The 200 Gbit/s passive optical network(PON)is most likely to be the next-generation scheme following 50G PON.The costeffective direct detection(DD)system is the economical choice.However,larger-capacity DD systems wil...The 200 Gbit/s passive optical network(PON)is most likely to be the next-generation scheme following 50G PON.The costeffective direct detection(DD)system is the economical choice.However,larger-capacity DD systems will face much more serious power fading caused by chromatic dispersion(CD)combined with square-law DD and thereby significantly increases the complexity of equalization algorithms.In this paper,a 200 Gbit/s Nyquist 4-level pulse amplitude modulation(PAM4)single side-band(SSB)modulation-DD downlink scheme is designed,and a low complexity quadratic-nonlinear equalizer is proposed for this system.The computational complexity of the quadratic nonlinear equalizer is about 28%of that of the conventional Volterra nonlinear equalizer,while still exhibiting excellent nonlinear equalization ability.Simulation results for the 200 Gbit/s system with 20 km fiber transmission show that it can achieve a power budget of 29 dB,while a 30.4 dB power budget is obtained in the 50 Gbit/s experimental transmission.展开更多
Colitis-associated colorectal cancer(CAC)is a major contributor to cancer-related mortality worldwide.Titanium dioxide(TiO_(2),E171),a widely used food additive,has been insufficiently studied regarding its effects on...Colitis-associated colorectal cancer(CAC)is a major contributor to cancer-related mortality worldwide.Titanium dioxide(TiO_(2),E171),a widely used food additive,has been insufficiently studied regarding its effects on macrophages within colon tumors during CAC development.In this study,CAC mouse models were used to investigate the biological impact of dietary E171 on macrophages in vivo,while lipopolysaccharide(LPS)-stimulated RAW264.7 macrophage cell lines were employed to elucidate the underlying mechanisms in vitro.We found that dietary E171 intake accelerated CAC development,exacerbated inflammatory responses and oxidative stress,and upregulated CAC-associated genes,including S100a8,S100a9,Lcn2,S100a11,Cxcl2,and interleukin-1α(Il-1α).E171 also increased the expression of S100A8,S100A9,NOD-like receptor family pyrin domain-containing 3(NLRP3),and gasdermin-D Nterminal(GSDMD-N)in macrophages within colon tumors.In inflammatory macrophages,E171 exposure enhanced cell viability,increased reactive oxygen species(ROS)levels,and elevated the expression and secretion of S100A8 and S100A9,consistent with in vivo histological observations.Furthermore,E171-induced secretion of S100A8 and S100A9 in macrophages was suppressed by specific inhibitors,including N-acetylcysteine(NAC,ROS inhibitor),MCC950(NLRP3 inhibitor),Z-YVAD-FMK(caspase 1 inhibitor),disulfiram(GSDMD inhibitor),and transfection of NLRP3 small interfering ribonucleic acid(siRNA).These results indicate that dietary E171 promotes CAC development by activating macrophages,with S100A8 and S100A9 serving as key mediators,and the NLRP3/caspase 1/GSDMD pathway acting as a critical mechanism.展开更多
基金ZTE Industry-University-Institute Cooperation Funds under Grant No.HC-CN-20230105001National Natural Science Foundation of China under Grant No.62001045。
文摘The 200 Gbit/s passive optical network(PON)is most likely to be the next-generation scheme following 50G PON.The costeffective direct detection(DD)system is the economical choice.However,larger-capacity DD systems will face much more serious power fading caused by chromatic dispersion(CD)combined with square-law DD and thereby significantly increases the complexity of equalization algorithms.In this paper,a 200 Gbit/s Nyquist 4-level pulse amplitude modulation(PAM4)single side-band(SSB)modulation-DD downlink scheme is designed,and a low complexity quadratic-nonlinear equalizer is proposed for this system.The computational complexity of the quadratic nonlinear equalizer is about 28%of that of the conventional Volterra nonlinear equalizer,while still exhibiting excellent nonlinear equalization ability.Simulation results for the 200 Gbit/s system with 20 km fiber transmission show that it can achieve a power budget of 29 dB,while a 30.4 dB power budget is obtained in the 50 Gbit/s experimental transmission.
基金supported by the National Natural Science Foundation of China(Nos.81974441 and 82203619)the Science and Technology Planning Project of Shenzhen Municipality(Nos.JCYJ20190814105619048 and JCYJ20220530154202005)。
文摘Colitis-associated colorectal cancer(CAC)is a major contributor to cancer-related mortality worldwide.Titanium dioxide(TiO_(2),E171),a widely used food additive,has been insufficiently studied regarding its effects on macrophages within colon tumors during CAC development.In this study,CAC mouse models were used to investigate the biological impact of dietary E171 on macrophages in vivo,while lipopolysaccharide(LPS)-stimulated RAW264.7 macrophage cell lines were employed to elucidate the underlying mechanisms in vitro.We found that dietary E171 intake accelerated CAC development,exacerbated inflammatory responses and oxidative stress,and upregulated CAC-associated genes,including S100a8,S100a9,Lcn2,S100a11,Cxcl2,and interleukin-1α(Il-1α).E171 also increased the expression of S100A8,S100A9,NOD-like receptor family pyrin domain-containing 3(NLRP3),and gasdermin-D Nterminal(GSDMD-N)in macrophages within colon tumors.In inflammatory macrophages,E171 exposure enhanced cell viability,increased reactive oxygen species(ROS)levels,and elevated the expression and secretion of S100A8 and S100A9,consistent with in vivo histological observations.Furthermore,E171-induced secretion of S100A8 and S100A9 in macrophages was suppressed by specific inhibitors,including N-acetylcysteine(NAC,ROS inhibitor),MCC950(NLRP3 inhibitor),Z-YVAD-FMK(caspase 1 inhibitor),disulfiram(GSDMD inhibitor),and transfection of NLRP3 small interfering ribonucleic acid(siRNA).These results indicate that dietary E171 promotes CAC development by activating macrophages,with S100A8 and S100A9 serving as key mediators,and the NLRP3/caspase 1/GSDMD pathway acting as a critical mechanism.
