The purpose of this study was to investigate the time course of changes in human tendon properties and metabolism during resistance training and detraining. Nine men (21-27 years) completed 3 months of isometric plantar flexion training and another 3 months of detraining. At the beginning and on every 1 month of training and detraining periods, the stiffness, blood circulation (blood volume and oxygen saturation), serum procollagen type 1 C-peptide (P1P; reflects synthesis of type 1 collagen), echointensity (reflects collagen content), and MRI signal intensity (reflects collagen structure) of the Achilles tendon were measured. Tendon stiffness did not change until 2 months of training, and the increase (50.3%) reached statistical significance at the end of the training period. After 1 month of detraining, tendon stiffness had already decreased to pre-training level. Blood circulation in the tendon did not change during the experimental period. P1P increased significantly after 2 months of training. Echointensity increased significantly by 9.1% after 2 months of training, and remained high throughout the experiment. MRI signal intensity increased by 24.2% after 2 months and by 21.4% after 3 months of training, but decreased to the pre-training level during the detraining period. These results suggested that the collagen synthesis, content, and structure of human tendons changed at the 2-month point of training period. During detraining, the sudden decrease in tendon stiffness might be related to changes in the structure of collagen fibers within the tendon.

Background: This study evaluated the relationship between inflammation, intra-hepatic oxidative stress, oxidative DNA damage and the progression of liver carcinogenesis in hepatitis C virus (HCV)-infected humans.Methods: Non-cancerous liver tissues were collected from 30 patients with an HCV-associated solitary hepatocellular carcinoma (HCC) who received curative tumor removal. After surgery, the patients were followed at monthly intervals at the outpatient clinic. Distribution of the inflammatory cells (CD68+), the number of 8-hydroxydeoxyguanosine (8-OHdG) DNA adducts and 4-hydroxynonenal (HNE) protein adducts and the expression of apurinic/ apyrimidinic endonuclease (APE) were determined by immunohistochemical analysis in serial liver sections from tumor-free parenchyma at the surgical margin around the tumor.Results: Significant positive correlations were observed between the number of CD68+ cells, the amount of HNE protein adducts, and the number of 8-OHdG adducts in liver tissue of patients with HCC and HCV. The cumulative disease-free survival was significantly shorter in patients with the highest percentage of 8-OHdG-positive hepatocytes. Using a Cox proportional hazard model, 8-OHdG, HNE and CD68 were determined to be good biomarkers for predicting disease-free survival in patients with HCC and HCV.Conclusions: These results support the hypothesis that HCV-induced inflammation causes oxidative DNA damage and promotes hepatocarcinogenesis which directly affects the clinical outcome. Since patients with greater intra-hepatic oxidative stress had a higher incidence of HCC recurrence, we suggest that oxidative stress biomarkers could potentially be used as a useful clinical diagnostic tool to predict the duration of disease-free survival in patients with HCV-associated HCC.

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Platelet-dependent thrombin level is enhanced in smokers, even when not smoking, when compared with non-smokers and increases immediately after smoking. Increases in nicotine and cotinine levels caused by smoking induced a prothrombotic state in smokers via increased platelet-dependent thrombogenesis.