10,918 research outputs found
Mimpi Tokoh Hashimoto Jun dalam Tanpen Ren'ai shōsetsu (Kari) karya Kato Shigeaki
Get PDFPembahasan dalam skripsi ini yaitu tentang mimpi tokoh Hashimoto Jun dalam tanpen Ren'ai shōsetsu (kari) karya Kato Shigeaki. Penelitian ini menggunakan penelitian kualitatif dengan metode kajian pustaka. Tujuan dari penelitian ini yaitu mengetahui bagaimana mimpi dan pengaruhnya terhadap tokoh Hashimoto Jun dalam tanpen Ren'ai shōsetsu (kari) karya Kato Shigeaki.
Penelitian ini menggunakan teori mimpi oleh Sigmund Freud. Berdasarkan hasil penelitian, ditemukan bahwa mimpi yang dialami oleh tokoh Hashimoto Jun terjadi karena penekanan, penyangkalan, dan pemenuhan harapan. Adapun pengaruh mimpi terhadap tokoh Hashimoto Jun yaitu (1) kecanduan dalam mengkonsumsi minuman keras, (2) kecanduan mengkonsumsi obat tidur, dan (3) kehidupan yang tidak normal.
Kata kunci : Kato Shigeaki, fenomena mimpi, mimpi manifes, laten, Ren'ai shōsetsu (kari
FIGURE 2 in A new Western Pacific Tonguefish (Pleuronectiformes: Cynoglossidae): The first Pleuronectiform discovered at active Hydrothermal Vents
No full textFIGURE 2. Blind-side view of holotype of Symphurus thermophilus, new species, holotype NSMT-P 70849, 98.7 mm SL, adult female collected at Kaikata Seamount, Minami-Ensei Knoll, Mid–Okinawa Trough, Western Pacific.Published as part of Munroe, Thomas A. & Hashimoto, Jun, 2008, A new Western Pacific Tonguefish (Pleuronectiformes: Cynoglossidae): The first Pleuronectiform discovered at active Hydrothermal Vents, pp. 43-59 in Zootaxa 1839 (1) on page 46, DOI: 10.11646/zootaxa.1839.1.2, http://zenodo.org/record/512762
Aspectos ultrasonográficos da tireóide na doença de hashimoto.
Get PDFTrabalho de Conclusão de Curso - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde, Departamento de Clínica Médica, Curso de Medicina, Florianópolis, 200
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
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
Get PDFG 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
Association Kikuchi disease with Hashimoto thyroiditis: a case report and literature review
Get PDFKikuchi-Fujimoto disease (KFD) is a benign and self-limited disease characterized by fever and lymphadenopathy. The etiology of KFD is unknown, but an autoimmune cause has been suggested. Hashimoto thyroiditis is the most common autoimmune thyroid disorder in children and is known to be associated with other autoimmune diseases. Only a few cases of Hashimoto thyroiditis associated with KFD have been documented. We report a case of a 16-year-old girl who was first diagnosed with KFD and developed Hashimoto thyroiditis 2 years and 6 months later during her follow-up period. Physicians of patients with KFD should consider the possibility of autoimmune diseases like Hashimoto’s thyroiditis
author
No full textauthorIn other places [Old Joe, the trapper] pointed out otter (or, as he pronounced it, "author") slidesPRINTED ITEM G.M.Story April 1959Not UsedNot UsedWithdrawn[see 'otter']Checked by Jordyn Hughes on Thu 09 Jun 201
JNK and ERK8 as downstream effectors of receptor tyrosine kinases
No full textMAP kinases are a super-family of serine-threonine protein kinases expressed in all eukaryotic cells. In mammals, there are many MAP kinases with different biological functions, grouped in distinctly regulated groups, ERK1/2 (extracellular signal related kinase, ERK), JNKs (jun amino terminal kinase, JNK), p38 and “atypical” MAP kinases. The MAP kinase transduction system is particularly important in growth factors signaling, which in turn control cell growth, proliferation, differentiation, survival and migration by activating receptor tyrosine kinase (RTK) family members, as platelet-derived growth factor (PDGF) and RET.
In the first report, we show that JNK is required for PDGF induction of c-myc expression. Furthermore, we identify a phylogenetically conserved AP-1 responsive element in the human, mouse and even drosophila c-myc promoter. Such element binds, in vivo, to members of the Jun family of transcription factors, c-Jun and JunD, as indicated by chromatin immunoprecipitation analysis. Finally, we show that, through this element, PDGF is able to control the activity of the c-myc transcription factor promoter in an AP-1 dependent fashion, implying the existence of a novel signaling pathway linking the PDGF receptor, through JNK and Jun proteins, to nuclear events culminating in the expression of the c-myc proto-oncogene.
In the second report, we show that RET/PTC3 activates Erk8, a new member of “atypical” MAP kinases group, by an Abl-dependent but Src-independent mechanism and demonstrate a key role for Tyr981 of RET/PTC3 in the initiation of such signaling pathway. Also, by using an alternative Erk8 splice variant, Erk8, lacking the C-terminal domain, we establish a role for this region in the activation of this MAP kinase by RET/PTC3. Finally, the use of a dominant interfering molecule for Erk8 revealed that RET/PTC3 requires this MAP kinase to stimulate the c-jun transcription factor promoter
New insights into patterns of first metastatic sites influencing survival of patients with hormone receptor-positive, HER2-negative breast cancer: a multicenter study of 271 patients
No full text主査：松村謙臣 教授 学内授与番号：医第1351号
Jun Yamamura, Shunji Kamigaki, Junya Fujita, Hiroki Osato, Hironobu Manabe, Yumiko Tanaka, Wataru Shinzaki, Yukihiko Hashimoto & Yoshifumi Komoike, New insights into patterns of first metastatic sites influencing survival of patients with hormone receptor-positive, HER2-negative breast cancer: a multicenter study of 271 patients, BMC Cancer, 2021 Apr 29; 21(1):476. doi: 10.1186/s12885-021-08219-3. 掲載application/pd
Jia ru ju he wu dui jun yun tuan liu ji jun yun tuan liu dui liu de ying xiang
No full textWong, Chai Kwok = 加入聚合物對均勻湍流及均勻湍流對流的影響 / 黃濟國.Thesis M.Phil. Chinese University of Hong Kong 2013.Includes bibliographical references (leaves 89-91).Abstracts also in Chinese.Title from PDF title page (viewed on 01, November, 2016).Wong, Chai Kwok = Jia ru ju he wu dui jun yun tuan liu ji jun yun tuan liu dui liu de ying xiang / Huang Jiguo
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