Background The incidence of gallstone increases with increasing age. No studies have been reported in the elderly population with laparoscopic cholecystectomy from developing nations. The aim of this study was to compare perioperative outcomes of laparoscopic cholecystectomy between the elderly (≥60 years old) and the young (<60 years old). Methods From July 2015 to June 2016, a retrospective review of medical records of 78 elderly patients (≥60 years old) and 164 young patients (<60 years old) who underwent laparoscopic cholecystectomy was done. The patients' demographics and perioperative outcomes were analyzed. Results Median ages were 65 years (range: 60–80) and 45 years (range: 21–59) for the elderly group and the young group. The majority of patients were female (62.8 and 72%). There were no significant differences in the conversion rate (9 and 7.9%, P = 0.78), postoperative complications (17.9 and 14.6%, P = 0.50), and length of stay in the hospital (4 days for both groups, P = 0.35) between the two groups. There was no mortality in either of the groups. Conclusion Our results of laparoscopic cholecystectomy in elderly patients are comparable with those in young patients. Therefore, laparoscopic cholecystectomy is safe even in the elderly population.

The dysregulated expression of glycolysis-related genes (GRGs) is closely related to the occurrence of diverse tumors and regarded as a novel target of tumor therapy. However, the role of GRGs in colon cancer is unclear. We obtained 226 differential GRGs (DE-GRGs) from The Cancer Genome Atlas (TCGA) database. Cox regression analysis was used to construct a DE-GRG prognostic model, including P4HA1, PMM2, PGM2, PPARGC1A, PPP2CB, STC2, ENO3, and CHPF2. The model could accurately predict the overall survival rate of TCGA and GSE17536 patient cohorts. The risk score of the model was closely related to a variety of clinical traits and was an independent risk factor for prognosis. Enrichment analysis revealed the activation of a variety of glycolysis metabolism and immune-related signaling pathways in the high-risk group. High-risk patients displayed low expression of CD4+ memory resting T cells and resting dendritic cells and high expression of macrophages M0 compared with the expression levels in the low-risk patients. Furthermore, patients in the high-risk group had a higher tumor mutation load and tumor stem cell index and were less sensitive to a variety of chemotherapeutic drugs. Quantitative reverse transcription polymerase chain reaction and immunohistochemistry analyses validated the expression of eight GRGs in 43 paired clinical samples. This is the first multi-omics study on the GRGs of colon cancer. The establishment of the risk model may benefit the prognosis and drug treatment of patients.

Background: Hepatoblastoma is a common hepatic tumor occurring in children between 0-5 years. Accumulating studies have shown lncRNA's potential role in distinct cancer progression and development, including hepatoblastoma. SnoRNA host gene 9 (SNHG9) is associated with the progression of distinct human cancers, but, its specific molecular mechanisms in hepatoblastoma is not unknown. Methods: In this study, we estimated SNHG9 expression in hepatoblastoma tissue and cell lines by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Next, we downregulated and upregulated SNHG9 expression in hepatoblastoma cell lines and then determined cell proliferation (CCK-8), colony formation, and cellular apoptosis activity. The dual luciferase reporter activity, RNA immunoprecipitation (RIP), biotin RNA pull down and Spemann's Pearson correlation coefficient assay were performed to establish the interaction between SNHG9, WNt3a and miR-23a-5p. A xenograft in-vivo tumorgenicity test was performed to elucidate the role of SNHG9 hepatoblastoma in tumorigenesis. SNHG9 role in Cisplatin drug resistance in hepatoblastoma was also determined. Results: SNHG9 was significantly upregulated in hepatoblastoma tissue and cell lines. SNHG9 overexpression on HUH6 & HepG2 resulted in a significant increase in cell proliferation and clonogenic activity while SNHG9 knock down resulted in a sustained inhibition of cell proliferation and clonogenic activity. Dual luciferase activity, RNA immunoprecipitation and biotin pull down confirmed the direct interaction of miR-23a-5p with SNHG9. The xenograft tumorgenicity test showed SNHG9 downregulation significantly inhibited the tumor growth in BALB/c mice. ROC and Kaplan-Meier analysis showed potential prognostic and diagnostic importance of SNHG9 in hepatoblastoma. Conclusion:We concluded that SNHG9/miR-23a-5p/Wnt3a axis promotes the progression hepatoblastoma tumor.

Introduction: Oesophageal resection were notoriously complicated and produces a cohort of patients prone to postoperative complications and here we would like to focus on the implementation and effectiveness of early chest tube removal in ERAS after oesophago-gastrectomy considering the various aspect like pleural effusion and reducing the length of hospital stay which ultimately lead to reducing the economic burden on patient.Methods: An ERAS programme was devised and implemented with the support of a dedicated in-hospital task-force. The patients underwent esophago-gastrectomy were randomly divided into two groups: the ERAS group and the control group (non-ERAS). The ERAS group was treated with early removal of the chest tube after surgery, and the control group was treated with traditional way and outcomes were compared between them.Results: The length of hospital stay and the cost of hospitalization in the ERAS group were significantly lower than those in the control group（p<0.05. However, there was no statistical significant difference in the incidences of pleural effusion between the two groups（p＞0.05).Conclusions: The introduction of early chest tube removal as an ERAS programme after oesophago-gastrectomy would not increase the risk of pleural effusion and would not increase the total length of stay and cost of hospitalisation without jeopardising patient safety or clinical outcomes.

Hepatoblastoma is the most common type of hepatic tumors occurring in children between 0 -5 years.And the exact pathophysiology of the disease is still mysterious. Accumulating studies on LncRNA have shown its pivotal role in the development and progression of distinct human cancers. However, the role of LINC01023 in hepatoblastoma is unknown.Methods: The relative expression of LINC01023, miR-378a-5p, and Wnt3 on hepatoblastoma tissue and cell lines was determined by quantitative polymerase chain reaction (qRT-PCR). The effect of LINC01023 downregulation and upregulation on cell proliferation, colony formation and apoptosis activities in HUH6 and HepG2 Cells was assessed by CKK8, clonogenic and ow cytometry analysis, respectively. Dual luciferase, RNA immunoprecipitation (RIP), and RNA pull-down were performed to con rm the interaction between LINC01023 and miR-378a-5p. Similarly, Dual luciferase assay was performed to con rmed the interaction between Wnt3 and miR-378a-5p. The xenograft tumorgenicity test was performed to elucidate the tumorgenicity potential of LINC01023.Results: LINC01023 was signi cantly upregulated in hepatoblastoma tissue and cell lines rather than in adjacent normal hepatic tissue and QSG7701 cell lines. LINC01023 silencing attenuated cell proliferation, colony formation and increased cell apoptosis. Conversely, LINC01023 upregulation results in signi cant increase in cell proliferation, and colony formation activities however, a signi cant reduction apoptosis activity. Interaction between the LINC01023 and WNT3 was con rmed by dual luciferase assay.Xenograft animal tumorgenicity test con rmed the in-vivo tumorigenesis potential of LINC01203. Conclusion:To the best of our knowledge, this study is the rst study demonstrating the role of LINC01023 in hepatoblastoma tumorigenesis through the LINC01023/miR-378a-5p/Wnt3 axis. It could be a potential therapeutic target and a prognostic biomarker in hepatoblastoma.