9,816 research outputs found
Mme UCHIDA Jun, Professeure invitée à l’EHESS en juin 2018
No full textProfesseur UCHIDA Jun, de l’Université de Stanford, historienne du Japon et spécialiste de l'époque moderne sera directrice d'étude invitée à l’EHESS en juin 2018. Elle est l’auteure de Brokers of Empire: Japanese Settler Colonialism in Korea, 1876–1945 (Harvard University Asia Center, 2014). Son projet de recherche en cours porte sur l’histoire de la diaspora des marchands de la région d’Ômi et du commerce de textiles qu’ils firent dans tout l’archipel. En réunissant des sources dans l’actue..
Scolia (Discolia) minowai Uchida 1933
No full text<i>38.</i> <i>Scolia</i> (<i>Discolia</i>) <i>minowai</i> Uchida, 1933 <p> <i>Scolia minowai</i> Uchida, 1933: 246, ♂, China (types in Entomological Museum, Sapporo).</p> <p> <i>Scolia minowai</i>: Yamane, 1995: 43.</p> <p> <b>Distribution.</b> China (Taiwan).</p>Published as part of <i>Liu, Zhen, Achterberg, Cornelis Van, He, Jun-Hua & Chen, Xue-Xin, 2021, A checklist of Scoliidae (Insecta: Hymenoptera) from China, pp. 101-126 in Zootaxa 4966 (2)</i> on page 116, DOI: 10.11646/zootaxa.4966.2.1, <a href="http://zenodo.org/record/4736250">http://zenodo.org/record/4736250</a>
Provincializing Empire
No full textProvincializing Empire explores the global history of Japanese expansion through a regional lens. It rethinks the nation-centered geography and chronology of empire by uncovering the pivotal role of expeditionary merchants from Ōmi (present-day Shiga Prefecture) and their modern successors. Tracing their lives from the early modern era, and writing them into the global histories of empire, diaspora, and capitalism, Jun Uchida offers an innovative analysis of expansion through a story previously untold: how the nation’s provincials built on their traditions to create a transpacific diaspora that stretched from Seoul to Vancouver, while helping shape the modern world of transoceanic exchange.
“Provincializing Empire offers a stimulating and persuasive account of the longue durée of Japanese capitalist development, connecting Japanese historiography to important conversations on the history of racial capitalism and geographies of space, place, and scale.” — DAVID AMBARAS, author of Japan’s Imperial Underworlds: Intimate Encounters at the Borders of Empire
“Wide-ranging yet richly documented, Provincializing Empire offers a powerful new transregional history of Japanese capitalism, challenging claims about the developmental state. It tells the fascinating story of a merchant diaspora whose growth was entwined with Japanese imperialism, and of the invented traditions that sustained provincial identity amid global commercial expansion.” — JORDAN SAND, author of Tokyo Vernacular: Common Spaces, Local Histories, Found Objects
""A tour de force! Jun Uchida's lucid narrative illuminates the multidirectional movements of settler-migrant merchants from peripheral Japan that cut across the prescribed borders of empires and nation-states. Empirically rich and theoretically sophisticated, Provincializing Empire calls into question many assumptions about Japanese imperialism and offers a less spatially bounded story of grassroots expansionism."" — EIICHIRO AZUMA, author of In Search of Our Frontier: Japanese America and Settler Colonialism in the Construction of Japan's Borderless Empire
""Provincializing Empire is a wonderfully creative model for connecting local and global history. Uchida frames her stimulating account of Japanese overseas commercial expansion, colonialism, and diaspora not as the top-down story of state policy but as the local history of a mercantile community."" — DAVID L. HOWELL, Robert K. and Dale J. Weary Professor of Japanese History, Harvard University
Proto-oncogene c-jun expression is induced by AML1-ETO in a JNK dependent manner:possible role in the pathogenesis of acute myeloid leukemia
No full textOverexpression 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
Paraprotis dendrova Uchida 1978
No full textParaprotis dendrova Uchida, 1978 (Fig. 14 A) Paraprotis dendrova Uchida, 1978: 16 –17, plas 3, 4 [Sabiura, Japan]. Paraprotis dendrova. —Nishi 1992 a: 18–19, fig. 3 A–D [Okinawa, Japan]; 1996: 309, fig. 4 e [Okinawa, Japan]; Nishi & Yamasu 1992 a: 85 [Ryukyu Islands, Japan; brooding]; Rouse 2005: 168, 173, 175, fig. 3 B [Okinawa, Japan]. Material examined. SAM E 3591, G 243, Patch Reef on the way to Palfrey Island, coll. G. Rouse & E. Kupriyanova, 1 Nov 2005; ZMA V.Pol. 4538, Granite Head, 14 ° 39 'S, 145 ° 27 'E, from underside of boulders on rock, little sand, subtidally, coll. H. ten Hove, 18 Jun 1983 (3, carrying eggs/embryos). Diagnosis. Operculum absent. Ocellar clusters (2–3 per radiole) present. A spiral projection for brood attachment originates from the right side of the mouth, carrying up to 50 embryos (Fig. 14 A). Collar non-lobed. Remarks. This small (tube about 1 mm wide) cryptic species lacks an operculum and is easily recognizable only when the brooding appendage is present. Distribution. Okinawa, Japan, Qld, Australia. New record for Australia.Published as part of Kupriyanova, Elena K., Sun, Yanan, Ten Hove, Harry A., Wong, Eunice & Rouse, Greg W., 2015, Serpulidae (Annelida) of Lizard Island, Great Barrier Reef, Australia, pp. 275-353 in Zootaxa 4019 (1) on page 301, DOI: 10.11646/zootaxa.4019.1.13, http://zenodo.org/record/28949
Proline-rich tyrosine kinase 2 mediates gonadotropin-releasing hormone signaling to a specific extracellularly regulated kinase-sensitive transcriptional locus in the luteinizing hormone beta-subunit gene
No full textG protein-coupled receptor regulation of gene transcription primarily occurs through the phosphorylation of transcription factors by MAPKs. This requires transduction of an activating signal via scaffold proteins that can ultimately determine the outcome by binding signaling kinases and adapter proteins with effects on the target transcription factor and locus of activation. By investigating these mechanisms, we have elucidated how pituitary gonadotrope cells decode an input GnRH signal into coherent transcriptional output from the LH beta-subunit gene promoter. We show that GnRH activates c-Src and multiple members of the MAPK family, c-Jun NH2-terminal kinase 1/2, p38MAPK, and ERK1/2. Using dominant-negative point mutations and chemical inhibitors, we identified that calcium-dependent proline-rich tyrosine kinase 2 specifically acts as a scaffold for a focal adhesion/cytoskeleton-dependent complex comprised of c-Src, Grb2, and mSos that translocates an ERK-activating signal to the nucleus. The locus of action of ERK was specifically mapped to early growth response-1 (Egr-1) DNA binding sites within the LH beta-subunit gene proximal promoter, which was also activated by p38MAPK, but not c-Jun NH2-terminal kinase 1/2. Egr-1 was confirmed as the transcription factor target of ERK and p38MAPK by blockade of protein expression, transcriptional activity, and DNA binding. We have identified a novel GnRH-activated proline-rich tyrosine kinase 2-dependent ERK-mediated signal transduction pathway that specifically regulates Egr-1 activation of the LH beta-subunit proximal gene promoter, and thus provide insight into the molecular mechanisms required for differential regulation of gonadotropin gene expression
Alexeter shakojiensis Uchida 1930
No full textAlexeter shakojiensis Uchida, 1930 Fig. 37 Diagnosis Face approximately 1.6 to 1.7 × as wide as long. Malar space about 0.4× as long as basal width of mandible. Postocellar line approximately 0.6 to 0.7 × as long as ocular-ocellar line. Areolet triangular, with long petiole; fore wing with vein 1cu-a slight distal to M&RS; hind wing vein 1-cu 2.3× as long as cu-a. Lateromedian longitudinal carinae of propodeum distinct, almost parallel. First metasomal tergite approximately 2.7 to 2.8 × as long as posterior width. Hind legs (tarsus pale yellow), tergites reddish brown. Material examined CHINA • 1 ♀; Benxi, Liaoning; 1 Jul. 1993; leg. Zhen-Lu Liu; GSFGPM • 6 ♀♀; Mengoutou, Beijing; 29 Aug. to 22 Sept. 2008; Tao Wang leg.; GSFGPM • 1 ♀, 1 ♂; Mengoutou, Beijing; 4 Aug. to 8 Sept. 2009; Tao Wang leg.; GSFGPM • 1 ♀; Zhouzhi, Shaanxi; 4 Aug. 2009; leg. Mao-Ling Sheng; GSFGPM • 1 ♂; Yanqing, Beijing; 12 Jun. 2012; leg. Shi-Xiang Zong; GSFGPM.Published as part of T., Li & S. P., Sun, 2022, The genus Alexeter Förster (Hymenoptera, Ichneumonidae) in China, with descriptions of three new species, pp. 81-103 in European Journal of Taxonomy 789 (81) on page 99, DOI: 10.5852/ejt.2022.789.1633, http://zenodo.org/record/590636
A critical step for JNK activation: isomerization by the prolyl isomerase Pin1
No full textc-Jun N-terminal kinase (JNK) is activated by dual phosphorylation of both threonine and tyrosine residues in the phosphorylation loop of the protein in response to several stress factors. However, the precise molecular mechanisms for activation after phosphorylation remain elusive. Here we show that Pin1, a peptidyl-prolyl isomerase, has a key role in the JNK1 activation process by modulating a phospho-Thr-Pro motif in the phosphorylation loop. Pin1 overexpression in human breast cancer cell lines correlates with increased JNK activity. In addition, small interfering RNA (siRNA) analyses showed that knockdown of Pin1 in a human breast cancer cell line decreased JNK1 activity. Pin1 associates with JNK1, and then catalyzes prolyl isomerization of the phospho-Thr-Pro motif in JNK1 from trans- to cis-conformation. Furthermore, Pin1 enhances the association of JNK1 with its substrates. As a result, Pin1 -/- cells are defective in JNK activation and resistant to oxidative stress. These results provide novel insights that, following stress-induced phosphorylation of Thr in the Thr-Pro motif of JNK1, JNK1 associates with Pin1 and undergoes conformational changes to promote the binding of JNK1 to its substrates, resulting in cellular responses from extracellular signals.Cell Death and Differentiation advance online publication, 10 June 2011; doi:10.1038/cdd.2011.82.open
Supplemental Material, DS1_VET_10.1177_0300985819875749 - Chronic Inflammatory and Proliferative Lesions of the Gallbladder in Aged Pigs
No full textSupplemental Material, DS1_VET_10.1177_0300985819875749 for Chronic Inflammatory and Proliferative Lesions of the Gallbladder in Aged Pigs by Nanako Ushio, James K. Chambers, Ken-ichi Watanabe, Takuya E. Kishimoto, Takanori Shiga, Jun-You Li, Hiroyuki Nakayama and Kazuyuki Uchida in Veterinary Pathology</p
Arthula Cameron
No full textGenus Arthula Cameron Arthula Cameron, 1900. Type species: Arthula brunneocornis Cameron, 1900, by monotypy. Orientocryptus Uchida, 1931. Type species: Orientocryptus formosanus Uchida, 1931, by original designation. Kuniocryptus Sonan, 1937. Type species: Orientocryptus flavofasciatus Uchida, 1931, by original designation. The genus Arthula is one of three closely related genera forming the subtribe Sphecophagina, and is characterized by the basal transverse carina of propodeum being strong, and the short and broad 2 r-m of the forewing being opposite or slightly basad of 2 m-cu (also see Townes et al. 1965, Gauld 1984). Three valid species have been previously recognized in the genus: A. brunneocornis Cameron, from India, A. formosanus (Uchida), from Taiwan, and A. flavofasciata (Uchida), known as a parasitoid on paper wasps of the genus Polistes in Taiwan and Japan.Published as part of Ubaidillah, Rosichon, Yamaguchi, Goshi & Kojima, Jun-Ichi, 2009, A new Arthula Cameron (Ichneumonidae, Cryptinae) parasitoid of Ropalidia plebeiana Richards (Vespidae) and host of Amoturoides breviscapus Girault (Torymidae) (Hymenoptera), pp. 45-50 in Zootaxa 2274 on page 46, DOI: 10.5281/zenodo.19104
- …
