Objective:To compare the clinical efficacy of laparoscopic Miles surgery through extraperitoneal stoma and intraperitoneal stoma.Methods:The medical records of 140 patients with low rectal cancer after laparoscopic Miles surgery admitted to Gastrointestinal Surgery of Northern Jiangsu People′s Hospital of Jiangsu Province from January 2018 to December 2022 were retrospectively analyzed. Among them, 80 were males and 60 were females, aged 50 to 75 years old, with an average age of 63.95 years old. They were divided into observation group (extraperitoneal stoma, n=70) and control group (intraperitoneal stoma, n=70) based on the stoma method. Through telephone, WeChat, outpatient follow-up and other contact methods, the intraoperative and postoperative recovery, the incidence of perioperative complications (stoma edema, stoma ischemia, peristoma inflammation, perineal/pelvic infection, lung infection) and the incidence of complications at 6 months and 1 year after surgery (stoma stricture, parastoma hernia/internal hernia, stoma prolapse/retraction), and the difference in the ability of artificial anus to control defecation at 1 year after surgery were compared between the two groups. SPSS27.0 statistical software was used for data analysis and processing. Results:(1) Incidence of individual complications such as lung infection between the two groups of patients during the perioperative period (4.3% vs 4.3%, χ2=0.17, P=0.676), stoma edema (25.7% vs 21.4%, χ2=0.36, P=0.550), stoma ischemia (7.1% vs 7.1%, χ2=0.00, P=1.000), peristomal inflammation (20.0% vs. 18.6%, χ2=0.05, P=0.830), perineal/pelvic infection (15.7% vs 27.1%, χ2=2.72, P=0.099), there was no difference between the two groups. There was still no difference in the overall complication rate between the two groups (72.9% vs 78.6%, χ2=0.62, P=0.430). (2) After follow-up to 6 months after surgery, the overall complication rate was 5.7% in the observation group compared with 22.9% in the control group ( χ2=7.06, P=0.008). In particular, the incidence of post-operative parastomal hernia/internal hernia did not occur in the observation group, while 8.6% of patients in the control group occurred (18.6% vs 42.9%, χ2=4.35, P=0.037). (3) After follow-up to 1 year after surgery, the overall complication rate in the observation group was lower than that in the control group ( χ2=8.59, P=0.003). The incidence of parastomal hernia/internal hernia after operation in the observation group was lower than that in the control group (2.9% vs 14.3%, χ2=4.47, P=0.034). (4) At the one-year follow-up, the overall excellent and good rate in the evaluation of bowel function in the observation group was higher than that in the control group (71.4% vs 48.6%, χ2=7.62, P=0.006). Conclusions:In laparoscopic Miles surgery for patients with rectal cancer, choosing extraperitoneal stoma has achieved good results, which can reduce the risk of complications 6 months or even 1 year after surgery, especially in preventing and controlling parastomal hernia/internal hernia. It has significant advantages, and at the same time, it can also promote the recovery of patients′ bowel function and reduce other related complications, thereby ensuring patient safety.

With obesity rates climbing worldwide, metabolic and bariatric surgery has evolved over seven decades into a pivotal therapeutic approach for treating severe obesity and related disorders. Recent research highlights that new anti-diabetic and weight-loss drugs, especially GLP-1 receptor agonists (GLP-1 RA), are catalyzing a paradigm shift in obesity management. Within this context, the key scientific challenge in metabolic surgery is thoroughly investigating how pharmacological interventions and surgical procedures work together in weight management, especially evaluating if new drugs can match bariatric surgery's long-term effectiveness, complication management, and metabolic changes. Resolving this interdisciplinary debate will influence precision medicine in obesity treatment and reshape future multidisciplinary care models for metabolic disorders.

Objective:To explore the effects and potential mechanisms of cell growth regulator 1 ( CGREF1) with an EF hand domain in colorectal cancer proliferation and migration. Methods:Fifty paraffin specimens of colorectal cancer tissues and corresponding paracancerous tissues were selected from January 2023 to January 2024 from the Northern Jiangsu People's Hospital Affiliated to Yangzhou University for analysis, and TCGA, GDSC, KMPLOT and STRING databases were used to explore the expression, prognosis, immune microenvironment, drug sensitivity and related signaling pathway functions of CGREF1 in colorectal cancer. Tissue and cellular expression levels of CGREF1 were analyzed by immunohistochemistry and qRT-PCR. Lentiviral-mediated CGREF1 overexpression in SW-620 cells (OE- CGREF1 vs NC groups) was functionally characterized through CCK-8 proliferation assays, colony formation tests, and scratch wound healing migration assays, with mechanistic investigation via Western blot analysis of apoptosis markers, invasion-related proteins, and RAS/RAF/ERK pathway components. In vivo tumorigenicity was assessed by subcutaneous injection of control or CGREF1-overexpressing SW620 cells in nude mice ( n=3 per group) with tumor growth monitoring. Software of GraphPad Prism 9 was used for statistical analysis of experimental data. Results:CGREF1CGREF1RASERK Studies based on databases, clinical samples and colorectal cancer cell line analyses demonstrated that CGREF1 is downregulated in colorectal cancer, where low CGREF1 expression showed positive correlation with tumor diameter and invasion depth. CGREF1 is closely related to tumor immune infiltration microenvironment and sensitivity to multiple anti-tumor drugs. Overexpression of CGREF1 promoted cell apoptosis while inhibiting cell proliferation, invasion and migration. Overexpression of CGREF1 downregulated the expression levels of RAS, ERK and P-P38/MAPK pathway proteins. CGREF1 inhibited tumor growth in vivo. Conclusion:CGREF1 can inhibit the proliferation, colony formation, and migration of CRC cells through the RAS/ERK/MAPK pathway.

The FCHO1 protein, encoded by the FCHO1 gene, is a pioneer protein that plays an important role in the initial stage of clathrin-mediated endocytosis. In recent years, it has been found that defects in the FCHO1 gene or abnormal expression levels of the FCHO1 protein are closely related to certain human diseases. This article will review the latest research results of FCHO1 in malignant tumors, immunodeficiency diseases, neurodegenerative diseases of the nervous system, and cardiovascular diseases, providing a theoretical basis for the development of new targets for the diagnosis and treatment of related diseases.

Objective To investigate the regulatory role and mechanism of mitochondrial riboso-mal protein S35(MRPS35)in the proliferation,invasion,and migration of colon cancer cells.Meth-ods A total of 120 colon cancer tissues and adjacent normal tissues from patients undergoing radical resection for colon cancer were collected.Human colon cancer cell lines(HCT116,SW480,SW620)and a human normal colon epithelial cell line(NCM460)were cultured.Bioinformatics analysis,real-time quantitative polymerase chain reaction,Western blot,immunohistochemical(IHC)analysis,and cellular functional experiments(plate clone formation assay,scratch test,Transwell migration assay,CCK-8 cell viability assay)were conducted to evaluate the expression and regulatory mechanism of MRPS35 in colon cancer.Results Bioinformatics analysis showed that the expression level of the MRPS35 gene was higher in colorectal cancer tissues than in adjacent normal tissues(P＜0.05).The relative expression levels of MRPS35 mRNA and MRPS35 protein were higher in human colon cancer cell lines(HCT116,SW480,SW620)than in NCM460 cells(P＜0.05).The relative ex-pression level of MRPS35 protein was higher in colon cancer tissues than that in adjacent normal tis-sues(P＜0.05).The expression level of MRPS35 was significantly correlated with tumor diameter,tumor differentiation,and T stage(P=0.002,0.021,0.036).Patients with high MRPS35 expres-sion had a higher overall survival rate than those with low MRPS35 expression(Log-rank P=0.015).After knockdown of MRPS35,the abilities of colon cancer cell cloning,proliferation,invasion,and migration were significantly enhanced.Furthermore,the expression of Wnt1,β-Catenin,and their downstream target proteins increased significantly after MRPS35 knockdown.Conclusion MRPS35 is significantly overexpressed in both colon cancer tissues and colon cancer cells,and it may inhibit the occurrence and development of colon cancer by regulating the Wnt/β-Catenin signaling pathway.Therefore,MRPS35 has the potential to become a novel biomarker and therapeutic target for colon cancer.

Objective:To evaluate safety and efficacy of B-type suture method ileostomy.Methods:Clinical data from 204 patients undergoing laparoscopic low anterior resection combined with protective ileostomy was analysed. Patients were divided into B-type suture ileostomy group ( n=67) and traditional ileostomy group ( n=137). Results:compared with traditional ileostomy group, B-type suture ileostomy group showed statistically significant differences in total operation time [(164±26) min vs. (172±24) min, t=2.229, P=0.027], ileostomy time [(12.7±2.3) min vs. (14.8±2.2) min, t=-6.565, P<0.001], blood loss [(57±20) ml vs. (69±31) ml, t=-2.797, P=0.006], postoperative hospital stay [(10.2±1.9) d vs. (11.8±2.3) d, t=-4.851, P<0.001], specimen incision infection rate (0 vs. 5.1%, P=0.047), postoperative body pain [82 (79-84) vs. 78 (76-80), Z=-5.805, P<0.001], and ileostomy incorporation time [(46±11) min vs. (51±12) min, t=-2.540, P=0.012]. Conclusion:B-type suture ileostomy for prophylactic ileostomy in laparoscopic low anterior resection for rectal cancer is safe and feasible.

Objective:To investigate the risk factors for postsurgical gastroparesis syndrome (PGS) after laparoscopic complete mesocolic excision (CME) for right colon cancer.Methods:The clinical data of 358 patients who underwent laparoscopic CME for right colon cancer were retrospectively analyzed. Univariate and multivariate logistics regression were used to analyze the independent risk factors for PGS.Results:PGS occurred in 19 patients (4.8%). Logistic regression analysis showed that preoperative anxiety score (PAS-7)≥14 ( OR=6.450, P=0.039), preoperative serum albumin<35 g/L ( OR=9.302, P=0.011), colon cancer at hepatic flexura ( OR=9.782, P=0.007), No.206 group lymph node dissection ( OR=8.317, P=0.004), and intra-abdominal infection ( OR=5.755, P=0.043) were independent risk factors for PGS. Conclusion:Patient's preoperative health status, tumor location, scope of lymph node dissection and postoperative intra-abdominal infection are all risk factors related to PGS after CME for right colon cancer.

Alongside significant progress in laparoscopic imaging systems such as 3D and 4K laparoscopy, as well as the da Vinci surgical robot system, laparoscopic distal gastrectomy shows promising efficacy in early distal gastric cancer treatment. Our nation exhibits a notably low rate of early gastric cancer detection, yet confronts a substantial cohort of advanced gastric cancer patients. Investigating the oncology safety of laparoscopic techniques for advanced distal gastric cancer tumors holds paramount significance. As medical engineering progresses and surgeons′ skills improve, the widespread adoption of minimally invasive techniques, establishment of quality control systems, and appropriate digestive tract reconstruction after surgery will enhance early recovery, long-term survival outcomes, and postoperative quality of life for patients.

G-protein signaling modulator 2 is a member of the GPSM family, with emerging significance in various diseases including Chadley-McCullough syndrome, rheumatoid arthritis, and systemic lupus erythematosus. Furthermore, its involvement extends to tumor pathogenesis, encompassing non-small-cell lung cancer, breast cancer, hepatocellular carcinoma, pancreatic carcinoma, serous ovarian cancer, Ewing's sarcoma, and osteosarcoma, influencing proliferation, invasion, and metastasis. There is no relevant review on the mechanism of GPSM2 in tumor progression. This paper will summarize the research progress on GPSM2 in tumors in recent years, focusing on its role and mechanism, with the aim of providing references and guidance for further research.

Objective To investigate the effects of long non-coding RNA (lncRNA) taurine up-regulated gene 1 (TUG1) on the proliferation, migration, and angiogenesis of gastric cancer cells. Methods The expression levels of LncRNA TUG1 in gastric cancer tissues and adjacent non-cancerous tissues were analyzed based on public databases. The expression of lncRNA TUG1 in gastric cancer cell lines was detected by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). SGC-7901 gastric cancer cells were transfected with si-TUG1 and si-NC, and the effects of knocking down lncRNA TUG1 on cell proliferation, colony formation, migration, and angiogenesis were analyzed using the Cell Counting Kit-8 (CCK-8) assay, colony formation assay, Transwell assay, and Matrigel tube formation assay. The correlation between alkB homolog 5 (ALKBH5) gene and lncRNA TUG1 was analyzed based on public databases. The regulatory relationship between ALKBH5 and lncRNA TUG1 was verified using Actinomycin D experiments. The effects of knocking down ALKBH5 on the proliferation, colony formation, migration, and angiogenesis of gastric cancer cells were analyzed through cell function experiments. Results LncRNA TUG1 was up-regulated in gastric cancer tissues and cell lines. After knocking down lncRNA TUG1, the proliferation, colony formation, migration, and angiogenesis abilities of SGC-7901 cells were lower than those of control cells(P < 0.05). Database analysis results showed that ALKBH5 was positively correlated with lncRNA TUG1 expression in gastric cancer (r=0.37, P < 0.05). Compared with control cells, the RNA stability of lncRNA TUG1 in SGC-7901 cells with knocked-down ALKBH5 decreased, and the cell proliferation, colony formation, migration, and angiogenesis abilities were also reduced (P < 0.05). Conclusion ALKBH5 promotes the proliferation, colony formation, migration, and angiogenesis of gastric cancer cells by inducing the expression of lncRNA TUG1.