Browsing by Author "Tercan, M."

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Defibrotide Activity in Experimental Frostbite Injury
(Churchill Livingstone, 1998) Özyazgan, I.; Tercan, M.; Bekerecioǧlu, M.; Melli, M.; Üstün, H.; Günay, G.K.
The pathogenesis of frostbite injury has not been completely elucidated although the available evidence suggests it is an inflammatory reaction following reperfusion injury. Defibrotide given i.p. at 40 mg/kg/day for three days to rabbits, the ears of which were subjected to frostbite, decreased the presence of inflammatory cells (mast cells -76%; neutrophils -40.4%) and increased prostaglandin I2 (PGI2) (as 6-Keto-PGF(1α)) in the involved skin. Thromboxane A2 (TxA2) (as TxB2)was unaffected. These data strengthen the view that an inflammatory process is the underlying cause of frostbite injury and that Defibrotide is active in pathological situations involving an inflammatory process like in frostbite.
Squamous Carcinoma in a Pressure Sore With a Very Short Latency Period
(2003) Tan, O.; Atik, B.; Bekerecioglu, M.; Tercan, M.; Bayram, I.
Malignancy in a chronic pressure sore is rare among Marjolin's ulcers. Carcinomas arising in pressure sores are highly aggressive and usually fatal. Although carcinomas in pressure sores are generally well-differentiated squamous carcinomas, they can show quite an aggressive course and do not respond either to chemotherapy or radiotherapy. The mortality rate is high despite wide surgical resection. It must be kept in mind that carcinomas may arise in pressure sores and treatment must be early and aggressive. We report a squamous carcinoma arising in a pressure sore that had a very short latency period. The related literature was reviewed.