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Background and Objectives: Hepatocellular carcinoma (HCC) is a major global health concern, and emerging evidence suggests that TIGIT and NKG2A are potential immune checkpoints with implications for HCC progression. This study aimed to evaluate the prognostic significance of TIGIT and NKG2A expression in HCC patients who underwent radical liver resection. Methods: We conducted a retrospective analysis of 144 HCC patients who underwent radical liver resection. TIGIT and NKG2A expression levels were assessed using the immunoreactive score. Cox proportional hazards models were utilized to analyze the association between TIGIT/NKG2A expression and clinical characteristics, relapse‐free survival (RFS), and overall survival (OS). Prognostic models for OS and RFS was developed and validated using concordance index and calibration curves. Additionally, the random forest algorithm was employed to identify independent risk factors for OS and RFS and their correlation with predicted survival. Results: TIGIT and NKG2A expression were identified as independent risk factors for RFS, while TIGIT expression alone significantly impacted OS. The prognostic models showed good discriminative ability, with concordance indices exceeding 0.7 for predicting 1‐, 3‐, and 5‐year OS or RFS. Calibration curves confirmed the reliability of the nomograms for OS and RFS prediction. The areas under the ROC curve consistently exceeded 0.7 for predicting OS and RFS. Elevated levels of TIGIT and NKG2A expression were associated with diminished RFS, highlighting their importance as prognostic factors. Conclusions: Our study establishes the prognostic significance of TIGIT and NKG2A expression in predicting OS and RFS following radical liver resection for HCC patients. The developed prognostic models incorporating TIGIT and NKG2A expression hold promise for improving risk stratification and clinical management of HCC patients. [ABSTRACT FROM AUTHOR]

Objective. To compare the survival time of patients with portal vein thrombosis after splenectomy for portal hypertension in cirrhosis and explore the influencing factors of the Shengjing classification. Methods. Clinical data of 108 patients with portal vein thrombosis after splenectomy in the department of general surgery of our hospital from November 2011 to December 2018 were selected, and a retrospective analysis was performed. Results. Among 108 patients with postoperative PVST formation, 9 had type Ia, 32 type Ib, 39 type IIa, 20 type IIb, 5 type IIIa, 3 type IIIb, and 0 type IV. Survival analysis showed that the difference in survival time distribution among the Shengjing typing groups was statistically significant (P < 0.05). The higher the classification level, the shorter the survival time and the higher the risk of death. The results of a single-factor analysis showed that there were statistically significant differences in the PVST Shengjing typing groups between the preoperative group with or without hepatitis, preoperative d-dimer level, and postoperative day 14 fibrinogen (FIB) level (P < 0.05). Multivariate logistic regression analysis showed that the OR value of higher PVST Shengjing typing in patients with hepatitis was 4.634 times higher than that in patients without hepatitis (95% CI: 1.593-13.478, χ 2 = 7.922 , P = 0.005 < 0.05). Preoperative d-dimer volume increased by 1 μg/L; the OR value of higher grade PVST Shengjing typing was 1.001 times higher (95% CI: 1.000-1.002) than that of lower grade PVST Shengjing typing ( χ 2 = 8.369 , P = 0.004 < 0.05). Conclusions. The survival time of patients with portal vein system thrombosis after splenectomy was significantly different among Shengjing typing groups, and the higher the classification level, the shorter the survival time and the higher the risk of death. In patients with portal hypertension in cirrhosis and PVST formation after splenectomy, if the preoperative d-dimer level is high or accompanied by hepatitis virus, the formation of PVST will involve a wide range, the disease is more serious, and the prognosis is also poor, so corresponding preventive measures should be taken to avoid the aggravation of PVST. [ABSTRACT FROM AUTHOR]

To establish a stable animal model of associating liver partition and portal vein ligation for staged hepatectomy (ALPPS), as well as to explore whether Endocan and HGF/c‐Met signalling pathway participate in the regeneration of residual liver through hepatic stem cells after ALPPS procedure. C57BL/6J male mice weighing 18‐22 g were used in this study. The liver regeneration index was expressed as the ratio of Future Liver Remnant (FLR)/Body weight (BW) × 100%. Expression of hepatic stem cell marker CK19 was assessed by immunohistochemical method. Serum levels of vascular endothelial growth factor (VEGF) and Endocan were detected by ELISA. VEGF, Endocan and c‐Met contents in residual liver were observed by Western blot analysis. The expression levels of Endocan and HGF/c‐Met pathway‐related genes were evaluated by qRT‐PCR. Compared with the portal vein ligation (PVL) group and sham group, the ALPPS group had more CK19 positive cells and a higher liver regeneration index (P <.05). The serum levels of VEGF in the ALPPS group were increased significantly (P <.05) from the first day and decreased from the second day after surgery, and maintained consistently higher than that of the sham group (P <.05). Western blot showed that the expressions of VEGF and Endocan in ALPPS group were significantly higher than those in both sham and PVL groups at different time points. The Endocan plays a role in the rapid regeneration of residual liver after ALPPS, likely through the interaction with the HGF/c‐Met pathway to affect the hepatic stem cell population. Significance of the study: Our animal study provides valuable insights on the effect of Endocan in the process of rapid regeneration of residual liver after ALPPS, which would lead to the possible expansion of clinical research on ALPPS surgery and further studies on its molecular underpinning during liver regeneration. [ABSTRACT FROM AUTHOR]

Objective. This study aimed to assess whether a single dose of ertapenem prophylaxis was more effective than other antibiotics to prevent surgical site infection (SSI) after selective hepatectomy for hepatocellular carcinoma (HCC). Methods. The data from HCC patients with open hepatectomy between January 2012 and June 2017 in Shengjing Hospital were retrospectively analyzed. These patients were divided into two groups: ertapenem (ER) group, where a single dose of ER was administered; non-ertapenem (NER) group, where NER antibiotics were administered. The SSI rates were compared between two groups before and after matching the propensity scores. Results. The enrolled patients consisted of 78 in the ER group and 197 in the NER group. After matching the propensity scores, each group was down-selected to 65 patients. The SSI rate among the matched 130 patients was 14.6%, 7.7% occurred in the ER group and 21.5% in the NER group (P<0.05). The SSI rates in organ/space of the ER and NER groups were 3.1% and 13.8%, respectively (P<0.05). Conclusions. A single dose of ER before surgery was more effective in mitigating SSI after selective hepatectomy compared with other antibiotics use. The results imply that the selection of both antibiotics and administration timing is important for the efficacy in preventing SSI. [ABSTRACT FROM AUTHOR]

Background/Aims. Hepatic ischemia-reperfusion (I/R) injury is a serious concern during hepatic vascular occlusion. The objectives of this study were to assess effects of three techniques for hepatic vascular occlusion on I/R injury and to explore the underlying mechanisms. Methods. Liver cirrhotic rats had undertaken Pringle maneuver (PR), hemihepatic vascular occlusion (HH), or hepatic blood inflow occlusion without hemihepatic artery control (WH). Levels of tumor necrosis factor alpha (TNF-α), nuclear factor kappa B (NF-κB), toll-like receptor 4 (TLR4), TIR-domain-containing adapter-inducing interferon-β (TRIF), and hemeoxygenase 1 (HMOX1) were assayed. Results. The histopathologic analysis displayed that liver harm was more prominent in the PR group, but similar in the HH and WH groups. The HH and WH groups responded to hepatic I/R inflammation similarly but better than the PR group. Mechanical studies suggested that TNF-α/NF-κB signaling and TLR4/TRIF transduction pathways were associated with the differential effects. In addition, the HH and WH groups had significantly higher levels of hepatic HMOX1 (P<0.05) than the PR group. Conclusions. HH and WH confer better preservation of liver function and protection than the Pringle maneuver in combating I/R injury. Upregulation of HMOX1 may lead to better protection and clinical outcomes after liver resection. [ABSTRACT FROM AUTHOR]

The aim of this study is to explore the hepatoprotective effect of intraportal prostaglandin E1 (PGE1) on liver ischemia reperfusion (IR) injury using an extrahepatic cholestatic model, observing oxidative stress markers, proinflammatory factors, apoptotic marker proteins, and an adhesion molecule. The extrahepatic cholestatic model was induced by common bile duct ligation. After seven days, rats were subjected to ischemia by Pringle maneuver for 15 min, followed by 1, 6, or 24 h of reperfusion. Prostaglandin E1 (PGE group) or normal saline (NS group) was continuously infused from 15 min before liver ischemia to 1 h after reperfusion. After reperfusion, histopathological evaluation of the liver was performed, as were measurements of bilirubin, biochemical enzymes, oxidative stress markers (GSH and MDA), proinflammatory factors (MPO, TNF-α, and IL-1β), apoptotic marker proteins (Bcl-2 and Bax), and the adhesion molecule (ICAM-1). PGE1 pretreatment attenuated IR injury in extrahepatic cholestatic liver probably by suppressing MDA, MPO, TNF-α, IL-1β, ICAM-1, and Bax levels and improving GSH and Bcl-2 levels. In conclusion, PGE1 protects extrahepatic cholestatic liver from IR injury by improving hepatic microcirculation and reducing oxidative stress damage, intrahepatic neutrophil infiltration, and hepatocyte apoptosis. [ABSTRACT FROM AUTHOR]