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Abstract Objective To evaluate the effect of the contrast-enhancement-boost (CE-boost) postprocessing technique on improving the image quality of obese patients in computed tomography pulmonary angiography (CTPA) compared to hybrid iterative reconstruction (HIR) and model-based iterative reconstruction (MBIR) algorithms. Methods This prospective study was conducted on 100 patients who underwent CTPA for suspected pulmonary embolism. Non-obese patients with a body mass index (BMI) under 25 were designated as group 1, while obese patients (group 2) had a BMI exceeding 25. The CE-boost images were generated by subtracting non-contrast HIR images from contrast-enhanced HIR images to improve the visibility of pulmonary arteries further. The CT value, image noise, signal-to-noise ratio (SNR), and contrast-to-noise ratio (CNR) were quantitatively assessed. Two chest radiologists independently reviewed the CT images (5, best; 1, worst) across three subjective characteristics including diagnostic confidence, subjective image noise, and vascular contrast. The Friedman test and Dunn-Bonferroni correction were used for statistical analysis. Results The CE-boost had significantly higher CT values than HIR and MBIR in both groups (all p

Abstract The vacancy effect in quantum spin liquid (QSL) has been extensively studied. A finite density of random vacancies in the Kitaev model can lead to a pileup of low-energy density of states (DOS), which is generally experimentally determined by a scaling behavior of thermodynamic or magnetization quantities. Here, we report detailed muon spin relaxation (μSR) results of H3LiIr2O6, a Kitaev QSL candidate with vacancies. The absence of magnetic order is confirmed down to 80 mK, and the spin fluctuations are found to be persistent at low temperatures. Intriguingly, the time-field scaling law of longitudinal-field (LF)-μSR polarization is observed down to 0.1 K. This indicates a dynamical scaling, whose critical exponent of 0.46 is excellently consistent with the scaling behavior of specific heat and magnetization data. All the observations point to the finite DOS with the form $$N(E)\sim {E}^{-\nu }$$ N ( E ) ∼ E − ν , which is expected for the Kitaev QSL in the presence of vacancies. Our μSR study provides a dynamical fingerprint of the power-law low-energy DOS and introduces a crucial new insight into the vacancy effect in QSL.

Abstract Background Silicosis is an irreversible fibrotic disease of the lung caused by chronic exposure to silica dust, which manifests as infiltration of inflammatory cells, excessive secretion of pro-inflammatory cytokines, and pulmonary diffuse fibrosis. As the disease progresses, lung function further deteriorates, leading to poorer quality of life of patients. Currently, few effective drugs are available for the treatment of silicosis. Bicyclol (BIC) is a compound widely employed to treat chronic viral hepatitis and drug-induced liver injury. While recent studies have demonstrated anti-fibrosis effects of BIC on multiple organs, including liver, lung, and kidney, its therapeutic benefit against silicosis remains unclear. In this study, we established a rat model of silicosis, with the aim of evaluating the potential therapeutic effects of BIC. Methods We constructed a silicotic rat model and administered BIC after injury. The FlexiVent instrument with a forced oscillation system was used to detect the pulmonary function of rats. HE and Masson staining were used to assess the effect of BIC on silica-induced rats. Macrophages-inflammatory model of RAW264.7 cells, fibroblast-myofibroblast transition (FMT) model of NIH-3T3 cells, and epithelial-mesenchymal transition (EMT) model of TC-1 cells were established in vitro. And the levels of inflammatory mediators and fibrosis-related proteins were evaluated in vivo and in vitro after BIC treatment by Western Blot analysis, RT-PCR, ELISA, and flow cytometry experiments. Results BIC significantly improved static compliance of lung and expiratory and inspiratory capacity of silica-induced rats. Moreover, BIC reduced number of inflammatory cells and cytokines as well as collagen deposition in lungs, leading to delayed fibrosis progression in the silicosis rat model. Further exploration of the underlying molecular mechanisms revealed that BIC suppressed the activation, polarization, and apoptosis of RAW264.7 macrophages induced by SiO2. Additionally, BIC inhibited SiO2-mediated secretion of the inflammatory cytokines IL-1β, IL-6, TNF-α, and TGF-β1 in macrophages. BIC inhibited FMT of NIH-3T3 as well as EMT of TC-1 in the in vitro silicosis model, resulting in reduced proliferation and migration capability of NIH-3T3 cells. Further investigation of the cytokines secreted by macrophages revealed suppression of both FMT and EMT by BIC through targeting of TGF-β1. Notably, BIC blocked the activation of JAK2/STAT3 in NIH-3T3 cells required for FMT while preventing both phosphorylation and nuclear translocation of SMAD2/3 in TC-1 cells necessary for the EMT process. Conclusion The collective data suggest that BIC prevents both FMT and EMT processes, in turn, reducing aberrant collagen deposition. Our findings demonstrate for the first time that BIC ameliorates inflammatory cytokine secretion, in particular, TGF-β1, and consequently inhibits FMT and EMT via TGF-β1 canonical and non-canonical pathways, ultimately resulting in reduction of aberrant collagen deposition and slower progression of silicosis, supporting its potential as a novel therapeutic agent.

BackgroundThis study aimed to observe the effects of repetitive transcranial magnetic stimulation (rTMS) on cognitive function and thyroid hormone levels in early older stroke patients with low thyroid hormone levels, and to investigate the correlation between the changes in thyroid hormone levels and the improvements in cognitive function after stroke.MethodsForty older stroke patients who met the inclusion criteria were recruited and randomized into a magnetic-stimulation group (rTMS group) and a sham-stimulation group (Sham group). The rTMS group received low-frequency true stimulation and the Sham group received low-frequency sham stimulation. Patients’ cognitive scores, activity of daily living(ADL) scores, and their levels of triiodothyronine (T3), free triiodothyronine (FT3), thyroxin (T4), free thyroxine (FT4), and thyroid stimulating hormone (TSH) were assessed before the intervention, after the 4-week intervention, and after an additional 4 weeks of follow-up; Repeated measurement analysis of variance was used to compare the changes of each index in the two groups at different times and the correlations between patiens’ cognitive function scores and their changing hormone levels were subsequently investigated.ResultsThirty-one patients were included in this study: 16 patients in rTMS group and 15 patients in the Sham group. Repeated-measures ANOVA showed that patients’ T3,FT3 and TSH levels tended to increase at 4-week intervention and at the follow up (p

Introduction: Immunoglobulin A nephropathy (IgAN) patients with lower estimated glomerular filtration rate (eGFR) and higher proteinuria are at a higher risk for end-stage kidney disease (ESKD) and their prognosis is still unclear. We aim to develop and validate prognostic models in IgAN patients with CKD stage 3 or 4 and proteinuria≥1.0 g/d. Methods: Patients who came from Xijing Hospital, spanning December 2008 to January 2020 were divided into training and test cohorts randomly, with a ratio of 7:3, achieving ESKD and death as study endpoints. Created prediction models for IgAN patients based on 66 clinical and pathological characteristics using the random survival forests (RSF), survival support vector machine (SSVM), eXtreme Gradient Boosting (XGboost), and Cox regression models. The concordance index (C-index), integrated Brier scores (IBS), net reclassification index (NRI), and integrated discrimination improvement (IDI) were used to evaluate discrimination, calibration, and risk classification respectively. Results: A total of 263 patients were enrolled. The median follow-up time was 57.3 months, with 124 (47.1%) patients experiencing combined events. Age, blood urea nitrogen, serum uric acid, serum potassium, glomeruli sclerosis ratio, hemoglobin, and tubular atrophy/interstitial fibrosis were identified as risk factors. The RSF model predicted the prognosis with a C-index of 0.871 (0.842, 0.900) in training cohort and 0.810 (0.732, 0.888) in test cohort, which was higher than the models built by SSVM model (0.794 (0.753, 0.835) and 0.805 (0.731, 0.879) respectively), XGboost model (0.840 (0.797, 0.883) and 0.799 (0.723, 0.875) respectively) and Cox regression (0.776 (0.727, 0.825) and 0.793 (0.713, 0.873) respectively). NRI and IDI showed that the RSF model exhibited superior performance than the Cox model. Conclusion: Our model introduced seven risk factors that may be useful in predicting the progression of IgAN patients with CKD stage 3 or 4 and proteinuria ≥1.0g/d. The RSF model is applicable for identifying the progression of IgAN and has outperformed than SSVM, XGboost, and Cox models.

Atmospheric fine particulate matter (PM2.5) can harm various systems in the human body. Due to limitations in the current understanding of epidemiology and toxicology, the disease types and pathogenic mechanisms induced by PM2.5 in various human systems remain unclear. In this study, the disease types induced by PM2.5 in the respiratory, circulatory, endocrine, and female and male urogenital systems have been investigated and the pathogenic mechanisms identified at molecular level. The results reveal that PM2.5 is highly likely to induce pulmonary emphysema, reperfusion injury, malignant thyroid neoplasm, ovarian endometriosis, and nephritis in each of the above systems respectively. The most important co-existing gene, cellular component, biological process, molecular function, and pathway in the five systems targeted by PM2.5 are Fos proto-oncogene (FOS), extracellular matrix, urogenital system development, extracellular matrix structural constituent conferring tensile strength, and ferroptosis respectively. Differentially expressed genes that are significantly and uniquely targeted by PM2.5 in each system are BTG2 (respiratory), BIRC5 (circulatory), NFE2L2 (endocrine), TBK1 (female urogenital) and STAT1 (male urogenital). Important disease-related cellular components, biological processes, and molecular functions are specifically induced by PM2.5. For example, response to wounding, blood vessel morphogenesis, body morphogenesis, negative regulation of response to endoplasmic reticulum stress, and response to type I interferon are the top uniquely existing biological processes in each system respectively. PM2.5 mainly acts on key disease-related pathways such as the PD-L1 expression and PD-1 checkpoint pathway in cancer (respiratory), cell cycle (circulatory), apoptosis (endocrine), antigen processing and presentation (female urogenital), and neuroactive ligand-receptor interaction (male urogenital). This study provides a novel analysis strategy for elucidating PM2.5-related disease types and is an important supplement to epidemiological investigation. It clarifies the risks of PM2.5 exposure, elucidates the pathogenic mechanisms, and provides scientific support for promoting the precise prevention and treatment of PM2.5-related diseases.

An edible film using gellan gum, black rice anthocyanins, and titanium dioxide as raw materials were prepared. The effect of edible film on blueberries coating preservation was investigated. Firstly, scanning electron microscopy revealed that there were no obvious cracks or delamination in the cross sections of the gellan gum film (GG), gellan gum, and black rice anthocyanin, composite film (GG-BRA), and gellan gum, black rice anthocyanin, and titanium dioxide composite film (GG-BRA-TiO2). Fourier transform infrared spectroscopy further showed that gellan gum was interacted with black rice anthocyanin and titanium dioxide through non covalent bond. The antibacterial experiment indicated that the GG-BRA-TiO2 composite film had a good antibacterial activity, in which size of the antibacterial circle for Staphylococcus aureus, E. coli and bread's yeast were 4.14, 2.77 and 3.55 (mm), respectively. Secondly, the composite film was used for the preservation of blueberries. The results showed that the GG-BRA and GG-BRA-TiO2 coating groups could slow down the rate of physicochemical properties changes during blueberry fruit storage. Among them, the preservation effect of GG-BRA-TiO2 composite film was better than that of GG-BRA composite film. After 10 days of storage, the weight loss rate, hardness, anthocyanins, total phenols, and the activity of polyphenol oxidase were decreased by 1.56%, 23.69%, 18.44%, 12.71%, and 14.00% compared to the control group, respectively. Therefore, GG-BRA-TiO2 composite film showed good water resistance and antibacterial properties and could be used as a promising coating and preservation material in food packaging.

Abstract Baicalein is a natural flavonoid abundant in various foods and dietary plants, including Tuber aestivum and Oroxylum indicum. In this study, we investigated the role of baicalein in enhancing the insulin‐sensitizing effect of metformin in mice with prediabetes. Baicalein, when combined with 25% of normal‐dose metformin, achieved a diabetes‐reversion rate of 80%, which was 1.86‐fold that of normal‐dose metformin. Mechanistically, baicalein enhanced the insulin‐sensitizing effect of metformin on lipid metabolism by inhibiting de novo lipogenesis through the AMP‐activated protein kinase/SREBP‐1c/FASN pathway and by inducing fatty‐acid β‐oxidation through the upregulation of ACSL1, CPT1A, EHHADH, and acyl‐CoA dehydrogenases (ACADL/ACADM/ACADS). Meanwhile, baicalein enhanced the insulin‐sensitizing effect of metformin via the modulation of the gut microenvironment by enriching probiotics, especially Akkermansia by 53.4‐fold, depleting opportunistic pathogens, and strengthening the intestinal barrier. The improved gut microenvironment led to the alleviation of chronic endotoxemia, as evidenced by decreased levels of lipopolysaccharide and proinflammatory cytokines. Furthermore, baicalein enhanced the effect of metformin on decreasing the circulating level of branched‐chain amino acids (BCAAs), which further improved insulin sensitivity by normalizing the mTORC1/p70S6K/IRS1 signaling pathway and de novo lipogenesis. Moreover, the role of baicalein in enhancing the insulin‐sensitizing effect of metformin was verified by an oleic acid‐induced steatosis model and a BCAA‐induced insulin resistance model in hepatocytes. Our study laid a theoretical foundation for developing baicalein into a dietary supplement for diabetes prevention. The diverse mechanisms of food‐derived flavonoids can be applied in the development of dietary supplements to enhance the efficacy of oral hyperglycemic agents currently used in clinics.

The thermal behavior of the cladding layer and the flow behavior of the molten pool significantly affect the geometry, temperature distribution and microstructure of the cladding track, thus affecting the mechanical properties of the cladding. Based on the interaction between the laser and powders, a calculation method of the cross-sectional area of the cladding track is proposed. The droplet energy method and the moving grid method are first combined to establish the surface growth model of the cladding track, to calculate the geometry of the cladding track. Then, the temperature field and flow field of the cladding track are studied. The driving forces of the molten pool flow including shear viscosity, gravity, buoyancy, surface tension at the gas-liquid boundary and pressure between liquids are considered to carry out the dynamics study of the molten pool. According to the force condition of the infinitesimal in the molten pool, the dynamic rules and boundary rules of the molten pool are established, so as to solve the flow field of the molten pool. In addition, the calculated geometry of the cladding track is compared with the experimental result to verify the accuracy of the model, and the microhardness of the cladding track is measured. The results show that the relative error between the simulation and the experiment is less than 6%, and the microhardness of the cladding layer is significantly improved. This work can provide a method for studying the morphology, temperature field, and flow field of laser cladding.

Abstract Background 99mTc radiolabeled nanobody NM-02 (99mTc-NM-02) is a novel single photon emission computed tomography (SPECT) probe with a high affinity and specificity for human epidermal growth factor receptor 2 (HER2). In this study, a clinical imaging trial was conducted to investigate the relationship between 99mTc-NM-02 uptake and HER2 expression in patients with breast cancer. Methods Thirty patients with pathologically confirmed breast cancer were recruited and imaged with both 99mTc-NM-02 SPECT/computed tomography (CT) and 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)/CT. According to the treatment conditions before recruitment, patients were divided into two groups, the newly diagnosed group (n = 24) and the treated group (n = 6). The maximal standard uptake value (SUVmax) of 18F-FDG and SUVmax and mean SUV (SUVmean) of 99mTc-NM-02 in the lesions were determined to analyze the relationship with HER2 expression. Results No meaningful relationship was observed between 18F-FDG uptake and HER2 expression in 30 patients with breast cancer. 99mTc-NM-02 uptake was positively correlated with HER2 expression in the newly diagnosed group, but no correlation was observed in the treated group. 99mTc-NM-02 uptake in HER2-positive lesions was lower in those with effective HER2-targeted therapy compared with the newly diagnosed group. 99mTc-NM-02 SPECT/CT detected brain and bone metastases of breast cancer with a different imaging pattern from 18F-FDG PET/CT. 99mTc-NM-02 showed no non-specific uptake in inflamed tissues and revealed intra- and intertumoral HER2 heterogeneity by SPECT/CT imaging in 9 of the 30 patients with breast cancer. Conclusions 99mTc-NM-02 SPECT/CT has the potential for visualizing whole-body HER2 overexpression in untreated patients, making it a promising method for HER2 assessment in patients with breast cancer. Trial registration NCT04674722, Date of registration: December 19, 2020.

Abstract Background Disorders of the gut microbiome could be responsible for the progression of multiple organ dysfunction syndrome. In this study, we examined the effect of esmolol on the gut microbiome in a rat model of sepsis induced by cecal ligation and puncture (CLP). Methods The animals (n = 32) were randomly divided into 3 groups: Sham group (sham operation + normal saline treatment, n = 8), CLP group (cecal ligation and puncture + normal saline treatment, n = 12), and CLP + ESM group (cecal ligation and puncture + esmolol treatment, n = 12). After 24 h, feces in the colon were collected for 16S rRNA gene sequencing and nitric oxide analysis. In addition, colon was removed for immunohistochemical staining of inducible nitric oxide synthase (iNOS). Results Four rats in the CLP group and two rats in the CLP + ESM group died. The abundance of Lactobacillus in the CLP + ESM group was higher than CLP group (P = 0.048). In the linear discriminant analysis effect size analysis, Norank f Muribaculaceae, Escherichia–Shigella and Lactobacillus were the predominant bacteria in the Sham group, CLP group and CLP + ESM group, respectively. The iNOS expression in colonocytes stained by brown in the CLP group were much more than Sham group (P = 0.001). Compared to CLP group, the iNOS expression in colonocytes reduced after esmolol treatment (P = 0.013). The concentration of nitric oxide in colon feces was different in Sham group, CLP group and CLP + ESM group (1.31 ± 0.15μmmol/l vs. 1.98 ± 0.27μmmol/l vs. 1.51 ± 0.14μmmol/l, P = 0.001). In addition, the concentration of nitric oxide in CLP group was higher than Sham group (P = 0.001) or CLP + ESM group (P = 0.001). Conclusions Esmolol increased the fecal abundance of Lactobacillus in a rat model of sepsis. Moreover, esmolol reduced the iNOS expression of colonocytes and the nitric oxide concentration of colon feces.

Abstract The clinical implications of extrachromosomal DNA (ecDNA) in cancer therapy remain largely elusive. Here, we present a comprehensive analysis of ecDNA amplification spectra and their association with clinical and molecular features in multiple cohorts comprising over 13,000 pan-cancer patients. Using our developed computational framework, GCAP, and validating it with multifaceted approaches, we reveal a consistent pan-cancer pattern of mutual exclusivity between ecDNA amplification and microsatellite instability (MSI). In addition, we establish the role of ecDNA amplification as a risk factor and refine genomic subtypes in a cohort from 1015 colorectal cancer patients. Importantly, our investigation incorporates data from four clinical trials focused on anti-PD-1 immunotherapy, demonstrating the pivotal role of ecDNA amplification as a biomarker for guiding checkpoint blockade immunotherapy in gastrointestinal cancer. This finding represents clinical evidence linking ecDNA amplification to the effectiveness of immunotherapeutic interventions. Overall, our study provides a proof-of-concept of identifying ecDNA amplification from cancer whole-exome sequencing (WES) data, highlighting the potential of ecDNA amplification as a valuable biomarker for facilitating personalized cancer treatment.

PBX1 is a transcription factor that can promote the occurrence of various tumors and play a reg-ulatory role in tumor growth, metastasis, invasion, and drug resistance. Furthermore, a variant generated by fusion of E2A and PBX1, E2A-PBX1, has been found in 25% of patients with childhood acute lymphoblastic leukemia. Thus, PBX1 is a potential therapeutic target for many cancers. Here, we describe the structure of PBX1 and E2A-PBX1 as well as the molecular mecha-nisms whereby these proteins promote tumorigenesis to provide future research directions for developing new treatments. We show that PBX1 and E2A-PBX1 induce the development of highly malignant and difficult-to-treat solid and blood tumors. The development of specific drugs against their targets may be a good therapeutic strategy for PBX1-related cancers. Furthermore, we strongly recommend E2A-PBX1 as one of the genes for prenatal screening to reduce the incidence of childhood hematological malignancies.

IntroductionThe research on plant leaf morphology is of great significance for understanding the development and evolution of plant organ morphology. As a relict plant, the G. biloba leaf morphology typically exhibits bifoliate and peltate forms. However, throughout its long evolutionary history, Ginkgo leaves have undergone diverse changes.MethodsThis study focuses on the distinct “trumpet” leaves and normal fan-shaped leaves of G. biloba for analysis of their phenotypes, photosynthetic activity, anatomical observations, as well as transcriptomic and metabolomic analyses.ResultsThe results showed that trumpet-shaped G. biloba leaves have fewer cells, significant morphological differences between dorsal and abaxial epidermal cells, leading to a significantly lower net photosynthetic rate. Additionally, this study found that endogenous plant hormones such as GA, auxin, and JA as well as metabolites such as flavonoids and phenolic acids play roles in the formation of trumpet-shaped G. biloba leaves. Moreover, the experiments revealed the regulatory mechanisms of various key biological processes and gene expressions in the trumpet-shaped leaves of G. biloba.DiscussionDifferences in the dorsal and abdominal cells of G. biloba leaves can cause the leaf to curl, thus reducing the overall photosynthetic efficiency of the leaves. However, the morphology of plant leaves is determined during the primordia leaf stage. In the early stages of leaf development, the shoot apical meristem (SAM) determines the developmental morphology of dicotyledonous plant leaves. This process involves the activity of multiple gene families and small RNAs. The establishment of leaf morphology is complexly regulated by various endogenous hormones, including the effect of auxin on cell walls. Additionally, changes in intracellular ion concentrations, such as fluctuations in Ca2+ concentration, also affect cell wall rigidity, thereby influencing leaf growth morphology.

IntroductionRoad cracks significantly shorten the service life of roads. Manual detection methods are inefficient and costly. The YOLOv5 model has made some progress in road crack detection. However, issues arise when deployed on edge computing devices. The main problem is that edge computing devices are directly connected to sensors. This results in the collection of noisy, poor-quality data. This problem adds computational burden to the model, potentially impacting its accuracy. To address these issues, this paper proposes a novel road crack detection algorithm named EMG-YOLO.MethodsFirst, an Efficient Decoupled Header is introduced in YOLOv5 to optimize the head structure. This approach separates the classification task from the localization task. Each task can then focus on learning its most relevant features. This significantly reduces the model’s computational resources and time. It also achieves faster convergence rates. Second, the IOU loss function in the model is upgraded to the MPDIOU loss function. This function works by minimizing the top-left and bottom-right point distances between the predicted bounding box and the actual labeled bounding box. The MPDIOU loss function addresses the complex computation and high computational burden of the current YOLOv5 model. Finally, the GCC3 module replaces the traditional convolution. It performs global context modeling with the input feature map to obtain global context information. This enhances the model’s detection capabilities on edge computing devices.ResultsExperimental results show that the improved model has better performance in all parameter indicators compared to current mainstream algorithms. The EMG-YOLO model improves the accuracy of the YOLOv5 model by 2.7%. The mAP (0.5) and mAP (0.9) are improved by 2.9% and 0.9%, respectively. The new algorithm also outperforms the YOLOv5 model in complex environments on edge computing devices.DiscussionThe EMG-YOLO algorithm proposed in this paper effectively addresses the issues of poor data quality and high computational burden on edge computing devices. This is achieved through optimizing the model head structure, upgrading the loss function, and introducing global context modeling. Experimental results demonstrate significant improvements in both accuracy and efficiency, especially in complex environments. Future research can further optimize this algorithm and explore more lightweight and efficient object detection models for edge computing devices.

Cadmium (Cd) is a widespread environmental toxicant that poses significant threat to public health. After intake, Cd is distributed throughout the body via blood and lymphatic circulation. However, the effect of Cd on lymphatic vessels has not been revealed. In this study, mice were exposed to 10 μM cadmium chloride through drinking water immediately after corneal alkali burn. In vivo analyses showed that Cd treatment enhances the alkali burn-induced corneal lymphangiogenesis, which is characterized by increased expression of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), prospero-related homeobox 1 (PROX-1) and vascular endothelial growth factor receptor 3 (VEGFR3). In vitro, the proliferation and migration of human dermal lymphatic endothelial cells (HDLECs) are increased by 1 μM Cd treatment, while inhibited by 10 μM Cd treatment. At a concentration of 1 μM, Cd specifically induces phosphorylation of signal transducer and activator of transcription 3 (STAT3), but has no effect on the MAPK, AKT, or NF-κB signaling pathway. In the presence of the STAT3 inhibitor STATTIC, Cd fails to induce HDLECs proliferation and migration. In addition, Cd upregulates VEGFR3 expression and its gene promoter activity in a STAT3-dependent manner. Our study suggests that low-dose Cd promotes lymphangiogenesis through activation of the STAT3 signaling pathway.