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        Study on three-dimensional numerical simulation of shell and tube heat exchanger of the surface ship under marine conditions

        Liao Yi,Cai Qi,He Shaopeng,Wang Mingjun,Xiao Hongguang,Gong Zili,Wang Cong,Jia Zhen,Feng Tangtao,Qiu Suizheng 한국원자력학회 2023 Nuclear Engineering and Technology Vol.55 No.4

        Shell-and-tube heat exchanger (STHX) is widely used by virtue of its simple structure and high reliability, especially in a space-constrained surface ship. For the STHX of the surface ship, roll, pitch and other motion of the ship will affect the heat transfer performance, resistance characteristics and structural strength of the heat exchanger. Therefore, it is urgent to carry out numerical simulation research on three-dimensional thermal hydraulic characteristics of surface ship STHX under the marine conditions. In this paper, the numerical simulation of marine shell and tube heat exchanger of surface ship was carried out using the porous media model. Firstly, the mathematical physical model and numerical method are validated based on the experimental data of a marine engine cooling water shell and tube heat exchanger. The simulation results are in good agreement with the experimental results. The prediction errors of pressure drop and heat transfer are less than 10% and 1% respectively. The effect of marine conditions on the heat transfer characteristics of the heat exchanger is investigated by introducing the additional force model of marine condition to evaluate the effect of different motion parameters on the heat transfer performance of the heat exchanger. This study could provide a reference for the optimization of marine heat exchanger design.

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        Crocin alleviates neurotoxicity induced by bupivacaine in SH-SY5Y cells with inhibition of PI3K/AKT signaling

        Lin Lili,Chen Zhen,Li Jun,Peng Jianye,Wang Jian,Feng Mingjun,Liu Tiancheng,Zhang Mengli,Wu Xian,Ai Fen,Shen Caijie 한국유전학회 2024 Genes & Genomics Vol.46 No.1

        Background Bupivacaine, a common local anesthetic, can cause neurotoxicity and permanent neurological disorders. Crocin has been widely reported as a potential neuroprotective agent in neural injury models. Objective The aim of this study was to investigate the role and regulatory mechanism of crocin underlying bupivacaine-induced neurotoxicity. Method Human neuroblastoma SH-SY5Y cells were treated with bupivacaine and/or crocin for 24 h, followed by detecting cell viability using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. The effect of crocin or bupivacaine on SH-SY5Y cell proliferation was measured by Ki67 immunofluorescence assay. The levels of apoptosis-related proteins and the markers in the PI3K/Akt signaling pathway were examined using western blot analysis. The activities of caspase 3, catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were tested using respective commercial assay kits. Flow cytometry analysis was executed for detecting SH-SY5Y cell apoptosis. Result Crocin attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells. Meanwhile, crocin inhibited SH-SY5Y cell apoptosis induced by bupivacaine via repressing the activity of caspase-3, reducing Bax expression, and elevating Bcl-2 expression. Moreover, crocin mitigated oxidative stress in SH-SY5Y cells by increasing the content of CAT, SOD, GSH-Px and reducing the content of MDA. Additionally, crocin protected against bupivacaine-induced dephosphorylation of Akt and GSK-3β. The protective effects of crocin against bupivacaine-induced neurotoxicity in SH-SY5Y cells were counteracted by the Akt inhibitor. Conclusion These results suggested that crocin may exert a neuroprotective function by promoting cell proliferation and suppressing apoptosis and oxidative stress in SH-SY5Y cells. Thus, crocin might become a promising drug for the treatment of bupivacaine-induced neurotoxicity. Background Bupivacaine, a common local anesthetic, can cause neurotoxicity and permanent neurological disorders. Crocin has been widely reported as a potential neuroprotective agent in neural injury models. Objective The aim of this study was to investigate the role and regulatory mechanism of crocin underlying bupivacaine-induced neurotoxicity. Method Human neuroblastoma SH-SY5Y cells were treated with bupivacaine and/or crocin for 24 h, followed by detecting cell viability using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. The effect of crocin or bupivacaine on SH-SY5Y cell proliferation was measured by Ki67 immunofluorescence assay. The levels of apoptosis-related proteins and the markers in the PI3K/Akt signaling pathway were examined using western blot analysis. The activities of caspase 3, catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were tested using respective commercial assay kits. Flow cytometry analysis was executed for detecting SH-SY5Y cell apoptosis. Result Crocin attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells. Meanwhile, crocin inhibited SH-SY5Y cell apoptosis induced by bupivacaine via repressing the activity of caspase-3, reducing Bax expression, and elevating Bcl-2 expression. Moreover, crocin mitigated oxidative stress in SH-SY5Y cells by increasing the content of CAT, SOD, GSH-Px and reducing the content of MDA. Additionally, crocin protected against bupivacaine-induced dephosphorylation of Akt and GSK-3β. The protective effects of crocin against bupivacaine-induced neurotoxicity in SH-SY5Y cells were counteracted by the Akt inhibitor. Conclusion These results suggested that crocin may exert a neuroprotective function by promoting cell proliferation and suppressing apoptosis and oxidative stress in SH-SY5Y cells. Thus, crocin might become a promising drug for the treatment of bupivacaine-induced neurotoxicity.

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