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    Öğe
    Acute toxic effects of methyl alcohol on the rat brain: The protective effects of caffeic acid phenethyl ester
    (Acta Medica Mediterranea, 2014) Çevik M.U.; Varol S.; Yücel Y.; Akil E.; Uzar E.; Kaplan I.; Can Y.U.
    Background: Efficiency of caffeic acid phenethyl ester (CAPE) in reducing free radicals generated by oxidative stress has been previously reported. In the present study, the protective effect of CAPE on methyl alcohol (MeOH) induced oxidative damages on rat brain were presented. Methods: The rats were randomly divided into four groups as follows: Control, methotrexate (MTX) alone, MTX+MeOH, and MTX+MeOH+CAPE (CAPE treatment). All animals except the control group were treated with MTX for 7 days. MTX was diluted in sterile saline and administered (0.3 mg/kg/day) intraperitoneally (ip). At the eighth day, MeOH was administered (3gm/Kg) (ip) in MeOH+MTX and CAPE treatment groups. Four hours after MeOH administration in the CAPE group rats were treated with 10 ?mol/kg CAPE (ip), serum physiologic (i.p.) in MeOH+MTX group. After eight hours, rats were anaesthetized and sacrificed. Malondialdehyde (MDA) levels, paraoxonase-1 (PON-1. activity were measured on the cerebral tissue. Results: MTX+MeOH group compared to the MTX alone group; a statistically significant increase in MDA levels (p= 0.042. were detected. In addition, MTX+MeOH group than MTX MTX alone group in led to a statistically significant decrease in PON-1 activity (p= 0.018.. CAPE treatment, significantly decrease in MDA levels was compared with MeOH+MTX (p= 0.001.. However, CAPE treatment caused an increase on PON-1 activity in MeOH group, which was statistically significant (p= 0.009.. Conclusion: Consequently, it was demonstrated for the first time that CAPE prevents acute MeOH intoxication induced brain injury by reducing the increase in lipid peroxidation, and elevating the decrease in PON-1 activity.
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    Öğe
    Heparin-induced thrombocytopenia and cerebrovasculer thromboembolia
    (2007) Al B.; Akil A.; Aritürk Z.; Akil E.
    Heparin-lnduced Thrombocytopenia is formed as a result of heparin and platelet- factor 4 complexes and the complex which antibodies interaction against. It threats life by causing artery and venous thromboembolia. It is diagnosed with clinical findings and the laboratory consequences that support clinical findings. When it is diagnosed the heparin therapy must be stopped. Nowadays, there are many drugs used as anticoagulation therapy such as lepirudin, argatroban danaparoid,-bivalurudin and fondaparinux. In this study, we discussed a patient with unstable angina pectoris in whom Heparin-lnduced Thrombocytopenia and cerebrovasculer thromboembolia was developed after heparin was applied.
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    Öğe
    The plasma level of parathormon and homocysteine in migraine patients; Another aspect on migraine-stroke associaton
    (Acta Medica Mediterranea, 2015) Varol S.; Akil E.; Yunce M.; Kaplan B.; Özdemir H.H.; Arslan D.; Yilmaz A.
    The pathogenesis of migraine has been well studied and it is associated with oxidative stress, neurogenic inflammation, and endothelial dysfunction. To the best of our knowledge, no studies have focused on the impact of the parathormone (PTH) and homocysteine levels in migrane patients. To determine migraine-stroke association, our study focused on the levels of PTH and homocysteine in the blood of migraine patients. Fifty five migraine patients in the presence or absence of aura were included. The patients in the migraine group were divided into subgroups: (I) migraine in the attack period (with and without aura) (n = 23), and (II) migraine in the interictal period (with and without aura) (n = 32). As a control, 30 healthy volunteers were also enrolled in the study. As a result, we found that PTH and homocysteine levels of the migraine patients were increased significantly when compared with healthy volunteers (p = 0.001). The PTH and homocysteine levels of the patients with aura were higher than patients without aura in the migraine group (p < 0.05). There were no statistically significant differences between PTH/homocysteine levels and migraine duration or migraine attack frequency (p > 0.05). There was a positive correlation between PTH and homocysteine levels in the migraine patients (p = 0.001, r = 0.49). To summarize, we found statistically significant increases in PTH and homocysteine blood levels of migraine patients versus healthy volunteers. These results may help to understand the pathogenesis of migraine ischemia, and potentially identify new prognostic markers for this condition.