39,285 research outputs found
Kwangtung 1:50,000 [cartographic material] /
No full textVarious eds. Relief shown by contours and spot heights.; Sheets individually titled at top margin, e.g. Tang Cun = Tang-tsun.; Sheets individually numbered at top margin, e.g. Sheet 7621-II.; Original published: Beijing? : Jun shi wei yuan hui jun ling bu lu di ce liang zong ju, surveyed in 1927, published 1938.; Includes index map to adjoining sheets.; Some of National Library of Australia's copies mounted on linen.Alternate title: Guangdong 1:50,000Title on index map: Guangdong wu wan fen yi di xing tuAlternate title: Series L78
Context-Aware Information Retrieval for Enhanced Situation Awareness
Get PDFIn the coalition forces, users are increasingly challenged with the issues of information overload and correlation of information from heterogeneous sources. Users might need different pieces of information, ranging from information about a single building, to the resolution strategy of a global conflict. Sometimes, the time, location and past history of information access can also shape the information needs of users. Information systems need to help users pull together data from disparate sources according to their expressed needs (as represented by system queries), as well as less specific criteria. Information consumers have varying roles, tasks/missions, goals and agendas, knowledge and background, and personal preferences. These factors can be used to shape both the execution of user queries and the form in which retrieved information is packaged. However, full automation of this daunting information aggregation and customization task is not possible with existing approaches. In this paper we present an infrastructure for context-aware information retrieval to enhance situation awareness. The infrastructure provides each user with a customized, mission-oriented system that gives access to the right information from heterogeneous sources in the context of a particular task, plan and/or mission. The approach lays on five intertwined fundamental concepts, namely Workflow, Context, Ontology, Profile and Information Aggregation. The exploitation of this knowledge, using appropriate domain ontologies, will make it feasible to provide contextual assistance in various ways to the work performed according to a user’s taskrelevant information requirements. This paper formalizes these concepts and their interrelationships
Gou tou jun shi Zhang Chunqiao
No full text三元里文化室绘.文字: 阴谋夺权 狗头军师 张春桥;下款:三元里文化室绘.裝裱後高寬: 135 x 41 cm.San yuan li wen hua shi hui.Wen zi : Yin mou duo quan gou tou jun shi Zhang Chunqiao; Xia kuan : San yuan li wen hua shi hui.Zhuang biao hou gao kuan : 135 x 41 cm
Yong yu you hua zhi bei chao leng yuan zi hun he wu de guang xue ou ji jing
No full textChen, Jun = 用於優化製備超冷原子混合物的光學偶極阱 / 陳軍.Thesis M.Phil. Chinese University of Hong Kong 2014.Includes bibliographical references (leaves 109-117).Abstracts also in Chinese.Title from PDF title page (viewed on 29, November, 2016).Chen, Jun = Yong yu you hua zhi bei chao leng yuan zi hun he wu de guang xue ou ji jing / Chen Jun
Proto-oncogene c-jun expression is induced by AML1-ETO in a JNK dependent manner:possible role in the pathogenesis of acute myeloid leukemia
Get PDFOverexpression of proto-oncogene c-jun and constitutive activation of the Jun NH2-terminal kinase (JNK) signaling pathway have been implicated in the leukemic transformation process. However, c-jun expression has not been investigated in acute myeloid leukemia (AML) cells containing the most common chromosomal translocations. t(8;21) is one of the most common AML-associated translocation and results in the AML1-ETO fusion protein. Overexpression of AML1-ETO in NIH3T3 cells leads to increased phosphorylation of Ser63 in c-Jun, which is generally JNK dependent. The role of the JNK signaling pathway for the functional properties of AML1-ETO is, however, unknown.
In the present study we found high expression levels of c-jun mRNA in t(8;21), t(15;17) or inv(16) positive patient cells by microarray analysis. Within t(8;21) positive patient samples, there was a correlation between AML1-ETO and c-jun mRNA expression levels. In myeloid U937 cells, c-jun mRNA and c-Jun protein expression levels increased upon induction of AML1-ETO. AML1-ETO transactivated the human c-jun promoter through the proximal AP-1 site via activating the JNK signaling pathway. JNK targets c-Jun and ATF-2, which also bind to the proximal AP-1 site in U937 cells, were also phosphorylated upon AML1-ETO induction. Furthermore, AML1-ETO induction increased the DNA binding capacity of c-Jun and ATF-2 to the proximal AP-1 site of the c-jun promoter, which might result in their enhanced transactivation capacities.
Interference with JNK and c-Jun activation by using JIP-1 or a JNK inhibitor reduced the transactivation capacity of AML1-ETO on the c-jun promoter and the pro-apoptotic function of AML1-ETO in U937 cells. AML1-ETO seems to activate the JNK signaling pathway by inducing the expression of a cytoplasmic factor, possibly G-CSF, because supernatant of AML1-ETO expressing cells was sufficient to induce phosphorylation of JNK and c-Jun in wildtype U937 cells.
This data demonstrates a novel mechanism of how AML1-ETO might exert positive effects on target gene expression and identifies the proto-oncogene c-jun as a common target gene in AML patient cells.Überexpression des Proto-Onkogens c-jun und konstitutive Aktivierung des Jun NH2-terminalen Kinase (JNK)-Signaltransduktionsweges sind wichtig für die leukämische Transformation in der Chronischen Myeloischen Leukämie. Die Expression von c-jun bei Akuter Myeloischer Leukämie (AML) mit den häufigsten reziproken Translokationen ist jedoch unbekannt. Bei einer der häufigsten AML Translokation t(8;21) wurde in Fibroblastenzellen gezeigt, daß das AML1-ETO-Fusionsgen die Phosphorylierung des Serin 63 in c-Jun erhöht. Die Rolle des JNK-Signalweges, der c-Jun am Serin 63 phosphorylieren kann, für die Funktion von AML1-ETO wurde bisher jedoch nicht untersucht. Weiterhin kann aktiviertes c-Jun durch eine positive Rückkoppelungsschleife über den c-jun Promotor zur Erhöhung der c-Jun Expression führen.
In der vorliegenden Arbeit konnten wir zeigen, daß AML Patientenzellen mit den häufigen Translokationen: t(8;21), t(15;17) oder inv(16) mehr c-jun mRNA besitzen im Vergleich zu Knochenmarkszellen gesunder Probanden. Weiterhin fanden wir eine hohe Korrelation zwischen der AML1-ETO und der c-jun mRNA bei t(8;21) positiven Patientenzellen. Induktion von AML1-ETO in der myeloischen U937 Zellinie erhöhte sowohl c-jun mRNA als auch c-Jun Proteinexpression. Damit konnten wir zeigen, daß AML1-ETO die Erhöhung der c-jun Expression bewirkt. Wir untersuchten den molekularen Mechanismus in U937 Zellen mittels transienter Transfektionen und fanden, daß AML1-ETO den c-jun Promotor durch die proximale AP-1 Seite transaktiviert. Diese Transaktivierung erfolgte indirekt über Aktivierung des JNK-Signaltransduktionsweges durch AML1-ETO. AML1-ETO-Induktion führte auch zur Phosphorylierung der JNK-Zielproteine c-Jun und ATF-2. Diese konnten im Gelretardierungsassay an die proximale AP-1 Seite des c-jun Promotors binden und wurden durch AML1-ETO-Induktion in ihrer Bindungsfähigkeit verstärkt. Deshalb nehmen wir an, daß die Transaktivierungskapazität des c-jun Promotors durch AML1-ETO über die Aktivierung des JNK-Signalweges läuft
Globalization and China’s Economic and Financial Development
Get PDFThis paper surveys China’s globalization in terms of in and out flows of goods, capital, information/technology and people from both the Chinese and the Western, especially American, points of view. It includes a discussion of the issue of revaluation of the RMB.
Supplementary material - Supplemental material for Chemical Investigation of the Secondary Metabolites of <i>Streptomyces</i> sp. 4205
No full textSupplemental material, Supplementary material, for Chemical Investigation of the Secondary Metabolites of Streptomyces sp. 4205 by Cheng-Zhen Gu, Jing Lv, Sheng-Hao Yuan, Yuan-Yuan Song, Chong-Ren Yang, Ying-Jun Zhang, and Ren-Sen Zeng in Natural Product Communications</p
Supplemental_Material – Supplemental material for Unstable shoes for the treatment of lower back pain: a meta-analysis of randomized controlled trials
No full textSupplemental material, Supplemental_Material for Unstable shoes for the treatment of lower back pain: a meta-analysis of randomized controlled trials by Deng-Yan Bai, Zhi-Guo Yuan, Jian-Jun Shao, Tao Zhu and Hai-Jun Zhang in Clinical Rehabilitation</p
Crosstalk between c-Jun and TAp73alpha/beta contributes to the apoptosis–survival balance
Get PDFThe p53-family member p73 plays a role in various cellular signaling pathways during development and growth control and it can have tumor suppressor properties. Several isoforms of p73 exist with considerable differences in their function. Whereas the functions of the N-terminal isoforms (TA and delta Np73) and their opposing pro- and antiapoptotic roles have become evident, the functional differences of the distinct C-terminal splice forms of TAp73 have remained unclear. Here, we characterized the global genomic binding sites for TAp73alpha and TAp73beta by chromatin immunoprecipitation sequencing as well as the transcriptional responses by performing RNA sequencing. We identified a specific p73 consensus binding motif and found a strong enrichment of AP1 motifs in close proximity to binding sites for TAp73alpha. These AP1 motif-containing target genes are selectively upregulated by TAp73alpha, while their mRNA expression is repressed upon TAp73beta induction. We show that their expression is dependent on endogenous c-Jun and that recruitment of c-Jun to the respective AP1 sites was impaired upon TAp73beta expression, in part due to downregulation of c-Jun. Several of these AP1-site containing TAp73alpha-induced genes impinge on apoptosis induction, suggesting an underlying molecular mechanism for the observed functional differences between TAp73alpha and TAp73beta
Transforming growth factor beta (TGF beta) mediates schwann cell death in vitro and in vivo: Examination of c-jun activation, interactions with survival signals, and the relationship of TGF beta-mediated death to schwann cell differentiation
No full textIn some situations, cell death in the nervous system is controlled by an interplay between survival factors and negative survival signals that actively induce apoptosis. The present work indicates that the survival of Schwann cells is regulated by such a dual mechanism involving the negative survival signal transforming growth factor beta (TGF beta), a family of growth factors that is present in the Schwann cells themselves. We analyze the interactions between this putative autocrine death signal and previously defined paracrine and autocrine survival signals and show that expression of a dominant negative c-Jun inhibits TGF beta -induced apoptosis. This and other findings pinpoint activation of c-Jun as a key downstream event in TGF beta -induced Schwann cell death. The ability of TGF beta to kill Schwann cells, like normal Schwann cell death in vivo, is under a strong developmental regulation, and we show that the decreasing ability of TGF beta to kill older cells is attributable to a decreasing ability of TGF beta to phosphorylate c-Jun in more differentiated cells
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