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In this article we discuss how an interdisciplinary research team partnered with a variety of stakeholders concerned with and/or affected by the impacts of climate change in the Red River Delta of Vietnam. The research, undertaken from 2016 to 2018, drew upon a wide range of methods to investigate systemically these impacts – with a view to the research inputting into the development of (more) sustainable ways of living. The research solicited various accounts of the experience of climate change in the community, set up learning processes in community meetings, and created an interface with government officials positioned at commune, district, provincial, and national levels. The intention was to offer support towards developing a learning process (broadly defined as including learnings/systemic inquiry across organizational levels of the society) to pursue options for sustainable living. The article offers our post-facto reflections which render more explicit (to ourselves and for the benefit of audiences) how the research team, with Hoang as lead researcher, facilitated the inquiry process towards developing a synthesis which underscored the assets for resilience to climate change and supported interventions to strengthen such (defined) assets.

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DNA damage checkpoint genes, such as p53, are frequently mutated in human cancer, but the selective pressure for their inactivation remains elusive. We analysed a panel of human lung hyperplasias, all of which retained wild-type p53 genes and had no signs of gross chromosomal instability, and found signs of a DNA damage response, including histone H2AX and Chk2 phosphorylation, p53 accumulation, focal staining of p53 binding protein 1 (53BP1) and apoptosis. Progression to carcinoma was associated with p53 or 53BP1 inactivation and decreased apoptosis. A DNA damage response was also observed in dysplastic nevi and in human skin xenografts, in which hyperplasia was induced by overexpression of growth factors. Both lung and experimentally-induced skin hyperplasias showed allelic imbalance at loci that are prone to DNA double-strand break formation when DNA replication is compromised (common fragile sites). We propose that, from its earliest stages, cancer development is associated with DNA replication stress, which leads to DNA double-strand breaks, genomic instability and selective pressure for p53 mutations.  相似文献   
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The mechanisms by which eukaryotic cells sense DNA double-strand breaks (DSBs) in order to initiate checkpoint responses are poorly understood. 53BP1 is a conserved checkpoint protein with properties of a DNA DSB sensor. Here, we solved the structure of the domain of 53BP1 that recruits it to sites of DSBs. This domain consists of two tandem tudor folds with a deep pocket at their interface formed by residues conserved in the budding yeast Rad9 and fission yeast Rhp9/Crb2 orthologues. In vitro, the 53BP1 tandem tudor domain bound histone H3 methylated on Lys 79 using residues that form the walls of the pocket; these residues were also required for recruitment of 53BP1 to DSBs. Suppression of DOT1L, the enzyme that methylates Lys 79 of histone H3, also inhibited recruitment of 53BP1 to DSBs. Because methylation of histone H3 Lys 79 was unaltered in response to DNA damage, we propose that 53BP1 senses DSBs indirectly through changes in higher-order chromatin structure that expose the 53BP1 binding site.  相似文献   
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为了从不锈钢粉尘中回收利用Fe,Cr和Ni等,对不锈钢粉尘热压块制备及其自还原过程进行了研究.在热压温度为200℃,热压压力为35 MPa条件下,抗压强度达到900 N/个以上.高温条件下,煤热解产生的挥发分可参与不锈钢粉尘还原反应,当还原温度为1 400,1 450℃时,挥发分还原作用率达到0.4.据XRD分析和热力学计算,自还原过程中含铬物质的物相转变顺序为Fe Cr2O4,Cr2O3,Cr7C3,[Cr]Fe-Cr-Ni-C.当还原温度为1 450℃,烟煤中固定碳与粉尘中可去除氧的物质量的比(xc/xo)为0.72时,不锈钢粉尘热压块不能完全还原;当xc/xo大于0.8,还原20 min时,不锈钢粉尘热压块能完全还原.  相似文献   
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辽宁本溪地区条带状铁矿(BIF)与其玄武质火山围岩之间的时空关联非常密切.对于玄武质火山围岩高场强元素(HFSE)的研究表明:wNb/wTa比值(7.00~19.93)表现出明显的分异,而wZr/wHf比值(33.46~38.28)则变化不大;从弓长岭到南芬、歪头山样品的wNb/wTa比值变化具有明显的循序性.这种高场强元素的迁移和分异特征反映出俯冲作用与盆地演化之间的关联.研究区玄武质火山围岩(wNb/wYb)N比值大于1(1.21~18.45,平均2.72),这进一步表明,其形成的构造背景为陆内弧后盆地提供了有利于BIF形成的条件.  相似文献   
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