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BACKGROUND: Reducing or preventing postoperative morbidity in patients with gastric cancer (GC) is particularly important in perioperative treatment plans. AIM: To identify risk factors for early postoperative complications of GC post-distal gastrectomy and to establish a nomogram prediction model. METHODS: This retrospective study included 131 patients with GC who underwent distal gastrectomy at the Second Hospital of Shandong University between January 2019 and February 2023. The factors influencing the development of complications after distal gastrectomy in these patients were evaluated using univariate and multivariate logistic regression analysis. Based on the results obtained, a predictive nomogram was established. The nomogram was validated using internal and external (n = 45) datasets. Its sensitivity and specificity were established by receiver operating characteristic curve analysis. Decision curve (DCA) analysis was used to determine its clinical benefit and ten-fold overfitting was used to establish its accuracy and stability. RESULTS: Multivariate logistic regression analysis showed that hypertension, diabetes, history of abdominal surgery, and perioperative blood transfusion were independent predictors of postoperative complications of distal gastrectomy. The modeling and validation sets showed that the area under the curve was 0.843 [95% confidence interval (CI): 0.746-0.940] and 0.877 (95%CI: 0.719-1.000), the sensitivity was 0.762 and 0.778, respectively, and the specificity was 0.809 and 0.944, respectively, indicating that the model had good sensitivity and specificity. The C-indexes of the modeling and validation datasets were 0.843 (95%CI: 0.746-0.940) and 0.877 (95%CI: 0.719-1.000), respectively. The calibration curve (Hosmer Lemeshow test: χ2 = 7.33) showed that the model had good consistency. The results of the DCA analysis indicated that this model offered good clinical benefits. The accuracy of 10-fold cross-validation was 0.878, indicating that the model had good accuracy and stability. CONCLUSION: The nomogram prediction model based on independent risk factors related to postoperative complications of distal gastrectomy can facilitate perioperative intervention for high-risk populations and reduce the incidence of postoperative complications.

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BACKGROUND: Overexpression of SQSTM1 (sequestosome 1, P62) and nuclear factor-κB (NF-κB) plays an important role in the invasion and metastasis of a variety of malignant tumors. AIM: To explore the expression of P62 and NF-κB in pancreatic cancer and their relationship with clinicopathological features. METHODS: The expression levels of P62 and NF-κB were analyzed by immunohistochemistry with a tissue chip containing 40 cases of human pancreatic carcinoma. Then we analyzed the correlation among P62 expression, phospho-P65 expression, and clinicopathological features of pancreatic carcinoma samples. RESULTS: P62 expression was mainly observed in the cytoplasm of pancreatic carcinoma cells. Phosphorylated P65 (phospho-P65) was mainly expressed in the nucleus and cytoplasm of pancreatic carcinoma cells. There was a significant difference in P62 expression among T stages. And a significant difference in phosphor-P65 expression among pathology types was noted. In the cases with strongly positive P62 expression, significant differences were found in age. And there were significant differences in T stage and tumor-node-metastasis stage in the cases with strongly positive phosphor-P65 expression. CONCLUSION: In pancreatic carcinoma, P62 expression is significantly correlated with T stage. It may be a valuable malignant indicator for human pancreatic carcinoma.

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Gastric cancer (GC) is one of the leading types of cancer in terms of mortality cases worldwide. Doxorubicin (Dox), a common chemotherapy drug, is frequently used to treat GC; however, acquired resistance to Dox hinders the chemotherapeutic outcome and causes shorter survival in GC patients. Several Dox-resistant GC cell lines, including SGC7901, SNU-1 and SNU-5 were generated to investigate the mechanism of Dox resistance in GC. Various methods were used to test the response of Dox-resistant GC cells and parental cells, including flow cytometry, Cell Counting kit-8 assay, reverse transcription polymerase chain reaction and western blot analysis. In the present study, various Dox-resistant cells presented reduced apoptosis and cell cycle arrest in response to Dox treatment. Western blot results revealed that cyclin D1 was upregulated in Dox-resistant cells, whereas inhibition or depletion of cyclin D1 re-sensitized the resistant cells to Dox treatment, which indicated that the induction of cyclin D1 expression was a result of the Dox resistance in GC cells. Furthermore, it was observed that a transcription activated form of p73 (TAp73), is the upstream modulator of cyclin D1, manipulating the cyclin D1 transcription with the assistance of activator protein 1 (AP-1). Overall, the present study data provided a rational strategy to overcome the Dox resistance in GC treatment by inhibiting cyclin D1 expression.

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AIM: To investigate the effect of ischaemia and reperfusion (I/R) injury on the Ca2+-ATPase activation in the intestinal tissue of a rat autologous orthotopic liver transplantation model and to determine if hypoxia preconditioning (HP) therapy induces HIF-1α to protect rat intestinal tissue against I/R injury. METHODS: Rats received non-lethal hypoxic preconditioning therapy to induce HIF-1α expression. We used an autologous orthotopic liver transplantation model to imitate the I/R injury in intestinal tissue. Then, we detected the microstructure changes in small intestinal tissues, Ca2+-ATPase activity, apoptosis, and inflammation within 48 h postoperatively. RESULTS: HIF-1α expression was significantly increased in intestinal tissue at 12 h postoperatively in rats that were exposed to a hypoxic environment for 90 min compared with a non-HP group (HP vs AT, P = 0.0177). Pathological analysis was performed on the intestinal mucosa cells, and the cells in the HP group appeared healthier than the cells in the AT group. The Ca2+-ATPase activity in the small intestinal cells in the AT group was significantly lower after the operation, and the Ca2+-ATPase activity in the HP group recovered faster than that in the AT group at 6 h postoperatively (HP vs AT, P = 0.0106). BCL-2 expression in the HP group was significantly higher than that in the AT group at 12 h postoperatively (HP vs AT P = 0.0010). The expression of the inflammatory factors NO, SOD, IL-6, and TNF-α was significantly lower in the HP group than in the AT group. CONCLUSION: Hypoxia-induced HIF-1α could protect intestinal mucosal cells against mitochondrial damage after I/R injury. HP could improve hypoxia tolerance in small intestinal mucosal cells and increase Ca2+-ATPase activity to reduce the apoptosis of and pathological damage to intestinal cells. HP could be a useful way to promote the earlier recovery of intestinal function after graft procedure.

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AIM: To evaluate the safety and feasibility of enhanced recovery after surgery (ERAS) for total laparoscopic uncut Roux-en-Y gastrojejunostomy after distal gastrectomy. METHODS: The clinical data of 42 patients who were divided into an ERAS group (n = 20) and a control group (n = 22) were collected. The observed indicators included operation conditions, postoperative clinical indexes, and postoperative serum stress indexes. Measurement data following a normal distribution are presented as mean ± SD and were analyzed by t-test. Count data were analyzed by χ2 test. RESULTS: The operative time, volume of intraoperative blood loss, and number of patients with conversion to open surgery were not significantly different between the two groups. Postoperative clinical indexes, including the time to initial anal exhaust, time to initial liquid diet intake, time to out-of-bed activity, and duration of hospital stay of patients without complications, were significantly different between the two groups (t = 2.045, 8.685, 2.580, and 4.650, respectively, P < 0.05 for all). However, the time to initial defecation, time to abdominal drainage-tube removal, and the early postoperative complications were not significantly different between the two groups. Regarding postoperative complications, on the first and third days after the operation, the white blood cell count (WBC) and C reactive protein (CRP) and interleukin-6 (IL-6) levels in the ERAS group were significantly lower than those in the control group. CONCLUSION: The perioperative ERAS program for total laparoscopic uncut Roux-en-Y gastrojejunostomy after distal gastrectomy is safe and effective and should be popularized. Additionally, this program can also reduce the duration of hospital stay and improve the degree of comfort and satisfaction of patients.

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OBJECTIVE: To investigate the expression of glioma-associated oncogene homolog 1(Gli-1) in colon cancer and its association with clinicopathological parameters and postoperative liver metastasis. METHODS: Expression of Gli-1 was detected by immunohistochemistry in paraffin-embedded specimens of 96 cases of colon cancer. Relationship between Gli-1 expression and clinicopathological parameters, postoperative liver metastasis were analyzed. RESULTS: Gli-1 protein expression was significantly increased in colon cancer tissues compared to normal colon tissues (P=0.037). Gli-1 expression in colon tissues was increased in patients with lymph node metastases (P=0.022) and higher T stages (P=0.030). Postoperative live metastasis-free survival period was significantly longer in low Gli-1 expression group than that of high Gli-1 expression group (48.22±10.03 months vs 20.46±6.32 months, P=0.001). Multivariate analysis showed that Gli-1 expression level is an independent prognostic factor for postoperative live metastasis-free survival. CONCLUSION: Colon cancer is associated with an upregulation of Gli-1 protein expression in colon tissues. In patients with colon cancer, Gli-1 expression level is closely related to lymph node metastases, T stages and postoperative live metastasis-free survival periods, indicative of a possible role of Gli-1 expression in colon cancer progression.

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