Smoke veil prior regularized surgical field desmoking without paired in-vivo data.

Though deep learning-based surgical smoke removal methods have shown significant improvements in effectiveness and efficiency, the lack of paired smoke and smoke-free images in real surgical scenarios limits the performance of these methods. Therefore, methods that can achieve good generalization performance without paired in-vivo data are in high demand. In this work, we propose a smoke veil prior regularized two-stage smoke removal framework based on the physical model of smoke image formation. More precisely, in the first stage, we leverage a reconstruction loss, a consistency loss and a smoke veil prior-based regularization term to perform fully supervised training on a synthetic paired image dataset. Then a self-supervised training stage is deployed on the real smoke images, where only the consistency loss and the smoke veil prior-based loss are minimized. Experiments show that the proposed method outperforms the state-of-the-art ones on synthetic dataset. The average PSNR, SSIM and RMSE values are 21.99±2.34, 0.9001±0.0252 and 0.2151±0.0643, respectively. The qualitative visual inspection on real dataset further demonstrates the effectiveness of the proposed method.

Cerebral ischemia increases bone marrow CD4+CD25+FoxP3+ regulatory T cells in mice via signals from sympathetic nervous system.

Recent evidence has shown that an increase in CD4(+)CD25(+)FoxP3(+) regulatory T (Treg) cells may contribute to stroke-induced immunosuppression. However, the molecular mechanisms that underlie this increase in Treg cells remain unclear. Here, we used a transient middle cerebral artery occlusion model in mice and specific pathway inhibitors to demonstrate that stroke activates the sympathetic nervous system, which was abolished by 6-OHDA. The consequent activation of ß2-adrenergic receptor (AR) signaling increased prostaglandin E2 (PGE2) level in bone marrow. ß2-AR antagonist prevented the upregulation of PGE2. PGE2, which acts on prostaglandin E receptor subtype 4 (EP4), upregulated the expression of receptor activator for NF-κB ligand (RANKL) in CD4(+) T cells and mediated the increase in Treg cells in bone marrow. Treatment of MCAO mice with RANKL antagonist OPG inhibited the increase in percent of bone marrow Treg cells. PGE2 also elevated the expression of indoleamine 2,3 dioxygenase in CD11C(+) dendritic cells and promoted the development of functional Treg cells. The effect was neutralized by treatment with indomethacin. Concurrently, stroke reduced production of stromal cell-derived factor-1 (SDF-1) via ß3-AR signals in bone marrow but increased the expression of C-X-C chemokine receptor (CXCR) 4 in Treg and other bone marrow cells. Treatment of MCAO mice with ß3-AR antagonist SR-59230A reduced the percent of Treg cells in peripheral blood after stroke. The disruption of the CXCR4-SDF-1 axis may facilitate mobilization of Treg cells and other CXCR4(+) cells into peripheral blood. This mechanism could account for the increase in Treg cells, hematopoietic stem cells, and progenitor cells in peripheral blood after stroke. We conclude that cerebral ischemia can increase bone marrow CD4(+)CD25(+)FoxP3(+) regulatory T cells via signals from the sympathetic nervous system.