We present a theoretical investigation of weak-value amplification(WVA)under decoherence,quantifying its metrological capabilities through the quantum Fisher information(QFI).By modeling decoherence via Kraus operator...We present a theoretical investigation of weak-value amplification(WVA)under decoherence,quantifying its metrological capabilities through the quantum Fisher information(QFI).By modeling decoherence via Kraus operators acting before and after the weak measurement interaction,we derive exact expressions for the QFI governing parameter estimation of a weak coupling strength.These analytical results reveal the fundamental limitation imposed by decoherence on the QFI achievable via WVA.From these results,the optimal post-selection state that maximizes the QFI can be derived for different noise environments.Through paradigmatic examples,including amplitude damping and depolarizing channels,we demonstrate a key distinction:the optimal post-selection evolves with the noise strength in the amplitude damping channel,but is fixed in the depolarizing channel.This work provides both theoretical insights and practical guidance for optimizing metrological schemes based on WVA in realistic decoherent environments.展开更多
AIM:To explore the changes in early retinal development after the occurrence of ischemia.METHODS:Human retinal organoids(hROs)of day 18 or day 30 were treated with oxygen-glucose deprivation and reperfusion(OGD/R)to s...AIM:To explore the changes in early retinal development after the occurrence of ischemia.METHODS:Human retinal organoids(hROs)of day 18 or day 30 were treated with oxygen-glucose deprivation and reperfusion(OGD/R)to simulate the retinal ischemia.All hROs were maintained normally until day 60 to evaluate changes in ischemic injuries during retinal development.Paraffin section staining was used for detecting changes in organoid structure and cell number.Real-time quantitative polymerase chain reaction(RT-qPCR)and Western blot(WB)analyses were used to observe the change in the expression of retinal cell markers.RESULTS:In hROs,OGD/R induced the decrease of proliferating cells,inhibited the expression of proliferated marker Ki67 and promoted early apoptosis of retinal cells(P<0.05).Under OGD/R condition,the progenitor cell layer and ganglion cell layer of hROs lost normal structure,and the number of neural stem cells(SOX2^(+)),retinal progenitor cells(CHX10^(+))and retinal ganglion cells(TUJ1^(+)/BRN3^(+)/ATOH7^(+))decreased(P<0.05).The expression of corresponding retinal cell markers also decreased(P<0.05).Organoids treated with OGD/R on day 30 had similar injuries in retinal structure and retinal cell markers to those on day 18.Long-term observations revealed that day 18-treated organoids remained disorganized progenitor and ganglion cell layers by day 60,with no recovery in proliferating cell nuclear antigen(PCNA)protein expression.RT-qPCR showed persistently low Ki67 transcription levels(P<0.001),while other retinal cell markers recovered or exceeded normal levels,indicating a limited self-repair happened in the development of hROs.In contrast,day 30-treated organoids exhibited normal structure and marker expression by day 60,with transcription levels of retinal cell markers returning to normal(P>0.05),demonstrating complete recovery from OGD/R damage.CONCLUSION:Retinal ischemia damage the retinal development in the short-term.After the restoration of retinal blood supply,the retinal ischemic damage can be recovered during subsequent development.However,retinal ischemic injuries at different developmental stages exhibit varying degrees of reversibility.The earlier ischemic injury occurs,the more difficult it is to repair retinal cell and structure damage.展开更多
基金Project supported by the National Natural Science Foundation of China(Grant Nos.12175052 and 12405010)Hangzhou Joint Fund of the Zhejiang Provincial Natural Science Foundation of China(Grant No.LHZSD24A050001)+4 种基金the Hangzhou Leading Youth Innovation and Entrepreneurship Team Project(Grant No.TD2024005)the HZNU scientific Research and Innovation Team Project(Grant No.TD2025003)the Guizhou Province Higher Education Teaching Content and Curriculum System Reform Project(Grant No.2023233)the Guizhou Education Department Young Talent in Science and Technology Program(Grant Nos.QianJiaoJi[2024]174 and QianJiaoJi[2024]178)Guizhou Provincial Theoretical Innovation Project(Grant No.GZLCLH-2025-ZX)。
文摘We present a theoretical investigation of weak-value amplification(WVA)under decoherence,quantifying its metrological capabilities through the quantum Fisher information(QFI).By modeling decoherence via Kraus operators acting before and after the weak measurement interaction,we derive exact expressions for the QFI governing parameter estimation of a weak coupling strength.These analytical results reveal the fundamental limitation imposed by decoherence on the QFI achievable via WVA.From these results,the optimal post-selection state that maximizes the QFI can be derived for different noise environments.Through paradigmatic examples,including amplitude damping and depolarizing channels,we demonstrate a key distinction:the optimal post-selection evolves with the noise strength in the amplitude damping channel,but is fixed in the depolarizing channel.This work provides both theoretical insights and practical guidance for optimizing metrological schemes based on WVA in realistic decoherent environments.
基金Supported by the National Natural Science Foundation of China(No.82070937).
文摘AIM:To explore the changes in early retinal development after the occurrence of ischemia.METHODS:Human retinal organoids(hROs)of day 18 or day 30 were treated with oxygen-glucose deprivation and reperfusion(OGD/R)to simulate the retinal ischemia.All hROs were maintained normally until day 60 to evaluate changes in ischemic injuries during retinal development.Paraffin section staining was used for detecting changes in organoid structure and cell number.Real-time quantitative polymerase chain reaction(RT-qPCR)and Western blot(WB)analyses were used to observe the change in the expression of retinal cell markers.RESULTS:In hROs,OGD/R induced the decrease of proliferating cells,inhibited the expression of proliferated marker Ki67 and promoted early apoptosis of retinal cells(P<0.05).Under OGD/R condition,the progenitor cell layer and ganglion cell layer of hROs lost normal structure,and the number of neural stem cells(SOX2^(+)),retinal progenitor cells(CHX10^(+))and retinal ganglion cells(TUJ1^(+)/BRN3^(+)/ATOH7^(+))decreased(P<0.05).The expression of corresponding retinal cell markers also decreased(P<0.05).Organoids treated with OGD/R on day 30 had similar injuries in retinal structure and retinal cell markers to those on day 18.Long-term observations revealed that day 18-treated organoids remained disorganized progenitor and ganglion cell layers by day 60,with no recovery in proliferating cell nuclear antigen(PCNA)protein expression.RT-qPCR showed persistently low Ki67 transcription levels(P<0.001),while other retinal cell markers recovered or exceeded normal levels,indicating a limited self-repair happened in the development of hROs.In contrast,day 30-treated organoids exhibited normal structure and marker expression by day 60,with transcription levels of retinal cell markers returning to normal(P>0.05),demonstrating complete recovery from OGD/R damage.CONCLUSION:Retinal ischemia damage the retinal development in the short-term.After the restoration of retinal blood supply,the retinal ischemic damage can be recovered during subsequent development.However,retinal ischemic injuries at different developmental stages exhibit varying degrees of reversibility.The earlier ischemic injury occurs,the more difficult it is to repair retinal cell and structure damage.
