In wastewater treatment process(WWTP), the accurate and real-time monitoring values of key variables are crucial for the operational strategies. However, most of the existing methods have difficulty in obtaining the r...In wastewater treatment process(WWTP), the accurate and real-time monitoring values of key variables are crucial for the operational strategies. However, most of the existing methods have difficulty in obtaining the real-time values of some key variables in the process. In order to handle this issue, a data-driven intelligent monitoring system, using the soft sensor technique and data distribution service, is developed to monitor the concentrations of effluent total phosphorous(TP) and ammonia nitrogen(NH_4-N). In this intelligent monitoring system, a fuzzy neural network(FNN) is applied for designing the soft sensor model, and a principal component analysis(PCA) method is used to select the input variables of the soft sensor model. Moreover, data transfer software is exploited to insert the soft sensor technique to the supervisory control and data acquisition(SCADA) system. Finally, this proposed intelligent monitoring system is tested in several real plants to demonstrate the reliability and effectiveness of the monitoring performance.展开更多
The effluent total phosphorus(ETP) is an important parameter to evaluate the performance of wastewater treatment process(WWTP). In this study, a novel method, using a data-derived soft-sensor method, is proposed to ob...The effluent total phosphorus(ETP) is an important parameter to evaluate the performance of wastewater treatment process(WWTP). In this study, a novel method, using a data-derived soft-sensor method, is proposed to obtain the reliable values of ETP online. First, a partial least square(PLS) method is introduced to select the related secondary variables of ETP based on the experimental data. Second, a radial basis function neural network(RBFNN) is developed to identify the relationship between the related secondary variables and ETP. This RBFNN easily optimizes the model parameters to improve the generalization ability of the soft-sensor. Finally, a monitoring system, based on the above PLS and RBFNN, named PLS-RBFNN-based soft-sensor system, is developed and tested in a real WWTP. Experimental results show that the proposed monitoring system can obtain the values of ETP online and own better predicting performance than some existing methods.展开更多
Background:Hepatic ischemia-reperfusion injury(HIRI)remains a common complication during liver transplantation(LT)in patients.As a key downstream effector of the Hippo pathway,Yes-associated protein(YAP)has been repor...Background:Hepatic ischemia-reperfusion injury(HIRI)remains a common complication during liver transplantation(LT)in patients.As a key downstream effector of the Hippo pathway,Yes-associated protein(YAP)has been reported to be involved in various physiological and pathological processes.However,it remains elusive whether and how YAP may control autophagy activation during ischemia-reperfusion.Methods:Human liver tissues from patients who had undergone LT were obtained to evaluate the correlation between YAP and autophagy activation.Both an in vitro hepatocyte cell line and in vivo liver-specific YAP knockdown mice were used to establish the hepatic ischemia-reperfusion models to determine the role of YAP in the activation of autophagy and the mechanism of regulation.Results:Autophagy was activated in the post-perfusion liver grafts during LT in patients,and the expression of YAP positively correlated with the autophagic level of hepatocytes.Liver-specific knockdown of YAP inhibited hepatocytes autophagy upon hypoxia-reoxygenation and HIRI(P<0.05).YAP deficiency aggravated HIRI by promoting the apoptosis of hepatocytes both in the in vitro and in vivo models(P<0.05).Attenuated HIRI by overexpression of YAP was diminished after the inhibition of autophagy with 3-methyladenine.In addition,inhibiting autophagy activation by YAP knockdown exacerbated mitochondrial damage through increasing reactive oxygen species(P<0.05).Moreover,the regulation of autophagy by YAP during HIRI was mediated by AP1(c-Jun)N-terminal kinase(JNK)signaling through binding to the transcriptional enhanced associate domain(TEAD).Conclusions:YAP protects against HIRI by inducing autophagy via JNK signaling that suppresses the apoptosis of hepatocytes.Targeting Hippo(YAP)-JNK-autophagy axis may provide a novel strategy for the prevention and treatment of HIRI.展开更多
The constitutive androstane receptor(CAR, NR3 I1) belongs to nuclear receptor superfamily.It was reported that CAR agonist TCPOBOP induces hepatomegaly but the underlying mechanism remains largely unknown. Yes-associa...The constitutive androstane receptor(CAR, NR3 I1) belongs to nuclear receptor superfamily.It was reported that CAR agonist TCPOBOP induces hepatomegaly but the underlying mechanism remains largely unknown. Yes-associated protein(YAP) is a potent regulator of organ size. The aim of this study is to explore the role of YAP in CAR activation-induced hepatomegaly and liver regeneration.TCPOBOP-induced CAR activation on hepatomegaly and liver regeneration was evaluated in wildtype(WT) mice, liver-specific YAP-deficient mice, and partial hepatectomy(PHx) mice. The results demonstrate that TCPOBOP can increase the liver-to-body weight ratio in wild-type mice and PHx mice.Hepatocytes enlargement around central vein(CV) area was observed, meanwhile hepatocytesproliferation was promoted as evidenced by the increased number of KI67+cells around portal vein(PV)area. The protein levels of YAP and its downstream targets were upregulated in TCPOBOP-treated mice and YAP translocation can be induced by CAR activation. Co-immunoprecipitation results suggested a potential proteineprotein interaction of CAR and YAP. However, CAR activation-induced hepatomegaly can still be observed in liver-specific YAP-deficient(Yape/e) mice. In summary, CAR activation promotes hepatomegaly and liver regeneration partially by inducing YAP translocation and interaction with YAP signaling pathway, which provides new insights to further understand the physiological functions of CAR.展开更多
基金Supported by the National Natural Science Foundation of China(61622301,61533002)Beijing Natural Science Foundation(4172005)Major National Science and Technology Project(2017ZX07104)
文摘In wastewater treatment process(WWTP), the accurate and real-time monitoring values of key variables are crucial for the operational strategies. However, most of the existing methods have difficulty in obtaining the real-time values of some key variables in the process. In order to handle this issue, a data-driven intelligent monitoring system, using the soft sensor technique and data distribution service, is developed to monitor the concentrations of effluent total phosphorous(TP) and ammonia nitrogen(NH_4-N). In this intelligent monitoring system, a fuzzy neural network(FNN) is applied for designing the soft sensor model, and a principal component analysis(PCA) method is used to select the input variables of the soft sensor model. Moreover, data transfer software is exploited to insert the soft sensor technique to the supervisory control and data acquisition(SCADA) system. Finally, this proposed intelligent monitoring system is tested in several real plants to demonstrate the reliability and effectiveness of the monitoring performance.
基金Supported by the National Science Foundation of China(61622301,61533002)Beijing Natural Science Foundation(4172005)Major National Science and Technology Project(2017ZX07104)
文摘The effluent total phosphorus(ETP) is an important parameter to evaluate the performance of wastewater treatment process(WWTP). In this study, a novel method, using a data-derived soft-sensor method, is proposed to obtain the reliable values of ETP online. First, a partial least square(PLS) method is introduced to select the related secondary variables of ETP based on the experimental data. Second, a radial basis function neural network(RBFNN) is developed to identify the relationship between the related secondary variables and ETP. This RBFNN easily optimizes the model parameters to improve the generalization ability of the soft-sensor. Finally, a monitoring system, based on the above PLS and RBFNN, named PLS-RBFNN-based soft-sensor system, is developed and tested in a real WWTP. Experimental results show that the proposed monitoring system can obtain the values of ETP online and own better predicting performance than some existing methods.
基金supported by grants from the National Natural Science Foundation of China(Nos.82100691,82070673,and 81870447)the Guangdong Natural Science Foundation(No.2021A1515010726)+1 种基金the China Postdoctoral Science Foundation(No.2021M693631)the Medical Scientific Research Foundation of Guangdong Province of China(No.A2021160).
文摘Background:Hepatic ischemia-reperfusion injury(HIRI)remains a common complication during liver transplantation(LT)in patients.As a key downstream effector of the Hippo pathway,Yes-associated protein(YAP)has been reported to be involved in various physiological and pathological processes.However,it remains elusive whether and how YAP may control autophagy activation during ischemia-reperfusion.Methods:Human liver tissues from patients who had undergone LT were obtained to evaluate the correlation between YAP and autophagy activation.Both an in vitro hepatocyte cell line and in vivo liver-specific YAP knockdown mice were used to establish the hepatic ischemia-reperfusion models to determine the role of YAP in the activation of autophagy and the mechanism of regulation.Results:Autophagy was activated in the post-perfusion liver grafts during LT in patients,and the expression of YAP positively correlated with the autophagic level of hepatocytes.Liver-specific knockdown of YAP inhibited hepatocytes autophagy upon hypoxia-reoxygenation and HIRI(P<0.05).YAP deficiency aggravated HIRI by promoting the apoptosis of hepatocytes both in the in vitro and in vivo models(P<0.05).Attenuated HIRI by overexpression of YAP was diminished after the inhibition of autophagy with 3-methyladenine.In addition,inhibiting autophagy activation by YAP knockdown exacerbated mitochondrial damage through increasing reactive oxygen species(P<0.05).Moreover,the regulation of autophagy by YAP during HIRI was mediated by AP1(c-Jun)N-terminal kinase(JNK)signaling through binding to the transcriptional enhanced associate domain(TEAD).Conclusions:YAP protects against HIRI by inducing autophagy via JNK signaling that suppresses the apoptosis of hepatocytes.Targeting Hippo(YAP)-JNK-autophagy axis may provide a novel strategy for the prevention and treatment of HIRI.
基金supported by the Natural Science Foundation of China (Grant numbers:82025034 and 81973392)the National Key Research and Development Program (Grant number:2017YFE0109900, China)+5 种基金the Shenzhen Science and Technology Program (Grant number:KQTD20190929174023858, China)the Natural Science Foundation of Guangdong (Grant number:2017A030311018, China)the 111 project (Grant number:B16047, China)the Key Laboratory Foundation of Guangdong Province (Grant number:2017B030314030, China)the Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program (Grant number:2017BT01Y093, China)the National Engineering and Technology Research Center for New drug Druggability Evaluation (Seed Program of Guangdong Province, Grant number:2017B090903004, China)。
文摘The constitutive androstane receptor(CAR, NR3 I1) belongs to nuclear receptor superfamily.It was reported that CAR agonist TCPOBOP induces hepatomegaly but the underlying mechanism remains largely unknown. Yes-associated protein(YAP) is a potent regulator of organ size. The aim of this study is to explore the role of YAP in CAR activation-induced hepatomegaly and liver regeneration.TCPOBOP-induced CAR activation on hepatomegaly and liver regeneration was evaluated in wildtype(WT) mice, liver-specific YAP-deficient mice, and partial hepatectomy(PHx) mice. The results demonstrate that TCPOBOP can increase the liver-to-body weight ratio in wild-type mice and PHx mice.Hepatocytes enlargement around central vein(CV) area was observed, meanwhile hepatocytesproliferation was promoted as evidenced by the increased number of KI67+cells around portal vein(PV)area. The protein levels of YAP and its downstream targets were upregulated in TCPOBOP-treated mice and YAP translocation can be induced by CAR activation. Co-immunoprecipitation results suggested a potential proteineprotein interaction of CAR and YAP. However, CAR activation-induced hepatomegaly can still be observed in liver-specific YAP-deficient(Yape/e) mice. In summary, CAR activation promotes hepatomegaly and liver regeneration partially by inducing YAP translocation and interaction with YAP signaling pathway, which provides new insights to further understand the physiological functions of CAR.