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Microethnography of Resilience in African Nomadic Pastoralism
This article describes microethnography based on living-in fieldwork among East African pastoral societies, focusing on the process of recovering from catastrophic situations in life and the natural society, and clarifies the original source of resilience at individual and collective levels. At the beginning of the 21st century, the Karimojong cluster was catastrophically affected by the so-called “humanitarian” intervention of external societies. Animals, which are fraught with values that cannot be captured in terms of production and reproduction alone, and have the meaning of supporting me as , have made it possible to restore life based on everyday body arrangements and rebuild nomadism based on animal resistance
経皮的心肺補助装置導入後24時間以内の最大乳酸値および最小乳酸値はICU内死亡の予測因子である:後方視的観察研究
長崎大学学位論文 [学位記番号]博(医歯薬)甲第1203号 [学位授与年月日]令和2年3月4
ヒト血管内皮細胞とヒト脂肪幹細胞を用いた再細胞化ラット肺における細胞外マトリックスと異種抗原の変化
長崎大学学位論文 [学位記番号]博(医歯薬)甲第1204号 [学位授与年月日]令和2年3月4
Chiral bifunctional sulfide-catalyzed asymmetric bromoaminocyclizations
A BINOL-derived chiral bifunctional sulfide catalyst bearing a phenylurea moiety was applied to enantioselective bromoaminocyclization reactions of 2-allylaniline derivatives, which provide optically active 2-substituted indoline products as important motifs for biologically active compounds. A protecting group on the nitrogen of the 2-allylaniline substrate was carefully optimized, and highly enantioselective reactions were achieved by employing thep-biphenylsulfonyl-protected substrates. The origin of the good level of enantioselectivity for the present bromoaminocyclization was also investigated on the basis of DFT calculations. The resultant optically active 2-(bromomethyl)indoline products could be transformed to various 2-substituted indolines with no loss of the optical purity
RECNA長崎被爆・戦後史研究会公開・総括シンポジウム 私たちは何を継承すべきか 長崎の被爆・戦後史研究から見えてくるもの
RECNA長崎被爆・戦後史研究会公開・総括シンポジウム 2020年2月15日(土) 於 長崎大学文教キャンパス 教養教育講義棟A-13教室64-65ページに掲載の長崎新聞記事について、長崎新聞社からの許諾を得て登録しています
Pathological roles of c-Met in bladder cancer: Association with cyclooxygenase-2, heme oxygenase-1, vascular endothelial growth factor-A and programmed death ligand 1
c-Met is a receptor tyrosine kinase that binds a specific ligand, namely hepatocyte growth factor (HGF). The HGF/c-Met system is important for malignant aggressiveness in various types of cancer, including bladder cancer (BC). However, although phosphorylation is the essential step required for biological activation of c-Met, pathological roles of phosphorylated c-Met at the clinical and molecular levels in patients with BC are not fully understood. In the present study, the expression levels of c-Met and the phosphorylation of two of its tyrosine residues (pY1234/pY1235 and pY1349) were immunohistochemically examined in 185 BC tissues. The associations between these expression levels and cancer cell invasion, metastasis, and cyclooxygenase-2 (COX-2), heme oxygenase-1 (HO-1), VEGF-A and programmed death ligand 1 (PD-L1) levels were investigated. c-Met was associated with muscle invasion (P=0.021), as well as the expression levels of HO-1 (P=0.028) and PD-L1 (P<0.001), whereas pY1349 c-Met was associated with muscle invasion (P=0.003), metastasis (P=0.025), and COX-2 (P=0.017), HO-1 (P=0.031) and PD-L1 (P=0.001) expression. By contrast, pY1234/1235 c-Met was associated with muscle invasion and metastasis (P=0.006 and P=0.012, respectively), but not with the panel of cancer-associated molecules. Furthermore, COX-2 and PD-L1 expression were associated with muscle invasion and metastasis, respectively (P=0.045 and P=0.036, respectively). Hence, c-Met serves important roles in muscle invasion by regulating HO-1 and PD-L1, whereas its phosphorylation at Y1349 is associated with muscle invasion and metastasis via the regulation of COX-2, HO-1 and PD-L1 in patients with BC. Furthermore, phosphorylation at Y1234/1235 may lead to muscle invasion and metastasis via alternate mechanisms associated with c-Met and pY1349 c-Met
Gene regulatory landscape in osteoblast differentiation
The development of osteoblasts, a bone-forming cell population, occurs in conjunction with development of the skeleton, which creates our physical framework and shapes the body. In the past two decades, genetic studies have uncovered the molecular framework of this process—namely, transcriptional regulators and signaling pathways coordinate the cell fate determination and differentiation of osteoblasts in a spatial and temporal manner. Recently emerging genome-wide studies provide additional layers of understanding of the gene regulatory landscape during osteoblast differentiation, allowing us to gain novel insight into the modes of action of the key regulators, functional interaction among the regulator-bound enhancers, epigenetic regulations, and the complex nature of regulatory inputs. In this review, we summarize current understanding of the transcriptional regulation in osteoblasts, in terms of the gene regulatory landscape