The stomach is the main digestive organ in humans. Patients with gastric cancer often develop digestive problems, which result in poor nutrition. Nutritional status is closely related to postoperative complications and quality of life (QoL) in patients with gastric cancer. The controlling nutritional status (CONUT) score is a novel tool to evaluate the nutritional status of patients. However, the relationship of the CONUT score with postoperative complications, QoL, and psychological status in patients with gastric cancer has not been investigated. The present follow-up study was conducted in 106 patients who underwent radical gastrectomy in our hospital between 2014 and 2019. The CONUT score, postoperative complications, psychological status, postoperative QoL scores, and overall survival (OS) of patients with gastric cancer were collected, and the relationship between them was analyzed. A significant correlation was observed between the CONUT score and postoperative complications of gastric cancer (P < 0.001), especially anastomotic leakage (P = 0.037). The multivariate regression analysis exhibited that the CONUT score (P = 0.002) is an independent risk factor for postoperative complications. The CONUT score was correlated with the state anxiety questionnaire (S-AI) for evaluating psychological status (P = 0.032). However, further regression analysis exhibited that the CONUT score was not an independent risk factor for psychological status. Additionally, the CONUT score was associated with postoperative QoL. The multivariate regression analysis exhibited that the CONUT score was an independent risk factor for the global QoL (P = 0.048). Moreover, the efficiency of CONUT score, prognostic nutrition index, and serum albumin in evaluating complications, psychological status, and QoL was compared, and CONUT score was found to outperform the other measures (Area Under Curve, AUC = 0.7368). Furthermore, patients with high CONUT scores exhibited shorter OS than patients with low CONUT scores (P = 0.005). Additionally, the postoperative complications (HR 0.43, 95% CI 0.21–0.92, P = 0.028), pathological stage (HR 2.26, 95% CI 1.26–4.06, P = 0.006), and global QoL (HR 15.24, 95% CI 3.22–72.06, P = 0.001) were associated with OS. The CONUT score can be used to assess the nutritional status of patients undergoing gastric cancer surgery and is associated with the incidence of postoperative complications and QoL.

Objective:To investigate the role of microRNA (miRNA)-101a in the liver fibrosis induced by activated hepatic stellate cell (HSC), through upregulating IRE1α signaling pathway.Methods:Carbon tetrachloride (CCl 4) induced liver fibrosis model of mice was established. RT-PCR was used to measure the mRNA level of miRNA-101a in liver tissue of mice. Protein level of α smooth muscle actin(αSMA), collagen I and IRE1α were investigated by Western blot. It was divide into Vehicle, TGFβ1, TGFβ1+ miRNA-NC and TGFβ1+ miRNA-M groups. TGFβ1+ miRNA-NC and TGFβ1+ miRNA-M group were transfected with miRNA-101a mimic negative control and miRNA-101a mimic, respectively. After the corresponding treatments, mRNA level of miRNA-101a was detected by RT-PCR, the protein level of αSMA、collagen I and IRE1α were measured by Western blot. Results:Compared to normal mice, the fibrotic deposition in liver tissue of CCl 4 group was increased significantly [(0.17±0.06) vs. (2.09±0.39), P<0.001)]. Protein level of αSMA, collagen I and IRE1α was increased significantly in the model group [(1.00±0.23) vs. (4.09±0.80), (1.00±0.21) vs. (4.98±1.19), (1.00±0.24) vs. (3.27±0.65), all P<0.001)]. While the mRNA level of miRNA-101a was decreased (1.00±0.05) vs. (0.43±0.05), P<0.001). In vitro study, we found that TGFβ1 could inhibit the mRNA expression of miRNA-101a, induced HSC-T6 activation and then up-regulated protein expression of αSMA, collagen I and IRE1α. Compared to TGFβ1+ miRNA-NC group, the expression of miRNA-101a in TGFβ1+ miRNA-M group increased significantly [(0.59±0.19) vs. (1.89±0.20), P<0.001)]. The protein levels of αSMA, collagen I were reduced by over expression of miRNA-101a [(2.65±0.69) vs. (0.84±0.13), (3.15±0.59) vs. (1.31±0.25), all P<0.05)], and the protein content of IRE1α was down-regulated [ (2.63±0.47) vs. (1.03±0.15), P<0.001)]. Conclusion:miRNA-101a may play a critical role in the inhibition of HSC activation and liver fibrogenesis by blocking IRE1α signaling pathway.

Nutritional risk screening and nutritional status assessment is important in assessing the risk of complications and prognosis of patients undergoing gastrointestinal surgery. Especially, due to the poor basic nutritional status, elderly patients and cancer patients have high incidence of postoperative complications, affecting the prognosis and even leading to death. At present, there are a wide variety of nutritional risk screening and assessment methods, each with its own advantages and focuses. In view of the individualized characteristics of patients with gastrointestinal cancer, it is helpful to find more effective and suitable tools for rapid and accurate nutritional status assessment and risk screening, which will help to reduce the operation related complications and improve the prognosis of patients.

Objective:To investigate the expression of serum Glypican-1 (GPC-1) in pancreatic cancer and the diagnostic value of combined CA19-9 and CEA in pancreatic cancer.Methods:Sixty patients with pancreatic cancer were recruited in Qingdao Municipal Hospital from October 2018 to July 2020, while thirty-one patients with benign pancreatic lesions and fifty healthy controls were selected in the same period. The expression of GPC-1 in serum was detected by ELISA. The levels of serum CA19-9 and CEA were detected by immunochemiluminescence assay, and the expression levels of serum GPC-1, CA19-9and CEA were analyzed and compared. The receiver operating characteristic curve (ROC) was used to evaluate the early diagnostic value of GPC-1, CA19-9, CEA alone and in combination for pancreatic cancer and pancreatic cancer with negative serological markers.Results:The expression level of serum GPC-1in patients with pancreatic cancer was correlated with vascular invasion, pancreatic duct dilatation, TNM staging, lymph node and distant metastasis (all P<0.05). Serum GPC-1, CA19-9, and CEA were all highly expressed in pancreatic cancer (P<0.05). The diagnostic value of GPC-1 was higher than CA19-9 and CEA in the diagnosis of pancreatic cancer with a single index; when distinguishing pancreatic cancer from healthy control group and benign pancreatic lesions, GPC-1+CA19-9, GPC-1+CEA or their combination was significantly higher than any single index, with the highest diagnostic value (AUC was 0.916 and 0.870, respectively). The expression of GPC-1 in patients with single or double negative of CA19-9 and CEA was higher than that in healthy controls and patients with benign pancreatic lesions, the difference was statistically significant (P<0.05). When GPC-1 was used to distinguish the patients with single negative or double negative pancreatic cancer of CA19-9 and CEA, and healthy control and benign pancreatic lesions, the AUC was 0.683-0.825, the sensitivity was 71.4%-87.5%, the specificity was 65.0%-82.9%, the accuracy was 73.9%-84.7%.Conclusions:The high expression of serum GPC-1 in pancreatic cancer is positively correlated with vascular invasion, pancreatic duct dilatation, TNM staging, lymph nodes and distant metastasis. The combined detection of serum GPC-1, CA19-9 and CEA can improve the diagnostic value of pancreatic cancer and make up for the deficiency of traditional single serological marker detection. It is a convenient and sensitive auxiliary screening method for pancreatic cancer.

Objective:To investigate the effect of propofol on the proliferation, migration and invasion of human gastric cancer cells and its molecular mechanism.Methods:The cell viabilities of human gastric MGC-803 and HGC-27 cells under different concentration of propofol were detected by methyl thiazolyl tetrazolium (MTT) method. MGC-803 cells were divided into control group and propofol group. Hoechst 33258 staining and electron microscopy were used to detect the apoptosis rates of the two groups of cells. Transwell experiment was used to detect the migration and invasion rates of the two groups of cells. The cells were then divided into control group, propofol group and propofol + miR-195i group. Real-time fluorescent quantitative PCR (qRT-PCR) was used to detect the relative expression of miR-195 in the cells. Western blotting was used to detect the expressions of Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway proteins.Results:At 24 h, the cell viabilities of MGC-803 cells under the action of 0, 1, 5, 10 and 20 mg/L propofol respectively were (100.00±4.96)%, (94.63±3.15)%, (77.38±6.73)%, (63.82±8.42)% and (35.94±7.01)%, with a statistically significant difference ( F=5.148, P<0.001). The cell viabilities of MGC-803 cells under the action of 5, 10 and 20 mg/L propofol were decreased significantly compared to that under the action of 0 mg/L propofol (all P<0.05). At the same time, the effects of propofol for 48 and 72 h could also significantly reduce the viabilities of MGC-803 cells. Similar results were also detected in HGC-27 cells. The results of Hoechst 33258 staining showed that the percentage of positive cells in the control group was (3.73±1.81)%, and that in the propofol group was (25.44±1.05)%, with a statistically significant difference ( t=6.415, P<0.001). The results of electron microscopy showed that the apoptosis rate in the control group was (4.60±1.36)%, and that in the propofol group was (28.15±1.99)%, with a statistically significant difference ( t=10.729, P<0.001). Transwell results showed that the cell migration rate in the control group was (53.94±4.62)%, and that in the propofol group was (21.28±3.98)%; the cell invasion rate in the control group was (62.38±6.75)%, and that in the propofol group was (33.81±4.92)%, and there were statistically significant differences ( t=4.628, P<0.001; t=6.418, P<0.001). qRT-PCR results showed that the relative expressions of miR-195 in the control group, propofol group and propofol + miR-195i group were 0.58±0.09, 1.24±0.22 and 0.63±0.16, with a statistically significant difference ( F=1.547, P=0.001). miR-195 expression was increased significantly in the propofol group compared to the control group ( P<0.001). Compared with the propofol group, miR-195 expression in the propofol + miR-195i group was decreased significantly ( P<0.001). Western blotting results showed that the relative expressions of phosphorylase Janus kinase 1 (p-JAK1) protein in the control group, propofol group and propofol + miR-195i group were 1.18±0.36, 0.27±0.08 and 0.58±0.11; the relative expressions of phosphorylase signal transducer and activator of transcription 3 (p-STAT3) protein in the three groups were 0.83±0.16, 0.21±0.07 and 0.72±0.13, and there were statistically significant differences ( F=1.655, P<0.001; F=2.520, P<0.001). The expressions of p-JAK1 and p-STAT3 protein in the propofol group were decreased significantly compared to the control group ( P<0.001; P=0.001). The expressions of p-JAK1 and p-STAT3 protein in the propofol + miR-195i group were increased significantly compared to the propofol group ( P=0.003; P=0.004). Conclusion:Propofol can inhibit the cell proliferation, migration and invasion of gastric cancer MGC-803 cells, and promote its apoptosis. Its mechanism may be related to the promotion of miR-195 expression and inhibition of JAK/STAT signal pathway activity.