ObjectiveTo investigate the therapeutic effect of sitravatinib on carbon tetrachloride （CCl₄）-induced liver fibrosis in mice. MethodsA total of 30 male C57BL/6J mice， aged 8 weeks， were randomly divided into control group， CCl₄ model group， and low- （5 mg/kg）， middle- （10 mg/kg）， and high-dose （20 mg/kg） sitravatinib groups. All mice except those in the control group were given intraperitoneal injection of CCl₄ for 4 consecutive weeks to induce liver fibrosis， and since the first day of modeling， the mice in the low-， middle-， and high-dose sitravatinib groups were given sitravatinib at the corresponding dose by gavage every day. The serum levels of total cholesterol （TC）， triglyceride （TG）， and alanine aminotransferase （ALT） were measured for the mice in each group； hepatic hydroxyproline content was measured； HE staining， Masson staining， and Sirius Red staining were used to observe liver histopathological changes； quantitative real-time PCR and Western blot were used to measure the mRNA and protein expression levels of α-smooth muscle actin （α-SMA） and collagen type I alpha 1 （Col1a1） in liver tissue. The therapeutic effect of sitravatinib was assessed based on the above results. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the control group， the model group had significant increases in the levels of TC， TG， and ALT （all P<0.05）， and there were no significant differences in the levels of TC， TG， and ALT between the model group and the low-， middle-， and high-dose sitravatinib groups （all P>0.05）. Hepatic hydroxyproline content decreased after sitravatinib intervention， with a significant difference between the middle-/high-dose sitravatinib groups and the CCl₄ model group （both P<0.05）. Histopathological staining showed that the sitravatinib treatment groups had a reduction in collagen deposition， along with thinning and fragmentation of fibrous septa， and in the high-dose sitravatinib group， 4 mice had a fibrosis stage of S0—S1 and 2 mice had a fibrosis stage of S2—S3， suggesting a certain degree of alleviation of liver fibrosis degree compared with the CCl₄ model group （mainly S3—S4）. The measurement of related molecules showed that sitravatinib downregulated the mRNA and protein expression levels of α-SMA and Col1a1 （all P<0.05）. ConclusionSitravatinib can effectively alleviate CCl₄-induced liver fibrosis in mice， possibly by inhibiting hepatic stellate cell activation and collagen synthesis.

Objective To analyze the main causes and risk factors of unplanned reoperation after liver transplantation. Methods The clinical data of 242 liver transplant recipients in the First Affiliated Hospital of Anhui Medical University from January 2015 to December 2024 were retrospectively analyzed. According to whether unplanned reoperation was performed during the same hospitalization after surgery, the recipients were divided into the reoperation group (n=36) and the non-reoperation group (n=206). The preoperative, intraoperative and postoperative data of the two groups, as well as donor and graft-related data, were compared to analyze the risk factors of unplanned reoperation after liver transplantation and the survival status of the two groups. Results Among the 242 liver transplant recipients, 36 underwent unplanned reoperations, with a total of 54 procedures including various laparotomies, endoscopic and interventional surgeries, among which there were 20 laparotomies, 18 endoscopic surgeries and 16 interventional surgeries. The most common cause of unplanned reoperation was biliary complications (20 times), followed by vascular complications (17 times). Compared with the non-reoperation group, the reoperation group had longer graft cold ischemia time, higher postoperative fatality rate of recipients, longer length of stay in the intensive care unit and postoperative hospital stay, and higher total hospitalization costs (all P<0.05). The incidence of unplanned reoperation was higher in recipients who underwent split liver transplantation (P<0.05). Multivariate analysis showed that intraoperative blood loss ≥1 000 mL, positive culture of graft perfusate and split liver transplantation were independent risk factors for unplanned reoperation (all P<0.05). The postoperative 7-day, 1-month, 3-month and 6-month survival rates of recipients in the reoperation group and the non-reoperation group were 100% vs. 98.1%, 88.9% vs. 94.2%, 69.4% vs. 90.8% and 66.7% vs. 90.8%, respectively, and the postoperative survival rate of recipients in the reoperation group was lower than that in the non-reoperation group (P<0.05). Conclusions The main causes of unplanned reoperation after liver transplantation are biliary complications, vascular complications, abdominal incision infection and intra-abdominal hemorrhage. Intraoperative massive blood loss, positive culture of graft perfusate and split liver transplantation are the risk factors associated with unplanned reoperation after liver transplantation.

ObjectiveCerebrospinal fluid (CSF) plays a crucial role in maintaining the homeostasis of the central nervous system (CNS). CSF rapidly exchanges with interstitial fluid (ISF) via the glymphatic system within the brain parenchyma. CSF-ISF circulation and its associated mechanisms are often referred to as the brain lymphatic system. This system is connected directly to meningeal lymphatic vessels (mLVs), jointly performing the function of clearing metabolic waste from the CNS. Emerging evidence indicates that this system is closely associated with the onset and progression of neurodegenerative diseases (NDs) such as Alzheimer’s disease (AD). Importantly, abnormal CSF circulation is not only a downstream consequence of AD pathology, but also a risk factor. In AD, the dynamics of CSF flow within the CNS are diminished, immune dysregulation occurs, and this may increase the risk of AD by exacerbating the burden of amyloid β-protein (Aβ). In the mouse model of AD, impaired CSF flow compromises this clearance function, leading to cognitive deficits. Clinically, acupuncture at cognition-related acupoints is commonly used for the prevention and treatment of AD. However, whether its therapeutic effects are mediated through the modulation of CSF dynamics remains unclear. This study aimed to evaluate the impact of acupuncture on CSF flow and investigate its acupoint specificity. MethodsMice were randomly assigned to experimental groups for the different electroacupuncture groups with the following acupoints: Baihui point (GV 20), Ear point, Neiguan point (PC 6), and Tianshu point (ST 25). Wild-type mice on a C57BL/6J background were used as controls. Fluorescent tracer was injected into the cisterna magna to label CSF flow. Fluorescence imaging was employed to assess the distribution of CSF within the brain before and after acupuncture stimulation. ResultsFollowing tracer injection into the cisterna magna, fluorescence signals rapidly reached the cerebellum and medulla—the regions closest to the injection site. Fluorescence intensity was higher in ventral brain regions compared to dorsal regions, likely due to greater vascular density in ventral areas facilitating CSF-ISF exchange. Electroacupuncture at the GV 20 produced the most pronounced enhancement of CSF across the whole brain, while stimulation at the ST 25 primarily augmented flow within subcortical regions. In contrast, electroacupuncture at the Ear point or the PC 6 had no observable effect on CSF in mice. ConclusionElectroacupuncture promotes CSF flow into the brain parenchyma in an acupoint-specific manner, with GV 20 exhibiting the most pronounced enhancement of CSF dynamics. These findings suggest that acupuncture-mediated facilitation of CSF flow may represent a potential therapeutic strategy for preventing or delaying age-related cognitive decline.

ObjectiveCerebrospinal fluid (CSF) plays a crucial role in maintaining the homeostasis of the central nervous system (CNS). CSF rapidly exchanges with interstitial fluid (ISF) via the glymphatic system within the brain parenchyma. CSF-ISF circulation and its associated mechanisms are often referred to as the brain lymphatic system. This system is connected directly to meningeal lymphatic vessels (mLVs), jointly performing the function of clearing metabolic waste from the CNS. Emerging evidence indicates that this system is closely associated with the onset and progression of neurodegenerative diseases (NDs) such as Alzheimer’s disease (AD). Importantly, abnormal CSF circulation is not only a downstream consequence of AD pathology, but also a risk factor. In AD, the dynamics of CSF flow within the CNS are diminished, immune dysregulation occurs, and this may increase the risk of AD by exacerbating the burden of amyloid β-protein (Aβ). In the mouse model of AD, impaired CSF flow compromises this clearance function, leading to cognitive deficits. Clinically, acupuncture at cognition-related acupoints is commonly used for the prevention and treatment of AD. However, whether its therapeutic effects are mediated through the modulation of CSF dynamics remains unclear. This study aimed to evaluate the impact of acupuncture on CSF flow and investigate its acupoint specificity. MethodsMice were randomly assigned to experimental groups for the different electroacupuncture groups with the following acupoints: Baihui point (GV 20), Ear point, Neiguan point (PC 6), and Tianshu point (ST 25). Wild-type mice on a C57BL/6J background were used as controls. Fluorescent tracer was injected into the cisterna magna to label CSF flow. Fluorescence imaging was employed to assess the distribution of CSF within the brain before and after acupuncture stimulation. ResultsFollowing tracer injection into the cisterna magna, fluorescence signals rapidly reached the cerebellum and medulla—the regions closest to the injection site. Fluorescence intensity was higher in ventral brain regions compared to dorsal regions, likely due to greater vascular density in ventral areas facilitating CSF-ISF exchange. Electroacupuncture at the GV 20 produced the most pronounced enhancement of CSF across the whole brain, while stimulation at the ST 25 primarily augmented flow within subcortical regions. In contrast, electroacupuncture at the Ear point or the PC 6 had no observable effect on CSF in mice. ConclusionElectroacupuncture promotes CSF flow into the brain parenchyma in an acupoint-specific manner, with GV 20 exhibiting the most pronounced enhancement of CSF dynamics. These findings suggest that acupuncture-mediated facilitation of CSF flow may represent a potential therapeutic strategy for preventing or delaying age-related cognitive decline.

Background: and Purpose Vertebrobasilar fusiform aneurysms (VBFAs) carry substantial morbidity and mortality, but optimal management for unruptured VBFAs remains unclear. We compared the safety and efficacy of conservative management (CM), stent-assisted coiling (SAC), and flow diverters (FDs) in patients with unruptured VBFAs, focusing on long-term prognosis. Methods: This study included data from a nationwide Chinese cohort of patients with vertebrobasilar dissecting aneurysms. Inverse probability of treatment weighting (IPTW) balanced confounders across groups. The primary outcome was poor prognosis (modified Rankin Scale score >2). Secondary outcomes included aneurysm rupture, ischemic stroke, compression symptoms, and VBFA-related deaths. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup and sensitivity analyses were performed. Results: Among 1,115 patients with unruptured VBFAs, 838 (median age, 54 years; 655 men) were included. After IPTW, baseline characteristics were balanced. Median follow-up was 54 months. FD was associated with a lower risk of poor prognosis than CM (OR, 0.48 [95% CI, 0.30 to 0.77]; p=0.002), with no difference between CM and SAC. FD also reduced aneurysm rupture (OR, 0.20 [95% CI, 0.07 to 0.60]; p=0.004) and compression symptoms (OR, 0.30 [95% CI, 0.13 to 0.68]; p=0.004) versus CM. Time-to-event analyses further revealed significant differences in vertebral artery lesions and Type I–II VBFAs, whereas no significant differences were observed in basilar or vertebrobasilar junction lesions or in Type III–IV VBFAs. Conclusions Compared with CM, FD was associated with improved long-term outcomes in unruptured VBFAs, particularly in vertebral artery lesions and Type I–II VBFAs, although residual confounding cannot be excluded.

Objective: To explore the independent risk factors of allogeneic blood transfusion during perioperative period of cytoreductive surgery in patients with ovarian cancer, and to construct a predictive model to facilitate clinical risk assessment and optimize perioperative blood management. Methods: Clinical data of 156 patients who underwent cytoreductive surgery for ovarian cancer in our hospital from January 2020 to December 2025 were retrospectively collected. The patients were divided into transfusion group (n=51) and non-transfusion group (n=105) according to whether they received allogeneic blood transfusion during perioperative period. The 1∶1 propensity score matching (PSM) was used to correct the confounding factors. Independent sample t test or Mann-Whitney U test was used for measurement data, and chisquare test was used for enumeration data. Variables with P<0.05 in univariate analysis were included in binary logistic regression for multivariate analysis to determine independent risk factors. A nomogram model for perioperative allogeneic blood transfusion risk prediction was constructed based on independent risk factors. Bootstrap method (100 samples) was used for internal calibration verification. ROC curve was used to evaluate the discrimination efficiency, and decision curve analysis (DCA) was used to evaluate the clinical net benefit of the model. Results: After propensity matching, the baseline data of the two groups were balanced and comparable. Multivariate logistic regression analysis showed that preoperative prothrombin time (PT) (OR=2.666, 95%CI 1.249~5.693, P=0.011), preoperative hemoglobin (Hb) (OR=0.953, 95%CI 0.923~0.984, P=0.003), intraoperative blood loss (OR=1.004, 95%CI 1.001-1.006, P=0.004), preoperative anemia grade (OR=3.052, 95%CI 1.007-9.252, P=0.049) were independent influencing factors of perioperative allogeneic blood transfusion. The nomogram model based on the above four factors was significant (LR χ =58.617, P<0.001), and the internal calibration curve showed that the predicted probability of the model was in good agreement with the actual probability (mean absolute error=0.042). The area under the ROC curve (AUC) was 0.890, indicating good discrimination efficiency. DCA showed that the clinical net benefit of the model was better than that of the unified transfusion/non-transfusion strategy in the 0-0.45 risk threshold range. Conclusion: Intraoperative blood loss, preoperative PT, preoperative Hb and preoperative anemia grade are independent risk factors for perioperative allogeneic blood transfusion in patients undergoing cytoreductive surgery for ovarian cancer. The nomogram model based on the above factors has good predictive efficacy and clinical hierarchical decision-making value, which can provide reference for clinical implementation of individualized blood management for high-risk patients and reduction of unnecessary blood transfusion rate.

ObjectiveTo investigate whether the inhibitory effect of Panax quinquefolium saponins （PQS） on non-small cell lung cancer （NSCLC） is enhanced under graphene-mediated far-infrared therapy （GFIR）， and to analyze its relationships with mitochondrial dysfunction， mitochondrial DNA （mtDNA） leakage， and the activation of cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathways. MethodsIn the cell experiments， the cell-counting kit 8 （CCK-8） was employed to assess the inhibitory effects of PQS alone or in combination with GFIR （PQS+GFIR） on A549 cell viability. The scratch assay and the colony formation assay were adopted to evaluate cell migration and colony formation capabilities， respectively. Flow cytometry was employed to assess apoptosis， mitochondrial membrane potential， and reactive oxygen species （ROS） levels. Immunofluorescence （IF） assay was performed to assess mitochondrial localization. Real-time polymerase China reaction（PCR） was used to detect mitochondrial DNA （mtDNA） leakage. A STING knockdown cell model was established by transfecting cells with small interfering RNA （siRNA）， and the knockdown efficiency was assessed by Real-time PCR and Western blot. The cell viability and apoptosis following gene knockdown were assessed through the CCK-8 assay and flow cytometry. In the animal experiments， an allogeneic xenograft mouse model was established with Lewis lung cancer cells. Mice were randomized into a control group， a model group， a cisplatin group， a low-dose PQS （PQS-Low， 90 mg·kg^-1） group， a high-dose PQS （PQS-High， 180 mg·kg^-1） group， a low-dose PQS combined with GFIR （PQS-Low+GFIR， 90 mg·kg^-1） group， and a high-dose PQS combined with GFIR （PQS-High+GFIR， 180 mg·kg^-1） group. Treatment lasted for 14 days， and the fluorescence intensity was monitored at the tumor site by small-animal in vivo imaging during the treatment period. Flow cytometry was utilized to determine the proportions of T-lymphocyte subsets， B-lymphocyte levels， and peripheral blood NK cell levels in the spleens of mice. Immunohistochemical （IHC） staining was performed to assess the infiltration of CD3⁺， CD4⁺， and CD8⁺ T-lymphocytes in the tumor tissue. Enzyme-linked immunosorbent assay （ELISA） was conducted to measure the levels of interferon-α （IFN-α）， interferon-β （IFN-β）， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6） in mouse tumors. The mRNA levels of cGAS， STING， TANK-binding kinase 1 （TBK1）， interferon regulatory factor 3 （IRF3）， interferon beta 1 （IFNB1）， and nuclear factor κB p65 （NF-κB p65） were determined by Real-time PCR. The protein levels of cGAS， STING， p-STING， TBK1， p-TBK1， IRF3， p-IRF3， NF-κB p65， and p-NF-κB p65 were quantified via Western blot. ResultsThe cell experiment results showed that compared with the control group， PQS inhibited the viability and migration of A549 cells， promoted apoptosis， affected mitochondrial localization， reduced mitochondrial membrane potential， increased the ROS level， and promoted mtDNA leakage. Following STING knockdown， the reductions in cell viability and the apoptosis-inducing effects caused by PQS were partially reversed （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group showed inhibited A549 cell migration and colony formation， exacerbated apoptosis， downregulated mitochondrial membrane potential， elevated ROS levels， and promoted mtDNA leakage. After STING knockdown， the reduced A549 cell viability and abnormal apoptosis phenotype were further reversed （P<0.05， P<0.01）. The animal experiment results showed that compared with the control group， the model group mice exhibited reduced proportions of T-lymphocyte subsets， CD19⁺ B-lymphocyte levels， and peripheral blood NK1.1⁺ cell levels in the spleen （P<0.01）. Compared with the model group， the PQS group showed increased immune cell parameters in mice （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group exhibited enhanced levels of the aforementioned indicators （P<0.01）. Compared with the model group， the PQS group showed significantly reduced fluorescence intensity in transplanted tumors， significantly upregulated expression of CD3 and CD4 in the tumor tissue， elevated levels of IFN-α and IL-6 in tumors， and upregulated mRNA levels of cGAS， STING， TBK1， IRF3， IFNB1， and NF-κB p65 as well as upregulated protein level of cGAS and phosphorylation level of STING in tumors （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group demonstrated further reduced tumor fluorescence intensity， elevated levels of CD3， CD4， and CD8 as well as cytokine levels in tumor tissue， and upregulated mRNA levels of genes related to the cGAS/STING pathway as well as upregulated protein level of cGAS and phosphorylation levels of STING， TBK1， IRF3， and NF-κB p65 （P<0.05， P<0.01） ConclusionGFIR enhances the inhibitory effect of PQS on NSCLC， potentially through mitochondrial dysfunction， mtDNA leakage， and activation of the cGAS/STING signaling pathway.

ObjectiveTo investigate whether the inhibitory effect of Panax quinquefolium saponins （PQS） on non-small cell lung cancer （NSCLC） is enhanced under graphene-mediated far-infrared therapy （GFIR）， and to analyze its relationships with mitochondrial dysfunction， mitochondrial DNA （mtDNA） leakage， and the activation of cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathways. MethodsIn the cell experiments， the cell-counting kit 8 （CCK-8） was employed to assess the inhibitory effects of PQS alone or in combination with GFIR （PQS+GFIR） on A549 cell viability. The scratch assay and the colony formation assay were adopted to evaluate cell migration and colony formation capabilities， respectively. Flow cytometry was employed to assess apoptosis， mitochondrial membrane potential， and reactive oxygen species （ROS） levels. Immunofluorescence （IF） assay was performed to assess mitochondrial localization. Real-time polymerase China reaction（PCR） was used to detect mitochondrial DNA （mtDNA） leakage. A STING knockdown cell model was established by transfecting cells with small interfering RNA （siRNA）， and the knockdown efficiency was assessed by Real-time PCR and Western blot. The cell viability and apoptosis following gene knockdown were assessed through the CCK-8 assay and flow cytometry. In the animal experiments， an allogeneic xenograft mouse model was established with Lewis lung cancer cells. Mice were randomized into a control group， a model group， a cisplatin group， a low-dose PQS （PQS-Low， 90 mg·kg^-1） group， a high-dose PQS （PQS-High， 180 mg·kg^-1） group， a low-dose PQS combined with GFIR （PQS-Low+GFIR， 90 mg·kg^-1） group， and a high-dose PQS combined with GFIR （PQS-High+GFIR， 180 mg·kg^-1） group. Treatment lasted for 14 days， and the fluorescence intensity was monitored at the tumor site by small-animal in vivo imaging during the treatment period. Flow cytometry was utilized to determine the proportions of T-lymphocyte subsets， B-lymphocyte levels， and peripheral blood NK cell levels in the spleens of mice. Immunohistochemical （IHC） staining was performed to assess the infiltration of CD3⁺， CD4⁺， and CD8⁺ T-lymphocytes in the tumor tissue. Enzyme-linked immunosorbent assay （ELISA） was conducted to measure the levels of interferon-α （IFN-α）， interferon-β （IFN-β）， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6） in mouse tumors. The mRNA levels of cGAS， STING， TANK-binding kinase 1 （TBK1）， interferon regulatory factor 3 （IRF3）， interferon beta 1 （IFNB1）， and nuclear factor κB p65 （NF-κB p65） were determined by Real-time PCR. The protein levels of cGAS， STING， p-STING， TBK1， p-TBK1， IRF3， p-IRF3， NF-κB p65， and p-NF-κB p65 were quantified via Western blot. ResultsThe cell experiment results showed that compared with the control group， PQS inhibited the viability and migration of A549 cells， promoted apoptosis， affected mitochondrial localization， reduced mitochondrial membrane potential， increased the ROS level， and promoted mtDNA leakage. Following STING knockdown， the reductions in cell viability and the apoptosis-inducing effects caused by PQS were partially reversed （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group showed inhibited A549 cell migration and colony formation， exacerbated apoptosis， downregulated mitochondrial membrane potential， elevated ROS levels， and promoted mtDNA leakage. After STING knockdown， the reduced A549 cell viability and abnormal apoptosis phenotype were further reversed （P<0.05， P<0.01）. The animal experiment results showed that compared with the control group， the model group mice exhibited reduced proportions of T-lymphocyte subsets， CD19⁺ B-lymphocyte levels， and peripheral blood NK1.1⁺ cell levels in the spleen （P<0.01）. Compared with the model group， the PQS group showed increased immune cell parameters in mice （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group exhibited enhanced levels of the aforementioned indicators （P<0.01）. Compared with the model group， the PQS group showed significantly reduced fluorescence intensity in transplanted tumors， significantly upregulated expression of CD3 and CD4 in the tumor tissue， elevated levels of IFN-α and IL-6 in tumors， and upregulated mRNA levels of cGAS， STING， TBK1， IRF3， IFNB1， and NF-κB p65 as well as upregulated protein level of cGAS and phosphorylation level of STING in tumors （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group demonstrated further reduced tumor fluorescence intensity， elevated levels of CD3， CD4， and CD8 as well as cytokine levels in tumor tissue， and upregulated mRNA levels of genes related to the cGAS/STING pathway as well as upregulated protein level of cGAS and phosphorylation levels of STING， TBK1， IRF3， and NF-κB p65 （P<0.05， P<0.01） ConclusionGFIR enhances the inhibitory effect of PQS on NSCLC， potentially through mitochondrial dysfunction， mtDNA leakage， and activation of the cGAS/STING signaling pathway.

Objective Jejunal interposition is an important option for restoring gastrointestinal continuity in patients with complex esophageal cancer in whom the stomach is unavailable for reconstruction due to previous gastrectomy, tumor involvement, failed gastric conduit, or other constraints. Although the jejunum offers a caliber similar to the esophagus, a rich blood supply, and preserved peristaltic function, anatomical variations in mesenteric length and vascular arcades render long-segment and high-level reconstruction susceptible to excessive tension, mesenteric torsion, venous congestion, and inadequate distal perfusion. This consensus aims to provide standardized recommendations for the application of jejunal interposition in this specific patient population. Methods This consensus was developed in accordance with the WHO Handbook for Guideline Development and Chinese national guideline development standards, with reference to the Appraisal of Guidelines for Research & Evaluation Ⅱ(AGREE Ⅱ), Reporting Items for Practice Guidelines in Healthcare (RIGHT), and Scientific, Transparent and Applicable Rankings (STAR) checklists. The project was registered on the international practice guidelines registry platform (PREPARE-2026CN1384). The working group systematically searched Chinese and English evidence addressing 12 clinical questions. Evidence was graded using the Oxford Centre for Evidence-Based Medicine (OCEBM) 2009 system, with structured appraisal of risk of bias, inconsistency, indirectness, and imprecision. Recommendations were formulated through two rounds of Delphi surveys and a face-to-face consensus meeting, with an agreement threshold of ≥75%. Results The consensus generated 12 recommendations covering indications, selection between jejunum and colon, preoperative assessment, surgical approach and reconstruction route, pedicled jejunal interposition (PJI), supercharged pedicled jejunal interposition (SPJ), indocyanine green (ICG) perfusion assessment, perioperative nutrition, management of anastomotic leakage, long-term follow-up, and special treatment scenarios. Given that the available direct evidence is predominantly derived from single-center retrospective cohorts and case series, recommendations extrapolated from general esophagectomy or other gastrointestinal surgical evidence are deliberately phrased with caution. Conclusion Jejunal interposition is a safe and effective approach for digestive tract reconstruction in patients with complex esophageal cancer in whom the stomach is unavailable. This consensus emphasizes that clinical decision-making should be individualized based on the patient's prior treatment history, reconstruction height, vascular anatomy, technical availability, and institutional experience in the Chinese context.

Objective To investigate the effect of tritiated water on the immune system of zebrafish and its potential molecular mechanism. Methods Zebrafish embryos (2.5 to 3 hours post-fertilization [hpf]) were exposed to 3.7 × 10⁴ Bq/mL tritiated water (tritiated water group), and those exposed to E3 culture medium were used as the control group. The mortality rate, hatching rate, deformity rate, heart rate, body length, yolk sac area, neutrophil count in the tail, immune-related gene expression, and immune-related protein expression of zebrafish in the two groups were determined. Then transcriptome technology was used to further analyze the possible mechanism of tritiated water affecting the immune system of zebrafish. Results Compared with the control group, zebrafish at 72 hpf in the tritiated water group had no significant changes in the mortality rate, hatching rate, deformity rate, body length, and yolk sac area((t = 0.9045, 0.5000, 1.0000, 0.7238, 0.0337, P = 0.4169, 0.6433, 0.3739, 0.4785, 0.9735), but had significantly increased heart rate(t = 4.575，P = 0.002). At 4 days post-fertilization (dpf), the neutrophil count in the tail of zebrafish in the tritiated water group was significantly increased(t = 2.563，P = 0.0196), the mRNA expression of TNF-α was significantly decreased(t = 2.891, P = 0.045), the protein expression of nuclear factor-kappa B (NF-κB) was significantly increased(t = 3.848, P = 0.018), and the protein expression of NLRP3 was significantly decreased(t = 14.98, P = 0.001). At 7 dpf, the neutrophil count in the tail and the protein expression levels of NF-κB, NLRP3, and interleukin-1β were significantly decreased(t = 3.772, 7.048, 15.620, 4.423, P = 0.014, 0.002, 0.0001, 0.012). Transcriptome sequencing revealed that differentially expressed genes were mainly enriched in the “neutrophil activation” and “platelet activation pathways” at 4 dpf and in the “neutrophil apoptosis”, “ferroptosis”, and “necroptosis” pathways at 7 dpf. Conclusion Tritiated water exposure induces a temporally dynamic immune response in zebrafish, potentially affecting immune homeostasis by regulating neutrophil activation and apoptosis, as well as the expression of NF-κB and NLRP3.