An integrated bioinformatics analysis to identify the shared biomarkers in patients with obstructive sleep apnea syndrome and nonalcoholic fatty liver disease.

Background: Obstructive sleep apnea (OSA) syndrome and nonalcoholic fatty liver disease (NAFLD) have been shown to have a close association in previous studies, but their pathogeneses are unclear. This study explores the molecular mechanisms associated with the pathogenesis of OSA and NAFLD and identifies key predictive genes. Methods: Using the Gene Expression Omnibus (GEO) database, we obtained gene expression profiles GSE38792 for OSA and GSE89632 for NAFLD and related clinical characteristics. Mitochondrial unfolded protein response-related genes (UPRmtRGs) were acquired by collating and collecting UPRmtRGs from the GeneCards database and relevant literature from PubMed. The differentially expressed genes (DEGs) associated with OSA and NAFLD were identified using differential expression analysis. Gene Set Enrichment Analysis (GSEA) was conducted for signaling pathway enrichment analysis of related disease genes. Based on the STRING database, protein-protein interaction (PPI) analysis was performed on differentially co-expressed genes (Co-DEGs), and the Cytoscape software (version 3.9.1) was used to visualize the PPI network model. In addition, the GeneMANIA website was used to predict and construct the functional similar genes of the selected Co-DEGs. Key predictor genes were analyzed using the receiver operating characteristic (ROC) curve. Results: The intersection of differentially expressed genes shared between OSA and NAFLD-related gene expression profiles with UPRmtRGs yielded four Co-DEGs: ASS1, HDAC2, SIRT3, and VEGFA. GSEA obtained the relevant enrichment signaling pathways for OSA and NAFLD. PPI network results showed that all four Co-DEGs interacted (except for ASS1 and HDAC2). Ultimately, key predictor genes were selected in the ROC curve, including HDAC2 (OSA: AUC = 0.812; NAFLD: AUC = 0.729), SIRT3 (OSA: AUC = 0.775; NAFLD: AUC = 0.750), and VEGFA (OSA: AUC = 0.812; NAFLD: AUC = 0.861) (they have a high degree of accuracy in predicting whether a subject will develop two diseases). Conclusion: In this study, four co-expression differential genes for OSA and NAFLD were obtained, and they can predict the occurrence of both diseases. Transcriptional mechanisms involved in OSA and NAFLD interactions may be better understood by exploring these key genes. Simultaneously, this study provides potential diagnostic and therapeutic markers for patients with OSA and NAFLD.

Active fraction of Polyrhachis vicina (Rogers) inhibits osteoclastogenesis by targeting Trim38 mediated proteasomal degradation of TRAF6.

BACKGROUND: Reactive Oxygen Species (ROS) is a key factor in the pathogenesis of osteoporosis (OP) primarily characterized by excessive osteoclast activity. Active fraction of Polyrhachis vicina Rogers (AFPR) exerts antioxidant effects and possesses extensive promising therapeutic effects in various conditions, however, its function in osteoclastogenesis and OP is unknown. PURPOSE: The aim of this study is to elucidate the cellular and molecular mechanisms of AFPR in OP. STUDY DESIGN AND METHODS: CCK8 assay was used to evaluate the cell viability under AFPR treatment. TRAcP staining, podosome belts staining and bone resorption were used to test the effect of AFPR on osteoclastogenesis. Immunofluorescence staining was used to observe the effect of AFPR on ROS production. si-RNA transfection, coimmunoprecipitation and Western-blot were used to clarify the underlying mechanisms. Further, an ovariectomy (OVX) -induced OP mice model was used to identify the effect of AFPR on bone loss using Micro-CT scanning and histological examination. RESULTS: In the present study, AFPR inhibited osteoclast differentiation and bone resorption induced by nuclear factor-κB receptor activator (NF-κB) ligand (RANKL) in dose-/ time-dependent with no cytotoxicity. Meanwhile, AFPR decreased RANKL-mediated ROS levels and enhanced ROS scavenging enzymes. Mechanistically, AFPR promoted proteasomal degradation of TRAF6 by significantly upregulating its K48-linked ubiquitination, subsequently inhibiting NFATc1 activity. We further observed that tripartite motif protein 38 (TRIM38) could mediate the ubiquitination of TRAF6 in response to RANKL. Moreover, TRIM38 could negatively regulate the RANKL pathway by binding to TRAF6 and promoting K48-linked polyubiquitination. In addition, TRIM38 deficiency rescued the inhibition of AFPR on ROS and NFATc1 activity and osteoclastogenesis. In line with these results, AFPR reduced OP caused by OVX through ameliorating osteoclastogenesis. CONCLUSION: AFPR alleviates ovariectomized-induced bone loss via suppressing ROS and NFATc1 by targeting Trim38 mediated proteasomal degradation of TRAF6. The research offers innovative perspectives on AFPR's suppressive impact in vivo OVX mouse model and in vitro, and clarifies the fundamental mechanism.

Hecogenin alleviates LPS-induced osteolysis via regulating pyroptosis and ROS involved Nrf2 activation.

Reactive oxidative species (ROS) generation triggers pyroptosis and induces development of inflammatory osteolysis. Hecogenin (HG) has anti-inflammatory and antioxidative property, but its effects on inflammatory osteolysis remains unclear. In our study, we investigated the mechanism of HG on pyroptosis and its effect on inflammatory osteolysis in vitro and in vivo. The impact of HG on osteoclastogenesis was evaluated using cytotoxicity, TRAcP staining and bone resorption assays. The RNA-sequencing was employed to identify potential signaling pathways, and then RT-qPCR, western blot, immunofluorescence, and ELISA were used to verify. To determine the protective effect of HG in vivo, Lipopolysaccharide (LPS)-induced animal models were utilized, along with micro-CT and histological examination. HG suppressed RANKL-induced osteoclast differentiation, bone resorption, NFATc1 activity and downstream factors. RNA-sequencing results showed that HG inhibited osteoclastogenesis by modulating the inflammatory response and macrophage polarization. Furthermore, HG inhibited the NF-κB pathway, and deactivated the NLRP3 inflammasome. HG activated the expression of nuclear factor E2-related factor 2 (Nrf2) to eliminate ROS generation. Importantly, the inhibitory effect of HG on NLRP3 inflammasome could be reversed by treatment with the Nrf2 inhibitor ML385. In vivo, HG prevented the mice against LPS-induced osteolysis by suppressing osteoclastogenesis and inflammatory factors. In conclusion, HG could activate Nrf2 to eliminate ROS generation, inactivate NLRP3 inflammasome and inhibit pyroptosis, thereby suppressing osteoclastogenesis in vitro and alleviating inflammatory osteolysis in vivo, which indicating that HG might be a promising candidate to treat inflammatory osteolysis.

Climate-adaptive crop distribution can feed food demand, improve water scarcity, and reduce greenhouse gas emissions.

Optimizing crop distribution stands as a pivotal approach to climate change adaption, enhancing crop production sustainability, and has been recognized for its immense potential in ensuring food security while minimizing environmental impacts. Here, we developed a climate-adaptive framework to optimize the distribution of staple crops (i.e., wheat, maize, and rice) to meet the multi-dimensional needs of crop production in China. The framework considers the feasibility of the multiple cropping systems (harvesting more than once on a cropland a year) and adopts a multi-dimensional approach, incorporating goals related to crop production, water consumption, and greenhouse gas (GHG) emissions. By optimizing, the total irrigated area of three crops would decrease by 7.7 % accompanied by a substantial 69.8 % increase in rain-fed areas compared to the baseline in 2010. This optimized strategy resulted in a notable 10.0 % reduction in total GHG emissions and a 13.1 % decrease in irrigation water consumption while maintaining consistent crop production levels. In 2030, maintaining the existing crop distribution and relying solely on yield growth would lead to a significant maize production shortfall of 27.0 %, highlighting a looming challenge. To address this concern, strategic adjustments were made by reducing irrigated areas for wheat, rice, and maize by 2.3 %, 12.8 %, and 6.1 %, respectively, while simultaneously augmenting rain-fed areas for wheat and maize by 120.2 % and 55.9 %, respectively. These modifications ensure that production demands for all three crops are met, while yielding a 6.9 % reduction in GHG emissions and a 15.1 % reduction in irrigation water consumption. This optimization strategy offers a promising solution to alleviate severe water scarcity issues and secure a sustainable agricultural future, effectively adapting to evolving crop production demands in China.

Potential benefits of cropping pattern change in the climate-sensitive regions of rice production in China.

Rice production is a primary contributor to global greenhouse gas emissions, with unclear pathways towards carbon neutrality. Here, through a comprehensive assessment of direct greenhouse gas (GHG) emission using DNDC model and indirect GHG emission using emission factor methods, we estimated the annual crop yield, GHG emission amount and intensity, and economic benefits of different cropping patterns in the climate-sensitive regions of rice production in China. Through the expansion of single-rice and cropping pattern change from the wheat-rice to wheat-rice-rice in the climate-sensitive regions of single and triple-cropping cultivations, the total grain yield increased by 4.4 % and 4.5 % compared with the current national grain production, the GHG emission would increase by 2.4 % and 5.4 % of the current national GHG emissions from rice and wheat production, the net economic benefits could increase 0.9 % and decrease 2.0 % of the national output value of rice and wheat production. The study takes the entire-life cycle of crop growth as the principal line, and could provide a valuable reference for the regulation of the cropping pattern and the formulation of carbon reduction policies in the climate-sensitive region.

Dauricine attenuates ovariectomized-induced bone loss and RANKL-induced osteoclastogenesis via inhibiting ROS-mediated NF-κB and NFATc1 activity.

BACKGROUND: Osteoclast plays an important role in maintaining the balance between bone anabolism and bone catabolism. The abnormality of osteoclast is closely related to osteolytic bone diseases such as osteoporosis, rheumatoid arthritis and tumor bone metastasis. PURPOSE: We aim to search for natural compound that may suppress osteoclast formation and function. STUDY DESIGN: In this study, we assessed the impact of Dauricine (Dau) on the formation and function of osteoclasts in vitro, as well as its potential in preventing bone loss in an ovariectomy mouse model in vivo. METHODS: Multiple in vitro experiments were carried out, including osteoclastogenesis, podosomal belt formation, bone resorption assay, RNA-sequencing, real-time quantitative PCR, ROS level detection, surface plasmon resonance assay, luciferase assay and western blot. To verify the effect in vivo, an ovariectomized mouse model (OVX model) was constructed, and bone parameters were measured using micro-CT and histology. Furthermore, metabolomics analysis was performed on blood serum samples from the OVX model. RESULTS: In vitro experiments demonstrated that Dau inhibits RANKL-induced osteoclastogenesis, podosomal belt formation, and bone resorption function. RNA-sequencing results revealed that Dau significantly suppresses genes related to osteoclast. Functional enrichment analysis indicated that Dau's inhibition of osteoclasts may be associated with NF-κB signaling pathway and reactive oxygen metabolism pathway. Molecular docking, surface plasmon resonance assay and western blot analysis further confirmed that Dau inhibits RANKL-induced osteoclastogenesis by modulating the ROS/NF-κB/NFATc1 pathway. Moreover, administration of Dau to OVX-induced mice validated its efficacy in treating bone loss disease. CONCLUSION: Dau prevents OVX-induced bone loss by inhibiting osteoclast activity and bone resorption, potentially offering a new approach for preventing and treating metabolic bone diseases such as osteoporosis. This study provides innovative insights into the inhibitory effects of Dau in an in vivo OVX model and elucidates the underlying mechanism.

Tempol alleviates acute lung injury by affecting glutathione synthesis through Nrf2 and inhibiting ferroptosis in lung epithelial cells.

As a life-threatening disease, acute lung injury (ALI) may progress to chronic pulmonary fibrosis. For the treatment of lung injury, Tempol is a superoxide dismutase mimetic and intracellular redox agent that can be a potential drug. This study investigated the regulatory mechanism of Tempol in the treatment of ALI. A mouse model of ALI was established, and HE staining was used to examine histomorphology. The CCK-8 assay was used to measure cell viability, and oxidative stress was assessed by corresponding kits. Flow cytometry and dichlorodihydrofluorescein diacetate staining assays were used to detect reactive oxygen species (ROS) levels. Protein expression levels were measured by Western blot analysis and ELISA. Pulmonary vascular permeability was used to measure the lung wet/dry weight ratio. The level of oxidative stress was increased in ALI mice, and the level of ferroptosis was upregulated. Tempol inhibited this effect and alleviated ALI. The administration of Tempol alleviated the pathological changes in ALI, inhibited pulmonary vascular permeability, and improved lung injury in ALI mice. The upregulation of genes essential for glutathione (GSH) metabolism induced by lipopolysaccharide (LPS) was inhibited by Tempol. In addition, nuclear factor-related factor 2 (Nrf2) is activated by Tempol therapy to regulate the de novo synthesis pathway of GSH, thereby alleviating LPS-induced lung epithelial cell damage. The results showed that Tempol alleviated ALI by activating the Nrf2 pathway to inhibit oxidative stress and ferroptosis in lung epithelial cells. In conclusion, this study demonstrates that Tempol alleviates ALI by inhibiting ferroptosis in lung epithelial cells through the effect of Nrf2 on GSH synthesis.

Cichoric acid targets RANKL to inhibit osteoclastogenesis and prevent ovariectomy-induced bone loss.

BACKGROUND AND AIM: Osteoporosis, a systemic metabolic bone disease, is characterized by the decline of bone mass and quality due to excessive osteoclast activity. Currently, drug-targeting osteoclasts show promising therapy for osteoporosis. In this study, we investigated the effect of cichoric acid (CA) on receptor activator of nuclear kappa-B ligand (RANKL)-induced osteoclastogenesis and the bone loss induced by ovariectomy in mice. EXPERIMENTAL PROCEDURE: Molecular docking technologies were employed to examine the interaction between CA and RANKL. CCK8 assay was used to evaluate the cell viability under CA treatment. TRAcP staining, podosome belt staining, and bone resorption assays were used to test the effect of CA on osteoclastogenesis and osteoclast function. Further, an OVX-induced osteoporosis mice model was employed to identify the effect of CA on bone loss using micro-CT scanning and histological examination. To investigate underlying mechanisms, network pharmacology was applied to predict the downstream signaling pathways, which were verified by Western blot and immunofluorescence staining. KEY RESULTS: The molecular docking analysis revealed that CA exhibited a specific binding affinity to RANKL, engaging multiple binding sites. CA inhibited RANKL-induced osteoclastogenesis and bone resorption without cytotoxic effects. Mechanistically, CA suppressed RANKL-induced intracellular reactive oxygen species, nuclear factor-kappa B, and mitogen-activated protein kinase pathways, followed by abrogated nuclear factor activated T-cells 1 activity. Consistent with this finding, CA attenuated post-ovariectomy-induced osteoporosis by ameliorating osteoclastogenesis. CONCLUSIONS AND IMPLICATIONS: CA inhibited osteoclast activity and bone loss by targeting RANKL. CA might represent a promising candidate for treating osteoclast-related diseases, such as osteoporosis.

Chronic intermittent hypoxia-induced oxidative stress activates TRB3 and phosphorylated JNK to mediate insulin resistance and cell apoptosis in the pancreas.

This study explores the potential mechanisms of obstructive sleep apnoea (OSA) complicates type 2 diabetes mellitus (T2DM) by which chronic intermittent hypoxia (CIH) induces insulin resistance and cell apoptosis in the pancreas through oxidative stress. Four- and eight-week CIH rat models were established, and Tempol (100 mg/kg/d), was used as an oxidative stress inhibitor. This study included five groups: 4-week CIH, 4-week CIH-Tempol, 8-week CIH, 8-week CIH-Tempol and normal control (NC) groups. Fasting blood glucose and insulin levels were measured in the serum. The expression levels of 8-hidroxy-2-deoxyguanosine (8-OHdG), tribbles homologue 3 (TRB3), c-Jun N-terminal kinase (JNK), phosphorylated JNK (p-JNK), insulin receptor substrate-1 (IRS-1), phosphorylated IRS-1 (Ser307) (p-IRS-1ser307 ), protein kinase B (AKT), phosphorylated AKT (Ser473) (p-AKTser473 ), B cell lymphoma protein-2 (Bcl-2), cleaved-caspase-3 (Cl-caspase-3), and the islet cell apoptosis were detected in the pancreas. CIH induced oxidative stress in the pancreas. Compared with that in the NC group and CIH-Tempol groups individually, the homeostasis model assessment of insulin resistance (HOMA-IR) and apoptosis of islet cells was increased in the CIH groups. CIH-induced oxidative stress increased the expression of p-IRS-1Ser307 and decreased the expression of p-AKTSer473 . The expression levels of TRB3 and p-JNK were higher in the CIH groups than in both the CIH-Tempol and NC groups. Meanwhile, the expressions of Cl-caspase-3 and Bcl-2 were upregulated and downregulated, respectively, in the CIH groups. Hence, the present study demonstrated that CIH-induced oxidative stress might not only induce insulin resistance but also islet cell apoptosis in the pancreas through TRB3 and p-JNK.

4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol) alleviates lung injury by inhibiting SIRT6-HIF-1α signaling pathway activation through the upregulation of miR-212-5p expression.

OBJECTIVE: Obstructive sleep apnea is closely related to oxidative stress. 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol) can scavenge reactive oxygen species (ROS) and ameliorate oxidative damage in the body. The mechanism by which Tempol alleviates chronic intermittent hypoxia-induced lung injury has rarely been reported. This study aimed to confirm the molecular mechanism by which Tempol alleviates lung injury. METHODS: The levels of miR-212-5p and Sirtuin 6 (SIRT6) in injured lungs were analyzed using bioinformatics. In vitro, intermittent hypoxia (IH) treatment induced hypoxia in BEAS-2B cells and we established a model of chronic intermittent hypoxia (CIH) in mouse using a programmed hypoxia chamber. We used HE staining to observe the morphology of lung tissue, and the changes in lung fibers were observed by Masson staining. The levels of inflammatory factors in mouse serum were detected by ELISA, and the levels of the oxidative stress indicators GSH, MDA, SOD and ROS were detected using commercially available kits. Moreover, a real-time qPCR assay was used to detect miR-212-5p expression, and Western blotting was used to detect the levels of SIRT6, HIF-1α and apoptosis-related proteins. CCK-8 was used to detect cell proliferation. Subsequently, we used flow cytometry to detect cell apoptosis. Dual-luciferase gene reporters determine the on-target binding relationship of miR-212-5p and SIRT6. RESULTS: SIRT6 was highly expressed in CIH-induced lung injury, as shown by bioinformatics analysis; however, miR-212-5p expression was decreased. Tempol promoted miR-212-5p expression, and the levels of SIRT6 and HIF-1α were inhibited. In BEAS-2B cells, Tempol also increased proliferation, inhibited apoptosis and inhibited oxidative stress in BEAS-2B cells under IH conditions. In BEAS-2B cells, these effects of Tempol were reversed after transfection with an miR-212-5p inhibitor. miR-212-5p targeted and negatively regulated the level of SIRT6 and overexpression of SIRT6 effectively reversed the enhanced influence of the miR-212-5p mimic on Tempol's antioxidant activity. Tempol effectively ameliorated lung injury in CIH mice and inhibited collagen deposition and inflammatory cell infiltration. Likewise, the therapeutic effect of Tempol could be effectively reversed by interference with the miR-212-5p inhibitor. CONCLUSION: Inhibition of the SIRT6-HIF-1α signaling pathway could promote the effect of Tempol by upregulating the level of miR-212-5p, thereby alleviating the occurrence of lung injury and providing a new underlying target for the treatment of lung injury.

Tussilagone inhibits osteoclastogenesis by modulating mitochondrial function and ROS production involved Nrf2 activation.

Reactive Oxygen Species (ROS) play an essential role in the pathogenesis of osteoporosis mainly characterized by excessive osteoclasts (OCs) activity. OCs are rich in mitochondria for energy support, which is a major source of total ROS. Tussilagone (TSG), a natural Sesquiterpenes from the flower of Tussilago farfara, has plentiful beneficial pharmacological characteristics with anti-inflammatory and anti-oxidative activity, but its effects and mechanism in osteopathology are still unclear. In our study, we investigated the regulation of ROS generated from the mitochondria in OCs. We found that TSG inhibited OCs differentiation and bone resorption without any cytotoxicity. Mechanistically, TSG reduced RANKL-mediated total ROS level by down-regulating intracellular ROS production and mitochondrial function, leading to the suppression of NFATc1 transcription. We also found that nuclear factor erythroid 2-related factor 2 (Nrf2) could enhance ROS scavenging enzymes in response to RANKL-induced oxidative stress. Furthermore, TSG up-regulated the expression of Nrf2 by inhibiting its proteosomal degradation. Interestingly, Nrf2 deficiency reversed the suppressive effect of TSG on mitochondrial activity and ROS signaling in OCs. Consistent with this finding, TSG attenuated post-ovariectomy (OVX)- and lipopolysaccharide (LPS) induced bone loss by ameliorating osteoclastogenesis. Taken together, TSG has an anti-bone resorptive effect by modulating mitochondrial function and ROS production involved Nrf2 activation.

Selective Anchoring by Surface Sulfur Species Coupled with Rapid Interface Electron Transfer for Ultrahigh Capacity Extraction of Uranium from Seawater.

Improving the adsorption selectivity, enhancing the extraction capacity, and ensuring the structural stability of the adsorbent are the key to realize the high efficiency recovery of uranium. In this work, we utilized the strong Lewis acid-base interaction between S2- and U(VI)O22+ coupling rapid electron transfer at the MnS/U(VI)O22+ solid-liquid interface to achieve excellent selectivity, high adsorption capacity, and rapid extraction of uranium. The as-synthesized MnS adsorbent exhibited an ultrahigh uranium extraction capacity (2457.05 mg g-1) and a rapid rate constant (K = 9.11 × 10-4 g h-1 mg-1) in seawater with 100.7 ppm of UO2(NO3)2 electrolyte. The kinetic simulation reveals that this adsorption process is a chemical adsorption process and conforms to a pseudo-second-order kinetic model, indicating electron transfer at the MnS/U(VI)O22+ solid-liquid interface. The relevant (quasi) in situ spectroscopic characterization and theoretical calculation results further revealed that the outstanding uranium extraction property of MnS could be attributed to the highly selective UO22+ adsorption of MnS with lower adsorption energy as a result of the strong interaction between S2- and UO22+ and the rapid mass transfer and interface electron transfer from S2- and low-valent Mn(II) to U(VI)O22+.

Tempol attenuates chronic intermittent hypoxia-induced lung injury through the miR-145-5p/Nrf2 signaling pathway.

This study mainly explored the effect of Tempol on OSA-induced lung injury and the specific molecular mechanism. A hypoxia/reoxygenation (H/R) cell model and an IH-induced lung injury model in rats were constructed. The expression of miRNAs and related proteins was detected by RT‒qPCR and Western blotting. HE and Masson staining were used to observe the pathological changes in lung tissues. The expression levels of inflammatory cytokines were detected by ELISA. Apoptotic cells were observed by TUNEL. The ROS levels were detected by a DCFH-DA probe. Tempol administration effectively reduced the pathological changes in lung tissue and the progression of pulmonary fibrosis in rats with lung injury and reduced the expression of inflammatory factors in lung tissue. miR-145-5p was significantly upregulated in rats with IH-induced lung injury, and Tempol treatment inhibited the expression of miR-145-5p. Transfection with the miR-145-5p inhibitor effectively inhibited H/R cell apoptosis and autophagy, while transfection with the miR-145-5p mimic had the opposite effect. Targeting miR-145-5p negatively regulates the expression of Nrf2. Transfection of the miR-145-5p mimic weakened the inhibitory effects of Tempol on apoptosis and autophagy in H/R cells. Overexpression of the Nrf2 mimic reversed the effects of the miR-145-5p mimic on Tempol to a certain extent. It was also confirmed in animal experiments that overexpression of Nrf2 reversed the inhibitory effect of the miR-145-5p mimic on Tempol's lung injury relief effect. Tempol alleviates lung injury induced by chronic interstitial hypoxia by regulating the miR-145-5p/Nrf2 molecular axis and inhibiting autophagy.

Effects of climate change on wind erosion in the three provinces of Northeast China.

The three provinces of Northeast China are crucial to national commodity grain production. Soils in those areas have begun to severely degrade after long-term high-intensity use, with wind erosion as one of the main reasons. Based on meteorological and soil data from 1981 to 2019, we evaluated the spatial-temporal characteristics of wind erosion on bare land in the three provinces of Northeast China by using the revised wind erosion equation (RWEQ), and analyzed the contributions of meteorological factors to wind erosion on bare land. The results showed that, the meteorological factors of wind erosion were overall high in southwestern part and low in northeastern part of the region. In general, wind erosion in the region was substantial, especially in Liaoning. During the 39 years, wind erosion significantly increased throughout the whole year and during the growing season, at a rate of 129 and 105 t·km-2 per decade, respectively. The obvious increase in wind erosion was observed in the northwest Liaoning, Liaohe Plain, and Changbai Mountain area. Wind speed and air temperature were the main factors affecting wind erosion during the year and non-growing season, which contributed less during the growing season when precipitation contributed the most. We concluded that climate change has aggravated soil wind erosion in the three provinces of Northeast China.

Tyrosine phosphorylation of band 3 impairs the storage quality of suspended red blood cells in the Tibetan high-altitude polycythemia population.

Due to environmental hypoxia on the Tibetan Plateau, local residents often exhibit a compensative increase in hemoglobin concentration to maintain the body's oxygen supply. However, increases in hemoglobin and hematocrit (Hct) pose a serious challenge to the quality of stored suspended red blood cells (SRBCs) prepared from the blood of high-hemoglobin populations, especially populations at high altitude with polycythemia in Tibet. To explore the difference in storage quality of SRBCs prepared from plateau residents with a high hemoglobin concentration, blood donors were recruited from Tibet (> 3600 m) and Chengdu (≈ 500 m) and divided into a high-altitude control (HAC) group, high-altitude polycythemia (HAPC) group and lowland control (LLC) group according to their hemoglobin concentration and altitude of residence. The extracellular acidification rate (ECAR), pyruvate kinase (PK) activity and band 3 tyrosine phosphorylation were analyzed on the day of blood collection. Then, whole-blood samples were processed into SRBCs, and storage quality parameters were analyzed aseptically on days 1, 14, 21 and 35 of storage. Overall, we found that tyrosine 21 phosphorylation activated glycolysis by releasing glycolytic enzymes from the cytosolic domain of band 3, thus increasing glucose consumption and lactate accumulation during storage, in the HAPC group. In addition, band 3 tyrosine phosphorylation impaired erythrocyte deformability, accompanied by the highest hemolysis rate in the HAPC group, during storage. We believe that these results will stimulate new ideas to further optimize current additive solutions for the high-hemoglobin population in Tibet and reveal new therapeutic targets for the treatment of HAPC populations.

Establishment of a reference interval for total carbon dioxide using indirect methods in Chinese populations living in high-altitude areas: A retrospective real-world analysis.

BACKGROUND: Hypoxia leads to different concentrations of the bicarbonate buffer system in Tibetan people. Indirect methods were used to establish the reference interval (RI) for total carbon dioxide (tCO2) based on big data from the adult population of Tibet, a high-altitude area in Western China. METHODS: Anonymous tCO2 test data (n = 442,714) were collected from the People's Hospital of the Tibet Autonomous Region from January 2018, to December 2021. Multiple linear regression and variance component analyses were performed to assess the effects of sex, age, and race on tCO2 levels. Indirect methods, including Hoffmann, Bhattacharya, expectation maximization (EM), kosmic and refineR, were used to calculate the total RI and ethnicity-partitioned RI. RESULTS: A total of 230,821 real-world tCO2 test results were eligible. Sex, age, and race were significantly associated with the tCO2 levels. The total and ethnically-partitioned RIs estimated using the five indirect methods were comparable. The total RI of tCO2 was 14-24 mmol/L (calculated using Hoffmann and refineR) and 15-24 mmol/L (Bhattacharya, EM and kosmic). For Han nationality, the RIs were 14-25 mmol/L (calculated using Hoffmann and Bhattacharya), 16-23 mmol/L (EM), 15-24 mmol/L (kosmic), and 14.2-24.5 mmol/L (refineR). For the Tibetan population, the RIs were 14-24 mmol/L (calculated using Hoffmann and refineR), 15-24 mmol/L (Bhattacharya and kosmic), and 15-23 mmol/L (EM). The established RIs were significantly lower than those living at lower altitudes area (22-29 mmol/L) that was provided by the manufacturer. CONCLUSION: The tCO2 RI of the populations living on the Tibetan Plateau was significantly lower than those at the lower altitudes. The RIs established using indirect methods are suitable for clinical applications in Tibet.

The heat stress during anthesis and the grain-filling period of spring maize in Northeast China is projected to increase toward the mid-21st century.

BACKGROUND: Against the background of global warming, heat stress has become more frequent, which adversely affects the growth and development of spring maize plants in Northeast China. To adapt the regional maize production to climate change, it is imperative to understand the spatio-temporal characteristics of heat stress. In the present study, we analyzed three of the indices for heat stress, including the number of heat stress days, heating degree days (HDD, the total heat degree-days during critical stages), and the percentage of stations with heat stress. RESULTS: From 1981 to 2019, the number of heat stress days varied greatly among the study years, ranging from 0 to 14 and 27 days, respectively. The average HDD was 7.8 and 5.0 °C day from 1981 to 2000, respectively, and the main hot-spots of heat stress occurred in the southwest regions. Moreover, compared with 1981-2000, the region of HDD during anthesis higher than 10 °C day in 2041-2060 under the SSP1-2.6 and SSP5-8.5 climate scenarios increased by 9.1-50.1% and 0.1-28.6%. The average HDD during the critical stages from 2041 to 2060 increased under the SSP5-8.5 climate scenario, being 1.5 times higher than that during 1981-2000. HDD during maize anthesis and the grain-filling period showed an overall increasing trend with years. About 19% and 58% of the study locations showed heat stress during the past 39 years, respectively. CONCLUSION: Heat stress during anthesis and the grain-filling period for spring maize in Northeast China is projected to increase toward the mid-21st century. © 2023 Society of Chemical Industry.

Electrocatalytic Mechanism of Defect in Spinels for Water and Organics Oxidation.

Spinels display promising electrocatalytic ability for oxygen evolution reaction (OER) and organics oxidation reaction because of flexible structure, tunable component, and multifold valence. Unfortunately, limited exposure of active sites, poor electronic conductivity, and low intrinsic ability make the electrocatalytic performance of spinels unsatisfactory. Defect engineering is an effective method to enhance the intrinsic ability of electrocatalysts. Herein, the recent advances in defect spinels for OER and organics electrooxidation are reviewed. The defect types that exist in spinels are first introduced. Then the catalytic mechanism and dynamic evolution of defect spinels during the electrochemical process are summarized in detail. Finally, the challenges of defect spinel electrocatalysts are brought up. This review aims to deepen the understanding about the role and evolution of defects in spinel for electrochemical water/organics oxidation and provide a significant reference for the design of efficient defect spinel electrocatalysts.

Spatial and temporal variations of extreme climate index in the Songhua River Basin during 1961-2020.

Understanding climate change and extreme climate is of great significance for ensuring food security and socio-economic development of the Songhua River Basin. Based on the daily precipitation, maximum temperature and minimum temperature data during 1961-2020 from 69 meteorological stations in and around the Songhua River Basin, we analyzed the temporal and spatial variations of extreme temperature and precipitation in the Songhua River Basin using 27 extreme climate indices recommended by the World Meteorological Organization, and linear trend method, Mann-Kendall trend test and ordinary Kriging interpolation methodology. The results showed that, from 1961 to 2020, except for cold speel duration, the extreme cold index in the study area showed a downward trend, while the extreme warm index, extreme value index and other temperature indices showed an upward trend. The increasing trend of the minimum temperature was greater than that of the maximum temperature. Icing days, cold speel duration and warm speel duration showed an increasing trend from south to north, while the minimum value of maximum temperature and that of minimum temperature showed opposite spatial characteristics. The high value areas of summer days and tropical nights were mainly distributed in the southwestern region, while there was no obvious spatial variations of cool days, warm nights, and warm days. Overall, except for cold speel duration, other extreme cold indices had a rapid decreasing trend in the north and west of the Songhua River Basin. In the warm index, summer days, warm nights, warm days, and warm speel duration had a rapid upward trend in the north and west, and tropical nights had the fastest rise in the southwest. In the extreme value index, the maximum of temperature rose fastest in the northwest, while the minimum rose fastest in the northeast. Except for consecutive dry days, the rest of precipitation indices showed an increasing trend, and the fastest rising areas were mainly in the north-central part of the Nenjiang River Basin, while some areas in the south of the Nenjiang River Basin became dry. Heavy precipitation days, very heavy precipitation days, heaviest precipitation days, consecutive wet days, very wet day precipitation, extremely wet day precipitation, and annual precipitation showed a gradual decreasing pattern from southeast to northwest. Overall, the Songhua River Basin was warming and wetting, but there were some differences among different regions, especially the northern and southern parts of the Nenjiang River Basin.

UPLC/Q-TOF-MS-based metabolomics evaluate the efficacy of oroxylin A against postmenopausal osteoporosis.

Post-menopausal osteoporosis (PMOP) is a common metabolic bone malady characterized by bone mass loss and bone microarchitectural deterioration; however, there is currently no effective drug for its management. According to our previous study, oroxylin A (OA) could effectively protect ovariectomized (OVX)-osteoporotic mice from bone loss; however, its therapeutic targets are still unclear. From a metabolomic perspective, we studied serum metabolic profiles to discover potential biomarkers and OVX-related metabolic networks, which could assist us to comprehend the impact of OA on OVX. Five metabolites were identified as biomarkers associated with 10 related metabolic pathways, including phenylalanine, tyrosine and tryptophan biosynthesis, and phenylalanine, tryptophan and glycerophospholipid metabolism. After OA treatment, the expression of multiple biomarkers changed, with lysophosphatidylcholine (18:2) being a major significantly regulated biomarker. Our study demonstrated that OA's effects on OVX are probably related to the regulation of phenylalanine, tyrosine and tryptophan biosynthesis. Our findings explain the role of OA against PMOP in terms of metabolism and pharmacology and provide a pharmacological foundation for OA treatment of PMOP.