Colorectal cancer is one of the malignant tumors, and postoperative recurrence or metastasis is a key factor to the survival of patients. Patients who underwent colorectal cancer surgery between January 2016 and December 2020 were included. Multivariate Logistic regression was used to analysis statistically, including recurrence or metastasis, liver metastasis, lung metastasis and death respectively. 419 cases of colorectal cancer were included in the clinical study according to the screening criteria. Multivariate Logistic regression analysis showed that Mesocolon fascia infiltration (OR,2.769; 95

BACKGROUND:Bacterial communities and their metabolites are increasingly recognized as key contributors to cardiovascular disease, yet their role and mechanistic involvement in abdominal aortic aneurysm (AAA) pathogenesis remain insufficiently defined. METHODS:Dental plaques from patients with AAA and matched healthy controls were subjected to metagenomic sequencing, and corresponding plasma samples underwent untargeted metabolomic profiling. In vivo, mice were topically exposed in the oral cavity to Fusobacterium nucleatum (Fn) followed by AngII (angiotensin II) infusion to evaluate its impact on AAA progression. A homologous recombination-based ilvE deletion strategy was used to confirm the role of Fn in isoleucine biosynthesis. Molecular assays were performed to assess ferroptosis-related signatures and histone acetylation in smooth muscle cells, while chromatin immunoprecipitation-quantitative polymerase chain reaction verified the specific acetylation target. In addition, dietary restriction of isoleucine was introduced in the AAA murine model to explore therapeutic relevance. RESULTS:Patients with AAA showed a marked enrichment of Fn in dental plaque, and topical application of Fn aggravated AngII-induced AAA in mice. Elevated plasma isoleucine concentrations were observed in both human AAA and experimental models. Genetic deletion of ilvE in Fn diminished bacterial isoleucine release and mitigated AAA development in mice. Mechanistic analyses revealed that Fn-derived isoleucine promoted ferroptosis in smooth muscle cells through H3K9ac (histone H3 lysine 9 acetylation)-dependent transcriptional activation of ACSL4 (acyl-CoA [coenzyme A] synthetase long-chain family member 4), a core regulator of ferroptosis. Dietary isoleucine restriction in the AngII-induced model reduced H3K9ac, suppressed ferroptosis, and alleviated aneurysmal progression. CONCLUSIONS:Fn-derived isoleucine drives ferroptosis in smooth muscle cells via H3K9ac-mediated activation of ACSL4, delineating a microbiota-metabolite-epigenetic axis in AAA pathogenesis and nominating dental plaque Fn abundance and circulating isoleucine as exploratory biomarker candidates requiring larger, independent validation.

Diabetic foot ulceration (DFU) imposes major global health burdens due to high morbidity and recurrence rates. Current therapies (debridement and offloading) show limited efficacy, highlighting the need to uncover molecular mechanisms of diabetic wound repair. Multi-omics analyses of DFU and healthy skin identify fibroblast-derived COL16A1 as a wound healing mediator. In vitro, COL16A1 overexpression or knockdown in fibroblasts is employed to assess its regulatory effects on cellular function and collagen secretory capacity. In vivo, localized adenoviral delivery of COL16A1 is administered to evaluate its therapeutic impact on wound closure in diabetic mice. DNA pull-down plus LC-MS/MS, ChIP-qPCR, and luciferase reporter assays are systematically implemented to delineate the upstream regulatory mechanism of COL16A1 expression. Transcriptomic profiling of skin specimens identifies fibroblast-derived COL16A1 as a key regulatory gene in DFU repair. Subsequent in vitro and in vivo experiments demonstrate COL16A1 enhances fibroblast activation and restores normal repair processes in diabetic wounds. Notably, Brahma-related gene 1 (BRG1) is identified as the key transcription factor governing COL16A1 expression. BRG1 directly binds to the COL16A1 promoter, upregulating its transcription and thereby accelerating diabetic wound healing. BRG1-COL16A1 axis is a critical regulatory pathway and proposes novel therapeutic targets for chronic diabetic wounds.

Uncontrolled proliferation, local invasion, and distant metastasis are hallmarks of malignancies, and they play crucial roles in tumor progression. Dynamin 1 (DNM1) is a member of the dynamin guanosine-5′-triphosphatease (GTPase) subfamily that regulates membrane fission, cytokinesis, and vesicle secretion. However, its function in colorectal-cancer (CRC) progression remains unclear. We used public datasets and a tissue microarray (TMA) cohort to analyze differential expression of DNM1 between CRC tissues and adjacent nontumor tissues (NTs). The role of DNM1 in CRC cells was determined by in vitro experiments, including colony formation, Cell Counting Kit-8 (CCK-8), and Transwell assays. Ribonucleic acid sequencing (RNA-seq) and bioinformatics analysis were performed to investigate mechanisms that DNM1 may be involved in. KLF5 was identified as an upstream transcriptional activator of DNM1 through a combination of bioinformatic screening and functional experiments. Xenograft and metastatic models were established to investigate the effects of DNM1 on tumor growth and metastasis. We found that DNM1 expression was upregulated in CRC tissues, which significantly correlated with poor patient prognoses. DNM1 overexpression (OE) enhanced the proliferation, migration, and invasion capabilities of CRC cells both in vitro and in vivo, whereas DNM1 knockdown (KD) yielded the opposite results. Mechanistically, we identified Krüppel-like factor 5 (KLF5) as an upstream transcription factor that activates DNM1 transcription. Furthermore, DNM1 was shown to mediate the activation of epithelial–mesenchymal transition (EMT) and the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. DNM1 promotes CRC progression and malignant phenotypes, and targeting the KLF5/DNM1/Akt axis may represents a promising strategy to improve patient outcomes.

Background: Colorectal liver metastasis (CRLM) exhibits highly heterogeneity, with clinically and molecularly defined subgroups that differ in their prognosis.The aim of this study is to explore whether leftsided tumors is clinically and gnomically distinct from right-sided tumors in CRLM.Methods: This retrospective study included 1,307 patients who underwent primary tumor and metastases resection at three academic centers in China from January 1, 2012, to December 31, 2020.Propensity score matching with 1:1 ratio matching was performed.The prognostic impact of tumor sidedness was determined after stratifying by the KRAS mutational status.Moreover, whole-exome sequencing (WES) of 200 liver tumor tissues were performed to describe the heterogeneity across the analysis of somatic and germline profiles.Results: The median follow-up was 68 months.Matching yielded 481 pairs of patients.Compared to right-sided CRLM, left-sided patients experienced with better 5-year overall survival (OS) in surgery responsiveness, with a 14.6 lower risk of death [hazard ratio (HR), 1.36, 95% confidence interval (CI), 1.10-1.69,P=0.004].Interaction between tumor sidedness and KRAS status was statistically significant: leftsidedness was associated with better prognosis among KRAS wild-type patients (HR 1.71; 95% CI: 1.20-2.45;P=0.003), but not among KRAS mutated-type patients.Integrated molecular analyses showed that rightsided tumors more frequently harbored TP53, APC, KRAS, and BRAF alterations, and identified a critical role of KRAS mutation in correlation with their survival differences.Higher pathogenic germline variants were identified in the right-sided tumors compared with left-sided tumors (29.3% vs. 15.5%,P=0.001). Conclusions:We demonstrated that the prognostic impacts of tumor sidedness in CRLM is restricted patients with KRAS wild-type tumors.Tumor sidedness displays considerable clinical and molecular heterogeneity that may associate with their therapy benefits and prognosis.

Background. Few large‐sample studies have examined the use of fecal management systems (FMSs) in intensive care units (ICUs) or evaluated the associated complications. This study aims to assess the effectiveness and safety of FMS for stool diversion in ICU patients with fecal incontinence (FI). Methods. We enrolled 381 FI patients, assigning them to either an FMS group (n = 134), which used a fecal management device, or a usual care (UC) group (n = 247) that received standard care including regular perianal cleaning. Results. The FMS group reported lower incidence and severity of incontinence‐associated dermatitis (IAD) and higher Braden Scale scores (10.42 ± 2.77) compared to the UC group (9.71 ± 2.56), indicating reduced pressure ulcer risk. Notably, FMS‐associated complications were minimal, with only 5 patients (3.73%) affected; one required surgical intervention for rectal mucosal bleeding. Conclusions. FMS significantly reduced stool‐associated skin irritation, lowered the incidence of IAD and pressure injuries, and improved nurses’ convenience compared to UC.

The purpose of this study was to explore the effect of electroacupuncture (EA) at Baliao point on short-term complications, such as anal pain and swelling, after procedure for prolapse and hemorrhoids (PPH) in patients with mixed hemorrhoids. A total of 124 eligible patients undergoing PPH surgery were included in this study and randomly divided into a control group (n = 67) and an EA group (n = 57), with patients in the control group receiving only PPH surgery and patients in the EA group receiving PPH surgery and EA at Baliao point. The visual analogue scale (VAS) scores of EA group at 8, 24, 48, and 72 h after operation were significantly lower than those of control group. The anal distension scores at 8, 48, and 72 h after operation were also significantly lower than those of control group. The number of postoperative analgesic drug administration per patient was also significantly lower in the EA group. The incidence of urinary retention and tenesmus in EA group was significantly lower than that in control group within the first day after surgery. EA treatment at the Baliao point can alleviate short-term anal pain and anal swelling after the procedure for prolapse and hemorrhoids, reduce the incidence of urinary retention, and decrease the use of postoperative analgesic drugs. This study was approved and registered by the Chinese Clinical Trial Center, Registration number: ChiCTR2100043519, Registration time: February 21, 2021 ( https://www.chictr.org.cn/ ).

Background:Ileostomy is often used in low rectal cancer to protect the anastomosis and reduce the incidence of anastomotic leakage. However, the closure of the stoma causes physical and psychological damage to patients. An intestine diversion tube with a double-balloon was designed to remove the need for ileostomy and a secondary surgery, and we sought to verify its effectiveness and safety.Methods:An intestine diversion tube with a double-balloon was designed, and the experiment was performed in 5 groups of experiment pigs by the same group of physicians. The tube was placed into the ileum through the cecum during surgery. All the animals were anatomized after being anesthetized on the 14th day postoperatively to check the anastomosis and abdominal cavity. The postoperative complications included anastomotic leakage, abdominal or pelvic infection, anastomotic stenosis, postoperative bleeding, intestinal obstruction, reoperation, electrolyte disorder, drainage tube blockage, and drainage tube fall off.Results:No serious postoperative complications occurred in the 5 animal groups. The average daily drainage tube volume was 188.6 mL, the average drainage tube removal time was 13.4 days, and the average first defecation time was 2.6 days. Postoperative drainage was smooth, and no anastomotic leakage, other complications, or animal deaths occurred.Conclusions:The use of the intestine diversion tube with a double-balloon was feasible in animal experiments and was safe and effective. The procedure is simple, and suitable for popularization and application in the clinic.

Background: Graphene oxide (GO) has been widely used in the field of biomedicine and has shown great potential in drug delivery. Oral administration is an important mode of administration, but there are few studies on the effects of oral GO on gastrointestinal tract and gut microbiota. This study sought to explore the effects of oral GO on the gastrointestinal tract and gut microbiota. Methods: In total, 20 C57BL/6 male mice, aged 5 weeks old, were randomly divided into the following 4 groups (n=5): the control group, the GO30 group, the GO60 group, and the GO120 group. The GO sample solution was administered intragastrically at the doses of 30, 60, or 120 mg/kg every 3 days, and the control group was given an equal volume of distilled water. On the 16th day, mouse feces were taken for 16S ribosomal ribonucleic acid (rRNA) sequencing analysis, and the mice were dissected, and the heart, liver, kidney, and colon removed for histological analysis. Additionally, the ultrastructure of the colon was observed by transmission electron microscopy. Results: No obvious damage was observed in the hearts, livers, and kidneys of the mice. However, the intestinal ultrastructure of the mice in the GO group was damaged. The main manifestations were an uneven arrangement and local atrophy of the microvilli, swelling of the mitochondria and endoplasmic reticulum, and the widening of the intercellular spaces. The damage was positively correlated with increasing GO doses. The 16S rRNA sequencing results showed that the structure of the gut microbiota in the GO group was altered, and the contents of Alistipes, Enterobacteriaceae, Eubacterium, and Xanthobacteraceae were decreased. Conclusions: The oral administration of GO had no obvious toxicity effects on the hearts, livers, and kidneys of the mice. However, it did destroy the ultrastructure of the mouse colon and shift the structure of the gut microbiota, decreasing the contents of Alistipes, Enterobacteriaceae, Eubacterium, and Xanthobacteraceae.

Background: Rectal cancer is usually treated by surgery, but recurrence or metastasis seriously affect the quality of life and survival of patients. Identifying the risk factors for postoperative recurrence or metastasis of rectal cancer has important guiding value for the treatment of rectal cancer. However, the research on risk factors of postoperative recurrence or metastasis of rectal cancer has not been unified. Methods: The data of all patients undergoing rectal cancer surgery in The Fifth People's Hospital of Shanghai, Fudan University, from 2016 to 2020 were collected and analyzed. A total of 185 patients were included for statistical analysis and were divided into a recurrence or metastasis group and a non-recurrence or metastasis group. Patients were followed up according to National Comprehensive Cancer Network (NCCN) guidelines by enhanced CT or MRI, and colonoscopy. The cut-off of the research was recurrence, metastasis, or death. Logistic regression analysis and Cox regression analysis were used to analyze the risk factors related to postoperative recurrence or metastasis of rectal cancer, and the survival curve was drawn. Results: Multiple logistic regression analysis showed involvement of the mesorectal fascia (MRF) [OR (odds ratio) =2.9, 95% confidence interval (CI): 1.16-7.29, P=0.023], nerve and vascular invasion (OR =1.7, 95% CI: 1.08-2.59, P=0.022), intraoperative blood transfusion (OR =3.7, 95% CI: 1.45-9.40, P=0.006), and Dukes staging (OR =2.3, 95% CI: 1.26-4.35, P=0.007) were independent risk factors for postoperative recurrence or metastasis of rectal cancer. Involvement of mesenteric fascia infiltration (OR =11.5, 95% CI: 1.49-88.79, P=0.019) and Dukes stage (OR =3.0, 95% CI: 1.46-6.26, P=0.003) were independent risk factors for liver metastasis, while nerve and vascular invasion (OR =2.4, 95% CI: 1.19-5.00, P=0.015) was an independent risk factor for pulmonary metastasis. Conclusions: Postoperative recurrence or metastasis of rectal cancer is related to many factors. These findings have clinical guiding value and significance for the follow up and prognosis of patients with rectal cancer after surgery. Large-scale prospective clinical studies are needed.

ImportanceSimultaneous or delayed resection of synchronous liver metastasis (SLM) with primary colorectal cancer (CRC) remains a controversial topic.ObjectiveTo investigate the outcomes of simultaneous vs delayed resection in patients with resectable SLM.Design, Setting, and ParticipantsThis comparative effectiveness research study included 1569 patients with resectable SLM who underwent curative-intent liver resection at 3 independent centers in China between January 1, 2000, to December 31, 2019. A 1:1 propensity score matching was performed. Follow-up was completed on August 31, 2021, and the data were analyzed from April 1 to 30, 2022.Main Outcomes and MeasuresPrimary outcome was the percentage of patients with at least 1 major complication within 60 days after surgery. Secondary outcomes were intraoperative and postoperative complications, overall survival (OS), and cancer-specific survival (CSS) rates.ResultsAmong the 1569 patients included, 1057 (67.4%) underwent delayed resection (719 men [68.0%] with a mean [SD] age of 57.4 [11.2] years), and 512 patients (310 men [60.5%] with a mean [SD] age of 57.1 [10.5] years) underwent simultaneous resection. Matching yielded 495 pairs of patients underwent simultaneous resection. The percentage of major perioperative complications did not differ between the simultaneous and delayed resection groups (34.1% vs 30.0%; P = .89). The OS rates were 65.2% at 3 years, 47.1% at 5 years, and 38.0% at 8 years for the delayed resection group and 78.0% at 3 years, 65.4% at 5 years, and 63.1% at 8 years for the simultaneous resection group (hazard ratio [HR], 1.42; 95% CI, 1.10-1.85, P = .003). The CSS rates were 68.3% at 3 years, 48.5% at 5 years, and 37.1% at 8 years for the delayed resection group and 79.2% at 3 years, 67.2% at 5 years, and 65.9% at 8 years for the simultaneous resection group (HR, 1.45; 95% CI, 1.14-1.98; P = .004). On subgroup analysis comparing the 2 strategies according to the KRAS sequence variation status, the OS rates (HR, 1.61; 95% CI, 1.45-2.18; P < .001) and CSS rates (HR, 1.62; 95 CI, 1.40-1.87; P = .003]) in the simultaneous resection group were significantly better than those in the delayed resection group in patients with KRAS wild-type tumors.Conclusions and RelevanceResults of this study suggest that complication rates did not differ when CRC and SLM were resected simultaneously and that the survival benefits of simultaneous resection were restricted to patients with KRAS wild-type tumors. Integrating molecular features into the treatment decision is a basis for accurate, individualized treatments.

Gemcitabine resistance (GR) in pancreatic cancer (PC) results in poor patient outcomes. SMAD family member (Smad4) dysregulation is a significant role of GR in PC, and EZH2 is involved in Smad4 expression in tumor progression. Interestingly, lncRNA small nucleolar RNA host gene 16 (SNHG16) might interact with EZH2, indicating a potential pathway to overcome gemcitabine-resistant PC progression. We investigated the role of the SNHG16/EZH2/Smad4 pathway in gemcitabine-resistant PC cells (PANC-1/GR and SW1990/GR). First, we found that SNHG16 was upregulated both in wild-type PC cells and in gemcitabine-resistant PC cells. SNHG16 overexpression reduced gemcitabine cytotoxicity and apoptosis in PC cells. Meanwhile, SNHG16 upregulation caused p-Akt elevation and Smad4 reduction. However, SNHG16 silencing induced the opposite trend. Then, we found that EZH2 was enriched in SNHG16 based on RIP and RNA pulldown. In particular, SNHG16 overexpression promoted the interaction between EZH2 and the Smad4 promoter according to Chromatin immunoprecipitation-quantitative polymerase chain reaction. Finally, both EZH2 inhibition and Smad4 upregulation increased gemcitabine cytotoxicity and apoptosis in PC cells during SNHG16 overexpression. Moreover, both treatments decreased p-Akt and increased Smad4. Collectively, lncRNA SNHG16 decreased Smad4 to induce GR in PC via EZH2-mediated epigenetic modification.

Aim: To investigate the anticancer effects and action mechanism of graphene oxide (GO) in colorectal cancer (CRC). Materials & methods: Anticancer effects and mechanisms of GO in CRC were investigated both in vivo and in vitro. Results: GO significantly inhibited tumor growth both in vitro and in vivo. GO was able to enter HCT116 cells through endocytosis. GO treatment resulted in cytotoxicity, reactive oxygen species (ROS) production, apoptosis, autophagy and activation of the AMPK/mTOR/ULK1 signal pathway. However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways. Conclusion: GO exerts anticancer effects against CRC via ROS-dependent AMPK/mTOR/ULK-1 pathway-related autophagy and apoptosis.

目的 探讨骨桥蛋白(OPN)在胃癌组织中的表达及其与胃癌预后关系.方法 选取1995年1月至1996年12月间上海中山医院及2011年1月至2015年12月间上海复旦大学附属上海市第五人民医院收治的住院胃癌患者.收集患者的原发灶肿瘤组织及癌旁非肿瘤组织,根据国际抗癌联盟(UICC/AJCC)胃癌TNM分期标准确定肿瘤分期,应用免疫组织化学染色法(EnVision二步法)检测OPN的表达,所有病例随访时间为至少5年或直到死亡.结果 纳入研究的患者共145例,平均年龄56岁,其中,男性93例.免疫组织化学染色法结果显示,OPN阳性表达率为59.3％(86/145),OPN表达率与有无浆膜侵犯(67.8％vs.46.6％)、淋巴结转移与否(75.7％vs.44.0％)以及与胃癌的临床分期有关(69.9％vs.48.6％),差异均有统计学意义(均P<0.05),但与胃癌发生部位、组织分型无关,差异无统计学意义(P>0.05).OPN基因表达阴性组5年生存率显著高于OPN基因表达阳性组,差异有统计学意义(P<0.05).结论 OPN胃癌组织中表达与胃癌浸润转移、临床分期有关,OPN表达阳性患者5年生存率较低.

Background Colorectal cancer (CRC), one of the most common malignancies worldwide, is associated with poor survival and has a high mortality rate. Taxol is a chemotherapeutic agent that has been clinically applied as a first-line drug against diverse cancers. Yet, development of drug resistance has become the major challenge for anti-cancer treatments. F-box and WD40 domain protein 7 (Fbxw7) is a known tumor suppressor which is frequently downregulated in cancers. However, the biological roles and mechanisms of Fbxw7 in Taxol resistance are still under investigation. Methods We report that Fbxw7 is significantly inactivated in CRC tumors and cell lines compared with normal tissues and colon cells. Expressions of Fbxw7 and Nox1 were detected from human colon tumors and cells by qRT-PCR and Western blot. Glycolysis rate was assessed by glucose uptake and lactate product assay. Interactions between Fbxw7 and Nox1 were determined by co-immunoprecipitation (Co-IP). Chemosensitivity and resistance of colon cancer cells were determined by MTT assay and Annexin V-FITC assay. Results Overexpression of Fbxw7 sensitized colon cancer cells to Taxol. Moreover, we observed a negative correlation between Fbxw7 and glucose metabolism. From the established Taxol-resistant (TR) cell line from HCT-116, Fbxw7 was found to be markedly downregulated in HCT-116 TR cells. We detected that NADPH oxidase 1 (Nox1), a superoxide-generating NADPH oxidase, is negatively regulated by Fbxw7. The Co-IP assay showed that Fbxw7 interacted with Nox1, which was observed to be significantly upregulated in CRC tissues. Nox1 therefore promotes the Taxol resistance and glucose metabolism of colon cancer cells. Finally, rescue experiments demonstrated that the Fbxw7-promoted Taxol sensitivity was partially through the Nox1-glycolysis axis. Restoration of Nox1 in Fbxw7-overexpressed TR colon cancer cells significantly recovered the Taxol resistance, which could be further overridden by glycolysis inhibition. Conclusions Collectively, this study uncovered that targeting the Fbxw7-Nox1-glucose metabolism axis could be an effective strategy against chemoresistant colon cancer.

BACKGROUND:Colorectal cancer (CRC) is the third most common cancer, according to recently published literature. While the incidence and the mortality of CRC has decreased due to effective cancer screening measures, there has been an increase in the number of young patients diagnosed with colon cancer due to unclear reasons. As a target molecule of the Wnt signaling pathway, Ascl2 is an important marker of CRC stem cells and plays an important role in maintaining the nature of colon cancer stem/precursor cells. However, the role of Ascl2 in autophagy in CRC cells is rarely elucidated.METHODS:In this study, we found that Ascl2 was increased in CRC compared with adjacent tissue. Downregulation of Ascl2 in CRC cells could suppress proliferation and invasion, and induce apoptosis, of CRC cells. Moreover, we found that autophagy-relative protein LC3 increased after Ascl2 knockdown. Furthermore, we treated CRC cells with autophagy inhibitors 3-MA (3-Methyladenine) and CQ (Chloroquine).RESULTS:The results showed that autophagy inhibitors could prevent apoptosis, which was induced by Ascl2 knockdown. Finally, we confirmed that the downregulation of Ascl2 in CRC cells could alleviate the pathological process in vivo by xenograft experiment.CONCLUSIONS:Our findings indicated that si-Ascl2 (small/short interfering) exerted a tumor suppression function in CRC by inducing autophagic cell death, and suggest that Ascl2 targeted therapy represents a novel strategy for CRC treatment.

Transanal minimally invasive surgery (TAMIS) is mainly used for benign tumors of the rectum, but there are few reports on treating malignant tumors of the rectum with a large volume. The aim of this study was to evaluate the feasibility and safety of TAMIS for resection of rectal malignant tumors. A 57-year-old patient was pathologically diagnosed as rectal malignancy before surgery. Computed tomography (CT), magnetic resonance imaging (MRI), fludeoxyglucose-18F (18F-FDG), and endoscopic mucosal biopsy were performed to assess the tumor location and preoperative size. There were no contraindications in all preoperative examinations. We applied TAMIS technology to perform the operation on this patient, And the operative time, the amount of blood loss, the length of hospital stay, the cost of hospital stay, surgical complications, postoperative complications and other relevant data were all collected. The operation was successful, the operation time was 45 min, 10 mL of intraoperative blood loss, and the length of stay was 3 days, a tumor of a maximum diameter of 4 cm being completely removed. There were no related complications or recurrence during postoperative follow-up. The pathological results were tubular villous adenoma with low-grade intraepithelial neoplasia, and a focal area of high-grade intraepithelial neoplasia. The pathological stage was T1N0M0. At 3-month follow-up there were no signs of recurrence. The patient was followed up for 5 years after the operation and there was no tumor recurrence or metastasis in other parts and no other discomfort. TAMIS is less commonly used in rectal malignancies, especially for tumors with larger diameters. We successfully performed complete resection of a 4-cm rectal malignant tumor with TAMIS. Given its low risk, low cost, simple operation, and few complications, TAMIS can be used for more indications of rectum diseases.

目的 观察肌电生物反馈治疗在直肠癌术后患者排尿功能中的影响.方法 将我院普外科2016年9月～2019年3月收集的50例直肠癌术后女性患者作为研究对象,进行肌电生物反馈治疗及干预,评价干预前后患者排尿功能的差异.结果 通过肌电生物反馈对50例直肠癌术后女性患者进行干预治疗,患者术后排尿功能主要在排尿次数、OABSS评分以及尿垫重量等指标方面,与干预前进行对比分析,有统计学差异.结论 肌电生物反馈对直肠癌术后患后排尿功能有一定改善价值和意义.

BACKGROUND Transanal minimally invasive surgery (TAMIS) is a good choice for resection of rectal neoplasms. Endoscopic mucosal resection (EMR) is also widely used in the treatment of benign rectal tumors such as rectal polyps and rectal adenomas. However, no studies have compared the outcome of TAMIS and EMR. AIM To compare the short-term outcomes after TAMIS and EMR for rectal carcinoid and benign tumors (including rectal polyps and adenomas). METHODS From January 2014 to January 2019, 44 patients who received TAMIS and 53 patients who received EMR at The Fifth People’s Hospital of Shanghai were selected. Primary outcomes (surgical-related) were operating time, blood loss, length of postoperative hospital stay, rate of resection margin involvement and lesion fragmentation rate. The secondary outcomes were complications such as hemorrhage, urinary retention, postoperative infection and reoperation. RESULTS No significant differences were observed in terms of blood loss (12.48 ± 8.00 mL for TAMIS vs 11.45 ± 7.82 mL for EMR, P = 0.527) and length of postoperative hospital stay (3.50 ± 1.87 d for TAMIS vs 2.72 ± 1.98 d for EMR, P = 0.065) between the two groups. Operating time was significantly shorter for EMR compared with TAMIS (21.19 ± 9.49 min vs 49.95 ± 15.28 min, P = 0.001). The lesion fragmentation rate in the EMR group was 22.6% (12/53) and was significantly higher than that (0%, 0/44) in the TAMIS group (P = 0.001). TAMIS was associated with a higher urinary retention rate (13.6%, 6/44 vs 1.9%, 1/53 P = 0.026) and lower hemorrhage rate (0%, 0/44 vs 18.9%, 10/53 P = 0.002). A significantly higher reoperation rate was observed in the EMR group (9.4%, 5/53 vs 0%, 0/44 P = 0.036). CONCLUSION Compared with EMR, TAMIS can remove lesions more completely with effective hemostasis and lower postoperative hemorrhage and reoperation rates. TAMIS is a better choice for the treatment of rectal carcinoids.