Desorption dynamics of deuterium molecules from the Si(100)-(3×1) dideuteride surface

We measured polar angle ()-resolved time-of-flight spectra of D2 molecules desorbing from the Si(100)-(3×1) dideuteride surface. The desorbing D2 molecules exhibit a considerable translational heating with mean desorption kinetic energies of 0.25 eV, which is mostly independent of the desorption angles for 0°30°. The observed desorption dynamics of deuterium was discussed along the principle of detailed balance to predict their adsorption dynamics onto the monohydride Si surface

Coverage dependent desorption dynamics of deuterium on Si(100) surfaces: Interpretation with a diffusion-promoted desorption model

We studied coverage dependence of time-of-flight (TOF) spectra of D2 molecules thermally desorbed from the D/Si(100) surface. The mean translational energies Et of desorbed D2 molecules were found to increase from 0.20±0.05 eV to 0.40±0.04 eV as the desorption coverage window was decreased from 1.0 MLD0.9 ML to 0.2 MLD0 ML, being consistent with the kinetics switch predicted in the interdimer mechanism. The measured TOF spectra were deconvoluted into 2H, 3H, and 4H components by a curve fitting method along the principle of detailed balance. As a result, it turned out that the desorption kinetics changes from the 4H to the 3H situation at high coverage above D = 0.9 ML, while the 2H desorption is dominant for a quite wide coverage region up to D = 0.8 ML. A dynamic desorption mechanism by which the desorption is promoted by D-atom diffusion to dangling bonds was proposed

生成物の状態選別ベクトル相関による二分子反応の立体動力学に関する研究

京都大学0048新制・課程博士博士(理学)甲第7684号理博第2069号新制||理||1098(附属図書館)UT51-99-G278京都大学大学院理学研究科化学専攻(主査)教授 梶本 興亜, 教授 廣田 襄, 教授 加藤 重樹学位規則第4条第1項該当Doctor of ScienceKyoto UniversityDA

Protective role of ALDH2 against acetaldehyde-derived DNA damage in oesophageal squamous epithelium.

Acetaldehyde is an ethanol-derived definite carcinogen that causes oesophageal squamous cell carcinoma (ESCC). Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme that eliminates acetaldehyde, and impairment of ALDH2 increases the risk of ESCC. ALDH2 is produced in various tissues including the liver, heart, and kidney, but the generation and functional roles of ALDH2 in the oesophagus remain elusive. Here, we report that ethanol drinking increased ALDH2 production in the oesophagus of wild-type mice. Notably, levels of acetaldehyde-derived DNA damage represented by N(2)-ethylidene-2'-deoxyguanosine were higher in the oesophagus of Aldh2-knockout mice than in wild-type mice upon ethanol consumption. In vitro experiments revealed that acetaldehyde induced ALDH2 production in both mouse and human oesophageal keratinocytes. Furthermore, the N(2)-ethylidene-2'-deoxyguanosine levels increased in both Aldh2-knockout mouse keratinocytes and ALDH2-knockdown human keratinocytes treated with acetaldehyde. Conversely, forced production of ALDH2 sharply diminished the N(2)-ethylidene-2'-deoxyguanosine levels. Our findings provide new insight into the preventive role of oesophageal ALDH2 against acetaldehyde-derived DNA damage