Highlights
Muscular contractions stimulate reactive oxygen species production in active muscle fibers and skeletal muscles are a primary source of reactive oxygen species production during exercise.
Prolonged or high intensity exercise can result in both: (1) oxidative damage in skeletal muscle fibers and (2) accelerated muscle fatigue.
Exercise-induced increases in the production of reactive oxygen species in skeletal muscle plays a required role in skeletal muscle adaptation to endurance training.
Based on the available evidence, it appears unlikely that rigorous and prolonged exercise results in an oxidative stress level that is detrimental to human health.
Aim: COVID-19 is a pandemic that causes high morbidity and mortality, especially in severe patients. In this study, we aimed to search and explain the relationship between biochemical markers, which are more common, easily available and applicable to diagnose and to stage the disease. Materials & methods: In this study, 609 patients were evaluated retrospectively. 11 biochemical parameters were included in analysis to explain the relationship with severity of disease. Results: Nearly, all the parameters that have been evaluated in this study were statistically valuable as a predictive parameter for severe disease. Areas under the curve of blood urea nitrogen (BUN)/albumin ratio (BAR), CALL score and lymphocyte/C-reactive protein ratio were 0.795, 0.778 and 0.770. The BUN/BAR and neutrophil/albumin ratios provide important prognostic information for decision-making in severe patients with COVID-19. Conclusion: High BUN/BAR and neutrophil/albumin ratios may be a better predictor of severity COVID-19 than other routinely used parameters in admission.
Mechanical ventilation (MV) is a life-saving intervention for many critically ill patients. Unfortunately, prolonged MV results in rapid diaphragmatic atrophy and contractile dysfunction, collectively termed ventilator-induced diaphragm dysfunction (VIDD). Recent evidence reveals that endurance exercise training, performed prior to MV, protects the diaphragm against VIDD. While the mechanism(s) responsible for this exercise-induced protection against VIDD remain unknown, increased diaphragm antioxidant expression may be required. To investigate the role that increased antioxidants play in this protection, we tested the hypothesis that elevated levels of the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) is required to achieve exercise-induced protection against VIDD. Cause and effect was investigated in two ways. First, we prevented the exercise-induced increase in diaphragmatic SOD2 via delivery of an antisense oligonucleotide targeted against SOD2 post-exercise. Second, using transgene overexpression of SOD2, we determined the effects of increased SOD2 in the diaphragm independent of exercise training. Results from these experiments revealed that prevention of the exercise-induced increases in diaphragmatic SOD2 results in a loss of exercise-mediated protection against MV-induced diaphragm atrophy and a partial loss of protection against MV-induced diaphragmatic contractile dysfunction. In contrast, transgenic overexpression of SOD2 in the diaphragm, independent of exercise, did not protect against MV-induced diaphragmatic atrophy and provided only partial protection against MV-induced diaphragmatic contractile dysfunction. Collectively, these results demonstrate that increased diaphragmatic levels of SOD2 are essential to achieve the full benefit of exercise-induced protection against VIDD.
Previous studies have demonstrated a significant association between red blood cell distribution width (RDW) and acute pulmonary embolism. To the authors' knowledge no study has been reported in patients with deep venous thrombosis (DVT). A total of 431 lower extremity venous duplex examinations were included in the study. Of these, 216 examinations with the diagnosis of DVT were compared to 215 examinations with normal duplex findings with respect to RDW. The two groups were well matched. DVT group had a higher median value and the interquartile range (25th and 75th) of RDW (%) level [14.9 (14.2-16.7)] compared to control group [14.4 (13.6-15.2); P < 0.001], respectively. Patients were divided into tertiles based on RDW. DVT was detected in 42 patients (31.6%) in the lowest tertile, in 81 (53.3%) in the middle tertile, and in 93 (63.7%) in the highest tertile (P < 0.001). In multivariate analysis after adjustment for confounding variables, RDW was the only parameter to predict the presence of DVT [odds ratio (OR) 1.37; 95% confidence interval (CI) 1.21-1.55; P < 0.001]. After removing patients with chronic DVT, the interquartile range (25th and 75th) of the RDW (%) level was also higher in the DVT group [15.0 (14.2-16.7)] compared with the control group [14.4 (13.6-15.2); P < 0.001], respectively. In addition, in proximal DVT, the significant difference continued to be present, although this significance was lost in distal DVT [14.4% (13.6-15.2) vs. 16.1% (15.1-17.4), P < 0.001 and 14.4% (13.6-15.2) vs. 14.3% (14.2-14.7), P = 0.959]. In multivariate analysis, RDW was an independent predictor of risk of proximal DVT (OR 1.60; 95% CI 1.39-1.84; P < 0.001). RDW (%) level was significantly higher in patients with bilateral DVT than in patients with unilateral DVT [16.0 (14.8-17.1) vs. 14.4 (14.2-14.8), P < 0.001, respectively]. In receiver operating characteristics curve analysis, RDW more than 14.9% had 85% sensitivity and 73% specificity in predicting proximal DVT. RDW, an inexpensive and easily measurable laboratory variable, was independently and significantly associated with the presence and severity of DVT, especially nonchronic proximal DVT. The mechanism of association requires, however, further study.
We report a 17-year-old male patient with erythromelanosis follicularis faciei et colli (EFFC), oral leucokeratosis and diabetes mellitus without islet cell antibody. His sister also had minimal findings of EFFC and minimal follicular papules on her shoulders and extensor surfaces of the arms. The father had only fine follicular papules, but no erythromelanosis. Skin and mucous membrane lesions of the proband were investigated histopathologically. Interestingly, in peripheral lymphocyte cultures of the family members, chromosomal breakage was not observed spontaneously, but it was seen with nitrogen mustard, although this disease may be of autosomal recessive inheritance. Thus, we suggest that EFFC may be a polyaetiological disorder (i.e. familial and environmental) and might be considered one of the chromosomal instability syndromes.
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