熱帯低気圧の暖気核に関する力学的研究

学位の種別: 課程博士審査委員会委員 : (主査)東京大学教授 新野 宏, 東京大学教授 佐藤 正樹, 東京大学教授 高薮 縁, 東京大学教授 羽角 博康, 東京大学准教授 三浦 裕亮University of Tokyo(東京大学

Thermal desorption of structured water layer on epitaxial graphene

Thermal desorption of the structured water layer on graphene was observed in this study via electrical conductivity measurements. Specifically, a structured water layer was formed on the graphene surface via deionized water treatment, following which we examined the thermal desorption process of the layer using sheet resistance measurements. The water molecules acting as a p-type dopant were strongly adsorbed on graphene, forming a solid layer. Consequently, the layer was completely removed from the graphene surface at 300⁡°C. The thermal desorption spectrum of the structured water layer on graphene was quantitatively obtained by converting the measured sheet resistance to carrier density change

Interaction between anti-Alzheimer and antipsychotic drugs in modulating extrapyramidal motor disorders in mice

AbstractAntipsychotics are often used in conjunction with anti-Alzheimer drugs to treat the behavioral and psychological symptoms of dementia (BPSD). Here, we examined the effects of cholinesterase inhibitors (ChEIs), donepezil and galantamine, on antipsychotic-induced extrapyramidal side effects (EPS) in mice. The effects of serotonergic agents on the EPS drug interaction were also evaluated. Donepezil (0.3–3 mg/kg) did not induce EPS signs by itself; however, it significantly potentiated bradykinesia induction with a low dose of haloperidol (0.5 mg/kg) in dose-dependent and synergistic manners. Galantamine (0.3–3 mg/kg) elicited mild bradykinesia at a high dose and dose-dependently augmented haloperidol-induced bradykinesia. The EPS potentiation by galantamine was blocked by trihexyphenidyl (a muscarinic antagonist), but not by mecamylamine (a nicotinic antagonist). In addition, the bradykinesia potentiation by galantamine was significantly reduced by (±)-8-hydroxy-2-(di-n-propylamino)-tetralin (a 5-HT1A agonist), ritanserin (a 5-HT2 antagonist), and SB-258585 (a 5-HT6 antagonist). The present results give us a caution for the antipsychotics and ChEIs interaction in inducing EPS in the treatment of BPSD. In addition, second generation antipsychotics, which can stimulate 5-HT1A receptors or antagonize 5-HT2 and 5-HT6 receptors, seem to be favorable as an adjunctive therapy for BPSD

Controlled structure of anatase TiO2 nanoparticles by using organic additives in a microwave process

Synthesis of anatase nanoparticles was carried out in a microwave system. Crystal morphology was controlled by organic additives including PAAc (polyacrylic acid) and PVP (polyvinylpyrrolidone). Modified TiO2 particles were compared to the bare TiO2 anatase structure. The synthesis of materials via the microwave system has great advantages due to the short reaction period and low energy requirement and is therefore an environmentally friendly process compared to the hydrothermal process. The decomposition of acetaldehyde was studied to determine the photocatalytic activity of the modified anatase TiO2 material

A FUNDAMENTAL RESEARCH ON THE EFFECTS OF A FLOATING BERTH ON REDUCTION OF TSUNAMI DAMAGES IN A HARBOR -REDUCTION EFFECTS OF THE BREAKING OF MOORING LINES AND RUNNING ON A QUAY

ABSTRACT Tsunami consecutively brings about several types of disasters, which is described as "disaster chain." In the case that vessels are moored to the quay, the breaking of the mooring line possibly causes drift or collision with other vessels. There is also a case that a mooring tether of the vessel moored to the floating pier is not broken in the damage of tsunami, which was confirmed at Shiogama port in Miyagi when the East Japan Great Earthquake occurred on March 11, 2011. The objectives of this paper are to clarify the reduction effect of mooring line force when a vessel is moored to a floating berth. The three-dimensional MPS method is used with advantages of floating berth considered. We simulated a vessel with the cargo carrier of 3,000t. Especially, by changing the wave elevation and the incident angle, the responses of the mooring tension which acts on the vessel moored to a floating berth and to the quay respectively are compared, and its reducing efficiency is examined. A conclusion is reached that, when tsunami incident wave angle is 90 degrees, mooring vessels to a floating berth can be expected as a solution to reduce the problems of vessel's running onto a quay, in comparison with mooring them at a quay wall. Also, we propose suitable anchoring methods according to the size of the vessels

Self-pulsation and excitability of blue-violet InGaN lasers

This article gives a review of our latest results on the self-pulsation and excitability properties of blue-violet lasers. A number of investigations of the phenomena in InGaN lasers with different designs are described. The bifurcations, which are the origin of the phenomena, are identified and the effects of the lasers parameters on device dynamics are discussed. It is shown how different laser structures can be used to control device behaviour and the dependence of self-pulsation and excitability behaviour on laser geometry is discussed. Finally, agreement between the results of numerical calculations and experimental measurements on self-pulsation is demonstrated

UCP3 ト Hax-1 ノ ソウゴ サヨウ ニヨル ミトコンドリア ノ カルシウム ノ ウド ノ チョウセツ

Mitochondrial Ca２＋ plays an important role in the regulations of various cellular functions. Uncoupling protein ３ （UCP３） is primarily expressed in the inner membrane of skeletal muscle mitochondria. Recently, it has been reported that UCP３ is associated with Ca２＋ uptake into mitochondria. However, the mechanisms by which UCP３ regulates mitochondrial Ca２＋ uptake are not well understood. Here we report that UCP３interacts with HS‐１associated protein X‐１ （Hax‐１）, an anti-apoptotic protein that is localized in mitochondria, which is involved in cellular responses to Ca２＋. The hydrophilic sequences within the loop２, matrix-localized hydrophilic domain of mouse UCP３are necessary for binding to Hax‐１of the C-terminal domain in adjacent to mitochondrial innermembrane. Interestingly, interaction of these proteins occurs the calciumdependent manner. Moreover, NMR spectrum of the C-terminal domain of Hax‐１was dramatically changed by removal of Ca２＋, suggesting that the C-terminal domain of Hax‐１ underwent a Ca２＋-induced conformation change. In the Ca２＋-free states, C-terminal Hax‐１ didn’t change the structure, suggesting that Ca２＋ binding may induce the change of protein structure of Hax‐１ C-terminus. These studies identify a novel UCP３‐Hax‐１complex regulates the influx of Ca２＋ into mitochondria. Thus, the efficacy of UCP３‐Hax‐１in mitochondrial calcium regulation may provide a novel therapeutic approach against mitochondrial dysfunction-related disease

Impact of glycemic control with sitagliptin on the 2‑year progression of arterial stiffness : a sub‑analysis of the PROLOGUE study

Background: No conclusive evidence has been obtained yet on the significance of the effects of dipeptidyl peptidase-4 (DPP-4 inhibitor) treatment on the arterial stiffness in clinical settings. In addition, the effects of good glycemic control on the arterial stiffness have also not been clarified yet. As a sub-analysis of the PROLOGUE study, we examined the effect of a DPP-4 inhibitor (sitagliptin) on the 2-year progression of the arterial stiffness and also to determine the effect of good glycemic control on the rate of progression of the arterial stiffness. Methods: In the PROLOGUE study, the study participants were either allocated to add-on sitagliptin treatment or to continued treatment with conventional anti-diabetic agents. Among the 463 participants of the PROLOGUE study, we succeeded in measuring the brachial-ankle pulse wave velocity (baPWV) at least two times during the 2-year study period in 96 subjects. Results: The changes in the baPWV during the study period were similar between the both groups (i.e., with/without staglipitin), overall. On the other hand, when the study subjects were divided into two groups according to the glycemic control status during the study period {good glycemic control group (GC) = hemoglobin (Hb)A1c <7.0 at both 12 and 24 months after the treatment randomization; poor glycemic control group (PC) = HbA1c ≥7.0 at either 12 months, 24 months, or both}, the 2-year increase of the baPWV was marginally significantly larger in the PC group (144 ± 235 cm/s) as compared to that the GC group (−10 ± 282 cm/s) (p = 0.036). Conclusion: While the present study could not confirm the beneficial effect of sitagliptin per se on the arterial stiffness, the results suggested that good glycemic control appears to be beneficial for delaying the annual progression of the arterial stiffness

Flavones Prevent LPS-Induced Muscle Atrophy

Muscle atrophy is a complex process that occurs as a consequence of various stress events. Muscle atrophy-associated genes (atrogenes) such as atrogin-1/MAFbx and MuRF-1 are induced early in the atrophy process, and the increase in their expression precedes the loss of muscle weight. Although antioxidative nutrients suppress atrogene expression in skeletal muscle cells, the inhibitory effects of flavonoids on inflammation-induced atrogin-1/MAFbx expression have not been clarified. Here, we investigated the inhibitory effects of flavonoids on lipopolysaccharide (LPS)-induced atrogin-1/MAFbx expression. We examined whether nine flavonoids belonging to six flavonoid categories inhibited atrogin-1/MAFbx expression in mouse C2C12 myotubes. Two major flavones, apigenin and luteolin, displayed potent inhibitory effects on atrogin-1/MAFbx expression. The pretreatment with apigenin and luteolin significantly prevented the decrease in C2C12 myotube diameter caused by LPS stimulation. Importantly, the pretreatment of LPS-stimulated myoblasts with these flavones significantly inhibited LPS-induced JNK phosphorylation in C2C12 myotubes, resulting in the significant suppression of atrogin-1/MAFbx promoter activity. These results suggest that apigenin and luteolin, prevent LPS-mediated atrogin-1/MAFbx expression through the inhibition of the JNK signaling pathway in C2C12 myotubes. Thus, these flavones, apigenin and luteolin, may be promising agents to prevent LPS-induced muscle atrophy

Chronic exposure of VEGF inhibitors promotes the malignant phenotype of colorectal cancer cells

VEGF-targeting anti-angiogenic drugs have enabled significant advances in cancer therapy. However, acquired resistance to VEGF-targeting drugs occurs, leading to disease progression. How tumors become the resistance remains fully uncertain. One of possible mechanisms for the resistance may be the direct effect of VEGF inhibitors on tumor cells expressing VEGF receptors (VEGF-R). We investigated here the direct effect of chronic VEGF inhibition on phenotype changes in cancer cells. To chronically inhibit cancer cell-derived VEGF, human colon cancer HCT116 cells were chronically exposed (3 months) to anti-VEGF neutralizing monoclonal antibody (HCT/mAb cells, blockade of VEGF alone) or VEGF-R tyrosine kinase inhibitor foretinib (HCT/fore cells, blockade of all VEGF family). HCT/mAb cells redundantly increased VEGF family member (VEGF, PlGF, VEGF-B, VEGF-R1 and VEGF-R2) and induced a resistance to hypoxia-induced apoptosis. By contrast, HCT/fore cells did not show the redundant increase in VEGF family member, but significantly increased a VEGF-independent pro-angiogenic factor FGF-2. HCT/fore cells showed increased migration and invasion activities in addition to a resistance to hypoxia-induced apoptosis. The resistance to apoptosis was significantly suppressed by inhibition of hypoxia-inducible factor-1α in HCT/mAb cells, but not in HCT/fore cells. These findings suggest that chronic inhibition of VEGF/VEGF-R accelerates malignant phenotypes of colon cancer cells