Transseptal Subperichondrial Endoscopic Hypophysectomy With Preservation of Vital Nasal Structures.

INTRODUCTION: Pituitary surgery involving different techniques is often applied to the excision of benign adenomas. Operative interventions involved various approaches and techniques. Endoscopic transsphenoidal approach is the less traumatic route to the sella turcica, avoiding brain retraction, and also permitting good visualization, with lower rates of morbidity and mortality. Although mortality of pituitary surgery decreased by advances in surgical techniques morbidities such as synechiae formation, anosmia, bleeding, nasal septal perforations, drying, and incrustation due to traumatization of the nasal structures such as septum, nasal mucosa, and middle concha are the current problems in pituitary surgery. Here, the authors described an endoscopic transseptal subpericondrial hypophysectomy with minimal damage to normal anatomy and physiology and discussed advantages of this technique. METHODS: The authors performed endoscopic transseptal subpericondrial hypophysectomy to 2 patients and evaluated intraoperative and postoperative results. RESULTS: No complication was noted during surgery or postoperative period with endoscopic transseptal subpericondrial hypophysectomy technique. CONCLUSIONS: Endoscopic transseptal subpericondrial hypophysectomy is a safe technique and, requires only a short surgery time and does not require the removal of any physiological tissue or cause any bleeding.

Selenium protects cerebral cells by cisplatin induced neurotoxicity.

PURPOSE: To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium. METHODS: Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time. RESULTS: Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity. CONCLUSION: Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity.

Selenium protects cerebral cells by cisplatin induced neurotoxicity

PURPOSE: To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium. METHODS: Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time. RESULTS: Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity. CONCLUSION: Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity. .

Borax partially prevents neurologic disability and oxidative stress in experimental spinal cord ischemia/reperfusion injury.

OBJECTIVES: The aim of this study is to investigate the potential effects of borax on ischemia/reperfusion injury of the rat spinal cord. METHODS: Twenty-one Wistar albino rats were divided into 3 groups: sham (no ischemia/reperfusion), ischemia/reperfusion, and borax (ischemia/reperfusion + borax); each group was consist of 7 animals. Infrarenal aortic cross clamp was applied for 30 minutes to generate spinal cord ischemia. Animals were evaluated functionally with the Basso, Beattie, and Bresnahan scoring system and inclined-plane test. The spinal cord tissue samples were harvested to analyze tissue concentrations of nitric oxide, nitric oxide synthase activity, xanthine oxidase activity, total antioxidant capacity, and total oxidant status and to perform histopathological examination. RESULTS: At the 72nd hour after ischemia, the borax group had significantly higher Basso, Beattie, and Bresnahan and inclined-plane scores than those of ischemia/reperfusion group. Histopathological examination of spinal cord tissues in borax group showed that treatment with borax significantly reduced the degree of spinal cord edema, inflammation, and tissue injury disclosed by light microscopy. Xanthine oxidase activity and total oxidant status levels of the ischemia/reperfusion group were significantly higher than those of the sham and borax groups (P < .05), and total antioxidant capacity levels of borax group were significantly higher than those of the ischemia/reperfusion group (P < .05). There was not a significantly difference between the sham and borax groups in terms of total antioxidant capacity levels (P > .05). The nitric oxide levels and nitric oxide synthase activity of all groups were similar (P > .05). CONCLUSIONS: Borax treatment seems to protect the spinal cord against injury in a rat ischemia/reperfusion model and improve neurological outcome.