Since the discovery of generalized Snell’s law in 2011[1],metasurfaces have opened up the mainstream of arbitrary wavefront manipulation in electromagnetism.Using a gradient-index metasurface,the parallel wavenumber ...Since the discovery of generalized Snell’s law in 2011[1],metasurfaces have opened up the mainstream of arbitrary wavefront manipulation in electromagnetism.Using a gradient-index metasurface,the parallel wavenumber kx of reflected wave can be not equal to the incident one(kx=ξ+k0sinθi,where k0 andθi are the incident wavenumber and angle,andξis the phase gradient of metasurface in its supercell)[1].Whenξ>k0,the reflected wave becomes a surface wave bounded on the metasurface(where|kx|>k0,kz is imaginary,and z is normal to the metasurface)[2].However,as research of metasurfaces continually evolves,some articles have pointed out that such graded metasurfaces suffer from a series of problems[3-6].In particular,multiple metallic resonators are adopted in a subwavelength supercell,resulting in impedance mismatch,moderate conversion efficiency,wave absorption,and fabrication complexity.Hence,although the approach of graded metasurfaces has been demonstrated in the microwave regime,it is hard to extend to infrared and optical ranges with shorter wavelengths.To solve this problem,Ra’di et al.[7]devised metagratings with periodic arrays of bianisotropic scatterers and showed that they enable wave front engineering with unitary efficiency and significantly lower fabrication demands.展开更多
The Wnt/β-catenin signaling pathway appears to be particularly important for bone homeostasis,whereas nuclear accumulation ofβ-catenin requires the activation of Rac1,a member of the Rho small GTPase family.The aim ...The Wnt/β-catenin signaling pathway appears to be particularly important for bone homeostasis,whereas nuclear accumulation ofβ-catenin requires the activation of Rac1,a member of the Rho small GTPase family.The aim of the present study was to investigate the role of RhoA/Rho kinase(Rock)-mediated Wnt/β-catenin signaling in the regulation of aging-associated bone loss.We find that Lrp5/6-dependent and Lrp5/6-independent RhoA/Rock activation by Wnt3a activates Jak1/2 to directly phosphorylate Gsk3βat Tyr216,resulting in Gsk3βactivation and subsequentβ-catenin destabilization.In line with these molecular events,RhoA loss-or gain-of-function in mouse embryonic limb bud ectoderms interacts genetically with Dkk1 gain-of-function to rescue the severe limb truncation phenotypes or to phenocopy the deletion ofβ-catenin,respectively.Likewise,RhoA loss-of-function in pre-osteoblasts robustly increases bone formation while gain-of-function decreases it.Importantly,high RhoA/Rock activity closely correlates with Jak and Gsk3βactivities but inversely correlates withβ-catenin signaling activity in bone marrow mesenchymal stromal cells from elderly male humans and mice,whereas systemic inhibition of Rock therefore activates theβ-catenin signaling to antagonize aging-associated bone loss.Taken together,these results identify RhoA/Rock-dependent Gsk3βactivation and subsequentβ-catenin destabilization as a hitherto uncharacterized mechanism controlling limb outgrowth and bone homeostasis.展开更多
Following publication of the original article(Shi et al.2021),the authors have identified errors in Figs.1d and 3i which occurred during the figure assembly process.Theβ-actin bands in Fig.1d were mistakenly compiled...Following publication of the original article(Shi et al.2021),the authors have identified errors in Figs.1d and 3i which occurred during the figure assembly process.Theβ-actin bands in Fig.1d were mistakenly compiled from similar experiments in a previous publication by the same group(Gong et al.2014),conducted within the same time frame as the experiments in Fig.1d.To address this,the authors made corrections in Fig.1d in this revision.Furthermore,theβ-catenin band in Fig.3a was inadvertently reused in Fig.3i,and the new Fig.3 containing the correctβ-catenin in Fig.3i has been provided below.It’s important to note that despite these corrections,all the results and conclusions in this article remain consistent and unaffected.The authors deeply regret any inconvenience caused by these errors and sincerely apologize for them.展开更多
文摘Since the discovery of generalized Snell’s law in 2011[1],metasurfaces have opened up the mainstream of arbitrary wavefront manipulation in electromagnetism.Using a gradient-index metasurface,the parallel wavenumber kx of reflected wave can be not equal to the incident one(kx=ξ+k0sinθi,where k0 andθi are the incident wavenumber and angle,andξis the phase gradient of metasurface in its supercell)[1].Whenξ>k0,the reflected wave becomes a surface wave bounded on the metasurface(where|kx|>k0,kz is imaginary,and z is normal to the metasurface)[2].However,as research of metasurfaces continually evolves,some articles have pointed out that such graded metasurfaces suffer from a series of problems[3-6].In particular,multiple metallic resonators are adopted in a subwavelength supercell,resulting in impedance mismatch,moderate conversion efficiency,wave absorption,and fabrication complexity.Hence,although the approach of graded metasurfaces has been demonstrated in the microwave regime,it is hard to extend to infrared and optical ranges with shorter wavelengths.To solve this problem,Ra’di et al.[7]devised metagratings with periodic arrays of bianisotropic scatterers and showed that they enable wave front engineering with unitary efficiency and significantly lower fabrication demands.
基金This work was supported by 973 Program(No.2018YFC1004404)National Natural Science Foundation of China(Nos.31071292,31271561,31571493,81741043,31871395,and 31801207).
文摘The Wnt/β-catenin signaling pathway appears to be particularly important for bone homeostasis,whereas nuclear accumulation ofβ-catenin requires the activation of Rac1,a member of the Rho small GTPase family.The aim of the present study was to investigate the role of RhoA/Rho kinase(Rock)-mediated Wnt/β-catenin signaling in the regulation of aging-associated bone loss.We find that Lrp5/6-dependent and Lrp5/6-independent RhoA/Rock activation by Wnt3a activates Jak1/2 to directly phosphorylate Gsk3βat Tyr216,resulting in Gsk3βactivation and subsequentβ-catenin destabilization.In line with these molecular events,RhoA loss-or gain-of-function in mouse embryonic limb bud ectoderms interacts genetically with Dkk1 gain-of-function to rescue the severe limb truncation phenotypes or to phenocopy the deletion ofβ-catenin,respectively.Likewise,RhoA loss-of-function in pre-osteoblasts robustly increases bone formation while gain-of-function decreases it.Importantly,high RhoA/Rock activity closely correlates with Jak and Gsk3βactivities but inversely correlates withβ-catenin signaling activity in bone marrow mesenchymal stromal cells from elderly male humans and mice,whereas systemic inhibition of Rock therefore activates theβ-catenin signaling to antagonize aging-associated bone loss.Taken together,these results identify RhoA/Rock-dependent Gsk3βactivation and subsequentβ-catenin destabilization as a hitherto uncharacterized mechanism controlling limb outgrowth and bone homeostasis.
文摘Following publication of the original article(Shi et al.2021),the authors have identified errors in Figs.1d and 3i which occurred during the figure assembly process.Theβ-actin bands in Fig.1d were mistakenly compiled from similar experiments in a previous publication by the same group(Gong et al.2014),conducted within the same time frame as the experiments in Fig.1d.To address this,the authors made corrections in Fig.1d in this revision.Furthermore,theβ-catenin band in Fig.3a was inadvertently reused in Fig.3i,and the new Fig.3 containing the correctβ-catenin in Fig.3i has been provided below.It’s important to note that despite these corrections,all the results and conclusions in this article remain consistent and unaffected.The authors deeply regret any inconvenience caused by these errors and sincerely apologize for them.
