The requirement of the mitochondrial protein NDUFS8 for angiogenesis.

Mitochondria are important for the activation of endothelial cells and the process of angiogenesis. NDUFS8 (NADH:ubiquinone oxidoreductase core subunit S8) is a protein that plays a critical role in the function of mitochondrial Complex I. We aimed to investigate the potential involvement of NDUFS8 in angiogenesis. In human umbilical vein endothelial cells (HUVECs) and other endothelial cell types, we employed viral shRNA to silence NDUFS8 or employed the CRISPR/Cas9 method to knockout (KO) it, resulting in impaired mitochondrial functions in the endothelial cells, causing reduction in mitochondrial oxygen consumption and Complex I activity, decreased ATP production, mitochondrial depolarization, increased oxidative stress and reactive oxygen species (ROS) production, and enhanced lipid oxidation. Significantly, NDUFS8 silencing or KO hindered cell proliferation, migration, and capillary tube formation in cultured endothelial cells. In addition, there was a moderate increase in apoptosis within NDUFS8-depleted endothelial cells. Conversely, ectopic overexpression of NDUFS8 demonstrated a pro-angiogenic impact, enhancing cell proliferation, migration, and capillary tube formation in HUVECs and other endothelial cells. NDUFS8 is pivotal for Akt-mTOR cascade activation in endothelial cells. Depleting NDUFS8 inhibited Akt-mTOR activation, reversible with exogenous ATP in HUVECs. Conversely, NDUFS8 overexpression boosted Akt-mTOR activation. Furthermore, the inhibitory effects of NDUFS8 knockdown on cell proliferation, migration, and capillary tube formation were rescued by Akt re-activation via a constitutively-active Akt1. In vivo experiments using an endothelial-specific NDUFS8 shRNA adeno-associated virus (AAV), administered via intravitreous injection, revealed that endothelial knockdown of NDUFS8 inhibited retinal angiogenesis. ATP reduction, oxidative stress, and enhanced lipid oxidation were detected in mouse retinal tissues with endothelial knockdown of NDUFS8. Lastly, we observed an increase in NDUFS8 expression in retinal proliferative membrane tissues obtained from human patients with proliferative diabetic retinopathy. Our findings underscore the essential role of the mitochondrial protein NDUFS8 in regulating endothelial cell activation and angiogenesis.

Influences of tobacco straw return with lime on microbial community structure of tobacco-planting soil and tobacco leaf quality.

Soil amendment is an important strategy for improving soil quality and crop yield. From 2014 to 2019, we conducted a study to investigate the effects of tobacco straw return with lime on soil nutrients, soil microbial community structure, tobacco leaf yield, and quality in southern Anhui, China. A field experiment was conducted with four treatments: straw removed (CK), straw return (St), straw return with dolomite (St + D), and straw return with lime (St + L). Results showed that after 5 years of application, the St + L significantly increased the soil pH by 16.9%, and the contents of soil alkaline nitrogen (N) and available potassium (K) by 17.2% and 23.0%, respectively, compared with the CK. Moreover, the St + L significantly increased tobacco leaf yield (24.0%) and the appearance (9.1%) and sensory (5.9%) quality of flue-cured tobacco leaves. The addition of soil conditioners (straw, dolomite, and lime) increased both the total reads and effective sequences of soil microorganisms. Bacterial diversity was more sensitive to changes in the external environment compared to soil fungi. The application of soil amendments (lime and straw) promoted the growth of beneficial microorganisms in the soil. Additionally, bacterial species had greater competition and limited availability of resources for survival compared to fungi. The results showed that soil microorganisms were significantly influenced by the presence of AK, AN, and pH contents. These findings can provide an effective method for improving the quality of flue-cured tobacco leaves and guiding the amelioration of acidic soil in regions where tobacco-rice rotation is practiced.

Straw Addition Enhances Crop Yield, Soil Aggregation, and Soil Microorganisms in a 14-Year Wheat-Rice Rotation System in Central China.

Straw return utilizes waste resources to reduce the use of chemical fertilizers worldwide. However, information is still lacking on the relative impact of straw return on soil fertility, the nutrient composition of different soil aggregates, and soil microbial communities. Therefore, this study aimed to understand the effects of different management practices on the crop yield, soil fertility, and soil community composition in a 14-year wheat-rice rotation system. The treatments included a control (without fertilizer and straw addition), chemical fertilization (NPK), straw return without fertilizer (S), and straw addition with chemical fertilizer (NPKS). The results showed that NPKS improved the wheat and rice yield by 185.12% and 88.02%, respectively, compared to the CK treatment. Additionally, compared to the CK treatment, the N, P, and K contents of the wheat stem were increased by 39.02%, 125%, and 20.23% under the NPKS treatment. Compared to the CK treatment, SOM, TN, TP, AN, AP, AK, CEC, AFe, AMn, ACu, and AZn were increased by 49.12%, 32.62%, 35.06%, 22.89%, 129.36%, 48.34%, 13.40%, 133.95%, 58.98%, 18.26% and 33.33% under the NPKS treatment, respectively. Moreover, straw addition promoted the creation and stabilization of macro-aggregates in crop soils. The relative abundance of macro-aggregates (0.25-2 mm) increased from 37.49% to 52.97%. Straw addition was associated with a higher proportion of aromatic and carbonyl carbon groups in the soil, which, in turn, promoted the formation of macro-aggregates. Redundancy analysis showed that straw return significantly increased the microbial community diversity. These findings demonstrate that straw addition together with chemical fertilizer could increase the crop yield by improving soil fertility, soil aggregate stability, and the diversity of fungi.

Extraction of Coastal Levees Using U-Net Model with Visible and Topographic Images Observed by High-Resolution Satellite Sensors.

Coastal levees play a role in protecting coastal areas from storm surges and high waves, and they provide important input information for inundation damage simulations. However, coastal levee data with uniformity and sufficient accuracy for inundation simulations are not always well developed. Against this background, this study proposed a method to extract coastal levees by inputting high spatial resolution optical satellite image products (RGB images, digital surface models (DSMs), and slope images that can be generated from DSM images), which have high data availability at the locations and times required for simulation, into a deep learning model. The model is based on U-Net, and post-processing for noise removal was introduced to further improve its accuracy. We also proposed a method to calculate levee height using a local maximum filter by giving DSM values to the extracted levee pixels. The validation was conducted in the coastal area of Ibaraki Prefecture in Japan as a test area. The levee mask images for training were manually created by combining these data with satellite images and Google Street View, because the levee GIS data created by the Ibaraki Prefectural Government were incomplete in some parts. First, the deep learning models were compared and evaluated, and it was shown that U-Net was more accurate than Pix2Pix and BBS-Net in identifying levees. Next, three cases of input images were evaluated: (Case 1) RGB image only, (Case 2) RGB and DSM images, and (Case 3) RGB, DSM, and slope images. Case 3 was found to be the most accurate, with an average Matthews correlation coefficient of 0.674. The effectiveness of noise removal post-processing was also demonstrated. In addition, an example of the calculation of levee heights was presented and evaluated for validity. In conclusion, this method was shown to be effective in extracting coastal levees. The evaluation of generalizability and use in actual inundation simulations are future tasks.

High performance solar-blind UV detector with Mg0.472Zn0.528O/Mg0.447Zn0.553O double layer structure on MgO substrate.

Mg0.472Zn0.528O/Mg0.447Zn0.553O double layer structure UV detectors are made on single structure MgO substrate by PLD method, and the effect of different thickness top MgZnO layer on the UV response characteristics of the detector are studied. Compared with the single layer MgZnO detector that made by Mg0.3Zn0.7O target, the Mg0.472Zn0.528O/Mg0.447Zn0.553O double layer detector with 30 nm top layer, shows much higher deep UV response (21.3 A W-1at 265 nm), much smaller dark current(66.9 pA) and much higher signal-to-noise ratio (2.8 × 105) at 25 V bias voltage. And the device also shows relative high response (23.1 A W-1) at 235 nm deep UV light at 25 V bias voltage, which is mainly attributed by the bottom MgZnO layer with higher Mg composition. When the top layer is 66.7 nm thick, the response of the Mg0.472Zn0.528O/Mg0.447Zn0.553O detector reached 228.8 A W-1at 255 nm under 25 V bias voltage, the signal-to-noise ratio of which is 10573 under 20 V bias voltage, and the near UV response of the device is also big because of more h-MgZnO in top MgZnO layer. When the top layer reached 90.2 nm, there are much more h-MgZnO in the top MgZnO layer, the peak response of the Mg0.472Zn0.528O/Mg0.447Zn0.553O detector is just 6.65 A W-1at 320 nm under 25 V bias voltage, the signal-to-noise ratio of which is 1248. The high Mg composition bottom MgZnO decrease the dark current of the Mg0.472Zn0.528O/Mg0.447Zn0.553O detector, both the 2DEG effect of the double layer structure and the amplify effect of the mix-phase MgZnO top layer, increased theIuvand deep UV response of the Mg0.472Zn0.528O/Mg0.447Zn0.553O detector. Therefore, the double layer Mg0.472Zn0.528O/Mg0.447Zn0.553O detector is more sensitive at faint deep UV light compared with previous reported MgZnO detectors, and the MgxZn1-xO/MgyZn1-yO detector shows similarIuvand signal-noise-ratio at faint deep UV light as high-temperature fabricated AlxGa1-xN/AlyGa1-yN detectors.

Gene and stem cell therapy for inherited cardiac arrhythmias.

Inherited cardiac arrhythmias are a group of genetic diseases predisposing to sudden cardiac arrest, mainly resulting from variants in genes encoding cardiac ion channels or proteins involved in their regulation. Currently available therapeutic options (pharmacotherapy, ablative therapy and device-based therapy) can not preclude the occurrence of arrhythmia events and/or provide complete protection. With growing understanding of the genetic background and molecular mechanisms of inherited cardiac arrhythmias, advancing insight of stem cell technology, and development of vectors and delivery strategies, gene therapy and stem cell therapy may be promising approaches for treatment of inherited cardiac arrhythmias. Recent years have witnessed impressive progress in the basic science aspects and there is a clear and urgent need to be translated into the clinical management of arrhythmic events. In this review, we present a succinct overview of gene and cell therapy strategies, and summarize the current status of gene and cell therapy. Finally, we discuss future directions for implementation of gene and cell therapy in the therapy of inherited cardiac arrhythmias.

CD137 Signaling Mediates Pulmonary Artery Endothelial Cell Proliferation Under Hypoxia By Regulating Mitochondrial Dynamics.

Altered mitochondrial dynamics affect pulmonary artery endothelial cells (PAECs) proliferation, contributing to the development of pulmonary hypertension. CD137 signaling promotes mitochondrial fission. We hypothesize CD137 signaling is involved in the excessive proliferation of PAECs. The levels of CD137 protein were increased in the lung tissue of hypoxic mice and hypoxic-stimulated PAECs. Activation of CD137 signal in hypoxic-PAECs upregulated the levels of hypoxia-inducible factor-2α (HIF-2α), glucose transporters type 4, the lactate transporter monocarboxylate transporter 4, key glycolysis rate-limiting enzymes and promoted mitochondrial division; moreover, increased glucose uptake, lactic acid and ATP production and proliferative cells were observed in these PAECs. Whereas, knockdown HIF-2α reversed CD137 signal-mediated effects in PAECs mentioned above. Compared with wild-type mice, the proliferation of PAECs and the percentage of vascular lateral wall thickness decreased in CD137 knockout mice. Together, CD137 signal participated in pulmonary vascular remodeling through the regulation of mitochondrial dynamics dependent on HIF-2α in PAECs.

Alterations in the composition and metabolite profiles of the saline-alkali soil microbial community through biochar application.

Saline-alkali soil poses significant chanllenges to sustainable development of agriculture. Although biochar is commonly used as a soil organic amendment, its microbial remediation mechanism on saline-alkali soil requires further confirmation. To address this, we conducted a pot experiment using cotton seedlings to explore the potential remediation mechanism of rice straw biochar (BC) at three different levels on saline-alkaline soil. The results showed that adding of 2% biochar greatly improved the quality of saline-alkaline soil by reducing pH levels, electrical conductivity (EC), and water-soluble ions. Moreover, biochar increased the soil organic matter (SOM), nutrient availability and extracellular enzyme activity. Interestingly, it also reduced soil salinity and salt content in various cotton plant tissues. Additionally, biochar had a notable impact on the composition of the microbial community, causing changes in soil metabolic pathways. Notably, the addition of biochar promoted the growth and metabolism of dominant salt-tolerant bacteria, such as Proteobacteria, Bacteroidota, Acidobacteriota, and Actinobacteriota. By enhancing the positive correlation between microorganisms and metabolites, biochar alleviated the inhibitory effect of salt ions on microorganisms. In conclusion, the incorporation of biochar significantly improves the soil microenvironment, reduces soil salinity, and shows promise in ameliorating saline-alkaline soil conditions.

A novel tsRNA-5008a promotes ferroptosis in cardiomyocytes that causes atrial structural remodeling predisposed to atrial fibrillation.

Atrial fibrillation (AF) is an extremely common clinical arrhythmia disease, but whether its mechanism is associated with ferroptosis remains unclear. The tRNA-derived small RNAs (tsRNAs) are involved in a variety of cardiovascular diseases, however, their role and mechanism in atrial remodeling in AF have not been studied. We aimed to explore whether tsRNAs mediate ferroptosis in AF progression. The AF models were constructed to detect ferroptosis-related indicators, and Ferrostatin-1 (Fer-1) was introduced to clarify the relationship between ferroptosis and AF. Atrial myocardial tissue was used for small RNA sequencing to screen potential tsRNAs. tsRNA functioned on ferroptosis and AF was explored. Atrial fibrosis and changes in the cellular structures and arrangement were observed in AF mice model, and these alterations were accompanied by ferroptosis occurrence, exhibited by the accumulation of Fe2+ and MDA levels and the decrease of expression of FTH1, GPX4, and SLC7A11. Blocking above ferroptosis activation with Fer-1 resulted in a significant improvement for AF. A total of 7 tsRNAs were upregulated (including tsRNA-5008a) and 2 tsRNAs were downregulated in atrial myocardial tissue in the AF group compared with the sham group. We constructed a tsRNA-mRNA regulated network, which showed tsRNA-5008a targeted 16 ferroptosis-related genes. Knockdown of tsRNA-5008a significantly suppressed ferroptosis through targeting SLC7A11 and diminished myocardial fibrosis both in vitro and in vivo. On the contrary, tsRNA-5008a mimics promoted ferroptosis in cardiomyocytes. Collectively, tsRNA-5008a involved in AF through ferroptosis. Our study provides novel insights into the role of tsRNA-5008a mediated ferroptosis in AF progression.

Inhibition of Sema4D attenuates pressure overload-induced pathological myocardial hypertrophy via the MAPK/NF-κB/NLRP3 pathways.

Sema4D (CD100) is closely related to pathological and physiological processes, including tumor growth, angiogenesis and cardiac development. Nevertheless, the role and mechanism of Sema4D in cardiac hypertrophy are still unclear to date. To assess the impact of Sema4D on pathological cardiac hypertrophy, TAC surgery was performed on C57BL/6 mice which were transfected with AAV9-mSema4D-shRNA or AAV9-mSema4D adeno-associated virus by tail vein injection. Our results indicated that Sema4D knockdown mitigated cardiac hypertrophy, fibrosis and dysfunction when exposed to pressure overload, and Sema4D downregulation markedly inhibited cardiomyocyte hypertrophy induced by angiotensin II. Meanwhile, Sema4D overexpression had the opposite effect in vitro and in vivo. Furthermore, analysis of signaling pathways showed that Sema4D activated the MAPK pathway during cardiac hypertrophy induced by pressure overload, and the pharmacological mitogen-activated protein kinase kinase 1/2 inhibitor U0126 almost completely reversed Sema4D overexpression-induced deteriorated phenotype, resulting in improved cardiac function. Further research indicated that myocardial hypertrophy induced by Sema4D was closely related to the expression of the pyroptosis-related proteins PP65, NLRP3, caspase-1, ASC, GSDMD, IL-18 and IL-1ß. In conclusion, our study demonstrated that Sema4D regulated the process of pathological myocardial hypertrophy through modulating MAPK/NF-κB/NLRP3 pathway, and Sema4D may be the promising interventional target of cardiac hypertrophy and heart failure.

Effects of triglyceride glucose (TyG) and TyG-body mass index on sex-based differences in the early-onset heart failure of ST-elevation myocardial infarction.

BACKGROUND AND AIM: Heart failure (HF) is an important complication of ST-elevation myocardial infarction (STEMI), including early- and late-onset HF. This study aimed to investigate the association between insulin resistance (IR)-related parameters triglyceride glucose (TyG) and TyG-body mass index (TyG-BMI) index and early-onset HF in STEMI between sexes. METHODS AND RESULTS: This cross-sectional study included patients with STEMI who underwent primary percutaneous coronary intervention (PCI) between January 2016 and September 2022. Patients were divided into tertiles according to TyG/TyG-BMI index levels in males and females. The presence of early-onset HF was compared between tertiles in both sexes. Moreover, patients were stratified according to the tertiles of TyG/Tyg-BMI index. Differences in early-onset HF of STEMI were compared between males and females in each tertile group. 1118 patients were included in this study, 20.3% of whom were females. The incidence rate of early-onset HF was significantly higher in females than in males (29% vs. 14.8%). TyG-BMI index was negatively correlated with early-onset HF. In both females and males, there was no difference in the occurrence of early-onset HF between the highest and lowest TyG/TyG-BMI index groups. Sex disparity was observed in females who had a significantly higher prevalence of early-onset HF than males in each TyG/TyG-BMI index tertile group; however, after adjustment, the differences disappeared. CONCLUSIONS: For patients with STEMI who undergo primary PCI, the incidence of early-onset HF is higher in females than in males. The TyG/TyG-BMI index do not contribute to the difference in early-onset HF between sexes.

Downregulation of B4GALT5 attenuates cardiac fibrosis through Lumican and Akt/GSK-3ß/ß-catenin pathway.

Virtually all forms of cardiac disease exhibit cardiac fibrosis as a common trait, which ultimately leads to adverse ventricular remodeling and heart failure. To improve the prognosis of heart disease, it is crucial to halt the progression of cardiac fibrosis. Protein function is intricately linked with protein glycosylation, a vital post-translational modification. As a fundamental member of the ß1,4-galactosyltransferase gene family (B4GALT), ß1,4-galactosyltransferase V (B4GALT5) is associated with various disorders. In this study, significant levels of B4GALT5 expression were observed in cardiac fibrosis induced by transverse aortic constriction (TAC) or TGFß1 and the activation of cardiac fibroblasts (CFs). Subsequently, by administering AAV9-shB4GALT5 injections to TAC animals, we were able to demonstrate that in vivo B4GALT5 knockdown decreased the transformation of CFs into myofibroblasts (myoFBs) and reduced the deposition of cardiac collagen fibers. In vitro tests revealed the same results. Conversely, both in vivo and in vitro experiments indicated that overexpression of B4GALT5 stimulates CFs activation and exacerbates cardiac fibrosis. Initially, we elucidated the primary mechanism by which B4GALT5 regulates the Akt/GSK-3ß/ß-catenin pathway and directly interacts with laminin, thereby affecting cardiac fibrosis. Our findings demonstrate that B4GALT5 promotes cardiac fibrosis through the Akt/GSK-3ß/ß-catenin pathway and reveal laminin as the target protein of B4GALT5.

An enhanced visualization image acquisition method for samples with poor conductivity under a conventional scanning electron microscope.

The low-vacuum and low-accelerating-voltage modes are the most simple and practical ways to directly analyze poorly conductive samples in conventional scanning electron microscopy (SEM). However, structural feature information may disappear or be obscured in these imaging modes, making it challenging to identify and analyze some local microstructures of poorly conductive samples. To overcome this challenge, an enhanced visualization image acquisition method for samples with poor conductivity is proposed based on the image registration and multi-sensor fusion technology. Experiments demonstrate that the proposed method can effectively obtain enhanced visualization images containing clearer terrain information than the SEM source images, thereby providing new references for measuring and analyzing microstructures.

Brevilin A ameliorates sepsis-induced cardiomyopathy through inhibiting NLRP3 inflammation.

Background: Sepsis is a systemic inflammatory disease, and Brevilin A (BA) has a powerful anti-inflammatory effect. However, whether BA has a similar effect on septic cardiomyopathy remains unclear. This study aimed to investigate the effect and mechanism of BA in septic cardiomyopathy. Methods: First, a model of septic cardiomyopathy was constructed in vitro and in vivo. The expression of the cardiac injury markers, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammation factors and its upstream modulator NF-κB was detected by real-time polymerase chain reaction and western blotting. Cardiac function was measured using echocardiography, cell viability was detected using the methyl thiazolyl tetrazolium assay. To further investigate the effects of BA on septic cardiomyopathy, different concentrations of BA were used. The experiment was divided into control group, LPS induced- group, LPS+2.5, 5.0, 10.0 µM BA treatment group of the vitro model, and the Sham, CLP, CLP+10, 20, 30 mg/kg BA treatment groups of the rat vivo model. Lastly, cardiac injury, NLRP3 inflammation, and cardiac function were assessed in each group. Results: The mRNA and protein expression of cardiac inflammation and injury genes were significantly increased in the in vitro and in vivo sepsis cardiomyopathy models. When different concentrations of BA were used in sepsis cardiomyopathy in vivo and in vitro, the above-mentioned myocardial inflammation and injury factors were suppressed to varying degrees, cell viability increased, cardiac function improved, and the survival rate of rats also increased. Conclusion: BA ameliorated sepsis cardiomyopathy by inhibiting NF-κB/NLRP3 inflammation activation.

Effect of co-application of straw and various nitrogen fertilizers on N2O emission in acid soil.

In order to explore the alteration of N transformation and N2O emissions in acid soil with the co-application of straw and different types of nitrogen (N) fertilizers, an incubation experiment was carried out for 40 days. There are totally five treatments in the study: (a) without straw and N fertilizer (N0), (b) straw alone application (SN0), (c) straw with NH4Cl (SN1), (d) straw with NaNO3 (SN2), and (e) straw with NH4NO3 (SN3). N2O emissions, soil physicochemical properties, and abundance/activity of ammonia-oxidizing archaea (AOA) were measured. The results showed that the combined application of straw and N enhanced N2O emissions, particularly, SN2 and SN3 treatments. Moreover, the soil pH was lower in co-application treatments and the average decreasing rate was 9.69%. Specially, the pH was lowest in the SN1 treatment. The results of correlation analysis indicated a markedly negative relationship between pH and N2O, as well as a negative relationship between pH and net mineralization rate. These findings suggest that pH alteration can affect the N transformation process in soil and thus influence N2O emissions. In addition, the dominant AOA at the genus level in the SN2 treatment was Nitrosopumilus, and Candidatus nitrosocosmicus in the SN3 treatment. The reshaped AOA structure can serve as additional evidence of the changes in the N transformation process. In conclusion, as the return of straw, the cumulation of N2O from arable acid soil depends on the form of N fertilizer. It is also important to consider how N fertilizer is applied to reduce the possibility of N being lost in the soil as gas.

UGCG modulates heart hypertrophy through B4GalT5-mediated mitochondrial oxidative stress and the ERK signaling pathway.

Mechanical pressure overload and other stimuli often contribute to heart hypertrophy, a significant factor in the induction of heart failure. The UDP-glucose ceramide glycosyltransferase (UGCG) enzyme plays a crucial role in the metabolism of sphingolipids through the production of glucosylceramide. However, its role in heart hypertrophy remains unknown. In this study, UGCG was induced in response to pressure overload in vivo and phenylephrine stimulation in vitro. Additionally, UGCG downregulation ameliorated cardiomyocyte hypertrophy, improved cardiomyocyte mitochondrial oxidative stress, and reduced the ERK signaling pathway. Conversely, UGCG overexpression in cardiomyocytes promoted heart hypertrophy development, aggravated mitochondrial oxidative stress, and stimulated ERK signaling. Furthermore, the interaction between beta-1,4-galactosyltransferase 5 (B4GalT5), which catalyses the synthesis of lactosylceramide, and UGCG was identified, which also functions as a synergistic molecule of UGCG. Notably, limiting the expression of B4GalT5 impaired the capacity of UGCG to promote myocardial hypertrophy, suggesting that B4GalT5 acts as an intermediary for UGCG. Overall, this study highlights the potential of UGCG as a modulator of heart hypertrophy, rendering it a potential target for combating heart hypertrophy.

" Assessing the impact of biochar on microbes in acidic soils: Alleviating the toxicity of aluminum and acidity".

In arable soils, anthropogenic activities such as fertilizer applications have intensified soil acidification in recent years. This has resulted in frequent environmental problems such as aluminum (Al) and H+ stress, which negatively impact crop yields and quality in acidic soils. Biochar, as a promising soil conditioner, has attracted much attention globally. The present study was conducted in a greenhouse by setting up 2% biochar rate to investigate how biochar relieves Al3+ hazards in acidic soil by affecting soil quality, soil environment, and soil microbiomes. The addition of biochar significantly improved soil fertility and enzyme activities, which were attributed to its ability to enhance the utilization of soil carbon sources by influencing the activity of soil microorganisms. Moreover, the Al3+ contents were significantly decreased by 66.61-88.83% compared to the C0 level (without biochar treatment). In particular, the results of the 27Al NMR suggested that forms of AlVI (Al(OH)2+, Al(OH)+ 2, and Al3+) were increased by 88.69-100.44% on the surface of biochar, reducing the Al3+ stress on soil health. The combination of biochar and nitrogen (N) fertilizer contributed to the augmentation of bacterial diversity. The application of biochar and N fertilizer increased the relative abundance of the majority of bacterial species. Additionally, the application of biochar and N fertilizer had a significant impact on soil microbial metabolism, specifically in the biosynthesis of secondary metabolites (lipids and organic acids) and carbon metabolic ability. In conclusion, biochar can enhance soil microbial activity and improve the overall health of acidic soil by driving microbial metabolism. This study offers both theoretical and technical guidance for enhancing biochar in acidified soil and promoting sustainable development in farmland production.

Identify Tcea3 as a novel anti-cardiomyocyte hypertrophy gene involved in fatty acid oxidation and oxidative stress.

Background: Chronic pressure overload triggers pathological cardiac hypertrophy that eventually leads to heart failure. Effective biomarkers and therapeutic targets for heart failure remain to be defined. The aim of this study is to identify key genes associated with pathological cardiac hypertrophy by combining bioinformatics analyses with molecular biology experiments. Methods: Comprehensive bioinformatics tools were used to screen genes related to pressure overload-induced cardiac hypertrophy. We identified differentially expressed genes (DEGs) by overlapping three Gene Expression Omnibus (GEO) datasets (GSE5500, GSE1621, and GSE36074). Correlation analysis and BioGPS online tool were used to detect the genes of interest. A mouse model of cardiac remodeling induced by transverse aortic constriction (TAC) was established to verify the expression of the interest gene during cardiac remodeling by RT-PCR and western blot. By using RNA interference technology, the effect of transcription elongation factor A3 (Tcea3) silencing on PE-induced hypertrophy of neonatal rat ventricular myocytes (NRVMs) was detected. Next, gene set enrichment analysis (GSEA) and the online tool ARCHS4 were used to predict the possible signaling pathways, and the fatty acid oxidation relevant pathways were enriched and then verified in NRVMs. Furthermore, the changes of long-chain fatty acid respiration in NRVMs were detected using the Seahorse XFe24 Analyzer. Finally, MitoSOX staining was used to detect the effect of Tcea3 on mitochondrial oxidative stress, and the contents of NADP(H) and GSH/GSSG were detected by relevant kits. Results: A total of 95 DEGs were identified and Tcea3 was negatively correlated with Nppa, Nppb and Myh7. The expression level of Tcea3 was downregulated during cardiac remodeling both in vivo and in vitro. Knockdown of Tcea3 aggravated cardiomyocyte hypertrophy induced by PE in NRVMs. GSEA and online tool ARCHS4 predict Tcea3 involved in fatty acid oxidation (FAO). Subsequently, RT-PCR results showed that knockdown of Tcea3 up-regulated Ces1d and Pla2g5 mRNA expression levels. In PE induced cardiomyocyte hypertrophy, Tcea3 silencing results in decreased fatty acid utilization, decreased ATP synthesis and increased mitochondrial oxidative stress. Conclusion: Our study identifies Tcea3 as a novel anti-cardiac remodeling target by regulating FAO and governing mitochondrial oxidative stress.

Can the co-application of biochar and different inorganic nitrogen fertilizers repress N2O emissions in acidic soil?

The sole application of nitrogen (N) fertilizer with lower N2O emission potential or combined with biochar may help for mitigating N2O production. However, how biochar applied with various inorganic N fertilizers affected N2O emission in acidic soil remains unclear. Thus, we examined N2O emission, soil N dynamics and relating nitrifiers (i.e., ammonia-oxidizing archaea, AOA) in acidic soil. The study contained three N fertilizers (including NH4Cl, NaNO3, NH4NO3) and two biochar application rates (i.e., 0% and 0.5%). The results indicated that the alone application of NH4Cl produced more N2O. Meanwhile, the co-application of biochar and N fertilizers enhanced N2O emission as well, especially in the combined treatment of biochar and NH4NO3. Soil pH was decreased with the application of various N fertilizers, especially with NH4Cl, and the average decrease rate was 9.6%. Meanwhile, correlation analysis showed a negative relationship between N2O and pH, dramatically, which might indicate that the alteration of pH was one factor relating to N2O emission. However, there was no difference between the same N addition treatments with or without biochar on pH. Interestingly, in the combined treatment of biochar and NH4NO3, the lowest net nitrification rate and net mineralization rate appeared during days 16-23. Meanwhile, the highest emission rate of N2O in the same treatment also appeared during days 16-23. The accordance might indicate that N transformation alteration was another factor relating to N2O emissions. In addition, compared to NH4NO3 alone application, co-applied with biochar had a lower content of Nitrososphaera-AOA, which was a main contributor to nitrification. The study emphasizes the importance of using a suitable form of N fertilizers and further indicates that two factors, namely alteration of pH and N transformation rate, are related to N2O emission. Moreover, in future studies, it is necessary to explore the soil N dynamics controlled by microorganisms.

Fucoxanthin alleviated atherosclerosis by regulating PI3K/AKT and TLR4/NFκB mediated pyroptosis in endothelial cells.

Fucoxanthin, a type of natural xanthophyll carotenoid, is mainly present in seaweeds and various microalgae. This compound has been proved to possess multiple functions including antioxidation, anti-inflammation and anti-tumor. Atherosclerosis is widely deemed as a chronic inflammation disease, and as the basis of vascular obstructive disease. However, there is rare research about fucoxanthin's effects on atherosclerosis. In this study, we demonstrated that the plaque area of mice treated with fucoxanthin was significantly reduced compared to the group that did not receive fucoxanthin. In addition, Bioinformatics analysis showed that PI3K/AKT signaling might be involved in the protective effect of fucoxanthin, and this hypothesis was then verified in vitro endothelial cell experiments. Besides, our further results showed that endothelial cell mortality measured by TUNEL and flow cytometry was significantly increased in the oxidized low-density lipoprotein (ox-LDL) treatment group while significantly decreased in the fucoxanthin treatment group. In addition, the pyroptosis protein expression level in the fucoxanthin group was significantly lower than that in the ox-LDL group, which indicated that fucoxanthin improved the pyroptosis level of endothelial cells. Furthermore, it was revealed that TLR4/NFκB signaling were also participated in the protection of fucoxanthin on endothelial pyroptosis. Moreover, the protection of fucoxanthin on endothelial cell pyroptosis was abrogated when PI3K/AKT was inhibited or TLR4 was overexpressed, which further suggested the anti-pyroptosis effect of fucoxanthin was mediated through regulations of PI3K/AKT and TLR4/NFκB signaling.