Abalone shell-derived Mg-doped mesoporous hydroxyapatite microsphere drug delivery system loaded with icariin for inducing apoptosis of osteosarcoma cells.

Hydroxyapatite (HAP) porous microspheres with very high specific surface area and drug loading capacity, as well as excellent biocompatibility, have been widely used in tumour therapy. Mg2+ is considered to be a key factor in bone regeneration, acting as an active agent to stimulate bone and cartilage formation, and is effective in accelerating cell migration and promoting angiogenesis, which is essential for bone tissue repair, anti-cancer, and anti-infection. In this study, abalone shells from a variety of sources were used as raw materials, and Mg2+-doped abalone shell-derived mesoporous HAP microspheres (Mg-HAP) were prepared by hydrothermal synthesis as Mg2+/ icariin smart dual delivery system (ICA-Mg-HAP, IMHA). With increasing of Mg2+ doping, the surface morphology of HAP microspheres varied from collapsed macroporous to mesoporous to smooth and non-porous, which may be due to Mg2+ substitution or coordination in the HAP lattice. At 30% Mg2+ doping, the Mg-HAP microspheres showed a more homogeneous mesoporous morphology with a high specific surface area (186.06 m2/g). The IMHA microspheres showed high drug loading (7.69%) and encapsulation rate (83.29%), sustained Mg2+ release for more than 27 days, sustained and stable release of icariin for 60 hours, and good responsiveness to pH (pH 6.4 > pH 5.6). In addition, the IMHA delivery system stimulated the rapid proliferation of bone marrow mesenchymal stem cells and induced apoptosis in MG63 cells by blocking the G2 phase cycle of osteosarcoma cells and stimulating the high expression of apoptotic genes (Bcl-2, caspase-3, -8, -9). This suggests that the abalone shell-based IMHA may have potential applications in drug delivery and tumour therapy.

Multi-response kinetic study of Maillard reaction hazards in the glucose-lysine model system.

BACKGROUND: Nε-carboxymethyllysine (CML), Nε-carboxyethyllysine (CEL) and α-aminoadipic acid (AAA) are important foodborne hazards and their intake can cause a variety of diseases in humans. It is extremely important to investigate the formation mechanism of CML, CEL and AAA, as well as their association with each other when aiming to control their production. RESULTS: A multi-response kinetic model was developed within the glucose-lysine Maillard reaction model system. The concentrations of glucose, lysine, glyoxal (GO), methylglyoxal (MGO), CML, CEL and AAA were quantified at different temperature (100-160 °C) and at different intervals (0-60 min). The experimental data were fitted to the proposed model to calculate kinetic parameters for the corresponding steps. The results indicated that the production of CML was primarily relied on the direct oxidative cleavage of the Amadori product, rather than the reaction between GO and Lys, whereas CEL and AAA were generated through the reaction of MGO with Lys. Significantly, the reaction between α-dicarbonyl compounds and Lys preferentially generated CML and CEL, resulting in the lower concentrations of AAA compared to CML and CEL. CONCLUSION: The multi-response kinetic model developed in the present study can be applied well to the Maillard reaction. The relationship between the formation mechanisms of CML, CEL and AAA is also explained. © 2024 Society of Chemical Industry.

Comparative Epigenetic Profiling Reveals Distinct Features of Mucosal Melanomas Associated with Immune Cell Infiltration and Their Clinical Implications.

Mucosal melanoma exhibits limited responsiveness to anti-PD-1 therapy. However, a subgroup of mucosal melanomas, particularly those situated at specific anatomic sites like primary malignant melanoma of the esophagus (PMME), display remarkable sensitivity to anti-PD-1 treatment. The underlying mechanisms driving this superior response and the DNA methylation patterns in mucosal melanoma have not been thoroughly investigated. We collected tumor samples from 50 patients with mucosal melanoma, including 31 PMME and 19 non-esophageal mucosal melanoma (NEMM). Targeted bisulfite sequencing was conducted to characterize the DNA methylation landscape of mucosal melanoma and explore the epigenetic profiling differences between PMME and NEMM. Bulk RNA sequencing and multiplex immunofluorescence staining were performed to confirm the impact of methylation on gene expression and immune microenvironment. Our analysis revealed distinct epigenetic signatures that distinguish mucosal melanomas of different origins. Notably, PMME exhibited distinct epigenetic profiling characterized by a global hypermethylation alteration compared with NEMM. The prognostic model based on the methylation scores of a 7-DMR panel could effectively predict the overall survival of patients with PMME and potentially serve as a prognostic factor. PMME displayed a substantial enrichment of immune-activating cells in contrast to NEMM. Furthermore, we observed hypermethylation of the TERT promoter in PMME, which correlated with heightened CD8+ T-cell infiltration, and patients with hypermethylated TERT were likely to have improved responses to immunotherapy. Our results indicated that PMME shows a distinct methylation landscape compared with NEMM, and the epigenetic status of TERT might be used to estimate prognosis and direct anti-PD-1 treatment for mucosal melanoma. SIGNIFICANCE: This study investigated the intricate epigenetic factor of mucosal melanomas contributed to the differential immune checkpoint inhibitor response, and found that PMME exhibited a global hypermethylation pattern and lower gene expression in comparison to NEMM. TERT hypermethylation may contribute to the favorable responses observed in patients with mucosal melanoma undergoing immunotherapy.

Construction of heterogeneous interfaces for water activation and dissociation to synergistically boost overall water splitting.

Construction of heterogeneous interfaces with dual active components to synergistically promote both hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) is an effective strategy for facilitating electrochemical water splitting, but the appropriate active component regulation via simple synthesis procedures is still challenging. Herein, the Co and Co2Mo3O8 active components are screened to construct effective heterogeneous interfaces and successfully integrated on Ni foam by thermal reduction of cobalt molybdate precursor. And this bifunctional electrode (Co/Co2Mo3O8/NF) required overpotentials of only 164 and 360 mV to drive the 100 mA cm-2 for HER and OER in alkaline media, respectively. Theoretical calculations showed that the electron transfer occurred from Co to Co2Mo3O8 at the interface, then the formed interfacial cobalt atoms with deficient electron were beneficial for water activation, and reduced energy barrier of water dissociation under the synergistic effect of Co2Mo3O8. Notably, the alkaline electrolyzer based on symmetric Co/Co2Mo3O8/NF electrodes generated 100 mA cm-2 at a voltage of only 1.75 V, surpassing commercially available precious-metal Pt/RuO2-based catalysts.

Dysfunction of Nrf2-regulated cellular defence system and JNK activation induced by high dose of fly Ash particles are associated with pulmonary injury in mouse lungs.

The mechanisms of the exposure to fine particulate matter (PM) as a risk factor for pulmonary injury are not fully understood. The transcription factor, NF-E2-related factor 2 (Nrf2), plays a key role in protection lung against PM insult and cancer chemoprevention. In this study, F3-S fly ash particles from a municipal waste incinerator were evaluated as a PM model. We found that F3-S triggered hierarchical oxidative stress responses involving the prolonged activation of the cytoprotective Nrf2 transcriptional program via Keap1 Cys151 modification, and c-Jun NH2-terminal kinase (JNK) phosphorylation at higher doses. In mouse lungs exposed to fly ash particles at a low dose (10-20 mg/kg), Nrf2 signalling was upregulated, while in those exposed to a high fly ash particle dose (40 mg/kg), there was significant activation of JNK, and this correlated with Nrf2 phosphorylation and the downregulation of antioxidant response element (ARE)-driven genes. The JNK inhibitor, SP600125, reversed Nrf2 phosphorylation, and downregulation of detoxifying enzymes. Silencing JNK expression in mouse lungs using adenoviral shRNA inhibited JNK activation and Nrf2 phosphorylation, promoted ARE-driven gene expression, and reduced pulmonary injury. Furthermore, we found that the 452-515 amino acid region within the Neh1 domain of Nrf2 was required for its interaction with P-JNK. We demonstrated that Nrf2 was an important P-JNK target in fly ash-induced pulmonary toxicity. JNK phosphorylated Nrf2, leading to a dysfunction of the Nrf2-mediated defence system.

Clinical value of FAT1 mutations to indicate the immune response in colorectal cancer patients.

Immunotherapy is currently approved for CRC whose tumors have high MSI-H. To find additional biomarkers for immunotherapy in CRC, targeted sequencing was performed on tumor tissues from a discovery cohort of 161 CRC patients. Validation cohorts from the cBioPortal were also used for survival and tumor cell infiltration analyses. The FAT1-mutated CRC group often co-occurred with MSI events and displayed a higher tumor mutational burden compared to the FAT1 wild-type CRC. Overall survival was higher in patients with FAT1 mutations than in patients with wild type FAT1. The altered PI3K-AKT pathway and immune pathways were enriched in the FAT1-mutated CRC. A higher infiltration rate of immune cells including CD4+ T cells, CD8+ T cells, macrophages M1 and regulatory T cells were also observed in the colorectal tumors with FAT1 mutation compared to tumors with wild type FAT1. The results showed that CRC patients with FAT1 mutations exhibited an immunotherapy-favorable profile.

Downregulation of VEGFA accelerates AGEs-mediated nucleus pulposus degeneration through inhibiting protective mitophagy in high glucose environments.

Intervertebral disc degeneration (IVDD) contributes largely to low back pain. Recent studies have highlighted the exacerbating role of diabetes mellitus (DM) in IVDD, mainly due to the influence of hyperglycemia (HG) or the accumulation of advanced glycation end products (AGEs). Vascular endothelial growth factor A (VEGFA) newly assumed a distinct impact in nonvascular tissues through mitophagy regulation. However, the combined actions of HG and AGEs on IVDD and the involved role of VEGFA remain unclear. We confirmed the potential relation between VEGFA and DM through bioinformatics and biological specimen detection. Then we observed that AGEs induced nucleus pulposus (NP) cell degeneration by upregulating cellular reactive oxygen species (ROS), and HG further aggravated ROS level through breaking AGEs-induced protective mitophagy. Furthermore, this adverse effect could be strengthened by VEGFA knockdown. Importantly, we identified that the regulation of VEGFA and mitophagy were vital mechanisms in AGEs-HG-induced NP cell degeneration through Parkin/Akt/mTOR and AMPK/mTOR pathway. Additionally, VEGFA overexpression through local injection with lentivirus carrying VEGFA plasmids significantly alleviated NP degeneration and IVDD in STZ-induced diabetes and puncture rat models. In conclusion, the findings first confirmed that VEGFA protects against AGEs-HG-induced IVDD, which may represent a therapeutic strategy for DM-related IVDD.

A beneficial adaptive role for CHOP in driving cell fate selection during ER stress.

Cellular stresses elicit signaling cascades that are capable of either mitigating the inciting dysfunction or initiating cell death. During endoplasmic reticulum (ER) stress, the transcription factor CHOP is widely recognized to promote cell death. However, it is not clear whether CHOP also has a beneficial role during adaptation. Here, we combine a new, versatile, genetically modified Chop allele with single cell analysis and with stresses of physiological intensity, to rigorously examine the contribution of CHOP to cell fate. Paradoxically, we find that CHOP promotes death in some cells, but proliferation-and hence recovery-in others. Strikingly, this function of CHOP confers to cells a stress-specific competitive growth advantage. The dynamics of CHOP expression and UPR activation at the single cell level suggest that CHOP maximizes UPR activation, which in turn favors stress resolution, subsequent UPR deactivation, and proliferation. Taken together, these findings suggest that CHOP's function can be better described as a "stress test" that drives cells into either of two mutually exclusive fates-adaptation or death-during stresses of physiological intensity.

A quick guide to networking for scientists.

Networking is an important skill for finding social relationships relevant to one's career. However, networking can be difficult to navigate as different social situations and career levels require unique skill sets. Here, we provide tips for effective networking at conferences, dinners, and other events.

Diversity, Equity and Inclusion in the Laboratory: Strategies to Enhance Inclusive Laboratory Culture.

Building a diverse laboratory that is equitable is critical for the retention of talent and the growth of trainees professionally and personally. Here, we outline several strategies including enhancing understanding of cultural competency and humility, establishing laboratory values, and developing equitable laboratory structures to create an inclusive laboratory environment to enable trainees to achieve their highest success.

Interference with the HNF4-dependent gene regulatory network diminishes endoplasmic reticulum stress in hepatocytes.

BACKGROUND: In all eukaryotic cell types, the unfolded protein response (UPR) upregulates factors that promote protein folding and misfolded protein clearance to help alleviate endoplasmic reticulum (ER) stress. Yet, ER stress in the liver is uniquely accompanied by the suppression of metabolic genes, the coordination and purpose of which are largely unknown. METHODS: Here, we combined in silico machine learning, in vivo liver-specific deletion of the master regulator of hepatocyte differentiation HNF4α, and in vitro manipulation of hepatocyte differentiation state to determine how the UPR regulates hepatocyte identity and toward what end. RESULTS: Machine learning identified a cluster of correlated genes that were profoundly suppressed by persistent ER stress in the liver. These genes, which encode diverse functions including metabolism, coagulation, drug detoxification, and bile synthesis, are likely targets of the master regulator of hepatocyte differentiation HNF4α. The response of these genes to ER stress was phenocopied by liver-specific deletion of HNF4α. Strikingly, while deletion of HNF4α exacerbated liver injury in response to an ER stress challenge, it also diminished UPR activation and partially preserved ER ultrastructure, suggesting attenuated ER stress. Conversely, pharmacological maintenance of hepatocyte identity in vitro enhanced sensitivity to stress. CONCLUSIONS: Together, our findings suggest that the UPR regulates hepatocyte identity through HNF4α to protect ER homeostasis even at the expense of liver function.

Asian Americans in STEM are not a monolith.

Despite tremendous diversity, Asian Americans in STEM are grouped and viewed as a homogeneous monolith, facing stereotypes and disparities. We propose solutions that include disaggregating the Asian American grouping and recognizing the diverse individual ethnic subgroups that comprise Americans of Asian ancestry to implement change within the STEM field.

Ameliorating Osteoarthritis in Mice Using Silver Nanoparticles.

Knee osteoarthritis (KOA) is one of the most commonly encountered degenerative diseases of the joints in people over 45 years of age. Currently, there are not any effective therapeutics for KOA,and the only end-point strategy is total knee arthroplasty (TKA); therefore, KOA is associated with economic burdens and societal costs. The immune inflammatory response is involved in the occurrence and development of KOA. We previously established a mouse model of KOA using type II collagen. Hyperplasia of the synovial tissue was present in the model, alongside a large number of infiltrated inflammatory cells. Silver nanoparticles have substantial anti-inflammatory effects and have been widely used in tumor therapy and surgical drug delivery. Therefore, we evaluated the therapeutic effects of silver nanoparticles in a collagenase II-induced KOA model. The experimental results showed that silver nanoparticles significantly reduced synovial hyperplasia and the infiltration of neutrophils in the synovial tissue. Hence, this work demonstrates the identification of a novel strategy for OA and provides a theoretical basis for preventing the progress of KOA.

A comparative analysis of near-infrared image colorization methods for low-power NVIDIA Jetson embedded systems.

The near-infrared (NIR) image obtained by an NIR camera is a grayscale image that is inconsistent with the human visual spectrum. It can be difficult to perceive the details of a scene from an NIR scene; thus, a method is required to convert them to visible images, providing color and texture information. In addition, a camera produces so much video data that it increases the pressure on the cloud server. Image processing can be done on an edge device, but the computing resources of edge devices are limited, and their power consumption constraints need to be considered. Graphics Processing Unit (GPU)-based NVIDIA Jetson embedded systems offer a considerable advantage over Central Processing Unit (CPU)-based embedded devices in inference speed. For this study, we designed an evaluation system that uses image quality, resource occupancy, and energy consumption metrics to verify the performance of different NIR image colorization methods on low-power NVIDIA Jetson embedded systems for practical applications. The performance of 11 image colorization methods on NIR image datasets was tested on three different configurations of NVIDIA Jetson boards. The experimental results indicate that the Pix2Pix method performs best, with a rate of 27 frames per second on the Jetson Xavier NX. This performance is sufficient to meet the requirements of real-time NIR image colorization.

ScRNA-seq revealed targeting regulator of G protein signaling 1 to mediate regulatory T cells in Hepatocellular carcinoma.

BACKGROUND: Regulatory T cells (Tregs) are central to determine immune response, thus targeting Tregs for immunotherapy is a promising strategy against tumor development and metastasis. OBJECTIVES: The objective of this study was to identify genes for targeting Tregs to improve the outcome of HCC. METHODS: We integrated expression data from different samples to remove batch effects and further applied embedding function in Scanpy to conduct sub-clustering of CD4+ T cells in HCC for each of two independent scRNA-seq data. The activity of transcription factors (TFs) was inferred by DoRothEA. Gene expression network analysis was performed in WGCNA R package. We finally used R packages (survminer and survival) to conduct survival analysis. Multiplex immunofluorescence analysis was performed to validate the result from bioinformatic analyses. RESULTS: We found that regulator of G protein signaling 1 (RGS1) expression was significantly elevated in Tregs compared to other CD4+ T cells in two independent public scRNA-seq datasets, and increased RGS1 predicted inferior clinical outcome of HCC patients. Multiplex immunofluorescence analysis supported that the higher expression of RGS1 in HCC Tregs in tumor tissue compared to it in adjacent tissue. Moreover, RGS1 expression in Tregs was positively correlated with the expression of marker genes of Tregs, C-X-C chemokine receptor 4 (CXCR4), and three CXCR4-dependent genes in both scRNA-seq and bulk RNA-seq data. We further identified that these three genes were selectively expressed in Tregs as compared to other CD4+ T cells. The activities of two transcription factors, recombination signal binding protein for immunoglobulin kappa J region (RBPJ) and yin yang 1 (YY1), were significantly different in HCC Tregs with RGS1 high and RGS1 low. CONCLUSIONS: Our findings suggested that RGS1 may regulate Treg function possibly through CXCR4 signaling and RGS1 could be a potential target to improve responses for immunotherapy in HCC.

Spleen Toxicity of Organophosphorus Flame Retardant TDCPP in Mice and the Related Mechanisms.

Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) is an organophosphorus flame retardant that has been utilized in recent years as a primary replacement for polybrominated diphenyl ethers (PBDEs) in a wide variety of fire-sensitive applications. However, the impact of TDCPP on the immune system has not been fully determined. As the largest secondary immune organ in the body, the spleen is considered to be an important study endpoint for determining immune defects in the body. The aim of this study is to investigate the effect of TDCPP toxicity on the spleen and its possible molecular mechanisms. In this study, for 28 consecutive days, TDCPP was administered intragastrically (i.g), and we assessed the general condition of mice by evaluating their 24 h water and food intake. Pathological changes in spleen tissues were also evaluated at the end of the 28-day exposure. To measure the TDCPP-induced inflammatory response in the spleen and its consequences, the expression of the critical players in the NF-κB pathway and mitochondrial apoptosis were detected. Lastly, RNA-seq was performed to identify the crucial signaling pathways of TDCPP-induced splenic injury. The results showed that TDCPP intragastric exposure triggered an inflammatory response in the spleen, likely through activating the NF-κB/IFN-γ/TNF-α/IL-1ß pathway. TDCPP also led to mitochondrial-related apoptosis in the spleen. Further RNA-seq analysis suggested that the TDCPP-mediated immunosuppressive effect is associated with the inhibition of chemokines and the expression of their receptor genes in the cytokine-cytokine receptor interaction pathway, including four genes of the CC subfamily, four genes of the CXC subfamily, and one gene of the C subfamily. Taken together, the present study identifies the sub-chronic splenic toxicity of TDCPP and provides insights on the potential mechanisms of TDCPP-induced splenic injury and immune suppression.

A beneficial adaptive role for CHOP in driving cell fate selection during ER stress.

Cellular stresses elicit signaling cascades that are capable of either mitigating the inciting dysfunction or initiating cell death. During endoplasmic reticulum (ER) stress, the transcription factor CHOP is widely recognized to promote cell death. However, it is not clear whether CHOP also has a beneficial role during adaptation. Here, we have combined a new, versatile, genetically modified Chop allele with single cell analysis and with stresses of physiological intensity, to rigorously examine the contribution of CHOP to cell fate. Paradoxically, we found that CHOP promoted death in some cells, but proliferation-and hence recovery-in others. Strikingly, this function of CHOP conferred to cells a stress-specific competitive growth advantage. The dynamics of CHOP expression and UPR activation at the single cell level suggested that CHOP maximizes UPR activation, which in turn favors stress resolution, subsequent UPR deactivation, and proliferation. Taken together, these findings suggest that CHOP's function can be better described as a "stress test" that drives cells into either of two mutually exclusive fates-adaptation or death-during stresses of physiological intensity.

Coupling of Oxygen Vacancies and Heterostructure on Fe3 O4 via an Anion Doping Strategy to Boost Catalytic Activity for Lithium-Sulfur Batteries.

The sluggish reaction kinetics and severe shutting behaviors of sulfur cathodes are the major roadblocks to realizing the practical application of lithium-sulfur (Li-S) batteries and need to be solved through designing/constructing rational sulfur hosts. Herein, an effective alternative material of Fe3 O4- x /FeP in-situ embedded in N-doped carbon-tube (Fe3 O4- x /FeP/NCT) is proposed. In this fabricated heterostructure, NCT skeleton works as a sulfur host provides physical barrier for lithium polysulfides (LiPSs), while Fe3 O4- x /FeP heterostructure with abundant oxygen vacancies provides double active centers to simultaneously accelerate e- /Li+ diffusion/transport kinetics and catalysis for LiPSs. Through the respective advantages, Fe3 O4- x /FeP/NCT exhibits synergy enhancement effect for restraining sulfur dissolution and enhancing its conversion kinetics. Furthermore, the promoted ion diffusion kinetics, enhanced electrical conductivity, and increased active sites of Fe3 O4- x /FeP/NCT are enabled by oxygen vacancies as well as the heterogeneous interfacial contact, which is clearly confirmed by experimental and first-principles calculations. By virtue of these superiorities, the constructed cathode shows excellent long-term cycling stability and a high-rate capability up to 10 C. Specially, a high areal capacity of 7.2 mAh cm-2 is also achieved, holding great promise for utilization in advanced Li-S batteries in the future.

Response of soil nutrients retention and rice growth to biochar in straw returning paddy fields.

Applying straw to agricultural production to improve soil productivity and crop yields is significant. However, the straw-only application is possibly not a practical choice for achieving environmental protection and high yield. This study evaluated the applicability of straw combined with biochar to the paddy field. Two-year pot experiments were conducted to examine the effect of straw combined with different proportions (0, 5, 20, 40 t ha-1) of biochar on soil nitrogen retention, phosphorous availability, rice yield, and physiological parameters. Five treatments were included: control (CK), 7 t ha-1 straw + 0 t ha-1 biochar (ST), 7 t ha-1 straw + 5 t ha-1 biochar (SC1), 7 t ha-1 straw + 20 t ha-1 biochar (SC2), 7 t ha-1 straw + 40 t ha-1 biochar (SC3). The results indicated that the biochar had an encouraging effect on paddy fields with straw returning: (1) SC3 treatment significantly increased ammonium nitrogen (NH4+-N) and nitrate nitrogen (NO3--N) content in soils compared to ST, increasing by 30.19% and 42.72%, while SC2 treatment increased by 25.84% and 30.40%, respectively; (2) Regarding soil phosphorus availability, ST treatment showed a negative effect, while proper biochar application rate (20 t ha-1) effectively increased Olsen-P content (18.24%); (3) No significant difference among these treatments was observed in the photosynthetic characteristics. Notably, 20 t ha-1 biochar application (SC2) effectively enhanced rice components (stem, ear) dry biomass, improved rice yield (10.14%), and Harvest index (HI: 4.99%). Hence, the appropriate rate (20 t ha-1) of biochar combined with straw (7 t ha-1) returning is a promising strategy for increasing nitrogen retention and phosphorous availability, alleviating N and P losses and promoting rice growth and yield. These findings are expected to provide a new perspective in that straw-returning with biochar achieves high efficiency, ecological, and sustainable development of agriculture.

High-resolution crop yield and water productivity dataset generated using random forest and remote sensing.

Accurate and high-resolution crop yield and crop water productivity (CWP) datasets are required to understand and predict spatiotemporal variation in agricultural production capacity; however, datasets for maize and wheat, two key staple dryland crops in China, are currently lacking. In this study, we generated and evaluated a long-term data series, at 1-km resolution of crop yield and CWP for maize and wheat across China, based on the multiple remotely sensed indicators and random forest algorithm. Results showed that MOD16 products are an accurate alternative to eddy covariance flux tower data to describe crop evapotranspiration (maize and wheat RMSE: 4.42 and 3.81 mm/8d, respectively) and the proposed yield estimation model showed accuracy at local (maize and wheat rRMSE: 26.81 and 21.80%, respectively) and regional (maize and wheat rRMSE: 15.36 and 17.17%, respectively) scales. Our analyses, which showed spatiotemporal patterns of maize and wheat yields and CWP across China, can be used to optimize agricultural production strategies in the context of maintaining food security.