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  1. Article ; Online: Water hammer in pipelines based on different friction models.

    Jiang, Dan / Zeng, Chen / Lu, Qixia / Guo, Qing

    Scientific reports

    2024  Volume 14, Issue 1, Page(s) 953

    Abstract: Water hammer in pipelines is a difficult problem in fluid transmission field. Especially, there exists some friction items of pipeline transient model such that the simulation model is not consistent to the experimental results. By using the friction ... ...

    Abstract Water hammer in pipelines is a difficult problem in fluid transmission field. Especially, there exists some friction items of pipeline transient model such that the simulation model is not consistent to the experimental results. By using the friction model proposed by Kagawa and the model of impulse response function, the pressure transients are calculated with and without cavitation. The corresponding simulation results involving pressure, velocity, steady and dynamic frictions, cavitation volume are analyzed to reveal the effect of friction item on pressure transients. Moreover, the features of steady and dynamic frictions are captured in pipelines with upstream and downstream valves. The comparative simulation results of two friction models have verified that the friction model using an impulse response function has higher consistency between simulation and experimental results of pipeline transients.
    Language English
    Publishing date 2024-01-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-024-51409-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: MCOLN1/TRPML1 in the lysosome: a promising target for autophagy modulation in diverse diseases.

    Qi, Jiansong / Li, Qingqing / Xin, Tianli / Lu, Qixia / Lin, Jinyi / Zhang, Yang / Luo, Haiting / Zhang, Feifei / Xing, Yanhong / Wang, Wuyang / Cui, Derong / Wang, Mengmeng

    Autophagy

    2024  , Page(s) 1–11

    Abstract: MCOLN1/TRPML1 is a nonselective cationic channel specifically localized to the late endosome and lysosome. With its property of mediating the release of several divalent cations such as ... ...

    Abstract MCOLN1/TRPML1 is a nonselective cationic channel specifically localized to the late endosome and lysosome. With its property of mediating the release of several divalent cations such as Ca
    Language English
    Publishing date 2024-03-24
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2024.2333715
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Blunting TRPML1 channels protects myocardial ischemia/reperfusion injury by restoring impaired cardiomyocyte autophagy.

    Xing, Yanhong / Sui, Zhongheng / Liu, Yucheng / Wang, Meng-Meng / Wei, Xiangqing / Lu, Qixia / Wang, Xinyan / Liu, Nan / Lu, Chen / Chen, Rong / Wu, Mengmei / Wang, Yuqing / Zhao, Yu-Hong / Guo, Feng / Cao, Jun-Li / Qi, Jiansong / Wang, Wuyang

    Basic research in cardiology

    2022  Volume 117, Issue 1, Page(s) 20

    Abstract: Accumulating evidence suggests that autophagy dysfunction plays a critical role in myocardial ischemia/reperfusion (I/R) injury. However, the underling mechanism of malfunctional autophagy in the cardiomyocytes subjected to I/R has not been well defined. ...

    Abstract Accumulating evidence suggests that autophagy dysfunction plays a critical role in myocardial ischemia/reperfusion (I/R) injury. However, the underling mechanism of malfunctional autophagy in the cardiomyocytes subjected to I/R has not been well defined. As a result, there is no effective therapeutic option by targeting autophagy to prevent myocardial I/R injury. Here, we used both an in vitro and an in vivo I/R model to monitor autophagic flux in the cardiomyocytes, by exposing neonatal rat ventricular myocytes to hypoxia/reoxygenation and by subjecting mice to I/R, respectively. We observed that the autophagic flux in the cardiomyocytes subjected to I/R was blocked in both in vitro and in vivo models. Down-regulating a lysosomal cationic channel, TRPML1, markedly restored the blocked myocardial autophagic flux induced by I/R, demonstrating that TRPML1 directly contributes to the blocked autophagic flux in the cardiomyocytes subjected to I/R. Mechanistically, TRPML1 is activated secondary to ROS elevation following ischemia/reperfusion, which in turn induces the release of lysosomal zinc into the cytosol and ultimately blocks the autophagic flux in cardiomyocytes, presumably by disrupting the fusion between autophagosomes and lysosomes. As a result, the inhibited myocardial autophagic flux induced by TRPML1 disrupted mitochondria turnover and resulted in mass accumulation of damaged mitochondria and further ROS release, which directly led to cardiomyocyte death. More importantly, pharmacological and genetic inhibition of TRPML1 channels greatly reduced infarct size and rescued heart function in mice subjected to I/R in vivo by restoring impaired myocardial autophagy. In summary, our study demonstrates that secondary to ROS elevation, activation of TRPML1 results in autophagy inhibition in the cardiomyocytes subjected to I/R, which directly leads to cardiomyocyte death by disrupting mitochondria turnover. Therefore, targeting TRPML1 represents a novel therapeutic strategy to protect against myocardial I/R injury.
    MeSH term(s) Animals ; Apoptosis ; Autophagy ; Mice ; Myocardial Reperfusion Injury/drug therapy ; Myocardium ; Myocytes, Cardiac ; Rats ; Reactive Oxygen Species
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2022-04-07
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-022-00930-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.30: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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