Պարարտ բջիջ (Armenian Wikipedia)

Analysis of information sources in references of the Wikipedia article "Պարարտ բջիջ" in Armenian language version.

refsWebsite

Global rank Armenian rank

41nih.gov

4^th place

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28doi.org

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6semanticscholar.org

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428^th place

5archive.org

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3web.archive.org

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1purl.org

7,712^th place

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1memidex.com

low place

1cell.com

2,814^th place

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1sciencedirect.com

149^th place

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1harvard.edu

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1merckvetmanual.com

9,011^th place

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1uni-sz.bg

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1worldcat.org

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archive.org

Marieb EN, Hoehn K (2004). Human Anatomy and Physiology (6th ed.). San Francisco: Pearson Benjamin Cummings. էջ 805. ISBN 978-0-321-20413-4.
Denburg JA (1998). Allergy and allergic diseases: the new mechanisms and therapeutics. Totowa, NJ: Humana Press. ISBN 978-0-89603-404-4.
Li W, Deanin GG, Margolis B, Schlessinger J, Oliver JM (July 1992). «FcεR1-mediated tyrosine phosphorylation of multiple proteins, including phospholipase Cγ1 and the receptor βγ2 complex, in RBL-2H3 rat basophilic leukemia cells». Molecular and Cellular Biology. 12 (7): 3176–82. doi:10.1128/MCB.12.7.3176. PMC 364532. PMID 1535686.
Akin C, Valent P, Metcalfe DD (2010). «Mast cell activation syndrome: Proposed diagnostic criteria». J. Allergy Clin. Immunol. 126 (6): 1099–104.e4. doi:10.1016/j.jaci.2010.08.035. PMC 3753019. PMID 21035176.
Dachman WD, Bedarida G, Blaschke TF, Hoffman BB (March 1994). «Histamine-induced venodilation in human beings involves both H1 and H2 receptor subtypes». The Journal of Allergy and Clinical Immunology. 93 (3): 606–14. doi:10.1016/S0091-6749(94)70072-9. PMID 8151062.

cell.com

Pundir, Priyanka; Liu, Rui; Vasavda, Chirag; Serhan, Nadine; Limjunyawong, Nathachit; Yee, Rebecca; Zhan, Yingzhuan; Dong, Xintong; Wu, Xueqing; Zhang, Ying; Snyder, Solomon H; Gaudenzio, Nicolas; Vidal, Jorge E; Dong, Xinzhong (July 2019). «A Connective Tissue Mast-Cell-Specific ReceptorDetects Bacterial Quorum-Sensing Moleculesand Mediates Antibacterial Immunity». Cell Host & Microbe. 26 (1): 114–122. doi:10.1016/j.chom.2019.06.003. PMC 6649664. PMID 31278040. Վերցված է 2021 թ․ հուլիսի 7-ին.

doi.org

da Silva EZ, Jamur MC, Oliver C (2014). «Mast cell function: a new vision of an old cell». J. Histochem. Cytochem. 62 (10): 698–738. doi:10.1369/0022155414545334. PMC 4230976. PMID 25062998. «Mast cells can recognize pathogens through different mechanisms including direct binding of pathogens or their components to PAMP receptors on the mast cell surface, binding of antibody or complement-coated bacteria to complement or immunoglobulin receptors, or recognition of endogenous peptides produced by infected or injured cells (Hofmann and Abraham 2009). The pattern of expression of these receptors varies considerably among different mast cell subtypes. TLRs (1–7 and 9), NLRs, RLRs, and receptors for complement are accountable for most mast cell innate responses»
Polyzoidis S, Koletsa T, Panagiotidou S, Ashkan K, Theoharides TC (2015). «Mast cells in meningiomas and brain inflammation». J Neuroinflammation. 12 (1): 170. doi:10.1186/s12974-015-0388-3. PMC 4573939. PMID 26377554. «MCs originate from a bone marrow progenitor and subsequently develop different phenotype characteristics locally in tissues. Their range of functions is wide and includes participation in allergic reactions, innate and adaptive immunity, inflammation, and autoimmunity [34]. In the human brain, MCs can be located in various areas, such as the pituitary stalk, the pineal gland, the area postrema, the choroid plexus, thalamus, hypothalamus, and the median eminence [35]. In the meninges, they are found within the dural layer in association with vessels and terminals of meningeal nociceptors [36]. MCs have a distinct feature compared to other hematopoietic cells in that they reside in the brain [37]. MCs contain numerous granules and secrete an abundance of prestored mediators such as corticotropin-releasing hormone (CRH), neurotensin (NT), substance P (SP), tryptase, chymase, vasoactive intestinal peptide (VIP), vascular endothelial growth factor (VEGF), TNF, prostaglandins, leukotrienes, and varieties of chemokines and cytokines some of which are known to disrupt the integrity of the blood-brain barrier (BBB) [38–40].

[The] key role of MCs in inflammation [34] and in the disruption of the BBB [41–43] suggests areas of importance for novel therapy research. Increasing evidence also indicates that MCs participate in neuroinflammation directly [44–46] and through microglia stimulation [47], contributing to the pathogenesis of such conditions such as headaches, [48] autism [49], and chronic fatigue syndrome [50]. In fact, a recent review indicated that peripheral inflammatory stimuli can cause microglia activation [51], thus possibly involving MCs outside the brain.»{{cite journal}}: CS1 սպաս․ չպիտակված ազատ DOI (link)
Franco CB, Chen CC, Drukker M, Weissman IL, Galli SJ (2010). «Distinguishing mast cell and granulocyte differentiation at the single-cell level». Cell Stem Cell. 6 (4): 361–8. doi:10.1016/j.stem.2010.02.013. PMC 2852254. PMID 20362540.
Prussin C, Metcalfe DD (February 2003). «4. IgE, mast cells, basophils, and eosinophils». The Journal of Allergy and Clinical Immunology. 111 (2 Suppl): S486–94. doi:10.1067/mai.2003.120. PMC 2847274. PMID 12592295.
Pal, Sarit; Gasheva, Olga Y.; Zawieja, David C.; Meininger, Cynthia J.; Gashev, Anatoliy A. (March 2020). «Histamine-mediated autocrine signaling in mesenteric perilymphatic mast cells». American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 318 (3): R590-604. doi:10.1152/ajpregu.00255.2019. PMC 7099465. PMID 31913658.
Moon TC, Befus AD, Kulka M (2014). «Mast cell mediators: their differential release and the secretory pathways involved». Front Immunol. 5: 569. doi:10.3389/fimmu.2014.00569. PMC 4231949. PMID 25452755. «Two types of degranulation have been described for MC: piecemeal degranulation (PMD) and anaphylactic degranulation (AND) (Figures 1 and 2). Both PMD and AND occur in vivo, ex vivo, and in vitro in MC in human (78–82), mouse (83), and rat (84). PMD is selective release of portions of the granule contents, without granule-to-granule and/or granule-to-plasma membrane fusions. ... In contrast to PMD, AND is the explosive release of granule contents or entire granules to the outside of cells after granule-to-granule and/or granule-to-plasma membrane fusions (Figures 1 and 2). Ultrastructural studies show that AND starts with granule swelling and matrix alteration after appropriate stimulation (e.g., FcεRI-crosslinking).»
Figure 1: Mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 2: Model of genesis of mast cell secretory granules Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 3: Lipid body biogenesis Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Table 2: Stimuli-selective mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Ashmole I, Bradding P (May 2013). «Ion channels regulating mast cell biology». Clin. Exp. Allergy. 43 (5): 491–502. doi:10.1111/cea.12043. PMID 23600539. S2CID 1127584. «P2X receptors are ligand-gated non-selective cation channels that are activated by extracellular ATP. ... Increased local ATP concentrations are likely to be present around mast cells in inflamed tissues due to its release through cell injury or death and platelet activation [40]. Furthermore, mast cells themselves store ATP within secretory granules, which is released upon activation [41]. There is therefore the potential for significant Ca2+ influx into mast cells through P2X receptors. Members of the P2X family differ in both the ATP concentration they require for activation and the degree to which they desensitise following agonist activation [37, 38]. This opens up the possibility that by expressing a number of different P2X receptors mast cells may be able to tailor their response to ATP in a concentration dependent manner [37].»
Wilhelm M, Silver R, Silverman AJ (November 2005). «Central nervous system neurons acquire mast cell products via transgranulation». The European Journal of Neuroscience. 22 (9): 2238–48. doi:10.1111/j.1460-9568.2005.04429.x. PMC 3281766. PMID 16262662.
Wouters MM, Vicario M, Santos J (2015). «The role of mast cells in functional GI disorders». Gut. 65 (1): 155–168. doi:10.1136/gutjnl-2015-309151. PMID 26194403. «Functional gastrointestinal disorders (FGIDs) are characterized by chronic complaints arising from disorganized brain-gut interactions leading to dysmotility and hypersensitivity. The two most prevalent FGIDs, affecting up to 16–26% of worldwide population, are functional dyspepsia and irritable bowel syndrome. ... It is well established that mast cell activation can generate epithelial and neuro-muscular dysfunction and promote visceral hypersensitivity and altered motility patterns in FGIDs, postoperative ileus, food allergy and inflammatory bowel disease.
▸ Mast cells play a central pathophysiological role in IBS and possibly in functional dyspepsia, although not well defined.
▸ Increased mast cell activation is a common finding in the mucosa of patients with functional GI disorders. ...
▸ Treatment with mast cell stabilisers offers a reasonably safe and promising option for the management of those patients with IBS non-responding to conventional approaches, though future studies are warranted to evaluate efficacy and indications.»
Budzyński J, Kłopocka M (2014). «Brain-gut axis in the pathogenesis of Helicobacter pylori infection». World J. Gastroenterol. 20 (18): 5212–25. doi:10.3748/wjg.v20.i18.5212. PMC 4017036. PMID 24833851. «In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector»{{cite journal}}: CS1 սպաս․ չպիտակված ազատ DOI (link)
Kinet JP (1999). «The high-affinity IgE receptor (FcεRI): from physiology to pathology». Annual Review of Immunology. 17: 931–72. doi:10.1146/annurev.immunol.17.1.931. PMID 10358778.
Li W, Deanin GG, Margolis B, Schlessinger J, Oliver JM (July 1992). «FcεR1-mediated tyrosine phosphorylation of multiple proteins, including phospholipase Cγ1 and the receptor βγ2 complex, in RBL-2H3 rat basophilic leukemia cells». Molecular and Cellular Biology. 12 (7): 3176–82. doi:10.1128/MCB.12.7.3176. PMC 364532. PMID 1535686.
Pundir, Priyanka; Liu, Rui; Vasavda, Chirag; Serhan, Nadine; Limjunyawong, Nathachit; Yee, Rebecca; Zhan, Yingzhuan; Dong, Xintong; Wu, Xueqing; Zhang, Ying; Snyder, Solomon H; Gaudenzio, Nicolas; Vidal, Jorge E; Dong, Xinzhong (July 2019). «A Connective Tissue Mast-Cell-Specific ReceptorDetects Bacterial Quorum-Sensing Moleculesand Mediates Antibacterial Immunity». Cell Host & Microbe. 26 (1): 114–122. doi:10.1016/j.chom.2019.06.003. PMC 6649664. PMID 31278040. Վերցված է 2021 թ․ հուլիսի 7-ին.
Tatemoto, Kazuhiko; Nozaki, Yuko; Tsuda, Ryoko; Konno, Shinobu; Tomura, Keiko; Furuno, Masahiro; Ogasawara, Hiroyuki; Edamura, Koji; Takagi, Hideo; Iwamura, Hiroyuki; Noguchi, Masato; Naito, Takayuki (2006). «Immunoglobulin E-independent activation of mast cell is mediated by Mrg receptors». Biochemical and Biophysical Research Communications. 349 (4): 1322–1328. doi:10.1016/j.bbrc.2006.08.177. PMID 16979137. Վերցված է 2021 թ․ հուլիսի 7-ին.
Frieri M (2018). «Mast Cell Activation Syndrome». Clin Rev Allergy Immunol. 54 (3): 353–365. doi:10.1007/s12016-015-8487-6. PMID 25944644. S2CID 5723622. «Table 1
Classification of diseases associated with mast cell activation from Akin et al. [14]
1. Primary
  a. Anaphylaxis with an associated clonal mast cell disorder
  b. Monoclonal mast cell activation syndrome (MMAS), see text for explanation
2. Secondary
  a. Allergic disorders
  b. Mast cell activation associated with chronic inflammatory or neoplastic disorders
  c. Physical urticarias (requires a primary stimulation)
  d. Chronic autoimmune urticaria
3. Idiopathic (When mast cell degranulation has been documented; may be either primary or secondary. Angioedema may be associated with hereditary or acquired angioedema where it may be mast cell independent and result from kinin generation)
  a. Anaphylaxis
  b. Angioedema
  c. Urticaria
  d. Mast cell activation syndrome (MCAS)...
Recurrent idiopathic anaphylaxis presents with allergic signs and symptoms—hives and angioedema which is a distinguishing feature—eliminates identifiable allergic etiologies, considers mastocytosis and carcinoid syndrome, and is treated with H1 and H2 antihistamines, epinephrine, and steroids [21, 22].»
Akin C, Valent P, Metcalfe DD (2010). «Mast cell activation syndrome: Proposed diagnostic criteria». J. Allergy Clin. Immunol. 126 (6): 1099–104.e4. doi:10.1016/j.jaci.2010.08.035. PMC 3753019. PMID 21035176.
Kumar M, Duraisamy K, Chow BK (May 2021). «Unlocking the Non-IgE Mediated Pseudo-Allergic Reaction Puzzle with Mas-Related G-Protein Coupled Receptor Member X2 (MRGPRX2)». Cells. 10 (5): 1033. doi:10.3390/cells10051033. PMC 8146469. PMID 33925682.
Alm PE (April 1983). «Sodium fluoride evoked histamine release from mast cells. A study of cyclic AMP levels and effects of catecholamines». Agents and Actions. 13 (2–3): 132–7. doi:10.1007/bf01967316. PMID 6191542. S2CID 6977280.
Dachman WD, Bedarida G, Blaschke TF, Hoffman BB (March 1994). «Histamine-induced venodilation in human beings involves both H1 and H2 receptor subtypes». The Journal of Allergy and Clinical Immunology. 93 (3): 606–14. doi:10.1016/S0091-6749(94)70072-9. PMID 8151062.
Machen TE, Rutten MJ, Ekblad EB (February 1982). «Histamine, cAMP, and activation of piglet gastric mucosa». The American Journal of Physiology. 242 (2): G79–84. doi:10.1152/ajpgi.1982.242.2.G79. PMID 6175225.
Lee DM, Friend DS, Gurish MF, Benoist C, Mathis D, Brenner MB (September 2002). «Mast cells: a cellular link between autoantibodies and inflammatory arthritis». Science. 297 (5587): 1689–92. Bibcode:2002Sci...297.1689L. doi:10.1126/science.1073176. PMID 12215644. S2CID 38504601.
Horny HP, Sotlar K, Valent P (2007). «Mastocytosis: state of the art». Pathobiology. 74 (2): 121–32. doi:10.1159/000101711. PMID 17587883.
Theoharides TC, Angelidou A, Alysandratos KD, և այլք: (January 2012). «Mast cell activation and autism». Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1822 (1): 34–41. doi:10.1016/j.bbadis.2010.12.017. PMID 21193035.
Blumenkrantz N, Asboe-Hansen G (May 1975). «A selective stain for mast cells». The Histochemical Journal. 7 (3): 277–82. doi:10.1007/BF01003596. PMID 47855. S2CID 32711203.
Tomov, N.; Dimitrov, N. (2017). «Modified bismarck brown staining for demonstration of soft tissue mast cells» (PDF). Trakia Journal of Sciences. 15 (3): 195–197. doi:10.15547/tjs.2017.03.001.
Heneberg P (November 2011). «Mast cells and basophils: trojan horses of conventional lin- stem/progenitor cell isolates». Current Pharmaceutical Design. 17 (34): 3753–71. doi:10.2174/138161211798357881. PMID 22103846.
Lebduska P, Korb J, Tůmová M, Heneberg P, Dráber P (December 2007). «Topography of signaling molecules as detected by electron microscopy on plasma membrane sheets isolated from non-adherent mast cells». Journal of Immunological Methods. 328 (1–2): 139–51. doi:10.1016/j.jim.2007.08.015. PMID 17900607.
Fujimiya, Mineko; Inui, Akio (2000). «Peptidergic regulation of gastrointestinal motility in rodents». Peptides. Elsevier BV. 21 (10): 1565–1582. doi:10.1016/s0196-9781(00)00313-2. ISSN 0196-9781. PMID 11068106. S2CID 45185196.

harvard.edu

ui.adsabs.harvard.edu

Lee DM, Friend DS, Gurish MF, Benoist C, Mathis D, Brenner MB (September 2002). «Mast cells: a cellular link between autoantibodies and inflammatory arthritis». Science. 297 (5587): 1689–92. Bibcode:2002Sci...297.1689L. doi:10.1126/science.1073176. PMID 12215644. S2CID 38504601.

memidex.com

«labrocytes». Memidex. Արխիվացված է օրիգինալից 2018 թ․ նոյեմբերի 6-ին. Վերցված է 2011 թ․ փետրվարի 19-ին.

merckvetmanual.com

«Cutaneous Mast Cell Tumors». The Merck Veterinary Manual. 2006. Արխիվացված օրիգինալից 2007 թ․ մայիսի 23-ին. Վերցված է 2007 թ․ հուլիսի 8-ին.

nih.gov

pubmed.ncbi.nlm.nih.gov

da Silva EZ, Jamur MC, Oliver C (2014). «Mast cell function: a new vision of an old cell». J. Histochem. Cytochem. 62 (10): 698–738. doi:10.1369/0022155414545334. PMC 4230976. PMID 25062998. «Mast cells can recognize pathogens through different mechanisms including direct binding of pathogens or their components to PAMP receptors on the mast cell surface, binding of antibody or complement-coated bacteria to complement or immunoglobulin receptors, or recognition of endogenous peptides produced by infected or injured cells (Hofmann and Abraham 2009). The pattern of expression of these receptors varies considerably among different mast cell subtypes. TLRs (1–7 and 9), NLRs, RLRs, and receptors for complement are accountable for most mast cell innate responses»
Polyzoidis S, Koletsa T, Panagiotidou S, Ashkan K, Theoharides TC (2015). «Mast cells in meningiomas and brain inflammation». J Neuroinflammation. 12 (1): 170. doi:10.1186/s12974-015-0388-3. PMC 4573939. PMID 26377554. «MCs originate from a bone marrow progenitor and subsequently develop different phenotype characteristics locally in tissues. Their range of functions is wide and includes participation in allergic reactions, innate and adaptive immunity, inflammation, and autoimmunity [34]. In the human brain, MCs can be located in various areas, such as the pituitary stalk, the pineal gland, the area postrema, the choroid plexus, thalamus, hypothalamus, and the median eminence [35]. In the meninges, they are found within the dural layer in association with vessels and terminals of meningeal nociceptors [36]. MCs have a distinct feature compared to other hematopoietic cells in that they reside in the brain [37]. MCs contain numerous granules and secrete an abundance of prestored mediators such as corticotropin-releasing hormone (CRH), neurotensin (NT), substance P (SP), tryptase, chymase, vasoactive intestinal peptide (VIP), vascular endothelial growth factor (VEGF), TNF, prostaglandins, leukotrienes, and varieties of chemokines and cytokines some of which are known to disrupt the integrity of the blood-brain barrier (BBB) [38–40].

[The] key role of MCs in inflammation [34] and in the disruption of the BBB [41–43] suggests areas of importance for novel therapy research. Increasing evidence also indicates that MCs participate in neuroinflammation directly [44–46] and through microglia stimulation [47], contributing to the pathogenesis of such conditions such as headaches, [48] autism [49], and chronic fatigue syndrome [50]. In fact, a recent review indicated that peripheral inflammatory stimuli can cause microglia activation [51], thus possibly involving MCs outside the brain.»{{cite journal}}: CS1 սպաս․ չպիտակված ազատ DOI (link)
Franco CB, Chen CC, Drukker M, Weissman IL, Galli SJ (2010). «Distinguishing mast cell and granulocyte differentiation at the single-cell level». Cell Stem Cell. 6 (4): 361–8. doi:10.1016/j.stem.2010.02.013. PMC 2852254. PMID 20362540.
Prussin C, Metcalfe DD (February 2003). «4. IgE, mast cells, basophils, and eosinophils». The Journal of Allergy and Clinical Immunology. 111 (2 Suppl): S486–94. doi:10.1067/mai.2003.120. PMC 2847274. PMID 12592295.
Pal, Sarit; Gasheva, Olga Y.; Zawieja, David C.; Meininger, Cynthia J.; Gashev, Anatoliy A. (March 2020). «Histamine-mediated autocrine signaling in mesenteric perilymphatic mast cells». American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 318 (3): R590-604. doi:10.1152/ajpregu.00255.2019. PMC 7099465. PMID 31913658.
Moon TC, Befus AD, Kulka M (2014). «Mast cell mediators: their differential release and the secretory pathways involved». Front Immunol. 5: 569. doi:10.3389/fimmu.2014.00569. PMC 4231949. PMID 25452755. «Two types of degranulation have been described for MC: piecemeal degranulation (PMD) and anaphylactic degranulation (AND) (Figures 1 and 2). Both PMD and AND occur in vivo, ex vivo, and in vitro in MC in human (78–82), mouse (83), and rat (84). PMD is selective release of portions of the granule contents, without granule-to-granule and/or granule-to-plasma membrane fusions. ... In contrast to PMD, AND is the explosive release of granule contents or entire granules to the outside of cells after granule-to-granule and/or granule-to-plasma membrane fusions (Figures 1 and 2). Ultrastructural studies show that AND starts with granule swelling and matrix alteration after appropriate stimulation (e.g., FcεRI-crosslinking).»
Figure 1: Mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 2: Model of genesis of mast cell secretory granules Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 3: Lipid body biogenesis Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Table 2: Stimuli-selective mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Ashmole I, Bradding P (May 2013). «Ion channels regulating mast cell biology». Clin. Exp. Allergy. 43 (5): 491–502. doi:10.1111/cea.12043. PMID 23600539. S2CID 1127584. «P2X receptors are ligand-gated non-selective cation channels that are activated by extracellular ATP. ... Increased local ATP concentrations are likely to be present around mast cells in inflamed tissues due to its release through cell injury or death and platelet activation [40]. Furthermore, mast cells themselves store ATP within secretory granules, which is released upon activation [41]. There is therefore the potential for significant Ca2+ influx into mast cells through P2X receptors. Members of the P2X family differ in both the ATP concentration they require for activation and the degree to which they desensitise following agonist activation [37, 38]. This opens up the possibility that by expressing a number of different P2X receptors mast cells may be able to tailor their response to ATP in a concentration dependent manner [37].»
Wilhelm M, Silver R, Silverman AJ (November 2005). «Central nervous system neurons acquire mast cell products via transgranulation». The European Journal of Neuroscience. 22 (9): 2238–48. doi:10.1111/j.1460-9568.2005.04429.x. PMC 3281766. PMID 16262662.
Wouters MM, Vicario M, Santos J (2015). «The role of mast cells in functional GI disorders». Gut. 65 (1): 155–168. doi:10.1136/gutjnl-2015-309151. PMID 26194403. «Functional gastrointestinal disorders (FGIDs) are characterized by chronic complaints arising from disorganized brain-gut interactions leading to dysmotility and hypersensitivity. The two most prevalent FGIDs, affecting up to 16–26% of worldwide population, are functional dyspepsia and irritable bowel syndrome. ... It is well established that mast cell activation can generate epithelial and neuro-muscular dysfunction and promote visceral hypersensitivity and altered motility patterns in FGIDs, postoperative ileus, food allergy and inflammatory bowel disease.
▸ Mast cells play a central pathophysiological role in IBS and possibly in functional dyspepsia, although not well defined.
▸ Increased mast cell activation is a common finding in the mucosa of patients with functional GI disorders. ...
▸ Treatment with mast cell stabilisers offers a reasonably safe and promising option for the management of those patients with IBS non-responding to conventional approaches, though future studies are warranted to evaluate efficacy and indications.»
Carabotti M, Scirocco A, Maselli MA, Severi C (2015). «The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems». Ann Gastroenterol. 28 (2): 203–209. PMC 4367209. PMID 25830558.
Budzyński J, Kłopocka M (2014). «Brain-gut axis in the pathogenesis of Helicobacter pylori infection». World J. Gastroenterol. 20 (18): 5212–25. doi:10.3748/wjg.v20.i18.5212. PMC 4017036. PMID 24833851. «In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector»{{cite journal}}: CS1 սպաս․ չպիտակված ազատ DOI (link)
Kinet JP (1999). «The high-affinity IgE receptor (FcεRI): from physiology to pathology». Annual Review of Immunology. 17: 931–72. doi:10.1146/annurev.immunol.17.1.931. PMID 10358778.
Li W, Deanin GG, Margolis B, Schlessinger J, Oliver JM (July 1992). «FcεR1-mediated tyrosine phosphorylation of multiple proteins, including phospholipase Cγ1 and the receptor βγ2 complex, in RBL-2H3 rat basophilic leukemia cells». Molecular and Cellular Biology. 12 (7): 3176–82. doi:10.1128/MCB.12.7.3176. PMC 364532. PMID 1535686.
Pundir, Priyanka; Liu, Rui; Vasavda, Chirag; Serhan, Nadine; Limjunyawong, Nathachit; Yee, Rebecca; Zhan, Yingzhuan; Dong, Xintong; Wu, Xueqing; Zhang, Ying; Snyder, Solomon H; Gaudenzio, Nicolas; Vidal, Jorge E; Dong, Xinzhong (July 2019). «A Connective Tissue Mast-Cell-Specific ReceptorDetects Bacterial Quorum-Sensing Moleculesand Mediates Antibacterial Immunity». Cell Host & Microbe. 26 (1): 114–122. doi:10.1016/j.chom.2019.06.003. PMC 6649664. PMID 31278040. Վերցված է 2021 թ․ հուլիսի 7-ին.
Tatemoto, Kazuhiko; Nozaki, Yuko; Tsuda, Ryoko; Konno, Shinobu; Tomura, Keiko; Furuno, Masahiro; Ogasawara, Hiroyuki; Edamura, Koji; Takagi, Hideo; Iwamura, Hiroyuki; Noguchi, Masato; Naito, Takayuki (2006). «Immunoglobulin E-independent activation of mast cell is mediated by Mrg receptors». Biochemical and Biophysical Research Communications. 349 (4): 1322–1328. doi:10.1016/j.bbrc.2006.08.177. PMID 16979137. Վերցված է 2021 թ․ հուլիսի 7-ին.
Frieri M (2018). «Mast Cell Activation Syndrome». Clin Rev Allergy Immunol. 54 (3): 353–365. doi:10.1007/s12016-015-8487-6. PMID 25944644. S2CID 5723622. «Table 1
Classification of diseases associated with mast cell activation from Akin et al. [14]
1. Primary
  a. Anaphylaxis with an associated clonal mast cell disorder
  b. Monoclonal mast cell activation syndrome (MMAS), see text for explanation
2. Secondary
  a. Allergic disorders
  b. Mast cell activation associated with chronic inflammatory or neoplastic disorders
  c. Physical urticarias (requires a primary stimulation)
  d. Chronic autoimmune urticaria
3. Idiopathic (When mast cell degranulation has been documented; may be either primary or secondary. Angioedema may be associated with hereditary or acquired angioedema where it may be mast cell independent and result from kinin generation)
  a. Anaphylaxis
  b. Angioedema
  c. Urticaria
  d. Mast cell activation syndrome (MCAS)...
Recurrent idiopathic anaphylaxis presents with allergic signs and symptoms—hives and angioedema which is a distinguishing feature—eliminates identifiable allergic etiologies, considers mastocytosis and carcinoid syndrome, and is treated with H1 and H2 antihistamines, epinephrine, and steroids [21, 22].»
Akin C, Valent P, Metcalfe DD (2010). «Mast cell activation syndrome: Proposed diagnostic criteria». J. Allergy Clin. Immunol. 126 (6): 1099–104.e4. doi:10.1016/j.jaci.2010.08.035. PMC 3753019. PMID 21035176.
Kumar M, Duraisamy K, Chow BK (May 2021). «Unlocking the Non-IgE Mediated Pseudo-Allergic Reaction Puzzle with Mas-Related G-Protein Coupled Receptor Member X2 (MRGPRX2)». Cells. 10 (5): 1033. doi:10.3390/cells10051033. PMC 8146469. PMID 33925682.
Alm PE (April 1983). «Sodium fluoride evoked histamine release from mast cells. A study of cyclic AMP levels and effects of catecholamines». Agents and Actions. 13 (2–3): 132–7. doi:10.1007/bf01967316. PMID 6191542. S2CID 6977280.
Dachman WD, Bedarida G, Blaschke TF, Hoffman BB (March 1994). «Histamine-induced venodilation in human beings involves both H1 and H2 receptor subtypes». The Journal of Allergy and Clinical Immunology. 93 (3): 606–14. doi:10.1016/S0091-6749(94)70072-9. PMID 8151062.
Machen TE, Rutten MJ, Ekblad EB (February 1982). «Histamine, cAMP, and activation of piglet gastric mucosa». The American Journal of Physiology. 242 (2): G79–84. doi:10.1152/ajpgi.1982.242.2.G79. PMID 6175225.
Lee DM, Friend DS, Gurish MF, Benoist C, Mathis D, Brenner MB (September 2002). «Mast cells: a cellular link between autoantibodies and inflammatory arthritis». Science. 297 (5587): 1689–92. Bibcode:2002Sci...297.1689L. doi:10.1126/science.1073176. PMID 12215644. S2CID 38504601.
Horny HP, Sotlar K, Valent P (2007). «Mastocytosis: state of the art». Pathobiology. 74 (2): 121–32. doi:10.1159/000101711. PMID 17587883.
Theoharides TC, Angelidou A, Alysandratos KD, և այլք: (January 2012). «Mast cell activation and autism». Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1822 (1): 34–41. doi:10.1016/j.bbadis.2010.12.017. PMID 21193035.
Blumenkrantz N, Asboe-Hansen G (May 1975). «A selective stain for mast cells». The Histochemical Journal. 7 (3): 277–82. doi:10.1007/BF01003596. PMID 47855. S2CID 32711203.
Heneberg P (November 2011). «Mast cells and basophils: trojan horses of conventional lin- stem/progenitor cell isolates». Current Pharmaceutical Design. 17 (34): 3753–71. doi:10.2174/138161211798357881. PMID 22103846.
Lebduska P, Korb J, Tůmová M, Heneberg P, Dráber P (December 2007). «Topography of signaling molecules as detected by electron microscopy on plasma membrane sheets isolated from non-adherent mast cells». Journal of Immunological Methods. 328 (1–2): 139–51. doi:10.1016/j.jim.2007.08.015. PMID 17900607.
Fujimiya, Mineko; Inui, Akio (2000). «Peptidergic regulation of gastrointestinal motility in rodents». Peptides. Elsevier BV. 21 (10): 1565–1582. doi:10.1016/s0196-9781(00)00313-2. ISSN 0196-9781. PMID 11068106. S2CID 45185196.

ncbi.nlm.nih.gov

da Silva EZ, Jamur MC, Oliver C (2014). «Mast cell function: a new vision of an old cell». J. Histochem. Cytochem. 62 (10): 698–738. doi:10.1369/0022155414545334. PMC 4230976. PMID 25062998. «Mast cells can recognize pathogens through different mechanisms including direct binding of pathogens or their components to PAMP receptors on the mast cell surface, binding of antibody or complement-coated bacteria to complement or immunoglobulin receptors, or recognition of endogenous peptides produced by infected or injured cells (Hofmann and Abraham 2009). The pattern of expression of these receptors varies considerably among different mast cell subtypes. TLRs (1–7 and 9), NLRs, RLRs, and receptors for complement are accountable for most mast cell innate responses»
Polyzoidis S, Koletsa T, Panagiotidou S, Ashkan K, Theoharides TC (2015). «Mast cells in meningiomas and brain inflammation». J Neuroinflammation. 12 (1): 170. doi:10.1186/s12974-015-0388-3. PMC 4573939. PMID 26377554. «MCs originate from a bone marrow progenitor and subsequently develop different phenotype characteristics locally in tissues. Their range of functions is wide and includes participation in allergic reactions, innate and adaptive immunity, inflammation, and autoimmunity [34]. In the human brain, MCs can be located in various areas, such as the pituitary stalk, the pineal gland, the area postrema, the choroid plexus, thalamus, hypothalamus, and the median eminence [35]. In the meninges, they are found within the dural layer in association with vessels and terminals of meningeal nociceptors [36]. MCs have a distinct feature compared to other hematopoietic cells in that they reside in the brain [37]. MCs contain numerous granules and secrete an abundance of prestored mediators such as corticotropin-releasing hormone (CRH), neurotensin (NT), substance P (SP), tryptase, chymase, vasoactive intestinal peptide (VIP), vascular endothelial growth factor (VEGF), TNF, prostaglandins, leukotrienes, and varieties of chemokines and cytokines some of which are known to disrupt the integrity of the blood-brain barrier (BBB) [38–40].

[The] key role of MCs in inflammation [34] and in the disruption of the BBB [41–43] suggests areas of importance for novel therapy research. Increasing evidence also indicates that MCs participate in neuroinflammation directly [44–46] and through microglia stimulation [47], contributing to the pathogenesis of such conditions such as headaches, [48] autism [49], and chronic fatigue syndrome [50]. In fact, a recent review indicated that peripheral inflammatory stimuli can cause microglia activation [51], thus possibly involving MCs outside the brain.»{{cite journal}}: CS1 սպաս․ չպիտակված ազատ DOI (link)
Franco CB, Chen CC, Drukker M, Weissman IL, Galli SJ (2010). «Distinguishing mast cell and granulocyte differentiation at the single-cell level». Cell Stem Cell. 6 (4): 361–8. doi:10.1016/j.stem.2010.02.013. PMC 2852254. PMID 20362540.
Prussin C, Metcalfe DD (February 2003). «4. IgE, mast cells, basophils, and eosinophils». The Journal of Allergy and Clinical Immunology. 111 (2 Suppl): S486–94. doi:10.1067/mai.2003.120. PMC 2847274. PMID 12592295.
Pal, Sarit; Gasheva, Olga Y.; Zawieja, David C.; Meininger, Cynthia J.; Gashev, Anatoliy A. (March 2020). «Histamine-mediated autocrine signaling in mesenteric perilymphatic mast cells». American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 318 (3): R590-604. doi:10.1152/ajpregu.00255.2019. PMC 7099465. PMID 31913658.
Moon TC, Befus AD, Kulka M (2014). «Mast cell mediators: their differential release and the secretory pathways involved». Front Immunol. 5: 569. doi:10.3389/fimmu.2014.00569. PMC 4231949. PMID 25452755. «Two types of degranulation have been described for MC: piecemeal degranulation (PMD) and anaphylactic degranulation (AND) (Figures 1 and 2). Both PMD and AND occur in vivo, ex vivo, and in vitro in MC in human (78–82), mouse (83), and rat (84). PMD is selective release of portions of the granule contents, without granule-to-granule and/or granule-to-plasma membrane fusions. ... In contrast to PMD, AND is the explosive release of granule contents or entire granules to the outside of cells after granule-to-granule and/or granule-to-plasma membrane fusions (Figures 1 and 2). Ultrastructural studies show that AND starts with granule swelling and matrix alteration after appropriate stimulation (e.g., FcεRI-crosslinking).»
Figure 1: Mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 2: Model of genesis of mast cell secretory granules Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 3: Lipid body biogenesis Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Table 2: Stimuli-selective mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Wilhelm M, Silver R, Silverman AJ (November 2005). «Central nervous system neurons acquire mast cell products via transgranulation». The European Journal of Neuroscience. 22 (9): 2238–48. doi:10.1111/j.1460-9568.2005.04429.x. PMC 3281766. PMID 16262662.
Carabotti M, Scirocco A, Maselli MA, Severi C (2015). «The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems». Ann Gastroenterol. 28 (2): 203–209. PMC 4367209. PMID 25830558.
Budzyński J, Kłopocka M (2014). «Brain-gut axis in the pathogenesis of Helicobacter pylori infection». World J. Gastroenterol. 20 (18): 5212–25. doi:10.3748/wjg.v20.i18.5212. PMC 4017036. PMID 24833851. «In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector»{{cite journal}}: CS1 սպաս․ չպիտակված ազատ DOI (link)
Li W, Deanin GG, Margolis B, Schlessinger J, Oliver JM (July 1992). «FcεR1-mediated tyrosine phosphorylation of multiple proteins, including phospholipase Cγ1 and the receptor βγ2 complex, in RBL-2H3 rat basophilic leukemia cells». Molecular and Cellular Biology. 12 (7): 3176–82. doi:10.1128/MCB.12.7.3176. PMC 364532. PMID 1535686.
Pundir, Priyanka; Liu, Rui; Vasavda, Chirag; Serhan, Nadine; Limjunyawong, Nathachit; Yee, Rebecca; Zhan, Yingzhuan; Dong, Xintong; Wu, Xueqing; Zhang, Ying; Snyder, Solomon H; Gaudenzio, Nicolas; Vidal, Jorge E; Dong, Xinzhong (July 2019). «A Connective Tissue Mast-Cell-Specific ReceptorDetects Bacterial Quorum-Sensing Moleculesand Mediates Antibacterial Immunity». Cell Host & Microbe. 26 (1): 114–122. doi:10.1016/j.chom.2019.06.003. PMC 6649664. PMID 31278040. Վերցված է 2021 թ․ հուլիսի 7-ին.
Akin C, Valent P, Metcalfe DD (2010). «Mast cell activation syndrome: Proposed diagnostic criteria». J. Allergy Clin. Immunol. 126 (6): 1099–104.e4. doi:10.1016/j.jaci.2010.08.035. PMC 3753019. PMID 21035176.
Kumar M, Duraisamy K, Chow BK (May 2021). «Unlocking the Non-IgE Mediated Pseudo-Allergic Reaction Puzzle with Mas-Related G-Protein Coupled Receptor Member X2 (MRGPRX2)». Cells. 10 (5): 1033. doi:10.3390/cells10051033. PMC 8146469. PMID 33925682.

purl.org

անատոմիայի հիմնարար մոդել

sciencedirect.com

Tatemoto, Kazuhiko; Nozaki, Yuko; Tsuda, Ryoko; Konno, Shinobu; Tomura, Keiko; Furuno, Masahiro; Ogasawara, Hiroyuki; Edamura, Koji; Takagi, Hideo; Iwamura, Hiroyuki; Noguchi, Masato; Naito, Takayuki (2006). «Immunoglobulin E-independent activation of mast cell is mediated by Mrg receptors». Biochemical and Biophysical Research Communications. 349 (4): 1322–1328. doi:10.1016/j.bbrc.2006.08.177. PMID 16979137. Վերցված է 2021 թ․ հուլիսի 7-ին.

semanticscholar.org

api.semanticscholar.org

Ashmole I, Bradding P (May 2013). «Ion channels regulating mast cell biology». Clin. Exp. Allergy. 43 (5): 491–502. doi:10.1111/cea.12043. PMID 23600539. S2CID 1127584. «P2X receptors are ligand-gated non-selective cation channels that are activated by extracellular ATP. ... Increased local ATP concentrations are likely to be present around mast cells in inflamed tissues due to its release through cell injury or death and platelet activation [40]. Furthermore, mast cells themselves store ATP within secretory granules, which is released upon activation [41]. There is therefore the potential for significant Ca2+ influx into mast cells through P2X receptors. Members of the P2X family differ in both the ATP concentration they require for activation and the degree to which they desensitise following agonist activation [37, 38]. This opens up the possibility that by expressing a number of different P2X receptors mast cells may be able to tailor their response to ATP in a concentration dependent manner [37].»
Frieri M (2018). «Mast Cell Activation Syndrome». Clin Rev Allergy Immunol. 54 (3): 353–365. doi:10.1007/s12016-015-8487-6. PMID 25944644. S2CID 5723622. «Table 1
Classification of diseases associated with mast cell activation from Akin et al. [14]
1. Primary
  a. Anaphylaxis with an associated clonal mast cell disorder
  b. Monoclonal mast cell activation syndrome (MMAS), see text for explanation
2. Secondary
  a. Allergic disorders
  b. Mast cell activation associated with chronic inflammatory or neoplastic disorders
  c. Physical urticarias (requires a primary stimulation)
  d. Chronic autoimmune urticaria
3. Idiopathic (When mast cell degranulation has been documented; may be either primary or secondary. Angioedema may be associated with hereditary or acquired angioedema where it may be mast cell independent and result from kinin generation)
  a. Anaphylaxis
  b. Angioedema
  c. Urticaria
  d. Mast cell activation syndrome (MCAS)...
Recurrent idiopathic anaphylaxis presents with allergic signs and symptoms—hives and angioedema which is a distinguishing feature—eliminates identifiable allergic etiologies, considers mastocytosis and carcinoid syndrome, and is treated with H1 and H2 antihistamines, epinephrine, and steroids [21, 22].»
Alm PE (April 1983). «Sodium fluoride evoked histamine release from mast cells. A study of cyclic AMP levels and effects of catecholamines». Agents and Actions. 13 (2–3): 132–7. doi:10.1007/bf01967316. PMID 6191542. S2CID 6977280.
Lee DM, Friend DS, Gurish MF, Benoist C, Mathis D, Brenner MB (September 2002). «Mast cells: a cellular link between autoantibodies and inflammatory arthritis». Science. 297 (5587): 1689–92. Bibcode:2002Sci...297.1689L. doi:10.1126/science.1073176. PMID 12215644. S2CID 38504601.
Blumenkrantz N, Asboe-Hansen G (May 1975). «A selective stain for mast cells». The Histochemical Journal. 7 (3): 277–82. doi:10.1007/BF01003596. PMID 47855. S2CID 32711203.
Fujimiya, Mineko; Inui, Akio (2000). «Peptidergic regulation of gastrointestinal motility in rodents». Peptides. Elsevier BV. 21 (10): 1565–1582. doi:10.1016/s0196-9781(00)00313-2. ISSN 0196-9781. PMID 11068106. S2CID 45185196.

uni-sz.bg

tru.uni-sz.bg

Tomov, N.; Dimitrov, N. (2017). «Modified bismarck brown staining for demonstration of soft tissue mast cells» (PDF). Trakia Journal of Sciences. 15 (3): 195–197. doi:10.15547/tjs.2017.03.001.

web.archive.org

«labrocytes». Memidex. Արխիվացված է օրիգինալից 2018 թ․ նոյեմբերի 6-ին. Վերցված է 2011 թ․ փետրվարի 19-ին.
Moon TC, Befus AD, Kulka M (2014). «Mast cell mediators: their differential release and the secretory pathways involved». Front Immunol. 5: 569. doi:10.3389/fimmu.2014.00569. PMC 4231949. PMID 25452755. «Two types of degranulation have been described for MC: piecemeal degranulation (PMD) and anaphylactic degranulation (AND) (Figures 1 and 2). Both PMD and AND occur in vivo, ex vivo, and in vitro in MC in human (78–82), mouse (83), and rat (84). PMD is selective release of portions of the granule contents, without granule-to-granule and/or granule-to-plasma membrane fusions. ... In contrast to PMD, AND is the explosive release of granule contents or entire granules to the outside of cells after granule-to-granule and/or granule-to-plasma membrane fusions (Figures 1 and 2). Ultrastructural studies show that AND starts with granule swelling and matrix alteration after appropriate stimulation (e.g., FcεRI-crosslinking).»
Figure 1: Mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 2: Model of genesis of mast cell secretory granules Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Figure 3: Lipid body biogenesis Արխիվացված 29 Ապրիլ 2018 Wayback Machine
Table 2: Stimuli-selective mediator release from mast cells Արխիվացված 29 Ապրիլ 2018 Wayback Machine
«Cutaneous Mast Cell Tumors». The Merck Veterinary Manual. 2006. Արխիվացված օրիգինալից 2007 թ․ մայիսի 23-ին. Վերցված է 2007 թ․ հուլիսի 8-ին.

worldcat.org

Fujimiya, Mineko; Inui, Akio (2000). «Peptidergic regulation of gastrointestinal motility in rodents». Peptides. Elsevier BV. 21 (10): 1565–1582. doi:10.1016/s0196-9781(00)00313-2. ISSN 0196-9781. PMID 11068106. S2CID 45185196.