The automatic identification of underwater noncooperative targets without label records remains an arduous task considering the marine noise interference and the shortage of labeled samples.In particular,the data-driv...The automatic identification of underwater noncooperative targets without label records remains an arduous task considering the marine noise interference and the shortage of labeled samples.In particular,the data-driven mechanism of deep learning cannot identify false samples,aggravating the difficulty in noncooperative underwater target recognition.A semi-supervised ensemble framework based on vertical line array fusion and the sparse adversarial co-training algorithm is proposed to identify noncooperative targets effectively.The sound field cross-correlation compression(SCC)feature is developed to reduce noise and computational redundancy.Starting from an incomplete dataset,a joint adversarial autoencoder is constructed to extract the sparse features with source depth sensitivity,aiming to discover the unknown underwater targets.The adversarial prediction label is converted to initialize the joint co-forest,whose evaluation function is optimized by introducing adaptive confidence.The experiments prove the strong denoising performance,low mean square error,and high separability of SCC features.Compared with several state-of-the-art approaches,the numerical results illustrate the superiorities of the proposed method due to feature compression,secondary recognition,and decision fusion.展开更多
目的金铁锁具有较好的抗炎镇痛的药理作用,但对金铁锁的抗炎作用及机制尚不明确。本研究旨在通过LPS诱导的RAW264.7细胞炎症模型对金铁锁进行抗炎作用及机制研究。方法采用LPS诱导RAW264.7细胞炎症模型,在给予金铁锁三萜类化合物干预后...目的金铁锁具有较好的抗炎镇痛的药理作用,但对金铁锁的抗炎作用及机制尚不明确。本研究旨在通过LPS诱导的RAW264.7细胞炎症模型对金铁锁进行抗炎作用及机制研究。方法采用LPS诱导RAW264.7细胞炎症模型,在给予金铁锁三萜类化合物干预后,采用ELISE试剂盒检测细胞上清液中NO、PGE_(2)的水平,PCR检测细胞中COX-2,i NOS,IL-6,TNF-αm RNA的表达,用western blot分别检测细胞总蛋白、细胞质及细胞核内NF-κB信号通路相关蛋白(IKKβ、photo-IκBα、NF-κBp65、photo-NF-κBp65)的表达情况,考察金铁锁三萜类化合物的抗炎作用机制。结果金铁锁能明显降低RAW264.7细胞活化后细胞上清液中NO和PGE_(2)的水平,对细胞上清液中NO和PGE_(2)的水平无明显影响,能明显降低对RAW264.7细胞活化后COX-2、i NOS m RNA的表达水平;金铁锁能明显抑制IKKβ的活化,抑制p-IκBα蛋白的降解,同时也能降低总蛋白中p-NF-κB p65的表达量,从而抑制细胞质内NF-κB p65向核内的转移。结论金铁锁具有良好的抗炎镇痛作用,能够抑制炎症介质的释放及酶的基因表达,改善炎症部位的病变情况,其抗炎机制与抑制NF-κB信号通路的激活有关。展开更多
基金the National Natural Science Foundation of China(No.6210011631)in part by the China Postdoctoral Science Foundation(No.2021M692628)。
文摘The automatic identification of underwater noncooperative targets without label records remains an arduous task considering the marine noise interference and the shortage of labeled samples.In particular,the data-driven mechanism of deep learning cannot identify false samples,aggravating the difficulty in noncooperative underwater target recognition.A semi-supervised ensemble framework based on vertical line array fusion and the sparse adversarial co-training algorithm is proposed to identify noncooperative targets effectively.The sound field cross-correlation compression(SCC)feature is developed to reduce noise and computational redundancy.Starting from an incomplete dataset,a joint adversarial autoencoder is constructed to extract the sparse features with source depth sensitivity,aiming to discover the unknown underwater targets.The adversarial prediction label is converted to initialize the joint co-forest,whose evaluation function is optimized by introducing adaptive confidence.The experiments prove the strong denoising performance,low mean square error,and high separability of SCC features.Compared with several state-of-the-art approaches,the numerical results illustrate the superiorities of the proposed method due to feature compression,secondary recognition,and decision fusion.
文摘目的金铁锁具有较好的抗炎镇痛的药理作用,但对金铁锁的抗炎作用及机制尚不明确。本研究旨在通过LPS诱导的RAW264.7细胞炎症模型对金铁锁进行抗炎作用及机制研究。方法采用LPS诱导RAW264.7细胞炎症模型,在给予金铁锁三萜类化合物干预后,采用ELISE试剂盒检测细胞上清液中NO、PGE_(2)的水平,PCR检测细胞中COX-2,i NOS,IL-6,TNF-αm RNA的表达,用western blot分别检测细胞总蛋白、细胞质及细胞核内NF-κB信号通路相关蛋白(IKKβ、photo-IκBα、NF-κBp65、photo-NF-κBp65)的表达情况,考察金铁锁三萜类化合物的抗炎作用机制。结果金铁锁能明显降低RAW264.7细胞活化后细胞上清液中NO和PGE_(2)的水平,对细胞上清液中NO和PGE_(2)的水平无明显影响,能明显降低对RAW264.7细胞活化后COX-2、i NOS m RNA的表达水平;金铁锁能明显抑制IKKβ的活化,抑制p-IκBα蛋白的降解,同时也能降低总蛋白中p-NF-κB p65的表达量,从而抑制细胞质内NF-κB p65向核内的转移。结论金铁锁具有良好的抗炎镇痛作用,能够抑制炎症介质的释放及酶的基因表达,改善炎症部位的病变情况,其抗炎机制与抑制NF-κB信号通路的激活有关。
