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    Crustal deformation and kinematics of the Eastern Part of the North Anatolian Fault Zone (Turkey) from GPS measurements
    (Elsevier, 2012) Tatar, Orhan; Poyraz, Fatih; Gursoy, Halil; Cakir, Ziyadin; Ergintav, Semih; Akpinar, Zafer; Kocbulut, Fikret
    The North Anatolian Fault Zone (NAFZ) is a 1200 km long dextral strike-slip fault zone forming the boundary between the Eurasian and Anatolian plates. It extends from the Gulf of Saros (North Aegean) in the west to the town of Karliova in eastern Turkey. Although there have been numerous geodetic studies concerning the crustal deformation, velocity field and the slip rate of the NAFZ along its western and central segments, geodetic observations along the eastern section of the NAFZ are sparse. In order to investigate the GPS velocities and the slip rate along the eastern part of the NAFZ, a dense GPS network consisting of 36 benchmarks was installed between Tokat and Erzincan on both sides of the fault zone and measured from 2006 to 2008. Measurement results indicate that the slip rate of the NAFZ increases westwards within about 400 km from 16.3 +/- 2.3 mm/year to 24.0 +/- 2.9 mm/year, in consistence with the observation that the Anatolian block is being pulled by the Hellenic trench rather than being pushed by the Arabian plate as a result of continental collision between the Arabian and Eurasian plates in eastern Turkey since late Miocene. Modelling the GPS velocities shows that fault locking depth increases also in the same direction from 8.1 +/- 3.3 km to 12.8 +/- 3.9 km. Slip rate decreases as moving off the Hellenic trench. An average slip rate of 20.1 +/- 2.4 mm/year and a locking depth of 12.5 +/- 3.5 km are also estimated for the entire study area by using all of the GPS measurements obtained in this study. The GPS velocities are in good agreement with the kinematic models created by paleomagnetic studies in the region and complete the overall picture. (C) 2011 Elsevier B.V. All rights reserved.
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    The effect of dexmedetomidine on myocardial ischemia reperfusion injury in streptozotocin induced diabetic rats
    (Anaesthesia Pain & Intensive Care, 2015) Arslan, Mustafa; Poyraz, Fatih; Kiraz, Hasan Ali; Alkan, Metin; Kip, Gulay; Erdem, Ozlem; Ozer, Abdullah
    Objective: Ischemia/reperfusion (I/R) injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. The aim of the present study was to examine the potential cardio-protective effects of dexmedetomidine in a diabetic rat model of myocardial I/R injury. Methodology: A total of 18 streptozotocin (55 mg/kg) induced diabetic Wistar Albino rats were randomly divided into three equal groups as follows: the diabetic I/R group (DIR) in which myocardial I/R was induced by ligating the left anterior descending (LAD) coronary artery for 30 min, followed by 2 hours of reperfusion following left thoracotomy, the diabetic I/R dexmedetomidine group (DIRD) which were given 100 mu g/kg dexmedetomidine intraperitoneally 30 min before I/R induction by the same method and the diabetic control group (DC) which underwent sham operations without tightening of the coronary sutures. As a control group (C), 6 healthy age-matched Wistar Albino rats underwent sham operations similar to DC group. After the operation the rats were sacrificied and the myocardial tissues were histopathologically examined. Results: Microscopic myonecrosis findings were significantly different among groups (p= 0.008). Myonecrosis findings were significantly higher in DIR compared to C, DC and DIRD groups (p= 0.001, p=0.007 and p=0.037 respectively). Similarly microscopic inflammatory cell infiltration degrees showed significant differences among groups (p<0.0001). Compared to C, DC and DIRD groups, the microscopic inflammatory cell infiltration was significantly higher among DIR group (p<0.0001, p<0.0001 and p=0.009 respectively). Also myocardial tissue edema was significantly different among groups (p=0.002). The microscopic myocardial tissue edema levels were significantly higher in DIR group than C and DIRD groups (p<0.0001 and p=0.022 respectively). Tissue edema was also more prominent in DC compared to C group (p=0.022) Conclusion: Taken together our data indicate that dexmedetomidine may be helpful in reducing myocardial necrosis, myocardial inflammation and myocardial tissue edema resulting from ischemia/reperfusion injury.
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    Öğe
    The effect of levosimendan on myocardial ischemia[1] reperfusion injury in streptozotocin-induced diabetic rats
    (Co-Action Publishing, 2015) Kiraz, Hasan Ali; Poyraz, Fatih; Kip, Gülay; Erdem, Özlem; Alkan, Metin; Arslan, Mustafa; Özer, Abdullah
    Objective: Ischemia/reperfusion (I/R) injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. The aim of the present study was to examine the potential cardio protective effects of levosimendan in a diabetic rat model of myocardial I/R injury. Methods: A total of 18 streptozotocin-induced diabetic Wistar Albino rats (55 mg/kg) were randomly divided into three equal groups as follows: the diabetic I/R group (DIR) in which myocardial I/R was induced following left thoracotomy, by ligating the left anterior descending coronary artery for 60 min, followed by 2 h of reperfusion; the diabetic I/R levosimendan group (DIRL), which underwent I/R by the same method while taking levosimendan intraperitoneal 12 mg kg-1; and the diabetic control group (DC) which underwent sham operations without tightening of the coronary sutures. As a control group (C), six healthy age-matchedWistar Albino rats underwent sham operations similar to the DC group. Two hours after the operation, the rats were sacrificed and the myocardial tissue samples were examined by light microscopy for evidence of myonecrosis and inflammatory cell infiltration. Results: Myonecrosis findings were significantly different among groups (p = 0.008). Myonecrosis was more pronounced in the DIR group compared with the C, DC, and DIRL groups (p = 0.001, p = 0.007 and p = 0.037, respectively). Similarly, the degree of inflammatory cell infiltration showed significant difference among groups (p<0.0001). Compared with C, DC, and DIRL groups, the inflammatory cell infiltration was significantly higher among the DIR group (p<0.0001, p<0.0001, and p=0.020, respectively). Also, myocardial tissue edema was significantly different among groups (p=0.006). The light microscopic myocardial tissue edema levels were significantly higher in the DIR group than the C, DC, and DIRL groups (p=0.001, p=0.037, and p=0.014, respectively). Conclusion: Taken together, our data indicate that levosimendan may be helpful in reducing myocardial necrosis, myocardial inflammation, and myocardial tissue edema resulting from ischemia-reperfusion injury. © 2015 Hasan Ali Kiraz et al.
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    Öğe
    The effect of levosinnendan on myocardial ischemia reperfusion injury in streptozotocin-induced diabetic rats
    (Co-Action Publishing, 2015) Kiraz, Hasan Ali; Poyraz, Fatih; Kip, Gulay; Erdem, Ozlem; Alkan, Metin; Arslan, Mustafa; Ozer, Abdullah
    Objective: Ischemia/reperfusion (I/R) injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. The aim of the present study was to examine the potential cardio protective effects of levosimendan in a diabetic rat model of myocardial I/R injury. Methods: A total of 18 streptozotocin-induced diabetic Wistar Albino rats (55 mg/kg) were randomly divided into three equal groups as follows: the diabetic I/R group (DIR) in which myocardial I/R was induced following left thoracotomy, by ligating the left anterior descending coronary artery for 60 min, followed by 2 h of reperfusion; the diabetic I/R levosimendan group (DIRL), which underwent I/R by the same method while taking levosimendan intraperitoneal 12 mu g kg(-1); and the diabetic control group (DC) which underwent sham operations without tightening of the coronary sutures. As a control group (C), six healthy age-matched Wistar Albino rats underwent sham operations similar to the DC group. Two hours after the operation, the rats were sacrificed and the myocardial tissue samples were examined by light microscopy for evidence of myonecrosis and inflammatory cell infiltration. Results: Myonecrosis findings were significantly different among groups (p = 0.008). Myonecrosis was more pronounced in the DIR group compared with the C, DC, and DIRL groups (p = 0.001, p = 0.007 and p = 0.037, respectively). Similarly, the degree of inflammatory cell infiltration showed significant difference among groups (p < 0.0001). Compared with C, DC, and DIRL groups, the inflammatory cell infiltration was significantly higher among the DIR group (p < 0.0001, p < 0.0001, and p = 0.020, respectively). Also, myocardial tissue edema was significantly different among groups (p = 0.006). The light microscopic myocardial tissue edema levels were significantly higher in the DIR group than the C, DC, and DIRL groups (p = 0.001, p = 0.037, and p = 0.014, respectively). Conclusion: Taken together, our data indicate that levosimendan may be helpful in reducing myocardial necrosis, myocardial inflammation, and myocardial tissue edema resulting from ischemia reperfusion injury.