4,367,199 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
Crossing Boundaries, The Calligraphic Work of Manny Ling
No full textThis is an exhibition catalogue for a solo major exhibition by Dr Manny Ling. Accompanying the publication are two essays written by Professor John Strachen, a poet and Pro-Vice-Chancellor of Bath Spa University, and Dr Diego Navarro from the University of Carlos III in Madrid, Spain. 23 pieces of work are presented in this publication in full colour. The exhibition addresses the exploration and research conducted by Dr Manny Ling over the last decade on the contexts of cross-cultural calligraphy between East and West
Yin zhi wen ling yan ji
No full text[潘成雲原序].綫裝, 1函.框19.7x13.2公分, 9行25字, 小字雙行同. 白口, 左右雙邊, 單黑魚尾. 版心上鐫題名, 中鐫小題, 下鐫葉次. 行間有圈點.題名據版心.內封背頁鐫"光緖己亥仲春開雕", 並印有"千歲坊文光齋印板存甯城報德觀"前附《文昌帝君陰騭文》(周振翰錄), 《陰騭文原始》, 《陰騭文靈驗記》 ; 卷末附捐刊姓氏芳名.Xian zhuang, 1 han.Kuang 19.7 x 13.2 gong fen, 9 hang 25 zi, xiao zi shuang hang tong. Bai kou, zuo you shuang bian, dan hei yu wei. Ban xin shang juan ti ming, zhong juan xiao ti, xia juan ye ci. Hang jian you quan dian.Ti ming ju ban xin.Nei feng bei ye juan "Guangxu ji hai zhong chun kai diao", bing yin you "Qian sui fang Wen guang zhai yin ban cun Ning Cheng Bao de guan"Qian fu "Wenchang di jun yin zhi wen" (Zhou Zhenhan lu), "Yin zhi wen yuan shi", "Yin zhi wen ling yan ji" ; juan mo fu juan kan xing shi fang ming.[Pan Chengyun yuan xu]
Soutenance de thèse : Lee Ju-ling
No full textLe 5 mai 2014 à 14h, Lee Ju-ling soutiendra sa thèse de doctorat intitulée : La nudité dans l’image : pouvoir et représentations du corps à Taïwan (1895-1987). Cette thèse a été préparée sous la direction du professeur Christian Henriot dans le cadre de l’Institut d’Asie Orientale. La soutenance aura lieu à l’Institut Française de l’Éducation (IFÉ) situé dans le site de l’ENS de Lyon (site R. Descartes). Résumé : Cette étude au croisement de l’histoire et des études visuelles porte sur le co..
C-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis
No full textUnderstanding the regulation of the apoptotic program in neurons by intracellular pathways is currently a subject of great interest. Recent results suggest that c-Jun N-terminal kinases (JNK), mitogen-activated protein kinases and the transcription factor c-Jun are important regulators of this cell death program in post-mitotic neurons following survival-factor withdrawal. Our study demonstrates that ceramide levels increase upon survival-factor withdrawal in primary cultured cortical neurons. Furthermore, survival-factor withdrawal or addition of exogenous c2-ceramide induces JNK pathway activation in these cells. Western blot analyses of JNK and c-Jun using phospho-specific antibodies reveal that JNK and subsequent c-Jun phosphorylation occur hours before the initiation of apoptosis, reflected morphologically by neurite retraction and fragmentation, cell-body shrinkage and chromatin fragmentation. Immunocytochemistry using the same antibodies shows that phospho-JNK are localized in the neurites of control neurons and translocate to the nucleus where phospho-c-Jun concurrently appears upon ceramide-induced apoptosis. To determine if ceramide-induced c-Jun activation is responsible for the induction of the apoptotic program, we performed transient transfections of a dominant negative form of c-Jun, truncated in its transactivation region. Our results show that DNc-Jun partially protects cortical neurons from ceramide-induced apoptosis. Treatment of dominant negative c-Jun-expressing neurons with the pharmacological inhibitor of p38 kinase, SB203580, completely blocked neuronal death. Thus our data show that p38 and JNK/c-Jun pathways cooperate to induce neuronal apoptosis
sj-docx-1-ict-10.1177_15347354241237973 – Supplemental material for Clinical Efficacy and Gut Microbiota Regulating-Related Effect of Si-Jun-Zi Decoction in Postoperative Non-Small Cell Lung Cancer Patients: A Prospective Observational Study
No full textSupplemental material, sj-docx-1-ict-10.1177_15347354241237973 for Clinical Efficacy and Gut Microbiota Regulating-Related Effect of Si-Jun-Zi Decoction in Postoperative Non-Small Cell Lung Cancer Patients: A Prospective Observational Study by Yiyun He, Ao Qi, Yifeng Gu, Congmeng Zhang, Yichao Wang, Wenxiao Yang, Ling Bi, Yabin Gong, Lijing Jiao and Ling Xu in Integrative Cancer Therapies</p
Silver City, Aubrey Lee, Jr.
No full textThree year old Aubrey sits atop his burro in front of the Lee home.8 bit; 810 ppi; ScanMaker 9800X
C/EBPalpha downregualtes c-jun expression
No full textThe transcription factor C/EBPa is crucial for the differentiation of granulocytes. Conditional expression of C/EBPa triggers neutrophilic differentiation and C/EBPa can block TPA induced monocytic differentiation of bipotential myeloid cells. In C/EBPa knockout mice, no mature granulocytes are present. A dramatic increase of c-jun mRNA in C/EBPa knockout mice fetal liver was observed. c-jun, a component of the AP-1 transcription factor complex and a co-activator of the transcription factor PU.1, is important for monocytic differentiation. Here we report that C/EBPa downregulates c-jun expression to drive granulocytic differentiation. Ectopic increase of C/EBPa expression decreases c-jun mRNA level, and the human c-jun promoter activity is downregulated 8 fold in presence of C/EBPa. C/EBPa and c-jun interact through their leucine zipper domains and this interaction prevents c-jun from binding to DNA. This results in downregulation of c-jun’s capacity to autoregulate its own promoter through the proximal AP-1 site. Overexpression of c-jun prevents C/EBPa induced granulocytic differentiation. c-jun expression was higher in AML M2 patients with dominant negative C/EBPa mutations in comparison to AML M2 patients without C/EBPa mutations. Thus, we propose a model in which C/EBPa needs to downregulate c-jun expression and transactivation capacity for promoting granulocytic differentiation.Der Transkriptionsfaktor C/EBPa ist essentiell für die Differenzierung von Granulozyten. Die konditionelle Expression von C/EBPa induziert die neutrophile Differenzierung. Überdies kann C/EBPa die TPA-induzierte Differenzierung von myeloiden Vorläuferzellen zu Monozyten blockieren. In C/EBPa knockout Mäusen gibt es keine reifen Granulozyten. In der fötalen Leber von C/EBPa knockout Mäusen konnte eine stark erhöhte Expression der c-jun mRNA beobachtet werden. c-jun ist eine Komponente des AP-1 Transkriptionsfaktorkomplexes, ein Koaktivator des Transkriptionsfaktors PU.1 und ist wichtig für die Differenzierung von Monozyten. In dieser Arbeit zeigen wir, dass C/EBPa die c-jun Expression herunterreguliert und somit die Differenzierung von Granulozyten induziert. Die Überexpression von C/EBPa reduzierte die c-jun mRNA Menge und die Aktivität des humanen c-jun Promotors war in der Gegenwart von C/EBPa 8-fach herunterreguliert. C/EBPa und c-jun interagieren über ihre Leucin-Zipper Domänen und diese Interaktion verhindert die DNA-Bindung von c-jun. Dies resultiert in einer verminderten Kapazität von c-jun, den eigenen Promotor über die proximale AP-1 Stelle zu regulieren. Die Überexpression von c-jun blockiert die durch C/EBPa induzierte granulozytäre Differenzierung. Die c-jun Expression war in AML-M2 Patienten mit dominant-negativen Mutationen in C/EBPa im Vergleich zu AML-M2 Patienten ohne Mutationen in C/EBPa erhöht. Aufgrund dieser Daten schlagen wir ein Modell vor, in dem C/EBPa die Expression und Transaktivierungskapazität von c-jun herunterregulieren muß, um die granulozytäre Differenzierung zu induzieren
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