Interaction of Electron Beam with the Target in Scanning Electron Microscope

Based on the fundamental potential function of the power and exponential forms, a diffusion model of electron beams penetrating in a target has been proposed to take place throughout a hemisphere with a centre located at the most probable energy dissipation depth, related to the diffusion depth and the maximum energy dissipation depth, which is found to agree well with the empirical data of back-scattering coefficient as a function of the incident energy. Based on the energy retardation power formula concerning the penetration and the energy loss of an electron probe into solid targets, the secondary electron emission yield has been derived as functions of three parameters such as atomic number, first ionization (or plasmon loss for an insulator) and back-scattering coefficient. Accordingly, the energy-and angular-dependence of secondary electron emissions and the subsequent temperature-rise of the specimens are quantitatively discussed for various target materials in SEM

Ferromagnetism induced in anisotropic stacked kagome-lattice antiferromagnet Cs2_2Cu3_3CeF12_{12}

The magnetic properties of Cs$_2$Cu$_3$CeF$_{12}$ were investigated through magnetization and specific heat measurements. Cs$_2$Cu$_3$CeF$_{12}$ is composed of a buckled kagome lattice of Cu$^{2+}$, which is stacked along the b axis. The exchange network in the buckled kagome lattice is strongly anisotropic. Consequently, Cs$_2$Cu$_3$CeF$_{12}$ can be divided into two subsystems: alternating Heisenberg chains with strong antiferromagnetic exchange interactions and dangling spins. The dangling spins couple with one another via effective exchange interactions, which are mediated by chain spins. The dangling spins are further divided into two subsystems, DS1 and DS2. The dangling spins in DS1 undergo three-dimensional ferromagnetic ordering at 3.14 K, while those in DS2 remain paramagnetic down to 0.35 K. The effective interaction between the DS1 spins is approximately expressed by the ferromagnetic $XXZ$ model with the $z$ direction parallel to the crystallographic c axis. A magnetic phase diagram for $H {\parallel} c$ was obtained and was analyzed within the framework of the molecular field approximation. With increasing magnetic field, the dangling spins are polarized and the magnetization curve exhibits a wide plateau at one-third of the saturation magnetization.Comment: 10 pages, 12 figure

Influence of cataract surgery and blood pressure changes caused by sodium restriction on retinal vascular diameter

Takatoshi Tano1, Yoshimune Hiratsuka2, Koichi Ono1, Akira Murakami11Department of Ophthalmology, Juntendo University School of Medicine, Tokyo; 2National Institute of Public Health, Tokyo, JapanPurpose: To investigate the impact of cataract surgery and blood pressure changes induced by one week of sodium restriction on retinal vascular diameter.Methods: Fundus photographs of 200 patients were obtained before and one week after cataract surgery. For one week after admission, 100 patients received sodium restriction and 100 patients (ie, the control group) did not receive sodium restriction. The diameter of the retinal vessels and blood pressure were compared between the sodium restriction group and the control group. The vascular diameter was measured using an objective computer-based method.Results: Neither group had a significant change in the diameter of the retinal vessels after cataract surgery. Although there was no significant change in retinal arterial and venular diameter in the sodium restriction group, one-week sodium restriction significantly reduced mean blood pressure. However, multiple linear regression analyses indicated that an increase in retinal arteriolar diameter was significantly associated with diabetes, hyperlipidemia, and alcohol intake.Conclusion: Cataract surgery and blood pressure reduction induced by one week of sodium restriction resulted in no significant change in retinal arteriolar diameter.Keywords: cataract surgery, hypertension, retinal blood vessel diameter, retinal fundus camera, sodium restriction

骨肉腫細胞の生存と増殖はミトコンドリア局在BIG3-PHB2複合体形成に依存する

Previous studies reported the critical role of the brefeldin A–inhibited guanine nucleotide exchange protein 3–prohibitin 2 (BIG3-PHB2) complex in modulating estrogen signaling activation in breast cancer cells, yet its pathophysiological roles in osteosarcoma (OS) cells remain elusive. Here, we report a novel function of BIG3-PHB2 in OS malignancy. BIG3-PHB2 complexes were localized mainly in mitochondria in OS cells, unlike in estrogen-dependent breast cancer cells. Depletion of endogenous BIG3 expression by small interfering RNA (siRNA) treatment led to significant inhibition of OS cell growth. Disruption of BIG3-PHB2 complex formation by treatment with specific peptide inhibitor also resulted in significant dose-dependent suppression of OS cell growth, migration, and invasion resulting from G2/M-phase arrest and in PARP cleavage, ultimately leading to PARP-1/apoptosis-inducing factor (AIF) pathway activation–dependent apoptosis in OS cells. Subsequent proteomic and bioinformatic pathway analyses revealed that disruption of the BIG3-PHB2 complex might lead to downregulation of inner mitochondrial membrane protein complex activity. Our findings indicate that the mitochondrial BIG3-PHB2 complex might regulate PARP-1/AIF pathway-dependent apoptosis during OS cell proliferation and progression and that disruption of this complex may be a promising therapeutic strategy for OS