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杨敏之 《上海交通大学学报》1990,24(2):8-15
本文给出双极性电池堆电池数学模型.利用在模拟电流回路中的电流平衡和电势平衡建立常系数线性差分方程组,及其求解电池堆泄漏电流等,并对计算结果进行分析和讨论,调整各参数使电池堆达到最佳状态.采用本文的差分方程组法比Katz 和Szpak 等的矩阵法简单方便,并且更有效. 相似文献
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电池电动势是电化学中最基本的概念。顾宏邦同志先后发表了《电池电动势的探讨》与《电池电动势再探》两篇论文。他试图从电化学势出发,推出了“能统一两大学派的”表达电池电动势的“新公式”,并声称该公式说明了著名电化学家Conway、以及查全性的“臆断”和“不 相似文献
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陈悦 《宝鸡文理学院学报(自然科学版)》1996,16(3):35-36,3
对于一个有不止一种价态的过渡元素及其离子的氧化还原反应,可以对应两种电池,这两种电池的电动势相差简单整数倍;而由汞及其两种离子的溶液组成的两种电池的电动势是相等的。 相似文献
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Stem cells: iPS cells under attack 总被引:1,自引:0,他引:1
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Biomimetics,a term defined by Schmitt in 1960s,has been accompanying the development of humanity in learning from nat-ure to solve problems over billions of yea... 相似文献
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Several cell types have been proposed to create niches for haematopoietic stem cells (HSCs). However, the expression patterns of HSC maintenance factors have not been systematically studied and no such factor has been conditionally deleted from any candidate niche cell. Thus, the cellular sources of these factors are undetermined. Stem cell factor (SCF; also known as KITL) is a key niche component that maintains HSCs. Here, using Scf(gfp) knock-in mice, we found that Scf was primarily expressed by perivascular cells throughout the bone marrow. HSC frequency and function were not affected when Scf was conditionally deleted from haematopoietic cells, osteoblasts, nestin-cre- or nestin-creER-expressing cells. However, HSCs were depleted from bone marrow when Scf was deleted from endothelial cells or leptin receptor (Lepr)-expressing perivascular stromal cells. Most HSCs were lost when Scf was deleted from both endothelial and Lepr-expressing perivascular cells. Thus, HSCs reside in a perivascular niche in which multiple cell types express factors that promote HSC maintenance. 相似文献
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Can B cells turn on virgin T cells? 总被引:16,自引:0,他引:16
The first event in the initiation of an immune response is the capture and presentation of antigen to T cells. Such presentation involves two distinct steps: (1) display of the antigen, which requires uptake, processing and re-expression of the antigen in association with MHC molecules on the presenting cell surface; and (2) triggering, in which the presenting cell provides signals leading to the activation of the responding T cell. Two sorts of cells can capture antigens, the 'professional' antigen-presenting cells (APCs) such as dendritic cells and macrophages, and the B cells. Both types of cells can display antigens and the APCs are known to be able to trigger resting T cells. But despite in vitro evidence that certain B-cell types can reactivate previously-activated T cells, it is not yet clear whether a B cell can initiate an immune response by providing the signals necessary to activate a resting T cell. We reasoned that resting B cells should not have this capacity because of the problems this would present with tolerance to self idiotypes. By exploiting the unique properties of the avian haematopoietic system, we have examined the presenting capacity of B cells in vivo and found that resting B cells are indeed unable to activate resting T cells. 相似文献
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Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells 总被引:2,自引:0,他引:2
Recent advances have highlighted extensive phenotypic and functional similarities between normal stem cells and cancer stem cells. This raises the question of whether disease therapies can be developed that eliminate cancer stem cells without eliminating normal stem cells. Here we address this issue by conditionally deleting the Pten tumour suppressor gene in adult haematopoietic cells. This led to myeloproliferative disease within days and transplantable leukaemias within weeks. Pten deletion also promoted haematopoietic stem cell (HSC) proliferation. However, this led to HSC depletion via a cell-autonomous mechanism, preventing these cells from stably reconstituting irradiated mice. In contrast to leukaemia-initiating cells, HSCs were therefore unable to maintain themselves without Pten. These effects were mostly mediated by mTOR as they were inhibited by rapamycin. Rapamycin not only depleted leukaemia-initiating cells but also restored normal HSC function. Mechanistic differences between normal stem cells and cancer stem cells can thus be targeted to deplete cancer stem cells without damaging normal stem cells. 相似文献