The application value of capsule endoscopy in diagnosing small intestinal carcinoma.

OBJECTIVE: The aim of this study was to explore the clinical value of capsule endoscopy in the diagnosis of small intestine neoplastic lesions. MATERIALS AND METHODS: A retrospective analysis was conducted on the clinical data of 108 patients who underwent capsule endoscopic examination in the Endoscopy Center of Xinxiang Central Hospital from February 2010 to January 2014. The characteristics of different small bowel diseases were observed, and the prevalence rates of different small bowel lesions were calculated. RESULTS: Of the included 108 patients who received capsule endoscopic examination, 74 cases showed lesions, with a detection rate of 68.52%. Of these 74 patients, 56 cases (51.85%) suffered from small bowel diseases and 18 cases (16.67%) were manifested with other gastrointestinal lesions. Moreover, obvious lesion was not observed in 34 cases (31.48%). Among the patients with lesions, we observed seven cases of submucosal tumor in small intestines, five cases of small intestinal carcinoma, two cases of small intestinal polyps, two cases of small intestinal roundworm, eight cases of small intestine ulcer, one case of Crohn's disease, 18 cases of enteritis, two cases of small intestine diverticula, four cases of small intestine hemangioma, one case of small intestine vascular malformation, one case of intestinal lymphangiectasia, one case of small intestine compression, two cases of small intestine hemorrhage, and two cases of small intestinal lipoma. Among the patients who showed other gastrointestinal lesions, we observed one case of esophageal diverticula, three cases of gastric erosion, six cases of superficial gastritis, four cases of gastric ulcer, one case of pyloric ulcer, one case of colonic polyps, and two cases of colon tumor. CONCLUSION: Capsule endoscopy demonstrated a high diagnostic value for various small bowel diseases, including both tumor and inflammatory lesions. Given its simplicity, safety, and reliability, capsule endoscopy was an important examination tool for the diagnosis of small bowel diseases.

Application value of endoscopic submucosal dissection and endoscopic mucosal resection for treatment of rectal carcinoids.

OBJECTIVE: The objective of this study is to explore the clinical effect and safety of endoscopic submucosal dissection (ESD) and endoscopic mucosal resection (EMR) for treatment of rectal carcinoids. METHODS: A retrospective analysis was conducted on 42 patients with rectal carcinoids who were hospitalized and subjected to surgical treatment in our hospital from January 2010 to November 2015. The patients were categorized into two groups based on treatment received: ESD (n = 22) and EMR (n = 20). The patients were analyzed and compared to determine differences in lesion size, operation time, histopathologically curative resection rate, intraoperative complications, complete lesion resection rate, and postoperative recurrence rate between the two groups. RESULTS: Operation time (25.2 ± 20.1 min) and wound surface diameter (36.2 ± 10.1 mm) were significantly higher in the ESD group than those in the EMR group (12.6 ± 8.4 min and 18.6 ± 5.9 mm, respectively) (P < 0.05). The differences in complete lesion and histopathologically curative resection rates between the two groups were not statistically significant (P > 0.05). Delayed hemorrhage was the primary postoperative complication in both groups. Postoperative follow-up was performed for 3-71 months, and the median follow-up time was 45 months. Recurrence was noted 32 months after surgery in one patient in the EMR group (4.5%), whereas recurrence was not detected in the ESD group. CONCLUSION: ESD and EMR are safe and effective methods for treatment of rectal carcinoids. Moreover, ESD had less risk of recurrence, more complete resection rate which could provide more information for postoperative treatment.

Tumor suppressor microRNA-27a in colorectal carcinogenesis and progression by targeting SGPP1 and Smad2.

The aberrant expression of microRNAs (miRNAs) is associated with colorectal carcinogenesis, but the underlying mechanisms are not clear. This study showed that the miRNA-27a (miR-27a) was significantly reduced in colorectal cancer tissues and colorectal cancer cell lines, and that the reduced miR-27a was associated with distant metastasis and colorectal cancer clinical pathological stages-miR-27a was lower at stages III/IV than that at stage II. Bioinformatic and systemic biological analysis predicted several targets of miR-27a, among them SGPP1 and Smad2 were significantly affected. SGPP1 and Smad2 at mRNA and protein levels were negatively correlated with miR-27a in human colorectal cancer tissues and cancer cell lines. Increased miR-27a significantly repressed SGPP1 and Smad2 at transcriptional and translational levels. Functional studies showed that increasing miR-27a inhibited colon cancer cell proliferation, promoted apoptosis and attenuated cell migration, which were also linked to downregulation of p-STAT3 and upregulation of cleaved caspase 3. In vivo, miR-27a inhibited colon cancer cell growth in tumor-bearing mice. Taken together, this study has revealed miR-27a as a tumor suppressor and has identified SGPP1 and Smad2 as novel targets of miR-27a, linking to STAT3 for regulating cancer cell proliferation, apoptosis and migration in colorectal cancer. Therefore, miR-27a could be a useful biomarker for monitoring colorectal cancer development and progression, and also could have a therapeutic potential by targeting SGPP1, Smad2 and STAT3 for colorectal cancer therapy.

[Indoor deposition flux and congener profiles of polybrominated diphenyl ethers (PBDEs) in Shanghai, China].

Indoor dry deposition of eight homes and offices in the urban area of Shanghai, China were sampled with clean glass plate during July to August of 2008 to study the indoor deposition flux and congener profiles of polybrominated diphenyl ethers (PBDEs). 16 PBDEs congeners which including BDE-17, -28, -71, 47, -66, -77, -100, -99, -85, -118, -154, -153, -138, -183, -190 and BDE-209 were measured by GC-MS with negative chemical ionization (NCI) in selected ion monitoring (SIM) mode. The particulate deposition flux of PBDEs in homes and offices were (10.9 +/- 8.2) and (14.2 +/- 11.9) ng x (m2 x d)(-1) respectively. Deca-BDE (BDE-209) was the major compound, accounting for 88.2% -99.2% of the quantified PBDEs. The particulate deposition flux in the offices [(3.1 +/- 2.0) mg x (m2 x d)(-1)] was relatively lower than that of homes, but the concentration of PBDEs in the particles [(3361.6 +/- 1987.4) ng x g(-1)] was significantly higher than that of homes [(1169.1 +/- 647.1) ng x g(-1)]. The concentration of PBDEs in the indoor dry deposition of Shanghai ranked in the middle level comparing with other cities around the world. The indoor deposition flux of PBDEs was mainly correlated with the flux of particle deposition and the usage of electrical and electronic products, but not the interior decoration and the amount of furniture.

[Expression of cyclooxygenase-2 and relationship with mismatch repair gene and microsatellite instability in hereditary non-polyposis colorectal cancer].

OBJECTIVE: To investigate the expression of Cyclooxygenase (COX)-2 and the relationship between cox-2, mismatch repair gene (MMR) proteins and microsatellite instability (MSI) in HNPCC. METHODS: Twenty-eight cases of adenomas and 14 cases of carcinomas were collected from 33 HNPCC families patients by colonoscopy. Sporadic adenomas (n = 32) and carcinomas (n = 24) were used as a control group. The expressions of COX-2 and mismatch repair gene hMLH1, hMSH2, hMSH6 proteins were examined by immunohistochemistry. MS1 were analyzed by using PCR with BAT25, BAT26, D2S123, D5S346 and D17S250 loci. RESULTS: The COX-2 high-expression rates were 53.6% (15/28) and 42.9% (6/14) in HNPCC adenomas and carcinomas, and were 62.5% (20/32) and 91.7% (22/24) in sporadic adenomas and carcinomas. COX-2 expression was lower in HNPCC carcinomas than that of sporadic carcinomas (P < 0.05). MMR deficiency rate and positive rate of MSI-H were both 71.4% (10/14) respectively in HNPCC carcinomas. It was higher than that in sporadic colorectal carcinomas [both 12.5% (3/24)]. Eight (80.0%) COX-2 low-expression were observed in 10 HNPCC carcinomas with MMR-deficient system while 4 cox-2 high-expression cases were observed in 4 HNPCC carcinomas with MMR-proficient system. COX-2 expression was lower in HNPCC carcinomas and adenomas, sporadic carcinomas with MMR-deficient system than that of MMR-proficient (P < 0.05). The COX-2 low-expression rates were 80.0% (8/10), 66.7% (12/18) and 66.7% (2/3) in HNPCC adenomas, HNPCC carcinomas and sporadic carcinomas with MSI-H. Cox-2 expression was lower in HNPCC and sporadic carcinomas (adenocarcinomas) with MSI-H than that of MSS (P < 0.05). CONCLUSION: Compared with sporadic carcinomas, the COX-2 expression was lower in HNPCC carcinomas. There was negative correlation between COX-2 expression and MMR-deficient (MSI-H). The detection of COX-2, MMR protein and MSI is of important significance in further studying the pathogenesis and interventional therapy of colorectal neoplasms.

[Mutation of hMLH1 and hMSH2 genes in hereditary nonpolyposis colorectal cancer: analysis of 76 probands].

OBJECTIVE: To investigate the mutations of the mismatch repair genes hMLH1 and hMSH2 in hereditary nonpolyposis colorectal cancer (HNPCC). METHODS: The DNA samples of 76 probands of HNPCC families underwent PCR amplification and sequencing on 35 exons in hMLH1 and hMSH2 genes. RESULTS: (1) The overall mutation rate of the hMLH1 and hMSH2 genes was 33% (25/76). (2) 22 mutations were found, 16 in the hMLH1 gene and 6 in the hMSH2 gene. (3) The spectrum of mutation type included frame shift, nonsense, splice site, and missense mutations. Missense mutation was the most common mutation type. CONCLUSION: The hMLH1 and hMSH2 mutations in Chinese HNPCC families show a wide spectrum. It seems that hMLH1 gene is involved more frequently than hMSH2 gene. A certain number of HNPCC families can be benefited from the genetic screening for mutation of the mismatch repair genes.