Postoperative abdominal adhesions (PAAs) are the result of excessive or prolonged inflammation. M1 macrophages are the primary producers of proinflammatory cytokines; however, their direct contribution to PAAs and the underlying mechanism remain unclear. The results of our previous study and public database analysis revealed that peritoneal injury induced M1 macrophage infiltration with specific hematopoietic cell kinase (HCK) upregulation. In vivo HCK inhibition reduced M1 macrophage accumulation in peritoneal injury. Accordingly, in vitro, HCK inhibitors and HCK knockout suppressed M1 macrophage polarization by downregulating the NF-κB pathway. Transwell and FITC-gelatin degradation assay confirmed that HCK deficiency abolished macrophage migration and invasion by disrupting podosome assembly. Furthermore, the causal role of M1 macrophages in PAAs was confirmed by abdominal macrophage depletion and adoptive transfer. M1 macrophage HCK orchestrated the IL6-driven proadhesive mesothelial-to-mesenchymal transition (MMT) via the NF-κB pathway. Finally, perioperative HCK inhibition was verified to alleviate PAA formation through the suppression of MMT-derived myofibroblast transition. Overall, we demonstrated that targeting HCK in M1 macrophages alleviates postoperative abdominal adhesions by suppressing NF-κB/IL6 axis-driven MMT, providing a new target and available strategy for the prevention of PAAs.

Background:Survival prediction using radiomics and deep learning (DL) has shown promise, but its utility for predicting local recurrence among patients with primary retroperitoneal sarcoma (RPS) remains unexplored. This study sought to construct a DL framework leveraging preoperative CT to predict local recurrence-free survival (LRFS) in RPS. Methods:We retrospectively enrolled 115 primary RPS patients (2013-2024), splitting into training (N = 86) and validation (N = 29) sets. An end-to-end DL model was designed to forecast LRFS using contrast-enhanced CT images. The DL-based score (DL-score) was contrasted with a conventional handcrafted radiomics model (Rad-score) and clinical model. Integrated models combining DL-score or Rad-score with clinicopathological factors were constructed (DLCM and RSCM). Model evaluation included the C-index, time-dependent ROC, calibration, decision curve analysis and survival analysis. Results:The DL-score outperformed Rad-score and clinical model, yielding higher C-index (training: 0.778 vs. 0.716 vs. 0.721; validation: 0.730 vs. 0.654 vs. 0.648). The DL-score proved to be an independent predictor of LRFS in training sets (adjusted HR = 5.950, 95% CI: 2.800-12.644; p < 0.001) and effectively categorized patients into high- and low-risk categories (p < 0.0001, p = 0.012, respectively). The combined DLCM further improved the performance, attaining C-index of 0.848 (95% CI: 0.790-0.915) and 0.749 (95% CI: 0.601-0.878) in the training and validation sets, respectively. The DLCM exhibited strong calibration and clinical utility and was an effective prognostic tool for risk classification in both cohorts. Conclusions:The CT-based DL model effectively predicts LRFS preoperatively in RPS, aiding risk stratification and guiding individualized therapeutic strategies.

OBJECTIVE:Retroperitoneal sarcomas are located in the retroperitoneum, characterized by a low incidence rate but a high degree of aggressiveness. Currently, surgery stands as the only curative treatment. This literature aims to employ a bibliometric analysis to systematically evaluate the research hotspots and trends in retroperitoneal sarcomas surgery. METHODS:Authors retrieved publications related to retroperitoneal sarcomas surgery from the Web of Science Core Collection (WoSCC) and PubMed databases spanning the period from 2005 to 2024. Subsequently, R, VOSviewer and CiteSpace software were employed to conduct bibliometric and visual analysis on the included publications. RESULTS:A total of 689 publications were included from 203 countries/regions and 2678 institutions. The United States had the highest number of publications, and Fdn IRCCS Ist Nazl Tumori is the top research institutions. The most frequently co-cited keywords were "soft tissue sarcoma", "management" and "survival". The research themes over the past decade have primarily centered around "management", "prognostic factors" and "inferior vena cava". CONCLUSIONS:This study utilized three widely recognized bibliometric software tools to conduct a bibliometric analysis on retroperitoneal sarcomas surgery. The results emphasize the significance of precise diagnosis, vascular reconstruction and prognostic factors, providing practical information for other scholars to understand key directions and frontier information in this field.

BACKGROUND:Retroperitoneal liposarcoma (RLPS) is a mesenchymal-derived malignant tumor characterized by high aggressiveness and a propensity for local recurrence. Emerging evidence implicates aberrant fatty acid metabolism as a key driver of RLPS progression, yet the transcriptional regulators orchestrating this process remain poorly defined. METHODS:Bioinformatics integrating cellular experiments demonstrated the role of fatty acid metabolism in the progression of RLPS. Immunohistochemistry (IHC) and Western blotting (WB) were employed to validate the expression levels of ARNT2, and the role of ARNT2 in tumor progression was demonstrated through CCK8 assays, Transwell invasion assays and wound healing assays. Further experiments confirmed the transcriptional regulatory effect of ARNT2 on STRA6 and demonstrated its control over RLPS progression by modulating intracellular lipid droplet and triglyceride levels. RESULTS:Here, we identify ARNT2 as a novel oncogenic transcription factor that promotes RLPS growth by transcriptionally upregulating STRA6, thereby reprogramming fatty acid metabolism. Specifically, ARNT2 binds to the STRA6 promoter to enhance its activity, thereby upregulating fatty acid metabolic enzymes and promoting lipid droplet accumulation with elevated triglycerides. This metabolic shift fuels energy production and biomass synthesis in RLPS cells, ultimately accelerating tumor proliferation and invasion. CONCLUSION:This study identifies ARNT2 as a transcriptional modulator of fatty acid metabolism pathways, highlighting its potential as a viable molecular target for RLPS therapy.

The mechanism of tumor budding (TB) in gastric adenocarcinoma (GAC) and its relationship with biological indicators and prognostic significance, remains unclear. In this study, we conducted a comprehensive analysis using whole-slide imaging to evaluate TB in 75 cases of GAC. Our findings revealed the risk factors associated with TB in GAC and their impact on patient prognosis. The results indicate that the majority of cases exhibited a TB grade exceeding 10 (n=41), followed by 6-10 (n=15). Histologic grade (R=0.26, P=0.06), pT stage (R=0.56, P=0.00), neural invasion (R=0.29, P=0.01), marginal zone growth pattern (R=0.25, P=0.02), and basal zone growth pattern (R=0.38, P=0.001) are associated with TB in GAC. Logistic regression analysis revealed that the infiltrative growth pattern in both the marginal zone (odds ratio=5.90, 95% CI: 1.04-33.44, P=0.05) and basal zone (odds ratio=12.80, 95% CI: 2.03-80.68, P=0.01) were identified as risk factors for TB in GAC. Univariate analysis demonstrated a negative correlation between TB and TB grade with overall survival and progression-free survival in GAC patients. Furthermore, the multivariate COX analysis revealed that TB and TB grade, along with American Joint Committee on Cancer stage, lymph node metastasis, and pT stage, independently influenced the prognosis of GAC patients. In conclusion, a comprehensive evaluation of TB could serve as a significant histologic marker for risk stratification in GAC.

Introduction Intestinal ischemia–reperfusion injury (IRI) is a critical condition often requiring emergency intervention. Ferroptosis, a form of regulated cell death driven by phospholipid peroxidation, plays a central role in its pathogenesis. Objective This study aimed to explore whether CoQ10 could mitigate intestinal IRI by suppressing ferroptosis. Methods We analyzed serum CoQ10 levels and inflammatory cytokines in patients with mesenteric artery embolism. In mice, intestinal IRI was induced by transient superior mesenteric artery ligation following two weeks of CoQ10 pretreatment. Histology, ELISA, immunoblotting, and RNA sequencing were used to assess therapeutic effects. To explore mechanisms, we used CRISPR/Cas9 to generate FSP1 and COQ2 knockouts in enterocytes, along with targeted metabolomics and co-autoxidation assays. In vivo loss of FSP1 function was induced by AAV9 to evaluate its role in CoQ10-mediated protection. Results Utilizing both our own and publicly available intestinal IRI cohorts, we identified a correlation between elevated CoQ10 levels and reduced systemic inflammation, along with decreased oxidized lipid accumulation in ischemia–reperfusion-affected small intestines. Transcriptomic enrichment analyses and biochemical assays demonstrated that CoQ10 supplementation effectively mitigates IRI by modulating lipid metabolism and inhibiting lipid peroxidation and ferroptosis. To elucidate the mechanism of action of CoQ10 against lipid peroxidation and ferroptosis, we established an in vitro ferroptosis-associated intestinal IRI model using enterocytes, which revealed that the CoQ10-mediated suppression of ferroptosis is dependent on FSP1. Targeted metabolomics analyses and co-autoxidation assays indicated that FSP1 suppresses ferroptosis by reducing CoQ10, thereby preventing phospholipid peroxidation. Loss of function FSP1 generated by genetic and pharmacological mechanisms in enterocytes or mouse intestines led to a decrease in the levels of reduced CoQ10, negating the therapeutic effects of CoQ10 on intestinal IRI. Conclusion Our study reveals a crucial role of CoQ10 in ferroptosis and highlights the potential of CoQ10 as a promising target for intestinal IRI treatment.

The mechanism of tumor budding (TB) in gastric adenocarcinoma (GAC) and its relationship with biological indicators and prognostic significance, remains unclear. In this study, we conducted a comprehensive analysis using whole-slide imaging to evaluate TB in 75 cases of GAC. Our findings revealed the risk factors associated with TB in GAC and their impact on patient prognosis. The results indicate that the majority of cases exhibited a TB grade exceeding 10 (n=41), followed by 6-10 (n=15). Histologic grade (R=0.26, P =0.06), pT stage (R=0.56, P =0.00), neural invasion (R=0.29, P =0.01), marginal zone growth pattern (R=0.25, P =0.02), and basal zone growth pattern (R=0.38, P =0.001) are associated with TB in GAC. Logistic regression analysis revealed that the infiltrative growth pattern in both the marginal zone (odds ratio=5.90, 95% CI: 1.04-33.44, P =0.05) and basal zone (odds ratio=12.80, 95% CI: 2.03-80.68, P =0.01) were identified as risk factors for TB in GAC. Univariate analysis demonstrated a negative correlation between TB and TB grade with overall survival and progression-free survival in GAC patients. Furthermore, the multivariate COX analysis revealed that TB and TB grade, along with American Joint Committee on Cancer stage, lymph node metastasis, and pT stage, independently influenced the prognosis of GAC patients. In conclusion, a comprehensive evaluation of TB could serve as a significant histologic marker for risk stratification in GAC.

Primary hepatic perivascular epithelioid cell tumor (PEComa) is an exceptionally rare mesenchymal neoplasm of borderline malignancy, with limited documentation of its contrast-enhanced ultrasound (CEUS) features in medical literature. In this context, we present a 53-year-old male patient without chronic liver disease, who exhibited a well-circumscribed hypoechoic left hepatic lobe mass on conventional ultrasonography. Subsequent CEUS demonstrated characteristics indicative of malignant tumors, with specific manifestations during the arterial phase, thereby informing clinical decision-making toward surgical resection. Histopathological confirmation of capsular-invasive PEComa underscores the utility of CEUS in characterizing such lesions, particularly in middle-aged patients with incidental solitary hepatic masses lacking predisposing risk factors. These findings advocate for the integration of CEUS into diagnostic algorithms to enhance specificity in atypical hepatic tumor evaluations.

Ethnopharmacological relevance: Carthami flos is a dried flower of the Asteraceae plant Carthamus tinctorius (L.). Danhong injection, composed of Carthami flos and Danshen can prevent the formation of postoperative peritoneal adhesions. Quercetin (QUE), an active compound of Carthami flos, has also been proved to prevent postoperative abdominal and uterine cavity adhesions. However, whether QUE is the key component in Carthami flos and the mechanism in preventing postoperative peritoneal adhesions has not been studied. Aim of the study: To predict whether QUE is the key molecule in Carthami flos and explore the effect and mechanism of QUE in preventing postoperative peritoneal adhesions. Materials and methods: Drug composition and target analysis was used to predict the key component in Carthami flos. The method of cecum-sidewall abrasion was used to establish adhesion models, and the antiadhesion effect of QUE was evaluated with the adhesion scoring system. Network pharmacology was used to predict the targets and potential mechanism of QUE in preventing adhesion. The mechanism was further verified by immunofluorescence, Western blot, wound healing experiment, and molecular docking. Results: Quercetin was predicted to be the key to preventing postoperative peritoneal adhesions in Carthami flos. Animal experiments revealed that QUE effectively ameliorated adhesions and reduced the expression of mesothelial-mesenchymal transition (MMT) related markers and TGF-beta 1. Moreover, the TGF-beta 1/PI3K/AKT pathway was predicted via protein-protein interaction and Kyoto encyclopedia of Genes and Genomes enrichment analysis to play a crucial part in preventing adhesion by QUE. Furthermore, in vitro experiments and molecular docking demonstrated that QUE could block the TGF-beta 1/PI3K/AKT pathway through forming a stable combination with T beta R-II, thereby inhibiting MMT and ameliorating peritoneal adhesion. Conclusions: QUE can not only reduce postoperative TGF-beta 1 but also block the TGF-beta 1/PI3K/AKT pathway to inhibit MMT of mesothelial cells, and finally alleviate postoperative peritoneal adhesions. These findings may provide insights towards development of a safe and effective anti-adhesive drug for prevention of postoperative peritoneal adhesions.

Objective: Abdominal wall hernias are common abdominal diseases, and effective hernia repair is challenging. In clinical practice, synthetic meshes are widely applied for repairing abdominal wall hernias. However, postoperative complications, such as inflammation and adhesion, are prevalent. Although biological meshes can solve this problem to a certain extent, they face the problems of heterogeneity, rapid degradation rate, ordinary mechanical properties, and high-cost. Here, a novel electrospinning mesh composed of polylactic acid and silk fibroin (PLA-SF) for repairing abdominal wall hernias was manufactured with good physical properties, biocompatibility and low production cost. Materials and methods: FTIR and EDS were used to demonstrate that the PLA-SF mesh was successfully synthesized. The physicochemical properties of PLA-SF were detected by swelling experiments and in vitro degradation experiments. The water contact angle reflected the hydrophilicity, and the stress‒strain curve reflected the mechanical properties. A rat abdominal wall hernia model was established to observe degradation, adhesion, and inflammation in vivo. In vitro cell mesh culture experiments were used to detect cytocompatibility and search for affected biochemical pathways. Results: The PLA-SF mesh was successfully synthesized and did not swell or degrade over time in vitro. It had a high hydrophilicity and strength. The PLA-SF mesh significantly reduced abdominal inflammation and inhibited adhesion formation in rat models. The in vitro degradation rate of the PLA-SF mesh was slower than that of tissue remodeling. Coculture experiments suggested that the PLA-SF mesh reduced the expression of inflammatory factors secreted by fibroblasts and promoted fibroblast proliferation through the TGF-β1/Smad pathway. Conclusion: The PLA-SF mesh had excellent physicochemical properties and biocompatibility, promoted hernia repair of the rat abdominal wall, and reduced postoperative inflammation and adhesion. It is a promising mesh and has potential for clinical application.

A high postoperative recurrence rate seriously impedes colon cancer (CC) patients from achieving long-term survival. Here, we aimed to develop a Treg-related classifier that can help predict recurrence-free survival (RFS) and therapy benefits of stage I–III colon cancer. A Treg-related prognostic classifier was built through a variety of bioinformatic methods, whose performance was assessed by KM survival curves, time-dependent receiver operating characteristic (tROC), and Harrell’s concordance index (C-index). A prognostic nomogram was generated using this classifier and other traditional clinical parameters. Moreover, the predictive values of this classifier for immunotherapy and chemotherapy therapeutic efficacy were tested using multiple immunotherapy sets and R package “pRRophetic". A nine Treg-related classifier categorized CC patients into high- and low-risk groups with distinct RFS in the multiple datasets (all p < 0.05). The AUC values of 5-year RFS were 0.712, 0.588, 0.669, and 0.662 in the training, 1st, 2nd, and entire validation sets, respectively. Furthermore, this classifier was identified as an independent predictor of RFS. Finally, a nomogram combining this classifier and three clinical variables was generated, the analysis of tROC, C-index, calibration curves, and the comparative analysis with other signatures confirmed its predictive performance. Moreover, KM analysis exhibited an obvious discrepancy in the subgroups, especially in different TNM stages and with adjuvant chemotherapy. We detected the difference between the two risk subsets of immune cell sub-population and the response to immunotherapy and chemotherapy. We built a robust Treg-related classifier and generated a prognostic nomogram that predicts recurrence-free survival in stage I–III colon cancer that can identify high-risk patients for more personalized and effective therapy.

Intestinal ischemia-reperfusion injury occurs in acute intestinal obstruction, intussusception, acute mesenteric artery embolism, and other diseases and can lead to local intestinal necrosis, distant organ involvement, or systemic reactions, with high morbidity and mortality. Ferroptosis plays a crucial role in intestinal ischemia-reperfusion injury, and inhibition of ferroptosis may provide new approaches for treating the disease. SIRT3 protects cells from oxidative stress and may be involved in the process of ferroptosis. We hypothesized that resveratrol, an agonist of SIRT3, could ameliorate intestinal ischemia-reperfusion injury by compensating the GSH/GPX4 pathway. Intestinal ischemia-reperfusion (I/R) and Caco-2 hypoxia-reoxygenation models were established. Transmission electron microscopy was used to assess mitochondrial function; the Chiu’s score was used to evaluate the degree of intestinal mucosal injury based on HE staining; and Western blot was used to detect the SIRT3/FoxO3a pathway, tight junction proteins and ferroptosis-related protein expression. Sirt3-/- C57, shSIRT3-Caco-2 cells and siFoxO3a-Caco-2 cells were established. C11-BODIPY was used to detect lipid peroxide in cells; FD4 and IFABP were used to detect intestinal permeability; MitoSOX was used to detect ROS levels; and MitoTracker and immunofluorescence colocalization were used to detect SIRT3 levels. In the intestinal I/R model, I/R injury occurs mainly during the reperfusion period and leads to ferroptosis through the GSH/GPX4 pathway. Resveratrol could reduce ferroptosis and ameliorate I/R injury by activating SIRT3. In Sirt3-/- mice, more intestinal mucosal cells underwent ferroptosis, I/R injury was more severe, and resveratrol lost the ability to ameliorate I/R injury. In addition, hypoxia-reoxygenation increased RSL3-induced ferroptosis sensitivity in Caco-2 cells in vitro. In the presence of shSIRT3 or RSL3 alone, resveratrol could ameliorate Caco-2 ferroptosis, but not RSL3-induced shSIRT3-Caco-2 ferroptosis. Furthermore, resveratrol might activate the SIRT3/FoxO3a pathway, increase the expression of SOD2 and catalase, and inhibit ROS generation, thus reducing lipid peroxidation and ferroptosis. To date, this is the first study to show that resveratrol ameliorates intestinal ischemia-reperfusion injury by activating SIRT3 and reducing ferroptosis. Resveratrol can reduce intestinal ischemia-reperfusion injury by activating the SIRT3/FoxO3a pathway, increasing the expression of SOD2 and catalase, reducing ROS and LPO production, compensating for the GSH/GPX4 pathway and inhibiting ferroptosis.

OBJECTIVE:To evaluate the feasibility and application value of mixed reality technology (MR) in Primary retroperitoneal tumour (PRT) surgery.METHODS:From 276 patients who underwent PRT resection at the First Affiliated Hospital of Xi'an Jiaotong University, we screened 46 patients who underwent MR-assisted retroperitoneal tumour resection and 46 patients who underwent tumour resection without MR assistance. The intraoperative and postoperative recovery of the patients in both groups were compared, and the reliability and validity of the application of MR were further examined using the Likert scale.RESULTS:There was a significant difference in the mean intraoperative bleeding volume between the two groups, but it was reduced in the MR group. The results of the Likert scale showed higher scores in the MR group than non-MR group.CONCLUSIONS:MR can be used to assist PRT resection and has great potential to improve the rate of complete retroperitoneal tumour resection.

Background: There is no clear description of the evolution of the progression of abdominal adhesions over time.Method: The optimized model was selected using different adhesion scoring systems. Then, this model was used to observe the progression of abdominal adhesions. Visualized observation of abdominal adhesion evolution was performed by laparoscopy and computed tomography. The inflammatory cell infiltration and collagen fibers in adhesion tissues at different times were evaluated by hematoxylin-eosin and picrosirius red staining. RNA sequencing was used to predict potential key targets of abdominal adhesions at different times.Results: The abdominal adhesion model showed the highest reproducibility when it was established using a circular tool and an electric brush. Based on this model, we found that the inflammatory response was activated early in the process of adhesion formation, peaking on day 3 and then gradually decreasing until stabilization on day 7. Collagen and fibronectin formed on day 1 and gradually increased until remaining stable on day 7. In addition, the characteristic changes in the adhesion zone from initial congestion, edema and fragile tissue to later dense and stable tissue could be vividly observed in live mice by laparoscopy and artificial pneumoperitoneum CT. The RNA sequencing results revealed that Hck on day 1, Ndufs3 and Ndufs8 on day 3 and Aif1 on day 7 might play key roles in abdominal adhesion formation.Conclusion: The construction of a standard process for describing the evolution of abdominal adhesions based on an optimized mouse model will help to facilitate subsequent adhesion-related studies.

Background: Postoperative abdominal adhesion (PAA) is a common postoperative complication. Clinically, various methods have been used to prevent the occurrence of PAA, such as drugs and physiotherapy; however, no satisfactory results have been obtained. Luteolin (LUT) is a natural flavonoid that reduces inflammation and acts as an antioxidant. This research aimed to examine the impact and mechanism of LUT in reducing PAA. Methods: C57/BL6 mice were used in vivo experiments. PAA model was established using a brush friction method. Visual scoring and hematoxylin and eosin staining were used to score the severity of adhesions. Network pharmacology was used to infer potential targets and core pathways of LUT. Hydrogen peroxide (H2O2) was used to induce oxidative stress in vitro, while the reactive oxygen species (ROS) assay kit was used to evaluate oxidative stress levels. Western blotting, cell immunofluorescence, and multiple immunofluorescence assays were used to detect alpha-SMA, vimentin, E-cadherin, collagen I, or AKT phosphorylation level. Scratch assay was used to detect cell migration. Results: LUT reduced the degree of PAA in mice. It attenuated H2O2-induced ROS production and reversed mesothelial-mesenchymal transition (MMT) in HMrSV5 cells. Network pharmacology analysis showed that LUT likely exerted anti-adhesion activity by regulating the PI3K-Akt signaling pathway. Phosphorylated Akt levels were significantly reduced in LUT-treated HMrSV5 cells. LUT also significantly reduced the expression of vimentin and collagen I in adherent tissues and upregulated E-cadherin expression. Conclusion: LUT blocks the ROS/PI3K/AKT pathway, thereby inhibiting MMT and reducing PAA. To this end, LUT has potential in PAA therapy.

Objective:To summarize the clinicopathologic features and clinical diagnosis and treatment experience of retroperitoneal paraganglioma.Methods:This study retrospectively analyzed the clinical, pathological and follow-up data of 39 patients admitted to the First Affiliated Hospital of Xi'an Jiaotong University from 1 Oct 2012 to 1 Oct 2022 for retroperitoneal paragangliomas undergoing resection.Results:There were 19 males and 20 females with tumor being functional in 11 cases (28%) and non-functional in 28 cases (72%). CT angiography showed that the tumors were distributed around the abdominal aorta and inferior vena cava in most cases. All 39 patients underwent tumor rescetion.Patients in laparoscopic group had shorter operation time and postoperative hospital saty compared with open sugery [(135±66)min vs. (194±67)min, t=-2.529, P=0.016; (6.6±2.2)d vs.(9.6±4.8)d, t=-2.096, P=0.043], while there was no statistically significant difference between the two groups in terms of intraoperative blood loss [(152±151)ml vs. (361±608)ml, t=-1.169, P=0.250]. There were no major postoperative complications in the laparoscopic group, and pulmonary infection in 1 case and intestinal obstruction in 1 case in the open group. Thrity-six cases were followed up, ranging from 2 to 115 months, 1 patient in the laparoscopic group died 1 year after surgery due to recurrence and metastasis. In the open group, 1 case recurred 2 years later and was discharged after the second operation, and 1 case died of recurrence 2 years after surgery. Conclusions:Surgery is indicated for retroperitoneal paraganglioma. Adequate perioperative management is the key to the success of the operation. Laparoscopic surgery is superior to open surgery in terms of operation time and postoperative recovery .

BackgroundEarly tumor recurrence is one of the most significant poor prognostic factors for patients with HCC after R0 resection. The aim of this study is to identify risk factors of early recurrence, in addition, to develop a nomogram model predicting early recurrence of HCC patients.MethodsA total of 481 HCC patients after R0 resection were enrolled and divided into a training cohort (n = 337) and a validation cohort (n = 144). Risk factors for early recurrence were determined based on Cox regression analysis in the training cohort. A nomogram incorporating independent risk predictors was established and validated.ResultsEarly recurrence occurred in 37.8% of the 481 patients who underwent curative liver resection of HCC. AFP ≥ 400 ng/mL (HR: 1.662; P = 0.008), VEGF-A among 127.8 to 240.3 pg/mL (HR: 1.781, P = 0.012), VEGF-A > 240.3 pg/mL (HR: 2.552, P < 0.001), M1 subgroup of MVI (HR: 2.221, P = 0.002), M2 subgroup of MVI (HR: 3.120, P < 0.001), intratumor necrosis (HR: 1.666, P = 0.011), surgical margin among 5.0 to 10.0 mm (HR: 1.601, P = 0.043) and surgical margin < 5.0 mm (HR: 1.790, P = 0.012) were found to be independent risk factors for recurrence-free survival in the training cohort and were used for constructing the nomogram. The nomogram indicated good predictive performance with an AUC of 0.781 (95% CI: 0.729-0.832) and 0.808 (95% CI: 0.731-0.886) in the training and validation cohorts, respectively.ConclusionsElevated serum concentrations of AFP and VEGF-A, microvascular invasion, intratumor necrosis, surgical margin were independent risk factors of early intrahepatic recurrence. A reliable nomogram model which incorporated blood biomarkers and pathological variables was established and validated. The nomogram achieved desirable effectiveness in predicting early recurrence in HCC patients.

背景与目的:孤立性纤维肿瘤(SFT)是一种临床上较为少见的软组织肿瘤,既往文献报道SFT好发于胸膜,近年来研究表明其在全身多部位均可发生.由于SFT在腹膜后发生率低,故目前仍缺乏对腹膜后SFT的临床诊治的深入研究报道.因此.本文通过回顾7例腹膜后SFT患者资料,探讨该病的临床特点、诊治及预后,以期加强认识并引起重视.方法:回顾性分析西安交通大学第一附属医院2014年3月-2021年9月收治的7例手术或穿刺活检病理及免疫组化检查确诊为腹膜后SFT患者的临床及病理资料,总结分析患者的诊治及预后情况.结果:7例患者中,男4例,女3例;平均年龄(53.3±13.2)岁.临床表现缺乏特异性,1例无明显症状,其余6例因肿瘤压迫周围组织器官出现不同程度的症状,以腹胀、腹痛最为常见.术前5例患者行CTA检查,其中2例供血动脉来自髂内动脉分支,1例来自髂内动脉分支及腰动脉分支,1例来自肠系膜下动脉远端分支,1例来自脾动脉分支.6例患者行根治性手术切除,其中3例术前行介入栓塞术,3例行联合脏器切除.平均手术时间(372.5±91.3)min,平均出血量(1 200.0±1 031.5)mL,平均住院时间(25.7±9.3)d,术前栓塞患者与未栓塞患者术后平均住院时间分别为(10.3±4.2)d和(11.7±2.3)d,术后第1天平均引流量分别为(283.3±119.3)mL和(385.0±262.5)mL.未栓塞患者中术后出现肺部感染1例,腹膜后包裹性积液1例.肿瘤大小9 cm x7 cm×6 cm～25 cm×20 cmx 10 cm,镜下肿瘤细胞呈梭形,呈现不同程度异型性,疏密不均,偶可见薄壁"鹿角状"血管,间质常含有胶原纤维.免疫组化阳性率 CD34、Ki-67 均为 100％(7/7),CD99、vimentin 均为 100％(6/6),STAT6 为100％(5/5),Bcl-2为50％(3/6),S-100为14％(1/7).随访2～66个月,失访1例,其余患者均未见复发或转移征象.结论:腹膜后SFT多无特异性临床表现,影像学检查对术前评估及制定手术方案具有指导意义,最终确诊依赖于病理检查及免疫组织化学结果.根治性手术切除是主要治疗手段,术前栓塞对缩短术后住院时间、减少术后引流量及并发症的发生具有积极作用,风险分层指导下术后长期随访具有重要意义.

Background: The upregulation of programmed death-ligand 1 (PD-L1) and epidermal growth factor re-ceptor 2 (HER2) may play a role in gastric adenocarcinoma (GAC).Aim: To study PD-L1 and HER-2 expression and prognosis in GAC.Methods: PD-L1 and HER2 expression was determined in tumor tissues of 75 patients with GAC. The correlations between PD-L1, HER2 expression, and clinicopathological factors were analyzed.Results: The positive expression rate for PD-L1 was 57.3% (43/75) and the HER2 over-expression rate was 17.3% (13/75). PD-L1 expression negatively correlated with the grade of GAC differentiation (r = -0.26, P < 0.05). Approximately 85% of HER2-positive GACs were found to be PD-L1-positive and PD-L1 expression positively correlated with HER2 overexpression. The TNM stage and combined HER2 and PD -L1 expression were independent prognostic factors affecting the survival of patients with GAC. The me-dian overall survival and recurrence-free survival of groups I (HER2 overexpression and PD-L1 positive), II (HER2 overexpression and PD-L1 negative), III (No HER2 overexpression and PD-L1 positive) and IV (No HER2 overexpression and PD-L1 negative) were (47 (17-77), 15 (0-4 4), 81 (62-101), and 78 (60-98) months, respectively.Conclusion: PD-L1 expression is upregulated in more than half of patients with GAC. Anti-PD-L1 treat-ment combined with anti-HER2 therapy may benefit patients with locally advanced GAC with HER2 over -expression.(c) 2022 The Authors. Published by Elsevier Ltd on behalf of Editrice Gastroenterologica Italiana S.r.l. This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ )

Peritoneal adhesions (PAs) are a serious complication of abdominal surgery and negatively affect the quality of life of millions of people worldwide. However, a clear molecular mechanism and a standard therapeutic strategy for PAs have not been established. Here, we developed a standardized method to mimic the pathological changes in PAs and found that sirtuin 3 (SIRT3) expression was severely decreased in adhesion tissues, which was consistent with our bioinformatics analysis and patient adhesion tissue analysis. Thus, we hypothesized that activating SIRT3 could alleviate postsurgical PAs. Sirt3-deficient ( Sirt3 −/− ) mice exhibited many more PAs after standardized abdominal surgery. Furthermore, compared with wild-type ( Sirt3 +/+ ) mice, Sirt3-deficient ( Sirt3 −/− ) mice showed more prominent reactive oxygen species (ROS) accumulation, increased levels of inflammatory factors, and exacerbated mitochondrial damage and fragmentation. In addition, we observed NLRP3 inflammasome activation in the adhesion tissues of Sirt3 −/− but, not Sirt3 +/+ mice. Furthermore, mesothelial cells sorted from Sirt3 −/− mice exhibited impaired mitochondrial bioenergetics and redox homeostasis. Honokiol (HKL), a natural compound found in several species of the genus Magnolia , could activate SIRT3 in vitro. Then, we demonstrated that treatment with HKL could reduce oxidative stress and the levels of inflammatory factors and suppress NLRP3 activation in vivo, reducing the occurrence of postsurgical PAs. In vitro treatment with HKL also restored mitochondrial bioenergetics and promoted mesothelial cell viability under oxidative stress conditions. Taken together, our findings show that the rescue of SIRT3 by HKL may be a new therapeutic strategy to alleviate and block postsurgical PA formation.