Recent developments in spectral white-light interferometry(WLI)are reviewed.Firstly,the techniques for obtaining optical spectrum are introduced.Secondly,some novel measurement techniques are reviewed,including the im...Recent developments in spectral white-light interferometry(WLI)are reviewed.Firstly,the techniques for obtaining optical spectrum are introduced.Secondly,some novel measurement techniques are reviewed,including the improved peak-to-peak WLI,improved wavelength-tracking WLI,Fourier transform WLI,and 3×3 coupler based WLI.Furthermore,a hybrid measurement for the intensity-type sensors,interferometric sensors,and fiber Bragg grating sensors is achieved.It is shown that these developments have assisted in the progress of WLI.展开更多
To better understand the mechanisms of hydrogen peroxide(H_(2)O_(2))’s decomposition and reactive oxygen species(ROS)’s formation on the catalyst’s surface is always a critical issue for the environmental applicati...To better understand the mechanisms of hydrogen peroxide(H_(2)O_(2))’s decomposition and reactive oxygen species(ROS)’s formation on the catalyst’s surface is always a critical issue for the environmental application of Fenton/Fenton-like reaction.We here report a new approach to activate H_(2)O_(2) in a co-catalytic Fenton system with oxygen incorporated MoS2,namely MoS_(2−x) O_(x) nanosheets.The MoS_(2−x) O_(x) nanosheets assisted co-catalytic Fenton system exhibited superior degradation activity of emerging antibiotic contaminants(e.g.,sulfamethoxazole).Combining density functional theory(DFT)calculation and experimental investigation,we demonstrated that oxygen incorporation could improve the intrinsic conductivity of MoS_(2−x) O_(x) nanosheets and accelerate surface/interfacial charge transfer,which further leads to the efficacious activation of H_(2)O_(2).Moreover,by tuning the oxygen proportion in MoS_(2−x) O_(x) nanosheets,we are able to modulate the generation of ROS and further direct the oriented-conversion of H_(2)O_(2) to surface-bounded superoxide radical(·O_(2−surface)).It sheds light on the generation and transformation of ROS in the engineered system(e.g.,Fenton,Fenton-like reaction)for efficient degradation of persistent pollutants.展开更多
Objectives:In this study,we explored how adiponectin mediated urotensinⅡ(UⅡ)-induced tumor necrosis factor-α(TNF-α)andα-smooth muscle actin(α-SMA)expression and ensuing intracellular signaling pathways in advent...Objectives:In this study,we explored how adiponectin mediated urotensinⅡ(UⅡ)-induced tumor necrosis factor-α(TNF-α)andα-smooth muscle actin(α-SMA)expression and ensuing intracellular signaling pathways in adventitial fibroblasts(AFs).Methods:Growth-arrested AFs and rat tunica adventitia of vessels were incubated with UⅡand inhibitors of signal transduction pathways for 1-24 h.The cells were then harvested for TNF-αreceptor(TNF-α-R)messenger RNA(mRNA)and TNF-αprotein expression determination by reverse transcription-polymerase chain reaction(RT-PCR)and enzyme-linked immunosorbent assay(ELISA),respectively.Adiponectin and adiponectin receptor(adipoR)expression was measured by RT-PCR,quantitative real-time PCR(qPCR),immunohistochemical analysis,and cell counting kit-8(CCK-8)cell proliferation experiments.We then quantified TNF-αandα-SMA mRNA and protein expression levels by qPCR and immunofluorescence(IF)staining.RNA interference(RNAi)was used to explore the function of the adipoR genes.To investigate the signaling pathway,we applied western blotting(WB)to examine phosphorylation of adenosine 5’-monophosphate(AMP)-activated protein kinase(AMPK).In vivo,an adiponectin(APN)-knockout(APN-KO)mouse model mimicking adventitial inflammation was generated to measure TNF-αandα-SMA expression by application of qPCR and IF,with the goal of gaining a comprehensive atlas of adiponectin in vascular remodeling.Results:In both cells and tissues,UⅡpromoted TNF-αprotein and TNF-α-R secretion in a dose-and time-dependent manner via Rho/protein kinase C(PKC)pathway.We detected marked expression of adipoR1,T-cadherin,and calreticulin as well as a moderate presence of adipoR2 in AFs,while no adiponectin was observed.Globular adiponectin(gAd)fostered the growth of AFs,and acted in concert with UⅡto induceα-SMA and TNF-αthrough the adipoR1/T-cadherin/calreticulin/AMPK pathway.In AFs,gAd and UⅡsynergistically induced AMPK phosphorylation.In the adventitial inflammation model,APN deficiency up-regulated the expression ofα-SMA,UⅡreceptor(UT),and UⅡwhile inhibiting TNF-αexpression.Conclusions:From the results of our study,we can speculate that UⅡinduces TNF-αprotein and TNF-α-R secretion in AFs and rat tunica adventitia of vessels via the Rho and PKC signal transduction pathways.Thus,it is plausible that adiponectin is a major player in adventitial progression and could serve as a novel therapeutic target for cardiovascular disease administration.展开更多
基金This work was supported by the National Natural Scientific Foundation of China(51075037)the Program for New Century Excellent Talents(NCET)at the University of China and Chinese 863 Project(2008AA04Z406).
文摘Recent developments in spectral white-light interferometry(WLI)are reviewed.Firstly,the techniques for obtaining optical spectrum are introduced.Secondly,some novel measurement techniques are reviewed,including the improved peak-to-peak WLI,improved wavelength-tracking WLI,Fourier transform WLI,and 3×3 coupler based WLI.Furthermore,a hybrid measurement for the intensity-type sensors,interferometric sensors,and fiber Bragg grating sensors is achieved.It is shown that these developments have assisted in the progress of WLI.
基金the National Natural Science Foundation of China(Nos.42077293 and 22006088)Natural Science Foundation of Guangdong Province(Nos.2019A1515011692 and 2019QN01L797)+2 种基金Shenzhen Municipal Science and Technology Innovation Committee(Nos.JCYJ20190809181413713 and WDZC20200817103015002)Y.X.H.also thanks the financial support from Overseas Cooperation Research Fund of Tsinghua Shenzhen International Graduate School(Nos.HW2020002 and QD2021010N)This work was also supported by the China Postdoctoral Science Foundation(No.2019M66067).
文摘To better understand the mechanisms of hydrogen peroxide(H_(2)O_(2))’s decomposition and reactive oxygen species(ROS)’s formation on the catalyst’s surface is always a critical issue for the environmental application of Fenton/Fenton-like reaction.We here report a new approach to activate H_(2)O_(2) in a co-catalytic Fenton system with oxygen incorporated MoS2,namely MoS_(2−x) O_(x) nanosheets.The MoS_(2−x) O_(x) nanosheets assisted co-catalytic Fenton system exhibited superior degradation activity of emerging antibiotic contaminants(e.g.,sulfamethoxazole).Combining density functional theory(DFT)calculation and experimental investigation,we demonstrated that oxygen incorporation could improve the intrinsic conductivity of MoS_(2−x) O_(x) nanosheets and accelerate surface/interfacial charge transfer,which further leads to the efficacious activation of H_(2)O_(2).Moreover,by tuning the oxygen proportion in MoS_(2−x) O_(x) nanosheets,we are able to modulate the generation of ROS and further direct the oriented-conversion of H_(2)O_(2) to surface-bounded superoxide radical(·O_(2−surface)).It sheds light on the generation and transformation of ROS in the engineered system(e.g.,Fenton,Fenton-like reaction)for efficient degradation of persistent pollutants.
基金supported by the the National Natural Science Foundation of China(No.82003372)the Natural Science Foundation of Hubei Province(Nos.2018CFB747 and 2018CFB537)the Educational Commission of Hubei Province(Nos.B2017112 and B20181130),China.
文摘Objectives:In this study,we explored how adiponectin mediated urotensinⅡ(UⅡ)-induced tumor necrosis factor-α(TNF-α)andα-smooth muscle actin(α-SMA)expression and ensuing intracellular signaling pathways in adventitial fibroblasts(AFs).Methods:Growth-arrested AFs and rat tunica adventitia of vessels were incubated with UⅡand inhibitors of signal transduction pathways for 1-24 h.The cells were then harvested for TNF-αreceptor(TNF-α-R)messenger RNA(mRNA)and TNF-αprotein expression determination by reverse transcription-polymerase chain reaction(RT-PCR)and enzyme-linked immunosorbent assay(ELISA),respectively.Adiponectin and adiponectin receptor(adipoR)expression was measured by RT-PCR,quantitative real-time PCR(qPCR),immunohistochemical analysis,and cell counting kit-8(CCK-8)cell proliferation experiments.We then quantified TNF-αandα-SMA mRNA and protein expression levels by qPCR and immunofluorescence(IF)staining.RNA interference(RNAi)was used to explore the function of the adipoR genes.To investigate the signaling pathway,we applied western blotting(WB)to examine phosphorylation of adenosine 5’-monophosphate(AMP)-activated protein kinase(AMPK).In vivo,an adiponectin(APN)-knockout(APN-KO)mouse model mimicking adventitial inflammation was generated to measure TNF-αandα-SMA expression by application of qPCR and IF,with the goal of gaining a comprehensive atlas of adiponectin in vascular remodeling.Results:In both cells and tissues,UⅡpromoted TNF-αprotein and TNF-α-R secretion in a dose-and time-dependent manner via Rho/protein kinase C(PKC)pathway.We detected marked expression of adipoR1,T-cadherin,and calreticulin as well as a moderate presence of adipoR2 in AFs,while no adiponectin was observed.Globular adiponectin(gAd)fostered the growth of AFs,and acted in concert with UⅡto induceα-SMA and TNF-αthrough the adipoR1/T-cadherin/calreticulin/AMPK pathway.In AFs,gAd and UⅡsynergistically induced AMPK phosphorylation.In the adventitial inflammation model,APN deficiency up-regulated the expression ofα-SMA,UⅡreceptor(UT),and UⅡwhile inhibiting TNF-αexpression.Conclusions:From the results of our study,we can speculate that UⅡinduces TNF-αprotein and TNF-α-R secretion in AFs and rat tunica adventitia of vessels via the Rho and PKC signal transduction pathways.Thus,it is plausible that adiponectin is a major player in adventitial progression and could serve as a novel therapeutic target for cardiovascular disease administration.
