Remimazolam Dosing for Gastroscopy: A Randomized Noninferiority Trial.

BACKGROUND: Remimazolam, an ultra-short-acting benzodiazepine, may provide adequate sedation for endoscopy while causing less cardiovascular or respiratory disturbance than propofol. Although fixed-dose administration is suggested, body weight affects the volume of the central chamber and thus affects the sedation depth that can be achieved by the first dose. This study aimed to compare the efficacy and safety of different doses of remimazolam and propofol by body weight for sedation during gastroscopy. METHODS: This multicenter, randomized, single-blind, parallel-controlled noninferiority trial recruited patients from five centers between March 2021 and July 2022. A total of 1,883 patients scheduled to undergo gastroscopy were randomized to groups receiving 0.15 mg/kg remimazolam, 0.2 mg/kg remimazolam, or 1.5 mg/kg propofol. The noninferiority margin was set to 5%. The primary outcome was the success rate of sedation. Adverse events were recorded to evaluate safety. RESULTS: The sedation success rate of the 0.2 mg/kg remimazolam group was not inferior to that of the 1.5 mg/kg propofol group (98.7% vs. 99.4%; risk difference, -0.64%; 97.5% CI, -2.2 to 0.7%, meeting criteria for noninferiority). However, the sedation success rate of the 0.15 mg/kg remimazolam group was 88.5%, and that of the 1.5 mg/kg propofol group was 99.4% (risk difference, -10.8%; 97.5% CI, -14.0% to -8.0%), demonstrating inferiority. Simultaneously, the overall adverse events rate of remimazolam was lower than that of propofol, and the incidence of bradycardia, hypotension, subclinical respiratory depression, and hypoxia in the remimazolam groups was significantly lower than that in the propofol group. CONCLUSIONS: This trial established the noninferior sedation success rate of remimazolam (0.2 mg/kg but not 0.15 mg/kg) compared with propofol (1.5 mg/kg), with a superior safety profile.

Efficacy and safety of remimazolam tosylate for sedation during upper gastrointestinal endoscopy: study protocol for a multicenter randomized controlled trial.

BACKGROUND: Gastrointestinal endoscopy has been associated with difficult experiences and can leave patients with an unpleasant impression. Propofol and midazolam are the most commonly used intravenous anesthetics for sedation during gastrointestinal endoscopy. However, cardiac and pulmonary adverse events are the primary concerns associated with the use of these sedatives. Remimazolam tosylate is an ultra-short-acting benzodiazepine drug with a mild inhibitory effect on the respiratory and circulatory systems. These properties qualify remimazolam tosylate to be used as a replacement for propofol or midazolam as a sedative during gastrointestinal endoscopy. This study aims to describe the efficacy and safety of remimazolam tosylate as a sedative for upper gastrointestinal endoscopy. METHODS: A multicenter, randomized, single-blind, parallel-controlled, noninferiority clinical study will be conducted to evaluate the efficacy and safety of remimazolam tosylate as a sedative during upper gastrointestinal endoscopy. Participants (n = 1800) will be randomized to receive remimazolam tosylate at 0.15 mg/kg (experimental group 1), remimazolam tosylate at 0.2 mg/kg (experimental group 2), or propofol at 1.5 mg/kg (control group). Procedure success will be assessed and defined as the completion of upper gastrointestinal endoscopy without the administration of a rescue sedative agent or more than two top-up doses of the trial drug in any 5-min period after initial administration. Sedation quality will be evaluated using the Modified Observer's Assessment of Alertness/Sedation score. Adverse events will be recorded to evaluate safety. DISCUSSION: This study will determine the optimal dosage of remimazolam tosylate during upper gastrointestinal endoscopy and will describe its efficacy and safety. These findings may contribute to a more comfortable and safer experience for patients compared with that when the conventional sedative propofol is used. TRIAL REGISTRATION: ClinicalTrials.gov NCT04727034. Registered on February 18, 2021.

Perioperative acute myocardial infarction in patients after non-cardiac surgery in China: Characteristics and risk factors.

To examine the characteristics and short-term outcome of perioperative myocardial infarction (PMI), a single-center retrospective study was carried out. The electronic medical records of 278,939 patients aged 45 years or older who underwent non-cardiac surgery at Renji Hospital from January 2003 to December 2015 were screened based on diagnostic codes (ICD121, ICD121.0, ICD121.1, ICD121.2, ICD121.3, ICD121.4, or ICD121.9). The incidence and characteristics of PMI and mortality risk factors were analyzed after non-cardiac surgery. PMI was reported in 45 patients, with an incidence rate of 1.61 per 10,000 and a mortality rate of 75.6% (34/45). The PMI incidence rate increased significantly with age. The PMI incidence rate was the highest for vascular surgery (5.82 per 10,000 cases). PMI occurs mainly within 48 h of surgery, with most cases showing an onset in the general wards. Logistic analysis showed that the use of nitrates is the independent protective factor for the outcomes of patients with PMI. The incidence of PMI in non-cardiac surgery is approximately 2 of 10,000 in patients aged 45 years or older, and increased significantly with age. The use of nitrates might be helpful for their survival.

Simvastatin attenuates macrophage-mediated gemcitabine resistance of pancreatic ductal adenocarcinoma by regulating the TGF-ß1/Gfi-1 axis.

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with an intrinsic resistance to almost all chemotherapeutic drugs, including gemcitabine. An abundance of tumor-associated macrophages (TAMs), which can promote the resistance of PDAC to gemcitabine, has been observed in the microenvironments of several tumors. In this study, we confirmed that incubation in TAM-conditioned medium (TAM-CM) reduces the gemcitabine-induced apoptosis of PDAC cells. Simvastatin attenuated the TAM-mediated resistance of PDAC cells to gemcitabine. Further investigation found that simvastatin reversed the TAM-mediated down-regulation of Gfi-1 and up-regulation of CTGF and HMGB1. Simvastatin induced Gfi-1 expression, which increased the sensitivity of PDAC cells to gemcitabine by decreasing TGF-ß1 secretion by TAMs. A luciferase reporter assay and ChIP assay revealed that Gfi-1 directly repressed the transcription of CTGF and HMGB1. Simvastatin also reversed the effects of gemcitabine on the expression of TGF-ß1 and Gfi-1 and reduced the resistance of PDAC to gemcitabine in vivo. These results provide the first evidence that simvastatin attenuates the TAM-mediated gemcitabine resistance of PDAC by blocking the TGF-ß1/Gfi-1 axis. These findings suggest the TGF-ß1/Gfi-1 axis as a novel therapeutic target for treating PDAC.

MiR-451, a potential prognostic biomarker and tumor suppressor for gastric cancer.

BACKGROUND: The expression of microRNA-451 (miR-451) and its association with clinical pathological factors in GC remain still unclear. The purpose of this study was to investigate if miR-451 is a potential prognostic biomarker and tumor suppressor for gastric cancer. METHODS: Real-time quantitative RT-PCR (qRT-PCR) was applied to detect miR-451 expression in GC cell lines and primary tumor and paired non-cancerous tissues. The association of miR-451 expression with clinicopathological factors and prognosis was statistically analyzed. RESULTS: We found that miR-451 showed decreased expression in GC tissues and cell lines, and its down-regulation tended to be positively correlated with lymphatic metastasis, clinical staging and shorter overall survival of patients. In addition, forced expression of miR-451 in BGC-823 and MKN-45 cells did not impact on cell proliferation, but did reduce migration and invasion rates in BGC-823 cells. CONCLUSION: Our findings indicated that miR-451 may act as a novel prognostic marker and potential therapeutic target in human GC.

Immunohistochemical Study of Expression of Sohlh1 and Sohlh2 in Normal Adult Human Tissues.

The expression pattern of Sohlh1 (spermatogenesis and oogenesis specific basic helix-loop-helix 1) and Sohlh2 in mice has been reported in previous studies. Sohlh1 and Sohlh2 are specifically expressed in spermatogonia, prespermatogonia in male mice and oocytes of primordial and primary follicles in female mice. In this report, we studied the expression pattern of Sohlh1 and Sohlh2 in human adult tissues. Immunohistochemical staining of Sohlh1 and Sohlh2 was performed in 5 samples of normal ovaries and testes, respectively. The results revealed that Sohlh genes are not only expressed in oocytes and spermatogonia, but also in granular cells, theca cells, Sertoli cells and Leydig cells, and in smooth muscles of blood vessel walls. To further investigate the expression of Sohlh genes in other adult human tissues, we collected representative normal adult tissues developed from three embryonic germ layers. Compared with the expression in mice, Sohlhs exhibited a much more extensive expression pattern in human tissues. Sohlhs were detected in testis, ovary and epithelia developed from embryonic endoderm, ectoderm and tissues developed from embryonic mesoderm. Sohlh signals were found in spermatogonia, Sertoli cells and also Leydig cells in testis, while in ovary, the expression was mainly in oocytes of primordial and primary follicles, granular cells and theca cells of secondary follicles. Compared with Sohlh2, the expression of Sohlh1 was stronger and more extensive. Our study explored the expression of Sohlh genes in human tissues and might provide insights for functional studies of Sohlh genes.

Catenin-δ1, negatively regulated by miR-145, promotes tumour aggressiveness in gastric cancer.

Increasing evidence supports the association of catenin-δ1 (CTNND1, p120ctn) with tumour development and progression. However, the mechanism and clinical significance of CTNND1 deregulation in gastric cancer remain unknown. The expression level and cellular localization of CTNND1 were determined by immunohistochemistry in 126 human gastric cancer and 50 non-tumourous tissues. The cellular localization of CTNND1 and epithelial cadherin (E-cadherin) were detected by immunofluorescence. Cell proliferation, apoptosis, migration and invasion assays were performed to assess the effect of CTNND1 cDNA or CTNND1 siRNA transfection on gastric cancer cells. Luciferase assay, western blot analysis and in vivo assays were used to determine whether CTNND1 could be regulated by miR-145. The results demonstrate that the cytoplasmic localization of CTNND1 protein, rather than expression level, was indicative of higher clinical stage, positive lymph node metastasis and poorer prognosis in gastric cancers. CTNND1 could promote gastric cancer cell migration and invasion with little effect on cellular proliferation and apoptosis. CTNND1 was proved to be a direct target gene for miR-145. Besides suppressing cytoplasmic CTNND1 expression, miR-145 could recover the membranous localization of CTNND1 and E-cadherin. We conclude that cytoplasmic CTNND1 can serve as an independent prognostic factor for patients with gastric cancers. MiR-145 inhibits invasion of gastric cancer cells not only by down-regulating cytoplasmic CTNND1 expression but also by inducing the translocation of CTNND1 and E-cadherin from the cytoplasm to the cell membrane through down-regulating N-cadherin.

Diagnostic and prognostic value of circulating miR-18a in the plasma of patients with gastric cancer.

The aim of this manuscript is to analyze the diagnostic and prognostic value of circulating miR-18a in the plasma of patients with gastric cancer. In this study, 82 patients with gastric cancer and 65 healthy controls were enrolled in the study, and 10 ml of peripheral venous blood was collected for RNA extraction. miR-18a expression was determined using TaqMan quantitative real-time polymerase chain reaction assay and was further correlated with patients' clinicopathological parameters and the follow-up data. The results indicated that plasma miR-18a was upregulated in gastric cancer patients compared with healthy controls (P < 0.001). miR-18a yielded an area under the receiver-operating characteristic curve of 0.907 with 80.5 % sensitivity and 84.6 % specificity in discriminating gastric cancer from healthy controls. Plasma miR-18a expression was significantly associated with pathological grade (P = 0.036) and lymph node status (P = 0.025), but not with tumor stage (P = 0.075). Both log-rank test and univariate Cox regression analysis showed that the higher miR-18a expression in plasma was associated with shorter disease-free survival and disease-specific survival of the patients with gastric cancer (P = 0.023 and P = 0.027; P = 0.036 and P = 0.043, respectively), which was also not proven by multivariate Cox regression analysis (P = 0.238 and P = 0.160, respectively). In conclusion, this study showed that miR-18a may be a promising biomarker for the detection of gastric cancer and its upregulation may be potentially associated with unfavorable prognosis of bladder cancer, suggesting that miR-18a might serve as a potential biological marker for further risk stratification in the management of gastric cancer.

Stanniocalcin 2 expression predicts poor prognosis of hepatocellular carcinoma.

Previous studies have shown that the expression level of stanniocalcin 2 (STC2) is associated with tumor progression. However, to date, the association between STC2 and clinicopathological factors in hepatocellular carcinoma (HCC) has not been investigated. The clinical significance of STC2 was investigated in 30 fresh HCC samples using western blot analysis and in 240 HCC tissues using immunohistochemical analysis. The level of STC2 in cancerous tissue was higher than in the matched non-cancerous tissues. Using immunohistochemistry, the STC2-positive group exhibited a higher incidence of lymph node metastasis and venous invasion compared with the STC2-negative group. Kaplan-Meier survival analysis revealed that the positive expression of STC2 correlated with poor overall survival (OS) and disease-free survival of HCC patients (P<0.01). STC2 expression was observed to be an independent prognostic factor for OS in HCC patients by multivariate analysis (hazard ratio, 2.39; 95% confidence interval, 1.04-5.89; P=0.013). These data suggest that STC2 expression may be a useful indicator of poor prognosis in HCC patients.

Upregulation of microRNA-25 associates with prognosis in hepatocellular carcinoma.

BACKGROUND: Accumulating evidence has shown that up-regulation of microRNA-25(miR-25) is associated with the prognosis of several types of human malignant solid tumors. However, whether miR-25 expression has influence on the prognosis of hepatocellular carcinoma (HCC) is still unknown. METHODS: The differentially expressed amount of the miR-25 was validated in triplicate by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Survival rate was analyzed by log-rank test, and survival curves were plotted according to Kaplan-Meier. Multivariate analysis of the prognostic factors was performed with Cox regression model. RESULTS: The expression of miR-25 was significantly upregulated in HCC tissues when compared with adjacent normal tissues (p<0.0001). Patients who had high miR-25 expression had a shorter overall survival than patients who had low miR-25 expression (median overall survival, 31.0 months versus 42.9 months, p=0.0192). The multivariate Cox regression analysis indicated that miR-25 expression (HR=2.179; p=0.001), TNM stage (HR=1.782; p=0.014), and vein invasion (HR=1.624; p=0.020) were independent prognostic factors for overall survival. CONCLUSION: Our data suggests that the overexpression of miR-25 in HCC tissues is of predictive value on poor prognosis. VIRTUAL SLIDE: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1989618421114309.

CCR9 as a prognostic marker and therapeutic target in hepatocellular carcinoma.

The chemokine receptor CCR9 was recently implicated in tumor biology. In the present study, our objective was to evaluate the clinical significance and potential role of CCR9 in hepatocellular carcinoma (HCC). CCR9 expression was detected by immunohistochemistry, quantitative PCR (qPCR) and western blotting in HCC patients. The prognostic significance of CCR9 expression was assessed. The functional roles of CCR9 in HCC were investigated using MTT, BrdU, colony formation assay and flow cytometry. CCR9 was significantly elevated in HCC tissue samples. High CCR9 expression was correlated with multiple tumor nodes, high Edmondson-Steiner grade and vascular invasion. Multivariate analysis showed that CCR9 expression was an independent prognostic factor for the overall survival (OS) of HCC patients. Further investigations revealed that ectopic expression of CCR9 enhanced cell proliferation and tumorigenicity in HCC cells, whereas CCR9 silencing impaired cell proliferation and tumorigenicity, which was mediated through downregulation of the cell cycle regulators p21, p27 as well as upregulation of cyclin D1. These results suggest that CCR9 can act as a novel prognostic marker and therapeutic target for HCC.

HOXA10 promotes cell invasion and MMP-3 expression via TGFß2-mediated activation of the p38 MAPK pathway in pancreatic cancer cells.

BACKGROUND: HOXA10 is closely related to tumor progression in many human cancers. However, the role of HOXA10 in pancreatic cancer remains unclear. The aim of this study was to determine the involvement of HOXA10 in pancreatic cancer cell invasion and migration. METHODS: The effect of HOXA10 on the invasion and migration of pancreatic cancer cells was assessed by invasion and migration assays. The protein of transforming growth factor beta-2 (TGFß2) was neutralized by TGFß2 blocking antibody. The activation of p38 was inhibited by SB239063. RESULTS: HOXA10 could promote the invasion and migration of pancreatic cancer cells. Knockdown of HOXA10 decreased the expressions of TGFß2 and matrix metallopeptidase-3 (MMP-3) and suppressed the activation of p38. Conversely, overexpression of HOXA10 increased the levels of TGFß2 and MMP-3. Further experiments identified that TGFß2 contributed to the HOXA10-promoted invasion and migration and regulated MMP-3 expression and p38 activation. Additionally, inhibition of p38 suppressed cell invasion and MMP-3 expression in pancreatic cancer cells. CONCLUSIONS: HOXA10 promotes cell invasion and MMP-3 expression of pancreatic cancer cells via TGFß2-p38 MAPK pathway. Thus, HOXA10 could be a useful target for the treatment of pancreatic cancer.

The chiral bioconversion and preclinical pharmacokinetic analysis of (R)-(+)-rabeprazole in beagle dogs by HPLC and HPLC-MS/MS.

In order to accurately investigate the preclinical pharmacokinetics of (R)-(+)-rabeprazole sodium injection, a reliable high-performance liquid chromatography (HPLC) method was developed using a Chiral-AGP column to prove that there is no chiral bioconversion of (R)-(+)-rabeprazole to (S)-(-)-rabeprazole in beagle dogs after single intravenous administration of (R)-(+)-rabeprazole sodium injection. An HPLC-tandem mass spectrometry (HPLC-MS/MS) method for analysis of (R)-(+)-rabeprazole was developed and validated, and used to acquire the pharmacokinetic parameters in beagle dogs. (R)-(+)-Rabeprazole and internal standard omeprazole were extracted from plasma samples by protein precipitation and separated on a C18 column using methanol-5 mm ammonium acetate as mobile phase. Detection was performed using a turbo-spray ionization source and mass spectrometric positive multi-reaction monitoring mode. The linear relationship was achieved in the range from 2.5 to 5000 ng/mL. The method also afforded satisfactory results in terms of sensitivity, specificity, precision, accuracy and recovery as well as the stability of the analyte under various conditions, and was successfully applied to a preclinical pharmacokinetic study in beagle dogs after single intravenous administrations of (R)-(+)-rabeprazole sodium injection at 0.33, 2 and 6 mg/kg.

Severe acute cholangitis after endoscopic sphincterotomy induced by barium examination: A case report.

Endoscopic sphincterotomy (EST) is considered as a possible etiological factor for severe cholangitis. We herein report a case of severe cholangitis after endoscopic sphincterotomy induced by barium examination. An adult male patient presented with epigastric pain was diagnosed as having choledocholithiasis by ultrasonography. EST was performed and the stone was completely cleaned. Barium examination was done 3 d after EST and severe cholangitis appeared 4 h later. The patient was recovered after treated with tienam for 4 d. Barium examination may induce severe cholangitis in patients after EST, although rare, barium examination should be chosen cautiously. Cautions should be also used when EST is performed in patients younger than 50 years to avoid the damage to the sphincter of Oddi.

Comparing the effects of Bassini versus tension-free hernioplasty: 3 years' follow-up.

In order to compare the effects of Bassini and tension-free mesh hernioplasty, a total of 552 patients with inguinal hernia who were subjected to surgical treatment in our hospital were randomly divided into the following two groups: the Bassini group (n = 269) and the tension-free mesh group (n = 283). The recurrence rates, pain, discomfort, and other complications were recorded, and the causes of the complications were explored. The recurrence rate in the Bassini group was 8.9% (24/269), significantly higher than that in the tension-free repair group (2.8%, 8/283). In addition, the recurrence rates in the Bassini and tension-free groups before 2004 were 12.6% and 5.6%, respectively, which were markedly higher than the rates after 2004 (5.3% and 0.7%, respectively). The rate of postoperative discomfort and pain within the first three months was higher in the Bassini group compared to the tensionfree group (25.7% vs 18.5%, respectively). However, there was no difference after three months in the rate of postoperative discomfort and pain, incidence of infection, or scrotal edema between the two groups. The average hospital stay in the Bassini group was longer than that in the tension-free repair group (7.6±1.2 vs 4.5±2.2 days, respectively), but the cost was lower (4518.0±510 vs 6221.3±578 yuan, respectively). Thus, tension-free mesh hernioplasty is indicated for most inguinal hernia patients due to the low recurrence rate, rapid recovery time, and treatment success, but the traditional Bassini procedure has lower cost and other beneficial effects and is still suitable for some patients.

Clinical strategy for the management of solid pseudopapillary tumor of the pancreas: aggressive or less?

OBJECTIVE: To further delineate the clinicopathological and radiological features of solid pseudopapillary tumor (SPT) of the pancreas and summarize the surgical therapy strategy for this tumor. METHODS: A retrospective review of 18 pathologically confirmed cases of SPT was performed and the clinical and pathological features, radiological findings and surgical interventions were analyzed. RESULTS: The patients included 17 females and 1 male with a median age of 23 years. The median diameter of the lesions was 8.0 cm. Abdominal pain was the predominant complaint (8/18). The rest of the patients were asymptomatic and presented with a pancreatic mass detected incidentally. Radiological study revealed a well-demarcated mass which was composed of a solid-cystic portion. On post-contrast CT, the solid portions could be enhanced whereas the cystic parts remained unenhanced. With the preoperative diagnosis of SPT in 11 patients and pancreatic cyst, benign or malignant pancreatic tumor in the rest, pancreatic tumor resection was successfully completed. Surgical exploration findings, pathological characteristics and good prognosis of the patients with SPT, indicated its low-grade malignant potential. CONCLUSION: In combination with clinical findings, radiological features of SPT may help to make the correct diagnosis and differentiation from other pancreatic neoplasms. Once diagnosed, given the excellent prognosis and low-grade malignancy, less aggressive surgical resection of the primary lesion is proposed.

Factors influencing infectious complications after pancreatoduodenectomy.

BACKGROUND/PURPOSE: Rates of postoperative morbidity, particularly infectious complications, remain high after pancreatoduodenectomy. METHODS: Subjects comprised 101 patients who had undergone pancreatoduodenectomy, analyzed according to presence or absence of infectious postoperative complications. Nineteen perioperative variables were analyzed to identify risk factors associated with postoperative infectious complications. RESULTS: Postoperative infectious complications occurred in 56 patients (55%); among them 29 had serious infectious morbidity, including bacteremia (13%), intra-abdominal infection (18%) and pneumonia (12%). One patient (1%) died of multiple organ failure subsequent to a severe septic attack. Only body mass index (BMI) differed significantly between patients with and without serious infection. Logistic regression analysis identified BMI >25 as an independent factor for occurrence of serious postoperative infectious complications. BMI >25 was a common risk factor for individual infection, including bacteremia, intra-abdominal infection, and pneumonia. As for the influence of BMI on perioperative parameters, the high BMI significantly affected the operation time. Meanwhile preoperative biliary drainage had no influence on overall and individual infectious morbidities. CONCLUSIONS: This study demonstrates the need for careful postoperative monitoring in the patient with high BMI.

Lymphangiogenesis in gastric carcinoma correlates with prognosis.

Lymphatic metastasis is an important way that gastric carcinomas can spread. However, little is known about the mechanisms of lymphangiogenesis and its clinical significance in gastric carcinomas. In the present study, lymphatic vessel density (LVD), VEGF-C expression, and proliferative activity of lymphatic endothelium were determined in human gastric carcinomas and xenografts of gastric cancer cells in nude mice. The development of lymphangiogenesis and its correlation with patient prognosis were investigated. The results showed that lymphatic vessels were observed mainly in peripheral tumour tissue with significantly (p < 0.05) higher P-LVD (peri-tumoural-LVD) than I-LVD (intra-tumoural-LVD). The expression of VEGF-C was heterogeneous within tumours, with a significantly higher expression (immunostaining score) at the margin than at the tumour centre (p < 0.05). A significant correlation was found between VEGF-C expression at the margin (but not at the centre) and P-LVD (r = 0.72, p < 0.01). High proliferative activity of lymphatic endothelium was also observed in the peripheral tissues, with a significant correlation between proliferative activity of lymphatic endothelium and VEGF-C expression (p < 0.05). These data imply that the increased lymphatics may have been newly formed following stimulation by VEGF-C. High VEGF-C expression at the margin of gastric carcinomas could induce lymphangiogenesis in the peri-tumoural stroma and contribute to the increased P-LVD. The data from mice tumour xenografts also suggested that VEGF-C produced from the transplanted gastric carcinoma cells could induce lymphangiogenesis around them. In patients, VEGF-C expression at tumour margins was associated with nodal metastasis, lymphatic vessel invasion, poor recurrence-free survival, and poor overall survival, and could serve as an independent predictor for patients with gastric carcinoma.