Numerical modeling the process of deep slab dehydration and magmatism.

This study uses a 2D high-resolution thermo-mechanical coupled model to investigate the dynamic processes of deep plate hydration, dehydration, and subsequent magmatic activity in ocean-continent subduction zones. We reveal the pathways and temporal evolution of water transport to the deep mantle during the subduction process. Plate dehydration plays a critical role in triggering partial melting of the deep mantle and related magmatic activity. Our study shows significant differences in the volumes of melt produced at different depths, with dehydration reactions in deeper regions being weaker compared to shallower ones. It takes a longer time to reach the suitable P-T conditions for hydrous melting in the deep mantle. The results highlight the geophysical significance of water transport in deep subduction zones and its role in magmatic processes, particularly in the formation of magma chambers beneath continental plates.

miR-135b-5p promotes gastric carcinogenesis by targeting CLIP4-mediated JAK2/STAT3 signal pathway.

BACKGROUND: Gastric cancer (GC) is a common cancer worldwide; however, its molecular and pathogenic mechanisms remain unclear. MicroRNAs (miRNAs), which target key genes in GC, are associated with tumor promotion or suppression. Therefore, identifying new miRNA mechanisms could improve the novel diagnostic and therapeutic strategies for patients with GC. METHODS: To explore the biological functions of miR-135b-5p in GC, bioinformatic analysis and in vitro functional assays, including colony formation, wound healing, Transwell, and EdU assays, were used to assess the proliferative, invasive, and migratory capacities of GC cells. Target genes were predicted using RNA-seq and online databases. Dual-luciferase reporter assay, fluorescence in situ hybridization and western blotting were used to confirm the regulatory relationship between miR-135b-5p and CLIP4. The role of CLIP4 in tumor progression was assessed using clinical samples and both in vitro and in vivo assays. The tumor-suppressive mechanism of CLIP4 in GC was elucidated using rescue assays. RESULTS: Our study identified that miR-135b-5p as one of the top three over-expressed miRNAs in GC tissues, with RT-qPCR confirming its upregulation. Functional analysis showed that upregulated miR-135b-5p promoted malignant phenotypes in GC cells. Mechanistic research indicated that miR-135b-5p acts as a cancer promoter by targeting CLIP4. Moreover, our study suggested that CLIP4 exerts its tumor-suppressive function by inhibiting the JAK2/STAT3 signaling pathway. CONCLUSION: This study reveals a novel mechanism by which miR-135b-5p exerts its tumor-promoting functions by targeting CLIP4. The tumor-suppressive function of CLIP4 by inactivating the JAK2/STAT3 pathway is also elucidated. Regulatory mechanism of CLIP4 by miR-135b-5p provides a promising novel therapeutic strategy for GC patients.

Overexpression of programmed cell death ligand 1 reduces LPS-induced inflammatory cytokine upregulation and enhances osteo/odontogenic-differentiation of human dental pulp stem cells via upregulation of CCCTC-binding factor.

OBJECTIVE: The aim of this study was to explore the effect and mechanism of programmed cell death ligand 1 (PD-L1) in promoting the proliferation and osteo/odontogenic-differentiation of human dental pulp stem cells (hDPSCs) by mediating CCCTC-binding factor (CTCF) expression. DESIGN: The interaction between PD-L1 and CTCF was verified through co-immunoprecipitation. hDPSCs transfected with PD-L1 overexpression and CTCF knockdown vectors were treated with lipopolysaccharide or an osteogenic-inducing medium. Inflammatory cytokines and osteo/odontogenic-differentiation related genes were measured. Osteo/odontogenic-differentiation of hDPSCs was assessed using alkaline phosphatase (ALP) and alizarin red S staining. RESULTS: Overexpression of PD-L1 inhibited LPS-induced pro-inflammatory cytokine upregulation, cell proliferation, ALP activity, and calcium deposition in hDPSCs and elevated the expression of osteo/odontogenic-differentiation related genes; however, such expression patterns could be reversed by CTCF knockdown. Co-immunoprecipitation results confirmed the binding of PD-L1 to CTCF, indicating that PD-L1 overexpression in hDPSCs increases CTCF expression, thus inhibiting the inflammatory response and increasing osteo/odontogenic-differentiation of hDPSCs. CONCLUSION: PD-L1 overexpression in hDPSCs enhances the proliferation and osteo/odontogenic-differentiation of hDPSCs and inhibit the inflammatory response by upregulating CTCF expression.

Genomic context sensitizes regulatory elements to genetic disruption.

Genomic context critically modulates regulatory function but is difficult to manipulate systematically. The murine insulin-like growth factor 2 (Igf2)/H19 locus is a paradigmatic model of enhancer selectivity, whereby CTCF occupancy at an imprinting control region directs downstream enhancers to activate either H19 or Igf2. We used synthetic regulatory genomics to repeatedly replace the native locus with 157-kb payloads, and we systematically dissected its architecture. Enhancer deletion and ectopic delivery revealed previously uncharacterized long-range regulatory dependencies at the native locus. Exchanging the H19 enhancer cluster with the Sox2 locus control region (LCR) showed that the H19 enhancers relied on their native surroundings while the Sox2 LCR functioned autonomously. Analysis of regulatory DNA actuation across cell types revealed that these enhancer clusters typify broader classes of context sensitivity genome wide. These results show that unexpected dependencies influence even well-studied loci, and our approach permits large-scale manipulation of complete loci to investigate the relationship between regulatory architecture and function.

Integrative multi-omics profiling in human decedents receiving pig heart xenografts.

In a previous study, heart xenografts from 10-gene-edited pigs transplanted into two human decedents did not show evidence of acute-onset cellular- or antibody-mediated rejection. Here, to better understand the detailed molecular landscape following xenotransplantation, we carried out bulk and single-cell transcriptomics, lipidomics, proteomics and metabolomics on blood samples obtained from the transplanted decedents every 6 h, as well as histological and transcriptomic tissue profiling. We observed substantial early immune responses in peripheral blood mononuclear cells and xenograft tissue obtained from decedent 1 (male), associated with downstream T cell and natural killer cell activity. Longitudinal analyses indicated the presence of ischemia reperfusion injury, exacerbated by inadequate immunosuppression of T cells, consistent with previous findings of perioperative cardiac xenograft dysfunction in pig-to-nonhuman primate studies. Moreover, at 42 h after transplantation, substantial alterations in cellular metabolism and liver-damage pathways occurred, correlating with profound organ-wide physiological dysfunction. By contrast, relatively minor changes in RNA, protein, lipid and metabolism profiles were observed in decedent 2 (female) as compared to decedent 1. Overall, these multi-omics analyses delineate distinct responses to cardiac xenotransplantation in the two human decedents and reveal new insights into early molecular and immune responses after xenotransplantation. These findings may aid in the development of targeted therapeutic approaches to limit ischemia reperfusion injury-related phenotypes and improve outcomes.

Suture passer combined with two-hole laparoscopic peritoneal dialysis catheterization in patients undergoing peritoneal dialysis.

BACKGROUND: Laparoscopic techniques are being widely applied for peritoneal dialysis (PD) catheter (PDC) placement. The suture passer is a novel fixation tool that aims to reduce catheter migration. We compared the clinical value of the suture passer combined with two-hole laparoscopic PDC placement to open surgical placement by evaluating preoperative and postoperative conditions, as well as the onset of complications in both groups. METHODS: A retrospective study was conducted including 169 patients who underwent PDC placement surgery from January 2021 to May 2023. Based on the method employed, patients were divided into two groups: the suture passer combined with a two-hole laparoscopy group (SLG) and the open surgical group (SG). Comprehensive patient information, including general data, preoperative and postoperative indicators, peritoneal function after surgery, and the incidence rate of complications, were collected and analyzed. RESULTS: The SLG showed a statistically significant decrease in operative time, intraoperative blood loss, and 6-month postoperative drift rate compared to the SG (p < 0.05). No statistically significant differences were observed between the two groups in terms of sex, age, primary disease, hospitalization time, hospitalization costs, preoperative and postoperative examination indicators, peritonitis, and omental wrapping. CONCLUSIONS: Suture passer combined with two-hole laparoscopic PDC placement, characterized by simplicity and facilitating secure catheter fixation, was deemed safe and effective for patients undergoing PD. It reduces the catheter migration rate and improved surgical comfort. Overall, this technique demonstrates favorable outcomes in clinical practice.

Cellular dynamics in pig-to-human kidney xenotransplantation.

BACKGROUND: Xenotransplantation of genetically engineered porcine organs has the potential to address the challenge of organ donor shortage. Two cases of porcine-to-human kidney xenotransplantation were performed, yet the physiological effects on the xenografts and the recipients' immune responses remain largely uncharacterized. METHODS: We performed single-cell RNA sequencing (scRNA-seq) and longitudinal RNA-seq analyses of the porcine kidneys to dissect xenotransplantation-associated cellular dynamics and xenograft-recipient interactions. We additionally performed longitudinal scRNA-seq of the peripheral blood mononuclear cells (PBMCs) to detect recipient immune responses across time. FINDINGS: Although no hyperacute rejection signals were detected, scRNA-seq analyses of the xenografts found evidence of endothelial cell and immune response activation, indicating early signs of antibody-mediated rejection. Tracing the cells' species origin, we found human immune cell infiltration in both xenografts. Human transcripts in the longitudinal bulk RNA-seq revealed that human immune cell infiltration and the activation of interferon-gamma-induced chemokine expression occurred by 12 and 48 h post-xenotransplantation, respectively. Concordantly, longitudinal scRNA-seq of PBMCs also revealed two phases of the recipients' immune responses at 12 and 48-53 h. Lastly, we observed global expression signatures of xenotransplantation-associated kidney tissue damage in the xenografts. Surprisingly, we detected a rapid increase of proliferative cells in both xenografts, indicating the activation of the porcine tissue repair program. CONCLUSIONS: Longitudinal and single-cell transcriptomic analyses of porcine kidneys and the recipient's PBMCs revealed time-resolved cellular dynamics of xenograft-recipient interactions during xenotransplantation. These cues can be leveraged for designing gene edits and immunosuppression regimens to optimize xenotransplantation outcomes. FUNDING: This work was supported by NIH RM1HG009491 and DP5OD033430.

Self-Supported WO3@RuO2 Nanowires for Electrocatalytic Acidic Water Oxidation.

Developing catalysts with high catalytic activity and stability in acidic media is crucial for advancing hydrogen production in proton exchange membrane water electrolyzers (PEMWEs). To this end, a self-supported WO3@RuO2 nanowire structure was grown in situ on a titanium mesh using hydrothermal and ion-exchange methods. Despite a Ru loading of only 0.098 wt %, it achieves an overpotential of 246 mV for the oxygen evolution reaction (OER) at a current density of 10 mA·cm-2 in acidic 0.5 M H2SO4 while maintaining excellent stability over 50 h, much better than that of the commercial RuO2. After the establishment of the WO3@RuO2 heterostructure, a reduced overpotential of the rate-determining step from M-O* to M-OOH* is confirmed by the DFT calculation. Meanwhile, its enhanced OER kinetics are also greatly improved by this self-supported system in the absence of the organic binder, leading to a reduced interface resistance between active sites and electrolytes. This work presents a promising approach to minimize the use of noble metals for large-scale PEMWE applications.

A study on the treatment of brain tumors with BNCT using several moderators with different thicknesses.

Boron neutron capture therapy (BNCT) is an effective binary radiation therapy that depends on nuclear capture reactions. In recent years, BNCT can be performed without a reactor owing to the development of accelerator-based neutron sources. A new BNCT irradiation facility is proposed, which is based on a 15 mA 2.5 MeV proton accelerator with a 100 µm thickness natural lithium target as a neutron converter. A great quantity of studies has shown that neutron beams with different spectra have unique therapeutic effects on tumors. An appropriate neutron beam for BNCT is obtained by Beam Shaping Assembly (BSA) and the moderator plays a main role in determining the BSA outlet beam spectrum. To figure out the dose distribution in phantom with various kinds of neutron spectrum modes during BNCT, a series of cases are calculated by MCNPX code. The results give a database for treatment of brain tumors with BNCT by using different moderators.

On the genetic basis of tail-loss evolution in humans and apes.

The loss of the tail is among the most notable anatomical changes to have occurred along the evolutionary lineage leading to humans and to the 'anthropomorphous apes'1-3, with a proposed role in contributing to human bipedalism4-6. Yet, the genetic mechanism that facilitated tail-loss evolution in hominoids remains unknown. Here we present evidence that an individual insertion of an Alu element in the genome of the hominoid ancestor may have contributed to tail-loss evolution. We demonstrate that this Alu element-inserted into an intron of the TBXT gene7-9-pairs with a neighbouring ancestral Alu element encoded in the reverse genomic orientation and leads to a hominoid-specific alternative splicing event. To study the effect of this splicing event, we generated multiple mouse models that express both full-length and exon-skipped isoforms of Tbxt, mimicking the expression pattern of its hominoid orthologue TBXT. Mice expressing both Tbxt isoforms exhibit a complete absence of the tail or a shortened tail depending on the relative abundance of Tbxt isoforms expressed at the embryonic tail bud. These results support the notion that the exon-skipped transcript is sufficient to induce a tail-loss phenotype. Moreover, mice expressing the exon-skipped Tbxt isoform develop neural tube defects, a condition that affects approximately 1 in 1,000 neonates in humans10. Thus, tail-loss evolution may have been associated with an adaptive cost of the potential for neural tube defects, which continue to affect human health today.

Genomic context sensitizes regulatory elements to genetic disruption.

Enhancer function is frequently investigated piecemeal using truncated reporter assays or single deletion analysis. Thus it remains unclear to what extent enhancer function at native loci relies on surrounding genomic context. Using the Big-IN technology for targeted integration of large DNAs, we analyzed the regulatory architecture of the murine Igf2/H19 locus, a paradigmatic model of enhancer selectivity. We assembled payloads containing a 157-kb functional Igf2/H19 locus and engineered mutations to genetically direct CTCF occupancy at the imprinting control region (ICR) that switches the target gene of the H19 enhancer cluster. Contrasting activity of payloads delivered at the endogenous Igf2/H19 locus or ectopically at Hprt revealed that the Igf2/H19 locus includes additional, previously unknown long-range regulatory elements. Exchanging components of the Igf2/H19 locus with the well-studied Sox2 locus showed that the H19 enhancer cluster functioned poorly out of context, and required its native surroundings to activate Sox2 expression. Conversely, the Sox2 locus control region (LCR) could activate both Igf2 and H19 outside its native context, but its activity was only partially modulated by CTCF occupancy at the ICR. Analysis of regulatory DNA actuation across different cell types revealed that, while the H19 enhancers are tightly coordinated within their native locus, the Sox2 LCR acts more independently. We show that these enhancer clusters typify broader classes of loci genome-wide. Our results show that unexpected dependencies may influence even the most studied functional elements, and our synthetic regulatory genomics approach permits large-scale manipulation of complete loci to investigate the relationship between locus architecture and function.

Manipulating the 3D organization of the largest synthetic yeast chromosome.

Whether synthetic genomes can power life has attracted broad interest in the synthetic biology field. Here, we report de novo synthesis of the largest eukaryotic chromosome thus far, synIV, a 1,454,621-bp yeast chromosome resulting from extensive genome streamlining and modification. We developed megachunk assembly combined with a hierarchical integration strategy, which significantly increased the accuracy and flexibility of synthetic chromosome construction. Besides the drastic sequence changes, we further manipulated the 3D structure of synIV to explore spatial gene regulation. Surprisingly, we found few gene expression changes, suggesting that positioning inside the yeast nucleoplasm plays a minor role in gene regulation. Lastly, we tethered synIV to the inner nuclear membrane via its hundreds of loxPsym sites and observed transcriptional repression of the entire chromosome, demonstrating chromosome-wide transcription manipulation without changing the DNA sequences. Our manipulation of the spatial structure of synIV sheds light on higher-order architectural design of the synthetic genomes.

Mouse genome rewriting and tailoring of three important disease loci.

Genetically engineered mouse models (GEMMs) help us to understand human pathologies and develop new therapies, yet faithfully recapitulating human diseases in mice is challenging. Advances in genomics have highlighted the importance of non-coding regulatory genome sequences, which control spatiotemporal gene expression patterns and splicing in many human diseases1,2. Including regulatory extensive genomic regions, which requires large-scale genome engineering, should enhance the quality of disease modelling. Existing methods set limits on the size and efficiency of DNA delivery, hampering the routine creation of highly informative models that we call genomically rewritten and tailored GEMMs (GREAT-GEMMs). Here we describe 'mammalian switching antibiotic resistance markers progressively for integration' (mSwAP-In), a method for efficient genome rewriting in mouse embryonic stem cells. We demonstrate the use of mSwAP-In for iterative genome rewriting of up to 115 kb of a tailored Trp53 locus, as well as for humanization of mice using 116 kb and 180 kb human ACE2 loci. The ACE2 model recapitulated human ACE2 expression patterns and splicing, and notably, presented milder symptoms when challenged with SARS-CoV-2 compared with the existing K18-hACE2 model, thus representing a more human-like model of infection. Finally, we demonstrated serial genome writing by humanizing mouse Tmprss2 biallelically in the ACE2 GREAT-GEMM, highlighting the versatility of mSwAP-In in genome writing.

Interactions between MFAP5 + fibroblasts and tumor-infiltrating myeloid cells shape the malignant microenvironment of colorectal cancer.

BACKGROUND: The therapeutic targeting of the tumor microenvironment (TME) in colorectal cancer (CRC) has not yet been fully developed and utilized because of the complexity of the cell-cell interactions within the TME. The further exploration of these interactions among tumor-specific clusters would provide more detailed information about these communication networks with potential curative value. METHODS: Single-cell RNA sequencing, spatial transcriptomics, and bulk RNA sequencing datasets were integrated in this study to explore the biological properties of MFAP5 + fibroblasts and their interactions with tumor-infiltrating myeloid cells in colorectal cancer. Immunohistochemistry and multiplex immunohistochemistry were performed to confirm the results of these analyses. RESULTS: We profiled heterogeneous single-cell landscapes across 27,414 cells obtained from tumors and adjacent tissues. We mainly focused on the pro-tumorigenic functions of the identified MFAP5 + fibroblasts. We demonstrated that tumor-resident MFAP5 + fibroblasts and myeloid cells (particularly C1QC + macrophages) were positively correlated in both spatial transcriptomics and bulk RNA-seq public cohorts. These cells and their interactions might shape the malignant behavior of CRC. Intercellular interaction analysis suggested that MFAP5 + fibroblasts could reciprocally communicate with C1QC + macrophages and other myeloid cells to remodel unfavorable conditions via MIF/CD74, IL34/CSF1R, and other tumor-promoting signaling pathways. CONCLUSION: Our study has elucidated the underlying pro-tumor mechanisms of tumor-resident MFAP5 + fibroblasts and provided valuable targets for the disruption of their properties.

In-situ constructing self-supported NiO/RuO2 heterostructure for reinforced alkaline hydrogen evolution reaction.

Rationally designing a strongly coupled heterostructure with rich functional sites and high catalytic stability is essential for efficient energy conversion. This work synthesizes a self-supported NiO/RuO2 heterostructure for hydrogen production via facile dealloying following an in-situ electrochemical oxidation method. It only requires 88 ± 1 mV to drive a current density of -100 mA/cm2 in the alkaline electrolyte during hydrogen evolution reaction (HER), outperforming NiO, RuO2, and Pt foil. The higher anodic potential applied to the dealloyed ribbons results in lower overpotentials and faster reaction kinetics. Meanwhile, the catalytic activity and stability of the individual NiO can be significantly improved once coupled with a small amount of heterogeneous RuO2. The strong synergistic effect between NiO and RuO2 contributes to exposing abundant active sites, optimizing electronic structure, facilitating charge transfer at the interface, and most importantly, maintaining structural stability. These advantages make the self-supported NiO/RuO2 heterostructure a promising candidate for replacing the Pt-based catalysts.

Tumour Seeding Following Core Biopsy of a Mucoepidermoid Carcinoma of the Parotid: Radiological Evidence and a Surgical Approach to En-Bloc Dissection of the Mass and Tract.

Tumour seeding along the needle tract following core needle biopsy of the parotid is a recognised complication. We present a unique case of mucoepidermoid carcinoma of the parotid in an 18-year-old patient with associated tumour seeding within the core needle biopsy tract. Tumour seeding was confirmed both histologically and radiologically on magnetic resonance imaging as early as 35 days post-biopsy. The patient was treated successfully with a combination of surgery and adjuvant proton beam therapy. This case also visually demonstrates a surgical approach to en-block excision of the mass and tract.

A conditional counterselectable Piga knockout in mouse embryonic stem cells for advanced genome writing applications.

Overwriting counterselectable markers is an efficient strategy for removing wild-type DNA or replacing it with payload DNA of interest. Currently, one bottleneck of efficient genome engineering in mammals is the shortage of counterselectable (negative selection) markers that work robustly without affecting organismal developmental potential. Here, we report a conditional Piga knockout strategy that enables efficient proaerolysin-based counterselection in mouse embryonic stem cells. The conditional Piga knockout cells show similar proaerolysin resistance as full (non-conditional) Piga deletion cells, which enables the use of a PIGA transgene as a counterselectable marker for genome engineering purposes. Native Piga function is readily restored in conditional Piga knockout cells to facilitate subsequent mouse development. We also demonstrate the generality of our strategy by engineering a conditional knockout of endogenous Hprt. Taken together, our work provides a new tool for advanced mouse genome writing and mouse model establishment.

Element immiscibility assisted Ru@Ni3B as an efficient electrocatalyst toward alkaline and acidic hydrogen evolution reaction.

Based on the element immiscibility of Ni-Ru, xRu@Ni3B (x = 0, 0.2, 0.5, 1.0) were facilely synthesized through a one-step dealloying method. Of them, 1.0Ru@Ni3B requires overpotentials of 40 ± 0.2 and 72 ± 0.3 mV to reach a current density of -20 mA cm-2 for acidic and alkaline hydrogen evolution reaction, respectively, which are close to or even better than those of metallic Pt foil. In addition, it could maintain superior catalytic and chemical stability after 24 hours of testing. This work provides a promising strategy for improving the atomic utilization efficiency of highly active noble metals toward the hydrogen evolution reaction (HER).

Electrochemical incorporation of heteroatom into surface reconstruction induced Ni vacancy of NixO nanosheet for enhanced water oxidation.

Surface reconstruction of non-oxide oxygen evolution reaction (OER) electrocatalysts has been intensively studied to improve their catalytic performances. However, further modification of the reconstructed active surfaces for better catalytic performances has not been reported. In this work, NiSe nanorods are prepared on nickel foam (NiSe@NF) as the pre-catalyst for electrochemical OER. It is revealed that non-stoichiometric NiO nanosheets with abundant Ni vacancies (NixO) are formed on the surfaces of NiSe nanorods (NixO/NiSe@NF) via in-situ electrochemical oxidation. Furthermore, the OER performances are obviously improved after heteroatom Fe is incorporated electrochemically into NixO nanosheets ((FeNi)O/NiSe@NF). For OER to have a current density of 20 mA cm-2 in 1 M KOH solution, the as-prepared (FeNi)O/NiSe@NF electrode only needs an overpotential of 268 mV. Density functional theory (DFT) calculations reveal that the formation of Ni vacancy can increase the free energy of *OH. More importantly, the incorporation of heteroatom Fe into Ni vacancy can significantly decrease the free energy of *O, which enables Fe-NiO to have the lowest theoretical overpotential for OER in this work. The present work provides a facile and universal strategy to modify the reconstructed active oxides' surfaces for higher electrocatalytic performances.

A Nomogram Model for Predicting the Response to Transcatheter Arterial Embolization in Patients With Symptomatic Hepatic Hemangioma.

Background: Transcatheter arterial embolization (TAE) is regarded as an effective treatment for patients with symptomatic hepatic hemangioma. However, few studies have evaluated the efficacy of TAE alone for treating hepatic hemangioma. The aim of this study was to identify the factors that influence the response to TAE and formulate a quantitative nomogram to optimize the individualized management of hepatic hemangioma. Methods: We retrospectively studied 276 patients treated with TAE for hepatic hemangioma at our center from January 2011 to December 2019. The full cohort was randomly divided into training and validation cohorts. After assessing the potential predictive factors for the efficacy of TAE in the training cohort, a nomogram model was established and evaluated by discrimination and calibration. Results: During follow-up, the symptom relief rate was 100%. The tumor blood supply (p < 0.001), tumor number (p = 0.004), and tumor size (p = 0.006) were identified as significant predictors of the failure of tumor shrinkage in response to TAE. The nomogram model showed favorable discrimination and calibration, with a C-index of 0.775 (95% CI, 0.705-0.845) in the training cohort, which was further confirmed in the validation cohort (C-index 0.768; 95% CI, 0.680-0.856). The side effects of TAE were relatively minor and included mainly abdominal pain, nausea, vomiting, fever, and the presence of elevated hepatic transaminases. Conclusion: TAE is a safe and effective treatment for symptomatic hepatic hemangioma. The established nomogram performed well for the estimation of the effect of TAE in patients with hepatic hemangioma and can facilitate the selection of patients who would benefit most from the treatment.