Robust polarimetric dehazing algorithm based on low-rank approximation and multiple virtual-exposure fusion

Polarimetric dehazing is an effective way to enhance the quality of images captured in foggy weather.However,images of essential polarization parameters are vulnerable to noise,and the brightness of dehazed images is usually unstable due to different environmental illuminations.These two weaknesses reveal that current polarimetric dehazing algorithms are not robust enough to deal with different scenarios.This paper proposes a novel,to our knowledge,and robust polarimetric dehazing algorithm to enhance the quality of hazy images,where a low-rank approximation method is used to obtain low-noise polarization parameter images.Besides,in order to improve the brightness stability of the dehazed image and thus keep the image have more details within the standard dynamic range,this study proposes a multiple virtual-exposure fusion(MVEF)scheme to process the dehazed image(usually having a high dynamic range)obtained through polarimetric dehazing.Comparative experiments show that the proposed dehazing algorithm is robust and effective,which can significantly improve overall quality of hazy images captured under different environments.

Ligation of CD180 inhibits IFN-α signaling in a Lyn-PI3K-BTK-dependent manner in B cells

A hallmark of systemic lupus erythematosus （SLE） is the consistent production of various auto-antibodies by auto-reactive B cells. Interferon-α（IFN-α） signaling is highly activated in SLE B cells and plays a vital role in the antibody response by B cells. Previous studies have shown that CD180-negative B cells, which are dramatically increased in SLE patients, are responsible for the production of auto-antibodies. However, the association between CD180 and IFN-αsignaling remains unknown. In the present study, we explored the effect of CD180 on regulating the activation of IFN-α signaling in B cells. We found that the number of CD180-negative B cells was increased in MRIJMp-Fas（Ipr/Ipr） lupus-prone mice compared with wild-type mice. Phenotypic analysis showed that CD180-negative B cells comprised CD138＋ plasmablast/plasma cells and GL-7＋ germinal center （GC） B cells. Notably, ligation of CD180 significantly inhibited the I FN-α-induced phosphorylation of signal transducer and activator of transcription 2 （STAT-2） and expression of IFN-stimulated genes （ISGs） in a Lyn-PI3K-BTK-dependent manner in vitro. Moreover, ligation of CD180 could also inhibit IFN-α-induced ISG expression in B cells in vivo. Furthermore, the Toll-like receptor 7 and Toll-like receptor 9 signaling pathways could significantly downregulate CD180 expression and modulate the inhibitory effect of CD180 signaling on the activation of I FN-a signaling. Collectively, our results highlight the close association between the increased proportion of CD180-negative B cells and the activation of IFN-α signaling in SLE. Our data provide molecular insight into the mechanism of IFN-α signaling activation in SLE B cells and a potential therapeutic approach for SLE treatment.