he comparison between previous reported hepatic and the present blood transcriptome. Our study demonstrated that RES supplementation might improve the resistance to metabolism dysfunction via mitochondrial energy synthesis and/or the respiratory chain (e.g., ATPase).

The recent emergence and rapid global spread of coronavirus disease 2019 (COVID-19) is leading to public health crises worldwide. Alcohol consumption and cigarette smoking (CS) are two known risk factors in many diseases including respiratory infections.

We performed a multi-center study in the four largest hospitals designated for COVID-19 patients in Wuhan. There are totally 1547 patients diagnosed with COVID-19 enrolled in the study, alcohol consumption and CS history were evaluated among these patients. The epidemiology, laboratory findings and outcomes of patients contracted COVID-19 were further studied.

Our findings indicated that COVID-19 patients with a history of CS tend to have more severe outcomes than non-smoking patients. However, alcohol consumption did not reveal significant effects on neither development of severe illness nor death rates in COVID-19 patients.

CS is a risk factor for developing severe illness and increasing mortality during the SARS-CoV-2 infection. We believe that our findings will provide a better understanding on the effects of alcohol intake and CS exposure in COVID-19 patients.

CS is a risk factor for developing severe illness and increasing mortality during the SARS-CoV-2 infection. We believe that our findings will provide a better understanding on the effects of alcohol intake and CS exposure in COVID-19 patients.Novel coronavirus disease (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Its impact on patients with comorbidities is clearly related to fatality cases, and diabetes has been linked to one of the most important causes of severity and mortality in SARS-CoV-2 infected patients. Substantial research progress has been made on COVID-19 therapeutics; however, effective treatments remain unsatisfactory. This unmet clinical need is robustly associated with the complexity of pathophysiological mechanisms described for COVID-19. Several key lung pathophysiological mechanisms promoted by SARS-CoV-2 have driven the response in normoglycemic and hyperglycemic subjects. There is sufficient evidence that glucose metabolism pathways in the lung are closely tied to bacterial proliferation, inflammation, oxidative stress, and pro-thrombotic responses, which lead to severe clinical outcomes. It is also likely that SARS-CoV-2 proliferation is affected by glucose metabolism of type I and type II cells. This review summarizes the current understanding of pathophysiology of SARS-CoV-2 in the lung of diabetic patients and highlights the changes in clinical outcomes of COVID-19 in normoglycemic and hyperglycemic conditions.In endotherms, growth, reproduction, and survival are highly depended on energy metabolism. Maintenance of constant body temperature can be challenging for endotherms under continuously changing environmental conditions, such as low or high ambient temperatures or limited food. Thus, many birds may drop body temperature below normothermic values during the night, known as rest-phase hypothermia, presumably to decrease energy metabolism. Under the assumption of the positive link between aerobic metabolism and reactive oxygen species, it is reasonable to suggest that low body temperature, a proxy of energy metabolism, will affect oxidative stress of the birds. Aging may considerably affect behavior, performance and physiology in birds and still requires further investigation to understand age-specific changes along the lifespan of the organism. Until today, age-specific rest-phase hypothermic responses and their effect on oxidant-antioxidant status have never been investigated. We exposed 25 zebra finches (Taenpothesis on how aging may lead to an accumulation of oxidative damage; the impaired physiological capacity to thermoregulate with advancing age does increase the risk of oxidative stress under challenging conditions. When energy is limited, the risk to encounter oxidative stress is increasing via a compensation to defend normothermic body temperatures.Background This study examines the effects of sports drinks ingestion during high-intensity exercise for carbohydrate oxidation rate (CHO-O) among athletes. Methods PubMed, Embase, and the Cochrane library were searched for available papers published up to November 2019. The primary outcome is the carbohydrate oxidation rate (CHO-O), and the secondary outcome is the fat oxidation rate (Fat-O). Statistical heterogeneity among the included studies was evaluated using Cochran’s Q test and the I2 index. The random-effects model was used for all analyses, regardless of the I2 index. Results Five studies are included, with a total of 58 participants (range, 8-14/study). All five studies are randomized crossover trials. Compared to the control beverages, sports drinks have no impact on the CHO-O of athletes [weighted mean difference (WMD) = 0.29; 95% CI, -0.06 to 0.65, P = 0.106; I2 = 97.4%, P less then 0.001] and on the Fat-O of athletes (WMD = -0.074; 95% CI, -0.19 to 0.06, P = 0.297; I2 = 97.5%, P less then 0.001). Carbohydrate-electrolyte solutions increase CHO-O (WMD = 0.47; 95% CI, 0.08-0.87, P = 0.020; I2 = 97.8%, P less then 0.001) but not Fat-O (WMD = -0.14; 95% CI, -0.31 to 0.03, P = 0.103; I2 = 98.2%, P less then 0.001). Caffeine has a borderline effect on Fat-O (WMD = 0.05; 95% CI, 0.00-0.10, P = 0.050). Conclusions Compared with the control beverages, sports drinks show no significant improvement in CHO-O and Fat-O in athletes. Carbohydrate-electrolyte solutions increase CHO-O in athletes but not Fat-O.Over the years, various studies have been dedicated to the mathematical modeling of gas transport and exchange in the lungs. Indeed, the access to the distal region of the lungs with direct measurements is limited and, therefore, models are valuable tools to interpret clinical data and to give more insights into the phenomena taking place in the deepest part of the lungs. In this work, a new computational model of the transport and exchange of a gas species in the human lungs is proposed. It includes (i) a method to generate a lung geometry characterized by an asymmetric branching pattern, based on the values of several parameters that have to be given by the model user, and a method to possibly alter this geometry to mimic lung diseases, (ii) the calculation of the gas flow distribution in this geometry during inspiration or expiration (taking into account the increased resistance to the flow in airways where the flow is non-established), (iii) the evaluation of the exchange fluxes of the gaseous species of interest between the tissues composing the lungs and the lumen, and (iv) the computation of the concentration profile of the exchanged species in the lumen of the tracheobronchial tree. Even if the model is developed in a general framework, a particular attention is given to nitric oxide, as it is not only a gas species of clinical interest, but also a gas species that is both produced in the walls of the airways and consumed within the alveolar region of the lungs. First, the model is presented. Then, several features of the model, applied to lung geometry, gas flow and NO exchange and transport, are discussed, compared to existing works and notably used to give new insights into experimental data available in the literature, regarding diseases, such as asthma, cystic fibrosis, and chronic obstructive pulmonary disease.We previously constructed a perspiration ratemeter for the measurement of palmar sweating in human subjects. Although galvanic skin response (GSR) has been used to evaluate emotional responses in human subjects, little is known about the relationships between the phasic and baseline components in GSR and active palmar sweating. From the aforementioned, we aimed to investigate the relationships in human subjects with handgrip exercise and eyes closing or opening. Fifteen healthy volunteers (mean age 26.9 ± 8.7 years) participated in the present experiments. We investigated the effects of maximal handgrip exercise, eyes closing or opening, and self-awareness of drowsy on the GSR, active palmar sweating, R-R interval in electrocardiograph (ECG), and percentage of α wave in EEG. The faster phasic component in GSR completely agreed with the starting point of active palmar sweating. Handgrip exercise induced significantly faster spike in GSR, active palmar sweating, and decrease in R-R interval in ECG. Eyes closinginess in human subjects.Left ventricular (LV) myocardial dysfunction occurs after myocardial infarction (MI) is associated with the location, infarct size, and transmurality degrees of MI. The myocardial strain is a sensitive index used for the quantification of myocardium dysfunction. This study used Tissue-Tracking to evaluate whether the different location of MI would result in different myocardial dysfunction. One hundred patients diagnosed with MI who underwent cardiovascular magnetic resonance examination were included. The tissue-tracking indices, LV global radial strain (GRS), global circumferential strain (GCS), global longitudinal strain (GLS), and the infarct size (IS,% of LV mass) were quantified. There were 42 cases of anterior wall MI (AWMI) and 58 cases of non-anterior wall MI (NAWMI). The GCS of AWMI was significantly lower than that of NAWMI (P = 0.036). In the same level of infarct size, the myocardial strain of AWMI was not significantly different from NAWMI group (P > 0.05). The GRS and GCS were significantly different between transmurality > 50% group with transmurality ≤ 50% group (P less then 0.05). The present study demonstrated that LV MI is associated with reduced myocardial strain, and the infarct size and degrees of transmurality were both related to the decline of myocardial strain in patients with MI.A wide range of arrhythmogenic phenotypes have been associated with heterogeneous mechanical dyskinesis. Pro-arrhythmic effects are often associated with dysregulated intra-cellular calcium handling, especially via the development of intra- and inter-cellular calcium waves. Experimental evidence suggests that mechanical strain can contribute to the generation and maintenance of these calcium waves via a variety of mechano-electric coupling mechanisms. Most model studies of mechano-electric coupling mechanisms have been focused on mechano-sensitive ion channels, even though experimental studies have shown that intra- and inter-cellular calcium waves triggered by mechanical perturbations are likely to be more prevalent pro-arrhythmic mechanisms in the diseased heart. A one-dimensional strongly coupled computational model of electromechanics in rabbit ventricular cardiomyocytes showed that specific myocyte stretch sequences can modulate the susceptibility threshold for delayed after-depolarizations. In simulations of mechanically-triggered calcium waves in cardiomyocytes coupled to fibroblasts, susceptibility to calcium wave propagation was reduced as the current through the gap junction caused current drain from the myocytes. In 1D multi-cellular arrays coupled via gap junctions, mechanically-induced waves may contribute to synchronizing arrhythmogenic calcium waves and after-depolarizations.