Slower changes in vegetation phenology than precipitation seasonality in the dry tropics.

The dry tropics occupy ~40% of the tropical land surface and play a dominant role in the trend and interannual variability of the global carbon cycle. Previous studies have reported considerable changes in the dry tropical precipitation seasonality due to climate change, however, the accompanied changes in the length of the vegetation growing season (LGS)-the key period of carbon sequestration-have not been examined. Here, we used long-term satellite observations along with in-situ flux measurements to investigate phenological changes in the dry tropics over the past 40 years. We found that only ~18% of the dry tropics show a significant (p ≤ .1) increasing trend in LGS, while ~13% show a significant decreasing trend. The direction of the LGS change depended not only on the direction of precipitation seasonality change but also on the vegetation water use strategy (i.e. isohydricity) as an adaptation to the long-term average precipitation seasonality (i.e. whether the most of LGS is in the wet season or dry season). Meanwhile, we found that the rate of LGS change was on average ~23% slower than that of precipitation seasonality, caused by a buffering effect from soil moisture. This study uncovers potential mechanisms driving phenological changes in the dry tropics, offering guidance for regional vegetation and carbon cycle studies.

Exosomes derived from programmed cell death: mechanism and biological significance.

Exosomes are nanoscale extracellular vesicles present in bodily fluids that mediate intercellular communication by transferring bioactive molecules, thereby regulating a range of physiological and pathological processes. Exosomes can be secreted from nearly all cell types, and the biological function of exosomes is heterogeneous and depends on the donor cell type and state. Recent research has revealed that the levels of exosomes released from the endosomal system increase in cells undergoing programmed cell death. These exosomes play crucial roles in diseases, such as inflammation, tumors, and autoimmune diseases. However, there is currently a lack of systematic research on the differences in the biogenesis, secretion mechanisms, and composition of exosomes under different programmed cell death modalities. This review underscores the potential of exosomes as vital mediators of programmed cell death processes, highlighting the interconnection between exosome biosynthesis and the regulatory mechanisms governing cell death processes. Furthermore, we accentuate the prospect of leveraging exosomes for the development of innovative biomarkers and therapeutic strategies across various diseases.

Optimizing timing for quantification of intracranial aneurysm enhancement: a multi-phase contrast-enhanced vessel wall MRI study.

OBJECTIVES: Aneurysm wall enhancement (AWE) on high-resolution contrast-enhanced vessel wall MRI (VWMRI) is an emerging biomarker for intracranial aneurysms (IAs) stability. Quantification methods of AWE in the literature, however, are variable. We aimed to determine the optimal post-contrast timing to quantify AWE in both saccular and fusiform IAs. MATERIALS AND METHODS: Consecutive patients with unruptured IAs were prospectively recruited. VWMRI was acquired on 1 pre-contrast and 4 consecutive post-contrast phases (each phase was 9 min). Signal intensity values of cerebrospinal fluid (CSF) and aneurysm wall on pre- and 4 post-contrast phases were measured to determine the aneurysm wall enhancement index (WEI). AWE was also qualitatively analyzed on post-contrast images using previous grading criteria. The dynamic changes of AWE grade and WEI were analyzed for both saccular and fusiform IAs. RESULTS: Thirty-four patients with 42 IAs (27 saccular IAs and 15 fusiform IAs) were included. The changes in AWE grade occurred in 8 (30%) saccular IAs and 6 (40%) in fusiform IAs during the 4 post-contrast phases. The WEI of fusiform IAs decreased 22.0% over time after contrast enhancement (p = 0.009), while the WEI of saccular IAs kept constant during the 4 post-contrast phases (p > 0.05). CONCLUSIONS: When performing quantitative analysis of AWE, acquiring post-contrast VWMRI immediately after contrast injection achieves the strongest AWE for fusiform IAs. While the AWE degree is stable for 36 min after contrast injection for saccular IAs. CLINICAL RELEVANCE STATEMENT: The standardization of imaging protocols and analysis methods for AWE will be helpful for imaging surveillance and further treatment decisions of patients with unruptured IAs. KEY POINTS: Imaging protocols and measurements of intracranial aneurysm wall enhancement are reported heterogeneously. Aneurysm wall enhancement for fusiform intracranial aneurysms (IAs) is strongest immediately post-contrast, and stable for 36 min for saccular IAs. Future multi-center studies should investigate aneurysm wall enhancement as an emerging marker of aneurysm growth and rupture.

Associations between atherosclerotic luminal stenosis in the distal internal carotid artery and diffuse wall thickening in its upstream segment.

OBJECTIVES: Significant atherosclerotic stenosis or occlusion in the distal internal carotid artery (ICA) may induce diffuse wall thickening (DWT) in the upstream arterial wall. This study aimed to assess the association of atherosclerotic steno-occlusive diseases in the distal ICA with DWT in the upstream ipsilateral ICA. METHODS: Individuals with atherosclerotic stenosis in the distal ICA, detected by carotid MR vessel wall imaging using 3D pre- and post-contrast T1 volume isotropic turbo spin-echo acquisition (T1-VISTA) sequence, were enrolled. The associations of vessel wall thickening, the longitudinal extent of DWT, enhancement of the upstream ipsilateral ICA, and stenosis degree in the distal ICA were examined. RESULTS: Totally 64 arteries in 55 patients with atherosclerotic steno-occlusive distal ICAs were included. Significant correlations were found between distal ICA stenosis and DWT in the petrous ICA (r = 0.422, p = 0.001), DWT severity (r = 0.474, p < 0.001), the longitudinal extent of DWT in the ICA (r = 0.671, p < 0.001), enhancement in the petrous ICA (r = 0.409, p = 0.001), and enhancement degree (r = 0.651, p < 0.001). In addition, high degree of enhancement was correlated with both increased wall thickness and increased prevalence of DWT in the petrous ICA (both p < 0.001). CONCLUSIONS: DWT of the petrous ICA is commonly detected in patients with atherosclerotic steno-occlusive disease in the distal ICA. The degree of stenosis in the distal ICA is associated with wall thickening and its longitudinal extent in the upstream segments. CLINICAL RELEVANCE STATEMENT: Diffuse wall thickening is a common secondary change in atherosclerotic steno-occlusive disease in the intracranial carotid. This phenomenon constitutes a confounding factor in the distinction between atherosclerosis and inflammatory vasculopathies, and could be reversed after alleviated atherosclerotic stenosis. KEY POINTS: • Diffuse wall thickening of the petrous internal carotid artery is commonly detected in patients with atherosclerotic steno-occlusive disease in the distal internal carotid artery. • The phenomenon of diffuse wall thickening could be reversed after stenosis alleviation. • Carotid artery atherosclerosis with diffuse wall thickening should warrant a differential diagnosis from other steno-occlusive diseases, including moyamoya diseases and Takayasu aortitis.

Encapsulation and assessment of therapeutic cargo in engineered exosomes: a systematic review.

Exosomes are nanoscale extracellular vesicles secreted by cells and enclosed by a lipid bilayer membrane containing various biologically active cargoes such as proteins, lipids, and nucleic acids. Engineered exosomes generated through genetic modification of parent cells show promise as drug delivery vehicles, and they have been demonstrated to have great therapeutic potential for treating cancer, cardiovascular, neurological, and immune diseases, but systematic knowledge is lacking regarding optimization of drug loading and assessment of delivery efficacy. This review summarizes current approaches for engineering exosomes and evaluating their drug delivery effects, and current techniques for assessing exosome drug loading and release kinetics, cell targeting, biodistribution, pharmacokinetics, and therapeutic outcomes are critically examined. Additionally, this review synthesizes the latest applications of exosome engineering and drug delivery in clinical translation. The knowledge compiled in this review provides a framework for the rational design and rigorous assessment of exosomes as therapeutics. Continued advancement of robust characterization methods and reporting standards will accelerate the development of exosome engineering technologies and pave the way for clinical studies.

O-glycosylation of SARS-CoV-2 spike protein by host O-glycosyltransferase strengthens its trimeric structure.

Protein O-glycosylation, also known as mucin-type O-glycosylation, is one of the most abundant glycosylation in mammalian cells. It is initially catalyzed by a family of polypeptide GalNAc transferases (ppGalNAc-Ts). The trimeric spike protein (S) of SARS-CoV-2 is highly glycosylated and facilitates the virus's entry into host cells and membrane fusion of the virus. However, the functions and relationship between host ppGalNAc-Ts and O-glycosylation on the S protein remain unclear. Herein, we identify 15 O-glycosites and 10 distinct O-glycan structures on the S protein using an HCD-product-dependent triggered ETD mass spectrometric analysis. We observe that the isoenzyme T6 of ppGalNAc-Ts (ppGalNAc-T6) exhibits high O-glycosylation activity for the S protein, as demonstrated by an on-chip catalytic assay. Overexpression of ppGalNAc-T6 in HEK293 cells significantly enhances the O-glycosylation level of the S protein, not only by adding new O-glycosites but also by increasing O-glycan heterogeneity. Molecular dynamics simulations reveal that O-glycosylation on the protomer-interface regions, modified by ppGalNAc-T6, potentially stabilizes the trimeric S protein structure by establishing hydrogen bonds and non-polar interactions between adjacent protomers. Furthermore, mutation frequency analysis indicates that most O-glycosites of the S protein are conserved during the evolution of SARS-CoV-2 variants. Taken together, our finding demonstrate that host O-glycosyltransferases dynamically regulate the O-glycosylation of the S protein, which may influence the trimeric structural stability of the protein. This work provides structural insights into the functional role of specific host O-glycosyltransferases in regulating the O-glycosylation of viral envelope proteins.

Single-cell RNA sequencing of estrual mice reveals PM2.5-induced uterine cell heterogeneity and reproductive toxicity.

Fine particulate matter (PM2.5) exposure has been extensively linked to reproductive and developmental dysfunctions, yet the underlying mechanisms remain elusive. This study employed single-cell RNA sequencing (scRNA-seq) to investigate PM2.5-induced changes in uterine cell populations and gene expression profiles in mice during estrus and early pregnancy. Methodologically, we intranasally inoculated mice with 20 µL of 4.0 mg/mL PM2.5 suspension during their estrus and early pregnancy periods. Utilizing scRNA-seq analysis, we revealed significant alterations in cell type composition following PM2.5 exposure. Notably, we observed a marked decrease in the proportion of natural killer (NK) cells in PM2.5-exposed mice (2.00 % vs. 8.97 % in controls). Further functional enrichment analysis identified suppression of the IL-17 signaling pathway in NK cells as a key mechanism of PM2.5-induced toxicity. GSEA analysis showed in-depth details of the downregulated genes in this pathway, including Fosb, S100a8, Tnfaip3, IL-17a, and S100a9. PM2.5 exposure also disrupted intercellular communication within the uterine microenvironment, with the number of cell interactions decreasing from 483 to 315 and interaction strength reducing from 12.43 to 6.78 compared to controls. Histological examination revealed that PM2.5 exposure led to thinning of the endometrium and less prominent main branches in uterine tissues, and immunofluorescence assays corroborated the altered expression of IL-17 pathway components, showing enhanced Hsp90ab1 expression and reduced FOSB, S100A8, and S100A9 expression in PM2.5-exposed uterine tissues. These findings provide novel insights into the cellular mechanisms of PM2.5-induced reproductive toxicity, highlighting the IL-17 signaling pathway in uterine NK cells as a potential target for therapeutic interventions. Our results underscore the need for air quality regulations and open new avenues for developing biomarkers and targeted therapies to mitigate the reproductive risks associated with PM2.5 exposure.

Silica-induced macrophage pyroptosis propels pulmonary fibrosis through coordinated activation of relaxin and osteoclast differentiation signaling to reprogram fibroblasts.

Silica nanoparticle (SiNP) exposure induces severe pulmonary inflammation and fibrosis, but the pathogenesis remains unclear, and effective therapies are currently lacking. To explore the mechanism underlying SiNPs-induced pulmonary fibrosis, we constructed in vivo silica exposure animal models and in vitro models of silica-induced macrophage pyroptosis and fibroblast transdifferentiation. We found that SiNP exposure elicits upregulation of pulmonary proteins associated with pyroptosis, including NLRP3, ASC, IL-1ß, and GSDMD, while the immunofluorescence staining co-localized NLRP3 and GSDMD with macrophage-specific biomarker F4/80 in silica-exposed lung tissues. However, the NLRP3 inhibitor MCC950 and classical anti-fibrosis drug pirfenidone (PFD) were found to be able to alleviate silica-induced collagen deposition in the lungs. In in vitro studies, we exposed the fibroblast to a conditioned medium from silica-induced pyroptotic macrophages and found enhanced expression of α-SMA, suggesting increased transdifferentiation of fibroblast to myofibroblast. In line with in vivo studies, the combined treatment of MCC950 and PFD was demonstrated to inhibit the expression of α-SMA and attenuate fibroblast transdifferentiation. Mechanistically, we adopted high throughput RNA sequencing on fibroblast with different treatments and found activated signaling of relaxin and osteoclast differentiation pathways, where the expression of the dysregulated genes in these two pathways was examined and found to be consistently altered both in vitro and in vivo. Collectively, our study demonstrates that SiNP exposure induces macrophage pyroptosis, which subsequently causes fibroblast transdifferentiation to myofibroblasts, in which the relaxin and osteoclast differentiation signaling pathways play crucial roles. These findings may provide valuable references for developing new therapies for pulmonary fibrosis.

Reproductive and developmental implications of micro- and nanoplastic internalization: Recent advances and perspectives.

A growing body of evidence exhibits the ubiquitous presence and accumulation of micro- and nanoplastics (MNPs) in the air, drinking water, food, and even inside the body, which has raised concerns about their potential impact on reproductive and developmental health. To comprehensively examine the current state of knowledge regarding MNPs-induced reproductive and developmental toxicity, we conducted this systematic review by focusing on the prevalence of MNPs determined in reproductive tissues and their influences on parental reproduction and offspring development. Our findings demonstrate the detection of MNPs in various human reproductive tissues, including semen, placenta, and ovarian follicular fluid, as well as in reproductive tissues of diverse animal species. We show a potential relationship between MNP exposure and increased prevalence of infertility and adverse pregnancy outcomes based on the fact that MNPs exert detrimental effects on reproductive parameters, including sperm quality, ovarian function, and steroidogenesis. In male reproductive systems, MNPs disrupt testicular tissue structure, impair reproductive endocrinology, and reduce sperm quality. In females, MNPs affect ovarian tissue structure and function, interfere with hormone secretion, and impact the endometrium and embryo implantation. Additionally, MNPs cause developmental toxicity in animal models, affecting embryonic development and offspring health, and produce transgenerational effects. Notably, in-depth literature study suggests a crucial role for oxidative stress, inflammation, and epigenetic modification in MNPs-induced toxicity. In conclusion, we integrated systematic knowledge on MNPs-induced reproductive and developmental toxicity, and the systematic finding underscores future study to fully elucidate the risks posed by MNPs to reproductive and developmental health and to inform policy decisions and public health interventions aimed at mitigating their harmful effects.

Enabling Interfacial Lattice Matching by Selective Epitaxial Growth of CuS Crystals on Bi2WO6 Nanosheets for Efficient CO2 Photoreduction into Solar Fuels.

Photocatalytic CO2 reduction serves as an important technology for value-added solar fuel production; however, it is generally limited by interfacial charge transport. To address this limitation, a two-dimensional/two-dimensional (2D/2D) p-n heterojunction CuS-Bi2WO6 (CS-BWO) with highly connected and matched interfacial lattices was designed via a two-step hydrothermal tandem synthesis strategy. The integration of CuS with BWO created a robust interface electric field and provided fast charge transfer channels due to the work function difference, as well as highly connected and matched interfacial lattices. The p-n heterojunction promoted electron transfer from the Cu to Bi sites, leading to coordination of Bi sites with high electronic density and low oxidation state. The Bi sites in BWO nanosheets facilitated the adsorption and activation of CO2, and generation of high-coverage key intermediate b-CO32-, while broad light-harvesting CuS (CS) provide abundant photoinduced electrons that were injected into the conduction band of BWO for CO2 photoreduction reaction. Remarkably, the p-n heterojunction CS-BWO exhibited CO and CH4 yields of 135.7 and 62.5 µmol g-1, respectively, which were significantly higher than those of CS, BWO, and physical mixture CS-BWO nanosheets. This work provided an innovative design strategy for developing high-activity heterojunction photocatalyst for converting CO2 into value-added solar fuels.

Solar driven CO2 hydrogenation to HCOOH on (TiO2)n (n = 1-6) atomic clusters.

Artificial photosynthesis is a crucial reaction that addresses energy and environmental challenges by converting CO2 into fuels and value-added chemicals. However, efficient catalytic activity using earth-abundant materials can be challenging due to intrinsic limitations. Herein, we explore neutral (TiO2)n (n = 1-6) atomic clusters for CO2 hydrogenation via comprehensive ab initio calculations combined with time-dependent functional theory. Our results show that these (TiO2)n clusters exhibit outstanding thermodynamic stabilities and decent surficial activities for CO2 activation and H2 dissociation, both of which possess kinetic barriers down to 0-0.74 eV. We establish a relationship between the binding strength of *CO2 species and electron characterization for these (TiO2)n clusters. These clusters, which have a wide energy gap between the highest occupied molecular orbital (HOMO) and the lowest unoccpied molecular orbital (LUMO) that allows them to harvest the solar light in the ultraviolet regime, enabling efficient catalysis for driving the catalysis of CO2 conversion. They provide exclusive reaction channels and high selectivity for yielding HCOOH products via the carboxyl mechanism, involving the kinetic barrier of the limiting step of 0.74-1.25 eV. We also investigated the substrate effect on supported (TiO2)n clusters, with non-metallic substrates featuring inert surfaces serving as suitable options for anchoring (TiO2)n clusters while preserving their intrinsic activity and selectivity. These computational results have significant implications not only for meeting energy demands but also for mitigating carbon emissions by utilizing CO2 as an alternative feedstock rather than considering it solely as a greenhouse gas.

Atomic resolution of short-range sliding dynamics of thymine DNA glycosylase along DNA minor-groove for lesion recognition.

Thymine DNA glycosylase (TDG), as a repair enzyme, plays essential roles in maintaining the genome integrity by correcting several mismatched/damaged nucleobases. TDG acquires an efficient strategy to search for the lesions among a vast number of cognate base pairs. Currently, atomic-level details of how TDG translocates along DNA as it approaches the lesion site and the molecular mechanisms of the interplay between TDG and DNA are still elusive. Here, by constructing the Markov state model based on hundreds of molecular dynamics simulations with an integrated simulation time of ∼25 µs, we reveal the rotation-coupled sliding dynamics of TDG along a 9 bp DNA segment containing one G·T mispair. We find that TDG translocates along DNA at a relatively faster rate when distant from the lesion site, but slows down as it approaches the target, accompanied by deeply penetrating into the minor-groove, opening up the mismatched base pair and significantly sculpturing the DNA shape. Moreover, the electrostatic interactions between TDG and DNA are found to be critical for mediating the TDG translocation. Notably, several uncharacterized TDG residues are identified to take part in regulating the conformational switches of TDG occurred in the site-transfer process, which warrants further experimental validations.

Mechanistic insights into severe pulmonary inflammation caused by silica stimulation: The role of macrophage pyroptosis.

Respirable silica dust is a common hazard faced by occupational workers and prolonged exposure to this dust can lead to pulmonary inflammation, fibrosis and, in severe cases, silicosis. However, the underlying mechanism by which silica exposure causes these physical disorders is not yet understood. In this study, we aimed to shed light on this mechanism by establishing in vitro and in vivo silica exposure models from the perspective of macrophages. Our results showed that compared to the control group, silica exposure resulted in an upregulation of the pulmonary expression of P2X7 and Pannexin-1, but this effect was suppressed by treatment with MCC950, a specific inhibitor of NLRP3. Our in vitro studies showed that silica exposure induced mitochondrial depolarization in macrophages, which led to a reduction of intracellular ATP and an influx of Ca2+. Furthermore, we found that creating an extracellular high potassium environment by adding KCl to the macrophage medium inhibited the expression of pyroptotic biomarkers and pro-inflammatory cytokines such as NLRP3 and IL-1ß. Treatment with BBG, a P2X7 antagonist, also effectively inhibited the expression of P2X7, NLRP3, and IL-1ß. On the other hand, treatment with FCF, a Pannexin-1 inhibitor, suppressed the expression of Pannexin-1 but had no effect on the expression of pyroptotic biomarkers such as P2X7, NLRP3, and IL-1ß. In conclusion, our findings suggest that silica exposure triggers the opening of P2X7 ion channels, resulting in intracellular K+ efflux, extracellular Ca2+ influx, and the assembly of the NLRP3 inflammasome, ultimately leading to macrophage pyroptosis and pulmonary inflammation.

Construction of Graphene@Ag-MLF composite structure SERS platform and its differentiating performance for different foodborne bacterial spores.

A new surface-enhanced Raman spectroscopy (SERS) biosensor of Graphene@Ag-MLF composite structure has been fabricated by loading AgNPs on graphene films. The response of the biosensor is  based on plasmonic sensing. The results showed that the enhancement factor of three different spores reached 107 based on the Graphene@Ag-MLF substrate. In addition, the SERS performance was stable, with good reproducibility (RSD<3%). Multivariate statistical analysis and chemometrics were used to distinguish different spores. The accumulated variance contribution rate was up to 96.35% for the top three PCs, while HCA results revealed that the spectra were differentiated completely. Based on optimal principal components, chemometrics of KNN and LS-SVM were applied to construct a model for rapid qualitative identification of different spores, of which the prediction set and training set of LS-SVM achieved 100%. Finally, based on the Graphene@Ag-MLF substrate, the LOD of three different spores was lower than 102 CFU/mL. Hence, this novel Graphene@Ag-MLF SERS substrate sensor was rapid, sensitive, and stable in detecting spores, providing strong technical support for the application of SERS technology in food safety.

Ectopic expression of OsJAZ6, which interacts with OsJAZ1, alters JA signaling and spikelet development in rice.

Jasmonates (JAs) are key phytohormones that regulate plant responses and development. JASMONATE-ZIM DOMAIN (JAZ) proteins safeguard JA signaling by repressing JA-responsive gene expression in the absence of JA. However, the interaction and cooperative roles of JAZ repressors remain unclear during plant development. Here, we found that OsJAZ6 interacts with OsJAZ1 depending on a single amino acid in the so-called ZIM domain of OsJAZ6 in rice JA signaling transduction and JA-regulated rice spikelet development. In vivo protein distribution analysis revealed that the OsJAZ6 content is efficiently regulated during spikelet development, and biochemical and genetic evidence showed that OsJAZ6 is more sensitive to JA-mediated degradation than OsJAZ1. Through over- and mis-expression experiments, we further showed that the protein stability and levels of OsJAZ6 orchestrate the output of JA signaling during rice spikelet development. A possible mechanism, which outlines how OsJAZ repressors interact and function synergistically in specifying JA signaling output through degradation titration, is also discussed.

The OsJAZ1 degron modulates jasmonate signaling sensitivity during rice development.

Jasmonates (JAs) are crucial to the coordination of plant stress responses and development. JA signaling depends on JASMONATE-ZIM DOMAIN (JAZ) proteins that are destroyed by the SCFCOI1-mediated 26S proteasome when the JAZ co-receptor COI1 binds active JA or the JA-mimicking phytotoxin coronatine (COR). JAZ degradation releases JAZ-interacting transcription factors that can execute stress and growth responses. The JAZ proteins typically contain Jas motifs that undergo conformational changes during JA signal transduction and that are important for the JAZ-COI1 interaction and JAZ protein degradation. However, how alterations in the Jas motif and, in particular, the JAZ degron part of the motif, influence protein stability and plant development have not been well explored. To clarify this issue, we performed bioassays and genetic experiments to uncover the function of the OsJAZ1 degron in rice JA signaling. We found that substitution or deletion of core segments of the degron altered the OsJAZ1-OsCOI1b interaction in a COR-dependent manner. We show that these altered interactions function as a regulator for JA signaling during flower and root development. Our study therefore expands our understanding of how the JAZ degron functions, and provides the means to change the sensitivity and specificity of JA signaling in rice.

Monitoring nature's calendar from space: Emerging topics in land surface phenology and associated opportunities for science applications.

Vegetation phenology has been viewed as the nature's calendar and an integrative indicator of plant-climate interactions. The correct representation of vegetation phenology is important for models to accurately simulate the exchange of carbon, water, and energy between the vegetated land surface and the atmosphere. Remote sensing has advanced the monitoring of vegetation phenology by providing spatially and temporally continuous data that together with conventional ground observations offers a unique contribution to our knowledge about the environmental impact on ecosystems as well as the ecological adaptations and feedback to global climate change. Land surface phenology (LSP) is defined as the use of satellites to monitor seasonal dynamics in vegetated land surfaces and to estimate phenological transition dates. LSP, as an interdisciplinary subject among remote sensing, ecology, and biometeorology, has undergone rapid development over the past few decades. Recent advances in sensor technologies, as well as data fusion techniques, have enabled novel phenology retrieval algorithms that refine phenology details at even higher spatiotemporal resolutions, providing new insights into ecosystem dynamics. As such, here we summarize the recent advances in LSP and the associated opportunities for science applications. We focus on the remaining challenges, promising techniques, and emerging topics that together we believe will truly form the very frontier of the global LSP research field.

NF-κB mediates silica-induced pulmonary inflammation by promoting the release of IL-1ß in macrophages.

Long-term exposure to respirable silica particles causes pulmonary inflammation and fibrosis primarily promoted by cytokines released from alveolar macrophages, yet the underlying mechanism is still unclear. From the perspective of nuclear factor kappa B (NF-κB), we studied the mechanism of IL-1ß biosynthesis and release. Utilizing BAY 11-7082, an NF-κB specific inhibitor, we showed the alteration of macrophage viability and examined the expression of both IL-1ß and NF-κB in vitro. We found that silica nanoparticles (SiNPs) were internalized by macrophages and caused damage to cell integrity. The immunofluorescence assay showed that SiNPs exposure enhanced the expression of IL-1ß and NF-κB, which could be effectively suppressed by BAY 11-7082. Besides, we built silica exposure mouse model by intratracheally instilling 5 mg of SiNPs and checked the effect of silica exposure on pulmonary pathological changes. Consistently, we found an upregulation of IL-1ß and NF-κB after SiNPs exposure, along with the aggravated inflammatory cell infiltration, thickened alveolar wall, and enhanced expression of collagens. In conclusion, SiNPs exposure causes pulmonary inflammation and fibrosis that is regulated by NK-κB through upregulating IL-1ß in alveolar macrophages.

Leveraging sustainable development of agriculture with sustainable water management: The empirical investigation of "Five Water Cohabitation" of Zhejiang Province in China.

In 2013, the government of Zhejiang Province put forward a strategic project named "Five Water Cohabitation" (FWC) by integrating five water treatments: "sewage treatment," "flood prevention," "drainage system improvement," "water supply guarantee," and "water saving promotion." It has been eight years since the project was proposed and launched. The primary purpose of the present study is to investigate the performance and significant effects of the project on the sustainable development of agriculture. This study investigates the project's implementation from four aspects: environmental sustainability, resource sustainability, social sustainability, and economic sustainability. Furthermore, the difference-in-differences approach is applied to verify the treatment effect. Liaoning Province is chosen as the control group because it is also the traditionally agricultural province, and it has not implemented any large-scale water management projects. This study selects six sustainable variables, i.e., per capita GDP, urban-rural disparity, total water resources, domestic waste clearance, urbanization level, and health security level. The results show that the FWC project positively affects the sustainable development of agriculture for Zhejiang Province in economic sustainability, ecological sustainability, and social sustainability.

Uterine metabolic disorder induced by silica nanoparticles: biodistribution and bioactivity revealed by labeling with FITC.

Extensive application of nanomaterials has dramatically increased the risk of silica nanoparticle (SiNP, SiO2) exposure, yet their biological effect on reproduction has not been fully elucidated. By tracking the uterine biodistribution of SiNP in pregnant mice, this study was conducted to evaluate the biological effect of SiNP on reproduction. First, SiNP was conjugated with FITC, and then the FITC-SiNP was administrated to trophoblast (100 µg/mL, 24 h) in vitro and pregnant mice (0.25 mg/mouse, 2-24 h) in vivo. It was found that the FITC-SiNP was internalized by trophoblast and deposited in the uterus. The internalization of SiNP caused trophoblast dysfunction and apoptosis, while SiNP accumulation in the uterus induced diffuse inflammatory infiltration. The genome-wide alteration of gene expression was studied by high throughput sequencing analysis, where 75 genes were found to be dysregulated after SiNP exposure, among which ACOT2, SCD1, and CPT1A were demonstrated to regulate the biosynthesis of unsaturated fatty acids. Moreover, the suppression of unsaturated fatty acids caused mitochondrial overload of long-chain fatty acyl-CoA (LACoA), which further induced both trophoblast apoptosis and endometrial inflammation. In conclusion, the successful conjugation of FITC onto SiNP facilitated the tracking of SiNP in vitro and in vivo, while exposure to FITC-SiNP induced uterine metabolic disorder, which was regulated by the ACOT/CPT1A/SCD1 axis through the biosynthesis of unsaturated fatty acids signaling pathway.