Endometrial carcinosarcoma is a tumor characterized by the coexistence of carcinoma and sarcoma. It almost only occurs in postmenopausal women, and the average five-year survival rate is less than 30%. Endometrial carcinosarcoma is very aggressive and usually has high tumor recurrence and mortality rates. Endometrial carcinosarcoma often metastasizes to the lymph nodes, lungs and peritoneum. Here, we report a rare case of duodenal metastasis of endometrial carcinosarcoma.

To investigate the radiomics models for the differentiation of simple and non-simple acute appendicitis. This study retrospectively included 334 appendectomy cases (76 simple and 258 non-simple cases) for acute appendicitis. These cases were divided into training (n = 106) and test cohorts (n = 228). A radiomics model was developed using the radiomic features of the appendix area on CT images as the input variables. A CT model was developed using the clinical and CT features as the input variables. A combined model was developed by combining the radiomics model and clinical information. These models were tested, and their performance was evaluated by receiver operating characteristic curves and decision curve analysis (DCA). The variables independently associated with non-simple appendicitis in the combined model were body temperature, age, percentage of neutrophils and Rad-score. The AUC of the combined model was significantly higher than that of the CT model (P = 0.041). The AUC of the radiomics model was also higher than that of the CT model but did not reach a level of statistical significance (P = 0.053). DCA showed that all three models had a higher net benefit (NB) than the default strategies, and the combined model presented the highest NB. A nomogram of the combined model was developed as the graphical representation of the final model. It is feasible to use the combined information of clinical and CT radiomics models for the differentiation of simple and non-simple acute appendicitis.

Objective: Colon cancer is associated with multiple levels of molecular heterogeneity. RNA processing converts primary transcriptional RNA to mature RNA, which drives tumourigenesis and its maintenance. The characterisation of RNA processing genes in colon cancer urgently needs to be elucidated. Methods: In this study, we obtained 1033 relevant samples from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to explore the heterogeneity of RNA processing phenotypes in colon cancer. Firstly, Unsupervised hierarchical cluster analysis detected 4 subtypes with specific clinical outcomes and biological features via analysis of 485 RNA processing genes. Next, we adopted the least absolute shrinkage and selection operator (LASSO) as well as Cox regression model with penalty to characterise RNA processing-related prognostic features. Results: An RNA processing-related prognostic risk model based on 10 genes including FXR1, MFAP1, RBM17, SAGE1, SNRPA1, SRRM4, ADAD1, DDX52, ERI1, and EXOSC7 was identified finally. A composite prognostic nomogram was constructed by combining this feature with the remaining clinical variables including TNM, age, sex, and stage. Genetic variation, pathway activation, and immune heterogeneity with risk signatures were also analysed via bioinformatics methods. The outcomes indicated that the high-risk subgroup was associated with higher genomic instability, increased proliferative and cycle characteristics, decreased tumour killer CD8+ T cells and poorer clinical prognosis than the low-risk group. Conclusion: This prognostic classifier based on RNA-edited genes facilitates stratification of colon cancer into specific subgroups according to TNM and clinical outcomes, genetic variation, pathway activation, and immune heterogeneity. It can be used for diagnosis, classification and targeted treatment strategies comparable to current standards in precision medicine. It provides a rationale for elucidation of the role of RNA editing genes and their clinical significance in colon cancer as prognostic markers.

肠系膜下动脉（inferior mesenteric artery，IMA）结扎水平的选择和No.253淋巴结的清扫是全直肠系膜切除手术的关键步骤。多项研究表明，保留左结肠动脉（left colic artery，LCA）可显著减少术后并发症（包括吻合口漏和盆腔自主神经损伤）的发生率，提高吻合口残端边缘动脉的压力，减少直肠吻合口漏的发生率，且D3淋巴结清扫术所获得的淋巴结总数与高位结扎IMA 组没有显著区别［1-3］。然而，在保留LCA的情况下完整清扫No.253淋巴结，对于外科医师仍然是不小的挑战。这里，我们介绍一种腹腔镜下保留LCA 的No.253淋巴清扫技术——“Σ”法。

Objective:To evaluate CT and or MRI imaging in the diagnosis of lateral lymph node metastasis in patients of middle and low rectal cancer.Methods:In this study, 112 lateral lymph nodes were harvested in 79 patients with middle and low rectal cancer. The relationship between the preoperative imaging features of the lateral lymph nodes and the postoperative pathology was evaluated.Result:Thirty-eight cases (48%) were pathologically confirmed to have lateral lymph node metastasis. The diameter of metastasis-positive lateral lymph nodes was significantly larger than that of metastasis-negative lateral lymph nodes ( P<0.01). Multivariate analysis of clinical features and imaging features found that, tumors poorly differentiated, mucinous adenocarcinoma, signet ring cell carcinoma ( P=0.006), and the largest short diameter of the lateral lymph node ≥7 mm ( P=0.024), uneven density or signal ( P=0.022) were independent risk factors for lateral lymph node metastasis. Conclusion:Poor tumor differentiation, lateral lymph node maximum short diameter ≥7 mm, density or signal unevenness are independent risk factors for lateral lymph node metastasis in middle and low rectal carcinoma.

目的:通过多层CT血管成像技术(MSCTA)回顾性分析左结肠动脉(LCA)与肠系膜下静脉(IMV)的解剖位置分型、IMV回流变异情况及IMV于根部以上水平的分支情况.方法:回顾性收集2018年9月至2021年11月92例患者(其中左半结肠癌8例、乙状结肠癌25例、直肠癌59例)的腹部CT增强扫描结果,并进行血管重建与术后录像复习.其中男56例,女36例,中位年龄63(54,72)岁.分别记录肠系膜下动脉(IMA)的分型、LCA/IMV分型及LCA、IMV至IMA根部的距离,IMV的回流汇入位置,IMV于根部以上的分支数量.通过卡方检验分析患者各指标之间与LCA/IMV解剖位置分型的相关关系.结果:MSCTA技术准确判断肠系膜动脉分型情况及LCA与IMV的位置关系准确率达98.91％.其中95.65％(88/92)的病例存在LCA,4例患者LCA缺如;1例患者IMV属于边缘型,85.06％(74/87)的IMV行走于LCA后方,余者走行于前方.IMA根部距LCA的距离平均为(30.11±11.85)mm,距IMV的距离平均为(24.77±10.36)mm.于IMA根部水平LCA走行于IMV外侧者最多,占37.50％(33/88),其次为交叉型(30.68％,27/88)、远侧型(17.05％,15/88)与内侧型(13.64％,12/88).IMV、LCA边缘型最为少见,仅占1.14％(1/88).LCA内侧型中,IMV距IMA根部的距离远于其他各型(P<0.05).LCA远侧型中,LCA距IMA根部的距离远于其他各型(P<0.05).IMV汇入脾静脉是最常见的回流模式,占55.43％(51/92);34.78％(32/92)的IMV汇入肠系膜上静脉;6.52％(6/92)的IMV汇入SMV与脾静脉交汇位置;3.26％(3/92)的IMV汇入空肠第一支静脉.IMA根部水平以上IMV有2个分支的最多,占51.09％(47/92);1个分支者次之,占25.00％(23/92);3个及以上分支者占20.65％(19/92);0个分支仅占3.26％(3/92).单因素分析显示,LCA/IMV解剖位置分型与患者性别、身高、体重、BMI、IMV回流方式、IMV与LCA的前后关系等均不相关.结论:MSCTA技术能准确判断IMA、LCA与IMV的解剖位置分型.肠系膜下动、静脉血管解剖变异形式多样,LCA/IMV解剖位置分型与人体相关指标无明确相关关系,因此腹腔镜结直肠癌根治术前通过MSCTA技术了解上述情况十分必要.

BACKGROUND:Adenocarcinoma has the highest incidence among malignant tumors of the small intestine (SI). Squamous cell carcinoma (SCC) often occurs in organs covered with squamous epithelium. Primary or metastatic SCC originating from the SI is very rare, with very few cases reported in the literature.CASE SUMMARY:This case report involves a 69-year-old man who developed abdominal pain after lunch. After admission, an abdominal computed tomography scan revealed perforation of the alimentary canal and multiple abnormal low-density lesions in the liver. During laparotomy, an approximately 4 cm × 3 cm-sized solid tumor was found in the jejunum, located 30 cm from the Treitz ligament, with a perforation. An intestinal segment of approximately 15 cm was removed, including the perforated portion. The pathological result was SCC. In combination with liver imaging, a diagnosis of SI SCC with multiple liver metastases was considered. The patient died from hepatic failure 1 mo after the operation.CONCLUSION:SI tumors are very rare compared to those originating in other digestive organs. Due to its insidious onset, the diagnosis of this disease is usually delayed. Clinicians must pay close attention to digestive symptoms such as persistent abdominal pain and melena.

目的 探讨腹腔镜直肠癌根治术中行侧方淋巴结清扫(LLND)治疗局部进展期低位直肠癌的可行性、安全性及疗效.方法 回顾性分析2000年1月至2019年12月北京大学第一医院普通外科收治的行直肠癌根治术的200例进展期低位直肠癌病人的临床资料,术中均行LLND.根据手术方式分为腹腔镜组(77例)和开放组(123例),比较两组病人的近期疗效及中期肿瘤学结果.结果 与开放组比较,腹腔镜组病人手术时间缩短[240(110～550) min vs.310(140～780) min,Z=-8.714,P＜ 0.001],出血量减少[100(10～1200)mL vs.400(60～2500) mL,Z=-5.233,P＜ 0.001],术后尿潴留发生率降低(8.8％ vs.21.1％,x2=4.607,P=0.032),术后尿管拔除时间[4(1～12)d vs.5(2～24)d,Z=-2.722,P=0.006]和术后住院时间[11(6～59)d vs.16(7～64)d,Z=-2.274,P=0.023]均缩短.腹腔镜组单侧侧方淋巴结检出总数[5.5(1～17)枚vs.5.0(1～17)枚,Z=-2.134,P=0.033]和单侧髂内及闭孔动脉淋巴结检出数目[4(1～17)枚vs.3(1～11)枚,Z=-2.234,P=0.025]均增高.两组病人总生存率及无病生存率差异均无统计学意义(78.6％ vs.79.0％,69.8％ vs.71.3％,P＞0.05).结论 腹腔镜技术用于LLND有助于减少术中出血,更好地保护植物神经功能,病人术后恢复更快,可清扫更多的区域淋巴结,但中期肿瘤学结果与开放手术相当.

BACKGROUND Crohn's disease (CD) causes a range of digestive symptoms including recurrent diarrhea, abdominalgia, and flatulence, and severely impacts the quality of life of patients. Infliximab, a monoclonal antibody against tumor necrosis factor alpha, has recently been promoted as a therapeutic treatment for CD, but its safety margins remain uncertain. We report a case of rapidly progressive colorectal cancer that was diagnosed in a patient with CD who had previously been treated with infliximab. CASE SUMMARY This case report refers to a 40-year-old male with a 6-year history of CD. The patient underwent transverse colostomy because of inflammatory ileus in 2017. He subsequently received infliximab treatment in 2018. Ten months later, worsening contracture of the transverse colostomy was observed. Imaging tests indicated that the patient may have developed colon cancer with extensive peritoneal implantation. At the same time, colonoscopy revealed a rectal mass and pathological examination indicated well-differentiated adenocarcinoma. Palliative ileostomy was performed to improve defecation in 2019. During the operation, a small nodular mass in the mesentery of the small intestine was identified and pathological examination of the mass revealed advanced adenocarcinoma. The patient was diagnosed with advanced colorectal cancer and administered palliative chemotherapy. He died in June 2020. CONCLUSION We stress the importance of recognizing the possible occurrence of malignance in patients with CD receiving infliximab.

Aims: The present study investigated the effect of Escherichia coli Nissle 1917 (EcN) on irinotecan-induced intestinal barrier dysfunction and gut microbial dysbiosis in a mouse model and in the human colonic cells lines Caco-2. Materials and methods: Male BALB/c mice received irinotecan intraperitoneal injection with or without EcN administration intragastrically. Body weight, diarrhea severity, intestinal permeability and histopathological analysis of ileum epithelia of mice from different groups were assessed. The expression and localization of tight junction proteins were examined using western blot and immunofluorescence. Gut microbiota structure and diversity were measured with 16 S rRNA sequencing. Caco-2 monolayers were incubated with EcN culture supernatant (EcN(sup)) or SN-38 and the monolayer barrier function was assessed by transepithelial electrical resistance (TER) and FITC-dextran 4000 Da (FD-4) flux. Key findings: Pretreatment with EcN significantly attenuated irinotecan-induced weight loss and diarrhea in mice. In addition, EcN inhibited the increased intestinal permeability and decreased Claudin-1 expression in irinotecan-treated mice. Furthermore, irinotecan treatment decreased the diversity of gut microbiota and increased the relative abundance of Proteobacteria compared to control group. EcN administration ameliorated the gut microbiota dysbiosis. In Caco-2 monolayers, EcN(sup) ameliorated the decreased TER and increased FD-4 flux elicited by SN-38. Moreover, EcN(sup) attenuated SN-38-induced altered localization and distribution of Claudin-1 in Caco-2 monolayers. Significance: Our results indicated that the administration of EcN protected against irinotecan-induced intestinal injury by regulating intestinal barrier function and gut microbiota.

Long non-coding RNA (Lnc)TCF7 is a novel lncRNA that is involved in tumorigenesis. Previous studies have revealed that lncTCF7 serves an essential role in maintaining cancer stem cell self-renewal; however, the functions of lncTCF7 in colorectal cancer (CRC) remain unknown. Therefore, the present study aimed to investigate the role of lncTCF7 in CRC. LncTCF7 was upregulated in 52/58 CRC tissues, and its expression correlated with tumor size, lymph metastasis and tumor-node-metastasis stage in CRC. Knocking down lncTCF7 in colon cancer cell lines decreased cell proliferation, migration and invasion, while lncTCF7 overexpression showed opposite changes. In addition, lncTCF7 promoted cell proliferation in vivo. LncTCF7 activated the Wnt/β-catenin signaling pathway, which is essential for cancer development. Survival analysis revealed that patients with higher expression of lncTCF7 had significantly worse prognosis compared with patients with low expression. These findings indicate that lncTCF7 regulates CRC progression and support the notion of lncTCF7 as a CRC prognostic marker.

The long noncoding (lnc) RNA H19 was involved in the tumorigenesis of many types of cancer. However, the role of H19 in the tumorigenesis of colon cancer has not been fully illustrated. Recent studies suggested a potential relationship between H19 and vitamin D receptor (VDR) signaling. Considering the pivotal role of VDR signaling in the colon epithelium both physiologically and pathologically, the correlation between H19 and VDR signaling may have an important role in the development of colon cancer. In this study, the correlation between H19 and vitamin D receptor (VDR) signaling and the underlying mechanisms in colon cancer were investigated both in vitro and in vivo. The results suggested that VDR signaling was able to inhibit the expression of H19 through regulating C-Myc/Mad-1 network. H19, on the other hand, was able to inhibit the expression of VDR through micro RNA 675-5p (miR-675-5p). Furthermore, H19 overexpression induced resistance to the treatment with 1,25(OH)2D3 both in vitro and in vivo. Together, these results suggested that H19 overexpression might be one of the mechanisms underlying the development of resistance to the treatment with 1,25(OH)2D3 in the advanced stage of colon cancer.

Intestinal barrier injury has been reported to play a vital role in the pathogenesis of endotoxemia. This study aimed to investigate the protective effect of GYY4137, a newly synthesized H2S donor, on the intestinal barrier function in the context of endotoxemia both in vitro and in vivo. Caco-2 (a widely used human colon cancer cell line in the study of intestinal epithelial barrier function) monolayers incubated with lipopolysaccharide (LPS) or TNF-α/IFN-γ and a mouse model of endotoxemia were used in this study. The results suggested that GYY4137 significantly attenuated LPS or TNF-α/IFN-γ induced increased Caco-2 monolayer permeability. The decreased expression of TJ (tight junction) proteins induced by LPS and the altered localization of TJs induced by TNF-α/IFN-γ was significantly inhibited by GYY4137; similar results were obtained in vivo. Besides, GYY4137 promoted the clinical score and histological score of mice with endotoxemia. Increased level of TNF-α/IFN-γ in the plasma and increased apoptosis in colon epithelial cells was also attenuated by GYY4137 in mice with endotoxemia. This study indicates that GYY4137 preserves the intestinal barrier function in the context of endotoxemia via multipathways and throws light on the development of potential therapeutic approaches for endotoxemia.

BACKGROUND:Recently, long noncoding RNA (lncRNA) H19 has been reported to be related with VDR signaling and the development of inflammatory diseases including osteoarthritis. The aim of this study was to investigate the correlation between the expression level of H19 and VDR in ulcerative colitis (UC) tissues and to investigate the effect of H19 overexpression on intestinal epithelial barrier function.METHODS:The expression level of H19, miR-675-5p, and VDR in UC tissues and paired normal tissues collected from 12 patients with UC was investigated by quantitative real-time polymerase chain reaction. Caco-2 monolayers were used to test the effect of H19 and miR-675-5p overexpression on the intestinal epithelial barrier function and the status of tight junction proteins and VDR. Luciferase assay was used to validate the target site of miR-675-5p in the 3'UTR of VDR mRNA.RESULTS:The expression of H19 was found to be negatively correlated with the expression of VDR in UC tissues (r = 0.5369, P < 0.05). The expression of miR-675-5p was also found to be negatively correlated with the expression of VDR in UC tissues (r = 0.5233, P < 0.01). H19 overexpression increased Caco-2 monolayer permeability and decreased the expression of tight junction proteins and VDR, which was significantly attenuated by cotransfection with miR-675-5p inhibitors. The 3'UTR of VDR mRNA was validated to be one of the direct targets of miR-675-5p.CONCLUSIONS:This study reveals the destructive effect of H19 overexpression on intestinal epithelial barrier function and suggests a potential role of H19 in the development of UC. In addition, H19 overexpression may be one of the mechanisms underlying the decreased expression of VDR in UC tissues and the interaction between H19 and VDR signaling may provide potential therapeutic targets for UC.

Objective To investigate the effects of exogenous secreted protein acidic and rich in cysteine (SPARC) on proliferation,migration and invasion ability of human pancreatic cancer cell lines.Methods The cuhured Mia PaCa-2 and PANC-1 pancreatic cancer cells were established in the presence of different concentrations (0,0.5,1.0,3.0,5.0,10.0 mg/L) or absence of exogenous SPARC as experimental and control groups.The change of proliferation was measured by methyl thiazol tetrazolium (MTT) assay.The 24 h cultured Mia PaCa-2 and PANC-1 pancreatic cancer cells were established in the presence (5 mg/L) or absence of exogenous SPARC as experimental and control groups,and the change of migration ability was detected by single cell migration assay and the change of invasion ability by Matrigel invasion assay respectively.Results Exogenous SPARC could inhibit the proliferation of cells in a concentration-dependent manner.Cell proliferation was inhibited in the presence of 10.0 mg/L exogenous SPARC by (32.8 ± 7.4) ％ and (32.5 ± 1.8) ％ in Mia PaCa-2 and PANC-1,respectively.5.0 mg/L SPARC reduced the distance covered within 24 h by 26％ and 39％,and in the presence of 5.0 mg/L SPARC the number of invasive cells was inhibited by 30％ and 56％ in 24 h,respectively.Conclusion Exogenous SPARC could inhibit the proliferation,migration and invasion ability in pancreatic cancer cells,suggesting extracelluar matrix may affect biological functions of malignant tumors.

Secreted protein acidic and rich in cysteine (SPARC) is a glycoprotein which plays multiple roles in different types of cancer. Our previous study showed that SPARC overexpression inhibited the growth and angiogenesis of tumors, and reduced expression of vascular endothelial growth factor (VEGF). However, the relationship between SPARC expression and clinicopathological factors of gastric cancer (GC) is controversial, and the role of SPARC in GC remains unclear. We evaluated expression of SPARC in 65 human GC tissues using immunohistochemistry (IHC). The results indicated that SPARC expression was negatively correlated with clinicopathological factors of GC. In vitro assay showed that SPARC overexpression decreased proliferation and clonogenicity by suppressing CD44 expression. In addition, SPARC overexpression inhibited VEGF induced proliferation and arrested cell cycle of GC cells by reducing the activation of VEGFR2, ERK1/2 and AKT signaling pathways. SPARC suppressed the invasion and migration of GC by reducing MMP-7, MMP-9, N-cadherin, Sp1 and p-ERK1/2 expression. In the in vivo assay, cancer metastasis mouse models were established by tail vein injection. The results revealed that the lung metastases of SPARC-overexpressing GC cells in the mice were much fewer than those of control cells.

Objective To determine the mechanisms through which sodium butyrate (NaB) protects peritonitis mice against intestinal barrier injury.Methods Seventy B57 mice were divided randomly into NaB group,and control group.NaB was fed through gavage (0.2 g/kg,twice per day).NaB concentrations in the gastrointestine were measured in 24 h. Cecal ligation and puncture (CLP) surgeries were performed to generate peritonitis.Mortality was monitored.Gut permeability was represented by plasma concentration of orally administrated tracer FD40 at 4 h after operation.Ileal histological alterations were studied.Results (1) NaB concentration in chyme measurements showed significantly higher NaB concentrations in NaB group than in control group in the stomach (2.08 ±0.39 vs ＜0.01 mmol/kg,P ＜0.01 ),the jejunum ( 1.23 ±0.48 vs ＜0.01 mmol/kg,P ＜0.05),and the ileum ( 1.64 ±0.22 vs ＜0.01 mmol/kg,P ＜0.01 ).CLP-induced mortality was significantly decreased by oral NaB treatment (23.1％ vs 53.8％,P ＜0.05).Gut permeability was largely increased after CLP [ plasma FD40 concentration:sham (0.05 ±0.005) mg/L,CLP (0.230 ±0.020) mg/L].This increased permeability was partially prevented by NaB feeding [ plasma FD40 concentration (0.120 ± 0.020) mg/L,P ＜ 0.01 ].Histological study showed that ileal tissue injury following peritonitis was substantially alleviated by NaB,and that tissue restitution process was prompted by NaB.Conclusion NaB protects the intestinal barrier function in peritonitis mice.