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1.
Int Wound J ; 20(9): 3540-3549, 2023 Nov.
Article in English | MEDLINE | ID: mdl-37218367

ABSTRACT

This study comprehensively assessed the effect of enhanced recovery after surgery (ERAS) on wound infection and postoperative complications in patients undergoing liver surgery. The PubMed, EMBASE, MEDLINE, Cochrane Library, China National Knowledge Infrastructure (CNKI), VIP, and Wanfang electronic databases were searched to collect published studies on the use of ERAS in liver surgery until December 2022. Literature selection was performed independently by two investigators according to the inclusion and exclusion criteria, and quality evaluation and data extraction were performed. RevMan 5.4 software was used in this study. Compared with the control group, the ERAS group showed a significantly lower incidence of postoperative wound infection (odds ratio [OR]: 0.59, 95% confidence interval [CI]: 0.41-0.84, P = .004) and overall postoperative complication rate (OR: 0.43, 95% CI: 0.33-0.57, P < .001) and significantly shorter postoperative hospital stay (mean difference: -2.30, 95% CI: -2.92 to -1.68, P < .001). Therefore, ERAS was safe and feasible when applied to liver resection, reducing the incidence of wound infection and total postoperative complications, and shortening the length of hospital stay. However, further studies are required to investigate the impact of ERAS protocols on clinical outcomes.


Subject(s)
Enhanced Recovery After Surgery , Surgical Wound Infection , Humans , Hepatectomy/adverse effects , Length of Stay , Liver , Postoperative Complications/etiology , Surgical Wound Infection/prevention & control
2.
Can J Gastroenterol Hepatol ; 2022: 7750140, 2022.
Article in English | MEDLINE | ID: mdl-36051249

ABSTRACT

A retrospective cohort study was conducted to collect 465 patients with hepatitis B-related hepatocellular carcinoma who had undergone radical hepatectomy from January 1, 2012, to August 31, 2018, at the First Affiliated Hospital of the University of Science and Technology of China. The clinical, pathological, and follow-up information was collected to compare the basic characteristics of death and nondeath after radical resection. Kaplan-Meier curves were used for survival analysis and male and female subgroup analysis. The multivariate Cox proportional-hazards regression model was used to analyze independent risk factors related to postoperative death. Of the 465 patients with radical resection of hepatitis B-related hepatocellular carcinoma, 132 died, and 1-, 3-, and 5-year cumulative survival rates after operation were 92.1%, 78%, and 64%, respectively. In the male and female subgroup, 115 and 17 patients died, respectively. The 1-, 3-, and 5-year cumulative survival rates were 92.6%, 77.0%, and 62.6%, respectively, in men, and 89.6%, 78.8%, and 70.2%, respectively, in women. Multivariate Cox proportional-hazards regression analysis showed that microvascular invasion (MVI), Edmondson III/IV, BCLC stage B, and total bilirubin (TB) > 20.5 µmol/L were independent risk factors in patients with hepatitis B-related hepatocellular carcinoma after radical hepatectomy.


Subject(s)
Carcinoma, Hepatocellular , Hepatitis B , Liver Neoplasms , Carcinoma, Hepatocellular/pathology , Disease-Free Survival , Female , Hepatitis B/complications , Humans , Liver Neoplasms/pathology , Male , Neoplasm Invasiveness/pathology , Neoplasm Recurrence, Local/pathology , Prognosis , Retrospective Studies , Risk Factors , Treatment Outcome
3.
J Int Med Res ; 49(10): 3000605211047278, 2021 Oct.
Article in English | MEDLINE | ID: mdl-34617814

ABSTRACT

OBJECTIVE: To investigate the clinical significance of human leukocyte antigen (HLA)-E levels in oesophageal squamous cell carcinoma (ESCC). METHODS: The levels of HLA-E immunostaining in ESCC lesions and 47 corresponding adjacent normal tissues were measured using immunohistochemistry. The correlation between the levels of immunostaining and clinical parameters was analysed. RESULTS: This study analysed 110 paraffin-embedded primary tumour lesions and 47 case-controlled paracancerous tissues that were surgically resected from 110 patients with ESCC. Positive immunostaining for HLA-E was observed in 88.2% (97 of 110) of ESCC lesions and 29.8% (14 of 47) of normal oesophageal tissues. There was no correlation between HLA-E immunostaining in ESCC lesions and clinicopathological characteristics such as lymph node metastasis, tumour-node-metastasis stage and differentiation grade. Kaplan-Meier survival analysis revealed a significantly better prognosis in patients with higher levels of HLA-E immunostaining than in those with lower levels of HLA-E immunostaining; overall survival was 28.6 months (95% confidence interval [CI], 23.2, 34.0) versus 15.3 months (95% CI, 11.5, 19.1), respectively. Furthermore, multivariate analysis showed that the HLA-E level was an independent prognostic factor in patients with ESCC. CONCLUSION: A higher level of HLA-E immunostaining was associated with favourable survival in patients with ESCC.


Subject(s)
Carcinoma, Squamous Cell , Esophageal Neoplasms , Esophageal Squamous Cell Carcinoma , Carcinoma, Squamous Cell/diagnosis , Esophageal Neoplasms/diagnosis , HLA Antigens , Humans , Prognosis
6.
Cancer Manag Res ; 10: 1647-1655, 2018.
Article in English | MEDLINE | ID: mdl-29970964

ABSTRACT

PURPOSE: The aim of this study was to investigate whether the expression of the ligand-gated Ca2+ channel transient receptor potential vanilloid type-1 (TRPV1) in primary human renal cell carcinoma (RCC) is associated with clinicopathological features. PATIENTS AND METHODS: Fresh and frozen primary tumor and normal peritumoral kidney tissues from 127 patients diagnosed with RCC were analyzed for TRPV1 expression by quantitative reverse transcription polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry. RESULTS: Quantitative RT-PCR revealed that TRPV1 was decreased 3.20-fold in RCC tissue vs normal peritumoral kidney tissue (p=0.012). Significantly different TRPV1 mRNA expression was detected in RCC tissues of different Fuhrman grades and histopathological subtypes (F=4.282, p=0.015 and F=5.205, p=0.014, respectively). Decreased TRPV1 expression was correlated with RCC histopathological subtype (R=-0.554, p=0.003) and Fuhrman grade (R=-0.525, p=0.006). Western blot analysis of TRPV1 protein expression showed similar results. Immunohistochemical analysis showed strong expression of TRPV1 in kidney tubules but demonstrated weak or no immunostaining in RCC tissues. CONCLUSION: TRPV1 expression was decreased in RCC, which was significantly associated with tumor Fuhrman grades and histopathological subtypes. It seems to suggest that TRPV1 expression may be a valuable tool to predict the extent of RCC progression.

7.
Oncotarget ; 5(19): 9256-68, 2014 Oct 15.
Article in English | MEDLINE | ID: mdl-25211001

ABSTRACT

The expression of RNA polymerase II subunit 3 (Rpb3) was found frequent up-regulation in Hepatocellular carcinoma (HCC) tumors. Significant associations could also be drawn between increased expressions of Rpb3 and advance HCC staging and shorter disease-free survival of patients. Overexpression of Rpb3 increased HCC cell proliferation, migratory rate and tumor growth in nude mice, whereas suppression of Rpb3 using shRNA inhibited these effects. For mechanism study, we found that Rpb3 bound directly to Snail, downregulated E-cadherin, induced HCC cells epithelial-mesenchymal transition (EMT). In particular, N-terminus of Rpb3 blocked Rpb3 binding to Snail, inhibited Rpb3-high-expression HCC cells proliferation, migration, tumor growth in nude mice, and also inhibited DEN-induced liver tumorigenesis. Furthermore, N-terminus of Rpb3 did not inhibit normal liver cells or Rpb3-low-expression HCC cells proliferation. These findings suggest that N-terminus of Rpb3 selectively inhibits Rpb3-high-expression HCC cells proliferation. N-terminus of Rpb3 may be useful in treating patients diagnosed with Rpb3-high-expression HCC.


Subject(s)
Carcinoma, Hepatocellular/genetics , Liver Neoplasms/genetics , Peptide Fragments/pharmacology , RNA Polymerase II/metabolism , Transcription Factors/metabolism , Animals , Cadherins/biosynthesis , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Cell Transformation, Neoplastic/genetics , Epithelial-Mesenchymal Transition/genetics , Gene Expression Regulation, Neoplastic , Hep G2 Cells , Humans , Male , Mice , Mice, Inbred C57BL , Mice, Nude , Peptide Fragments/genetics , Protein Binding/genetics , RNA Interference , RNA Polymerase II/biosynthesis , RNA Polymerase II/genetics , RNA, Small Interfering , Snail Family Transcription Factors
8.
Biomed Res Int ; 2014: 547187, 2014.
Article in English | MEDLINE | ID: mdl-25006578

ABSTRACT

As a well-known neurotrophic factor, nerve growth factor (NGF) has also been extensively recognized for its acceleration of healing in cutaneous wounds in both animal models and randomized clinical trials. However, the underlying mechanisms accounting for the therapeutic effect of NGF on skin wounds are not fully understood. NGF treatment significantly accelerated the rate of wound healing by promoting wound reepithelialization, the formation of granulation tissue, and collagen production. To explore the possible mechanisms of this process, the expression levels of CD68, VEGF, PCNA, and TGF-ß1 in wounds were detected by immunohistochemical staining. The levels of these proteins were all significantly raised in NGF-treated wounds compared to untreated controls. NGF also significantly promoted the migration, but not the proliferation, of dermal fibroblasts. NGF induced a remarkable increase in the activity of PI3K/Akt, JNK, ERK, and Rac1, and blockade with their specific inhibitors significantly impaired the NGF-induced migration. In conclusion, NGF significantly accelerated the healing of skin excisional wounds in rats and the fibroblast migration induced by NGF may contribute to this healing process. The activation of PI3K/Akt, Rac1, JNK, and ERK were all involved in the regulation of NGF-induced fibroblast migration.


Subject(s)
Cell Movement/drug effects , Fibroblasts/pathology , MAP Kinase Signaling System/drug effects , Nerve Growth Factor/pharmacology , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Wound Healing/drug effects , Animals , Antigens, CD/metabolism , Antigens, Differentiation, Myelomonocytic/metabolism , Cell Proliferation/drug effects , Cells, Cultured , Collagen/biosynthesis , Dermis/pathology , Epithelium/drug effects , Epithelium/pathology , Extracellular Signal-Regulated MAP Kinases/metabolism , Fibroblasts/drug effects , Fibroblasts/enzymology , Granulation Tissue/drug effects , Granulation Tissue/pathology , Humans , JNK Mitogen-Activated Protein Kinases/metabolism , Male , Nerve Growth Factor/administration & dosage , Proliferating Cell Nuclear Antigen/metabolism , Rats, Sprague-Dawley , Transforming Growth Factor beta1/metabolism , Up-Regulation/drug effects , Vascular Endothelial Growth Factor A/metabolism , rac1 GTP-Binding Protein/metabolism
9.
Acta Pharmacol Sin ; 35(1): 82-8, 2014 Jan.
Article in English | MEDLINE | ID: mdl-23685956

ABSTRACT

AIM: To investigate the roles of P21-activated kinase 5 (PAK5) in proliferation and tumorigenicity of human hepatocellular carcinoma (HCC). METHODS: HCC and matched paraneoplastictis tissue samples were obtained from 30 patients. Human HCC cell lines SMMC7721, HepG2, Hep3B, SK-HEP-1, Huh-7, and liver cell line HL-7702 were examined. The expression of PAK5 gene was studied using real-time qPCR and Western blotting. Cell proliferation was quantified with the MTT assay. Cell cycle was analyzed with flow cytometry. The tumorigenicity of Lv-shRNA-transfected HepG2 cells was evaluated in BALB/cA nude mice. RESULTS: The mRNA level of PAK5 was significantly higher in 25 out of 30 HCC samples compared to the matched paraneoplastic tissues. The HCC cell lines showed varying expression of PAK5 protein, and the highest level was found in the HepG2 cells. PAK5 gene silencing in HepG2 cells markedly reduced the cell proliferation and colony formation, and induced cell cycle arrest in the G1 phase. Furthermore, PAK5 gene silencing suppressed the tumor formation in nude mice, and significantly decreased the expression of HCC-related genes Cyclin D1 and beta-catenin. CONCLUSION: PAK5 may play essential roles in the initiation and progression of human HCC. Thus, it may be an effective therapeutic target or perhaps serve as a clinical diagnostic or prognostic marker in human HCC.


Subject(s)
Carcinogenesis/metabolism , Carcinoma, Hepatocellular/enzymology , Cell Proliferation , Liver Neoplasms/enzymology , p21-Activated Kinases/physiology , Animals , Carcinoma, Hepatocellular/pathology , Hep G2 Cells , Humans , Liver Neoplasms/pathology , Mice , Mice, Inbred BALB C , Mice, Nude , Xenograft Model Antitumor Assays/methods
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