Laparoscopic-assisted colonoscopy: results and follow-up endoscopic success.

AIM: Incomplete colonoscopy occurs in 8-10% of attempted examinations. An incomplete colonoscopy is usually followed by radiological evaluation of the large bowel to complete the colonic assessment. Patients then found to have polyps of > 1 cm represent a significant management dilemma. This study describes our experience using laparoscopy to facilitate complete colonoscopy and polypectomy in patients with fixed angulation and the success of subsequent colonoscopies. METHOD: All patients from 2008 to 2012 with an incomplete colonoscopy because of fixed angulation and with polyps detected by subsequent imaging underwent standard laparoscopy with colonic mobilization by division of adhesions to facilitate direct vision. Completion of colonoscopy and polypectomy, intra-operative complications, postoperative morbidity and successful standard follow-up colonoscopy were studied. RESULTS: Twelve patients underwent the procedure. Complete colonoscopy to caecum was successful in all, with a median of 2 (range 1-5) polyps per patient and a mean polyp size of 22 mm. One iatrogenic enterotomy was repaired immediately, with no sequelae. Ten patients have since undergone colonoscopy under sedation, with complete colonic evaluation possible in nine of the patients. CONCLUSION: Laparoscopic-assisted colonoscopy allows safe polypectomy in patients with incomplete colonoscopy, without the need for segmental resection. This less-invasive procedure yields recovery times similar to those of colonoscopy alone, avoiding the morbidity of a segmental resection with the added benefit of successful routine colonoscopy in the future.

The influence of selenium and neuroleptics on the rat brain nuclear regulatory mechanism in carcinogenesis.

The potential clinical benefit of the antitumor effect of selenium (Se) has recently been confirmed in tumor-bearing animals and human tumor cells in culture. In clinical medicine, the reduced incidence of cancer among schizophrenic patients was attributed to neuroleptic medication. However, there has been little information on the effect of Se, carcinogen, and neuroleptic on the brain cells. This investigation was carried out on the brains of male Wistar rats treated with inorganic Se, 9,10-dimethyl-1,2-benzanthracene, and chlorpromazine. Chromatin was prepared and purified from isolated brain cell nuclei. Various protein species (histones and nonhistone proteins), RNA, and DNA were extracted by different extraction procedures. A higher relative content of nonhistone proteins was found in the group of animals treated with Se alone, carcinogen alone, and Se plus carcinogen administered simultaneously when compared with other experimental and control groups. The ratio of nonhistone proteins and histones of < 1.0 in the group of animals treated with neuroleptic + carcinogen or with neuroleptic indicates a lower content of nonhistone proteins when compared to histones. We obtained a more pronounced susceptibility to degradation by DNase I in the group of animals treated with neuroleptic + carcinogen or with neuroleptic compared to chromatin in the animals treated with carcinogen alone. We conclude that neuroleptic increases protein synthesis, as well as chromatin susceptibility to enzymatic degradation, thus achieving an opposite effect of carcinogen.