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Root exudates are an important pathway for plant-microbial interactions and are highly sensitive to climate change. However, how extreme drought affects root exudate and its components, as well as species-specific difference in response magnitude and direction, are poorly understood. In this study, root exudation rates of total carbon (C) and its components (e.g., sugar, organic acid, and amino acid) were measured under the control and drought treatments (i.e., 70% throughfall reduction) by in situ collection of four tree species with different growth rates in a subtropical forest. We also quantified soil properties, root morphological traits, and mycorrhizal infection rates to examine the driving factors underlying variations in root exudation. Our results showed that drought significantly decreased root exudation rates of total C, sugar, and amino acid by 17.8%, 30.8%, and 35.0%, respectively, but increased root exudation rate of organic acid by 38.6%. These changes were largely associated with drought-induced changes in tree growth rates, root morphological traits, and mycorrhizal infection rates. Specifically, trees with relatively high growth rates were more responsive to drought for root exudation rates compared to those with relatively low growth rates, which were closely related to root morphological traits and mycorrhizal infection rates. These findings highlight the importance of plant growth strategy in mediating drought-induced changes in root exudation rates. The trade-offs between root exudation rates, root morphological traits, and mycorrhizal symbioses in response to drought could be incorporated into land surface models to improve the prediction of climate change impacts on rhizosphere C dynamics in forest ecosystems.

Yulan Huang,* Shitong He,* Yitian Chen, Junli Sheng, Yuling Fu, Xialin Du, Yalong Yang, Honglin Liu, Zhenyu Han, Yingqi Huang, Qian Wen, Chaoying Zhou, Xinying Zhou, Shengfeng Hu, Li Ma Institute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, 510515, People’s Republic of China*These authors contributed equally to this workCorrespondence: Li Ma; Shengfeng HuInstitute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, 510515, People’s Republic of China, Email mali_61648322@smu.edu.cn; hushengfeng@smu.edu.cnBackground: As deubiquitinases (DUBs), ubiquitin C-terminal hydrolase (UCH)-L1 has been shown to play a crucial role in regulating diverse biological processes. However, its function in macrophage polarization remains unclear.Methods: We performed in vivo and in vitro experiments to investigate the role of ubiquitin carboxyl-terminal hydrolase L1 (UCHL1), a kind of DUBs, in macrophage differentiation by using UCHL1-deficiency mice.Results: We demonstrated that LPS stimulation induced UCHL1 expression in macrophages. The deficiency of UCHL1 expression decreased the expression of CD80 and CD86 but increased the expression of CD206. The expression of TNF-α, IL-6, iNOS, and IL-10 was downregulated, while that of Arg1, Ym1, and Fizz1 was upregulated in UCHL1 deficient macrophages. Moreover, we observed that UCHL1 promoted the degradation of p110α through autophagy, but paradoxically increased the activity of AKT, thereby promoting polarization of macrophages into pro-inflammatory states.Conclusion: In this study, we identified UCHL1 as a positive regulator of M1 macrophage polarization. Our findings may help in developing therapeutic interventions for the treatment of inflammatory diseases and pathogenic infections.Keywords: UCHL1, macrophages, AKT, p110α, autophagy

Objectives: This study was designated to establish a PCOS rat model with recombinant human insulin growth factor-1 (RH-IGF-1). We made assessment on the characteristics of hyperinsulinemia and hyperandrogenism in the rat model. Design: This study performed the characteristics of PCOS upon RH-IGF-1inejction and evaluated the disease process of PCOS syndrome caused by the insulin resistant pathological condition of IGF-1 based on the comparative study of in vivo test. Setting: The experiment was conducted in the experimental research center of Yinzhou NO.2 hospital, Ningbo, Zhejiang Province, China. Materials and Methods: Thirty-four female Sprague-Dawley (SD) immature rats aged 21 days, were randomly divided rats divided into two groups. Those treated with recombinant human insulin growth factor-1(RH-IGF-1) 2mg/100g daily were in RH-IGF-1 group(n=20), and those with 0.9% Sodium Chloride 0.2ml/100g daily were in the saline group (n =14). The experiment was carried out in two stages. In Stage I, rats were anesthetized upon the first estrous cycle in the saline group with tissue and blood samples collected(n=7), and rats in the RH-IGF-1 treated group were anesthetized on the 5th day after vaginal opening (VO) (n=10). In Stage II, rats in the saline group were anesthetized after three complete cycles (n=7), meanwhile, while on the 15th day after VO (n=10) for those in the RH-IGF-1 group. Results: We have found that compared with the control group, rats injected with RH-IGF-1 expressed an early vaginal opening, disordered estrous cycle, polycystic ovaries and significantly increased ovarian weight/body weight ratio. And from the perspective of hormone secretion, their androgen increased significantly and the insulin resistance index also elevated distinctly, possessing main characteristics similar to PCOS. Limitations: In this study, we were limited by the inability to examine IGF-1 in hypothalamus. IGF-1 in hypothalamus and in vitro experiments would be taken into consideration for further study in the future. Conclusions: These findings suggest that IGF-1 may be a key factor in the pathogenesis of PCOS, and the increase of androgen may be the pathological result, not the cause of polycystic ovary syndrome.

Both biochar and nitrogen (N) addition have been proposed for enhancing plant productivity and increasing carbon (C) sequestration. Although numerous studies have been conducted to examine responses of soil greenhouse gas (GHG) fluxes to biochar or N addition, biochar is often co‐applied with N fertilizer and the interactive effects of the two factors still remain unclear. In this study, we performed a meta‐analysis of manipulative experiments with 267 two‐factor observations to quantify the main and interactive effects of biochar and N addition on soil GHG fluxes at a global scale. Our results showed that biochar addition significantly increased soil CO2 emission by 10.1%, but decreased N2O emission by 14.7%. Meanwhile, N addition increased both soil CO2 and N2O emissions by 11.6% and 288%, respectively. The combination of biochar and N addition also exhibited significant positive effect on CO2 (+18.0%) and N2O (+148%) emissions, but there were non‐significant changes in CH4 fluxes. Consequently, antagonistic interaction between biochar and N addition was observed in soil GHG fluxes and their global warming potential (GWP), except for CH4 uptake showing an additive interaction. This synthesis highlights the importance of the interactive effects between biochar and N addition, providing a quantitative basis to develop sustainable strategies toward widespread application of biochar to preserve cropping system and mitigate climate change.

Mycobacterium tuberculosis, the pathogen that causes tuberculosis, exhibits complex host–pathogen interactions. Pattern recognition receptors and their downstream signaling pathways play crucial roles in determining the outcome of infection. In particular, the scaffold protein β-arrestin 2 mediates downstream signaling of G protein–coupled receptors. However, the role of β-arrestin 2 in conferring immunity against M. tuberculosis has not yet been explored. We found that β-arrestin 2 was upregulated in the lesioned regions of lung tissues in patients with tuberculosis. M. tuberculosis infection upregulated β-arrestin 2 expression in human macrophages, and silencing of β-arrestin 2 significantly enhanced bactericidal activity by enhancing the expression of proinflammatory cytokines such as TNF-α. β-Arrestin 2 was shown to inhibit the activation of the TLR2/ERK1/2 pathway and its transcriptional regulation activity upon M. tuberculosis infection. Furthermore, β-arrestin 2 transcriptionally regulates TNF-α by binding to CREB1. These observations revealed that the upregulation of β-arrestin 2 is critical for M. tuberculosis to escape immune surveillance through an unknown mechanism. Our research offers a novel interference modality to enhance the immune response against tuberculosis by targeting β-arrestin 2 to modulate the TLR2–β-arrestin 2–ERK1/2–CREB1–TNF-α regulatory axis.

Deubiquitinases (DUBs) regulate diverse biological processes and represent a novel class of drug targets. However, the biological function of only a small fraction of DUBs, especially in adaptive immune response regulation, is well-defined. In this study, we identified DUB ubiquitin-specific peptidase 12 (USP12) as a critical regulator of CD4+ T cell activation. USP12 plays an intrinsic role in promoting the CD4+ T cell phenotype, including differentiation, activation, and proliferation. Although USP12-deficient CD4+ T cells protected mice from autoimmune diseases, the immune response against bacterial infection was subdued. USP12 stabilized B cell lymphoma/leukemia 10 (BCL10) by deubiquitinating, and thereby activated the NF-κB signaling pathway. Interestingly, this USP12 regulatory mechanism was identified in CD4+ T cells, but not in CD8+ T cells. Our study results showed that USP12 activated CD4+ T cell signaling, and targeting USP12 might help develop therapeutic interventions for treating inflammatory diseases or pathogen infections.

To investigate the contributions of atmospheric particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) to heavy air pollution events in Fen-Wei Plain, China and identify their sources, a combination of wavelet analysis and low-atomic number (Z) particle electron probe X-ray microanalysis (EPMA) was utilized in a typical haze episode lasting 10 days (from Nov. 11 to 20, 2016) at Jinzhong, an inland city adjacent to Taiyuan, the capital of Shanxi Province. A 3-layer wavelet decomposition filtration was performed using the daubechies wavelet functions (db6) and the distribution of the real wavelet transformation coefficients and variance of wavelet series for various pollutants within 240 h was plotted. Five dominant periods of PM2.5 in mass concentration were observed, peaking at 101 h, 144 h, 50–51 h, 27–28 h, and 18 h in sequence from high to low in the wavelet variance chart. They were similar to those of PM10, SO2, and CO and partially overlapped with those of NO2, but different from those of O3, implying that PM2.5 have the same sources as PM10, SO2, and CO and have complicated relations with O3 and NO2. It was further found that the chemical compositions of PM2.5 in the dominant periods made great changes compared to the non-dominant periods. The relative number abundance of elemental carbon (EC) and droplets rich in CNOS (likely the mixture of carbonaceous matter with secondary aerosols such as NH4NO3 and (NH4)2SO4/NH4HSO4) in the first and second dominant period were significantly higher than that in other periods. It is concluded that coal and biomass combustion and secondary particles are still the main contributors to the wintertime heavy air pollution events in Fen-Wei Plain, suggesting that the wavelet analysis combined with low-Z particle EPMA is useful in examination of atmospheric particulate matter's origin, evolution, and roles played in haze events.

Vitamin B6 is necessary to maintain normal metabolism and immune response, especially the anti‐inflammatory immune response. However, the exact mechanism by which vitamin B6 plays the anti‐inflammatory role is still unclear. Here, we report a novel mechanism of preventing excessive inflammation by vitamin B6 via reduction in the accumulation of sphingosine‐1‐phosphate (S1P) in a S1P lyase (SPL)‐dependent manner in macrophages. Vitamin B6 supplementation decreased the expression of pro‐inflammatory cytokines by suppressing nuclear factor‐κB and mitogen‐activated protein kinases signalling pathways. Furthermore, vitamin B6–reduced accumulation of S1P by promoting SPL activity. The anti‐inflammatory effects of vitamin B6 were inhibited by S1P supplementation or SPL deficiency. Importantly, vitamin B6 supplementation protected mice from lethal endotoxic shock and attenuated experimental autoimmune encephalomyelitis progression. Collectively, these findings revealed a novel anti‐inflammatory mechanism of vitamin B6 and provided guidance on its clinical use.

Biomass allocation in plants is fundamental for understanding and predicting terrestrial carbon storage. Recent studies suggest that climate warming can differentially affect root and shoot biomass, and subsequently alter root: shoot ratio. However, warming effects on root: shoot ratio and their underlying drivers at a global scale remain unclear. Using a global synthesis of >300 studies, we here show that warming significantly increases biomass allocation to roots (by 13.1%), and two factors drive this response: mean annual precipitation of the site, and the type of mycorrhizal fungi associated with a plant. Warming-induced allocation to roots is greater in relatively drier habitats compared to shoots (by 15.1%), but lower in wetter sites (by 4.9%), especially for plants associated with arbuscular mycorrhizal fungi compared to ectomycorrhizal fungi. Root-biomass responses to warming predominantly determine the biomass allocation in terrestrial plants suggesting that warming can reinforce the importance of belowground resource uptake. Our study highlights that the wetness or dryness of a site and plants’ mycorrhizal associations strongly regulate terrestrial carbon cycle by altering biomass allocation strategies in a warmer world.

Water-dispersed glutaraldehyde (GA) non-conjugated chitosan polymer fluorophores (GCPF) with quantum yield of 16% is synthesized by stirring chitosan and GA for 6 h at room temperature in the present work. It is a facile and mild method and fluorescent GCPF can be stabled for two months. Owing to the spectral overlap of fluorescent spectrum of GCPF and absorption spectrum of picric acid (PA), a novel sensitive fluorescent method using fluorescent GCPF for PA detection from 10 nM to 50 μM via fluorescence resonance energy transfer (FRET) strategy is established. The distance between donor of GCPF and acceptor of PA (R0 value) is calculated to be 3.5 nm. FRET method using fluorescent GCPF possesses high sensitivity (LOD of 2.8 nM), and selectivity and fast response within 2 min. Moreover, fluorescent GCPF is also utilized in visual analysis of PA using cotton swabs. Fluorescence quenching effect can be observed by eyes irradiated with 365 nm ultraviolet light at cotton swabs and using GCPF solid on quartz glasses, which paves an effect and wide way for the application of fluorescent GCPF in our daily life.

It is the first time to develop electrochemiluminescence resonance energy transfer (ECRET) strategy using luminol-doped silica nanoparticles (luminol-SiNPs) for both “turn-off” detection of 2,4,6-trinitrophenol (TNP) and “turn-on” detection of anesthetic drug lidocaine hydrochloride (LDC). The spectral overlap of ECL emission of luminol-SiNPs with the absorption of TNP triggers ECRET from luminol-SiNPs to TNP and results in the decreased ECL signals. Besides, the specific interaction between TNP and LDC consumes TNP, accordingly prevents ECRET from luminol-SiNPs to TNP and achieves increasing ECL signals. The proposed ECRET strategy using luminol-SiNPs exhibits fast response (within 10 min), high sensitivity with LOD of 22.4 nM for TNP and 92.5 nM for LDC, respectively. It is also successfully applied in ECRET detection of TNP in lake water, LDC in human serum and commercial drug sample detections with satisfactory recoveries. More importantly, ECL of luminol-SiNPs is measured via linear sweep voltammetry by electrochemical reduction of dissolved oxygen at negative potential (– 1 V) and in no need of adding hydrogen peroxide (H2O2). Reactive oxygen species be generated in situ and make luminol-SiNPs system emit ECL, which makes ECL of the whole luminol-SiNPs system more stable than luminol-H2O2 system.

Roots and their rhizosphere considerably influence soil structure by regulating soil aggregate formation and stabilization. This study aimed to examine the rhizosphere effects on soil aggregation and explore potential mechanisms along secondary forest successions. Effects of roots and their rhizosphere on soil aggregation in two subtropical secondary forest successions were examined by separating soils into rhizosphere and bulk soils. Soil aggregate mean weight diameter (MWD), soil organic carbon (SOC), soil nutrients, and fine-root traits were simultaneously measured. Soil aggregate MWD increased significantly in the bulk soils along secondary forest successions, but did not differ in the rhizosphere soils. Rhizosphere effects on soil aggregate MWD (i.e., root-induced differences between the rhizosphere and bulk soils) were thus significantly higher at the early-successional stage of subtropical forest with low soil fertility than those at the late stages with high fertility. Rhizosphere significantly increased SOC and soil total nitrogen (TN) throughout the entire secondary forest successions, which was nonlinearly correlated with soil aggregate MWD. Principal components regression analysis showed that SOC was the primary abiotic factor and positively correlated with soil aggregate MWD. As for biotic factors, fine-root length density and N concentration were two important root traits having significant effects on soil aggregate stability. An improved conceptual framework was developed to advance our understanding of soil aggregation and rhizosphere effects, highlighting the roles of soil fertility (i.e., SOC and available nutrients), root traits, and forest age in driving soil aggregation. Impacts of root-derived organic compounds inputs to rhizosphere on soil aggregation were stronger at the early-successional stage of subtropical forest than those at the late stages. This succession-specific pattern in rhizosphere effects largely resulted from the nonlinear relationships between soil aggregate MWD and SOC concentration with a plateau at high SOC. Incorporating the SOC-dependent rhizosphere effects on biogeochemical cycle into Earth system models might improve the prediction of forest soil C dynamics.

Herein, the electrochemiluminescence (ECL) donor Ru(bpy)32+-doped silica nanoparticles (RuSiNPs) and acceptor methylene blue (MB) were combined to achieve electrochemiluminescence resonance energy transfer (ECRET) using the overlap of the ECL emission of RuSiNPs with the absorption of MB. Owing to the ECRET from RuSiNPs to MB, the ECL of RuSiNPs was quenched by MB. During the oxidation of glucose catalysed by MB only under an alkaline condition, MB with blue color is reduced to the colourless form methylene white by glucose; this is accompanied by the disappearance of absorbance at 650 nm. Accordingly, ECRET was inhibited after the addition of glucose to the RuSiNP and MB mixture. Therefore, the ECL “turn-on” detection of glucose was achieved via the proposed ECRET strategy. The proposed ECRET method exhibited high sensitivity for glucose detection with the limit of detection (LOD) of 85.4 nM, selectivity towards glucose in the presene of metal ions, anions, dopamine or uric acid, and fast response within 5 min; moreover, it was successfully applied for glucose detection in human serum samples, and the average recoveries of 99.33%, 99.73% and 100.07% were obtained. This widens the application of ECRET in bioanalysis.

Root exudates determine plant’s ability to acquire nutrients through influencing plant’s interactions with soil microorganisms. Recent studies suggest that plant’s associations with beneficial soil microorganisms explain variation in root exudation as plants opt to minimize the exudation cost through such symbiosis. Yet, we have a poor understanding of whether plants change their exudation rates through mycorrhizal symbiosis in soil environments with varying resource availability. Here, we report the effects of plant-mycorrhizal symbiosis on root exudation rates across a gradient of soil phosphorous (P) availability from a field experiment in subtropical forests. Root exudation rates were higher in plants partnering with arbuscular mycorrhizal fungi than those with ectomycorrhizal fungi, but this difference disappeared in soils with high P. Specific root surface area, specific root length and fine root vitality explained high root exudation in P-limited soils. These findings demonstrate that mycorrhizal symbiosis and root functional traits collectively determine the variation in root exudation in Plimited environments.

Predicting future carbon (C) dynamics in grassland ecosystems requires knowledge of how grazing and global climate change (e.g., warming, elevated CO2 , increased precipitation, drought, and N fertilization) interact to influence C storage and release. Here, we synthesized data from 223 grassland studies to quantify the individual and interactive effects of herbivores and climate change on ecosystem C pools and soil respiration (Rs). Our results showed that grazing overrode global climate change factors in regulating grassland C storage and release (i.e., Rs). Specifically, grazing significantly decreased aboveground plant C pool (APCP), belowground plant C pool (BPCP), soil C pool (SCP), and Rs by 19.1%, 6.4%, 3.1%, and 4.6%, respectively, while overall effects of all global climate change factors increased APCP, BPCP, and Rs by 6.5%, 15.3%, and 3.4% but had no significant effect on SCP. However, the combined effects of grazing with global climate change factors also significantly decreased APCP, SCP, and Rs by 4.0%, 4.7%, and 2.7%, respectively but had no effect on BPCP. Most of the interactions between grazing and global climate change factors on APCP, BPCP, SCP, and Rs were additive instead of synergistic or antagonistic. Our findings highlight the dominant effects of grazing on C storage and Rs when compared with the suite of global climate change factors. Therefore, incorporating the dominant effect of herbivore grazing into Earth System Models is necessary to accurately predict climate-grassland feedbacks in the Anthropocene.

HERC5 (homologous to mouse HERC6) is an E3 enzyme that mediates interferon-stimulated gene 15 (ISG15)-induced ISGylation of protein targets to inhibit protein function, thereby playing a vital role in various physiological functions. However, the direct role of HERC5 in macrophages after M. tuberculosis infection has not yet been studied. In the present study, we showed that HERC5 plays a vital role in promoting the inflammatory immune response. HERC5 deficiency in macrophages enhanced bacterial growth, both in vitro and in vivo. We demonstrated that HERC5 increased pro-inflammatory cytokine production in macrophages by positively regulating the PI3K-AKT signaling pathway. Finally, we found that HERC5 regulated PTEN ISGylation and degradation, thereby promoting activation of the PI3K-AKT signaling pathway. Our findings identified an essential role of HERC5 in the ISGylation of PTEN and contributed to our understanding of its protective effects against M. tuberculosis infection. Therefore, HERC5 is a potential target for therapeutic intervention against tuberculosis. Funding Information: This work was supported National Natural Science Foundation of China (81772150, 81901614, 82072242, 82070906), Guangdong Basic and Applied Basic Research Foundation (2019A1515011103). Declaration of Interests: The authors declare no competing financial interests. Ethics Approval Statement: All the mice were maintained under specific pathogen-free conditions with the approval of the Scientific Investigation Board of the Biosafety Management Committee of Southern Medical University

Deubiquitinases (DUBs) regulate diverse biological processes and represent a novel class of drug targets. However, the biological function of only a small fraction of DUBs, especially in adaptive immune response regulation, is well-defined. In this study, we identified DUB ubiquitin-specific peptidase 12 (USP12) as a critical regulator of CD4+ T cell activation. USP12 plays an intrinsic role in promoting the CD4+ T cell phenotype, including differentiation, activation, and proliferation. Although USP12-deficient CD4+ T cells protected mice from autoimmune diseases, the immune response against bacterial infection was subdued. USP12 stabilized B cell lymphoma/leukemia 10 (BCL10) by deubiquitinating, and thereby activated the NF-κB signaling pathway. Interestingly, this USP12 regulatory mechanism was identified in CD4+ T cells, but not in CD8+ T cells. Our study results showed that USP12 activated CD4+ T cell signaling, and targeting USP12 might help develop therapeutic interventions for treating inflammatory diseases or pathogen infections.

Extreme drought is likely to become more frequent and intense as a result of global climate change, which may significantly impact plant root traits and responses (i.e., morphology, production, turnover, and biomass). However, a comprehensive understanding of how drought affects root traits and responses remains elusive. Here, we synthesized data from 128 published studies under field conditions to examine the responses of 17 variables associated with root traits to drought. Our results showed that drought significantly decreased root length and root length density by 38.29% and 11.12%, respectively, but increased root diameter by 3.49%. However, drought significantly increased root:shoot mass ratio and root cortical aerenchyma by 13.54% and 90.7%, respectively. Our results suggest that drought significantly modified root morphological traits and increased root mortality, and the drought-induced decrease in root biomass was less than shoot biomass, causing higher root:shoot mass ratio. The cascading effects of drought on root traits and responses may need to be incorporated into terrestrial biosphere models to improve prediction of the climate-biosphere feedback.

Nitrogen (N) and phosphorus (P) have been demonstrated to limit terrestrial carbon (C) storage in terrestrial ecosystems. However, the reliable indicator to infer N and P limitation are still lacking, especially in subtropical forests. Here we used a terrestrial ecosystem (TECO) model framework in combination with a Bayesian approach to evaluate effects of nutrient limitation from added N/P processes and data sets on C storage capacities in two subtropical forests (Tiantong and Qianyanzhou [QYZ]). Three of the six simulation experiments were developed with assimilating data (TECO C model with C data [C-C], TECO C-N coupling model with C and N data [CN-CN], and TECO C-N-P model with C, N, and P data [CNP-CNP]), and the other three ones were simulated without assimilating data (C-only, CN-only, and CNP-only). We found that P dominantly constrained C storage capacities in Tiantong (42%) whereas N limitation decreased C storage projections in QYZ (44%). Our analysis indicated that the stoichiometry of wood biomass and soil microbe (e.g., N:P ratio) were more sensitive indicators of N or P limitation than that of other pools. Furthermore, effects of P-induced limitation were mainly on root biomass by additional P data and on both metabolic litter and soil organic carbon (SOC) by added P processes. N-induced effects were mainly from added N data that limited plant non-photosynthetic tissues (e.g., woody biomass and litter). The different effects of N and P modules on C storage projections reflected the diverse nutrient acquisition strategies associated with stand ages and plant species under nutrient stressed environment. These findings suggest that the interaction between plants and microorganisms regulate effects of nutrient availability on ecosystem C storage, and stoichiometric flexibility of N and P in plant and soil C pools could improve the representation of N and P limitation in terrestrial ecosystem models.

Knowledge of root: shoot ratio (R/S) is fundamental for our understanding of carbon allocation and storage in terrestrial ecosystems. Due to the periodic variation of water table and the difficulty of measuring belowground biomass (BGB), macrophyte biomass allocation in both coastal and inland wetlands remains unclear, especially at regional scale. In this study, 131 records of biomass allocation in wetlands were collected to examine general pattern of macrophyte R/S in relation to climate, soil, and hydrological factors in China using model selection and variance decomposition analysis. Our results showed that coastal wetlands supported higher aboveground biomass (AGB, 3.1 kg m−2) but a lower R/S (1.2) than inland ones (1.47 kg m−2 and 3.1, respectively). The positive relationships between AGB and BGB and between BGB and R/S in coastal wetlands were significantly different from those in inland wetlands, while only inland wetlands exhibited a significant negative correlation between R/S and AGB (R2 = 0.19, p

A sensitive electrochemiluminescent immunoassay for alkaline phosphatase (ALP) using p-nitrophenyl phosphate (PNPP) as substrate based on the electrochemiluminescence resonance energy transfer (ECRET) is developed. Luminol-doped silica nanoparticles (luminol-SiNPs) are prepared by water/oil (W/O) microemulsion method. PNPP convertes to p-nitrophenol (PNP) in the presence of ALP, which results in the absorption peak shifting from 360 nm to 450 nm. Herein the spectral overlap between absorption spectrum of PNP and electrochemiluminescence (ECL) spectrum of luminol-SiNPs (425 nm) makes energy transfer occur from luminol-SiNPs to PNP. In the optimized conditions, a linear relationship was obtained using this ECRET method at the concentration of ALP from 5 to 50 U/L (r = 0.9905) and with the limit of detection (LOD) of 0.8 U/L. This ECRET method exhibits sufficient specificity for ALP over other enzymes such as horseradish peroxidase, trypsin and lysozyme.

NOD-like receptor (NLR) family CARD domain containing 3 (NLRC3), an intracellular member of NLR family, is a negative regulator of inflammatory signaling pathways in innate and adaptive immune cells. Previous reports have shown that NLRC3 is expressed in dendritic cells (DCs). However, the role of NLRC3 in DC activation and immunogenicity is unclear. In the present study, we find that NLRC3 attenuates the antigen-presenting function of DCs and their ability to activate and polarize CD4+ T cells into Th1 and Th17 subsets. Loss of NLRC3 promotes pathogenic Th1 and Th17 responses and enhanced experimental autoimmune encephalomyelitis (EAE) development. NLRC3 negatively regulates the antigen-presenting function of DCs via p38 signaling pathway. Vaccination with NLRC3-overexpressed DCs reduces EAE progression. Our findings support that NLRC3 serves as a potential target for treating adaptive immune responses driving multiple sclerosis and other autoimmune disorders.

Mycobacterium tuberculosis, which primarily infects mononuclear phagocytes, remains the leading bacterial cause of enormous morbidity and mortality because of bacterial infections in humans throughout the world. The IL-1 family of cytokines is critical for host resistance to M. tuberculosis. As a newly discovered subgroup of the IL-1 family, although IL-36 cytokines have been proven to play roles in protection against M. tuberculosis infection, the antibacterial mechanisms are poorly understood. In this study, we demonstrated that IL-36γ conferred to human monocyte-derived macrophages bacterial resistance through activation of autophagy as well as induction of WNT5A, a reported downstream effector of IL-1 involved in several inflammatory diseases. Further studies showed that WNT5A could enhance autophagy of monocyte-derived macrophages by inducing cyclooxygenase-2 (COX-2) expression and in turn decrease phosphorylation of AKT/mTOR via noncanonical WNT signaling. Consistently, the underlying molecular mechanisms of IL-36γ function are also mediated by the COX-2/AKT/mTOR signaling axis. Altogether, our findings reveal a novel activity for IL-36γ as an inducer of autophagy, which represents a critical inflammatory cytokine that control the outcome of M. tuberculosis infection in human macrophages.

A method is presented for electrochemiluminescent (ECL) detection of the food additive curcumin via an energy transfer strategy and by using luminol-doped silica nanoparticles (luminol-NPs). The ECL emission of the luminol-NPs (peaking at 425 nm) is reduced in the presence of curcumin due to spectral overlap. The assay can be performed within 1 min, response is linear in the 0.1 to 100 µM curcumin concentration range, and the limit of detection is 32 nM. The method is selective over many ions, adenosine triphosphate, ascorbic acid, cysteine and folic acid. It was successfully applied to the determination of curcumin in spiked human serum and urine. The average recoveries range from 99.0 to 102.6%. Graphical abstract Electrochemiluminescence (ECL) "turn-off" detection of curcumin at levels as low as 32 nM via energy transfer using luminol-doped silica nanoparticles. No hydrogen peroxide (H

NOD‐like receptor (NLR) family CARD domain containing 3 (NLRC3), an intracellular member of NLR family, is a negative regulator of inflammatory signaling pathways in innate and adaptive immune cells. Previous reports have shown that NLRC3 is expressed in dendritic cells (DCs). However, the role of NLRC3 in DC activation and immunogenicity is unclear. In the present study, we find that NLRC3 attenuates the antigen‐presenting function of DCs and their ability to activate and polarize CD4(+) T cells into Th1 and Th17 subsets. Loss of NLRC3 promotes pathogenic Th1 and Th17 responses and enhanced experimental autoimmune encephalomyelitis (EAE) development. NLRC3 negatively regulates the antigen‐presenting function of DCs via p38 signaling pathway. Vaccination with NLRC3‐overexpressed DCs reduces EAE progression. Our findings support that NLRC3 serves as a potential target for treating adaptive immune responses driving multiple sclerosis and other autoimmune disorders.

Water-dispersed fluorescent silicon nanodots (SiNDs) were synthesized by a one-pot hydrothermal method starting from tetraethyl orthosilicate (TEOS) as silicon source and trisodium citrate as reducing reagent. The method is simple and convenient. The SiNDs, with excitation/emission peaks at 347/440 nm and with fluorescence quantum yield of 18% are shown to be viable fluorescent probes for picric acid (PA). The SiNDs strongly bind PA, and their blue fluorescence is quenched. The distance between the donor and acceptor (R0 value) is calculated from fluorescence data to be 2.1 nm. A fluorometric method was worked out that has a linear response in the 8 nM to 50 μM PA concentration range and a 0.92 nM limit of detection. The method has a fast response (2 min) and is well selective over other nitroaromatic compounds and metal ions. The average recoveries from spiked lake water samples ranged between 98.4 and 100.8%.

Global climate models predict that future precipitation regimes will largely change across the globe due to the intensification of the global water cycle under climate warming, which may generate considerable impacts on ecosystem carbon (C) dynamics. Although substantial manipulative experiments have been conducted to probe the responses of ecosystem C processes to altered precipitation, how soil C storage responds to both drought and irrigation is still unclear across biomes and the globe. A meta-analysis of 179 published studies was carried out to examine responses of soil C storage and associated C fluxes and pools to drought and irrigation. Our results showed that, on average across all biomes, drought and irrigation similarly induced minor increases in soil C pool (SCP) by 1.45% and 1.27%, respectively. However, drought and irrigation oppositely affected both C fluxes and plant C pools as well as in agroecosystems (e.g., croplands and grasslands). The drought-induced increases in root: shoot ratio and decreases in heterotrophic respiration and soil C turnover rate mostly contributed to minor increase in SCP, while an increase in newly fixed C inputs in soil was more important under irrigation. In addition, the relative changes in precipitation intensity in manipulative experiments were positively correlated with response ratios of plant C pool (PCP), net primary production (NPP), microbial biomass C, ecosystem, soil and heterotrophic respiration. The drought-induced responses of SCP exhibited a positive correlation with experimental duration but not under irrigation and for other C pools and fluxes. These results indicate that more attention should be paid to the responses of C allocation and turnover rate to drought and irrigation, which should be incorporated into land surface models to better project effects of altered precipitation on ecosystem C cycling in terrestrial ecosystems.

Nonstructural carbohydrates (NSC) play important roles in forest vulnerability to climate change, especially under increasing drought intensity and frequency. Understanding NSC dynamics is essential for accurately predicting the resistance and resilience of forests in response to drought. However, our knowledge of NSC responses to drought is still limited due to the lack of research in trees of different life stages. In this study, we conducted a throughfall exclusion experiment (TFE) with four subtropical evergreen tree species to examine drought effects on NSC in mature trees and understory seedlings. Our results showed the differential effects of drought on NSC dynamics of understory seedlings and mature trees. In the TFE experiment, mature trees of all four species were relatively homoeostatic with the insignificantly changed NSC pools, photosynthesis, and growth under the drought treatment compared to the control. In contrast, understory seedlings displayed significant decreases in total NSC and soluble sugars (−14.70 ± 3.66% and −16.93 ± 3.85%, respectively) with the exception of Lithocarpus glaber (L. glaber). The seedlings of L. glaber with the highest hydraulic resistance maintained or slightly increased NSC and its components in response to drought. Our study highlights the importance of life stage in assessing drought effects of trees on NSC storage and then forest C cycling, which could be incorporated into the dynamic global vegetation models (DGVMs) to better understand drought effects on forest C balance in the future.

Lanthanide coordination nanoparticles terbium(III) (Tb3+)-based fluorescent nanoparticles (luminol-Tb NPs) are synthesized via aggregation-induced fluorescence strategy. Fluorescence of luminol-Tb NPs is enhanced nearly 40 times compared with luminol, which is the effect of aggregation-induced fluorescence by Tb3+. Luminol-Tb NPs with high fluorescence is utilized in fluorescent “turn-off” detection of uric acid (UA) within 1 min from 0.1 to 50 μM with the limit of detection (LOD) of 28 nM. The fluorescence quenching effect may be ascribed to photoinduced electron transfer occurs from luminol-Tb NPs to UA. This fluorescent method exhibits high selectivity in UA detection towards metal ions, glucose, ascorbic acid, dopamine, creatinine, urea and cysteine. When it is also applied in detection of UA in serum samples, 5 μM, 10 μM and 30 μM UA are respectively added to serum samples and recoveries range from 97.5% to 101.3% in serum samples. It demonstrates the practical value of luminol-Tb NPs for UA detection in serum.

It is known that vitamin B1 (VB1) has a protective effect against oxidative retinal damage induced by anti-tuberculosis drugs. However, it remains unclear whether VB1 regulates immune responses during Mycobacterium tuberculosis (MTB) infection. We report here that VB1 promotes the protective immune response to limit the survival of MTB within macrophages and in vivo through regulation of peroxisome proliferator-activated receptor γ (PPAR-γ). VB1 promotes macrophage polarization into classically activated phenotypes with strong microbicidal activity and enhanced tumor necrosis factor-α and interleukin-6 expression at least in part by promoting nuclear factor-κB signaling. In addition, VB1 increases mitochondrial respiration and lipid metabolism and PPAR-γ integrates the metabolic and inflammatory signals regulated by VB1. Using both PPAR-γ agonists and deficient mice, we demonstrate that VB1 enhances anti-MTB activities in macrophages and in vivo by down-regulating PPAR-γ activity. Our data demonstrate important functions of VB1 in regulating innate immune responses against MTB and reveal novel mechanisms by which VB1 exerts its function in macrophages.

NLRC3, a member of the NLR family, has been reported as a negative regulator of inflammatory signaling pathways in innate immune cells. However, the direct role of NLRC3 in modulation of CD4+ T-cell responses in infectious diseases has not been studied. In the present study, we showed that NLRC3 plays an intrinsic role by suppressing the CD4+ T cell phenotype in lung and spleen, including differentiation, activation, and proliferation. NLRC3 deficiency in CD4+ T cells enhanced the protective immune response against Mycobacterium tuberculosis infection. Finally, we demonstrated that NLRC3 deficiency promoted the activation, proliferation, and cytokine production of CD4+ T cells via negatively regulating the NF-κB and MEK-ERK signaling pathways. This study reveals a critical role of NLRC3 as a direct regulator of the adaptive immune response and its protective effects on immunity during M. tuberculosis infection. Our findings also suggested that NLRC3 serves as a potential target for therapeutic intervention against tuberculosis., Author summary Accumulating evidence that NLRs play an intrinsic roles in regulating T cell responses in lungs and lymphoid tissues, however, to our known, contribution for NLRs modulation of T-cell responses directly in infectious diseases has not been studied. NLRC3, a member of the NLR family, has been reported as a negative regulator of inflammatory signaling pathways in innate immune cells. The direct role of NLRC3 in the modulation of CD4+ T-cell responses in infectious diseases has not been studied. In the present study, we focused on elucidating the roles of NLRC3 in shaping CD4+ T cell responses in vivo and in vitro, in particular during M. tuberculosis infection. We found that NLRC3 plays an intrinsic l roles by suppressing the CD4+ T cell phenotype in lungs and lymphoid tissues, including Th1 and Th17 differentiation, activation, and proliferation. NLRC3 deficiency in CD4+ T cells enhanced the protective immune response against M. tuberculosis infection. Finally, we demonstrated that NLRC3 deficiency promoted the activation, proliferation, and cytokine production of CD4+ T cells via negatively regulating the NF-κB and MEK-ERK signaling pathways. This study reveals a critical role of NLRC3 as a direct regulator of the adaptive immune response and its protective effects on immunity during M. tuberculosis infection. Our findings also suggested that NLRC3 serves as a potential target for therapeutic intervention against tuberculosis.

The aim of the present study was to investigate the treatment effects and associated mechanism of Bak Foong pills (BFPs) combined with metformin in the treatment of polycystic ovarian syndrome (PCOS). BFPs and/or metformin were administrated to treat the PCOS rats, and the weights and morphologies of the ovary, uterus and adrenal gland were measured. The levels of fasting blood glucose (FBG), serum testosterone (T), luteinizing hormone, fasting insulin (FIN) and insulin-like growth factor-1 were also measured, and the homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. The expression level of androgen receptor (AR) in the ovarian tissue, and the cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc) mRNA levels in the ovary and adrenal tissues were detected. The levels of T, FIN, FBG and HOMA-IR in the combination group were significantly reduced; the wet weights of the ovary and the adrenal gland were decreased significantly, while that of the uterus was increased, and the histological morphology benignly recovered. The rats of each treatment group all experienced restored ovulation. The AR expression level in the treatment group was reduced, and the P450scc mRNA levels in the ovary and the adrenal gland of the combined treatment group were decreased. BFPs combined with metformin significantly affected PCOS, and the possible mechanism involved in the treatment may have been through the reduction of P450scc generation. BFPs may reduce the androgen levels, thus allowing the ovary to restore ovulation.