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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19-48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30-500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.
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PMID:Lung mast cell density and distribution in chronically hypoxic animals. 13 66

Systemic mastocytosis occurred as a fatal event in a patient with long-standing polycythemia vera. The patient had been treated over the course of 21 yr with radioactive phosphorus. Possible relationships between mastocytosis and polycythemia vera, and also between mastocytosis and treatment with ionizing radiation, are discussed. Histopathologic and electron microscopic findings are illustrated. Difficulties in establishing the diagnosis of mast cell disease in this setting are also described.
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PMID:Systemic mastocytosis in a patient with polycythemia vera treated with radioactive phosphorus. 30 Feb 55

To investigate mechanisms of mast-cell proliferation, we have utilized infection of Lewis rats with the intestinal nematode, Nippostrongylus brasiliensis, which induces a pronounced intestinal mast-cell hyperplasia. Adoptive transfer of 2 x 10(8) immune mesenteric lymph node cells (IMLN), collected 14 days post infection with 3000 third stage larvae (L3), into rats concurrently given 3000 L3 hastened the expected intestinal mastocytosis by up to 4-5 days. IMLN exhibited this mastopoietic activity in the presence but not in the absence of concurrent infection. Normal mesenteric lymph node cells did not show similar mastopoietic activity. Intestinal mastocytosis was delayed by sub-lethal irradiation (400 rad) but IMLN reconstituted the mast-cell response of such animals. The mastopoietic activity could not be attributed to worm antigen as antigen administered intravenously had no significant effect on mastocytosis and furthermore, antigen could not be detected in mastopoietically active IMLN suspensions used as a possible antigen source in passive cutaneous anaphylaxis tests. Immune serum (14 days post primary infection with 3000 L3) also hastened mastocytosis in infected rats, whereas normal serum did not. The IMLN may be an enriched source of intestinal mast cell precursors and, in addition, may contain a cell type(s) which regulates the differentiation and proliferation of such precursors.
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PMID:Immunologically mediated intestinal mastocytosis in Nippostrongylus brasiliensis-infected rats. 31 19

The ultrastructural aspects of mast cells from skin lesions in 2 patients with mastocytoma were compared to those from lesions in 4 patients with mastocytosis, 3 with cutaneous and 1 with systemic involvement. In mastocytoma, the mast cells accumulated in a large mass. They revealed short cytoplasmic villi and were similar, morphologically, to mast cells of normal skin and gingiva. In the diffuse types of the disease, cutaneous and systemic, the cells were arranged in small groups. In addition to normal mast cells, there were also irregular or bizarre-shaped cells presenting long and twisted cytoplasmic protrusions. In the case with the systemic involvement and in 2 of 3 cases with apparently cutaneous diffuse lesions, the villi of adjacent cells interlaced and showed a tendency to form mast cell aggregates. The pathognomonic value of the above observation seems worthy of further investigations.
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PMID:Comparative ultrastructural study of mast cells in mastocytoma and mastocytosis. 40 98

We report the case of a 66-year-old male patient with portal hypertension related to systemic mastocytosis. The liver was enlarged; microscopic examination showed portal mast cell infiltration and fibrosis. Portal hypertension was evidenced by splenomegaly, esophageal varices, and increased wedged-free hepatic venous pressure gradient. Arteriography showed that portal vein was patent. Portal hypertension could be the consequence of intrahepatic block due to mast cell infiltration and/or fibrosis of the liver.
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PMID:Portal hypertension in systemic mastocytosis. 63 92

We report the case of a 15-month-old child suffering from diffuse cutaneous mastocytosis characterized by blisters and widespread skin involvement but without systemic manifestations. Skin biopsies were examined by electron microscopy. We observed various alterations in the morphology of mast cells and mast cell granules.
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PMID:[Diffuse cutaneous mastocytosis in childhood]. 66 67

Two patients with mast cell disease presented with unusual features. In one the absence of skin lesions made the diagnositic problem a challenging one. Certain of the laboratory findings, especially those related to the serum cholesterol concentration and platelet function tests, were particularyl interesting. Chemotherapy induced partial remission. The second patient had a long, relatively benign course complicated by two episodes of herpes zoster, the last being associated with the Landry-Guillain-Barre syndrome. In both patients the skeletal abnormalities were radiologically similar. When these are present they should be considereed sufficiently characteristic to indicate strongly a diagnosis of mastocytosis.
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PMID:Mastocytosis: unusual manifestation; clinical and radiologic changes. 80 88

Small bipsies of the skin were taken from patients with papulo-cutaneous mastocytosis. The mast cell tumours were then degranulated with compound 48/80 (250 mug/ml in saline), and with a Sorption microcalorimeter, relatively strong exothermic reactions were measured, whereas normal skin showed only 1/10th the intensity. Disodium chromoglicate (1%) had no inhibitory effect on this thermal reaction.
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PMID:Thermal effects from degranulation of mastcells in cutaneous mastocytosis. 83 33

Phospholipid preparations from the nematode Ascaris suum or cysts of Echinococcus granulosus (hydatid cysts) induced an eosinophilia when injected into the peritoneal cavity of rats. Peritoneal eosinophilia persisted throughout 21 days of daily injections of Ascaris lipid and was accompanied by blood eosinophilia, mast cell granule lysis and mast cell hyperplasia. The active material consisted of lecithin and lecithin plasmalogen, and in aqueous suspension had a membrane-like appearance. Electron microscopy revealed that the phospholipid was ingested by all types of cells in the peritoneal cavity, including mast cells, and was rapidly broken down by eosinophils. Phagocytosis was found to be complement dependent. The lipid combined with properdin in human serum and stimulated complement breakdown via the alternative complement pathway.
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PMID:Eosinophilia and mast cell hyperplasia induced by parasite phospholipid. 87 90

Exposure to acute hypoxia (barometric pressure 263 mmHg) for 8 hours did not lead to increased numbers of mast cells in the lungs of rats. In contrast, in adult rats kept for 35 days at a barometric pressure of 380 mmHg there was a proliferation of mast cells around the pulmonary blood vessels and in the alveolar septa. This hyperplasia of lung mast cells in response to chronic hypoxia was reversible on removal of the hypoxic stimulus. There was a correlation between the logarithm of the perivascular lung mast cell density (defined in the paper) and the logarithm of the right ventricular weight. There was no increase in the mast cells in the carotid bodies of the hypoxic rats. Young male, old male, young female, and old female rats which had been subjected for 39 days to a barometric pressure of 380 mmHg showed a proliferation of mast cells around the pulmonary blood vessels and in the alveolar walls. This response was greatest in the adult animals and independent of their sex. In the age and sex experiment there was a correlation between the perivascular lung mast cell density and the medial thickness of the muscular pulmonary arteries. Since mast cell hyperplasia has been reported as preceding right ventricular hypertrophy, it is conceivable that mast cell proliferation in the lung may be a defence mechanism to limit the severity of hypoxic pulmonary hypertension rather than to mediate it.
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PMID:Lung mast cells in rats exposed to acute hypoxia, and chronic hypoxia with recovery. 88 42


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