Methamphetamine causes lipid peroxidation and an increase in superoxide dismutase activity in the rat striatum

The administration of methamphetamine to experimental animals results in damage to nigrostriatal dopaminergic neurons. In the present study, we demonstrated that both the acute repeated and the chronic administration of methamphetamine causes an increase in thiobarbituric acid reactive substances, which are indicators of lipid peroxidation, and superoxide dismutase activity in the rat striatum. The results of present study strengthen the notion that reactive oxygen species may play an important role in the methamphetamine-induced neurotoxicity.     

Small arterial elasticity predicts the extent of coronary artery disease: Relationship with serum uric acid

BackgroundArterial elasticity has been previously linked to atherosclerotic vascular disease states. Serum uric acid level has been recently associated with increased arterial stiffness, but to what extent serum uric acid reflects angiographic coronary artery status and vessel compliance remains to be established. In this study we aimed to evaluate the association of arterial elasticity indexes, serum uric acid and the presence and extent of angiographic coronary artery disease (CAD) in patients with chronic stable angina.MethodsOne hundred and eight consecutive patients attending for elective coronary angiography were investigated. The severity of CAD was expressed using the Gensini score. Quantitative analysis of the arterial elasticity was performed by applanation tonometry. Serum uric acid was measured in all participants. Stepwise multiple linear regression analysis was used to identify the independent correlates of the Gensini score.ResultsAfter adjustment for age, gender, common cardiac risk factors and cardiovascular drugs, small artery elasticity index (SAEI) (p < 0.001) and serum uric acid (p < 0.001) were independently correlated with the severity of CAD. Stepwise multiple linear regression analysis was also used to identify independent correlates of the SAEI. Serum uric acid emerged as the only independent correlate of SAEI (p < 0.001).ConclusionsSAEI independently reflects the extent of CAD in patients with chronic stable angina. This relationship is chiefly mediated by serum uric acid. Our data add to the growing evidence that serum uric acid may be a marker of arterial stiffness and atherosclerotic burden.     

The first Susac's syndrome case in Turkey

Susac's syndrome is a vasospastic disease resulting from bilateral microangiopathy of the brain, cochlea and retina. It is characterized by encephalopathy, bilateral sensorineural fluctuating hearing loss and visual loss. It is very uncommon and usually affects women during young adulthood. Since all three symptoms of the triad may not be present, the clinical diagnosis is difficult. Therefore, neuroimaging, particularly magnetic resonance imaging, has an important role in establishing the diagnosis. In this case report, we present a young woman who had all the symptoms of Susac's syndrome. This is the first Susac's syndrome case reported in Turkey.     

5-Fluorouracil induces arterial vasoconstrictions but does not increase angiotensin II levels

Because the mechanisms of 5-Fluorouracil (5-FU) cardiotoxicity have not yet been completely identified, prophylactic options are not available. To our knowledge, there are no published data investigating the use of angiotensin converting enzyme (ACE) inhibitors for 5-Fluorouracil-associated cardiotoxicity. In this study, we aimed to evaluate the influence of 5-FU administration on the diameter of the brachial artery and the levels of angiotensin II. The patients were administered bolus 5-FU/leucovorin in the study group. Angiotensin II and troponin T assays, complete blood cell counts, hepatic and renal function tests were analyzed in five consecutive blood samples in the initiation, just after termination, and on 24, 48, and 72 h after termination of the regimen. Pre- and post-treatment angiotensin II and troponin T assays, complete blood cell counts, hepatic and renal function tests were also analyzed in the control group. Brachial arterial diameters were measured and recorded in all patients before and after the treatment. A total of 59 patients were included in this study. Thirty one out of 59 patients (52.5%) were in the 5-FU study group and the remaining 28 patients (47.5%) were in the control group. Basal and post-treatment brachial artery diameters in the 5-FU study group were 0.436 ± 0.51 and 0.423 ± 0.50 cm, respectively (P = 0.001). The corresponding values in the controls were 0.3954 ± 0.50 and 0.3957 ± 0.49 cm, basal and post-treatment, respectively (P = 0.979). Angiotensin II levels were not changed significantly at serial measurements (P = 0.496). Moreover, the corresponding measurements were not statistically different in both two groups treated with and without 5-FU (P = 0.372). The pathophysiology of 5-FU-induced cardiac toxicity has not yet been elucidated. In the present study, 5-FU-associated vasoconstriction was not dependent on angiotensin II levels, thus we suggest that the prophylactic administration of ACE inhibitors cannot prevent cardiotoxicity in these patients. The underlying mechanisms of cardiotoxicity related to 5-FU might be multifactorial; nevertheless, further prospective investigation for the toxic effects of fluoropyrimidines on the coronary endothelium and myocardium are needed.     

Preclinical safety evaluation of intravitreal injection of full-length humanized vascular endothelial growth factor antibody in rabbit eyes

PURPOSE: To evaluate the preclinical safety of intravitreal bevacizumab, which is a full-length humanized monoclonal antibody against the vascular endothelial growth factor (VEGF), in rabbit eyes over a short-term period. METHODS: Twenty-four rabbits were divided into two groups, each with two subgroups. The first group (groups 1 and 2) received 1.25 mg (0.05 mL) intravitreal bevacizumab, and the second group (groups 3 and 4) received 3.00 mg (0.12 mL) intravitreal bevacizumab. The right eyes were designated as the study eyes, and the left eyes served as a control and received the same volume of saline intravitreally. Groups 1 and 3 were labeled as early groups and scheduled to be terminated at 14 days. Groups 2 and 4, labeled as late groups, were scheduled to be terminated at 28 days. Besides electroretinography (ERG) and visually evoked potentials (VEP), central corneal thickness, intraocular pressure, fundus photography, and anterior segment imaging were performed at baseline and scheduled time points. Enucleated eyes were preserved for light and electron microscopic investigation. RESULTS: No anterior segment inflammation was observed, except in one eye in group 1 which showed a uveitic reaction. No evidence of retinal toxicity was seen with intravitreal bevacizumab at doses of 1.25 and 3.00 mg, by either ERG or light microscopy. Electron microscopic assessment revealed mitochondrial damage in the inner segments of photoreceptors. Immunohistochemical staining with bax and caspase-3 and -9 showed intensive apoptotic protein expression in all study sections and minimal expression in the control eyes. CONCLUSIONS: Although electrophysiologic investigation and light microscopy showed normal retinal function and structure, mitochondrial disruption in the inner segments of photoreceptors was detected by electron microscopy, and apoptotic expression was detected after the injection of intravitreal bevacizumab.     

The mean platelet volume in patients with essential and white coat hypertension

Mean platelet volume (MPV), a determinant of platelet function, is a newly emerging risk factor for atherothrombosis. The risk profile of white coat hypertension has not yet been completely clear. The present study was designed to evaluate MPV in white coat hypertensive subjects compared with essential hypertensive patients and normotensive subjects. We selected 36 essential hypertensive patients, 36 white coat hypertensive subjects and 36 normotensive control subjects matched for age, gender, and body mass index. MPV was very significantly higher in essential hypertensives and white coat hypertensives than in normotensives (P < 0.00); it was also higher in essential hypertensives than in white coat hypertensives (P < 0.05). Platelet counts were not different among the study groups (P > 0.05). MPV was positively correlated with ambulatory diastolic blood pressure in essential hypertension and white coat hypertension groups (P < 0.05). In conclusion, our data suggests one possible mechanism by which white coat hypertensive subjects may be at increased cardiovascular risk.     

Ectopic Thyroid Gland on the Ascending Aorta with a Partial Pericardial Defect: Report of a Case

Intrathoracic ectopic goiters are rare. To our knowledge, only two reports of thyroid tissue on the aorta have been reported in the English literature. A 42-year-old woman was found to have a right paracardiac mass. Sternotomy revealed a firm and encapsulated tumor attached to the anterolateral surface of the ascending aorta and a defect in the right superior part of the pericardium. The mass was completely excised and histopathologic examination confirmed a multinodular goiter. We discuss the features of this rare tumor.     

Acute exhaustive exercise does not alter lipid peroxidation levels and antioxidant enzyme activities in rat hippocampus, prefrontal cortex and striatum

Although regular physical exercise is beneficial to the body, it is well known that exhaustive exercise causes oxidative stress in muscle. Recent studies suggest that regular moderate physical exercise has the beneficial effects on brain. However, there is little information regarding whether or not exhaustive exercise could generate oxidative stress in brain and the findings are conflicting. The aim of this study was to investigate the effects of exhaustive exercise on thiobarbituric acid reactive substances, as an indicator of lipid peroxidation, in the hippocampus, prefrontal cortex and striatum. Additionally we examined antioxidant enzymes activities, superoxide dismutase and glutathione peroxidase, to assess the effects of reactive oxygen species. Exhaustive exercise did not change superoxide dismutase and glutathione peroxidase enzyme activities and thiobarbituric acid reactive substances levels neither immediately (0 min) nor at 3, 6, 12, 24 and 48 h after the cessation of exercise in the brain. These results indicate that acute exhaustive exercise may not cause significant lipid peroxidation in the hippocampus, prefrontal cortex and striatum during the post-exercise period.