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Whether the QT interval displays circadian rhythm after heart rate correction is unresolved and the relationship of QT interval to heart rate variability (HRV) is uncertain.<br /><br /> To test the hypothesis that there is a circadian rhythm to QT interval and HRV and determine the relationship between QTc and HRV.<br /><br /> The hourly average ECG data from 24-h ECGs were examined in individuals (50 without medications and 9 on beta blockers only) with no evidence of coronary artery disease or structural heart disease. The QT duration of normal QRS complexes from a series of 30-s windows was measured. The presence of circadian rhythm was tested by the data analytic approach of goodness of fit to a cosine function.<br /><br /> QT interval with and without heart rate correction showed a circadian rhythm for five heart rate adjustment formulae except for the Bazett formula. HRV also showed circadian rhythm but with different acrophages and nadirs depending on the HRV component. There were significant (p&lt;0.05) positive correlations of QTc with pNN50 rms-SD and SDNN and significant (p&lt;0.05) negative correlations with SDANN and Tri. The beta blocker group did not generally show circadian rhythm for QT interval or HRV.<br /><br /> QT, after heart rate adjustment, and HRV have circadian rhythmicity. There are significant correlations between QT interval and HRV indices. Circadian rhythm was blunted with beta blockers. The data are consistent with the concept of a predominance of parasympathetic activity to increase QTc and sympathetic activity to shorten QTc, even after 'correction' of the QT interval for heart rate.<br /><br />QT, after heart rate adjustment, and HRV have circadian rhythmicity. There are significant correlations between QT interval and HRV indices. Circadian rhythm was blunted with beta blockers. The data are consistent with the concept of a predominance of parasympathetic activity to increase QTc and sympathetic activity to shorten QTc, even after 'correction' of the QT interval for heart rate.Oxidative stress is one of the major causes of cellular senescence in mammalian cells. The excess amount of reactive oxygen species generated by oxygen metabolism is pathogenic and facilitates tissue aging. Lung tissue is more susceptible to oxidative stress than other organs because it is directly exposed to environmental stresses. The aging of lung tissues increases the risk of chronic diseases. Senescent cells accumulate in tissues during aging and contribute to aging-associated morbidity; however, the roles of cellular senescence in lung aging and diseases have not yet been elucidated in detail. To clarify the physiological role of oxidative stress-induced cellular senescence in aging-associated declines in pulmonary function, we herein investigated the effects of the antioxidant N-acetyl-L-cysteine (NAC) on lung cellular senescence and aging in mice. The administration of NAC to 1-year-old mice reduced the expression of senescence-associated genes in lung tissue. Pulmonary function and lung morphology were partly restored in mice administered NAC. Collectively, these results suggest that oxidative stress is a major inducer of cellular senescence in vivo and that the control of oxidative stress may prevent lung aging and diseases.Methylene blue (MB) is a blue cationic thiazine dye and currently used in different medical settings. Notably, there have been several attempts to introduce MB for attenuating pain in the last decade. Some clinical studies reported remarkable results, which, however, have been much debated. In addition, accumulating evidence have revealed that MB diminishes voltage-gated sodium channel currents. Accordingly, in the present study, we conducted in vivo experiments, including in vivo single nerve recording and behavioral test, to investigate whether MB dampens neural firing rates and ultimately contributes to pain relief. As a result, neural firing rates significantly decreased and finally converged to zero after MB administration. This event lasted longer than that of lidocaine and was dose-dependently modulated. Furthermore, there was a marked improvement in pain behaviors. The withdrawal threshold and latency of hind paws significantly rose post-MB administration. Therefore, these results demonstrate that MB lessens pain by significantly weakening neural excitability, which implies a strong possibility that this dye may be developed as a pain-relieving medication in the future. This is the first in vivo study to elucidate the effect of MB on nerves and pain relief.<br /><br /> Lysyl oxidase (LOX) is a metalloenzyme that requires Cu as a cofactor and it is responsible for the formation of collagen and elastin cross-linking. The objective of this work was to measure the LOX enzyme activity in the heart of bovines with Cu deficiency induced by high molybdenum and sulfur levels in the diet.<br /><br /> Eighteen myocardial samples were obtained from Cu-deficient (n = 9) and control (n = 9) Holstein bovines during two similar assays. The samples were frozen in liquid nitrogen and stored at -70 °C to measure enzymatic activity. A commercial kit was used, following producer instructions.<br /><br /> The results showed that LOX activity from the hearts of Cu-deficient bovines is 29 % lower than the ones of control bovines, being this difference statistically significant (p = 0.03).<br /><br /> To our knowledge, this is the first report that determined LOX enzymatic activity in bovine heart of Cu-deficient animals. The microscopic alterations found in these animals in our previous work, could be explained by a diminished LOX activity. The results are in agreement with other authors, who found a relationship between LOX activity and dietary Cu intake. [https://www.selleckchem.com/products/azd9291.html AZD9291] The information provided by this work could help to clarify the pathogenesis of cardiac lesions in cattle with dietary Cu deficiency.<br /><br />To our knowledge, this is the first report that determined LOX enzymatic activity in bovine heart of Cu-deficient animals. The microscopic alterations found in these animals in our previous work, could be explained by a diminished LOX activity. The results are in agreement with other authors, who found a relationship between LOX activity and dietary Cu intake. The information provided by this work could help to clarify the pathogenesis of cardiac lesions in cattle with dietary Cu deficiency.