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We report a case of urinary bladder perforation during colonoscopy. A 67-year-old female, who had undergone a transabdominal hysterectomy for uterine myomas 15 years ago, visited the emergency department with complaint of abdominal pain after a screening colonoscopy. Laparoscopic examination revealed severe adhesion between the sigmoid colon and the urinary bladder. The urinary bladder wall was weakened, and several perforation sites were found. The surgery was converted to a laparotomy. After a thorough examination, we performed primary repair for the perforation sites, followed by an omentopexy.
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We report a case of a goblet-cell carcinoid tumor of the appendix which metastasized to the peritoneum and was treated by using cytoreductive surgery (CRS) with intraperitoneal chemotherapy. A 47-year-old male presented with chronic constipation and was diagnosed as having a rectal adenocarcinoma with a signet-ring-cell component under colonoscopy. Computed tomography suggested peritoneal metastases with diffuse nodular parietal peritoneal thickening of the entire abdomen and focal invasion of the upper rectum by a seeding mass. CRS with intraperitoneal chemotherapy was done under the diagnosis of a rectal adenocarcinoma with peritoneal metastases. The pathologic diagnosis was a goblet-cell carcinoid tumor of the appendix with peritoneal metastasis. The histological discrepancy between a peritoneal metastatic mass and a rectal mass was due to the mixed histological pattern of a goblet-cell carcinoid tumor. A metastatic mass may not share identical immunohistochemical characteristics from its origin. This histologic discrepancy necessitates caution in diagnosing a distant metastasis of a goblet-cell carcinoid tumor.
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Surgical site infection (SSI) is one of the most common complications that can occur after stoma closure. Reports have described differences in the incidence of wound infection depending on the skin closure technique, but there is no consensus on the ideal closure technique for a stoma wound. The aim of this study was to compare the incidence of SSI and the patient satisfaction between a circumferential purse-string approximation (CPA) and a primary linear closure (PC) of a stoma wound.
This prospective nonrandomized trial enrolled 48 patients who underwent a stoma closure from February 2010 to October 2013. Patients were divided into two groups according to the stoma closing technique: the CPA group (n = 34) and the PC group (n = 14). The incidences of SSI for the two groups were compared, and the patients' satisfaction with the stoma closure was determined by using a questionnaire.
SSI occurred in 3 of 48 patients (6.3%) and was more frequent in the PC group than in the CPA group (3/14 [21.4%] vs. 0/34 [0%], P = 0.021). Time to complete healing after stoma closure in the CPA group was 32 days (range, 14-61 days). Patients in the CPA group were more satisfied with the resulting wound scar (P = 0.043).
After stoma closure, CPA was associated with a significantly lower incidence of wound infection and greater patient satisfaction compared to PC. However, with the CPA technique, the time to heal is longer than it is with PC.
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The aim of this study was to observe the clinical features of a bezoar-induced small bowel obstruction and to investigate the role of abdominal computed tomography (CT) in establishing the diagnosis.
We retrospectively reviewed 20 cases of bezoar-induced small bowel obstruction in our hospital from 1996 to 2010.
Thirteen patients (65%) had a history of abdominal surgery. Nine patients (45%) were diagnosed with a bezoar before surgery, seven patients were diagnosed by using abdominal CT, and two patients were diagnosed with a small bowel series. Abdominal CT was performed in 15 patients, and the diagnostic accuracy was 47% (7/15). Surgery revealed ten bezoars in the jejunum and 11 in the ileum. Two patients had bezoars found concurrently in the stomach. Spontaneous removal took place in two patients. An enterotomy and bezoar extraction was performed in 15 patients. Fragmentation and milking, a small bowel resection, and a Meckel's diverticulectomy were performed in one patient each. Early operative treatment was possible (P = 0.036) once the bezoar had been diagnosed by using abdominal CT. There tended to be fewer postoperative complications in patients who were diagnosed with a bezoar by using abdominal CT, but the result was not statistically significant (P = 0.712).
A preoperative diagnosis of bezoar-induced small bowel obstruction by using clinical features was difficult. Increased use of abdominal CT led to a more accurate diagnosis and to earlier surgery for bezoar-induced small bowel obstructions, thereby reducing the rate of complications.
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Evidence that indicates bile acid is a promoter of colon cancer exists. Deoxycholic acid (DCA) modifies apoptosis or proliferation by affecting intracellular signaling and gene expression. However, because previous studies have been based on studies on colon cancer cell lines, the effect of DCA on normal colonocytes is unknown.
Normal colonocytes and Caco-2 and HCT116 cells were treated with 20 µM and 250 µM of DCA, and the effect of different concentrations of DCA was measured based on the expression of cell-cycle-related proteins by using Western blots.
The expressions of CDK2 and cyclin D1 for different concentrations of DCA in normal colonocytes and colon cancer cells were similar, but the expressions of cyclin E and A were significantly different. In HCT116 colon cancer cells, the expression of cyclin E increased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin E was not changed or decreased. In HCT116 colon cancer cells, the expression of cyclin A was not changed or decreased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin A was increased at a DCA concentration of 20 µM.
The effect of DCA on stimulating cell proliferation suggests that DNA synthesis is stimulated by an increased expression of cyclin E in colon cancer cells. Our results suggest that a low dose of DCA induces cellular proliferation through increased expression of cyclin A and that a high dose of DCA induces decreased expression of cyclin E and CDK2 in normal colonocytes.
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Oxaliplatin is a third-generation platinum compound, and it has no nephrotoxicity and has reduced bone marrow toxicity. Cancer cells that are resistant to cisplatin are sensitive to oxaliplatin. Oxaliplatin is used widely for the treatment of colon cancers. Recently, oxaliplatin was reported to inhibit the expression of survivin, which protects cell apoptosis. However, there are no reports on the expressions of survivin variants and the changes in intracellular localization of survivin in cancer cells. We studied the expression of survivin caused by oxaliplatin in HCT116 colon cancer cells, and we observed the localization of survivin in the mitotic phase.
We treated the HCT116 colon cancer cells with 2.0 µM of oxaliplatin, and we studied the expressions of survivin protein, and survivin mRNA variants, as well as the changes in intracellular localization, by using the Western blot method, RT-PCR, immunocytochemistry, and flowcytometry.
Oxaliplatin inhibits the expression of the survivin protein and survivin mRNA in HCT116 colon cancer cells. The expression of the survivin-2B variants, which have no antiapoptotic activity but control cell mitosis by localization on a microtubule, is reduced continuously 2 days after treatment with oxaliplatin. In immunocytochemistry, expression of survivin in the cytoplasm is reduced and especially is not expressed in microtubules and contractile rings.
One of the mechanisms of oxaliplatin is to inhibit the expression of and to change the localization of survivin. Based on these results, we suggest that changes in the expression of survivin variants and in their localization are two effects of oxaliplatin.
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