Microparticle Formation and Crystallization Rate of HMX with Supercritical CO_2 Antisolvent Recrystallization

Microparticle formation and crystallization rate of 1,3,5,7-tetranitro-l,3,5,7-tetraazacyclooctane (HMX) in acetone solution using supercritical carbon dioxide antisolvent (GAS) recrystallization were studied. Scanning electronic microscopy, X-ray diffraction and infrared radiation were used to examine particle size, crystallinity and chemical structure. The results show that B-HMX microparticle in different average size (2-9.5um) and with narrow size distribution were obtained by controlling the expansibility, expansion speed, initial concentration and temperature during recrystallization of HMX. The formation of nuclei may be a main cause of consumption of solute when the solution is expanded rapidly enough and the equilibrium concentration is lower, in which almost monodisperse microparticle can be obtained.

MNX1通过调控ATG7诱导细胞自噬介导鼻咽癌放疗抵抗

目的探讨MNX1通过调控ATG7诱导细胞自噬介导鼻咽癌放疗抵抗的作用机制。方法采用人鼻咽癌抗辐射细胞系HONE-1-IR和辐射敏感细胞系HONE-1进行体外分析;检测细胞中MNX1的表达水平,比较自噬标志物LC3Ⅱ、ATG7和p62表达情况;并分析MNX1与ATG7调控细胞自噬的关系。结果与HONE-1细胞相比,HONE-1-IR细胞中MNX1 m RNA和蛋白水平均升高,LC3Ⅱ、ATG7和p62蛋白表达水平同样升高(P<0.05);下调MNX1抑制了自噬体的形成(P<0.05)。与阴性对照组相比,转染si MNX1的细胞增殖率和细胞活力明显降低(P<0.05);细胞集落形成率明显降低(P<0.05)。下调MNX1明显阻断了自噬体的形成,上调ATG7后,自噬体的抑制水平恢复到对照组的水平(P<0.05);在HONE-1-IR细胞中通过下调MNX1抑制了细胞的增殖和活力,而通过上调ATG7逆转了这种抑制(P<0.05)。结论MNX1通过上调ATG7调控细胞自噬参与放疗抵抗,通过敲低MNX1-ATG7轴可提高放疗抵抗细胞的敏感性,MNX1可作为增强放射敏感性的潜在治疗靶点。

1-亚硝基-3,5,7-三硝基-1,3,5,7-四氮杂环辛烷急性毒性研究

选用SD大鼠和白兔分别进行1-亚硝基-3,5,7-三硝基-1,3,5,7-四氮杂环辛烷(MNX)急性经口毒性、皮肤及眼刺激试验。结果发现,雄性和雌性大鼠MNX经口LD;分别为316 mg/kg、43 mg/kg;4只白兔皮肤刺激试验评分均为0,但3只染毒24 h后死亡;4只白兔眼刺激试验均出现轻微刺激症状,1只染毒48 h后恢复正常,其余3只死亡。提示MNX对雄性和雌性大鼠急性经口毒性等级分别为中等毒和高毒;对白兔皮肤无刺激性,对眼睛具有可逆性的轻度刺激。