Evaluation of quality of life issues after different management policies for vestibular schwannomas: what are we measuring?

PURPOSE: To compare the different quality of life measures used to report the outcomes of the different forms of management of vestibular schwannomas.METHODS: Literature search and critical evaluation of outcome measures and comparison between different studies.RESULTS: A total number of 6749 patients were included in 31 studies. Eighteen studies used the SF36 forms, 17 - custom questionnaires, 7 - the GBI and 8 used various other questionnaires. The most commonly reported handicaps included hearing loss, facial nerve paralysis, tinnitus, gait and balance disorders, pain and headache, psychological and cognitive problems, loss of taste and lacrimation and facial hypoesthesia.CONCLUSIONS: When evaluating QOL issues in patients with vestibular schwannoma, the type of intervention as well as the pre-interventional status should be considered. More specific comprehensive systems of evaluation should be devised through the cooperation of multiple centers with different management policies and variable patient populations as well

Spectrophotometric Determination of Trimipramine in Tablet Dosage Form via Charge Transfer Complex Formation

Purpose: To develop and validate simple, rapid and sensitive spectrophotometric procedures for determination of trimipramine in tablet dosage form.Methods: The methods were based on the interaction of trimipramine as n-electron donor with the ο-acceptor, iodine and various π-acceptors, namely: chloranil (CH), chloranilic acid (ChA), 2,3-dichloro-5, 6-dicyano-1, 4-benzoquinone (DDQ), and 7, 7,8, 8 tetracyanoquinodimethane (TCNQ), to form charge transfer complexes. The complexes obtained were measured spectrophotometrically at 292, 220, 520, 302, and 824 nm for I2, CH, ChA, DDQ, and TCNQ, respectively. Different variables affecting the reaction were carefully studied and optimized.Results: Beer's law was obeyed over the concentration ranges 1 - 5, 5 - 50, 15 - 100, 5- 50, and 10 -75 ppm for I2, CH, ChA, DDQ, and TCNQ respectively, with apparent molar absorptivities of 7.1 x 104, 0.3 x 104, 1.6 x 104, 0.26 x 104, and 0.1 x 104 l mol-1cm-1 respectively. The proposed methods were successfully applied to the determination of trimipramine with good accuracy and precision.Conclusion: The results demonstrated that the developed methods are as accurate, precise and reproducible as the pharmacopeial method. The methods would be valuable for routine application in quality control.Keywords: Charge-transfer complex, Trimipramine, Spectrophotometry (T and S

THERAPEUTIC POTENCY OF SWEET ORANGE JUICE OVER LIVER GENOTOXICITY INDUCED BY PESTICIDE LANNATE IN RATS

Objective: The aim of the present investigation was to study the potential effect of sweet orange juice against liver genotoxicity induced by lannate. Methods: adult 36 female rats were divided into 6 groups: group C (control group), group L (lannate group) injected intraperitoneal (i. p.) with 1 mg/kg b. wt. lannate for one day, group J (orange juice group) orally administered a dose of 0.1 ml/10 g b. wt. of orange juice for 48 h, group J+L received the orange juice prior to lannate, group J with L received lannate in continuous with the orange juice and group L+J received lannate prior to the orange juice. Tested parameters were DNA fragmentation, micronucleus, histopathology examination and biochemical analysis. Results: it was found that, the intake of lannate caused high DNA fragmentation and significant increase (P<0.001) in the number of micronucleated polychromatic erythrocytes in the bone marrow. Furthermore, lannate exhibited some pathological changes in the liver tissues as well as a significant (P<0.001) decrease in the total antioxidative capacity (TAC) and a significant increase in the total oxidative capacity (TOC). On the other hand, orange juice administration of all treatments (pre-treatment, continuous and post-treatment) gave some amelioration against liver damage induced by lannate. While the best results were evidenced in the continuous treatment group where the juice could attenuate liver DNA fragmentation and significantly decreased (P<0.001) the number of micronucleated polychromatic erythrocytes. In addition, it improved the induced degenerative histopathological changes as well as ameliorated the changes occurred in TAC and TOC significantly (P<0.001). Conclusion: the antigenotoxic impact of orange juice against lannate was therapeutic and hence can counteract the poisonous effect of the pesticide in people who exposed to it

Hepatocarcinogenic potential of the glucocorticoid antagonist RU486 in B6C3F1 mice: effect on apoptosis, expression of oncogenes and the tumor suppressor gene p53

BACKGROUND: Glucocorticoids inhibit hepatocellular proliferation and modulate the expression of oncogenes and tumor suppressor genes via mechanisms involving the glucocorticoid receptor. Glucocorticoids also produce a receptor-mediated inhibitory effect on both basal and hormone-stimulated expression of a newly discovered family of molecules important for shutting off cytokine action. We therefore hypothesized that inhibiting glucocorticoid receptors may disturb hepatocellular growth and apoptosis. Consequently, we investigated the effect of RU486, a potent antagonist of the glucocorticoid receptor, on basal levels of hepatocellular proliferation and apoptosis in male B6C3F1 mice. Furthermore, we evaluated the effect of this compound on cellular genes involved in the regulation of these important processes. RESULTS: Data show that treatment of male B6F3C1 mice with RU486 (2 mg/kg/d, ip) for 7 days dramatically inhibited liver cell proliferation by about 45% and programmed hepatocellular death by approximately 66%. RU 486 also significantly increased hepatic expression of the oncogenes mdm2 and JunB, while reducing that of the tumor suppressor gene p53. CONCLUSION: Exposure to RU486 may ultimately enhance the susceptibility of the liver to cancer risk by diminishing its ability to purge itself of pre-cancerous cells via apoptosis. This effect may be mediated through increases in the hepatic expression of the oncogene mdm2, coupled with decreases in that of the tumor suppressor gene p53. The decrease in hepatocellular proliferation caused by RU 486 may be related to effects other than its anti-glucocorticoid activity

Inhibition of Carrageenan-Induced Cutaneous Inflammation by PPAR Agonists Is Dependent on Hepatocyte-Specific Retinoid X ReceptorAlpha

It has been proposed that PPAR-dependent, accelerated catabolism of proinflammatory mediators may contribute to the fast resolution of inflammation. Because retinoid X receptors are obligate heterodimer partners of PPARs, we investigated the impact of deleting hepatocyte-specific RXRα on the antiedema effect of PPAR agonists. In wild-type mice (WT), pretreatment with the PPARα agonist perfluorooctanoic acid diminished carrageenan-induced paw edema by 66 ± 10%. This effect was essentially absent (13 ± 8%) in hepatocyte-specific RXRα-deficient mice. Similarly, pretreatment of WT mice with the PPARδ agonist L-783483 or the PPARγ agonist L-805645 caused 54 ± 1% and 38 ± 8% reduction in carrageenan-induced paw edema, respectively. These effects were also significantly diminished or absent in hepatocyte-specific RXRα-deficient mice. In contrast, aspirin reduced carrageenan-induced paw edema equally in WT and hepatocyte-specific RXRα-deficient mice. The identification of RXRα as an important factor involved in the antiedema effect produced by agonists of the three PPAR subtypes is a significant achievement towards the goal of designing novel, effective anti-inflammatory drugs