Relevant bibliographies by topics / Mast cells

Contents

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

Academic literature on the topic 'Mast cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Mast cells"

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Holgate, S. T. "Mast cells." Clinical Experimental Allergy 21, no. 5 (September 1991): 633–34. http://dx.doi.org/10.1111/j.1365-2222.1991.tb00864.x.

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Rao, Kavitha N., and Melissa A. Brown. "Mast Cells." Annals of the New York Academy of Sciences 1143, no. 1 (November 2008): 83–104. http://dx.doi.org/10.1196/annals.1443.023.

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Swedenborg, Jesper, Mikko I. Mäyränpää, and Petri T. Kovanen. "Mast Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 31, no. 4 (April 2011): 734–40. http://dx.doi.org/10.1161/atvbaha.110.213157.

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WEBER, SYLVIA, SABINE KRÜGER-KRASAGAKES, JÜRGEN GRABBE, TORSTEN ZUBERBIER, and BEATE M. CZARNETZKI. "MAST CELLS." International Journal of Dermatology 34, no. 1 (January 1995): 1–10. http://dx.doi.org/10.1111/j.1365-4362.1995.tb04366.x.

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Shea-Donohue, Terez, Jennifer Stiltz, Aiping Zhao, and Luigi Notari. "Mast Cells." Current Gastroenterology Reports 12, no. 5 (August 14, 2010): 349–57. http://dx.doi.org/10.1007/s11894-010-0132-1.

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Schlereth, Tanja, and Frank Birklein. "Mast Cells." Anesthesiology 116, no. 4 (April 1, 2012): 756–57. http://dx.doi.org/10.1097/aln.0b013e31824bb143.

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Metcalfe, D. D., D. Baram, and Y. A. Mekori. "Mast cells." Physiological Reviews 77, no. 4 (October 1, 1997): 1033–79. http://dx.doi.org/10.1152/physrev.1997.77.4.1033.

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Mast cells are found resident in tissues throughout the body, particularly in association with structures such as blood vessels and nerves, and in proximity to surfaces that interface the external environment. Mast cells are bone marrow-derived and particularly depend upon stem cell factor for their survival. Mast cells express a variety of phenotypic features within tissues as determined by the local environment. Withdrawal of required growth factors results in mast cell apoptosis. Mast cells appear to be highly engineered cells with multiple critical biological functions. They may be activated by a number of stimuli that are both Fc epsilon RI dependent and Fc epsilon RI independent. Activation through various receptors leads to distinct signaling pathways. After activation, mast cells may immediately extrude granule-associated mediators and generate lipid-derived substances that induce immediate allergic inflammation. Mast cell activation may also be followed by the synthesis of chemokines and cytokines. Cytokine and chemokine secretion, which occurs hours later, may contribute to chronic inflammation. Biological functions of mast cells appear to include a role in innate immunity, involvement in host defense mechanisms against parasitic infestations, immunomodulation of the immune system, and tissue repair and angiogenesis.
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Wershil, Barry K., and Stephen J. Galli. "Gastrointestinal Mast Cells." Gastroenterology Clinics of North America 20, no. 3 (September 1991): 613–27. http://dx.doi.org/10.1016/s0889-8553(21)00573-2.

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Norris, Alan. "Targeting mast cells." Expert Opinion on Investigational Drugs 13, no. 7 (July 2004): 739–41. http://dx.doi.org/10.1517/13543784.13.7.739.

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Mueller, Kristen L. "Mast Cells Revisited." Science 335, no. 6064 (January 5, 2012): 14.3–14. http://dx.doi.org/10.1126/science.335.6064.14-c.

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Dissertations / Theses on the topic "Mast cells"

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Dacre, Kirstie Jane. "Involvement of mast cells and mast cell serine proteinases in equine heaves." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29721.

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Mast cells release potent mediators upon degranulation, including serine proteinases. These proteinases play a pivotal role in the pathogenesis of human asthma. Due to the similarities between human asthma and equine heaves, a similar role for the mast cell in equine heaves is proposed. Clinical heaves horses had significantly increased BALF tryptase concentrations compared to controls or heaves horses in remission, whereas BALF tryptase concentrations of controls and heaves horses in remission did not significantly differ. Horses with other pulmonary diseases also had significantly elevated BALF tryptase concentrations compared to controls. Cloning and sequencing of these proteinases revealed an alanine 216 substitution in equine tryptase, which confers increased arginine substrate specificity and may restrict fibrinogenolysis in vivo. Probing of tryptase mRNA transcript regulation in control and heaves susceptible horses revealed no significant change in airway liminal cell pellet tryptase expression following hay/straw challenge of control or heaves horses. However, bronchiolar tissues from heaves horses in early resolution phase had significantly down-regulated tryptase transcripts compared to controls. Furthermore, immunohistochemistry revealed significant intra-epithelial recruitment of tryptase positive mast cells in heaves horses compared to controls, suggesting involvement of tissue mast cells in response to challenge. In vitro hay dust suspension (HDS) challenge induced significant airway luminal mast cell degranulation in heaves susceptible horses, however a similar dose response trend was also evident in control horses. The increased number of intra-epithelial mast cells in heaves horses may explain the divergent mast cell response to in vivo and in vitro challenges. HDS-induced mast cell degranulation in both control and heaves horses may suggest non-IgE mediated degranulation. Alternatively, both control and heaves horses may have been sensitised to HDS allergens and phenotypic diversity may ultimately determine response to challenge.
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Leskinen, Markus. "Mast cell-mediated apoptosis of smooth muscle cells and endothelial cells." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/leskinen/.

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Crummy, F. "Adenosine, mast cells and asthma." Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403238.

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Huntley, John Frederick. "Mast cells and intestinal nematodiasis." Thesis, University of Edinburgh, 1991. http://hdl.handle.net/1842/15070.

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Specific enzyme-linked immunosorbent assays (ELISA) for rat mast cell proteinase I and II (RMCP I and II), intestinal mast cell proteinase (IMCP) and sheep mast cell proteinase (SMCP) were developed. Sheep serum or lymph contained potent inhibitory factors which interfered with the ELISA for SMCP, whereas little or no effect was demonstrated in the rodent ELISA by homologous serum. Secretion of SMCP into gastric lymph was noted in immune sheep following oral challenge with Ostertagia circumcincta. Development of immunity to Haemonchus contortus in sheep, expressed as the ability to exclude larvae from the mucosal surface, was characterised by an increase in mucosal mast cells (MMC) and increased abomasal tissue concentrations of SMCP. Increased concentrations of SMCP were demonstrated in serum and mucus in immune, but not in naive, sheep following direct abomasal challenge with 1 x 106 L3 Haemonchus larvae. The abrogation of immune exclusion by treatment with corticosteroids was associated with a significant reduction in the number of MMC and concentrations of SMCP in abomasal tissue. Immune exclusion persisted for 6 weeks but had declined by 12 weeks following the cessation of larval challenge. This decline was associated with a significant reduction in the number of MMC and concentrations of SMCP in abomasal tissue. Ovine mast cells derived from in vitro culture of bone marrow cells (BMMC) were compared with MMC. BMMC contained similar constituents to MMC including SMCP, histamine, dopamine and arylsulphatase. BMMC contained an additional 3[H]-DFP reactive protein not demonstrated in MMC. In the mouse, the major source of IMCP was the gastrointestinal tract. During infection with Trichinella spiralis, secretion of IMCP was demonstrated. Murine mast cells of the gastrointestinal tract exhibited heterogeneity in their proteinase phenotype, with many cells apparently containing a mixture of proteinases. Heterogeneity in the proteinase expression of mast cells in the rat was also demonstrated, with mast cells containing either RMCP I, RMCP II or RMCP I and II. Cells expressing dual proteinase phenotype were observed in some non-mucosal locations. During a primary infection of Nippostrongylus brasiliensis, changes in the RMCP I and II concentrations occurred in almost all tissues of the rat. These included significant increases in RMCP II concentrations in mesenteric lymph node, lung and intestinal tract 12 days after infection. Other changes, including those of RMCP I concentrations in bone marrow, are described.
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Alswied, Abdullah M. "Calcium signalling in mast cells." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:cc8f5f8b-5cab-4391-bce3-9541ab371002.

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Mast cells play a central role in many allergic and in ammatory conditions. These cells are activated following an intracellular rise in calcium, such as that which occurs after the activation of cell-surface receptors. One such important receptor is cysteinyl leukotriene (CysLT) receptor type 1 (CysLT1), which is activated by lipid mediators such as CysLTs LTC4, LTD4, and LTE4. CysLT1 stimulation leads to the hydrolysis of membrane phospholipids such as phosphatidylinositol 4 5-bisphosphate (PIP2) via phospholipase C-β , which results in the generation of diacylglycerol and inositol trisphosphate. Inositol trisphosphate transiently increases cytosolic calcium levels by releasing calcium from its internal stores. This transient phase is followed by an influx of external calcium caused by the opening of store-operated calcium release-activated calcium (CRAC) channels in the plasma membrane. To understand how CRAC channels are involved in receptor- driven calcium responses, I investigated whether the opening of CRAC channels regulates the production of cellular phosphoinositide. Using cytoplasmic calcium ion (Ca2+) imaging in the mast cell line RBL-2H3, I found that LTC4 induced repetitive calcium oscillations that ran down in the absence of external calcium and were sustained by calcium entry through CRAC channels. The molecular characterisation of CRAC channel components in RBL-2H3 cells revealed that LTC4 -mediated calcium oscillations were maintained through calcium entry via Orai1 and that the calcium signal could not be maintained by Orai3 or other calcium- permeable channels. Furthermore, STIM1 (but not STIM2) was the only homologue that supported calcium oscillations in RBL-2H3 cells. The inhibition of the cellular phosphoinositide pool by lithium chloride (LiCl) reduces calcium oscillations. Adding the substrate inositol rescued these oscillations, but only when external calcium was present. Pharmacologically blocking CRAC channels with a low concentration of CRAC channel blockers prevented the recovery of oscillations in LiCl-treated cells, even when inositol was present. To further understand how calcium entry contributes to the production of PIP2, I investigated whether PI4P- or PI5P-specific pools support the oscillatory calcium signal induced by LTC4. Accordingly, by using pharmacological blockers, concluded that PIP2 used in LTC4 -mediated calcium signalling is produced via the conversion of PI4P into PIP2 by PI5K1 kinases and that the cellular PI5P pool does not contribute to the calcium signal. Moreover, the conversion of PI4P into PIP2 was possible only when there was calcium entry via CRAC channels. Characterisation of the expressed PI5K1 kinases in RBL-2H3 cells revealed expression of only PIP5K1a and PIP5K1? and that both kinases are needed to maintain the oscillatory calcium signal induced by LTC4 and to provide an overlapping function. To further expand current understanding of how calcium regulates PI5K1 kinases, I specifically investigated how calcium entry regulates PIP5K1?. This was accomplished by looking into PIP5K1?-regulating proteins, of which talin is a focal adhesion protein shown to activate PIP5K1?. In this thesis, I show that the cleavage and activation of talin depend on calcium entry via CRAC channels, thereby elucidating a possible mechanism in how CRAC channels mediating calcium entry are involved in phosphoinositide production. This thesis identifies a new role for CRAC channels in mast cell activation. The opening of CRAC channels and calcium entry are required for PIP2 production and thus the maintenance of agonist-mediated calcium signalling.
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Roy, Ananya. "Mast Cells as Sentinels : Role of serglycin and mast cell proteases in infection and inflammation." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-173508.

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Mast cells (MCs), normally classified into connective tissue MCs and mucosal MCs, are highly granulated cells found in the interface between the interior and the exterior environment of our body, e.g. skin, airways and gastro-intestinal tract. They react to bacteria, parasites, viruses, and allergens by degranulation and release of premade and newly synthesized inflammatory mediators. The MC-proteases (tryptases, chymases and carboxypeptidase A), histamine and serglycin (SG) proteoglycans are premade mediators. Among these, SG is also expressed in a variety of other immune and non-immune cells. Heparin and chondroitin sulphate glycosaminoglycan chains confer highly negative charge to SG, by which MC-proteases are retained in secretory granules. Deletion of SG cause impaired packing and storage of most MC-proteases. During challenge with Toxoplasma gondii the SG-deficient mice showed significant lower inflammatory cytokine levels in comparison to wild-type mice. Results were consistently similar in vitro, bringing forward the importance of SG in inflammatory cytokine and innate immune responses towards T. gondii. Infection with Trichinella spiralis in SG-/- mice caused increased intestinal enteropathy, a tendency of delayed worm expulsion and increased larval burden in the muscle tissue as compared to wild-type animals. An altered TH2 cytokine response was also observed, and all these effects were not repaired by wild-type MC reconstitution of the SG-/- mice. Altogether, our results suggest that SG is important for tissue homeostasis, and that SG expressing cells seem capable of switching from a SG-dependent storage mode to a SG-independent secretory mode upon infection. The chymase (MCPT4) expressed by connective tissue MC has been implicated to have a protective role during infection and in limiting inflammation. We explored a protective role by inducing T. gondii infection in the Mcpt4-null mice, and found MCPT4-mediated recruitment of neutrophils and eosinophils via control of cytokine signaling. Endogenous proteins “alarmins” released by dead cells can trigger tissue and cell damage. We conclusively show that chymase efficiently degrades Hsp70 both in vitro and in vivo and that the degradation of other alarmins, e.g. HMGB1, biglycan and IL-33 may also depend on chymase.
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Friend, Reuben. "SNARE proteins in human mast cells." Thesis, University of Sheffield, 2013. http://etheses.whiterose.ac.uk/5177/.

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Mast cells form an integral part of both innate and adaptive immunity; they help to orchestrate the inflammatory immune response through the release of a variety of inflammatory mediators. Adverse reaction to allergens can lead to activation of mast cells, causing degranulation and release of a range of pro-inflammatory mediators contributing to the onset of allergy. The most studied activation pathway in the adaptive immune response of mast cells is through the Immunoglobulin E (IgE) cell surface receptor FceRI. Crosslinking of FceRI leads to degranulation and de novo synthesis of mediators. Every eukaryotic cell undergoes constitutive secretion. Alongside this general process, cells such as neuronal endocrine and immune cells, including mast cells, perform regulated secretion. This enables the cell to rapidly release mediators stored in secretory granules upon stimulation by a particular extracellular ligand. Mediators released fall into two categories; pre-formed, contained within these secretory granules; monoamines such as histamine as well as many proteases, and de novo synthesized that are released through the constitutive secretory pathway, including prostaglandins, leukotrienes, cytokines and chemokines. Elucidating the mechanisms of mast cell mediator release is imperative for understanding many disease processes; however, knowledge of the precise mechanisms by which mast cell exocytosis is controlled remains elusive. The aim of this study was to identify and characterise Soluble NSF attachment protein receptor (SNARE) proteins involved in the release of inflammatory mediators in human mast cells. Using LAD 2 human mast cells and primary human lung mast cells (HLMCS), expression of a variety of syntaxins and Vesicle associated membrane proteins (VAMPs), as well as the ubiquitously expressed SNAP-23 were found. To study the roles of individual VAMPs in exocytosis a novel technique utilising pH sensitive pHluorins was developed. Using VAMPs tagged with pHluorins, the cellular distribution of VAMP-3 and VAMP-8 containing vesicles and their behaviour upon IgE stimulation in live cells was monitored. In unstimulated cells, VAMP- 3 and 8 were found to have distinct cellular distributions. Upon IgE stimulation both VAMP-3 and VAMP-8 containing vesicles translocated to the membrane and underwent membrane fusion, consistent with roles in exocytosis. However, their responses showed distinct time courses and calcium dependences. Importantly the VAMP-3 vesicle pool could be selectively targeted with a botulinum neurotoxin serotype B (BoNT)/B LC construct and in doing so inhibited the release of IL-6. The findings in this study support the notion that distinct vesicle pools, defined in part by expression of VAMP-3 and VAMP-8, regulate the release of inflammatory mediators from mast cells and that BoNTs might provide a novel means of targeting the release of chronic inflammatory mediators from mast cells for treatment of chronic inflammatory diseases.
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Tree-Booker, Claire. "TRPC channels in human mast cells." Thesis, University of Sheffield, 2011. http://etheses.whiterose.ac.uk/1927/.

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Mast cells have an important role in the immune system, but they are centrally involved in the pathophysiology of asthma, along with a number of other allergic diseases including rhinitis, eczema and irritable bowel disease (Metcalfe et al., 1997; Beaven, 2009). In the allergic response they are activated by IgE binding to high affinity receptors and subsequent crosslinking by antigen. A rise in intracellular Ca2+ is required for mast cells to become activated and release mediators into the surrounding areas, which give rise to the symptoms of allergic disease (Gilfillan & Tkaczyk, 2006). Elucidating the ion channels responsible for mast cell Ca2+ entry may unveil new therapeutic targets for the treatment of asthma and other allergic diseases. Store-operated Ca2+ entry (SOCE) is a major mechanism for mast cell Ca2+ influx and is known to involve highly Ca2+-selective Orai1 channels. TRPC channels are non-selective Ca2+ channels; TRPC1, 4 and 5 are thought to be involved in SOCE, whereas TRPC3, 6 and 7 are activated by diacylglycerol (DAG). Whilst a limited number of studies carried out in rodent mast cells suggest that TRPC channels could be important for Ca2+ entry and mediator release, their functional expression and roles in human mast cells have not been characterised. This study showed that the LAD 2 human mast cell line and primary human lung mast cells (HLMCs) express mRNA for TRPC6. TRPC6-like currents were demonstrated for the first time in HLMCs, in response to direct activation by the DAG analogue OAG, and downstream of Gq protein-coupled P2Y1 receptor stimulation by ADP. This study also revealed for the first time that TRPC1 channels are expressed in both LAD 2 cells and HLMCs, and that both TRPC1 and Orai1 channels are likely to be involved in SOCE. Importantly, this study also indicated that TRPC1 channels could be involved in Ca2+ entry and mediator release downstream of IgE receptor activation. TRPC channels could thus contribute to Ca2+ entry required for mast cell activation in allergic disease, and could represent a therapeutic target for the modulation of diseases such as asthma.
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Lin, Tzu-Yin. "The world according to mast cells – the role of Kit in normal and neoplastic canine mast cells." The Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1189098916.

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Wang, Yiyu [Verfasser]. "Analysis of mast cells and mast cell-mediator-related histological features in cholinergic urticaria / Yiyu Wang." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1189139715/34.

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Books on the topic "Mast cells"

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Krishnaswamy, Guha, and David S. Chi, eds. Mast Cells. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1592599672.

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Hughes, Michael R., and Kelly M. McNagny, eds. Mast Cells. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1568-2.

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Dvorak, Ann M. Human Mast Cells. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74145-6.

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D, Befus, Bienenstock John, Denburg Judah A, and Mast Cell Symposium (1985 : Alton, Ont.), eds. Mast cell differentiation and heterogeneity. New York: Raven Press, 1986.

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Guha, Krishnaswamy, and Chi David S, eds. Mast cells: Methods and protocols. Totowa, N.J: Humana Press, 2006.

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Gibbs, Bernhard F., and Franco H. Falcone, eds. Basophils and Mast Cells. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0696-4.

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Gibbs, Bernhard F., and Franco H. Falcone, eds. Basophils and Mast Cells. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1173-8.

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Ribatti, Domenico, and Enrico Crivellato. Mast Cells and Tumours. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1469-4.

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Foundation, Novartis. Mast Cells and Basophils. New York: John Wiley & Sons, Ltd., 2006.

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A, Kaliner Michael, and Metcalfe Dean D, eds. The Mast cell in health and disease. New York: Marcel Dekker, 1993.

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Book chapters on the topic "Mast cells"

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Ghably, Jack, Hana Saleh, Harsha Vyas, Emma Peiris, Niva Misra, and Guha Krishnaswamy. "Paul Ehrlich’s Mastzellen: A Historical Perspective of Relevant Developments in Mast Cell Biology." In Mast Cells, 3–10. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_1.

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Bandara, Geethani, Dean D. Metcalfe, and Arnold S. Kirshenbaum. "Growth of Human Mast Cells from Bone Marrow and Peripheral Blood-Derived CD34+ Pluripotent Hematopoietic Cells." In Mast Cells, 155–62. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_10.

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Lorentz, Axel, Gernot Sellge, and Stephan C. Bischoff. "Isolation and Characterization of Human Intestinal Mast Cells." In Mast Cells, 163–77. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_11.

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Haidl, Ian D., and Jean S. Marshall. "Human Mast Cell Activation with Viruses and Pathogen Products." In Mast Cells, 179–201. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_12.

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Kawakami, Yuko, and Toshiaki Kawakami. "Basic Techniques to Study FcεRI Signaling in Mast Cells." In Mast Cells, 205–18. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_13.

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Dráber, Pavel, and Petr Dráber. "Membrane-Cytoskeleton Dynamics in the Course of Mast Cell Activation." In Mast Cells, 219–37. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_14.

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Rios, Eon J., and Janet Kalesnikoff. "FcεRI Expression and Dynamics on Mast Cells." In Mast Cells, 239–55. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_15.

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Westerberg, Christine Möller, Maria Ekoff, and Gunnar Nilsson. "Regulation of Mast Cell Survival and Apoptosis." In Mast Cells, 257–67. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_16.

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Geldman, Alexander, and Catherine J. Pallen. "Protein Tyrosine Phosphatases in Mast Cell Signaling." In Mast Cells, 269–86. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_17.

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Maltby, Steven, Maximilian Plank, Catherine Ptaschinski, Joerg Mattes, and Paul S. Foster. "MicroRNA Function in Mast Cell Biology: Protocols to Characterize and Modulate MicroRNA Expression." In Mast Cells, 287–304. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1568-2_18.

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Conference papers on the topic "Mast cells"

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Farha, Samar, Jacqueline Sharp, Kewal Asosingh, Margaret Park, Jodi Hanson, Suzy A. Comhair, W. H. Wilson Tang, James Thomas, James E. Loyd, and Serpil C. Erzurum. "Mast Cells In Pulmonary Arterial Hypertension." 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.a4949.

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Reid, Alicia C., Arul Veerappan, Colleen Achong, Nathan O'Connor, and Randi B. Silver. "MAST CELLS, MAST CELL RENIN AND LOCAL ANGIOTENSIN II IN MONOCROTALINE-INDUCED PULMONARY ARTERIAL HYPERTENSION." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6329.

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Michels, NM, HW Chu, SC LaFasto, S. Case, M. Minor, and RJ Martin. "Mast Cells MediateMycoplasma PneumoniaeClearance after Acute Infection." 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.a3241.

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Paßlick, David, Hendrik Beckert, and Sebastian Reuter. "Mast Cells and SiO2 Nanoparticles – a Suitable Interaction?" In Herbsttagung der Sektion Zellbiologie in der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e. V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678387.

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Umarova, Bella. "MAST CELLS: ROLE IN PHYSIOLOGICAL AND PATHOLOGICAL PROCESSES." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m586.sudak.ns2019-15/416-417.

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Ntaliarda, G., I. Lilis, V. Papaleonidopoulos, I. Giopanou, M. Oplopoiou, M. Lianou, G. Giotopoulou, et al. "A requirement for mast cells in lung adenocarcinoma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.lsc-1144.

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Umarova, B. "MAST CELLS FROM INFLAMMATORY STIMULUS TO IMMUNE RESPONSE." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2358.sudak.ns2021-17/379.

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Messemaker, Tobias, Jolien Suurmond, Kim L. Habets, Marieke Heijink, Joris J. Schonkeren, Annemarie Dorjee, Martin Giera, Tom W. Huizinga, Rene E. Toes, and Fina Kurreeman. "03.19 Mast cells are reprogrammed through repeated triggering." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211049.19.

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Dahal, Bhola K., Djuro Kosanovic, Raj K. Savai, Hossain Ardeschir Ghofrani, Norbert Weissmann, Wolfgang M. Kuebler, Friedrich Grimminger, Werner Seeger, and Ralph T. Schermuly. "Role Of Mast Cells In Experimental Pulmonary Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6330.

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Berlin, Frida, Sofia Mogren, Lena Uller, and Cecilia Andersson. "Mast cell chymase induce functional and morphological alterations in bronchial epithelial cells." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa830.

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Reports on the topic "Mast cells"

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Theoharides, Theoharis. Role of Mast Cells in Mammary Gland Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada430366.

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Ho, Andrea Ming-Wei. Capillary electrophoretic study of individual exocytotic events in single mast cells. Office of Scientific and Technical Information (OSTI), February 1999. http://dx.doi.org/10.2172/348903.

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Ivanova, Ivelina G., Nikola S. Tomov, Nikolay D. Dimitrov, Dimitrinka Y. Atanasova, Dimitar P. Sivrev, and Ivaylo S. Stefanov. Distribution of Serotonin Positive Mast Cells in the Intrapulmonary Airways of Rats. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, February 2019. http://dx.doi.org/10.7546/crabs.2019.02.14.

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Noga, Edward J., Angelo Colorni, Michael G. Levy, and Ramy Avtalion. Importance of Endobiotics in Defense against Protozoan Ectoparasites of Fish. United States Department of Agriculture, September 2003. http://dx.doi.org/10.32747/2003.7586463.bard.

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Infectious disease is one of the most serious causes of economic loss in all sectors of aquaculture. There is a critical need to understand the molecular basis for protection against infectious disease so that safer, more reliable and more cost-effective strategies can be designed for their control. As part of this effort, the major goal of our BARD project was to determine the importance of endobiotics as a defense against protozoan ectoparasites in fish. Endobiotics, or antimicrobial polypeptides, are peptides and small proteins that are increasingly recognized as having a vital role in the innate defense of virtually all animals. One objective of our BARD project was to determine the antiparasitic potency of one specific group of endobiotics that were isolated from hybrid striped bass (Morone saxatilis x M chrysops). We found that these endobiotics, which we had previously named histone-like proteins (HLPs), exhibited potent activity against Amyloodinium and that the putative levels of HLPs in the skin were well within the levels that we found to be lethal to the parasite in vitro. We also found evidence for the presence of similar antibiotics in sea bream (Sparus aurata) and Mediterranean sea bass (Dicentrarchus labrax). We also examined the effect of chronic stress on the expression of HLP in fish and found that HLP levels were dramatically decreased after only one week of a crowding/high ammonia sublethal stress. We also began to explore the feasibility of upregulating endobiotics via immunostimulation. However, we did not pursue this objective as fully as we originally intended because we spent a much larger effort than originally anticipated on the last objective, the attempted isolation of novel endobiotics from hybrid striped bass. In this regard, we purified and identified four new peptide endobiotics. These endobiotics, which we have named piscidins (from "Pisces" meaning fish), have potent, broad-spectrum activity against a number of both fish and human pathogens. This includes not only parasites but also bacteria. We also demonstrated that these peptides are present in the mast cell. This was the first time that the mast cell, the most common tissue granulocyte in vertebrates, was shown to possess any type of endobiotic. This finding has important implications in explaining the possible function of mast cells in the immune response of vertebrates. In summary, the research we have accomplished in this BARD project has demonstrated that endobiotics in fish have potent activity against many serious pathogens in aquaculture and that there is considerable potential to use these compounds as stress indicators in aquaculture. There is also considerable potential to use some of these compounds in other areas of medicine, including treatment of serious infectious diseases of humans and animals.
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Lew, Chong Zhi, and Ting Chi Yeh. Pediatric Extracranial Germ Cell Tumor: Clinical Perspective of Autologous Hematopoietic Cell Transplantation. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0081.

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Review question / Objective: A large number of systematic reviews and meta-analyses (SRs/MAs) involving sodium-glucose cotransporter-2 inhibitors (SGLT-2is) in the treatment of heart failure with preserved ejection fraction (HFpEF) have different outcomes. Condition being studied: The efficacy of SGLT-2is on HFpEF is currently a hot topic. However, the results of SRs/MAs conducted on relevant randomized controlled trials (RCTs) are inconsistent. We aim to conduct an umbrella review of existing SRs/MAs, to comprehensively evaluate study quality, and to incorporate calculated data from RCTs to update the results of primary outcomes.
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Barefoot, Susan, Benjamin Juven, Thomas Hughes, Avraham Lalazar, A. B. Bodine, Yitzhak Ittah, and Bonita Glatz. Characterization of Bacteriocins Produced by Food Bioprocessing Propionobacteria. United States Department of Agriculture, August 1992. http://dx.doi.org/10.32747/1992.7561061.bard.

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Objectives were to further characterize activity spectra of dairy propionibacteria bacteriocins, jenseniin G and propionicin PLG-1, purify them, examine the role of cell walls in resistance, examine their interactions with cytoplasmic membrane, explain producer immunity, and clone the responsible genes. Inhibitory spectra of both bacteriocins were further characterized. Propionicin was most effective in controlling Gram-positive, rather than Gram-negative organisms; it controlled growth of sensitive cells both in a culture medium and a model food system. Jenseniin inhibited yogurt cultures and may help prevent yogurt over-acidification. Both were active against botulinal spores; jenseniin was sporostatic; propionicin was sporicidal. Jenseniin was produced in broth culture, was stable to pH and temperature extremes, and was purified. Its molecular mass (3649 Da) and partial amino acid composition (74%) were determined. A blocked jenseniin N-terminus prevented sequencing. Methods to produce propionicin in liquid culture were improved, and large scale culture protocols to yield high titers were developed. Methods to detect and quantify propionicin activity were optimized and standardized. Stability of partially purified propionicin was demonstrated and an improved purification scheme was developed. Purified propionicin had a 9328-Da molecular mass, contained 99 amino acids, and was significantly hydrophobic; ten N-terminal amino acids were identified. Propionicin and Jenseniin interacted with cytoplasmic membranes; resistance of insensitive species was cell wall-related. Propionicin and jenseniin acted similarly; their mode of action appeared to differ from nisin. Spontaneous jenseniin-resistant mutants were resistant to propionicin but nisin-sensitive. The basis for producer immunity was not resolved. Although bacteriocin genes were not cloned, a jenseniin producer DNA clone bank and three possible vectors for cloning genes in propionibacteria were constructed. In addition, transposon Tn916 was conjugatively transferred to the propionicin producer from chromosomal and plasmid locations at transfer frequencies high enough to permit use of Tn916 for insertional mutagenesis or targeting genes in propionibacteria. The results provide information about the bacteriocins that further supports their usefulness as adjuncts to increase food safety and/or quality.
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Tran, Emily, Jasmine J. Park, Nandini N. Kulkarni, and Vinay S. Gundlapalli. Left Facial Primary Leiomyosarcoma Misdiagnosed as Atypical Fibroxanthoma and Immunochemical Markers Relevant to Diagnosis: A Case Report. Science Repository, February 2024. http://dx.doi.org/10.31487/j.ajscr.2023.04.03.

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Soft tissue sarcomas are relatively rare neoplasms of mesenchymal origin that generally make up less than 2% of all adult malignant neoplasms. Atypical fibroxanthoma is a benign soft tissue tumor often confused with malignant variants of similar tumors such as leiomyosarcoma due to similar staining markers and cell morphology. We report a case of a 70-year-old caucasian male who initially presented with a 2 cm exophytic left facial lesion that was misdiagnosed as atypical fibroxanthoma upon biopsy. The patient underwent a wide local excision of the growing 11 cm mass and immediate reconstruction with a cervicofacial flap and full thickness skin graft. Pathological analysis of the specimen revealed the final diagnosis as confirmed primary leiomyosarcoma. Both the patient’s biopsy report and the surgical pathology report revealed similar negative findings (desmin, cytokeratin AE1/AE3, p63, SOX10) as well as similar positive findings (smooth muscle actin and CD68). Critical distinctions that led to a change in diagnosis from atypical fibroxanthoma to leiomyosarcoma emerged during the final pathological analysis, which revealed more widespread positive staining for smooth muscle actin and muscle-specific actin throughout the surgical specimen along with detailed cell and nucleus morphology of atypical spindle cells in the dermis and subcutis. This valuable information was not available during the initial biopsy when the lesion was smaller. It is possible that earlier diagnosis of primary leiomyosarcoma could have resulted in advanced pre-operative treatment and excision of the facial lesion, preventing involvement of surrounding areas such as the patient’s left eye, ear, and facial nerve.
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Greenbaum, Steve G. NMR Studies of Mass Transport in New Conducting Media for Fuel Cells. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada502750.

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Stewart, B. J. Mass Spectrometry Data Set for Renal Cell Carcinoma and Polycystic Kidney Disease Cell Models. Office of Scientific and Technical Information (OSTI), January 2017. http://dx.doi.org/10.2172/1342001.

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Frank, M. Single Cell Proteomics with Ultra-High Sensitivity Mass Spectrometry. Office of Scientific and Technical Information (OSTI), February 2005. http://dx.doi.org/10.2172/15011526.

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