Electrically tunable lasing based on defect mode in one-dimensional photonic crystal with conducting polymer and liquid crystal defect layer

This article may be downloaded for personal use only. Any other use requires prior permission of the author and AIP Publishing. This article appeared in Ryotaro Ozaki, Yuko Matsuhisa, Masanori Ozaki, and Katsumi Yoshino, Appl. Phys. Lett. 84, 1844 (2004) and may be found at https://doi.org/10.1063/1.1686891

Linearly polarized lasing in one-dimensional hybrid photonic crystal containing cholesteric liquid crystal

This article may be downloaded for personal use only. Any other use requires prior permission of the author and AIP Publishing. This article appeared in Yuko Matsuhisa, Ryotaro Ozaki, Yuuki Takao, and Masanori Ozaki, J. Appl. Phys. 101, 033120 (2007) and may be found at https://doi.org/10.1063/1.2434835

High Q defect mode and laser action in one-dimensional hybrid photonic crystal containing cholesteric liquid crystal

The authors have investigated the optical characteristics of a one-dimensional hybrid photonic crystal (1D HPC) containing cholesteric liquid crystal (CLC) as a defect by theoretical calculation and predicted the appearance of additional modes at the band edges of the CLC defect, whose Q factor was higher than those of the other defect modes. They have confirmed the appearance of the additional mode experimentally. Single-mode laser action with low pumping threshold was observed in a 1D HPC with a dye-doped CLC defect, which is based on the additional defect mode with a high Q factor peculiar to the CLC defect having periodic structure. This work is partially supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan.This article may be downloaded for personal use only. Any other use requires prior permission of the author and AIP Publishing. This article appeared in Yuko Matsuhisa, Ryotaro Ozaki, Katsumi Yoshino, Masanori Ozaki, Appl. Phys. Lett. 89, 101109 (2006) and may be found at https://doi.org/10.1063/1.2347114

Low-threshold and high efficiency lasing upon band-edge excitation in a cholesteric liquid crystal

A low threshold and high efficiency laser based on dye-doped cholesteric liquid crystals (CLCs) is demonstrated using an input excitation with the same handedness of circular polarization as the helical structure of the sample at the shorter wavelength band edge of the reflection band. The responsible mechanism originates from the dramatic increase of the optical density of state (DOS) at the band edges. The calculated DOS of the CLC system confirms the authors\u27 experimental results

Cholesteric liquid crystal laser in a dielectric mirror cavity upon band-edge excitation

Low threshold laser action of dye-doped cholesteric liquid crystals ( CLCs) is demonstrated using an input circularly polarized light whose handedness is the same as the cholesteric helix of the sample at the high-energy band edge of the reflection band. The mechanism originates from the dramatic increase of the photon density of state at the band edges. We also demonstrate an enhanced laser action of a CLC in a dielectric multilayer cavity. In such a device configuration, the band-edge excitation at high-energy band edge improves the lasing performance not only for the same handedness circularly polarized pump beam as the cholesteric helix but also for the opposite one. It stems from the polarization independence of the dielectric multilayers

MLH1-mediated recruitment of FAN1 to chromatin for the induction of apoptosis triggered by O6-methylguanine

O6 -Methylguanines (O6 -meG), which are produced in DNA by the action of alkylating agents, are mutagenic and cytotoxic, and induce apoptosis in a mismatch repair (MMR) protein-dependent manner. To understand the molecular mechanism of O6 -meG-induced apoptosis, we performed functional analyses of FANCD2 and FANCI-associated nuclease 1 (FAN1), which was identified as an interacting partner of MLH1. Immunoprecipitation analyses showed that FAN1 interacted with both MLH1 and MSH2 after treatment with N-methyl-N-nitrosourea (MNU), indicating the formation of a FAN1-MMR complex. In comparison with control cells, FAN1-knockdown cells were more resistant to MNU, and the appearances of a sub-G1 population and caspase-9 activation were suppressed. FAN1 formed nuclear foci in an MLH1-dependent manner after MNU treatment, and some were colocalized with both MLH1 foci and single-stranded DNA (ssDNA) created at damaged sites. Under the same condition, FANCD2 also formed nuclear foci, although it was dispensable for the formation of FAN1 foci and ssDNA. MNU-induced formation of ssDNA was dramatically suppressed in FAN1-knockdown cells. We therefore propose that FAN1 is loaded on chromatin through the interaction with MLH1 and produces ssDNA by its exonuclease activity, which contributes to the activation of the DNA damage response followed by the induction of apoptosis triggered by O6 -meG.福岡歯科大

Haploinsufficiency of SAMD9L, an Endosome Fusion Facilitator, Causes Myeloid Malignancies in Mice Mimicking Human Diseases with Monosomy 7

SummaryMonosomy 7 and interstitial deletion of 7q (−7/7q−) are well-recognized nonrandom chromosomal abnormalities frequently found among patients with myelodysplastic syndromes (MDSs) and myeloid leukemias. We previously identified candidate myeloid tumor suppressor genes (SAMD9, SAMD9-like = SAMD9L, and Miki) in the 7q21.3 subband. We established SAMD9L-deficient mice and found that SAMD9L+/− mice as well as SAMD9L−/− mice develop myeloid diseases resembling human diseases associated with −7/7q−. SAMD9L-deficient hematopoietic stem cells showed enhanced colony formation potential and in vivo reconstitution ability. SAMD9L localizes in early endosomes. SAMD9L-deficient cells showed delays in homotypic endosome fusion, resulting in persistence of ligand-bound cytokine receptors. These findings suggest that haploinsufficiency of SAMD9L and/or SAMD9 gene(s) contributes to myeloid transformation

The Frizzled 3 gene is associated with methamphetamine psychosis in the Japanese population

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