Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight patients with transfusion-dependent thalassemia major were given continuous intravenous infusions of the chelator, deferoxamine mesylate, to reduce iron overload. Within 5 to 9 days of starting the infusions, four patients developed a pulmonary syndrome of moderate to life-threatening severity characterized by tachypnea, hypoxemia, and a diffuse interstitial pattern on chest roentgenogram. Pulmonary function studies showed restrictive dysfunction. Lung biopsy showed diffuse abnormalities with alveolar damage, interstitial fibrosis, and inflammation. The inflammatory infiltrate comprised lymphocytes, eosinophils, and mast cells. Exposure of the biopsy specimen to fluorescein-conjugated anti-IgE antibody showed fixation of IgE to the mast cell surface, suggesting a hypersensitivity reaction. Detailed studies failed to identify an infectious agent. The temporal relationship between drug administration and lung disease, and the clinical similarities in the four affected patients, strongly suggested a cause and effect relationship. We recommend that therapy with continuous intravenous infusions of deferoxamine be monitored carefully with respect to pulmonary status.
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PMID:Pulmonary syndrome in patients with thalassemia major receiving intravenous deferoxamine infusions. 233 Sep 23

Mast cells were identified by electronmicroscopy in the alveolar wall of the lung in 20 subjects (10 normal, 10 abnormal). A quantitative and qualitative study was made of the mast cells. In the normal lung there was an average concentration of 350 mast cells/mm2 of alveolar wall and in the abnormal 523/mm2. Mast cells occupied approximately 1.6-2.1% of the area of the alveolar wall. There was marked variation in the structure of the mast cell granules but no differences between those in the normal and abnormal lungs. There was evidence that constant degranulation of mast cells may be occurring in the lung. The role that alveolar mast cells may play in the vasoconstrictor response to alveolar hypoxia is discussed. It is suggested that the tachypnoea present in asthma may partly be due to release of mediators from sensitised mast cells within the alveolar wall.
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PMID:Mast cells in the human alveolar wall: an electronmicroscopic study. 732 80

Tumor necrosis factor-alpha (TNF-alpha) has been implicated as an important mediator in the development of multiple system organ failure after either severe injury or infection. Using the rat cremaster muscle, we previously showed that systemically administered TNF-alpha caused hypotension, tachypnea, and microvascular protein leakage in association with leukocyte-endothelial adherence. In the current study, we hypothesized that topical administration of TNF-alpha to the cremaster muscle would cause microvascular protein leakage independent of changes in hemodynamic parameters. In addition, histological methods were used to study the role of neutrophils and mast cells in the TNF-alpha-induced microvascular protein leakage. Topically applied low-dose (1 ng/ml) TNF-alpha caused microvascular leakage in the cremaster, without changes in central hemodynamic parameters, but high-dose TNF-alpha (10 ng/ml) did not cause protein leakage. Histological studies did not demonstrate evidence of either neutrophil adhesion or mast cell degranulation in topically applied TNF-alpha-treated cremasters compared to controls. These data suggest that TNF-alpha-induced macromolecular leakage is a dose-dependent phenomenon which can occur independently of neutrophils or mast cell degranulation.
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PMID:Tumor necrosis factor causes microvascular protein leakage independently of neutrophils or mast cells. 801

The effects of intravenous (iv) administration of the synthetic opioid analgesic meperidine in conscious dogs and their relation to histamine stored in mast cells were studied in comparison with those induced by compound 48/80, potent mast cell degranulator. When 48/80 (0.5 mg/ kg) and meperidine (10 mg/kg) were injected iv into conscious dogs, an acute brief period of yelling, flare reaction, scratching, hypersalivation, urination, defecation, and tachypnea occurred after a latency of 30-35 sec. In addition, meperidine-treated dogs showed marked sedation. Dogs whose histamine stores were depleted by 48/80 manifested none of those effects induced by meperidine except sedation. Likewise, pretreatment with meperidine prevented the effects of a subsequent injection of 48/80. Sedation appeared to be independent of the histamine-releasing effect of meperidine, whereas other effects elicited by its intravenous injection of the drug were suppressed by 48/80 and thus were probably mediated via released histamine. We concluded that the peripheral effects of meperidine show histamine dependency and mast cells are a potential important site for the peripheral actions of meperidine as well.
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PMID:The role of mast cells in the genesis of acute manifestations following the intravenous injection of meperidine in dogs. 1960 96

A 9-year-old crossbred dog was presented with a 2-week history of diarrhoea and tachypnoea. Marked circulating eosinophilia was identified. Pleural and abdominal effusions were detected by radiography and ultrasonography and cytological examination of these fluids revealed a predominance of eosinophils. Splenic and hepatic cytology revealed mast cell neoplasia, which was confirmed as visceral mast cell tumour on post-mortem examination. Histological changes of myocardial inflammation, necrosis and fibrosis were found. These findings are consistent with Loeffler's endocarditis.
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PMID:Loeffler's endocarditis and bicavity eosinophilic effusions in a dog with visceral mast cell tumour and hypereosinophilia. 2380 8