排序方式: 共有75条查询结果,搜索用时 13 毫秒
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(接上期)上面提到的非定居移住民,是指从福建及浙江省南部的台州府等地流入奉化县山区的人,即所谓的“棚民”。在位于忠义乡以西的剡源乡,可以见到如下的记事 。剡源向乏水患,亦无劫案。自嘉庆初,闽、台(福建省与浙江省台州府———引用者)棚民相率来剡〔源乡〕,种靛青、种苞芦,日辟日广。如牛山之濯濯水,无所蓄迨。〔嘉庆〕末年,大雨连旬,山水骤注于溪,溪不能容,遂漂没田畴无算。……比年仙居、黄岩无业贫民偕来工作,寓居山厂,一不得食,抢劫之案,层见叠出。由此来看,自嘉庆初年( 1 8世纪末)以降,福建等地的棚民、浙江南部的贫民流入该地山… 相似文献
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Makoto Ue 《复旦学报(自然科学版)》2007,(5)
1 Results Electrochemical energy storage devices such as lithium-ion batteries[1-2] and double-layer capacitors[3-4] have attracted a great deal of attention because of their potential application to electric hybrid vehicles. They utilize nonaqueous electrolyte solutions comprising from organic solvents and lithium or quaternary ammonium salts with fluorine-containing anions. This is because the relatively large anions with electron-withdrawing atoms enable ionic dissociation in dipolar aprotic solvents... 相似文献
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A. Tsukui S. Fukuda K. Shimoji 《Cellular and molecular life sciences : CMLS》1992,48(11-12):1118-1121
The responses of basilar arteries (BAs) to serotonin were attenuated by high \(P_{CO_2 } \) (86±1 mm Hg) and the pH matched acidotic solution ( \(P_{CO_2 } \) 37±1 mm Hg), whereas the responses of middle cerebral arteries (MCAs) were not. High \(P_{CO_2 } \) decreased the basal tone of both arteries, and the changes in basal tone due to high \(P_{CO_2 } \) were not influenced by 3×10?7 M imipramine, 10?5 M pargyline or 10?4 M aspirin. The responses of BAs to serotonin were attenuated by high \(P_{CO_2 } \) in the presence of imipramine, pargyline and aspirin. The responses of MCAs to serotonin were not influenced by high \(P_{CO_2 } \) in the presence of pargyline and aspirin, but attenuated by high \(P_{CO_2 } \) in the presence of imipramine. 相似文献
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KakuzoIwamura MakotoHoriike TomoyaSibahara 《清华大学学报》2003,8(1):14-18
A genetic algorithm to solve the set covering problem proposed in the literature had some improvements which gave better solutions, i.e., better chromosomes in the first starting population, taking full account of domain specific knowledge with sound programming skill. We have further investigated the input data dependency of their genetic algorithm, i.e., the dependency on costs and density. We have found that for input problem data sets with densities greater than or equal to 3%, our genetic algorithm is still practical both in computing time and approximation ratio. 相似文献
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Tezuka H Abe Y Iwata M Takeuchi H Ishikawa H Matsushita M Shiohara T Akira S Ohteki T 《Nature》2007,448(7156):929-933
Immunoglobulin-A has an irreplaceable role in the mucosal defence against infectious microbes. In human and mouse, IgA-producing plasma cells comprise approximately 20% of total plasma cells of peripheral lymphoid tissues, whereas more than 80% of plasma cells produce IgA in mucosa-associated lymphoid tissues (MALT). One of the most biologically important and long-standing questions in immunology is why this 'biased' IgA synthesis takes place in the MALT but not other lymphoid organs. Here we show that IgA class-switch recombination (CSR) is impaired in inducible-nitric-oxide-synthase-deficient (iNOS-/-; gene also called Nos2) mice. iNOS regulates the T-cell-dependent IgA CSR through expression of transforming growth factor-beta receptor, and the T-cell-independent IgA CSR through production of a proliferation-inducing ligand (APRIL, also called Tnfsf13) and a B-cell-activating factor of the tumour necrosis factor (TNF) family (BAFF, also called Tnfsf13b). Notably, iNOS is preferentially expressed in MALT dendritic cells in response to the recognition of commensal bacteria by toll-like receptor. Furthermore, adoptive transfer of iNOS+ dendritic cells rescues IgA production in iNOS-/- mice. Further analysis revealed that the MALT dendritic cells are a TNF-alpha/iNOS-producing dendritic-cell subset, originally identified in mice infected with Listeria monocytogenes. The presence of a naturally occurring TNF-alpha/iNOS-producing dendritic-cell subset may explain the predominance of IgA production in the MALT, critical for gut homeostasis. 相似文献
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DAI (DLM-1/ZBP1) is a cytosolic DNA sensor and an activator of innate immune response 总被引:4,自引:0,他引:4
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Resolution of acute inflammation is an active process essential for appropriate host responses, tissue protection and the return to homeostasis. During resolution, specific omega-3 polyunsaturated fatty-acid-derived mediators are generated within resolving exudates, including resolvin E1 (RvE1) and protectin D1 (PD1). It is thus important to pinpoint specific actions of RvE1 and PD1 in regulating tissue resolution. Here we report that RvE1 and PD1 in nanogram quantities promote phagocyte removal during acute inflammation by regulating leukocyte infiltration, increasing macrophage ingestion of apoptotic polymorphonuclear neutrophils in vivo and in vitro, and enhancing the appearance of phagocytes carrying engulfed zymosan in lymph nodes and spleen. In this tissue terrain, inhibition of either cyclooxygenase or lipoxygenases--pivotal enzymes in the temporal generation of both pro-inflammatory and pro-resolving mediators--caused a 'resolution deficit' that was rescued by RvE1, PD1 or aspirin-triggered lipoxin A4 analogue. Also, new resolution routes were identified that involve phagocytes traversing perinodal adipose tissues and non-apoptotic polymorphonuclear neutrophils carrying engulfed zymosan to lymph nodes. Together, these results identify new active components for postexudate resolution traffic, and demonstrate that RvE1 and PD1 are potent agonists for resolution of inflamed tissues. 相似文献
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A quantitative trait locus regulating rice grain width 总被引:1,自引:0,他引:1
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Kitamura T Kometani K Hashida H Matsunaga A Miyoshi H Hosogi H Aoki M Oshima M Hattori M Takabayashi A Minato N Taketo MM 《Nature genetics》2007,39(4):467-475
Inactivation of TGF-beta family signaling is implicated in colorectal tumor progression. Using cis-Apc(+/Delta716) Smad4(+/-) mutant mice (referred to as cis-Apc/Smad4), a model of invasive colorectal cancer in which TGF-beta family signaling is blocked, we show here that a new type of immature myeloid cell (iMC) is recruited from the bone marrow to the tumor invasion front. These CD34(+) iMCs express the matrix metalloproteinases MMP9 and MMP2 and the CC-chemokine receptor 1 (CCR1) and migrate toward the CCR1 ligand CCL9. In adenocarcinomas, expression of CCL9 is increased in the tumor epithelium. By deleting Ccr1 in the background of the cis-Apc/Smad4 mutant, we further show that lack of CCR1 prevents accumulation of CD34(+) iMCs at the invasion front and suppresses tumor invasion. These results indicate that loss of transforming growth factor-beta family signaling in tumor epithelium causes accumulation of iMCs that promote tumor invasion. 相似文献