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基因性肥大细胞缺陷的W/Wv小鼠中的自发性胃溃疡

Spontaneous stomach ulcer in genetically mast-cell depleted W/Wv mice.

作者信息

Shimada M, Kitamura Y, Yokoyama M, Miyano Y, Maeyama K, Yamatodani A, Takahashi Y, Tatsuta M

出版信息

Nature. 1980 Feb 14;283(5748):662-4. doi: 10.1038/283662a0.

DOI:10.1038/283662a0
PMID:7354854
Abstract

Histamine has been implicated in the pathogenesis of gastroduodenal ulcers. Since mast cells contain a considerable amount of histamine as well as heparin and other biologically active substances, it seems reasonable to speculate that they are involved in this process. In fact, development of gastroduodenal ulcers was reported in dogs with mastocytoma, and an increase in mast-cell number was described in the vicinity of human gastroduodenal ulcers. Y.K. et al. have recently found that the number of mast cells in a unit length of the skin of W/Wv mutant mice is less than 1% of the value for the congeneic +/+ mice and that no mast cells are detected in the intestinal canal of W/Wv mice. Therefore, this mutant mouse was used to investigate the role of mast cells in the induction of gastroduodenal ulcers. As a preliminary experiment, we examined the stomach and duodenum of W/Wv mice without any treatments. Unexpectedly, we found the spontaneous development of perforating stomach ulcers in W/Wv mice, suggesting that mast cells do not necessarily have aggravating effects on the production of stomach ulcers.

摘要

组胺已被认为与胃十二指肠溃疡的发病机制有关。由于肥大细胞含有大量组胺以及肝素和其他生物活性物质,推测它们参与这一过程似乎是合理的。事实上,有报道称患有肥大细胞瘤的犬会发生胃十二指肠溃疡,并且在人类胃十二指肠溃疡附近观察到肥大细胞数量增加。Y.K.等人最近发现,W/Wv突变小鼠单位长度皮肤中的肥大细胞数量不到同基因+/+小鼠的1%,并且在W/Wv小鼠的肠道中未检测到肥大细胞。因此,本研究使用这种突变小鼠来探讨肥大细胞在胃十二指肠溃疡诱导中的作用。作为初步实验,我们检查了未经任何处理的W/Wv小鼠的胃和十二指肠。出乎意料的是,我们发现W/Wv小鼠出现了自发性穿孔性胃溃疡,这表明肥大细胞不一定对胃溃疡的产生有加重作用。

相似文献

1
Spontaneous stomach ulcer in genetically mast-cell depleted W/Wv mice.基因性肥大细胞缺陷的W/Wv小鼠中的自发性胃溃疡
Nature. 1980 Feb 14;283(5748):662-4. doi: 10.1038/283662a0.
2
Fate of bone marrow-derived cultured mast cells after intracutaneous, intraperitoneal, and intravenous transfer into genetically mast cell-deficient W/Wv mice. Evidence that cultured mast cells can give rise to both connective tissue type and mucosal mast cells.将骨髓来源的培养肥大细胞经皮内、腹腔内和静脉内注射转移至遗传性肥大细胞缺陷的W/Wv小鼠后的命运。有证据表明培养的肥大细胞可分化为结缔组织型和黏膜型肥大细胞。
J Exp Med. 1985 Sep 1;162(3):1025-43. doi: 10.1084/jem.162.3.1025.
3
Tissue histamine levels in male and female mast cell deficient mice (W/Wv) and in their littermates (Wv/+, W/+ and +/+).
Agents Actions. 1985 Oct;17(1):1-4. doi: 10.1007/BF01966671.
4
Development of large numbers of mast cells at sites of idiopathic chronic dermatitis in genetically mast cell-deficient WBB6F1-W/Wv mice.在基因性肥大细胞缺陷的WBB6F1-W/Wv小鼠的特发性慢性皮炎部位出现大量肥大细胞。
Blood. 1987 Jun;69(6):1661-6.
5
Decrease of mast cells in W/Wv mice and their increase by bone marrow transplantation.W/Wv小鼠中肥大细胞数量减少,而骨髓移植可使其数量增加。
Blood. 1978 Aug;52(2):447-52.
6
Clonal nature of mast-cell clusters formed in W/Wv mice after bone marrow transplantation.骨髓移植后W/Wv小鼠中形成的肥大细胞簇的克隆性质。
Nature. 1979 Sep 13;281(5727):154-5. doi: 10.1038/281154a0.
7
Mast-cell-deficient W/Wv mice exhibit a decreased rate of tumor angiogenesis.肥大细胞缺陷的W/Wv小鼠表现出肿瘤血管生成速率降低。
Int J Cancer. 1988 Jul 15;42(1):48-52. doi: 10.1002/ijc.2910420110.
8
Genetically mast cell-deficient W/Wv mice as a tool for studies of differentiation and function of mast cells.基因性肥大细胞缺陷的W/Wv小鼠作为研究肥大细胞分化和功能的工具。
Fed Proc. 1987 Apr;46(5):1920-3.
9
The role of mast cells in thioglycollate-induced inflammation.肥大细胞在巯基乙酸诱导的炎症中的作用。
J Immunol. 1988 Sep 15;141(6):2090-6.
10
Proliferation and differentiation in culture of mast cell progenitors derived from mast cell-deficient mice of genotype W/Wv.源自基因型为W/Wv的肥大细胞缺陷小鼠的肥大细胞祖细胞在培养中的增殖与分化。
J Cell Physiol. 1985 Feb;122(2):187-92. doi: 10.1002/jcp.1041220204.

引用本文的文献

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Mast Cells: Key Contributors to Cardiac Fibrosis.肥大细胞:心脏纤维化的关键贡献者。
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2
Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4 T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis.在对委内瑞拉类圆线虫的初次和二次免疫中,肥大细胞、嗜碱性粒细胞、IgE和IgG与CD4 T细胞和ILC2细胞的重要性差异。
Infect Immun. 2017 Apr 21;85(5). doi: 10.1128/IAI.00053-17. Print 2017 May.
3
Histamine from brain resident MAST cells promotes wakefulness and modulates behavioral states.
来自脑内常驻肥大细胞的组胺促进觉醒并调节行为状态。
PLoS One. 2013 Oct 18;8(10):e78434. doi: 10.1371/journal.pone.0078434. eCollection 2013.
4
Mast cells are critical for protection against peptic ulcers induced by the NSAID piroxicam.肥大细胞对于预防 NSAID 吡罗昔康引起的消化性溃疡至关重要。
PLoS One. 2011;6(8):e23669. doi: 10.1371/journal.pone.0023669. Epub 2011 Aug 12.
5
Restoration of gut motility in Kit-deficient mice by bone marrow transplantation.通过骨髓移植恢复Kit缺陷小鼠的肠道运动能力。
J Gastroenterol. 2009;44(8):834-41. doi: 10.1007/s00535-009-0077-z. Epub 2009 May 21.
6
Gastrointestinal stromal tumors: past, present, and future.胃肠道间质瘤:过去、现在与未来
J Gastroenterol. 2008;43(7):499-508. doi: 10.1007/s00535-008-2200-y. Epub 2008 Jul 23.
7
Mast cell-deficient W-sash c-kit mutant Kit W-sh/W-sh mice as a model for investigating mast cell biology in vivo.肥大细胞缺陷的W-sash c-kit突变体Kit W-sh/W-sh小鼠作为体内研究肥大细胞生物学的模型。
Am J Pathol. 2005 Sep;167(3):835-48. doi: 10.1016/S0002-9440(10)62055-X.
8
Gastrointestinal stromal tumors (GIST): a model for molecule-based diagnosis and treatment of solid tumors.胃肠道间质瘤(GIST):实体瘤分子诊断与治疗的模型
Cancer Sci. 2003 Apr;94(4):315-20. doi: 10.1111/j.1349-7006.2003.tb01439.x.
9
Allelic loss of 14q and 22q, NF2 mutation, and genetic instability occur independently of c-kit mutation in gastrointestinal stromal tumor.在胃肠道间质瘤中,14号染色体长臂(14q)和22号染色体长臂(22q)的等位基因缺失、神经纤维瘤病2型(NF2)基因突变以及基因不稳定性的发生独立于c-kit基因突变。
Jpn J Cancer Res. 2000 Dec;91(12):1241-9. doi: 10.1111/j.1349-7006.2000.tb00910.x.
10
Bile reflux due to disturbed gastric movement is a cause of spontaneous gastric ulcer in W/Wv mice.胃运动紊乱导致的胆汁反流是W/Wv小鼠自发性胃溃疡的一个原因。
Dig Dis Sci. 1999 Jun;44(6):1177-83. doi: 10.1023/a:1026684425642.