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Abstract Depth sensing plays a crucial role in various applications, including robotics, augmented reality, and autonomous driving. Monocular passive depth sensing techniques have come into their own for the cost-effectiveness and compact design, offering an alternative to the expensive and bulky active depth sensors and stereo vision systems. While the light-field camera can address the defocus ambiguity inherent in 2D cameras and achieve unambiguous depth perception, it compromises the spatial resolution and usually struggles with the effect of optical aberration. In contrast, our previously proposed meta-imaging sensor1 has overcome such hurdles by reconciling the spatial-angular resolution trade-off and achieving the multi-site aberration correction for high-resolution imaging. Here, we present a compact meta-imaging camera and an analytical framework for the quantification of monocular depth sensing precision by calculating the Cramér–Rao lower bound of depth estimation. Quantitative evaluations reveal that the meta-imaging camera exhibits not only higher precision over a broader depth range than the light-field camera but also superior robustness against changes in signal-background ratio. Moreover, both the simulation and experimental results demonstrate that the meta-imaging camera maintains the capability of providing precise depth information even in the presence of aberrations. Showing the promising compatibility with other point-spread-function engineering methods, we anticipate that the meta-imaging camera may facilitate the advancement of monocular passive depth sensing in various applications.

Background: Pyroptosis is an inflammatory form of regulated necrosis that has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the role of lipid peroxidation in pyroptosis and its underlying mechanisms in COPD remain unclear. Methods: In vitro, human bronchial epithelial cells (Beas-2b cells) were exposed to cigarette smoke extract (CSE) for 24 h. In vivo, mice were exposed to cigarette smoke (CS) for 4 weeks. To investigate the role of xCT, we used siRNA and AAV6 to conditionally knock down xCT in vitro and in vivo, respectively. Results: The administration of ferrostatin-1 (Fer-1), a ferroptosis inhibitor that inhibits lipid peroxidation, significantly reduced the cytotoxicity of CSE to Beas-2b cells and mitigated inflammatory exudation, lung injury and mucus hypersecretion in mice with CS-induced COPD. Fer-1 suppressed gasdermin D (GSDMD)-mediated pyroptosis caused by CS in vitro and in vivo. However, in Beas-2b cells and the lung epithelial cells of mice, conditional knockdown of xCT (a negative regulatory factor of lipid peroxidation) inhibited the xCT/GPx4 axis, leading to more severe lipid peroxidation and GSDMD-mediated pyroptosis during cigarette smoke exposure. Moreover, we found that CS promoted the degradation of xCT through the ubiquitin proteasome system (UPS) and that treatment with MG132 significantly inhibited the degradation of xCT and downregulated the expression of pyroptosis-related proteins. Conclusion: The results of this study suggested that the ubiquitination-mediated degradation of xCT drives GSDMD-mediated pyroptosis in COPD and is a potential therapeutic target for COPD.

Objective: Fine particulate matter (PM2.5) is a source of pollution worldwide, that causes inflammation and liver fibrosis. Melatonin, as the predominant hormone secreted by the pineal gland, can inhibit PM2.5-induced lung injury by activating nuclear factor erythroid 2-related factor 2 (Nrf2) to inhibit ferroptosis. However, the possible role of melatonin in PM2.5-induced liver damage remains unclear. Experimental approach: In vitro, the effects of melatonin on PM2.5-induced oxidative stress and LX-2 cell activation were examined. In vivo, a PM2.5-induced inflammation and liver fibrosis mouse model was used to evaluate the hepatoprotective effect of melatonin. Results: In vitro, melatonin induced the expression of Nrf2 and its downstream genes and inhibited PM2.5-induced reactive oxygen species (ROS) production and mitochondrial damage. Melatonin also ameliorated the PM2.5-induced oxidative stress and fibrogenic marker upregulation. However, the antifibrotic effect of melatonin was abolished in siNrf2-treated LX-2 cells. In vivo, we observed mitochondrial abnormalities and mitochondrial fragmentation, which were accompanied by increased PTEN-induced kinase 1 (PINK1) and Parkin expression, in PM2.5-treated mouse hepatocytes. These changes were partially reversed by melatonin. In addition, melatonin activated the Nrf2 signaling pathway and protected against PM2.5-induced oxidative stress. Furthermore, melatonin alleviated inflammation and liver fibrosis. Moreover, Nrf2-KO mice exhibited more severe inflammation and liver fibrosis after PM2.5 exposure than wild-type mice, and the protective effect of melatonin on PM2.5- treated Nrf2-KO mice was greatly compromised. Conclusion: These data suggest that melatonin effectively inhibits PM2.5-induced liver fibrosis by activating Nrf2 and inhibiting ROS-mediated mitophagy and inflammation.

Objective: Acetaminophen (APAP) is one of the world's popular and safe painkillers, and overdose can cause severe liver damage and even acute liver failure. The effect and mechanism of the xanthohumol on acetaminophen-induced hepatotoxicity remains unclear. Methods: The hepatoprotective effects of xanthohumol were studied using APAP-induced HepG2 cells and acute liver injury of mouse, seperately. Results: In vitro, xanthohumol inhibited H2O2- and acetaminophen-induced cytotoxicity and oxidative stress. Xanthohumol up-regulated the expression of Nrf2. Further mechanistic studies showed that xanthohumol triggered Nrf2 activation via the AMPK/Akt/GSK3β pathway to exert a cytoprotective effect. In vivo, xanthohumol significantly ameliorated acetaminophen-induced mortality, the elevation of ALT and AST, GSH depletion, MDA formation and histopathological changes. Xanthohumol effectively suppressed the phosphorylation and mitochondrial translocation of JNK, mitochondrial translocation of Bax, the activation o cytochrome c, AIF secretion and Caspase-3. In vivo, xanthohumol increased Nrf2 nuclear transcription and AMPK, Akt and GSK3β phosphorylation in vivo. In addition, whether xanthohumol protected against acetaminophen-induced liver injury in Nrf2 knockout mice has not been illustated. Conclusion: Thus, xanthohumol exerted a hepatoprotective effect by inhibiting oxidative stress and mitochondrial dysfunction through the AMPK/Akt/GSK3β/Nrf2 antioxidant pathway.

Urban airborne fine particulate matter (PM2.5) is a global pollution source that has been strongly related to multiple respiratory diseases involving various types of regulated cell death (RCD). However, the role of ferroptosis, a novel form of RCD, in PM2.5-induced acute lung injury (ALI), has not been elucidated. Herein, we define the role and mechanism of ferroptosis in a PM2.5-induced ALI model. First, we demonstrated that lipid peroxidation and iron accumulation were significantly enhanced in ALI models and were accompanied by activation of the AMP-activated protein kinase (AMPK)-Beclin1 signaling pathway and inhibition of the key subunit SLC7A11 of System Xc-. However, these abnormalities were partially reversed by ferroptosis inhibitors. We further revealed that Beclin1 knockdown or overexpression ameliorated or exacerbated PM2.5-induced ferroptosis, respectively. Mechanistically, we verified that Beclin1 blocks System Xc- activity to trigger ferroptosis by directly binding to SLC7A11. Finally, knockdown of Beclin1 by AAV-shRNA or inhibition of AMPK, an upstream activator of Beclin1, ameliorated PM2.5-induced ferroptosis and ALI. Taken together, our results revealed that ferroptosis plays a novel role in PM2.5-induced ALI and elucidated the specific mechanism involving the AMPK-Beclin1 pathway and System Xc-, which may provide new insight into the toxicological effects of PM2.5 on respiratory problems.

Microfluidic chips have been widely applied in biochemical analysis, DNA sequencing, and disease diagnosis due to their advantages of miniaturization, low consumption, rapid analysis, and automation. Injection molded microfluidic chips have attracted great attention because of their short processing time, low cost, and mass production. The microchannel is the critical element of a microfluidic chip, and thus the microchannel replicability directly affects the performance of the microfluidic chip. In the current paper, a new method is proposed to evaluate the replicability of the microchannel profile via the root mean square value of the actual profile curve and the ideal profile curve of the microchannel. To investigate the effects of injection molding parameters (i.e., mold temperature, melting temperature, holding pressure, holding time, and injection rate) on microchannel replicability, a series of single-factor experiments were carried out. The results showed that, within the investigated experimental range, the increase of mold temperature, melt temperature, holding pressure, holding time, and injection rate could improve microchannel replicability accuracy. Specifically, the microchannels along the flow direction of the polymer melt were significantly affected by the mold temperature and melt temperature. Moreover, the replicability of the microchannel was influenced by the distance from the injection gate. The effect of microchannel replication on electrophoresis was demonstrated by a protein electrophoresis experiment.