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Surface ozone (O3) pollution has adverse impacts on the yield of winter wheat. The North China Plain (NCP), one of the globally significant primary regions for winter wheat production, has been frequently plagued by severe O3 pollution in recent years. In this study, the effects of O3 pollution on winter wheat yield and economic impact were evaluated in the NCP during the 2015–2018 seasons using the regional atmospheric chemical transport model (WRF-Chem), O3 metrics including the phytotoxic surface O3 dose above 12 nmol m−2 s−1 (POD12), and the accumulated daytime O3 above 40 ppb (AOT40). Results showed that the modeled O3, exposure-based AOT40, and flux-based POD12 increased during the winter wheat growing season from 2015 to 2018. The annual average daytime O3, exposure-based AOT40, and flux-based POD12 were 44 ppb, 5.32 ppm h, and 1.78 mmol m−2, respectively. During 2015–2018, winter wheat relative production loss averaged 10.9% with AOT40 and 14.6% with POD12. This resulted in an average annual production loss of 12.4 million metric tons, valued at approximately USD 4.5 billion. This study enhances our understanding of the spatial sensitivity of winter wheat to O3 impacts, and suggests that controlling O3 pollution during the key growth stages of winter wheat or improving its O3 tolerance will enhance food security. [ABSTRACT FROM AUTHOR]

The gross primary production (GPP) of vegetation in urban areas plays an important role in the study of urban ecology. It is difficult however, to accurately estimate GPP in urban areas, mostly due to the complexity of impervious land surfaces, buildings, vegetation, and management. Recently, we used the Vegetation Photosynthesis Model (VPM), climate data, and satellite images to estimate the GPP of terrestrial ecosystems including urban areas. Here, we report VPM-based GPP (GPPvpm) estimates for the world's ten most populous megacities during 2000-2014. The seasonal dynamics of GPPvpm during 2007-2014 in the ten megacities track well that of the solar-induced chlorophyll fluorescence (SIF) data from GOME-2 at 0.5° × 0.5° resolution. Annual GPPvpm during 2000-2014 also shows substantial variation among the ten megacities, and year-to-year trends show increases, no change, and decreases. Urban expansion and vegetation collectively impact GPP variations in these megacities. The results of this study demonstrate the potential of a satellite-based vegetation photosynthesis model for diagnostic studies of GPP and the terrestrial carbon cycle in urban areas.

Thyroid cancer incidence increases worldwide annually, primarily due to factors such as ionizing radiation (IR), iodine intake, and genetics. Papillary carcinoma of the thyroid (PTC) accounts for about 80% of thyroid cancer cases. RET/PTC1 (coiled‐coil domain containing 6 [CCDC6]‐rearranged during transfection) rearrangement is a distinctive feature in over 70% of thyroid cancers who exposed to low doses of IR in Chernobyl and Hiroshima‒Nagasaki atomic bombings. This study aims to elucidate mechanism between RET/PTC1 rearrangement and IR in PTC. N‐thy‐ori‐3‐1 cells were subjected to varying doses of IR (2/1/0.5/0.2/0.1/0.05 Gy) of IR at different days, and result showed low‐dose IR‐induced RET/PTC1 rearrangement in a dose‐dependent manner. RET/PTC1 has been observed to promote PTC both in vivo and in vitro. To delineate the role of different DNA repair pathways, SCR7, RI‐1, and Olaparib were employed to inhibit non‐homologous end joining (NHEJ), homologous recombination (HR), and microhomology‐mediated end joining (MMEJ), respectively. Notably, inhibiting NHEJ enhanced HR repair efficiency and reduced IR‐induced RET/PTC1 rearrangement. Conversely, inhibiting HR increased NHEJ repair efficiency and subsequent RET/PTC1 rearrangement. The MMEJ did not show a markable role in this progress. Additionally, inhibiting DNA‐dependent protein kinase catalytic subunit (DNA‐PKcs) decreased the efficiency of NHEJ and thus reduced IR‐induced RET/PTC1 rearrangement. To conclude, the data suggest that NHEJ, rather than HR or MMEJ, is the critical cause of IR‐induced RET/PTC1 rearrangement. Targeting DNA‐PKcs to inhibit the NHEJ has emerged as a promising therapeutic strategy for addressing IR‐induced RET/PTC1 rearrangement in PTC. [ABSTRACT FROM AUTHOR]

Introduction: Radiation‐induced pulmonary fibrosis (RIPF) is a chronic, progressive, irreversible lung interstitial disease that develops after radiotherapy. Although several previous studies have focused on the mechanism of epithelial–mesenchymal transition (EMT) in lung epithelial cells, the essential factors involved in this process remain poorly understood. The DNA‐dependent protein kinase catalytic subunit (DNA‐PKcs) exhibits strong repair capacity when cells undergo radiation‐induced damage; whether DNA‐PKcs regulates EMT during RIPF remains unclear. Objectives: To investigate the role and molecular mechanism of DNA‐PKcs in RIPF and provide an important theoretical basis for utilising DNA‐PKcs‐targeted drugs for preventing RIPF. Methods: DNA‐PKcs knockout (DPK−/−) mice were generated via the Cas9/sgRNA technique and subjected to whole chest ionizing radiation (IR) at a 20 Gy dose. Before whole chest IR, the mice were intragastrically administered the DNA‐PKcs‐targeted drug VND3207. Lung tissues were collected at 1 and 5 months after IR. Results: The expression of DNA‐PKcs is low in pulmonary fibrosis (PF) patients. DNA‐PKcs deficiency significantly exacerbated RIPF by promoting EMT in lung epithelial cells. Mechanistically, DNA‐PKcs deletion by shRNA or inhibitor NU7441 maintained the protein stability of Twist1. Furthermore, AKT1 mediated the interaction between DNA‐PKcs and Twist1. High Twist1 expression and EMT‐associated changes caused by DNA‐PKcs deletion were blocked by insulin‐like growth factor‐1 (IGF‐1), an AKT1 agonist. The radioprotective drug VND3207 prevented IR‐induced EMT and alleviated RIPF in mice by stimulating the kinase activity of DNA‐PKcs. Conclusion: Our study clarified the critical role and mechanism of DNA‐PKcs in RIPF and showed that it could be a potential target for preventing RIPF. [ABSTRACT FROM AUTHOR]