COVID-19 is associated with acute and lethal pneumonia, causing the severe acute respiratory syndrome (SARS), which is not confined to the respiratory tract, as demonstrated by clinical evidence of the involvement of multiple organs, including the central nervous system (CNS). In this context, we hypothesized that both oligosymptomatic and symptomatic patients present an imbalance in the microbiota-gut (immune system) and nervous system axis, worsening the clinical picture. The brain constantly receives a direct and indirect influence from the intestine, more specifically from the immune system and intestinal microbiota. The presence of SARS-CoV-2 in the intestine and CNS, can contribute to both neurological disorders and gut immune system imbalance, events potentialized by an intestinal microbiota dysbiosis, aggravating the patient's condition and causing more prolonged harmful effects.Statistics released by the World Health Organization in 2018 show that the total death of people is 56.9 million worldwide in 2016. The first one is cardiovascular diseases, including ischemic heart disease and stroke, which accounted for 17.65 million people (31%) [1]. Treadmill Exercise Test is suitable for measuring the changes in Electrocardiography (ECG) initial, middle, and after exercise [2]. They are using it to distinguish chest pain without apparent causes, judging the severity of coronary artery disease, and screening personnel with coronary artery disease risk factors. The most important contribution of this study is to use the Hilbert Huang Transform (HHT) [3], a non-invasive method, to decompose the original ECG signals of inspectors through the Empirical Mode Decomposition (EMD) [4-7], not the commonly used of 12-lead ECG detection method. There is a total of 49 participants in 24 pseudo-positive persons; 4 were re-judged into positive, reducing 83.3% pseudo-positive persons who need to do the follow-up testing, significantly reducing the consumption of medical and time.Oral submucous fibrosis is the direct consequence of a sustained pro-inflammatory environment characterized by excessive collagen deposition causing tissue fibrosis, and progressive degeneration of vital structures including muscle. The pathogenesis of oral submucous fibrosis is largely mediated by the pro-inflammatory, pro-fibrotic cytokines, excessive oxidative stress, abnormal angiogenesis, and epithelial to mesenchymal transition. Mesenchymal stem cells largely known for their regenerative potential have shown to have an immunomodulatory, anti-fibrotic, anti-oxidative, and angiogenic potential. Thus, mesenchymal stem cells, when introduced in an oral submucous fibrosis micro-environment, could potentially counter the progressive fibrosis. The present hypotheses discuss the various pathogenic aspects of oral submucous fibrosis and the properties of mesenchymal stem cells which could aid in halting the disease progression.Toll-like receptor 7 is critical in recognition of single strand RNA viruses, including SARS CoV-2, and generation of anti-viral immunity.  https://www.selleckchem.com/pharmacological_MAPK.html  Coronaviruses evolved strategies to dampen the host immunity. Herein, we discuss the potential use of TLR7 agonists in the early stages of COVID-19 treatment.In the advent of COVID-19 pandemic, testing is highly essential to be able to identify, isolate, treat infected persons, and finally curb transmission of this infectious respiratory disease. Group testing has been used previously for various infectious diseases and recently reported for large-scale population testing of COVID-19. However, possible sample dilution as a result of large pool sizes has been reported, limiting testing methods' detection sensitivity. Moreover, the need to sample all individuals prior to pooling overburden the limited resources such as test kits. An alternative proposed strategy where test is performed on pooled samples from individuals representing different households is presented here. This strategy intends to improve group testing method through the reduction in the number of samples collected and pooled during large-scale population testing. Moreover, it introduces database system which enables continuous monitoring of the population's virus exposure for better decision making.We are proposing optimal training conditions that can lead to an increase in the number of serial sarcomeres (SSN) and muscle fascicle length (FL) in spastic muscles. Therapeutic interventions for increasing FL in clinical populations with neurological origin, in whom relative shortness of muscle fascicles contributed to the presentation of symptoms such as spasticity, contracture, and limited functional abilities, do not generally meet these conditions, and therefore, result in less than satisfactory outcomes. Based on a review of literature, we argue that protocols of exercise interventions that led to sarcomerogenesis, and increases in SSN and FL in healthy animal and human models satisfied three criteria 1) all involved eccentric exercise at appropriately high velocity; 2) resulted in positive strain of muscle fascicles; and 3) momentary deactivation in the stretched muscle. Accordingly, to increase FL in spastic muscles, new exercise protocols in which the three presumed criteria are satisfied, must be developed, and long-term muscle architectural and functional adaptations to such trainings must be examined.Chloroquine (CQ) and hydroxychloroquine (HCQ) were among the first drugs repurposed for the treatment of SARS-CoV-2 infection. A few in vitro studies confirmed that both drugs exhibited dose dependent anti-SARS-CoV-2 activities. These observations and the encouraging results from early poorly conducted observational studies created a major hype about the therapeutic potential of these drugs in the treatment of COVID-19 disease. This was further catalyzed by media and political influences leading to a widespread use of these agents. Subsequent randomized trials revealed lack of efficacy of these agents in improving the outcomes of COVID-19 or in preventing infection in post-exposure prophylaxis studies. Nevertheless, many ongoing trials continue to actively recruit tens of thousands of patients to receive HCQ worldwide. In this perspective, we address the possible mechanisms behind the lack of efficacy and the increased risk of cardiac toxicity of HCQ in COVID-19 disease. For the lack of efficacy, we discuss the fundamental differences of treatment initiation between in vitro and in vivo studies, the pitfalls of the pharmacological calculations of effective blood drug concentrations and related dosing regimens, and the possible negative effect of HCQ on the antiviral type-I interferon response.