维普中文期刊产品整合服务
4篇 您的检索式:作者名="Heting Jiang"
    题名 作者 年代 出处 被引量
1Strong dual-crosslinked hydrogels for ultrasound-triggered drug delivery显示文摘Hydrogels that can respond to dynamic forces either from endogenous biological activities or from external mechanical stimuli show great promise as novel drug delivery systems (DDS).However,it remains challenging to engineer hydrogels that specifically respond to externally applied mechanical forces with minimal basel drug leakage under normal stressful physiological conditions.Here we present an ultrasound responsive hydrogel-based DDS with special dual-crosslinked nanoscale network architecture.The covalent crosslinks endow the hydrogel high mechanical stability and greatly suppress deformation-triggered drug release.Meanwhile,the dynamic covalent boronate ester linkages between hydrogel backbone and the anti-inflammation compound,tannic acid (TA),allow effective ultrasound-triggered pulsetile release of TA.As such,the hydrogel shows distinct drug release profiles under compression and ultrasound.A proof-of-principle demonstration of the suppression of inflammation activation of macrophage upon ultrasound-triggered release of TA was also illustrated.We anticipate that this novel hydrogel-based drug delivery system can be used for the treatment of inflammatory diseases on load-bearing tissues,such as muscle and cartilage.Wenxu Sun Heting Jiang Xin Wu Zhengyu Xu Chen Yao Juan Wang Meng Qin Qing Jiang Wei Wang Dongquan Shi Yi Cao 2019Nano Research2019,12,1:3
2Ultrasonic vibration enabled under-liquid forming of metallic glasses显示文摘Advancements in forming technology offer significant advantages for the manufacturing industry,including enhanced efficiency,energy conservation,and improved material utilization[1].However,traditional additive manufacturing[2],thermoplastic forming[3],and laser cutting[4]encounter challenges when applied in under-liquid environments,mainly due to difficulties in temperature control and heat source provision.Xin Li Luyao Li Sajad Sohrabi Jia'nan Fu Zhen Li Zhe Chen Rongce Sun Yu Zhang Jinbiao Huang Heting Zhang Jian Zhu Xiangyan Chen Kaikai Song Jiang Ma 2024Science Bulletin2024,69,2:0
3Artificial intelligence-based non-invasive tumorsegmentation, grade stratification and prognosisprediction for clear-cell renal-cell carcinoma显示文摘Due to the complicated histopathological characteristics of clear-cell renal-cell carcinoma(ccRcC),non-invasive prognosis before operative treatment is crucial in selecting the appropriate treatment.A total of 126345 computerized tomography(cT)images from four independent patient cohorts were included for analysis in this study.We propose a V Bottieneck multi-resolution and focus-organ network(VB-MrFo-Net)using a cascade framework for deep learning analysis.The VB-MrFo-Net achieved better performance than VB-Net in tumor segmentation,with a Dice score of 0.87.The nuclear-grade prediction model performed best in the logistic regression classifier,with area under curve values from 0.782 to 0.746.Survival analysis revealed that our prediction model could significantly distinguish patients with high survival risk,with a hazard ratio(HR)of 2.49[95%confidence interval(CI):1.13-5.45,P=0.023]in the General cohort.Excellent performance had also been verified in the Cancer Genome Atlas cohort,the Clinical Proteomic Tumor Analysis Consortium cohort,and the Kidney Tumor Segmentation Challenge cohort,with HRs of 2.77(95%CI:1.58-4.84,P=0.0019),3.83(95%CI:1.22-11.96,P=0.029),and 2.80(95%CI:1.05-7.47,P=0.025),respectively.In conclusion,we propose a novel VB-MrFo-Net for the renal tumor segmentation and automatic diagnosis of ccRcc.The risk stratification model could accurately distinguish patients with high tumor grade and high survival risk based on non-invasive CT images before surgical treatments,which couid provide practical advicefordecidingtreatmentoptions.Siteng Chen Dandan Song Lei Chen Tuanjie Guo Beibei Jiang Aie Liu Xianpan Pan Tao Wang Heting Tang Guihua Chen Zhong Xue Xiang Wang Ning Zhang Junhua Zheng 2023Precision Clinical Medicine2023,6,3:0
4The endoplasmic reticulum membrane protein complex subunit Emc6 is essential for rhodopsin localization and photoreceptor cell survival显示文摘The endoplasmic reticulum(ER)membrane protein complex(EMC)is responsible for monitoring the biogenesis and synthetic quality of membrane proteins with tail-anchored or multiple transmembrane domains.The EMC subunit EMC6 is one of the core members of EMC and forms an enclosed hydrophilic vestibule in cooperation with EMC3.Despite studies demonstrating that deletion of EMC3 led to rhodopsin mislocalization in rod photoreceptors of mice,the precise mechanism leading to the failure of rhodopsin trafficking remains unclear.Here,we generated the first rod photoreceptor-specific knockout of Emc6(RKO)and cone photoreceptor-specific knockout of Emc6(CKO)mouse models.Deficiency of Emc6 in rod photoreceptors led to progressive shortening of outer segments(OS),impaired visual function,mislocalization and reduced expression of rhodopsin,and increased gliosis in rod photoreceptors.In addition,CKO mice displayed the progressive death of cone photoreceptors and abnormal localization of cone opsin protein.Subsequently,proteomics analysis of the RKO mouse retina illustrated that several cilium-related proteins,particularly anoctamin-2(ANO2)and transmembrane protein 67(TMEM67),were significantly down-regulated prior to OS degeneration.Detrimental rod photoreceptor cilia and mislocalized membrane disc proteins were evident in RKO mice.Our data revealed that in addition to monitoring the synthesis of rhodopsin-dominated membrane disc proteins,EMC6 also impacted rod photoreceptors'ciliogenesis by regulating the synthesis of membrane proteins associated with cilia,contributing to the mislocalization of membrane disc proteins.Kuanxiang Sun Lu Liu Xiaoyan Jiang Heting Wang Lin Wang Yeming Yang Wenjing Liu Lin Zhang Xiaohui Zhao Xianjun Zhu 2024Genes & Diseases2024,11,2:0
返回顶部 每页显示:
共1页 首页 上一页 第1页 下一页 末页 /1 跳转

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费