Low-temperature processed InGaZnO MES-FET for flexible device applications

Amorphous oxide semiconductor (AOSs) of an In-Ga-Zn-O (IGZO)1) is expected to be used as a channel material for thin-film transistors (TFTs) because the IGZO TFTs exhibit field-effect motility (μFE) of over 10 cm2/Vs and good uniformity even fabricate at room temperature. The oxide TFTs with metal-insulator-semiconductor (MIS) structure have been employed widely; however, maximum processing temperature of 300-400 °C is required to guarantee the performance and reliability of the TFTs. In contrast, metal-semiconductor field effect transistor (MES-FET) has several advantages especially for flexible devices since a Schottky gate can be formed at low temperature with AOSs. There are a few reports of AOSs based MES-FET2, 3); however, it has remained an issue to form stable and good Schottky contact on the AOSs. We reported the top-gated MES-FET with the IGZO channel, which was deposited by mist chemical vapour deposition at 350 °C, and sputtered silver oxide (AgOx) Schottky gate4). The μFE of 3.2 cm2/Vs and subthreshold swing (SS) of 356 mV/decade were achieved. However, a maximum processing temperature of the MES-FET was 350 °C, which was not suitable for flexible device applications. In this presentation, the IGZO MES-FET with AgOx Schottky gate was fabricated at a maximum processing temperature of 150 °C. We investigated the influences of deposition conditions and post-deposition annealing on electrical properties of the low-temperature processed IGZO MES-FET. Figure 1 shows a cross sectional view of the IGZO MES-FET. First, a 100 nm-thick IGZO film was deposited on glass substrate by DC magnetron sputtering without intentional substrate heating from InGaZnO (In:Ga:Zn=1:1:1 mol.%) target. Deposition pressure was kept at 1.0 Pa, while the O2 gas ratio [R(O2)=O2/(Ar+O2)] was varied at 0.66, 0.80, and 1.00%. The IGZO film was patterned into an active channel by conventional photolithography and wet etching. The IGZO channel was then annealed at 100 or 150 ºC for 1h in ambient air. A 120 nm-thick AgOx was deposited by DC reactive sputtering, and Au was deposited on the AgOx by thermal evaporation. The AgOx/Au stacked Schottky gate was patterned by lift-off. Finally, Mo source and drain electrodes was formed by lift-off. Channel width/length of the MES-FET was 100/10 μm. Figure 2 shows the (a) forward and reverse currents of the IGZO/AgOx Schottky diode and (b) on and off current of the IGZO MES-FET, as a function of the Hall carrier concentration (NHall) in the IGZO channel. The diode properties were well correlated with the NHall; however, on-current of the MES-FET depended on not only NHall but also the R[O2] of the IGZO deposition. Carrier transport mechanism of the IGZO MES-FET and control methods of electrical properties will be discussed at the conference. Please click Additional Files below to see the full abstract

Precipitation of calcium compounds onto rock surfaces in water with cementitious material

In this study, the precipitation of minerals onto rock surfaces was investigated to consider whether sealing of pores and cracks in rock can be accelerated. Cylindrical specimens were prepared and then kept in purified water with powders of high-strength and ultra-low-permeability concrete (HSULPC), which will be used to confine transuranic wastes in Japan. Then, the rock specimens were weighed and the surfaces of rock specimens were inspected under a microscope. It was recognized that precipitation occurred on the surface of the rock specimens. It was also shown that precipitation did not occur on rock specimens kept in water without HSULPC. The weight of all specimens stored in HSULPC increased, and the observed weight change was larger for rocks with higher porosities. It is concluded that precipitation of minerals occurs on the rock surface when the rock is kept in water with HSULPC powders. From the results obtained in this study, it is suggested that the sealing of pores and cracks in rock can be accelerated by the precipitation of calcium compounds using HSULPC. It is concluded that HSULPC is useful for underground radioactive waste disposal

Roles for B[a]P and FICZ in subchondral bone metabolism and experimental temporomandibular joint osteoarthritis via the AhR/Cyp1a1 signaling axis

Bone loss due to smoking represents a major risk factor for fractures and bone osteoporosis. Signaling through the aryl hydrocarbon receptor (AhR) and its ligands contributes to both bone homeostasis and inflammatory diseases. It remains unclear whether the same AhR signaling axis affects the temporomandibular joint (TMJ). The aim of this study was to investigate possible mechanisms which mediate bone loss in the TMJ due to smoking. In particular, whether benzo[a]pyrene (B[a]P), a carcinogen of tobacco smoke, induces expression of the AhR target gene, Cyp1a1, in mandibular condyles. Possible functions of an endogenous ligand of FICZ, were also investigated in a TMJ-osteoarthritis (OA) mouse model. B[a]P was administered orally to wild-type and AhR−/− mice and bone metabolism was subsequently examined. TMJ-OA was induced in wild-type mice with forceful opening of the mouth. Therapeutic functions of FICZ were detected with μCT and histology. Exposure to B[a]P accelerated bone loss in the mandibular subchondral bone. This bone loss manifested with osteoclastic bone resorption and upregulated expression of Cyp1a1 in an AhR-dependent manner. In a mouse model of TMJ-OA, FICZ exhibited a dose-dependent rescue of mandibular subchondral bone loss by repressing osteoclast activity. Meanwhile, in vitro, pre-treatment with FICZ reduced RANKL-mediated osteoclastogenesis. B[a]P regulates mandibular subchondral bone metabolism via the Cyp1a1. The AhR ligand, FICZ, can prevent TMJ-OA by regulating osteoclast differentiation

Roles for B[a]P and FICZ in subchondral bone metabolism and experimental temporomandibular joint osteoarthritis via the AhR/Cyp1a1 signaling axis

Bone loss due to smoking represents a major risk factor for fractures and bone osteoporosis. Signaling through the aryl hydrocarbon receptor (AhR) and its ligands contributes to both bone homeostasis and inflammatory diseases. It remains unclear whether the same AhR signaling axis affects the temporomandibular joint (TMJ). The aim of this study was to investigate possible mechanisms which mediate bone loss in the TMJ due to smoking. In particular, whether benzo[a]pyrene (B[a]P), a carcinogen of tobacco smoke, induces expression of the AhR target gene, Cyp1a1, in mandibular condyles. Possible functions of an endogenous ligand of FICZ, were also investigated in a TMJ-osteoarthritis (OA) mouse model. B[a]P was administered orally to wild-type and AhR(-/-) mice and bone metabolism was subsequently examined. TMJ-OA was induced in wild-type mice with forceful opening of the mouth. Therapeutic functions of FICZ were detected with mu CT and histology. Exposure to B[a]P accelerated bone loss in the mandibular subchondral bone. This bone loss manifested with osteoclastic bone resorption and upregulated expression of Cyp1a1 in an AhR-dependent manner. In a mouse model of TMJ-OA, FICZ exhibited a dose-dependent rescue of mandibular subchondral bone loss by repressing osteoclast activity. Meanwhile, in vitro, pre-treatment with FICZ reduced RANKL-mediated osteoclastogenesis. B[a]P regulates mandibular subchondral bone metabolism via the Cyp1a1. The AhR ligand, FICZ, can prevent TMJ-OA by regulating osteoclast differentiation

Construction of a genetic AND gate under a new standard for assembly of genetic parts

<p>Abstract</p> <p>Background</p> <p>Appropriate regulation of respective gene expressions is a bottleneck for the realization of artificial biological systems inside living cells. The modification of several promoter sequences is required to achieve appropriate regulation of the systems. However, a time-consuming process is required for the insertion of an operator, a binding site of a protein for gene expression, to the gene regulatory region of a plasmid. Thus, a standardized method for integrating operator sequences to the regulatory region of a plasmid is required.</p> <p>Results</p> <p>We developed a standardized method for integrating operator sequences to the regulatory region of a plasmid and constructed a synthetic promoter that functions as a genetic AND gate. By standardizing the regulatory region of a plasmid and the operator parts, we established a platform for modular assembly of the operator parts. Moreover, by assembling two different operator parts on the regulatory region, we constructed a regulatory device with an AND gate function.</p> <p>Conclusions</p> <p>We implemented a new standard to assemble operator parts for construction of functional genetic logic gates. The logic gates at the molecular scale have important implications for reprogramming cellular behavior.</p

A reporter system evaluates tumorigenesis, metastasis, β-catenin/MMP regulation, and druggability

Cancer invasion, metastasis, and therapy resistance are the crucial phenomena in cancer malignancy. The high-expression of matrix metalloproteinase 9 (MMP9) is a biomarker as well as a causal factor of cancer invasiveness and metastatic activity. However, a regulatory mechanism underlying MMP9 expression in cancer is not clarified yet. Additionally, a new strategy for anti-cancer drug discovery is becoming an important clue. In the present study, we aimed (i) to develop a novel reporter system evaluating tumorigenesis, invasiveness, metastasis, and druggability with a combination of three-dimensional (3D) tumoroid model and Mmp9 promoter and (ii) to examine pharmacological actions of anti-cancer medications using this reporter system. High expression and genetic amplification of MMP9 were found in colon cancer cases. We found that proximal promoter sequences of MMP9 in murine and human contained conserved binding sites for transcription factors β-catenin/TCF/LEF, glucocorticoid receptor (GR), and NF-κB. The murine Mmp9 promoter (-569 to +19) was markedly activated in metastatic colon cancer cells and additionally activated by tumoroid formation and by β-catenin signaling stimulator lithium chloride (LiCl). The Mmp9 promoter-driven fluorescent reporter cells enabled the monitoring of activities of MMP9/gelatinase, tumorigenesis, invasion, and metastasis in allogeneic/syngenic transplantation experiments. We also demonstrated pharmacological actions as follows. ids Dexamethasone and hydrocortisone, steroidal medications binding to GR, inhibited the Mmp9 promoter but did not inhibit tumorigenesis. On the other hand, an antimetabolite 5-fluorouracil, a golden standard for colon cancer chemotherapy, inhibited tumoroid formation but did not inhibit Mmp9 promoter activity. Notably, anti-malaria medication artesunate inhibited both tumorigenesis and the Mmp9 promoter in vitro, potentially through inhibition of β-catenin/TCF/LEF signaling. Thus, this novel reporter system enabled monitoring tumorigenesis, invasiveness, metastasis, key regulatory signalings such as β-catenin/MMP9 axis, and druggability

コーシーモンダイノカイノトクイテンノデンパニツイテ

京都大学0048新制・論文博士理学博士乙第1716号論理博第343号新制||理||136(附属図書館)2846UT51-46-B101(主査)教授 溝畑 茂, 教授 吉田 耕作, 教授 山口 昌哉学位規則第5条第2項該当Kyoto UniversityDA

Sur le prolongement analytique de la solution du probleme de Cauchy pourcertains operateurs differentiels de partie principale a coefficientspolynomiaux

In our preceding articles, by applying the results of Bieberbach, Fatou and Picard, we have constructed an example such that the domain of holomorphy of the solution admits an exterior point. Next we have studied the domain of holomorphy of the solution for differential operators with polynomial coefficients that concern the differential equations of Darboux-Halphen, of Chazy and of the modular function. In this article, we make some studies on the analytic continuation of the solution of the Cauchy problem for certain differential operators of principal part with polynomial coefficients