A1 in CDMCs. Interestingly, ketotifen, a ‘dual action’ drug possesses a similar pharmacological profile to nedocromil, but not promethazine, which does not act through the Anx-A1 release. Strong evidence supports the notion that the mechanisms of action of nedocromil are modulated by Anx-A1, thus the possibility that FPR2 might be involved in the acute actions of nedocromil was tested. Nedocromil inhibits the release of PGD2 through the activation of FPR2 but not the inhibition of histamine release. A possible explanation for this finding could be that Anx-A1 might be interacting with other FPR family members to exert the histamine inhibitory effects. Although only a small subset of the downstream intracellular signaling pathway of MAPK was tested, the results indicate that Anx-A1 differentially regulates the activation of p38 and JNK in CDMCs treated with nedocromil. These findings indicate a novel model system in which Anx-A1 mediates the pharmacological actions of anti-allergic drugs and thus has an important role in preventing the mast cell degranulation.
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El-Lati, Suhad George. "Morphological and biochemical aspects of degranulation of human skin mast cells." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316384.

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Biethahn, Katharina [Verfasser]. "Regulation of Fc epsilon receptor I-mediated mast cell degranulation / Katharina Biethahn." Kiel : Universitätsbibliothek Kiel, 2011. http://d-nb.info/1043358471/34.

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HADJADJ, BADRE. "Modelisation de la degranulation des basophiles humains et etude du controle optimal." Paris 6, 1994. http://www.theses.fr/1994PA066385.

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L'objectif de notre travail consiste a proposer des modeles mathematiques associes aux phenomenes de la degranulation des basophiles humains et de la liberation de l'histamine, puis a elaborer des techniques pour un controle optimal du systeme. Cela nous permet d'etudier l'effet de hautes dilutions sur ce systeme. Dans le chapitre 1 nous avons etabli un modele de simulation representant le phenomene en fonction des dilutions homeopathiques. Dans le chapitre 2 nous avons etudie un modele compartimental lineaire tres simplifie puis nous avons introduit un controle optimal. Dans le chapitre 3 un autre modele compartimental a ete propose qui prend en compte le phenomene du retro-controle negatif de l'histamine (feed-back). Puis a nouveau nous avons etudie le controle optimal du systeme. Finalement dans le chapitre 4 nous avons etudie et applique une methode decompositionnelle, dite technique d'adomian, sur les deux systemes differentiels associes aux modeles compartimentaux etudies
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Books on the topic "Degranulation"

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Dvorak, Ann M. Basophil and Mast Cell Degranulation and Recovery. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9525-7.

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Dvorak, Ann M. Basophil and mast cell degranulation and recovery. Plenum Press, 1991.

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Kühr, Joachim. Degranulation basophiler Leukozyten als Parameter bei allergischen Kindern. [s.n.], 1987.

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Geen, Jonathan L. The human basophil degranulation test as a method for the investigation of high dilution phenomena. National Library of Canada, 1990.

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Dvorak, Ann M. Basophil and Mast Cell Degranulation and Recovery. Springer, 2013.

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Dvorak, Ann M. Basophil and Mast Cell Degranulation and Recovery. Springer London, Limited, 2013.

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Richter, Johan. Cytokine-induced degranulation in human neutrophils: Role of cytosolic free calcium and leukocyte adhesion molecules. 1991.

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Kiel, Universität, ed. Untersuchungen zur chemotaktischen Aktivität und Degranulation neutrophiler Granulozyten durch Interleukin-8 und andere Chemotaxine bei entzündlichen Erkrankungen. 1999.

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Rustemeyer, Martina. Vergleichende Beurteilung des neuen Humanen Basophilen Degranulations-Tests (HBDT) mit dem Intracutantest und Radio-Allergo-Sorbens-Test (RAST) bei Insektengiftallergikern. 1989.

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Book chapters on the topic "Degranulation"

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Gooch, Jan W. "Degranulation." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13529.

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Renz, H., and B. Gierten. "Basophilen-Degranulation." In Springer Reference Medizin. Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_495.

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Renz, H., and B. Gierten. "Basophilen-Degranulation." In Lexikon der Medizinischen Laboratoriumsdiagnostik. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_495-1.

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Pedrycz, Witold. "Granulation-Degranulation Processes." In An Introduction to Computing with Fuzzy Sets. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-52800-3_11.

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Masilamani, Madhan, Mohanapriya Kamalakannan, and Hugh A. Sampson. "Basophil Degranulation Assay." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6925-8_11.

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Dvorak, Ann M. "Degranulation and Recovery from Degranulation of Basophils and Mast Cells." In Chemical Immunology and Allergy. KARGER, 2005. http://dx.doi.org/10.1159/000086519.

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Felix, Lindsey C., Sarah Almas, and Paige Lacy. "Regulatory Mechanisms in Neutrophil Degranulation." In Immunopharmacology and Inflammation. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77658-3_8.

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Dvorak, Ann M. "Degranulation of Basophils and Mast Cells." In Blood Cell Biochemistry. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9525-7_5.

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Hamawy, Majed M., та William D. Swaim. "FcεRI-Mediated Cell Degranulation, Proliferation and Adhesion". У IgE Receptor (FcεRI) Function in Mast Cells and Basophils. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-22022-1_9.

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Bedouhène, Samia, Pham My-Chan Dang, Margarita Hurtado-Nedelec, and Jamel El-Benna. "Neutrophil Degranulation of Azurophil and Specific Granules." In Methods in Molecular Biology. Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0154-9_16.

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Conference papers on the topic "Degranulation"

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Xu, Kaijie, and Weike Nie. "Bi-Fuzzy Clustering Algorithm by Augmented Granulation-Degranulation Mechanisms." In 2019 IEEE 4th International Conference on Signal and Image Processing (ICSIP). IEEE, 2019. http://dx.doi.org/10.1109/siprocess.2019.8868442.

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Xu, Jianshu, Yating Lin, Jiamin Gao, et al. "Single mast cell degranulation detection based on FRET probe." In Optics in Health Care and Biomedical Optics XI, edited by Qingming Luo, Xingde Li, Ying Gu, and Dan Zhu. SPIE, 2021. http://dx.doi.org/10.1117/12.2601190.

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Yang, Wenzhong, Seungrag Lee, Jiyong Lee, Yoonsung Bae, and Dugyoung Kim. "Silver nanoparticle-induced degranulation observed with quantitative phase microscopy." In BiOS, edited by Marek Osinski, Wolfgang J. Parak, Thomas M. Jovin, and Kenji Yamamoto. SPIE, 2010. http://dx.doi.org/10.1117/12.842925.

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Leily, Mohammad, Patrick Trimby-Smith, Rose-Marie Mackay, Laurie Lau, and Andrew Walls. "Inhibition of Mast Cell Degranulation by Surfactant Protein D." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2048.

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Tang, Shuzhen, Jianshu Xu, Yating Lin, et al. "Graphene oxide based FRET probe for mast cell degranulation." In Optics in Health Care and Biomedical Optics IX, edited by Qingming Luo, Xingde Li, Yuguo Tang, Ying Gu, and Dan Zhu. SPIE, 2019. http://dx.doi.org/10.1117/12.2537508.

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Fawzy, Ashraf, Vickram Tejwani, Nirupama Putcha, et al. "Platelet degranulation is associated with respiratory morbidity in COPD." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa3090.

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Costa, Raisa Ferreira, Emanuela Paz Rosas, Daniella Araújo de Oliveira, and Marcelo Moraes Valença. "Action of capsaicin in the degranulation of mast cells in dura mater of rats: literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.001.

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Abstract:
Introduction: Capsaicin is able to induce mast cell degranulation, an event probably related to the pathophysiology of a migraine attack. Objectives: The present review study aimed to address the mechanisms of action of capsaicin and other chemical inducers in mast cell degranulation and an interaction of nerves and events that happen in the dura mater with the activation of mast cells. Design: A survey was carried out in the literature, from 1980 to 2019, in different databases (SciELO, U.S. National Library of Medicine and the National Institutes Health (PubMed) and Web of Science) using the following terms: capsaicin, mast cell and dura mater. Methods: 36 articles were selected for this review. The inclusion criteria were experimental model studies in rats that described the mechanisms of action of chemical inducers, including capsaicin. Results: Studies indicate that the main mechanisms of action of capsaicin are chemical induction through the activation of TRPV1 channels, allowing calcium influx into neurons in the trigeminal ganglion of the dura mater, activating mast cell degranulation, releasing pro-inflammatory (e.g., histamine, oxide nitric) and vasoactive (e.g., CGRP and substance P) substances. Conclusion: Therefore, the use of capsaicin may be a tool to be used in na animal model to better understand the pathophysiology of migraine.
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Smith, SG, N. Jiwani, KJ Howie, et al. "The Effect of IL-5 Receptor Downregulation on Eosinophil Degranulation." 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.a3703.

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Li, Jiani, Bowei Wang, Jianjun Dong, et al. "Imaging of RBL-2H3 Cell Degranulation by Atomic Force Microscopy." In 2022 IEEE International Conference on Manipulation, Manufacturing and Measurement on the Nanoscale (3M-NANO). IEEE, 2022. http://dx.doi.org/10.1109/3m-nano56083.2022.9941640.

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Saha, Sriparna, and Sanghamitra Bandyopadhyay. "A New Cluster Validity Index Based on Fuzzy Granulation-degranulation Criteria." In 15th International Conference on Advanced Computing and Communications (ADCOM 2007). IEEE, 2007. http://dx.doi.org/10.1109/adcom.2007.19.

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