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    • 15. 发明申请
    • TEXTUAL QUERY BASED MULTIMEDIA RETRIEVAL SYSTEM
    • 基于文本查询的多媒体检索系统
    • WO2011034502A1
    • 2011-03-24
    • PCT/SG2010/000343
    • 2010-09-16
    • XU, DongTSANG, Wai HungLIU, YimingNANYANG TECHNOLOGICAL UNIVERSITY
    • XU, DongTSANG, Wai HungLIU, Yiming
    • G06F17/30
    • G06F17/30017G06F17/30253G06F17/30648G06F17/3071
    • A system and method are proposed for identifying multimedia files in a first database which are related to a textual term specified by a user. The textual term is used to search a second database of multimedia files, each of which is associated with a portion of text. The "second database" is usually composed of files from the databases of a very large number of servers connected via the internet. The multimedia files identified in the search are ones for which the corresponding associated text is relevant to the textual term. The identified multimedia files are used to generate a classifier engine. The classifier engine is then applied to the first database of multimedia files, thereby retrieving multimedia files in the first database which are relevant to the textual term. The user can optionally specify whether the retrieved multimedia files are relevant or not, and this permits a feedback process to improve the classifier engine.
    • 提出了一种用于识别第一数据库中与用户指定的文本词相关的多媒体文件的系统和方法。 文本术语用于搜索多媒体文件的第二个数据库,其中每个文件与一部分文本相关联。 “第二数据库” 通常由通过互联网连接的大量服务器的数据库中的文件组成。 搜索中标识的多媒体文件是对应的相关文本与文本词语相关的文件。 所识别的多媒体文件被用于生成分类器引擎。 然后将分类器引擎应用到多媒体文件的第一数据库,从而检索第一数据库中与文本术语相关的多媒体文件。 用户可以选择指定检索到的多媒体文件是否相关,这允许反馈过程改进分类器引擎。
    • 16. 发明申请
    • ATTENUATION OF HYPEROXIA-INDUCED CELL DEATH WITH MITOCHONDRIAL ALDEHYDE DEHYDROGENASE
    • 超氧化物歧化酶诱导的细胞死亡与麻醉醛糖脱氢酶的衰减
    • WO2007147168A2
    • 2007-12-21
    • PCT/US2007/071492
    • 2007-06-18
    • THE CHILDREN'S MERCY HOSPITALXU, DongTRUOG, William, E.
    • XU, DongTRUOG, William, E.
    • C12N15/09
    • C12N9/0008A61K48/00C12N2510/00
    • Oxygen toxicity is one of the major risk factors in Jhe development of the chronic lung disease or bronchopulmonary dysplasia in premature infants. Using proteoraic analysis, we discovered mitochondria! aldehyde dehydrogenase (mtALDR or ALDB2) was down-regulated in neonatal rat lung after hyperoxic exposure. To study the role of mtALDH in hyperoxie lung injury, we overexpressed ratALDH in human lung epithelial ceils (A549) and found thai mtALDH significantly reduced hyperoxia-induced cell death. Compared to control cells (Neo- A549), the.necrotic cell death in mtALDH overexpressing cells (mtALDH-A549) decreased from 25.3% to 6.5%, 50.5% to 9.1% and 52,4% to 15.06% after 24-, 48- and 72-hour hyperoxic exposure, respectively. The levels of intracellular and mitochondria-derived reactive oxygen species (ROS) in ratALDH-A549 cells after hyperoxic exposure were significantly lowered compared to Nεo-A549 cells. mtALDH overexpreasion significantly stimulated extracellular signal regulated kinase (HRK) phosphorylation, under nontoxic and hyperoxic conditions. inhibition of ERK phosphorylation partially eliminated the protective effect of mtALDH in hyperoxia-induced cell death, suggesting ERK activation by ratALDH conferred cellular resistance to hyperoxia. mtALDH overexpresaion augmented Akt phosphorylation and maintained She total Akt level in mt ALDH- A549 cells under.nonnoxie and hyperoxic conditions. Inhibition of FBK activation by LY294002 in miALüH-A549 cells significantly increased necrotic cell death after hyperoxic exposure, indicating that. POKVAkt activation by mtALDH played an important role in cell survival after hyperoxia. Taken together, these data demonstrate that πuALDH overexpression attenuates hyperøxia-induced cell death in lung epithelial cells through reduction of ROS, activation of ERK/MAPK and PBK/Akt cell survival signaling pathways.
    • 氧气毒性是早产儿慢性肺部疾病或支气管肺发育异常的主要危险因素之一。 使用蛋白质分析,我们发现线粒体! 醛脱氢酶(mtALDR或ALDB2)在高氧暴露后新生大鼠肺中下调。 为了研究mtALDH在高氧肺损伤中的作用,我们在人肺上皮细胞(A549)中过表达大鼠ALDH,发现mtALDH显着降低高氧诱导的细胞死亡。 与对照细胞(Neo-A549)相比,mtALDH过表达细胞(mtALDH-A549)中坏死性细胞死亡率从24.3%下降到25.3%,分别为25.5%,9.1%和52.4%,降幅达到15.06% - 和72小时高氧暴露。 与Neo-A549细胞相比,高氧暴露后大鼠HDH-A549细胞中细胞内和线粒体来源的活性氧(ROS)水平显着降低。 在无毒和高氧条件下,mtALDH过表达显着刺激细胞外信号调节激酶(HRK)磷酸化。 抑制ERK磷酸化部分消除了mtALDH在高氧诱导的细胞死亡中的保护作用,表明大鼠ALD的ERK活化赋予细胞对高氧的抗性。 mtALDH过表达增强Akt磷酸化,并维持她在无氧和高氧条件下的总ALDH-A549细胞中的总Akt水平。 在miALüH-A549细胞中LY294002对FBK活化的抑制显着增加了高氧暴露后的坏死细胞死亡,表明。 mtALDH的POKVAkt激活在高氧后细胞存活中起重要作用。 总之,这些数据表明,puALDH过表达通过减少ROS,激活ERK / MAPK和PBK / Akt细胞存活信号通路来减弱肺上皮细胞中的眼眶诱导的细胞死亡。