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Sun-induced chlorophyll fluorescence (SIF) is an important indicator of vegetation photosynthesis. While remote sensing enables large-scale monitoring of SIF, existing products face the challenge of trade-offs between temporal and spatial resolutions, limiting their applications. To select the optimal model for SIF data downscaling, we used a consistent dataset combined with vegetation physiological and meteorological parameters to evaluate four different regression methods in this study. The XGBoost model demonstrated the best performance during cross-validation (R2 = 0.84, RMSE = 0.137 mW/m2/nm/sr) and was, therefore, selected to downscale GOME-2 SIF data. The resulting high-resolution SIF product (HRSIF) has a temporal resolution of 8 days and a spatial resolution of 0.05° × 0.05°. The downscaled product shows high fidelity to the original coarse SIF data when aggregated (correlation = 0.76). The reliability of the product was ensured through cross-validation with ground-based and satellite observations. Moreover, the finer spatial resolution of HRSIF better matches the footprint of eddy covariance flux towers, leading to a significant improvement in the correlation with tower-based gross primary productivity (GPP). Specifically, in the mixed forest vegetation type with the best performance, the R2 increased from 0.66 to 0.85, representing an increase of 28%. This higher-precision product will support more effective ecosystem monitoring and research.

Multi-axis differential absorption spectroscopy (MAX-DOAS) has become an important tool for detecting trace gases in optical remote sensing. At present, the temporal resolution of the system using the traditional motor-rotated elevation telescope is extremely low. We focus on studying the atmospheric radiation transmission of fast synchronous MAX-DOAS (FS MAX-DOAS), which has greatly improved the temporal resolution on the ground and on mobile platforms and the influence of related parameters on the atmospheric mass factor (AMF), which is used to guide the design and experiments of the new system. The optimal elevation angle combination, the spectral resolution, and the specific effects of relevant parameters on the AMF during profile inversion by the new system were analyzed, and the feasibility of the new system for mobile MAX-DOAS was evaluated. The inversion results of the measured spectra collected by the system show that FS MAX-DOAS can meet the requirements of both ground and mobile platform observation scenarios. The results of our sensitivity study are of great significance for guiding experiments.

Background Ventilator-induced lung injury (VILI) is one of the severe complications in the clinic concerning mechanical ventilation (MV). Capsaicin (CAP) has anti-inflammatory and inhibitory effects on oxidative stress, which is a significant element causing cellular ferroptosis. Nevertheless, the specific role and potential mechanistic pathways through which CAP modulates ferroptosis in VILI remain elusive. Methods VILI was established in vivo, and the pulmonary epithelial cell injury model induced by circulation stretching (CS) was established in vitro. Both mice and cells were pretreated with CAP. Transmission electron microscopy, ELISA, Western blot, immunofluorescence, RT-PCR, fluorescent probes, and other experimental methods were used to clarify the relationship between iron death and VILI in alveolar epithelial cells, and whether capsaicin alleviates VILI by inhibiting iron death and its specific mechanism. Results Ferroptosis was involved in VILI by utilizing in vivo models. CAP inhibited ferroptosis and alleviated VILI's lung damage and inflammation, and this protective effect of CAP was dependent on maintaining mitochondrial redox system through SITR3 signaling. In the CS-caused lung epithelial cell injury models, CAP reduced pathological CS-caused ferroptosis and cell injury. Knockdown SIRT3 reversed the role of CAP on the maintaining mitochondria dysfunction under pathological CS and eliminated its subsequent advantageous impacts for ferroptosis against overstretching cells. Conclusion The outcomes showed that CAP alleviated ferroptosis in VILI via improving the activity of SITR3 to suppressing mitochondrial oxidative damage and maintaining mitochondrial redox homeostasis, illustrating its possibility as a novel therapeutic goal for VILI. Graphical Abstract

Regulatory B cells (Breg) critically orchestrate inflammatory resolution and tissue repair. This study investigates the therapeutic potential of transforming growth factor (TGF)-β1-producing Bregs in ventilator-induced lung injury (VILI), leveraging biomimetic nanotechnology to overcome limitations of conventional cytokine delivery. We engineered macrophage-derived microvesicle-encapsulated nanoparticles (TMNP) for pH-responsive, spatiotemporally controlled TGF-β1 release. Therapeutic efficacy was evaluated in a murine VILI model through longitudinal immunophenotyping, histopathology, and cytokine profiling at post-ventilation days 1 and 10 (PV1d, PV10d). VILI triggered biphasic pulmonary Breg expansion (PV1d: 7.83-fold . controls, < 0.001; PV10d resurgence) coinciding with peak injury. TMNP administration induced sustained TGF-β1 bioavailability (PV10d: 3.6-fold . free cytokine, < 0.001), attenuating histopathology (22.5% reduction in alveolar hemorrhage, < 0.01) and suppressing IL-6/TNF-α ( < 0.01). Treatment concomitantly expanded Breg populations and modulated T cell subset. TMNP orchestrates Breg-mediated immunoresolution through precision cytokine delivery and lymphocyte modulation, enabling dual-phase protection against ventilation-associated immunopathology. This paradigm represents a transformative approach for acute respiratory distress management.

Mechanical ventilation (MV) remains a cornerstone of critical care; however, its prolonged application can exacerbate lung injury, leading to ventilator-induced lung injury (VILI). Although previous studies have implicated ferroptosis in the pathogenesis of VILI, the underlying mechanisms remain unclear. This study investigated the roles of ferritinophagy in ferroptosis subsequent to VILI. Using C57BL/6J mice and MLE-12 cells, we established both in vivo and in vitro models of VILI and cyclic stretching (CS)-induced cellular injury. We assessed lung injury and the biomarkers of ferroptosis and ferritinophagy, after appropriate pretreatments. This study demonstrated that high tidal volumes (HTV) for 4 h enhanced the sensitivity to ferroptosis in both models, evidenced by increased intracellular iron levels, lipid peroxidation and cell death, which can be mitigated by ferrostatin-1 treatment. Notably, nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy contributed to ferroptosis in VILI. Inhibition of autophagy with 3-methyladenine or NCOA4 knockdown decreased intracellular Fe 2+ levels and inhibited lipid peroxidation, thereby attenuating CS-induced lung injury. Furthermore, it has also been observed that the AMPK/ULK1 axis can trigger ferritinophagy in VILI. Collectively, our study indicated that MV can induce ferroptosis by promoting NCOA4-dependent ferritinophagy, which could be a novel therapeutic target for the prevention and treatment of VILI.

This study employed dual-azimuth scanning MAX-DOAS to monitor vertical column densities of NO2 and HCHO in Shanghai during the summer and winter of 2023, and compared the results with Sentinel-5P TROPOMI data. Dual-azimuth scanning revealed a generally consistent trend in gas concentrations (r > 0.95), but concentrations at 90° were higher than those at 0°, especially near the surface. This suggests that averaging multiple azimuth angles is necessary to better represent regional pollution levels. During the observation period, diurnal patterns revealed that NO2 exhibited a “double peak” in the morning and evening, which was more pronounced in the summer, while HCHO peaked between 13:00 and 15:00. Comparisons with the TROPOMI data demonstrated overall good agreement. However, the probability of TROPOMI’s NO2 and HCHO measurements being lower than those of MAX-DOAS was 80% and 62.5%, respectively. Furthermore, TROPOMI tended to overestimate at high concentrations, with overestimation reaching 41.14% for NO2 when exceeding 9.54 × 1015 molecules/cm2 and 25.93% for HCHO when exceeding 1.26 × 1016 molecules/cm2. Sensitivity analysis of the sampling distance (0–40 km) between TROPOMI samples and the ground-based site, and the sampling time (±5 to ±60 min) relative to the TROPOMI overpass, revealed that using a sampling distance of 15–25 km for NO2 and 10–20 km for HCHO, along with appropriately shortening sampling times in the winter and extending them in the summer, can effectively enhance the consistency between satellite and ground-based observations. These findings not only reveal the spatiotemporal distribution characteristics of regional pollutants but optimize the sampling time and distance parameters for satellite–ground observation validation, providing data support for improving and enhancing the accuracy of satellite retrieval algorithms.

Tumor cells experience endoplasmic reticulum (ER) stress due to oncogene activation and stressors in the tumor microenvironment, such as hypoxia and acidosis. ER stress plays a crucial role in carcinogenesis. However, its oncogenic mechanism in esophageal squamous cell carcinoma (ESCC) remains poorly understood. The transcriptional regulation of CRELD2 by ATF4 was investigated using a dual-luciferase reporter assay. Cellular proliferation, migration, and invasion capacities of ESCC cells were systematically evaluated through assays of MTS, colony formation, wound healing, transwell invasion, and flow cytometry analysis. To elucidate the molecular mechanisms underlying CRELD2 regulation, a series of experimental approaches including immunofluorescence, qRT-PCR, Western blotting, and co-immunoprecipitation assays were performed. CRELD2 was identified as a significantly differentially expressed gene in ER-stressed ESCC cells, with its induction was mediated through the PERK-ATF4 pathway. CRELD2 exhibited oncogenic properties by enhancing ESCC cells proliferation, migration, and invasion, while also serving as a critical mediator of ER stress-regulated malignant behaviors. CRELD2 facilitated physical interaction with APMAP and promoted its cell membrane localization under ER stress. Notably, knockdown of APMAP significantly attenuated malignant phenotypes, mirroring the effects of CRELD2 depletion. Further investigations uncovered that APMAP activated TGF-β/SMAD pathway by binding to TAK1 in competition with transforming growth factor beta receptor I (TGFBR1). Concurrently, APMAP orchestrated TAK1/NF-κB signaling by enhancing TAK1 phosphorylation via facilitating the assembly of TAK1-TAB1-TAB2 ternary complexes. CRELD2, induced by the PERK-ATF4 pathway under ER stress, promotes localization of APMAP on the cell membrane, which subsequently triggers activation of TGF-β/SMAD and NF-κB signaling pathway, ultimately driving epithelial-mesenchymal transition and malignant progression of ESCC cells, and CRELD2 may serve as a promising therapeutic target for ESCC.

Understanding the spatiotemporal distribution and transport of atmospheric water vapor in urban areas is crucial for improving mesoscale models and weather and climate predictions. This study employs Multi-Axis Differential Optical Absorption Spectroscopy to monitor the dynamic distribution and transport flux of water vapor in Beijing within the tropospheric layer (0–4 km) from June 2021 to May 2022. The seasonal peaks in precipitable water occur in August, reaching 39.13 mm, with noticeable declines in winter. Water vapor was primarily distributed below 2.0 km and generally decreases with increasing altitude. The largest water vapor transport flux occurs in the southeast–northwest direction, whereas the smallest occurs in the southwest–northeast direction. The maximum flux, observed at about 1.2 km in the southeast–northwest direction during summer, reaches 31.77 g/m2/s (transported towards the southeast). Before continuous rainfall events, water vapor transport, originating primarily from the southeast, concentrates below 1 km. Backward trajectory analysis indicates that during the rainy months, there was a higher proportion of southeasterly winds, especially at lower altitudes, with air masses from the southeast at 500 m accounting for 69.11%. This study shows the capabilities of MAX-DOAS for remote sensing water vapor and offers data support for enhancing weather forecasting and understanding urban climatic dynamics.

NOX (NOX = NO + NO2) emissions measurements in Beijing are of great significance because they can aid in understanding how NOX pollution develops in mega-cities throughout China. However, NOX emissions in mega-cities are difficult to measure due to changes in wind patterns and moving sources on roads during measurement. To obtain good spatial coverage on different ring roads in Beijing over a short amount of time, two mobile differential optical absorption spectroscopy (DOAS) instruments were used to measure NOX emission flux from April 18th to 26th, 2018. In addition, a wind profile radar provided simultaneous wind field measurements for altitudes between 50 m and 1 km for each ring road measurement. We first determined NOX emission flux of different ring roads using wind field averages from measured wind data. The results showed that the NOX emission flux of Beijing’s fifth ring road, which represented the urban part, varied from (19.29 ± 5.26) × 1024 molec./s to (36.46 ± 12.86) × 1024 molec./s. On April 20th, NOX emission flux for the third ring was slightly higher than the fourth ring because the two ring roads were measured at different time periods. We then analyzed the NOX emission flux error budget and error sensitivity. The main error source was the wind field uncertainty. For some measurements, the main emission flux error source was either wind speed uncertainty or wind direction uncertainty, but not both. As Beijing’s NOX emissions came from road vehicle exhaust, we found that emission flux error had a more diverse sensitivity to wind direction uncertainty, which improved our knowledge on this topic. The NOX emission flux error sensitivity study indicated that more accurate measurements of the wind field are crucial for effective NOX emission flux measurements in Chinese mega-cities. Obtaining actual time and high resolved wind measurements is an advantage for mega-cities’ NOX emission flux measurements. The emission flux errors caused by wind direction and wind speed uncertainties were clearly distinguished. Other sensitivity studies indicated that NOX/NO2 ratio uncertainty dominated flux errors when the NOX/NO2 ratio uncertainty was >0.4. Using two mobile-DOAS and wind profile radars to measure NOx emission flux improved the quality of the emission flux measuring results. This approach could be applied to many other mega-cities in China and in others countries.

Background: The mechanism of sepsis especially non-survivors has not yet been identified. Objective: To identify the key genes concerned with non-survivor sepsis (NSS) and analyze its molecular mechanism. Methods: The original data were obtained from the GEO database to screen deferentially expressed genes (DEGs). GO and KEGG analysis were performed to analyze the functional annotation of DEGs. The protein-protein interaction (PPI) network and related analysis of hub genes were carried out. Further, hub genes were confirmed in the lipopolysaccharide (LPS)-induced septic mice by western blotting and immunohistochemistry. Results: We obtained 188 DEGs and 32 hub genes between NSS patients and healthy volunteers. Among of them, the top 10 hub genes including STAT1, ISG15, HERC1, EIF2AK2, RPL27, LY6E, IFI44L, XAF1, RSAD2 and HERC6 were studied, which predict sepsis based on receiver operator characteristic curve analysis. These hub genes were enriched in positive regulation of biomedical process including translation, response to virus and suppression of mitochondrial depolarization, etc.; cell component including mitochondrial inner membrane; molecular function containing ligase activity, etc. These hub genes are also enriched in influenza A infection and leukocyte trans-endothelial migration. The expression of these hub genes is better involved in a diagnosis of NSS, such as HERC6 (AUC = 0.9753, p = .0007), RPL27 (AUC = 0.9691, p = .0008), ISG15 (AUC = 0.9630, p = .0009), STAT1 (AUC = 0.9383, p = .0017), HERC1 (AUC = 0.9259, p = .0023), and XAF1 (AUC = 0.9259, p = .0023). Furthermore, 20 mg/kg of LPS injection up-regulated the expression of ISG15, RPL27, LY6E and HERC6 in the lung tissues compared with control mice. Conclusion: These identified 188 DEGs and 10 hub genes were associated with NSS, especially ISG15, RPL27, LY6E and HERC6 genes expressed in the lung as the most vulnerable organ.