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    Alteration of serum and cardiac tissue adropin, copeptin, irisin and TRPM2 expressions in DOX treated male rats
    (Informa Healthcare, 2015) Aydin, S.; Eren, M. N.; Kuloglu, T.; Aydin, S.; Yilmaz, M.; Gul, E.; Kalayci, M.
    Doxorubicin (DOX) cardiotoxicity is a significant side effect in cancer survivors. DOX and its metabolites alter cardiac gene expression and affect metabolic energy-related peptides. Adropin, copeptin, irisin and TRPM2 are produced locally in the heart and play a role in energy homeostasis. We investigated the fates of adropin, copeptin, irisin and TRPM2 in serum and cardiac tissues of DOX treated rats. Animals were divided into three groups of six: 1) untreated controls, 2) DOX treated and 3) saline treated. The rats were fed a standard diet ad libitum for 14 days then were sacrificed and heart and serum samples were taken. Adropin, copeptin, irisin levels in tissue homogenates and serum were measured using ELISA. Immunoreactivity of heart tissue adropin, copeptin, irisin and TRPM2 also were investigated. The peptides increased in both serum and cardiac tissue homogenates in animals treated with DOX compared to the other groups. DOX increased adropin in endocardial and myocardial cells, but it decreased expression of copeptin. DOX did not affect endocardial irisin and TRPM2 expressions, but myocardial irisin and TRPM2 expressions were increased. Serum adropin, irisin and copeptin were increased in DOX treated rats. Cardiac adropin, copeptin, irisin and TRPM2 are affected by DOX and may play a role in DOX cardiotoxicity.
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    Öğe
    How to Increase the Diagnostic Value of Malignancy-related Ascites: Discriminative Ability of the Ascitic Tumour Markers
    (Field House Publishing Llp, 2009) Tuzun, Y.; Yilmaz, M.; Dursun, M.; Canoruc, F.; Celik, Y.; Cil, T.; Boyraz, T.
    Making a differential diagnosis between malignant and non-malignant ascites is an important clinical issue, but cytological examination has a relatively low diagnostic sensitivity. This study aimed to find a discriminative model that distinguished between malignancy-related and non-malignant ascites. The study included 107 patients: 50 with nonmalignant and 57 with malignant ascites. Ascites was analysed using a range of tumour markers and standard cytology. Standardized canonical discriminant function coefficients were used to distinguish between ascites types. The combination of carbohydrate antigen (CA) 15-3, carcinoembryonic antigen (CEA) and cytokeratin 19 fragments (CYFRA-21.1) discriminated between malignancy-related ascites and non-malignant ascites with an accuracy of 98.8% compared with an accuracy of 77.8% for cytological examination. In conclusion, the use of a discriminant function constructed from a combination of CA15-3, CEA and CYFRA-21.1 could distinguish malignant from non-malignant ascites with greater accuracy than cytological examination. Further studies in larger population groups are warranted.