Global evidence for joint effects of multiple natural and anthropogenic drivers on soil nitrogen cycling.

Global soil nitrogen (N) cycling remains poorly understood due to its complex driving mechanisms. Here, we present a comprehensive analysis of global soil δ15N, a stable isotopic signature indicative of the N input-output balance, using a machine-learning approach on 10,676 observations from 2670 sites. Our findings reveal prevalent joint effects of climatic conditions, plant N-use strategies, soil properties, and other natural and anthropogenic forcings on global soil δ15N. The joint effects of multiple drivers govern the latitudinal distribution of soil δ15N, with more rapid N cycling at lower latitudes than at higher latitudes. In contrast to previous climate-focused models, our data-driven model more accurately simulates spatial changes in global soil δ15N, highlighting the need to consider the joint effects of multiple drivers to estimate the Earth's N budget. These insights contribute to the reconciliation of discordances among empirical, theoretical, and modeling studies on soil N cycling, as well as sustainable N management.

Shifts in soil ammonia-oxidizing community maintain the nitrogen stimulation of nitrification across climatic conditions.

Anthropogenic nitrogen (N) loading alters soil ammonia-oxidizing archaea (AOA) and bacteria (AOB) abundances, likely leading to substantial changes in soil nitrification. However, the factors and mechanisms determining the responses of soil AOA:AOB and nitrification to N loading are still unclear, making it difficult to predict future changes in soil nitrification. Herein, we synthesize 68 field studies around the world to evaluate the impacts of N loading on soil ammonia oxidizers and nitrification. Across a wide range of biotic and abiotic factors, climate is the most important driver of the responses of AOA:AOB to N loading. Climate does not directly affect the N-stimulation of nitrification, but does so via climate-related shifts in AOA:AOB. Specifically, climate modulates the responses of AOA:AOB to N loading by affecting soil pH, N-availability and moisture. AOB play a dominant role in affecting nitrification in dry climates, while the impacts from AOA can exceed AOB in humid climates. Together, these results suggest that climate-related shifts in soil ammonia-oxidizing community maintain the N-stimulation of nitrification, highlighting the importance of microbial community composition in mediating the responses of the soil N cycle to N loading.

Life expectancy and mental related burden of disease among people living with HIV/AIDS.

Mental health problems leads to serious disease burden among people living with HIV/AIDS (PLHIV). The study aimed at measuring the mental disorders-caused burden of disease based on PLHIV in mainland China. The data used was from the national HIV/AIDS case reporting system, life expectancy (LE) and LE-eliminated suicide were evaluated by the life-table method. The total YLLs and YLLs caused by suicide in each age group were calculated. The disability weights were estimated by the scale of depression symptoms (CES-D) from the multi-center cross-sectional survey, then calculated the corresponding YLDs as a burden of mental illness among PLHIV. Results showed that the LE had been prolonged by implementing antiviral therapy for PLHIV. The proportion of YLLs caused by suicide was the highest (5·46%) in the 15-24 age group. The YLDs in the 25-34 age group were the highest. The YLLs caused by suicide in males were higher than those in the same age group of females. The YLDs and YLLs were higher in heterosexual-infected PLHIV than in homosexual-infected PLHIV, except for YLLs in the 25-34 age group. In summary, this study first provided localized data on the disease burden caused by mental health problems among PLHIV.

Downregulation of miR-337-3p in hypoxia/reoxygenation neuroblastoma cells increases KCTD11 expression.

Neurodegeneration is linked to the progressive loss of neural function and is associated with several diseases. Hypoxia is a hallmark in many of these diseases, and several therapies have been developed to treat this disease, including gene expression therapies that should be tightly controlled to avoid side effects. Cells experiencing hypoxia undergo a series of physiological responses that are induced by the activation of various transcription factors. Modulation of microRNA (miRNA) expression to alter transcriptional regulation has been demonstrated to be beneficial in treating multiple diseases, and in this study, we therefore explored potential miRNA candidates that could influence hypoxia-induced nerve cell death. Our data suggest that in mouse neuroblasts Neuro-2a cells with hypoxia/reoxygenation (H/R), miR-337-3p is downregulated to increase the expression of Potassium channel tetramerization domain containing 11 (KCTD11) and subsequently promote apoptosis. Here, we demonstrate for the first time that KCTD11 plays a role in the cellular response to hypoxia, and we also provide a possible regulatory mechanism by identifying the axis of miR-337-3p/KCTD11 as a promising candidate modulator of nerve cell survival after H/R exposure.

CuCo2O4 nanoneedle arrays growth on carbon cloth as a non-enzymatic electrochemical sensor with low detection limit ketoprofen recognition.

An electrochemical sensor for detecting ketoprofen was constructed by in-situ grown copper cobaltate (CuCo2O4) nanoneedle arrays on a carbon cloth (CC) substrate. The resulting porous nanoneedle arrays not only expose numerous electrochemically active sites but also significantly enhance the electrochemical apparent active area and current transmission efficiency. By leveraging its electrochemical properties, the sensor achieves an impressive detection limit for ketoprofen of 0.7 pM, with a linear range spanning from 2 pM ~ 2 µM. Furthermore, the sensor exhibits remarkable reproducibility, anti-interference capabilities, and stability. Notably, the developed sensor also performed ketoprofen detection on real samples (including drug formulations and wastewater) and demonstrated excellent recognition ability. These exceptional performances can be attributed to the direct growth of CuCo2O4 nanoneedle arrays on the CC substrate, which facilitates a robust electrical connection, provides abundant electrocatalytic active sites, and expands the apparent active area. Consequently, these improvements contribute to the efficient trace detection capabilities of the ketoprofen sensor.

Revisiting the relationships between soil nitrous oxide emissions and microbial functional gene abundances.

A conceptual framework proposes that soil N2 O emissions are more likely related to microbial functional gene abundances based on laboratory experiments than in-situ observations. This framework has largely contributed to reconciling the disputation on linking soil N2 O emissions with functional gene abundances, but the direct evidence is lacking. Wei et al. (2023) provided new evidence to support this framework, showing that O2 dynamics were a better predictor of in-situ soil N2 O emissions than were functional gene abundances. Before the observations can inform N2 O modeling and support sustainable nitrogen management, however, some additional efforts are needed to revisit the relationships between in-situ soil N2 O emissions and functional gene abundances.

Role of creatine supplementation on the myofibre characteristics and muscle protein synthesis of grass carp (Ctenopharyngodon idellus).

To assess the role of dietary creatine on myofibre characteristics and protein synthesis in muscle, we fed grass carp (Ctenopharyngodon idellus, initial body weight: 88·47 ± 1·44 g) creatine-supplemented diets (1·84, 5·91, 8·48 and 15·44 g/kg diet) for 8 weeks. Creatine supplementation did not affect growth performance, but significantly increased creatine contents in muscle and liver. At 8·48 g/kg, creatine decreased the activities of alanine transaminase and aspartate aminotransferase in serum and improved hardness and chewiness of muscle due to shorter myofibre mean diameter, higher myofibre density and the frequencies of the diameters of classes I and III and collagen content, longer sarcomere length and upregulated mRNA levels of slow myosin heavy chains. Creatine supplementation upregulated the mRNA expressions of myogenic regulatory factors. The 8·48 g/kg creatine-supplemented diet significantly increased the contents of protein, total amino acids (AA), essential AA and free flavour AAs in muscle, the protein levels of insulin-like growth factor I, myogenic differentiation antigen and PPAR-γ coactlvator-1α in muscle and stimulated the phosphorylation of target of rapamycin (TOR) pathway in muscle. In summary, 8·48 mg/kg creatine improved fish health and skeletal muscle growth and increased hardness and protein synthesis in muscle of grass carp by affecting myofibre characteristics and the TOR signalling pathway. A second-order regression model revealed that the optimal dietary creatine supplementation of grass carp ranges between 8·48 and 12·04 g/kg.

A graphene-like semiconducting BC2P monolayer as a promising material for a Li-ion battery and CO2 adsorbent.

Searching for high-performance anode materials and CO2 adsorption materials are key factors for next-generation renewable energy technologies and mitigation of the greenhouse effect. Herein, we report a novel two-dimensional (2D) BC2P monolayer with great potential as an anode material for lithium-ion batteries (LIBs) and as a material for CO2 adsorption. The adsorption energies of Li atoms and CO2 molecules on the BC2P supercell are negative enough to assure stability and safety under operating conditions. More intriguingly, the BC2P monolayer possesses a very high theoretical capacity of 1018.8 mA g h-1 for LIBs. In addition, the diffusion energy barriers of Li on the BC2P supercell are 0.26 and 0.87 eV, showing good charge/discharge capability, and the electrode potential of Li is beneficial to their performance as an anode material. Moreover, four chemical and three physical adsorption sites were verified, indicating that the CO2 molecule was effectively adsorbed on the BC2P supercell. These desirable properties make the BC2P monolayer a promising 2D material for application in LIBs and for CO2 adsorbents aimed at highly efficient CO2 capture.

[Analysis of a Chinese pedigree affected with Hereditary coagulation factor â « deficiency due to compound heterozygous variants of F12 gene].

OBJECTIVE: To analyze the clinical phenotypes and genetic variants of a Chinese pedigree affected with Hereditary coagulation factor Ⅻ (FⅫ) deficiency. METHODS: A pedigree presented at the First Affiliated Hospital of Air Force Medical University on December 24,2021 was selected as the study subject. Activated partial thromboplastin time (APTT) and coagulation factor Ⅻ activity (FⅫ:C) were determine by a clotting method, and FⅫ antigen was detected with an ELISA assay. Following the extraction of genomic DNA, all exons and flanking regions of the F12 gene were subjected to Sanger sequencing. Clustalx-2.1-win, PROVEAN and Swiss-PDB Viewer software was used to analyze the conservation of amino acids at the variant sites, impact of of the variants on the amino acid substitutions and the protein structure. RESULTS: The APTT of the proband has prolonged to 70.2 s. Her FⅫ:C and FⅫ:Ag have decreased to 12% and 13%, respectively. DNA sequencing revealed that the proband has harbored c.346G>A (p.Gly97Ser) and c.1583C>A (p.Ser509Tyr) heterozygous compound missense variants in exons 5 and 13 of the F12 gene, respectively. Her father and sister were heterozygous carriers for the c.346G>A (p.Gly97Ser) variant, whilst her mother and brother were heterozygous for the c.1583C>A (p.Ser509Tyr) variant. CONCLUSION: The c.346G>A (p.Gly97Ser) and c.1583C>A (p.Ser509Tyr) compound heterozygous variants of the F12 gene probably underlay the pathogenesis of hereditary coagulation FⅫ deficiency in this pedigree.

Elevational shifts in foliar-soil δ15 N in the Hengduan Mountains and different potential mechanisms.

The natural abundance of stable nitrogen isotopes (δ15 N) provides insights into the N dynamics of terrestrial ecosystems, the determination of which is considered an effective approach for gaining a better understanding ecosystem N cycling. However, there is currently little information available regarding the patterns and mechanisms underlying the variation in foliar-soil δ15 N among mountain ecosystems. In this study, we examined the determinants of foliar-soil δ15 N in association with N transportation rates along an elevational gradient in the Hengduan Mountains. Despite the relatively high levels of available N produced from high N fixation and mineralization, we detected the lowest levels of foliar δ15 N at 3500 m a.s.l., reflecting the stronger vegetation N limitation at medium high elevations. The enhanced vegetation N limitation was driven by the combined effects of higher microbial immobilization and inherent plant dynamic (the shifts of δ15 N in vegetation preference, including vegetation community) with changing climate along the elevational gradient. Unexpectedly, we established that soil δ15 N was characterized by an undulating rise and uncoupled correlation with foliar δ15 N with increasing elevation, thereby indicating that litter input might not be a prominent driver of soil δ15 N. Conversely, soil nitrification and denitrification were found to make a more pronounced contribution to the pattern of soil δ15 N along the elevational gradient. Collectively, our results serve to highlight the importance of microbial immobilization in soil N dynamics and provide novel insights that will contribute to enhancing our understanding of N cycling as indicated by foliar-soil δ15 N along elevational gradients.

Detection and Gene Mutation Analysis of Three Variations in Two Unrelated Chinese Hereditary Coagulation Factor XI Deficiency Families.

INTRODUCTION: Three variations including a novel F11 gene variation were detected in two unrelated Chinese families with coagulation factor XI deficiency, and their possible pathogenesis was elucidated. METHODS: The genomic DNA of the probands' pedigrees was extracted, and all exons and flanking sequences of F11 gene were subjected to PCR amplification and Sanger sequencing. ClustalX-2.1-win, Mutation Taster, and Swiss-Pdb Viewer software were used to analyze the conservation and impact of the variations on protein function and structure. RESULTS: DNA sequencing showed that the proband one had p.Gly350Glu and p.Trp501stop complex heterozygous variations, while the proband two took p.Pro338Leu and p.Trp501stop compound heterozygous variations. Conservation, structural, and functional analysis of variant amino acids indicated that these three variations were harmful and probably affected the structure and function of the variable protein. CONCLUSIONS: Three variations including p.Pro338Leu, p.Gly350Glu, and p.Trp501stop responsible for the reduction of the FXI activities were herein detected. Notably, the p.Pro338Leu variation was discovered for the first time in the world. Furthermore, the p.Gly350Glu was first reported in China.

Overexpression of Kininogen-1 aggravates oxidative stress and mitochondrial dysfunction in DOX-induced cardiotoxicity.

BACKGROUND: Doxorubicin (DOX) is a widely used cancer chemotherapeutic drug with cardiotoxicity effect limiting its clinical use. DOX induced cardiotoxicity is mediated by oxidative stress and mitochondrial damage. Kininogen-1(KNG1) is an important pro-inflammatory and pro-oxidant factor, and studies have found that it can aggravate lung and brain damage. However, it has not been known in terms of cardiotoxicity. Therefore, the purpose of this study is to understand the mechanism of KNG1 in DOX-induced heart injury. METHODS: C57 mice were selected for intraperitoneal injection of DOX. The model was successfully established, and fresh ventricular tissues were isolated from the ctrl group and the DOX group for mass spectrometry analysis to screen for differentially expressed proteins. Nuclear Factor-Like 2 (Nrf2), Heme Oxygenase 1 (HO-1), 4-Hydroxynonenal (4-HNE) were used to evaluate oxidative stress level, Cytochrome C Oxidase Subunit 4 (COX4) was used to evaluate mitochondria function. Mitochondrial inner membrane potential (ΔΨm) was monitored with JC-1 fluorescence. RESULTS: KNG1 was identified as a core gene which was highly expressed in the DOX myocardial injury model. Following this, an overexpression adenovirus was constructed, and KNG1 was overexpressed in vivo (mice) and in vitro (neonatal mouse cardiomyocytes (NMCMs)). It was found that overexpression of KNG1 can aggravate heart oxidative stress and mitochondrial damage. Besides, a knockdown KNG1 model was constructed, and the low expression of KNG1 was performed in cytology. It was found that knockdown of KNG1 can improve cardiomyocyte oxidative stress and mitochondrial damage caused by DOX. Nrf2 is an important antioxidant factor. Further, following KNG1 knock down, Nrf2 was also knocked down, and found that its cardiomyocyte protective effect was weakened. CONCLUSION: The overexpression of KNG1 aggravates the oxidative stress and mitochondrial damage of the heart in vivo and in vitro, which might play a role by regulating Nrf2, providing a therapeutic target for DOX-induced cardiotoxicity.

Differential response of soil CO2 , CH4 , and N2 O emissions to edaphic properties and microbial attributes following afforestation in central China.

Land use change specially affects greenhouse gas (GHG) emissions, and it can act as a sink/source of GHGs. Alterations in edaphic properties and microbial attributes induced by land use change can individually/interactively contribute to GHG emissions, but how they predictably affect soil CO2 , CH4 , and N2 O emissions remain unclear. Here, we investigated the direct and indirect controls of edaphic properties (i.e., dissolved organic carbon [DOC], soil organic C, total nitrogen, C:N ratio, NH4+ -N, NO3- -N, soil temperature [ST], soil moisture [SM], pH, and bulk density [BD]) and microbial attributes (i.e., total phospholipid fatty acids [PLFAs], 18:1ω7c, nitrifying genes [ammonia-oxidizing archaea, ammonia-oxidizing bacteria], and denitrifying genes [nirS, nirK, and nosZ]) over the annual soil CO2 , CH4 , and N2 O emissions from the woodland, shrubland, and abandoned land in subtropical China. Soil CO2 and N2 O emissions were higher in the afforested lands (woodland and shrubland) than in the abandoned land, but the annual cumulative CH4 uptake did not significantly differ among all land use types. The CO2 emission was positively associated with microbial activities (e.g., total PLFAs), while the CH4 uptake was tightly correlated with soil environments (i.e., ST and SM) and chemical properties (i.e., DOC, C:N ratio, and NH4+ -N concentration), but not significantly related to the methanotrophic bacteria (i.e., 18:1ω7c). Whereas, soil N2 O emission was positively associated with nitrifying genes, but negatively correlated with denitrifying genes especially nosZ. Overall, our results suggested that soil CO2 and N2 O emissions were directly dependent on microbial attributes, and soil CH4 uptake was more directly related to edaphic properties rather than microbial attributes. Thus, different patterns of soil CO2 , CH4 , and N2 O emissions and associated controls following land use change provided novel insights into predicting the effects of afforestation on climate change mitigation outcomes.

Significance of the p.Phe218Ser and p.Gly304Glu F5 Variants in Hereditary Factor V Deficiency.

Hereditary factor V (FV) deficiency is a rare autosomal recessive bleeding disorder caused by F5 gene mutations. The objective of this study was to investigate the p.Phe218Ser and p.Gly304Glu variants found in 2 families with hereditary FV deficiency. The FV activity (FV:C) and FV antigen (FV:Ag) were measured by clotting and ELISA, respectively. The F5 gene and sequence conservation were analyzed by direct sequencing and ClustalX-2.1-win, respectively. One proband carried a homozygous p.Phe218Ser (c.653T>C) mutation, with FV:C and FV:Ag decreased to 11 and 14%, respectively. The other proband carried a heterozygous p.Gly304Glu (c.911G>A) mutation, with FV:C and FV:Ag reduced to 55 and 62%, respectively. Phe218 and Gly304 were highly conserved in the homologous gene in 9 other species. We hypothesized that the p.Phe218Ser and p.Gly304Glu variants are deleterious and responsible for the reduction in FV:C and FV:Ag.

Identification of differentially expressed genes associated with lung adenocarcinoma via bioinformatics analysis.

Lung adenocarcinoma (LUAD) with extremely high morbidity as well as mortality is still in the exploration stage of pathogenesis and treatment. This study aimed to screen and identify differentially expressed genes (DEGs) associated with LUAD via bioinformatics analysis. Three LUAD microarray datasets, GSE116959, GSE68571 and GSE40791, were selected from the Gene Expression Omnibus (GEO) database to analyze the DEGs. 128 DEGs were identified in all, incorporating 36 upregulated and 92 downregulated. Function and pathway enrichment analyses showed that metabolic pathways were their main signaling pathways. After that, seven hub genes including VWF, SPP1, PECAM1, TOP2A, CDK1, UBE2C and KIF23 were mined by the protein-protein interaction (PPI) network. Gene expression analysis, TNM and survival analysis of these hub genes were performed via Gene Expression Profiling Interactive Analysis (GEPIA) online database. Further analysis indicated that TOP2A, CDK1, UBE2C and KIF23 were related to the stage of LUAD patients and overall survival. Then, we verified the relative expression levels of TOP2A, CDK1, UBE2C and KIF23 in LUAD cell lines by qRT-PCR. In conclusion, this study indicated that the four hub genes screened out by bioinformatics analysis were differentially expressed in LUAD compared to normal sample and might be prognostic markers of LUAD.

Ionic liquid([C12mim][PF6])-assisted synthesis of TiO2 /Ti2O (PO4)2 nanosheets and the chemoresistive gas sensing of trimethylamine.

The architecture of PO43- modified 2D TiO2 nanosheets was constructed by ionic liquids (ILs)-assisted hydrothermal method. The nanosheet structure can be regulated by the addition of different amount of ionic liquid. Using the composite nanosheets  a chemoresistive gas sensor was prepared for trimethylamine (TMA) detection. Most reported TMA sensors need to be operated at a relatively high operating temperature, but in this paper, the as-synthesized PO43--modified 2D TiO2/Ti2O(PO4)2 nanosheet sensor has high response (S = 87.46), short response time (14.6 s), and good reproducibility to 100 ppm TMA gas, when the temperature is 170 °C. In contrast to the single-phase TiO2 sensor, the gas-sensing property of the composite one is obviously enhanced. Moreover, its response shows excellent linear relationship with TMA concentration from 0.2 to 500 ppm, and a detection limit of 0.2 ppm. The TMA detection mechanism was investigated by analyzing the changes of the surface adsorption oxygen content by XPS and gaseous products using gas chromatography after the sensor was in contact with TMA.

Low-dose nicotine promotes autophagy of cardiomyocytes by upregulating HO-1 expression.

Nicotine as a major component of addiction in cigarettes has been reported to play protective roles in some pathological processes. It is reported that activation of the nicotinic acetylcholine receptor also has a cardioprotective effect. Thus, in our study, we investigated the effect and mechanism of nicotine on the autophagy of cardiomyocytes, and whether nicotine protects cardiomyocytes against palmitic acid (PA) injury. The results indicated that low-dose nicotine promoted neonatal mouse cardiac myocytes (NMCMs) autophagy and accelerated autophagic flux while inhibiting NMCMs apoptosis, but high-dose nicotine inhibited autophagy and promoted apoptosis. Moreover, low-dose nicotine upregulated heme oxygenase-1 (HO-1) expression and knocking down HO-1 abolished the effects of nicotine on the autophagy and apoptosis of NMCMs. Methyllycaconitine citrate (α7-nAChR blocker, MLA) inhibited HO-1 expression and the effects of nicotine on autophagy and apoptosis of NMCMs. Furthermore, low-dose nicotine improved the inhibited autophagy and increased apoptosis induced by palmitic acid (PA) in NMCMs and these effects were reversed by knocking down HO-1. In conclusion, our data suggested that low-dose nicotine promoted autophagy and inhibited apoptosis of cardiomyocytes by upregulating HO-1.

Multifunctionality of biocrusts is positively predicted by network topologies consistent with interspecies facilitation.

The potential of biodiversity loss to impair the delivery of ecosystem services has motived ecologists to better understand the relationship between biodiversity and ecosystem functioning. Although increasing evidence underlines the collective contribution of different biodiversity components on the simultaneous performance of multiple functions (multifunctionality), we know little about the trade-offs between individual diversity effects and the extent to which they determine multifunctionality differentially. Here, at a subcontinental scale of 62 dryland sites, we show in phototrophic microbiota of biological soil crusts (biocrusts) that, whereas richness alone is unable to guarantee the maxima of multifunctional performance, interspecies facilitation and compositional identity are particularly stronger but often neglected predictors. The inconsistent effects of different biodiversity components imply that soil multifunctionality can be lost despite certain species remaining present. Moreover, we reveal a significant empirical association between species functional importance and its topological feature in co-occurrence networks, indicating a functional signal of species interaction. Nevertheless, abundant species tend to isolate and merely interact within small topological structures, but rare species were tightly connected in complicated network modules. Our findings suggest that abundant and rare species of soil phototrophs exhibit distinct functional relevance. These results give a comprehensive view of how soil constructive species drive multifunctionality in biocrusts and ultimately promote a deeper understanding of the consequences of biodiversity loss in real-world ecosystems.

Asymmetric response of soil methane uptake rate to land degradation and restoration: Data synthesis.

Land degradation and restoration profoundly affect soil CH4 uptake capacity in terrestrial ecosystems. However, a comprehensive assessment of the response of soil CH4 uptake to land degradation and restoration at global scale is not available. Here, we present a global meta-analysis with a database of 228 observations from 83 studies to investigate the effects of land degradation and restoration on the capacity of soil CH4 uptake. We found that land degradation significantly decreased the capacity of soil CH4 uptake, except the conversion of pasture to cropland where the soil CH4 uptake rate showed no response. In contrast, all types of land restoration significantly increased the capacity of soil CH4 uptake. Interestingly, the response of soil CH4 uptake rate to land degradation and restoration was asymmetric: the increased soil CH4 uptake rate in response to the land restoration was smaller compared to the decrease in CH4 uptake rate induced by the land degradation. The effect of land degradation on soil CH4 uptake rate was not dependent on the time since land use change, but the CH4 sink strength increased with the time since land restoration. The response of soil CH4 uptake rate to both land degradation and restoration was predominantly regulated by changes in the soil water-filled pore space, soil bulk density, and pH, whereas alterations in the substrate quantity and quality had negligible effect. Additionally, the effects of land degradation and restoration on soil CH4 uptake were strongly related to the mean annual precipitation and soil texture. Overall, our results provide novel insights for understanding of how land degradation and restoration can affect the CH4 sink strength of upland soils, and more importantly, our findings are beneficial to take measures to enhance the potential of soil CH4 uptake in response to global land use change.

SPR immunosensor combined with Ti4+@TiP nanoparticles for the evaluation of phosphorylated alpha-synuclein level.

A highly sensitive and specific surface plasmon resonance (SPR) method using one anti-alpha-synuclein antibody (anti-αS) and titanium phosphate nanoparticles (Ti4+@TiP) was developed for quantitative evaluation of phosphorylated αS level which was defined by the ratio of p-αS to total alpha-synuclein (t-αS) (p-αS/t-αS). The close affinities of anti-αS to αS (0.975 pM-1) and p-αS (0.938 pM-1) were obtained. Based on this fact , both αS forms were simultaneously captured and the t-αS was quantified using the anti-αS immobilized Au chip. With the selective recognition of Ti4+@TiP nanoparticles, the p-αS was quantified. The dynamic ranges of our method were 1.0~20.0 pg mL-1 for the detection of t-αS and 0.1~10.0 pg mL-1 for that of p-αS. The analysis of αS- and p-αS-spiked artificial cerebrospinal fluid samples revealed the high accuracy of the method. Furthermore, the concentrations of αS and p-αS in clinical CSF samples collected from three healthy donors were determined and displayed a high correlation with the results from a commercial ELISA kit, confirming the viability and of the proposed method. The method is convenient, economical, and practical for the evaluation of phosphorylated αS level with high sensitivity and selectivity. It is of great significance for the early diagnosis of PD and the evaluation of PD progression.Graphical abstract.