2 Profiting Approaches For Akt inhibitor Which Rarely ever Fails

Paired t-test was used to compare pre- and post-operative values of serum TAC. All P Selleck EPZ-6438 1]. The postoperative period was uneventful without any complication. In 26 cases (n = 86.6%), surgical wound healed within 2 weeks and for remaining four patient it took 3 weeks. Radiation therapy of 55�C65 grays was administered postoperatively to stage III (n = 6) and stage IV (n = 4) cancer patients. One patient with stage III oral carcinoma received both postoperative chemotherapy and radiation therapy as adjuvant treatment. The patients enrolled in the study were followed up for a period of 1-year. There was no mortality during this period. However, find more we could not estimate serum TAC again because of economic constraints and lack of patient compliance. Table 1 Site-wise distribution of oral carcinoma We found the mean value of serum TAC in oral cancer patients was161.9 �� 46.1 ��mol/l. The pre- and post-operative mean value of serum TAC in these patients were 161.9 �� 46.1 and 170.5 �� 45.1 ��mol/l respectively (two tailed P = 0.315). Among these cases, early stage carcinoma (stages I and II) was more common (n = 19, 63.3%). Montelukast Sodium In histology, four different types of squamous cell carcinoma (SCC) were detected viz. well-differentiated (n = 10), moderately differentiated (n = 12), poorly differentiated (n = 6) and verrucous carcinoma (n = 2). The pre- and post-operative serum TAC showed variation in different stages and histological types of cancer [Table 2]. In our study, the habits of smoking (n = 11), tobacco chewing (n = 7), both smoking and tobacco-chewing (n = 4), areca-quid (n = 5) and alcohol consumption (n = 4) were common among oral cancer patients. Table 2 Comparison of pre- and post-operative serum TAC in oral carcinoma patients DISCUSSION Antioxidants are cyto-protective chemicals that prevent the oxidative damage caused by free radicals.[9] Reactive oxygen and nitrogen species are oxygen and nitrogen derived free radicals are generated naturally as by-products of cellular metabolism. Under physiological conditions, the free radicals are rapidly neutralized by antioxidants. In oxidative stress, these free radicals are not counterbalanced adequately and remain in excess to cause damage by reacting with nucleic acids, proteins, polyunsaturated fatty acids and carbohydrates. Oxidative damage is implicated in the pathogenesis of several medical disorders viz. atherosclerosis, cancer, arthritis and neurodegenerative disorders.