Ni/Ni3C Core-Shell Nanochains and Its Magnetic Properties: One-Step Synthesis at low temperature

One-dimensional Ni/Ni3C core-shell nanoball chains with an average diameter by around 30 nm were synthesized by means of a mild chemical solution method using a soft template of trioctylphosphineoxide (TOPO). It was revealed that the uniform Ni nanochains were capped with Ni3C thin shells by about 1 to 4 nm in thickness and each Ni core consists of polygrains. The coercivity of the core-shell nanochains is much enhanced (600 Oe at 5 K) and comparable with single Ni nanowires due to the one-dimensional shape anisotropy. Deriving from the distinctive structure of Ni core and Ni3C shell, this architecture may possess a possible bi-functionality. This unique architecture is also useful for the study on the magnetization reversal mechanism of one-dimensional magnetic nanostructure.Comment: 17 pages, 6 figur

An appendix adenocarcinoma mimicking appendicitis

SummaryCancer of the appendix is very rare and is typically found incidentally in approximately 1% of patients who received appendectomies. Most of appendiceal tumors are carcinoid, adenoma, and lymphoma. Adenocarcinoma of the appendix accounts for only 10% of all primary appendiceal cancers and the treatment remains controversial. In this article, we report a 67-year-old man who presented with symptoms of appendicitis that was diagnosed as adenocarcinoma of the appendix Stage II. The patient was treated with right hemicolectomy. To date he remains asymptomatic

ANALYSIS OF ANGULAR MOMENTUM THE WHOLE BODY DURING GLIDE HITTING AND KICK HITTING IN BASEBALL

The purpose of this study were to analyze the biomechanical characteristics of glide and kick hitting in baseball which exerted by professional baseball players in Taiwan. Five professional baseball players were selected as the subjects. The experiment used two JVC-DV 9800 high-speed digital cameras(120 Hz).The video data was treated by Kwon3D 3.0 motion analysis system. The following are the main results: The kick hitting could get better rotation benefit and optimum. In the stride phase, angUlar momentum of the body is increasing by body inertia. In the rotation phase, the velocity increasing of the body center of gravity makes the angUlar momentum increase. The largest angular momentum appears right before the ball hi!. Because the body inertia in ball hitting moment was very small, the angUlar momentum was mainly affected by angular velocity. In the phase, the average value, largest value and hitting moment value of angular momentum with kick hitting are larger than those with glide hitting. Therefore, the kick hitting could get larger linear and angular momentum

Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction.

Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe the effects of mitochondria-specific, not cytoplasmic, Omi/HtrA2 on myocardial apoptosis and cardiac function. Transgenic mice overexpressing cardiac-specific mitochondrial Omi/HtrA2 were generated and they had increased myocardial apoptosis, decreased systolic and diastolic function, and decreased left ventricular remodeling. Transiently or stably overexpression of mitochondria Omi/HtrA2 in H9C2 cells enhance apoptosis as evidenced by elevated caspase-3, -9 activity and TUNEL staining, which was completely blocked by Ucf-101, a specific Omi/HtrA2 inhibitor. Mechanistic studies revealed mitochondrial Omi/HtrA2 overexpression degraded the mitochondrial anti-apoptotic protein HAX-1, an effect attenuated by Ucf-101. Additionally, transfected cells overexpressing mitochondrial Omi/HtrA2 were more sensitive to hypoxia and reoxygenation (H/R) induced apoptosis. Cyclosporine A (CsA), a mitochondrial permeability transition inhibitor, blocked translocation of Omi/HtrA2 from mitochondrial to cytoplasm, and protected transfected cells incompletely against H/R-induced caspase-3 activation. We report in vitro and in vivo overexpression of mitochondrial Omi/HtrA2 induces cardiac apoptosis and dysfunction. Thus, strategies to directly inhibit Omi/HtrA2 or its cytosolic translocation from mitochondria may protect against heart injury