Low-light image enhancement aims to improve the visibility of severely degraded images captured under insufficient illumination,alleviating the adverse effects of illumination degradation on image quality.Traditional ...Low-light image enhancement aims to improve the visibility of severely degraded images captured under insufficient illumination,alleviating the adverse effects of illumination degradation on image quality.Traditional Retinex-based approaches,inspired by human visual perception of brightness and color,decompose an image into illumination and reflectance components to restore fine details.However,their limited capacity for handling noise and complex lighting conditions often leads to distortions and artifacts in the enhanced results,particularly under extreme low-light scenarios.Although deep learning methods built upon Retinex theory have recently advanced the field,most still suffer frominsufficient interpretability and sub-optimal enhancement performance.This paper presents RetinexWT,a novel framework that tightly integrates classical Retinex theory with modern deep learning.Following Retinex principles,RetinexWT employs wavelet transforms to estimate illumination maps for brightness adjustment.A detail-recovery module that synergistically combines Vision Transformer(ViT)and wavelet transforms is then introduced to guide the restoration of lost details,thereby improving overall image quality.Within the framework,wavelet decomposition splits input features into high-frequency and low-frequency components,enabling scale-specific processing of global illumination/color cues and fine textures.Furthermore,a gating mechanism selectively fuses down-sampled and up-sampled features,while an attention-based fusion strategy enhances model interpretability.Extensive experiments on the LOL dataset demonstrate that RetinexWT surpasses existing Retinex-oriented deeplearning methods,achieving an average Peak Signal-to-Noise Ratio(PSNR)improvement of 0.22 dB over the current StateOfTheArt(SOTA),thereby confirming its superiority in low-light image enhancement.Code is available at https://github.com/CHEN-hJ516/RetinexWT(accessed on 14 October 2025).展开更多
Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postn...Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postnatal neurogenesis remains unclear.In this study,to define the precise role of transforming growth factor-βsignaling in postnatal neurogenesis at distinct stages of the neurogenic cascade both in vitro and in vivo,we developed two novel inducible and cell type-specific mouse models to specifically silence transforming growth factor-βsignaling in neural stem cells in(mGFAPcre-ALK5fl/fl-Ai9)or immature neuroblasts in(DCXcreERT2-ALK5fl/fl-Ai9).Our data showed that exogenous transforming growth factor-βtreatment led to inhibition of the proliferation of primary neural stem cells while stimulating their migration.These effects were abolished in activin-like kinase 5(ALK5)knockout primary neural stem cells.Consistent with this,inhibition of transforming growth factor-βsignaling with SB-431542 in wild-type neural stem cells stimulated proliferation while inhibited the migration of neural stem cells.Interestingly,deletion of transforming growth factor-βreceptor in neural stem cells in vivo inhibited the migration of postnatal born neurons in mGFAPcre-ALK5fl/fl-Ai9 mice,while abolishment of transforming growth factor-βsignaling in immature neuroblasts in DCXcreERT2-ALK5fl/fl-Ai9 mice did not affect the migration of these cells in the hippocampus.In summary,our data supports a dual role of transforming growth factor-βsignaling in the proliferation and migration of neural stem cells in vitro.Moreover,our data provides novel insights on cell type-specific-dependent requirements of transforming growth factor-βsignaling on neural stem cell proliferation and migration in vivo.展开更多
基金supported in part by the National Natural Science Foundation of China[Grant number 62471075]the Major Science and Technology Project Grant of the Chongqing Municipal Education Commission[Grant number KJZD-M202301901].
文摘Low-light image enhancement aims to improve the visibility of severely degraded images captured under insufficient illumination,alleviating the adverse effects of illumination degradation on image quality.Traditional Retinex-based approaches,inspired by human visual perception of brightness and color,decompose an image into illumination and reflectance components to restore fine details.However,their limited capacity for handling noise and complex lighting conditions often leads to distortions and artifacts in the enhanced results,particularly under extreme low-light scenarios.Although deep learning methods built upon Retinex theory have recently advanced the field,most still suffer frominsufficient interpretability and sub-optimal enhancement performance.This paper presents RetinexWT,a novel framework that tightly integrates classical Retinex theory with modern deep learning.Following Retinex principles,RetinexWT employs wavelet transforms to estimate illumination maps for brightness adjustment.A detail-recovery module that synergistically combines Vision Transformer(ViT)and wavelet transforms is then introduced to guide the restoration of lost details,thereby improving overall image quality.Within the framework,wavelet decomposition splits input features into high-frequency and low-frequency components,enabling scale-specific processing of global illumination/color cues and fine textures.Furthermore,a gating mechanism selectively fuses down-sampled and up-sampled features,while an attention-based fusion strategy enhances model interpretability.Extensive experiments on the LOL dataset demonstrate that RetinexWT surpasses existing Retinex-oriented deeplearning methods,achieving an average Peak Signal-to-Noise Ratio(PSNR)improvement of 0.22 dB over the current StateOfTheArt(SOTA),thereby confirming its superiority in low-light image enhancement.Code is available at https://github.com/CHEN-hJ516/RetinexWT(accessed on 14 October 2025).
基金supported by NIH grants,Nos.R01NS125074,R01AG083164,R01NS107365,and R21NS127177(to YL),1F31NS129204-01A1(to KW)and Albert Ryan Fellowship(to KW).
文摘Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postnatal neurogenesis remains unclear.In this study,to define the precise role of transforming growth factor-βsignaling in postnatal neurogenesis at distinct stages of the neurogenic cascade both in vitro and in vivo,we developed two novel inducible and cell type-specific mouse models to specifically silence transforming growth factor-βsignaling in neural stem cells in(mGFAPcre-ALK5fl/fl-Ai9)or immature neuroblasts in(DCXcreERT2-ALK5fl/fl-Ai9).Our data showed that exogenous transforming growth factor-βtreatment led to inhibition of the proliferation of primary neural stem cells while stimulating their migration.These effects were abolished in activin-like kinase 5(ALK5)knockout primary neural stem cells.Consistent with this,inhibition of transforming growth factor-βsignaling with SB-431542 in wild-type neural stem cells stimulated proliferation while inhibited the migration of neural stem cells.Interestingly,deletion of transforming growth factor-βreceptor in neural stem cells in vivo inhibited the migration of postnatal born neurons in mGFAPcre-ALK5fl/fl-Ai9 mice,while abolishment of transforming growth factor-βsignaling in immature neuroblasts in DCXcreERT2-ALK5fl/fl-Ai9 mice did not affect the migration of these cells in the hippocampus.In summary,our data supports a dual role of transforming growth factor-βsignaling in the proliferation and migration of neural stem cells in vitro.Moreover,our data provides novel insights on cell type-specific-dependent requirements of transforming growth factor-βsignaling on neural stem cell proliferation and migration in vivo.
