Numerical and Experimental Investigation On The Prevention of Co Deflagration

The exhaust gases from industrial furnaces contain a huge amount of heat and chemical enthalpy. However, it is hard to recover this energy since exhaust gases invariably contain combustible components such as carbon monoxide (CC). If the CO is unexpectedly ignited during the heat recovery process, deflagration or even detonation could occur, with serious consequences such as complete destruction of the equipment. In order to safely utilize the heat energy contained in exhaust gas, danger of its explosion must be fully avoided. The mechanism of gas deflagration and its prevention must therefore be studied. In this paper, we describe a numerical and experimental investigation of the deflagration process in a semi-opened tube. The results show that, upon ignition, a low-pressure wave initially spreads within the tube and then deflagration begins. For the purpose of preventing deflagration, an appropriate amount of nitrogen was injected into the tube at a fixed position. Both simulation and experimental results have shown that the injection of inert gas can successfully interrupt the deflagration process. The peak value of the deflagration pressure can thereby be reduced by around 50%. (C) 2008 Elsevier Ltd. All rights reserved.

Antioxidant N-acetylcysteine attenuates the acute liver injury caused by X-ray in mice

The aim of this study was to evaluate the protective effects of different doses and administration modes of N-acetylcysteine (NAC) against X-ray-induced liver damage in mice. Kun-Ming mice were divided into four groups, each composed of six animals: two control groups and two NAC-treated groups. An acute study was carried out to determine alterations in lipid peroxidation (determined by measuring malondiadehyde (MDA) level), glutathione (GSH) content and superoxide dismutase (SOD) activity (assayed by colorimetric method), and DNA damage (characterized by DNA-single strand break using with comet assay) as well as cell apoptosis (measured by flow cytometry) at 12 h after irradiation. The results showed that there were dose-related decreases in MDA level, DNA damage and cell apoptosis, and dose-dependent increases in GSH content and SOD activity in all NAC-treated groups compared to control groups, indicating that pre-treatment or post-treatment with NAC significantly attenuates the acute liver damage caused by X-ray. In addition, significant positive correlations were observed between MDA level and DNA damage or cell apoptosis, implying that lipid peroxidation plays a major role in X-ray-induced liver injury. The data suggest that NAC exerts its radioprotective effect by counteracting accumulated reactive oxygen species in the liver through its properties as a direct antioxidant and a GSH precursor, when administered before or after X-ray irradiation.

小肠电离辐射损伤研究进展；Advances in Small Intestinal Ionizing Radiation Injury Research

肠道的电离辐射损伤是腹部及盆腔肿瘤放射治疗过程中的剂量限制因素。综述了小肠电离辐射损伤的临床症状、小肠上皮及粘膜下层基质改变、信号分子表达变化、组织学变化和超微结构变化。简介了中国科学院近代物理研究所重离子束辐射生物医学重点实验室正在进行的有关小肠重离子辐射损伤及防护方面的研究工作。

两种保护剂对C离子诱导小鼠急性肝损伤的应答；Response of Two Protective Agents to Acute Injury Induced by ~(12)C~(6+) Ions in Mouse Liver

比较了N-乙酰半胱氨酸(NAC)及乙酰左旋肉毒碱(ALCAR)对12C6+离子照射小鼠的损伤效应,并探讨了其可能的作用机制。利用4Gy剂量的12C6+离子束对预先给予NAC(100mg/kg)和ALCAR(100mg/kg)保护的昆明小鼠进行单次全身照射。随后检测肝组织中总抗氧化能力(TAC)、DNA单链断裂和细胞凋亡率。结果显示,与照射对照组相比,提前给予NAC和ALCAR均极显著地增强了肝组织的抗氧化能力(P<0.001),减轻了12C6+离子导致的肝组织中DNA断裂(P<0.001)和细胞凋亡(P<0.001)。此外,还发现ALCAR组抗重离子辐照损伤的能力显著地高于NAC组(P<0.05)。实验结果提示了NAC和ALCAR可通过抵御组织内的氧化胁迫,阻止DNA链的断裂和细胞的凋亡,实现对C离子辐照损伤的保护效应。而且ALCAR比NAC可能更适合成为有潜力、有希望的抗C重离子辐射药物。