BackgroundTransitional cell carcinoma (TCC) accounts for around 95% of bladder cancers and is the 4th most common cancer among men and the tenth most common in women, in the US. There is a constant need to clarify current TCC incidence and mortality rates among different population groups for better clinical practice guidelines. We aimed to describe the TCC incidence and incidence-based mortality by demographic and tumor-related characteristics over the last 40 years in the US.MethodsWe obtained data from the SEER 18 registries to study TCC cases that were diagnosed between the years 1973 and 2014. We calculated incidence rates and incidence-based mortality rates in different demographic and tumor-related characteristics and expressed rates by 100,000 person-years. We then calculated the annual changes in incidence and incidence-based mortality rates and displayed them as annual percent changes (APCs).ResultsThere were 182,114 patients with TCC between 1973 and 2014 in the United States. Overall incidence rates of TCC increased 0.16% (95% CI, 0.02–0.30, p = .02) per year over the study period. However, the incidence declined significantly since 2007; (95%CI,-1.89- -0.77, p < .001), except among the elderly and African Americans, which increased significantly over the study period. Overall TCC mortality rates did not change over the study period. However, since 2000 it started to decrease significantly.ConclusionTCC incidence and incidence-based mortality rates had been showing significant increases over the previous decades. However, significant declines in both incidence and incidence-based mortality rates have been observed over the recent years, except in some patients with certain racial groups. Improved understanding of the etiological and ecological factors of TCC could lead to further declines in incidence and incidence-based mortality rates.Electronic supplementary materialThe online version of this article (10.1186/s12885-019-5267-3) contains supplementary material, which is available to authorized users.

Age-related myocardial dysfunction has important implications with impaired redox homeostasis. Current study focused on investigation of redox homeostasis and histopathological changes in the myocardium of mimetically (MA), naturally aged (NA), and young control (YC) rats. Chronic D-galactose administration to young male Wistar rats (5 months old) was used to set up experimental aging models. We investigated 16 different oxidative damage biomarkers which have evaluated redox homeostasis of cellular macromolecules such as protein, lipid, and DNA. As a protein oxidation biomarker, advanced oxidation end products, protein carbonyl groups, protein-bound advanced glycation end products, dityrosine, kynurenine, and N-formylkynurenine concentrations in MA and NA rats were found to be significantly higher compared to those in YC rats. On the other hand, the levels of protein thiol groups were not significantly different between groups, whereas lipid peroxidation biomarkers such as conjugated diens, lipid hydroperoxides, and malondialdehyde in MA and NA rats were found to be significantly higher in comparison to those in YCs. For the assessment of oxidative DNA damage, we analyzed eight hydroxy-5'-deoxyguanosine concentrations of MA and NA groups which were higher than YCs. As an antioxidant status in the MA and NA groups, Cu-Zn superoxide dismutase, ferric reducing antioxidant power, and total thiol levels were lower than those in the YCs. Only nonprotein thiol levels were not significantly different. We also observed similar histopathological changes in MA and NA rats. We concluded that the mimetic aging model could be considered as a reliable experimental model for myocardial senescence.

No abstract

No abstract

Objective. Endocan has been shown to be a marker for several cancers and may show degree of malignancy. The aim of this study is to assess tissue levels of endocan in common brain tumors, namely, meningiomas, low-grade gliomas (LGGs), and high-grade gliomas (HGGs). Patients and Methods. Endocan was assayed by commercially available enzyme linked immunosorbent assay (ELISA) kits in a total of 50 brain tumors (20 meningiomas, 19 LGGs, and 20 HGGs) and 15 controls. The results were compared to control brain tissues. Results. Each tumor group showed significant higher levels of endocan compared to controls (p < 0.05). In addition, endocan levels showed steady increase from the least (meningiomas) to the most (HGGs) malignant tumors and positive correlation was noted between the degree of malignancy and endocan level (p = 0.0001). Conclusion. Endocan, a vital molecule for angiogenesis, is expressed in common brain tumors and results suggest that endocan could be a marker for malignancy.