飞秒光纤光源的波分解复用 复用实验

为研究飞秒光源作为链路初始光源的可行性，使用阵列波导光栅（AWG）对265 fs光纤光源进行波分解复用 复用实验。实验光源波长为1 52765～1 56505 nm，通道数为48，通道间隔为080 nm。研究发现:在分波实验中，飞秒光纤光源经过AWG后，扫描谱线3 dB带宽为064 nm ，相邻通道串扰为2726 dB，比连续光源增大502 dB；在合波实验中，观察到AWG多端口端对宽带光源的波长选择作用，验证了AWG的色散特性，发现多光束的输出谱线总体轮廓未出现太大变形；在波分解复用 复用实验中，谱线最大损耗为251 dB，输出谱线轮廓和初始光谱基本一致，信号在传输过程中未出现明显失真，证明飞秒光源作为链路初始光源的可行性。     

基于科技查新数据的用户拓展及其关联聚类

科技查新用户数据是查新业务积累的真实而宝贵的资源,其充分利用不仅是查新业务管理的需要,可提升查新服务水平,同时还能用于挖掘更多的情报价值.调研发现,当前对科技查新用户数据的挖掘利用仍以基础性的业务管理分析为主,而增值情报价值的挖掘较少.为拓展成都文献情报中心科技查新客户群体和增值服务范围,做大做强查新业务,立足成都中心查新服务实践,依托于积累查新用户及其服务记录,在挖掘发现潜在服务对象的基础上,通过多维用户关联聚类,探讨了后期信息情报服务的精准营销与推送,分析了基于用户聚类的服务推荐存在的不足,展望了挖掘更多需求信息的推荐路径.     

QT工艺对一种B-Nb低碳贝氏体钢 组织及强韧性的影响

通过室温拉伸、摆锤冲击、光学及扫描电镜研究了QT(淬火+回火)工艺对实验钢晶界比例、晶粒尺寸、碳化物析出情况及强韧性的影响，并对其变体的分布及组合方式进行了分析.结果表明:随着回火温度的升高，实验钢强度逐渐降低，塑性逐渐提高;450T和500T钢断口为准解理型断裂，贝氏体板条间析出的碳化物及较低比例的大角度晶界使得冲击韧性较差;而600T和650T钢断口为韧窝断裂，组织中大角度晶界的比例增加，有效地阻碍了裂纹的扩展.变体分析表明，450T钢变体组合方式介于Bain group和CP(close packed)group之间，而600T钢变体之间呈现较明显的CP组合方式，同一CP group内的变体取向差较大，偏折了裂纹传播路径，提高了低温韧性.     

西安市夜间旅游公共服务体系构建与质量评价

旅游公共服务是随着旅游业诞生而产生的,旅游公共服务水平作为衡量地区旅游业发展质量和社会经济发展水平的重要指标之一,近年来受到国内外学者的广泛关注.夜间经济的发展与旅游公共服务水平息息相关,如何实现旅游公共服务设施由白昼场景向昼夜双场景的转换,从而实现夜间经济高质量发展必将成为学术界研究的热点.本文以夜间经济十强城市——西安市为研究对象,通过分发调查问卷收集相关信息数据,并运用SPSS进行数据分析、建立模型.聚焦夜间旅游公共服务质量的影响因子,发现西安市各项夜间旅游公共服务水平与夜间旅游公共服务总体水平成正相关,均逐年提升,其中夜间旅游公共交通服务、夜间旅游公共安全保障服务综合水平较高,对夜间旅游公共服务质量产生显著影响,而夜间旅游公共信息咨询服务水平相对较低,进而为西安市及相同案例区旅游公共服务体系优化提供针对性对策.     

Protein kinase D inhibitor CRT0066101 suppresses bladder cancer growth in vitro and xenografts via blockade of the cell cycle at G2/M

The protein kinase D (PKD) family of proteins are important regulators of tumor growth, development, and progression. CRT0066101, an inhibitor of PKD, has antitumor activity in multiple types of carcinomas. However, the effect and mechanism of CRT0066101 in bladder cancer are not understood. In the present study, we show that CRT0066101 suppressed the proliferation and migration of four bladder cancer cell lines in vitro. We also demonstrate that CRT0066101 blocked tumor growth in a mouse flank xenograft model of bladder cancer. To further assess the role of PKD in bladder carcinoma, we examined the three PKD isoforms and found that PKD2 was highly expressed in eight bladder cancer cell lines and in urothelial carcinoma tissues from the TCGA database, and that short hairpin RNA (shRNA)-mediated knockdown of PKD2 dramatically reduced bladder cancer growth and invasion in vitro and in vivo, suggesting that the effect of the compound in bladder cancer is mediated through inhibition of PKD2. This notion was corroborated by demonstrating that the levels of phospho-PKD2 were markedly decreased in CRT0066101-treated bladder tumor explants. Furthermore, our cell cycle analysis by flow cytometry revealed that CRT0066101 treatment or PKD2 silencing arrested bladder cancer cells at the G2/M phase, the arrest being accompanied by decreases in the levels of cyclin B1, CDK1 and phospho-CDK1 (Thr161) and increases in the levels of p27^Kip1 and phospho-CDK1 (Thr14/Tyr15). Moreover, CRT0066101 downregulated the expression of Cdc25C, which dephosphorylates/activates CDK1, but enhanced the activity of the checkpoint kinase Chk1, which inhibits CDK1 by phosphorylating/inactivating Cdc25C. Finally, CRT0066101 was found to elevate the levels of Myt1, Wee1, phospho-Cdc25C (Ser216), Gadd45α, and 14-3-3 proteins, all of which reduce the CDK1-cyclin B1 complex activity. These novel findings suggest that CRT0066101 suppresses bladder cancer growth by inhibiting PKD2 through induction of G2/M cell cycle arrest, leading to the blockade of cell cycle progression.     

Degradation of the mitochondrial complex I assembly factor TMEM126B under chronic hypoxia

Cell stress such as hypoxia elicits adaptive responses, also on the level of mitochondria, and in part is mediated by the hypoxia-inducible factor (HIF) 1α. Adaptation of mitochondria towards acute hypoxic conditions is reasonably well understood, while regulatory mechanisms, especially of respiratory chain assembly factors, under chronic hypoxia remains elusive. One of these assembly factors is transmembrane protein 126B (TMEM126B). This protein is part of the mitochondrial complex I assembly machinery. We identified changes in complex I abundance under chronic hypoxia, in association with impaired substrate-specific mitochondrial respiration. Complexome profiling of isolated mitochondria of the human leukemia monocytic cell line THP-1 revealed HIF-1α-dependent deficits in complex I assembly and mitochondrial complex I assembly complex (MCIA) abundance. Of all mitochondrial MCIA members, we proved a selective HIF-1-dependent decrease of TMEM126B under chronic hypoxia. Mechanistically, HIF-1α induces the E3-ubiquitin ligase F-box/WD repeat-containing protein 1A (β-TrCP1), which in turn facilitates the proteolytic degradation of TMEM126B. Attenuating a functional complex I assembly appears critical for cellular adaptation towards chronic hypoxia and is linked to destruction of the mitochondrial assembly factor TMEM126B.     

Prion protein cleavage fragments regulate adult neural stem cell quiescence through redox modulation of mitochondrial fission and SOD2 expression

Neurogenesis continues in the post-developmental brain throughout life. The ability to stimulate the production of new neurones requires both quiescent and actively proliferating pools of neural stem cells (NSCs). Actively proliferating NSCs ensure that neurogenic demand can be met, whilst the quiescent pool makes certain NSC reserves do not become depleted. The processes preserving the NSC quiescent pool are only just beginning to be defined. Herein, we identify a switch between NSC proliferation and quiescence through changing intracellular redox signalling. We show that N-terminal post-translational cleavage products of the prion protein (PrP) induce a quiescent state, halting NSC cellular growth, migration, and neurite outgrowth. Quiescence is initiated by the PrP cleavage products through reducing intracellular levels of reactive oxygen species. First, inhibition of redox signalling results in increased mitochondrial fission, which rapidly signals quiescence. Thereafter, quiescence is maintained through downstream increases in the expression and activity of superoxide dismutase-2 that reduces mitochondrial superoxide. We further observe that PrP is predominantly cleaved in quiescent NSCs indicating a homeostatic role for this cascade. Our findings provide new insight into the regulation of NSC quiescence, which potentially could influence brain health throughout adult life.     

墨西哥Perdido带上Wilcox组油藏富集模式分析

为了明确Perdido带上Wilcox组油藏富集控制因素，以上Wilcox组油藏为研究对象，通过有效供烃范围、油输导方式、圈闭形成与生排烃期匹配关系及保存条件对比分析，探讨了Perdido带上Wilcox组油藏富集控制因素及成藏模式。研究认为，供烃区规模对油藏规模控制作用明显；上Wilcox组油藏存在顺源式、向源式和背源式3种垂向运移方式，其中，顺源式和向源式运移有利于油藏富集；圈闭形成与生排烃期匹配较好的油藏，供烃充足，油藏规模大；保存是油藏富集的必要条件，遭受严重破坏的油藏规模小；建立了Perdido带上Wilcox组3种油藏成藏模式，其中，“双侧供烃-顺源输导”和“单侧供烃-向源输导”有利于油藏富集，是该区寻找规模性油藏的有利模式。     

Collaborative explanation,explanatory roles,and scientific explaining in practice

Scientific explanation is a perennial topic in philosophy of science, but the literature has fragmented into specialized discussions in different scientific disciplines. An increasing attention to scientific practice by philosophers is (in part) responsible for this fragmentation and has put pressure on criteria of adequacy for philosophical accounts of explanation, usually demanding some form of pluralism. This commentary examines the arguments offered by Fagan and Woody with respect to explanation and understanding in scientific practice. I begin by scrutinizing Fagan's concept of collaborative explanation, highlighting its distinctive advantages and expressing concern about several of its assumptions. Then I analyze Woody's attempt to reorient discussions of scientific explanation around functional considerations, elaborating on the wider implications of this methodological recommendation. I conclude with reflections on synergies and tensions that emerge when the two papers are juxtaposed and how these draw attention to critical issues that confront ongoing philosophical analyses of scientific explanation.