22 research outputs found
Photoemission Angular Distribution Beyond the Single Wavevector Description of Photoelectron Final States
We develop a novel simulation procedure for angle-resolved photoemission
spectroscopy (ARPES), where a photoelectron wave function is set to be an
outgoing plane wave in a vacuum associated with the emitted photoelectron wave
packet. ARPES measurements on the transition metal dichalcogenide
- are performed, and our simulations exhibit good
agreement with experiments. Analysis of our calculated final state wave
functions quantitatively visualizes that they include various waves due to the
boundary condition and the uneven crystal potential. These results show that a
more detailed investigation of the photoelectron final states is necessary to
fully explain the photon-energy- and light-polarization-dependent ARPES
spectra.Comment: 6+14 pages, 4+15 figure
Broken Screw Rotational Symmetry in the Near-Surface Electronic Structure of -Stacked Crystals
We investigate the electronic structure of - and
by angle-resolved photoemission spectroscopy (ARPES) and
photoemission intensity calculations. Although in bulk form, these materials
are expected to exhibit band degeneracy in the plane due to screw
rotation and time-reversal symmetries, we observe gapped band dispersion near
the surface. We extract from first-principles calculations the near-surface
electronic structure probed by ARPES and find that the calculated photoemission
spectra from the near-surface region reproduce the gapped ARPES spectra. Our
results show that the near-surface electronic structure can be qualitatively
different from the bulk one due to partially broken nonsymmorphic symmetries.Comment: 6+11 pages, 4+13 figure
In Vivo Detection of Mitochondrial Dysfunction Induced by Clinical Drugs and Disease-Associated Genes Using a Novel Dye ZMJ214 in Zebrafish
application/pdf内容の要旨・審査結果の要旨 / 三重大学大学院医学系研究科 生命医科学専攻 基礎医学系講座 薬理ゲノミクス分
In Vivo Detection of Mitochondrial Dysfunction Induced by Clinical Drugs and Disease-Associated Genes Using a Novel Dye ZMJ214 in Zebrafish
application/pdf要約 / 三重大学大学院医学系研究科 生命医科学専攻 基礎医学系講座 薬理ゲノミクス分
Resonant Tunneling Due to van der Waals Quantum-Well States of Few-Layer WSe2 in WSe2/h-BN/p+-MoS2 Junction
Activation of Sterol Regulatory Element Binding Factors by Fenofibrate and Gemfibrozil Stimulates Myelination in Zebrafish
Oligodendrocytes are major myelin-producing cells and play essential roles in the function of a healthy nervous system. However, they are also one of the most vulnerable neural cell types in the central nervous system (CNS), and myelin abnormalities in the CNS are found in a wide variety of neurological disorders, including multiple sclerosis, adrenoleukodystrophy, and schizophrenia. There is an urgent need to identify small molecular weight compounds that can stimulate myelination. In this study, we performed comparative transcriptome analysis to identify pharmacodynamic effects common to miconazole and clobetasol, which have been shown to stimulate myelination by mouse oligodendrocyte progenitor cells (OPCs). Of the genes differentially expressed in both miconazole- and clobetasol-treated mouse OPCs compared with untreated cells, we identified differentially expressed genes (DEGs) common to both drug treatments. Gene ontology analysis revealed that these DEGs are significantly associated with the sterol biosynthetic pathway, and further bioinformatics analysis suggested that sterol regulatory element binding factors (SREBFs) might be key upstream regulators of the DEGs. In silico screening of a public database for chemicals associated with SREBF activation identified fenofibrate, a peroxisome proliferator-activated receptor α (PPARα) agonist, as a drug that increases the expression of known SREBF targets, raising the possibility that fenofibrate may also stimulate myelination. To test this, we performed in vivo imaging of zebrafish expressing a fluorescent reporter protein under the control of the myelin basic protein (mbp) promoter. Treatment of zebrafish with fenofibrate significantly increased expression of the fluorescent reporter compared with untreated zebrafish. This increase was attenuated by co-treatment with fatostatin, a specific inhibitor of SREBFs, confirming that the fenofibrate effect was mediated via SREBFs. Furthermore, incubation of zebrafish with another PPARα agonist, gemfibrozil, also increased expression of the mbp promoter-driven fluorescent reporter in an SREBF-dependent manner. These results suggest that activation of SREBFs by small molecular weight compounds may be a feasible therapeutic approach to stimulate myelination