Reliability and Validity of Persian Version of State-Trait Anxiety Inventory Among High School Students.

OBJECTIVES: The aim of the present study was to assess the reliability and validity of the Persian version of the State-Trait Anxiety Inventory Form Y (STAI-Y) among high school students. METHODS: A sample of 492 high school students in Kermanshah city, Iran were randomly selected via multistage sampling. They were asked to complete the STAI-Y and Beck Anxiety Inventory (BAI) to determine the correlation coefficients. Data analysis was performed via descriptive statistics, factor analysis, Cronbach's coefficient alpha, and Pearson correlation coefficient. RESULTS: In the Persian version of STAI-Y, the Cronbach's alpha for internal consistency was 0.886 for trait anxiety and 0.846 for state anxiety. The convergent validity between STAI-Y and BAI was 0.612 for trait anxiety and 0.643 for state anxiety (p < 0.001). CONCLUSION: The reliability, internal consistency, and validity of the Persian version of the STAI-Y is good among high school students in Kermanshah.

Mitigation of statins-induced cytotoxicity and mitochondrial dysfunction by L-carnitine in freshly-isolated rat hepatocytes.

Statins are widely used as anti hyperlipidemic agents. Hepatotoxicity is one of their adverse effects appearing in some patients. No protective agents have yet been developed to treat statins-induced hepatotoxicity. Different investigations have suggested L-carnitine as a hepatoprotective agent against drugs-induced toxicity. This study was designed to evaluate the effect of L-carnitine on the cytotoxic effects of statins on the freshly-isolated rat hepatocytes. Hepatocytes were isolated from male Sprague-Dawley rats by collagenase enzyme perfusion via portal vein. Cells were treated with the different concentrations of statins (simvastatin, lovastatin and atorvastatin), alone or in combination with L-carnitine. Cell death, reactive oxygen species (ROS) formation, lipid peroxidation, and mitochondrial depolarization were assessed as toxicity markers. Furthermore, the effects of statins on cellular reduced and oxidized glutathione reservoirs were evaluated. In accordance with previous studies, an elevation in ROS formation, cellular oxidized glutathione and lipid peroxidation were observed after statins administration. Moreover, a decrease in cellular reduced glutathione level and cellular mitochondrial membrane potential collapse occurred. L-carnitine co-administration decreased the intensity of aforementioned toxicity markers produced by statins treatment. This study suggests the protective role of L-carnitine against statins-induced cellular damage probably through its anti oxidative and reactive radical scavenging properties as well as its effects on sub cellular components such as mitochondria. The mechanism of L-carnitine protection may be related to its capacity to facilitate fatty acid entry into mitochondria; possibly adenosine tri-phosphate or the reducing equivalents are increased, and the toxic effects of statins toward mitochondria are encountered.

Potentiation by nitric oxide synthase inhibitor and calcium channel blocker of aspartame-induced antinociception in the mouse formalin test.

By applying a 12 day regimen of the non-calorific sweetener, aspartame, in combination with representative compounds of the calcium channel blocker and nitric oxide synthase inhibitor, we tried to investigate using a formalin-test in mice the relative role of aspartame on pain and its mechanism of action. Verapamil (2, 3.5, 5, 7.5 mg/kg) induced significant (P < 0.01) antinociception in both phases of the formalin test. L-Nitro-arginine-methyl-ester (L-NAME) at the doses used, induced significant (P < 0.01) antinociception in early phase (1, 2, 5, 10 mg/kg) and late phase (5, 10 mg/kg). Twelve days of treatment in animals by aspartame (0.16% w/v) significantly induced antinociception in both phases of the formalin test. Both verapamil (5 mg/kg) and L-NAME (10 mg/kg) significantly (P < 0.01) potentiated aspartame-induced antinociception in both phases of formalin test. The present findings support the hypothesis that the activation of NMDA receptors by aspartame modulates pain-related behaviour via a nitric oxide/cGMP/glutamate release cascade. It is concluded that aspartame would be a good analgesic agent if it would be used in combination with a calcium channel blocker or NOS inhibitor.