AIM:To compare the clinical outcomes of patients with portal hypertension (PH) who underwent treatment with splenectomy plus simplified pericardial devascularisation (SSPD) or splenectomy plus traditional pericardial devascularisation (STPD).METHODS:We conducted a single-centre retrospective study of 1045 PH patients treated with either SSPD (S Group, 357 patients) or STPD (T Group, 688 patients) between January 2002 and February 2017. In all, 37 clinical indicators were compared to evaluate the efficacy of SSPD.RESULTS:Perioperative indicators in the S Group were significantly better than those in the T Group (P < 0.05). In both groups, the postoperative long-term portal vein diameter and Model for End-Stage Liver Disease score were significantly lower than those in the preoperative and postoperative short-term groups (P < 0.05). The incidence of complications in the S Group was significantly lower than that in the T Group (P < 0.05). Compared to the T Group, postoperative short-term WBC (white blood cell) and platelet counts were significantly lower and the short-term Hb (haemoglobin) level was significantly higher in the S Group (P < 0.05). In the S Group, postoperative long-term total bilirubin, direct bilirubin, alanine transaminase, and aspartate transaminase and postoperative serum creatinine and cystatin C levels were significantly lower than those in the T Group (P < 0.05), and postoperative albumin was significantly higher than that in the T Group (P < 0.05).CONCLUSION:Compared to STPD, SSPD is a simple and easy procedure resulting in less tissue damage. Patients recovered smoothly and steadily with fewer complications. Short-term liver and kidney function damage was less severe, and long-term liver function recovery was better. Therefore, SSPD is worthy of clinical promotion and application for the treatment of PH.

AIM To analyse the postoperative survival of patients with portal hypertension and determine the factors that influence survival and construct nomograms. METHODS We retrospectively followed 1045 patients who underwent splenectomy plus pericardial devascularisation (SPD) between January 2002 and December 2017. Two SPD types are used in our department: splenectomy plus simplified pericardial devascularisation (SSPD) and splenectomy plus traditional pericardial devascularisation (STPD). The Kaplan-Meier method and Cox regression analysis were used to evaluate the prognostic effects of multiple parameters on overall survival (OS), disease-specific survival (DSS) and bleeding-free survival (BFS). Significant prognostic factors were combined to build nomograms to predict the survival rate of individual patients. RESULTS Five hundred and fifty-seven (53.30%) patients were successfully followed with 192 in the SSPD group and 365 in the STPD group; 93 (16.70%) patients died, of whom 42 (7.54%) died due to bleeding. Postoperative bleeding was observed in 84 (15.10%) patients. The 5- and 10-year OS, DSS and BFS rates in the group of patients who underwent SSPD were not significantly different from those in patients who underwent STPD. Independent prognostic factors for OS were age, operative time, alanine transaminase level and albumin-bilirubin score. Independent prognostic factors for BFS were male sex, age, intraoperative blood loss and time to first flatus. Independent prognostic factors for DSS were the Comprehensive Complication Index and age. These characteristics were used to establish nomograms, which showed good accuracy in predicting 1-, 3- and 5-year OS and BFS. CONCLUSION SSPD achieves or surpasses the long-term survival effect of traditional pericardial devascularisation and is worthy of clinical promotion and application. Nomograms are effective at predicting prognosis.

Hypoxia-reoxygenation (H/R) injury hepatocyte models were established to simulate the ischemia/reperfusion injury of transplanted organ. Through the study of the molecular mechanism of H/R on the F-actin damage of the liver cytomembrane, the mechanism of F-actin damage induced by ischemia and reperfusion was studied from the level of cell and molecule.The hypoxic environment of cells in vitro was simulated by chemical hypoxia agent CoCl2. Liver cells were detected by MTT, H/R group was subdivided into 3 subgroups: H/R 2, 4, and 6 h. Changes of cell shape and the growth state, apoptosis, ultrastructural changes, and the changes in F-actin microfilament content were observed. Heat shock protein 27 (HSP27), Cofilin, and F-actin gene and protein levels were determined by real-time polymerase chain reaction and western blot assay, respectively.Cells showed circular adherence growth under normal circumstances, while the spindle cells and shedding cells were significantly increased in H/R groups. Apoptosis cells in H/R group were increased significantly with the extension of hypoxia time. The number of endoplasmic reticulum was decreased significantly in the H/R group, the mitochondrion hydropic was degenerated and the glycogen was disappeared. The F-actin fibers in the H/R group were disordered, the morphology of the fibers was obviously decreased, and the fluorescence staining decreased obviously (P < .05). The transcription and expression levels of HSP27, Cofilin, and F-actin were significantly lower than those in the control group (P < .05).These results demonstrate that H/R can affect the correct assembly of F-actin microfilaments and weakens the normal cycle of F-actin microfilaments through inhibiting the protein expression and gene transcription of HSP27 and Cofilin in hepatocytes, thereby changing the skeleton of F-actin microfilaments.

AIM: To study whether transfer of blood between the right gastroepiploic artery and gastroduodenal artery could lessens the damage to bile canaliculi.METHODS: Forty male Bama miniature pigs were divided into four groups as follows: a control group, two hepatic artery ischemia groups(1 h and 2 h), and a hepatic artery bridging group. The hemodynamics of the hepatic artery in the hepatic artery bridging group was measured using color Doppler ultrasound. Morphological changes in the bile canaliculus were observed by transmission electron microscopy. Cofilin, heat shock protein 27 and F-actin expression was detected by immunohistochemistry, Western blot, and real-time polymerase chain reaction. Terminal deoxynucleotidyl transferase-mediated nick end-labeling method was used to evaluate liver injury. RESULTS: The hemodynamics was not changed in the hepatic artery bridging group. The microvilli in the bile canaliculus were impaired in the two hepatic artery ischemia groups. The down-regulation of cofilin and F-actin and up-regulation of heat shock protein 27 were observed in the two hepatic artery ischemia groups, while there were no significant differences between thecontrol group and hepatic artery bridging group.CONCLUSION: Hepatic artery ischemia aggravates damage to bile canaliculi, and this damage can be diminished by a hepatic artery bridging duct.

Hepatic stellate cells (HSCs) are the primary sources of extracellular matrix (ECM) in normal and fibrotic liver. Peroxisome proliferator-activated receptor gamma (PPARγ) maintains HSCs in a quiescent state, and its downregulation induces HSC activation. MicroRNAs (miRNAs) can induce PPARγ mRNA degradation, but the mechanism by which miRNAs regulate PPARγ in rat HSCs is unclear. This study aimed to investigate some miRNAs which putatively bind to the 3′-untranslated region (3′-UTR) of PPARγ mRNA, and increase expression of ECM genes in rat HSCs. In carbon tetrachloride injection (CCl4) and common bile duct ligation (CBDL) liver fibrosis models, miRNAs miR-130a, miR-130b, miR-301a, miR-27b and miR-340 levels were found to be increased and PPARγ expression decreased. Overexpression of miR-130a and miR-130b enhanced cell proliferation by involving Runx3. MiR-130a and miR-130b decreased PPARγ expression by targeting the 3′-UTR of PPARγ mRNA in rat HSC-T6 cells. Transforming growth factor-β1 (TGF-β1) may mediate miR-130a and miR-130b overexpression, PPARγ downregulation, and ECM genes overexpression in cell culture. These findings suggest that miR-130a and miR-130b are involved in downregulation of PPARγ in liver fibrosis.

Pancreatic cancer (PC) is an aggressive and devastating disease with a poor prognosis. Cisplatin, a commonly used chemotherapeutic agent for solid tumors, is effective as a single agent or in combination with other drugs for the treatment of PC. Previous studies have suggested that Twist and growth differentiation factor 15 (GDF15) are involved in the progression of PC. However, the role of Twist and GDF15 in PC remains to be elucidated. In the present study, the individual effect of and interaction between Twist and GDF15 in PC cell invasion and chemoresistance to cisplatin was examined. Twist and/or GDF15 were stably overexpressed or knocked down in ASPC‑1 and BXPC‑3 human PC cells. Overexpression of Twist in the two cell lines markedly increased GDF15 expression, cell invasion, matrix metalloproteinase‑2 expression/activity and the half maximal inhibitory concentration (IC50) values of cisplatin, which was eradicated by GDF15 knockdown or the selective p38 mitogen‑activated protein kinase (MAPK) inhibitor SB203580 (10 µM). By contrast, Twist knockdown significantly decreased GDF15 expression, cell invasion, matrix metalloproteinase‑2 expression/activity and the IC50 values of cisplatin, which was completely reversed by overexpression of GDF15. In addition, while overexpression and knockdown of Twist increased and decreased p38 MAPK activity, respectively, GDF15 demonstrated no significant effect on p38 MAPK activity in PC cells. In conclusion, the present study, for the first time, to the best of our knowledge, demonstrated that Twist promotes PC cell invasion and cisplatin chemoresistance through inducing GDF15 expression via a p38 MAPK‑dependent mechanism. The present study provides new insights into the molecular mechanisms underlying PC progression and chemoresistance.

AIM:We undertook this meta-analysis to investigate the relationship between revascularization and outcomes after liver transplantation.METHODS:A literature search was performed using MeSH and key words. The quality of the included studies was assessed using the Jadad Score and the Newcastle-Ottawa Scale. Heterogeneity was evaluated by the χ(2) and I (2) tests. The risk of publication bias was assessed using a funnel plot and Egger's test, and the risk of bias was assessed using a domain-based assessment tool. A sensitivity analysis was conducted by reanalyzing the data using different statistical approaches.RESULTS:Six studies with a total of 467 patients were included. Ischemic-type biliary lesions were significantly reduced in the simultaneous revascularization group compared with the sequential revascularization group (OR = 4.97, 95%CI: 2.45-10.07; P < 0.00001), and intensive care unit (ICU) days were decreased (MD = 2.00, 95%CI: 0.55-3.45; P = 0.007) in the simultaneous revascularization group. Although warm ischemia time was prolonged in simultaneous revascularization group (MD = -25.84, 95%CI: -29.28-22.40; P < 0.00001), there were no significant differences in other outcomes between sequential and simultaneous revascularization groups. Assessment of the risk of bias showed that the methods of random sequence generation and blinding might have been a source of bias. The sensitivity analysis strengthened the reliability of the results of this meta-analysis.CONCLUSION:The results of this study indicate that simultaneous revascularization in liver transplantation may reduce the incidence of ischemic-type biliary lesions and length of stay of patients in the ICU.

Nonanastomotic strictures (NAS) are common biliary complications after liver transplantation (LT). Delayed rearterialization induces biliary injury in several hours. However, whether this injury can be prolonged remains unknown. The correlation of this injury with NAS occurrence remains obscure. Different delayed rearterialization times were compared using a porcine LT model. Morphological and functional changes in bile canaliculus were evaluated by transmission electron microscopy and real‐time PCR. Immunohistochemistry and TUNEL were performed to validate intrahepatic bile duct injury. Three months after LT was performed, biliary duct stricture was determined by cholangiography; the tissue of common bile duct was detected by real‐time PCR. Bile canaliculi were impaired in early postoperative stage and then exacerbated as delayed rearterialization time was prolonged. Nevertheless, damaged bile canaliculi could fully recover in subsequent months. TNF‐α and TGF‐β expressions and apoptosis cell ratio increased in the intrahepatic bile duct only during early postoperative period in a time‐dependent manner. No abnormality was observed by cholangiography and common bile duct examination after 3 months. Delayed rearterialization caused temporary injury to bile canaliculi and intrahepatic bile duct in a time‐dependent manner. Injury could be fully treated in succeeding months. Solo delayed rearterialization cannot induce NAS after LT.