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The Turkish Organ Transplantation and Burn Foundation was established in 1980. This was followed by the founding of the Turkish Transplantation and Burn Foundation Hospital in 1985. Under the aegis of this foundation and the Haberal Educational Foundation, Baskent University (BU) was founded in 1993 by Professor Mehmet Haberal, general surgeon and pioneer of organ transplantation in Turkey, and the President of the university since then.The BU Neurosurgery Department began functioning in January of 1995, with the advancement of the department and with contributions from the other hospitals in cities of Adana, Konya and Alanya. Just 13 years after its foundation, BU became one of the most prestigious universities of the country. While establishing new neurosurgery units within BU health care facilities, the neurosurgeons appointed to the new center spend few months in the neurosurgery department at the BU Ankara Hospital, central hospital, at first in order to get acquainted with the BU medical system. After the new neurosurgery unit begins to operate, senior neurosurgeons from Ankara are called to supervise junior colleagues during major surgical procedures. In addition to these exchanges, residents are sent routinely to these centers as part of the neurosurgical residency programme. As the system is very integrated, neurosurgeons from other centers of the BU also routinely come to Ankara Hospital and Research Center for educational purposes.BU as a whole and its health system model in particular are certainly unique in Turkey. The statistical data from all hospitals of the BU reveal growing patient demand and consumer satisfaction. more...

The aims were to investigate the early effects of graded, closed, mild head injury on neurofilament protein (NF160) and microtubule-associated protein-2 (MAP2) and to examine the levels of lipid peroxidation and the impact of mexilitine, inhibitor of lipid peroxidation, pretreatment on tissue damage.One hundred and twenty-six rats were divided into groups as follows: Group 1 (n = 14) were controls; group 2 (n = 56) sustained trauma alone; and group 3 (n = 56) were pretreated with mexilitine (50 mg/kg). Groups 2 and 3 were subdivided into subgroups (n = 14 each), which were subjected to 100 g/cm2, 125 g/cm2, 150 g/cm2, and 175 g/cm2 trauma forces, respectively. Two hours after trauma, the frontal lobes from all groups were removed and processed for lipid peroxidation HE staining, immunofluorescent labelling of neurofilaments and microtubules with anti-NF160 and anti-MAP2 antibodies.Compared to control findings, all the trauma-only animals showed increased lipid peroxidation levels and the elevations paralleled the amount of force applied. Administration of mexilitine significantly reduced the level of lipid peroxidation. In NF160 stainings, in group 2, the degree of impairment in axonal organization paralleled the different levels of force that were applied. Groups 3C and 3D (mexilitine pretreated) showed well-preserved axons and intact perikarya. In MAP2 stainings group 2 animals showed remarkably less MAP2 staining throughout the sections. There were no significant differences in MAP2 staining intensity or pattern among the group 2 subgroups. In contrast, in the sections from the group 3 animals, the level of MAP2 positivity was markedly preserved.In conclusion, our results show that the cytoskeletal proteins we investigated have different capacities for resisting injury, and that MAP2 is more vulnerable to injury than NF160. One of the reason for this cytoskeletal disruption may be increased lipid peroxidation. Inhibition of lipid peroxidation by pre-treatment with 50-mg/kg mexilitine significantly reduces the level of lipid peroxidation and may protect MAP2 and NF160 integrity in closed mild head injury. This protection is inversely proportional to the magnitude of the applied force. more...