Is intravenous infusion an unrecognized route for internal microplastic human exposure? A general assessment.

As newly recognized environmental pollutants, microplastics (MPs, ≤5 mm in length) have been reported in various human tissues and fluids, including the spleen, liver, heart, blood and blood clots, raising global concerns about their impact on human health. This study investigated the characteristics of MPs in intravenous infusion and the removal of MPs from infusion products by infusion sets fitted with different filters using micro-Fourier Transform Infrared Spectroscopy. MPs were detected in infusion products, with an average abundance of 1.24 ± 1.44 items/unit (2.91 ± 3.91 items/L). The primary types of MPs identified were fragmented particles of polyethene and polypropylene, ranging in size from 15-100 µm. Internal filters in infusion sets played a crucial role in removing MPs, particularly fibrous ones, resulting in a reduction in both abundance and particle size of MPs in the human body. Moreover, this study conducted a general assessment of intravenous microplastic exposure among hospital patients and estimated the global per-person input of MPs via intravenous administration. It is an opportunity for us to gain a deeper understanding of MPs in intravenous infusion and provides guides selecting infusion devices, increasing awareness of associated health risks.

Transforming contaminant ligands at water-solid interfaces via trivalent metal coordination.

In environmental matrices, the migration and distribution of contaminants at water-solid interfaces play a crucial role in their capture or dissemination. Scientists working in environmental remediation and wastewater treatment are increasingly aware of metal-contaminant coordination; however, interfacial behaviors remain underexplored. Here, we show that trivalent metal ions (e.g. Al3+ and Fe3+) mediate the migration of pollutant ligands (e.g. tetracycline (TC) and ofloxacin) to the organic solid interface. In the absence of Al3+, humic acid (HA) colloids (50 mg/L) capture 26.1 % of the TC in water (initial concentration: 10 mg/L) via weak intermolecular interactions (binding energy: -5.71 kcal/mol). Adding Al3+ (2.5 mg/L) significantly enhances the binding of TC to an impressive 94.2 % via Al3+ mediated coordination (binding energy: -84.89 kcal/mol). The significant increase in binding energy results in superior interfacial immobilization. However, excess free Al3+ competes for TC binding via direct binary coordination, as confirmed based on the unique fluorescence of Al3+-TC complexes. Density functional theory calculations reveal the intricate process of HA-Al3+ binding via carboxyl and phenolic hydroxyl sites. The HA-Al3+ flocs then leverage the remaining coordination capacity of Al3+ to chelate with TC. As well as providing insights into the pivotal role of metal ion on the self-purification of natural water bodies, our findings on the interfacial behavior of metal-contaminant coordination will propel coagulation technology to the capture of microscale pollutants.

Rhizospheric bacterial communities against microplastics (MPs): Novel ecological strategies based on the niche differentiation.

Considerable amounts of microplastics (MPs) are stocked in plant rhizospheres, yielding adverse effects on rhizospheric microorganisms and threatening plant health. However, the adaptation of the rhizospheric microbiota for MPs remains largely unknown. Here, to evaluate the adaptive strategies of rhizospheric bacterial communities against MPs, we characterized the spatial dissimilarities in MPs properties and bacterial communities from mangrove non-rhizosphere to rhizosphere to root hair sediments. Consequently, two strategies were uncovered: (1) Bacterial communities showed significant niche differentiation induced by the increasingly enriched MPs evaluated by piecewise structural equation modeling (piecewise SEM), as increasing specialization (10.2 % to 19.4 % to 23.0 % of specialists) and decreasing generalization (10.4 % to 10.2 % to 8.7 % of generalists). (2) A self-remediation strategy of enhancing microbial plastic-degrading potentials was determined in bacterial communities, tightly coupled to the increase of specialists (linear regression analysis, R2 = 0.54, P < 0.001) and increasing MPs weathering degrees visualized by the scanning electron microscopy (SEM) from non-rhizosphere to rhizosphere to root hair regions. Our study provides a novel insight into the ecological strategies that rhizospheric microbes utilize against MPs, and broadens our knowledge of the interaction between soil microbes and global MPs pollution.

XDL-ESI: Electrophysiological Sources Imaging via explainable deep learning framework with validation on simultaneous EEG and iEEG.

Electroencephalography (EEG) or Magnetoencephalography (MEG) source imaging aims to estimate the underlying activated brain sources to explain the observed EEG/MEG recordings. Solving the inverse problem of EEG/MEG Source Imaging (ESI) is challenging due to its ill-posed nature. To achieve a unique solution, it is essential to apply sophisticated regularization constraints to restrict the solution space. Traditionally, the design of regularization terms is based on assumptions about the spatiotemporal structure of the underlying source dynamics. In this paper, we propose a novel paradigm for ESI via an Explainable Deep Learning framework, termed as XDL-ESI, which connects the iterative optimization algorithm with deep learning architecture by unfolding the iterative updates with neural network modules. The proposed framework has the advantages of (1) establishing a data-driven approach to model the source solution structure instead of using hand-crafted regularization terms; (2) improving the robustness of source solutions by introducing a topological loss that leverages the geometric spatial information applying varying penalties on distinct localization errors; (3) improving the reconstruction efficiency and interpretability as it inherits the advantages from both the iterative optimization algorithms (interpretability) and deep learning approaches (function approximation). The proposed XDL-ESI framework provides an efficient, accurate, and interpretable paradigm to solve the ESI inverse problem with satisfactory performance in both simulated data and real clinical data. Specially, this approach is further validated using simultaneous EEG and intracranial EEG (iEEG).

Targeting Catechol-O-Methyltransferase Induces Mitochondrial Dysfunction and Enhances the Efficacy of Radiotherapy in Glioma.

Radiotherapy (RT) is commonly used to try to eliminate any remaining tumor cells following surgical resection of glioma. However, tumor recurrence is prevalent, highlighting the unmet medical need to develop therapeutic strategies to enhance the efficacy of RT in glioma. Focusing on the radiosensitizing potential of currently approved drugs known to cross the blood-brain barrier can facilitate rapid clinical translation. Here, we assessed the role of catechol-o-methyltransferase (COMT), a key enzyme to degrade catecholamines and a drug target for Parkinson's disease, in glioma treatment. Analysis of TCGA data showed significantly higher COMT expression levels in both low-grade glioma and glioblastoma compared to normal brain tissues. Inhibition of COMT by genetic knockout or FDA-approved COMT inhibitors significantly sensitized glioma cells to RT in vitro and in vivo. Mechanistically, COMT inhibition in glioma cells led to mitochondria dysfunction and increased mitochondrial RNA release into the cytoplasm, activating the cellular antiviral double-stranded RNA sensing pathway and type I interferon (IFN) response. Elevated type I IFNs stimulated the phagocytic capacity of microglial cells, enhancing RT efficacy. Given the long-established safety record of the COMT inhibitors, these findings provide a solid rationale to evaluate them in combination with RT in glioma patients.

Multi-Modal Electrophysiological Source Imaging With Attention Neural Networks Based on Deep Fusion of EEG and MEG.

The process of reconstructing underlying cortical and subcortical electrical activities from Electroencephalography (EEG) or Magnetoencephalography (MEG) recordings is called Electrophysiological Source Imaging (ESI). Given the complementarity between EEG and MEG in measuring radial and tangential cortical sources, combined EEG/MEG is considered beneficial in improving the reconstruction performance of ESI algorithms. Traditional algorithms mainly emphasize incorporating predesigned neurophysiological priors to solve the ESI problem. Deep learning frameworks aim to directly learn the mapping from scalp EEG/MEG measurements to the underlying brain source activities in a data-driven manner, demonstrating superior performance compared to traditional methods. However, most of the existing deep learning approaches for the ESI problem are performed on a single modality of EEG or MEG, meaning the complementarity of these two modalities has not been fully utilized. How to fuse the EEG and MEG in a more principled manner under the deep learning paradigm remains a challenging question. This study develops a Multi-Modal Deep Fusion (MMDF) framework using Attention Neural Networks (ANN) to fully leverage the complementary information between EEG and MEG for solving the ESI inverse problem, which is termed as MMDF-ANN. Specifically, our proposed brain source imaging approach consists of four phases, including feature extraction, weight generation, deep feature fusion, and source mapping. Our experimental results on both synthetic dataset and real dataset demonstrated that using a fusion of EEG and MEG can significantly improve the source localization accuracy compared to using a single-modality of EEG or MEG. Compared to the benchmark algorithms, MMDF-ANN demonstrated good stability when reconstructing sources with extended activation areas and situations of EEG/MEG measurements with a low signal-to-noise ratio.

VHL loss enhances antitumor immunity by activating the anti-viral DNA-sensing pathway.

von Hippel-Lindau (VHL), known as a tumor suppressor gene, is frequently mutated in clear cell renal cell carcinoma (ccRCC). However, VHL mutation is not sufficient to promote tumor formation. In most cases other than ccRCC, VHL loss alters cellular homeostasis and causes cell stress and metabolic changes by stabilizing hypoxia-inducible factor (HIF) levels, resulting in a fitness disadvantage. In addition, the function of VHL in regulating immune response is still not well established. In this study, we demonstrate that VHL loss enhances the efficacy of anti-programmed death 1 (PD1) treatment in multiple murine tumor models in a T cell-dependent manner. Mechanistically, we discovered that upregulation of HIF1α/2α induced by VHL loss decreased mitochondrial outer membrane potential and caused the cytoplasmic leakage of mitochondrial DNA, which triggered cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) activation and induced type I interferons. Our study thus provided mechanistic insights into the role of VHL gene loss in boosting antitumor immunity.

Predicting survival in patients with myelodysplastic/myeloproliferative neoplasms with SF3B1 mutation and thrombocytosis.

We investigated data from 180 consecutive patients with myelodysplastic/myeloproliferative neoplasms with SF3B1 mutation and thrombocytosis (MDS/MPN-SF3B1-T) who were diagnosed according to the 2022 World Health Organization (WHO) classification of myeloid neoplasms to identify covariates associated with survival. At a median follow-up of 48 months (95% confidence interval [CI] 35-61 months), the median survival was 69 months (95% CI 59-79 months). Patients with bone marrow ring sideroblasts (RS) < 15% had shorter median overall survival (OS) than did those with bone marrow RS ≥ 15% (41 months [95% CI 32-50 months] versus 76 months [95% CI 59-93 months]; P < 0.001). According to the univariable analyses of OS, age ≥ 65 years (P < 0.001), hemoglobin concentration (Hb) < 80 g/L (P = 0.090), platelet count (PLT) ≥ 800 × 10E + 9/L (P = 0.087), bone marrow RS < 15% (P < 0.001), the Revised International Prognostic Scoring System (IPSS-R) cytogenetic category intermediate/poor/very poor (P = 0.005), SETBP1 mutation (P = 0.061) and SRSF2 mutation (P < 0.001) were associated with poor survival. Based on variables selected from univariable analyses, two separate survival prediction models, a clinical survival model, and a clinical-molecular survival model, were developed using multivariable analyses with the minimum value of the Akaike information criterion (AIC) to specifically predict outcomes in patients with MDS/MPN-SF3B1-T according to the 2022 WHO classification.

Combination therapy with venetoclax and azacitidine for the treatment of myelodysplastic syndromes with DDX41 mutations.

Myelodysplastic syndromes (MDS) patients with DEAD-box helicase 41 (DDX41) mutations have been reported to be treated effectively with lenalidomide; however, there are no randomized studies to prove it. Venetoclax and azacitidine are safe and effective in high-risk MDS/AML. In this study, we evaluated the efficacy of venetoclax and azacitidine combination therapy in eight consecutive MDS patients with DDX41 mutations at our centre from March 2021 to November 2023. We retrospectively analyzed the genetic features and clinical characteristics of these patients. Our findings suggest that MDS patients with DDX41 mutation may benefit from the therapy, for six subjects received this regimen as initial therapy and five of the six subjects achieved complete remission.

Analysis of clinical features of heart failure in children with cardiomyopathy and improved ejection fraction.

Background: The prognosis of children with heart failure varies considerably. After treatment, left ventricular ejection fraction (LVEF) can be improved in some children. The aim of this study was to analyze the clinical features of children with heart failure accompanied by cardiomyopathy and recovered ejection fraction [heart failure with recovered ejection fraction (HFrecEF)] and to identify the predictors of improved LVEF. Methods: Children diagnosed with heart failure in Beijing Anzhen Hospital Affiliated to Capital Medical University from 2018 to 2021 were retrospectively enrolled. According to the baseline and change of LVEF, the patients were divided into two groups: a reduced ejection fraction (HFrEF) group and an HFrecEF group. The t-test was used to evaluate the difference between the two groups. The predictive factors of ejection fraction improvement were analyzed with a logistic regression model. Results: A total of 72 children were included in this study, including 31 (43.1%) in the HFrEF group and 41 (56.9%) in the HFrecEF group. Compared with children in the HFrEF group, children in the HFrecEF group were younger and had faster resting heart rates, lower creatinine, lower suppression of tumorigenicity 2 (ST2) expression, a lower platelet-to-lymphocyte (PLT:LYM) ratio, and smaller left atrial diameter. After a mean follow-up of 35.87 months, 26 cases returned to normal ejection fraction. In the HFrEF group, sudden cardiac death occurred in two cases, and four cases received heart transplantation. Logistic analysis showed that virus infection [odds ratio (OR) =1.279; 95% confidence interval (CI): 0.374-4.379; P=0.007], low ST2 expression (cutoff value =1.89 ng/mL: OR =1.042; 95% CI: 1.007-1.082; P=0.032), and treatment with intravenous immunoglobulin (IVIG) (OR =5.077; 95% CI: 1.458-17.684; P=0.011) were predictors of improvement in LVEF in patients with heart failure after treatment. Conclusions: In some patients with HFrecEF, LVEF eventually returned to normal. The combination of viral infection, low ST2 expression, and the application of IVIG therapy were found to be independent predictors of LVEF improvement in patients with heart failure after treatment.

Validation and comparison of 5th edition World Health Organization classification (WHO 2022) and International Consensus Classification proposals for MDS-SFB31.

The criteria of myelodysplastic syndromes (MDS) with mutated SFB31 (MDS-SFB31) proposed by the 5th edition of the WHO classification (WHO 2022) and the International Consensus Classification (ICC) need validation. We analysed 125 consecutive MDS cases with SFB31 mutation or ring sideroblasts (RS) ≥15% without excess blasts. We found that SFB31-negative MDS with RS had significantly different clinical features and worse prognosis. According to WHO 2022, the detection of ≥15% RS may substitute for SF3B1 mutation and our analyses support this proposal for similar prognosis of two groups after excluding high-risk genetic features referred by WHO 2022. Patients with variant allele frequency (VAF) <10% SFB31 tend to have briefer survival, supporting the VAF 10% threshold of ICC. Patients with multilineage dysplasia (MLD) had significantly shorter OS than those with single lineage dysplasia. MLD is still a powerful morphological marker of worse outcome in WHO 2022 and ICC-defined MDS-SF3B1.

Rejuvenating classical brain electrophysiology source localization methods with spatial graph Fourier filters for source extents estimation.

EEG/MEG source imaging (ESI) aims to find the underlying brain sources to explain the observed EEG or MEG measurement. Multiple classical approaches have been proposed to solve the ESI problem based on different neurophysiological assumptions. To support clinical decision-making, it is important to estimate not only the exact location of the source signal but also the extended source activation regions. Existing methods may render over-diffuse or sparse solutions, which limit the source extent estimation accuracy. In this work, we leverage the graph structures defined in the 3D mesh of the brain and the spatial graph Fourier transform (GFT) to decompose the spatial graph structure into sub-spaces of low-, medium-, and high-frequency basis. We propose to use the low-frequency basis of spatial graph filters to approximate the extended areas of brain activation and embed the GFT into the classical ESI methods. We validated the classical source localization methods with the corresponding improved version using GFT in both synthetic data and real data. We found the proposed method can effectively reconstruct focal source patterns and significantly improve the performance compared to the classical algorithms.

Secreted salt and hydrodynamic factors combine to affect dynamic fluctuations of microplastics on mangrove leaves.

Mangrove leaves have been acknowledged as crucial sink for coastal microplastics (MPs). Whereas, the temporal dynamics of MPs intercepted by mangrove leaves have remained poorly understood. Here, we detected MPs intercepted by submerged and non-submerged mangrove leaves over time and the potential driving factors. Abundance and characteristics of MPs interception by mangrove leaves exhibited dynamic fluctuations, with the coefficient of variation (CV) of submerged mangrove leaves (CV = 0.604; 1.76 n/g to 15.45 n/g) being approximately twofold higher than non-submerged mangrove leaves (CV = 0.377; 0.74 n/g to 3.28 n/g). Partial least squares path model (PLS-PM) analysis further illustrated that MPs abundance on submerged mangrove leaves were negative correlated to hydrodynamic factors (i.e., current velocity and tidal range). Intriguingly, secreted salt as a significantly driver of MPs intercepted by mangrove leaves. Results of this work highlights that MPs intercepted by mangrove leaves is characterized by dynamic fluctuations and reveals the importance of hydrodynamic factors and secreted salt. Overall, this work identifies the pivotal buffering role played by mangrove leaves in intercepting MPs, which provides basic knowledge for better understanding of microplastic pollution status and control from mangrove plants.

Review of Anaka Dworakowska & Viraktamath, 1975 (Hemiptera, Cicadellidae, Typhlocybinae) with the descriptions of five new species from China.

The dikraneurine leafhopper genus Anaka is reviewed based on a comparative morphological study. Five new species, Anakaauriculasp. nov., Anakacruciatasp. nov., Anakacurvatasp. nov., Anakarosaceasp. nov., and Anakaspiralissp. nov. from China are described and illustrated in detail. Additionally, a key to known Anaka species is provided along with a checklist of all species and their distributions.

Relevance Analysis of TPM2 and Clinicopathological Characteristics in Breast Cancer.

Background: The function of tropomyosin 2 (TPM2) in breast cancer is still far understudied. In this study, we aim to explore the roles of TPM2 in breast cancer progression. Methods: This research included 155 breast cancer tissues. The expression of TPM2 was analyzed by immunohistochemical staining and grading. The mRNA expression of TPM2 in pan-cancer was analyzed with The Cancer Genome Atlas (TCGA) data plate form. The differential expression of TPM2 protein and the differential promoter methylation level of TPM2 between breast cancer tissues and normal breast tissues were analyzed by the UALCAN online database. The relationship between TPM2 and signaling pathways was interpreted by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) pathway enrichment analyses. The survival curve of TPM2 was analyzed across the Kaplan-Meier plotter online database. Furthermore, the relationship between TPM2 expression and infiltrating macrophages was validated through in vitro co-culture experiments. Results: TPM2 expression was significantly down-regulated in breast cancer samples. In addition, TPM2 expression was correlated with lymph node metastasis and high-grade histopathological morphology. The receiver operating characteristic (ROC) curve indicated that TPM2 expression could well distinguish between normal breast tissue and breast cancer tissue. TPM2 may have potential value in breast cancer diagnosis. Bioinformatics analysis illustrated that TPM2 was mainly involved in extracellular matrix organization, collagen fibril organization, cell junction assembly, focal adhesion, cAMP signaling pathway, estrogen signaling pathway, Wnt signaling pathway, and adaptive immune system. TPM2 expression was correlated with immune infiltrating cells and immune checkpoint molecules. Our in vitro co-culture experiments showed that the M2 macrophages could upregulate the expression of TPM2. Conclusion: TPM2 may play key roles in breast cancer occurrence and development, especially in cancer metastasis. TPM2 may be a potential biomarker for breast cancer diagnosis.

Insight into the role of niche concept in deciphering the ecological drivers of MPs-associated bacterial communities in mangrove forest.

Myriad inherent and variable environmental features are controlling the assembly and succession of bacterial communities colonizing on mangrove microplastics (MPs). However, the mechanisms governing mangrove MPs-associated bacterial responses to environmental changes still remain unknown. Here, we assessed the dissimilarities of MPs-associated bacterial composition, diversity and functionality as well as quantified the niche variations of each taxon on plastispheres along river-mangrove-ocean and mangrove landward-to-seaward gradients in the Beibu Gulf, China, respectively. The bacterial richness and diversity as well as the niche breadth on mangrove sedimentary MPs dramatically decreased from landward to seaward regions. Characterizing the niche variations linked the difference of ecological drivers of MPs-associated bacterial populations and functions between river-mangrove-ocean (microplastic properties) and mangrove landward-to-seaward plastispheres (sediment physicochemical properties) to the trade-offs between selective stress exerted by inherent plastic substrates and microbial competitive stress imposed by environmental conditions. Notably, Rhodococcus erythropolis was predicted to be the generalist species and closely associated to biogeochemical cycles of mangrove plastispheres. Our work provides a reliable pathway for tackling the hidden mechanisms of environmental factors driving MPs-associated microbe from perspectives of niches and highlights the spatial dynamic variations of mangrove MPs-associated bacteria.

Transformation of 6PPDQ during disinfection: Kinetics, products, and eco-toxicity assessment.

N-phenyl-N'-(1,3-dimethyl butyl)-p-phenylenediamine-quinone (6PPDQ) currently arouses broad concerns because of its acute lethality to coho salmon and rainbow trout at environmentally relevant concentrations and the wide occurrence in runoff-impacted water. Investigation on the fate and transformation of 6PPDQ in various treatment processes is necessary for its risk assessment and control. Here, we explored the transformation of 6PPDQ during disinfection with its precursor 6PPD as a reference, focusing on kinetics, products, and toxicity variation. 6PPDQ readily reacted with hypochlorite and chlorine dioxide with second-order rate constants of 2580 ± 143 M-1 s-1 and 614 ± 52 M-1 s-1 (pH 7.0 and 25 °C), which are slightly lower than the reactions of 6PPD. We tentatively identified thirteen transformation products for 6PPDQ and eight for 6PPD in reaction with the two disinfectants. It seems that the quinone ring of 6PPDQ and the p-phenylenediamine moiety of 6PPD are reactive sites. The transformation of these compounds probably proceeds through Cl-substitution, ring cleavage, hydroxylation, and amine oxidation and hydrolysis. Tests with zebrafish embryos revealed that the transformation products of 6PPDQ could have higher eco-toxicity than the parent compound, while the toxicity of the 6PPD products remained nearly unchanged. The increased toxicity of 6PPDQ during disinfection highlights the necessity to substantially reduce its content before the disinfection of runoff-impacted water.

VHL loss enables immune checkpoint blockade therapy by boosting type I interferon response.

Despite a moderate mutation burden, clear cell renal cell carcinoma (ccRCC) responds well to immune checkpoint blockade (ICB) therapy. Here we report that loss-of-function mutations in the von Hippel-Lindau (VHL) gene, the most frequent in ccRCC, underlies its responsiveness to ICB therapy. We demonstrate that genetic knockout of the VHL gene enhanced the efficacy of anti-PD-1 therapy in multiple murine tumor models in a T cell-dependent manner. Mechanistically, we discovered that upregulation of HIF1α and HIF2α induced by VHL gene loss decreased mitochondrial outer membrane potential and caused the cytoplasmic leakage of mitochondrial DNA (mtDNA), which triggered cGAS-STING activation and induced type I interferons. Our study thus provided novel mechanistic insights into the role of VHL gene loss in potentiating ccRCC immunotherapy.

Correlation of Claudin18.2 expression with clinicopathological characteristics and prognosis in gastric cancer.

OBJECTIVES: Claudin18.2 (Cldn18.2) is a tight junction protein expressed in gastric epithelial cells and is an emerging target for gastric cancer (GC). This study aimed to analyze the correlation between Cldn18.2 and clinicopathological parameters in GC patients undergoing radical surgery. METHODS AND RESULTS: This study included 426 GC patients who underwent radical gastrectomy. The expression of Cldn18.2 was analyzed by immunohistochemical staining and grading. The statistical results indicated that the expression of Cldn18.2 was correlated with T stage, TNM stage, Lauren classification, and the expression level of Mucin-2 (MUC2), Mucin-5AC (MUC5AC), Mucin-6 (MUC6), human epidermal growth factor receptor 2 (HER2), P53 and trefoil factor 2 (TFF2). In addition, through data mining of the Cancer Genome Atlas (TCGA) database, it is suggested that Cldn18.2 expression level is significantly correlated with the expression level of MUC5AC, MUC6, and TFF2. Besides, Cldn18.2 is related to tumor immune infiltration, programmed cell death protein 1 (PD 1) pathway, cell cycle and Wnt signaling pathway. CONCLUSIONS: The expression of Cldn18.2 was closely related to gastric-type GC, so gastric-type GC patients may benefit more from targeted drugs targeting Cldn18.2. In GC cells, depletion of Cldn18.2 may influence cell cycle and immune response by affecting Wnt signaling pathway and PD 1 pathway.

Distinct microplastics abundance variation in root-associated sediments revealed the underestimation of mangrove microplastics pollution.

Mangrove sediment is acknowledged as the critical sink of microplastics (MPs). However, the potential effect of mangrove root systems on the MPs migration in sediment remains largely unknown. Here, our study characterized the spatial distribution of MPs trapped in root hair, rhizosphere, and non-rhizosphere zones, and analyzed their correlations with physicochemical properties of sediments. The significantly increased MPs abundances toward root systems shed light on the distinct effect on the migration of MPs exerted by mangrove root systems. Partial least squares path modeling (PLS-PM) analysis revealed that pore water content and pH influenced the abundances of different MP characteristics (shape, color, size, and type) and further promoted the accumulation of MPs toward the root systems. In different mangrove areas from landward to seaward, other sediment properties (median grain size, clay content, and salinity) also controlled MP distribution. Additionally, smaller-sized MPs (<1000 µm) were more easily transported to the root systems. Our study emphasizes the importance of considering root systems effect when investigating the mechanisms of MPs distribution and migration in mangrove sediments.