The Effect of N2O Emission Mitigation by Growing Soybeans Instead of Other Crops

农业是重要的温室气体排放源之一，而在农业生产过程中施用氮肥是引起农业温室气体排放的主要原因。因此，如何合理有效的施用氮肥对减少农业温室气体排放、减缓全球气候变化至关重要。鉴于此，对通过合理施用氮肥从而减少温室气体排放的减排措施进行成本效益分析，将有助于我们找到具有经济效益的农业温室气体减排方法。目前，相关减排措施研究主要集中在农田测土配方施肥、改良施肥（缓释肥和长效肥）上。得益于与豆类作物共生的根瘤菌具有的固氮作用，豆类作物相比其他农作物施用更少的氮肥，从而排放更少的氧化亚氮（N2O）。因此，对种植豆类作物替代其他农作物这一N2O减排措施的成本效益进行分析，可以考察该减排措施的减排潜力，丰富相...Greenhouse gas produced by agriculture plays an important role in greenhouse gas emissions, while using chemical fertilizer in agricultural activities is the main cause of producing agricultural greenhouse gas. Therefore, how to use chemical fertilizer reasonably and effectively is vital to reduce agricultural greenhouse gas emissions and slow down global warming. In view of this, a cost-benefit a...学位：经济学硕士院系专业：经济学院_人口、资源与环境经济学学号：1532013115221

CDK5-dependent BAG3 degradation modulates synaptic protein turnover

阿尔茨海默病（AD）是严重威胁人类健康的重大神经系统疾病，AD的发生发展与衰老密切相关，目前临床治疗方法十分有限。因此迫切需要从AD致病早期入手，发现和鉴定导致AD神经功能紊乱的机制和靶点，为AD的早期防治提供基础。张杰教授及其团队从高通量磷酸化蛋白质组学入手，系统研究了CDK5在神经细胞中的磷酸化底物，鉴定出了在蛋白质量控制中发挥重要功能的BAG3蛋白是CDK5的全新底物。课题组从磷酸化蛋白质组学入手，发现和阐明了细胞周期蛋白激酶5（CDK5）通过调控BAG3在维持突触蛋白水平调控中的作用机制，及其在阿尔茨海默病（AD）发生发展中的机理。 该研究是多个团队历时8年合作完成的，香港中文大学的周熙文教授、美国匹兹堡大学的Karl Herrup教授、美国Sanford-Burnham研究所的许华曦教授、美国梅奥医学中心的卜国军教授，厦门大学医学院的文磊教授、张云武教授、赵颖俊教授、薛茂强教授，军事医学科学院的袁增强教授等都参与了该工作。 厦门大学医学院2012级博士生周杰超等为文章的第一作者，张杰教授为通讯作者。Background Synaptic protein dyshomeostasis and functional loss is an early invariant feature of Alzheimer’s disease (AD), yet the unifying etiological pathway remains largely unknown. Knowing that cyclin-dependent kinase 5 (CDK5) plays critical roles in synaptic formation and degeneration, its phosphorylation targets were re-examined in search for candidates with direct global impacts on synaptic protein dynamics, and the associated regulatory network was also analyzed. Methods Quantitative phospho-proteomics and bioinformatics analyses were performed to identify top-ranked candidates. A series of biochemical assays were used to investigate the associated regulatory signaling networks. Histological, electrochemical and behavioral assays were performed in conditional knockout, shRNA-mediated knockdown and AD-related mice models to evaluate its relevance to synaptic homeostasis and functions. Results Among candidates with known implications in synaptic modulations, BCL2-associated athanogene-3 (BAG3) ranked the highest. CDK5-mediated phosphorylation on Ser297/Ser291 (Mouse/Human) destabilized BAG3. Loss of BAG3 unleashed the selective protein degradative function of the HSP70 machinery. In neurons, this resulted in enhanced degradation of a number of glutamatergic synaptic proteins. Conditional neuronal knockout of Bag3 in vivo led to impairment of learning and memory functions. In human AD and related-mouse models, aberrant CDK5-mediated loss of BAG3 yielded similar effects on synaptic homeostasis. Detrimental effects of BAG3 loss on learning and memory functions were confirmed in these mice, and such were reversed by ectopic BAG3 re-expression. Conclusions Our results highlight that neuronal CDK5-BAG3-HSP70 signaling axis plays a critical role in modulating synaptic homeostasis. Dysregulation of the signaling pathway directly contributes to synaptic dysfunction and AD pathogenesis.This work was supported by the National Science Foundation in China (Grant: 31571055, 81522016, 81271421 to J.Z.; 81801337 to L.L; 81774377 and 81373999 to L.W.); Fundamental Research Funds for the Central Universities of China-Xiamen University (Grant: 20720150062, 20720180049 and 20720160075 to J.Z.); Fundamental Research Funds for Fujian Province University Leading Talents (Grant JAT170003 to L.L); Hong Kong Research Grants Council (HKUST12/CRF/13G, GRF660813, GRF16101315, AoE/M-05/12 to K.H.; GRF16103317, GRF16100718 and GRF16100219 to H.-M,C.); Offices of Provost, VPRG and Dean of Science, HKUST (VPRGO12SC02 to K.H.); Chinese University of Hong Kong (CUHK) Improvement on Competitiveness in Hiring New Faculty Funding Scheme (Ref. 133), CUHK Faculty Startup Fund and Alzheimer’s Association Research Fellowship (AARF-17-531566) to H.-M, C. 该研究受到了国家自然科学基金、厦门大学校长基金、福建省卫生教育联合攻关基金等的资助

SNX14 deficiency-induced defective axonal mitochondrial transport in Purkinje cells underlies cerebellar ataxia and can be reversed by valproate

共济失调是一类以运动协调性紊乱为主要特征的神经系统症状，临床表现包括步态不稳、丧失平衡、吞咽困难、眼球运动异常、肌张力受损等。厦门大学医学院神经科学研究所王鑫教授团队首次从轴突线粒体运输这一全新视角揭示了一类遗传性共济失调的发病机制，并发现抗癫痫药--丙戊酸大幅度减缓模型小鼠的疾病进程，具有较强的转化应用价值，有望为共济失调提供新的治疗手段。 该研究工作由王鑫教授指导完成，厦门大学医学院助理教授张洪峰和博士生洪育娟共同完成主要实验工作。Loss-of-function mutations in SNX14 cause autosomal recessive spinocerebellar ataxia 20, which is a form of early-onset cerebellar ataxia that lacks molecular mechanisms and mouse models. We generated Snx14-deficient mouse models and observed severe motor deficits and cell-autonomous Purkinje cell degeneration. SNX14 deficiency disrupted microtubule organization and mitochondrial transport in axons by destabilizing the microtubule-severing enzyme spastin, which is implicated in dominant hereditary spastic paraplegia with cerebellar ataxia, and compromised axonal integrity and mitochondrial function. Axonal transport disruption and mitochondrial dysfunction further led to degeneration of high-energy-demanding Purkinje cells, which resulted in the pathogenesis of cerebellar ataxia. The antiepileptic drug valproate ameliorated motor deficits and cerebellar degeneration in Snx14-deficient mice via the restoration of mitochondrial transport and function in Purkinje cells. Our study revealed an unprecedented role for SNX14-dependent axonal transport in cerebellar ataxia, demonstrated the convergence of SNX14 and spastin in mitochondrial dysfunction, and suggests valproate as a potential therapeutic agent.We thank Tim Huang for helpful discussion, Wei Mo for sharing mouse lines, Li Zhong for sharing reagents, Aidong Han, Luming Yao, Caiming Wu, Mingxia Zhu, Qingfeng Liu, Lin Zhu, Shuo Zhang, Haiping Zheng, and Changchuan Xie for technical assistance, and Cui Li for providing bioinformatics software. We also thank Novogene Co., Ltd. and PTM Biolab Co., Ltd. for technical assistance in the transcriptomic and proteomic analyses, respectively. 厦门大学医学院许华曦、赵颖俊、张云武、杜丹教授在研究过程中给予大力帮助和支持。本研究工作得到国家重点研发计划项目、国家自然科学基金、福建省自然科学基金、厦门大学校长基金的资助和支持

中国当代小说在现代英语世界中的翻译与传播

当代中文小说开始走向海外市场.小说英译的海外评价和接受,能够推动中文小说在海外市场的传播范围,同时,也能展望中国当代小说今后的发展之路.中国当代小说海外译介仍存在众多局限,以鲁迅、木心的小说译介为代表,反映了中国当代小说在英译过程中,海外读者表现出的评价及接受特征,并通过此研究推动中国当代小说在海外,尤其是现代英语世界的传播.</p

一种渐变折射率减反射膜的制备方法

本发明设计一种渐变折射率减反射膜的制备方法，其特征在于包括在光学基片上镀铝膜，根据渐变折射率减反射膜的应用场合要求，设定拟制备的渐变折射率减反膜的层数、每层折射率和厚度；然后根据确定每层所需的阳极氧化深度、每层所需的阳极氧化时间、各层多孔氧化铝孔隙率值和定每层多孔氧化铝在阳极氧化后进行化学刻蚀的时间，根据上述参数反复进行阳极氧化和化学刻蚀，最后氧化退火；本发明在制备过程中可以通过精确控制阳极氧化和化学刻蚀的时间来控制不同膜层的厚度和折射率，可得到任意层数的折射率连续变化的减反射薄膜，因此，在可见和红外波段有很好的宽谱减反射效果

煤红外快速热解过程中床层对二次反应的影响

针对煤快速热解研究中样品添加量少(mg级)、焦油收集难等问题,本研究利用压片法制备微薄厚度(mm级)的煤层,并采用红外加热装置考察大添加量(g级)、微薄煤层的快速热解特性。对比堆积煤样和不同煤压片厚度(1.5~3 mm)与个数(1~2)的压片煤样热解特性发现,压片煤层热解过程的二次反应受到明显抑制,焦油产率急剧增加,在1000℃时达9.96%,为格金分析的1.5倍,实现油气产量的同步增长。模拟蒸馏分析发现,堆积状态下焦油以沥青质为主,而微薄煤层制焦油含大量轻油、酚油、萘油、洗油和蒽油。GC-MS和FTIR分析表明,随煤层厚度和个数的减少,焦油组分和含量提高,芳香烃类和含氧官能团吸收增加,进一步验证煤快速热解过程中煤层厚度对焦油产率和品质的影响,揭示在二次反应充分抑制下煤高温热解的初级反应特性

煤红外快速热解过程中床层对二次反应的影响

针对煤快速热解研究中样品添加量少(mg级)、焦油收集难等问题,本研究利用压片法制备微薄厚度(mm级)的煤层,并采用红外加热装置考察大添加量(g级)、微薄煤层的快速热解特性。对比堆积煤样和不同煤压片厚度(1.5~3 mm)与个数(1~2)的压片煤样热解特性发现,压片煤层热解过程的二次反应受到明显抑制,焦油产率急剧增加,在1000℃时达9.96%,为格金分析的1.5倍,实现油气产量的同步增长。模拟蒸馏分析发现,堆积状态下焦油以沥青质为主,而微薄煤层制焦油含大量轻油、酚油、萘油、洗油和蒽油。GC-MS和FTIR分析表明,随煤层厚度和个数的减少,焦油组分和含量提高,芳香烃类和含氧官能团吸收增加,进一步验证煤快速热解过程中煤层厚度对焦油产率和品质的影响,揭示在二次反应充分抑制下煤高温热解的初级反应特性

SNX12 Affects Aβ Generation Through Regulating Subcellular Localization of BACE1

不溶性β淀粉样蛋白(β-AMylOId,Aβ)的沉积是阿尔茨海默症(AlzHEIMEr′S dISEASE,Ad)的中心环节,Aβ是由β-分泌酶(bACE1)和γ-分泌酶顺序切割β淀粉样蛋白前体蛋白(β-AMylOId PrECurSOr PrOTEIn,APP)产生的,bACE1与APP在质膜、内含体/溶酶体、高尔基体反面膜囊(Tgn)以及早期分泌途径之间的转运很大程度上影响了Aβ的产生.通过WESTErn blOT和免疫荧光的方法探讨了SOrTIng nEXIn12(SnX12)对Aβ产生的影响及其作用机制.WESTErn blOT结果显示过表达SnX12后,分泌到细胞外的Aβ减少,γ-分泌酶的活性及PS1、nCT、PEn-2、APP和bACE1的蛋白水平没有明显变化,APP-βCTf水平降低,而下调SnX12时Aβ水平增加,与对照组相比,差异均具有统计学意义(P<0.05);免疫荧光结果表明,SnX12与bACE1在细胞内存在共定位,并且SnX12表达增加可以使bACE1和APP在细胞内处于同一区域的数量减少.这些结果表明,过表达SnX12通过调节bACE1在细胞内的定位,使细胞内处于同一区域的bACE1与APP的数量减少,导致经bACE1切割的APP减少,从而降低Aβ的产生.因此SnX12可能在Ad的发病过程中起着一定的调节作用.The deposition of insoluble β-amyloid(Aβ) is the key link of Alzheimer′s disease(AD).Aβ is produced by sequential proteolytic cleavage of the β-amyloid precursor protein(APP) by β-(BACE1) and γ-secretases.Aβ production is affected by the trafficking of BACE1 and APP among plasma membrane,endosome/lysosome,trans golgi network(TGN) and the early secretary pathways.Here this article used Western blot and immunofluorescence to investigate the effect of sorting nexin12(SNX12) on Aβ production and the underlying mechanism.Western blot data showed that overexpression of SNX12 resulted in a significant reduction in the levels of Aβ and APP-βCTF,but had no effect on the levels of γ-secretase components(including PS1,NCT and pen-2),APP,and BACE1;While knockdown of SNX12 increased the level of Aβ.Furthermore,immunofluorescence data showed that SNX12 colocalized with BACE1 and overexpression of SNX12 decreased the co-localization of APP and BACE1.This study demonstrates that overexpression of SNX12 can reduce the co-localization of APP and BACE1 by re-distributing the subcellular localization of BACE1,therefore reducing the cleavage of APP by BACE1 and Aβ generation.Taken together,our results suggest that SNX12 may involve in AD pathology.国家自然科学基金项目(30973150);国家重点基础研究发展计划(973)前期研究专项项目(2010CB535004);国家科技重大专项项目(2009ZX09103-731);福建省自然科学杰出青年基金项目(2009J06022