http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Publisher Correction: Direct imaging of the electron liquid at oxide interfaces
Song, Kyung,Ryu, Sangwoo,Lee, Hyungwoo,Paudel, Tula R.,Koch, Christoph T.,Park, Bumsu,Lee, Ja Kyung,Choi, Si-Young,Kim, Young-Min,Kim, Jong Chan,Jeong, Hu Young,Rzchowski, Mark S.,Tsymbal, Evgeny Y.,E Nature Publishing Group UK 2018 Nature nanotechnology Vol.13 No.7
In the version of this Letter originally published, in two instances in Fig. 1 the layers in the cross-sectional view of the (001) interface were incorrectly labelled: in Fig. 1b SrO<SUP>+</SUP> should have read SrO<SUP>0</SUP>; in Fig. 1c LaO<SUP>+</SUP>, AlO<SUB>2</SUB><SUP>–</SUP>, LaO<SUP>+</SUP>, TiO<SUB>2</SUB><SUP>0</SUP>, SrO<SUP>+</SUP>, TiO<SUB>2</SUB><SUP>0</SUP> should have read LaO<SUB>3</SUB><SUP>3–</SUP>, Al<SUP>3+</SUP>, LaO<SUB>3</SUB><SUP>3–</SUP>, Ti<SUP>4+</SUP>, SrO<SUB>3</SUB><SUP>4–</SUP>, Ti<SUP>4+</SUP>. In Fig. 3c the upper-right equation read –σ<SUB>s</SUB> = –e/2a<SUP>2</SUP> but should have read –σ<SUB>s</SUB> = e/2a<SUP>2</SUP> and in Fig. 3f the lower-right equation read –σ<SUB>s</SUB> = –e/2√3a<SUP>2</SUP> but should have read σ<SUB>s</SUB> = –e/2√3a<SUP>2</SUP>. These errors have now been corrected in the online version of the Letter.
FAM83H mutations cause ADHCAI and alter intracellular protein localization.
Lee, S-K,Lee, K-E,Jeong, T-S,Hwang, Y-H,Kim, S,Hu, J C-C,Simmer, J P,Kim, J-W Journal of Dental Research, Inc 2011 Journal of dental research Vol.90 No.3
<P>Mutations in a family with sequence similarity 83 member H (FAM83H) cause autosomal-dominant hypocalcification amelogenesis imperfecta (ADH CAI). All FAM83H ADHCAI-causing mutations terminate translation or shift the reading frame within the specific exon 5 segment that encodes from Ser(287) to Glu(694). Mutations near Glu(694) cause a milder, more localized phenotype. We identified disease-causing FAM83H mutations in two families with ADHCAI: family 1 (g.3115C>T, c.1993 C>T, p.Q665X) and family 2 (g.3151C>T, c.2029 C>T, p.Q677X). We also tested the hypothesis that truncation mutations alter the intracellular localization of FAM83H. Wild-type FAM83H and p.E694X mutant FAM83H fused to green fluorescent protein (GFP) localized in the cytoplasm of HEK293T cells, but the mutant FAM83H proteins (p.R325X, p.W460X, and p.Q677X) fused to GFP localized mainly in the nucleus with slight expression in the cytoplasm. We conclude that nuclear targeting of the truncated FAM83H protein contributes to the severe, generalized enamel phenotype.</P>
THE EVOLUTION OF LYMAN$\alpha$ FOREST CLOUDS AT z > 2
KIM T.-S.,Hu E. M.,COWIE L. L.,SONGAILA A. The Korean Astronomical Society 1996 Journal of The Korean Astronomical Society Vol.29 No.suppl1
Using the Keck 10 m telescope data with the HIRES spectrograph, we analyzed the evolution of Lyman$\alpha$ forest clouds at z > 2 down to the HI column density $10^{12.8}cm^{-2}$. The number density per unit column density does not change with redshifts at lower HI cloumn density ($N_{HI} < 10^{14}cm^{-2}$), while the forest clouds at higher column density disappear rapidly. The cutoff b value, the thermal temperature indicator, increases as redshift decreases. The correlation strength seems to be stronger as redshift decreases.
Guo, J.,Hu, X.,Liu, J.,Feng, T.,Yoon, E.Y.,Kim, H.S. PAS 2015 ARCHIVES OF METALLURGY Vol.60 No.2
<B>Abstract</B><P>Amorphous alloys or metallic glasses have attracted significant interest in the materials science and engineering communities due to their unique physical, mechanical, and chemical properties. The viscous flow of amorphous alloys exhibiting high strain rate sensitivity and homogeneous deformation is considered to be an important characteristic in thermoplastic forming processes performed within the supercooled liquid region because it allows superplastic-like deformation behavior. Here, the correlation between the superheated liquid fragility, and the onset temperature of crystallization for Al-based alloys, is investigated. The activation energy for viscous flow of the liquid is also investigated. There is a negative correlation between the parameter of superheated liquid fragility and the onset temperature of crystallization in the same Al-based alloy system. The activation energy decreases as the onset temperature of crystallization increases. This indicates that the stability of a superheated liquid can affect the thermal stability of the amorphous alloy. It also means that a liquid with a large superheated liquid fragility, when rapidly solidified, forms an amorphous alloy with a low thermal stability.</P>
Electronic and spin states ofSrRuO3thin films: An x-ray magnetic circular dichroism study
Agrestini, S.,Hu, Z.,Kuo, C.-Y.,Haverkort, M. W.,Ko, K.-T.,Hollmann, N.,Liu, Q.,Pellegrin, E.,Valvidares, M.,Herrero-Martin, J.,Gargiani, P.,Gegenwart, P.,Schneider, M.,Esser, S.,Tanaka, A.,Komarek, A American Physical Society 2015 Physical review. B, Condensed matter and materials Vol.91 No.7
( Lei Zhang ),( Ji T Gong ),( Hu Q Zhang ),( Quan H Song ),( Guang H Xu ),( Lei Cai ),( Xiao D Tang ),( Hai F Zhang ),( Fang E Liu ),( Zhan S Jia ),( Hong W Zhang ) 대한소화기기능성질환·운동학회 2015 Journal of Neurogastroenterology and Motility (JNM Vol.21 No.2
Background/Aims There are increasing evidences for gastrointestinal motility disorder (GIMD) and gastric stress ulcer induced by noise stress. The present study was to investigate the reversed effect of melatonin on GIMD and gastric stress ulcer induced by noise stress and potential mechanism. Methods Noise stress was induced on rats, and melatonin (15 mg/kg) was administered to rats by intraperitoneal injection. Differences were assessed in gastric residual rate (GRR), small intestine propulsion rate (SPR), Guth injury score, cortisol, gastrointestinal hormones (calcitonin-gene-related peptide and motilin) and oxidative stress markers (superoxide dismutase and malondialde hyde) in blood plasma as well as gastric mucosa homogenate with or without melatonin. The pathological examination of gastric mucosa was also performed. Results The GRR and SPR were improved by noise stress compared with control (P < 0.05). The pathological examination and Guth injury score revealed gastric stress ulcer. Moreover, the levels of cortisol, motilin and malondialdehyde in blood plasma and malondialdehyde in gastric mucosa homogenate were increased by noise stress (P < 0.05). CGRP and superoxide dismutase activity in both of blood plasma and gastric mucosa homogenate were significantly decreased (P< 0.05). Furthermore, melatonin reversed changes in GRR, SPR, pathological examination, Guth injury score, cortisol, motilin, CGRP, superoxide dismutase activity and malondialdehyde (P < 0.05). Conclusions Melatonin is effective in reversing the GIMD and gastric stress ulcer induced by noise stress. The underlying mechanism may be involved in oxidative stress and gastrointestinal hormones. (J Neurogastroenterol Motil 2015;21:189-199)
<i>LAMB3</i> Mutations Causing Autosomal-dominant Amelogenesis Imperfecta
Kim, J.W.,Seymen, F.,Lee, K.E.,Ko, J.,Yildirim, M.,Tuna, E.B.,Gencay, K.,Shin, T.J.,Kyun, H.K.,Simmer, J.P.,Hu, J.C.-C. SAGE Publications 2013 Journal of dental research Vol.92 No.10
<P>Amelogenesis imperfecta (AI) can be either isolated or part of a larger syndrome. Junctional epidermolysis bullosa (JEB) is a collection of autosomal-recessive disorders featuring AI associated with skin fragility and other symptoms. JEB is a recessive syndrome usually caused by mutations in both alleles of <I>COL17A1, LAMA3, LAMB3</I>, or <I>LAMC2</I>. In rare cases, heterozygous carriers in JEB kindreds display enamel malformations in the absence of skin fragility (isolated AI). We recruited two kindreds with autosomal-dominant amelogenesis imperfecta (ADAI) characterized by generalized severe enamel hypoplasia with deep linear grooves and pits. Whole-exome sequencing of both probands identified novel heterozygous mutations in the last exon of <I>LAMB3</I> that likely truncated the protein. The mutations perfectly segregated with the enamel defects in both families. In Family 1, an 8-bp deletion (c.3446_3453del GACTGGAG) shifted the reading frame (p.Gly 1149Glufs*8). In Family 2, a single nucleotide substitution (c.C3431A) generated an in-frame translation termination codon (p.Ser1144*). We conclude that enamel formation is particularly sensitive to defects in hemidesmosome/basement-membrane complexes and that syndromic and non-syndromic forms of AI can be etiologically related.</P>