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Period Express Estimation in Lively Syndication Techniques Taking into consideration Multiple Uncertainties.
DNA methylation, besides being considered as a biomarker to predict the risk of obesity and T2D, has been suggested also as a target for dietary and pharmacological treatments. The present observations may suggest further interventions in order to improve the outcome of COVID-19 in people affected by diabetes.According to WHO the worst of the COVID-19 pandemic is yet to come. Despite of the exceptional measures being undertaken by regulatory agencies to expedite vaccine development, we may be several months if not years away from an effective vaccine. In such unprecedented times, the only resort nations have at their disposal is to identify and repurpose existing drugs against COVID-19 based on their known clinical or pharmacological profile which can provide direct or corroborative evidence of favorable benefit risk in the management of COVID-19. Immune-mediated inflammation remains the hallmark of severe complications related to COVID-19 and while corticosteroids have shown preliminary evidence of benefit, they can act like a double-edged sword for majority of COVID-19 patients. Therefore, there is a need to identify 'non-steroid' potent and safe anti-inflammatory agents for use in therapeutic armamentarium against COVID-19. This article makes a case for one such existing drug, roflumilast, that can emerge as a steroid-sparing alternative against COVID-19.(1) Background RNA viruses and especially coronaviruses could act inside host cells not only by building their own proteins, but also by perturbing the cell metabolism. We show the possibility of miRNA-like inhibitions by the SARS-CoV-2 concerning for example the hemoglobin and type I interferons syntheses, hence highly perturbing oxygen distribution in vital organs and immune response as described by clinicians; (2) Hypothesis We hypothesize that short RNA sequences (about 20 nucleotides in length) from the SARS-CoV-2 virus genome can inhibit the translation of human proteins involved in oxygen metabolism, olfactory perception and immune system. (3) Methods We compare RNA subsequences of SARS-CoV-2 protein S and RNA-dependent RNA polymerase genes to mRNA sequences of beta-globin and type I interferons; (4) Results RNA subsequences longer than eight nucleotides from SARS-CoV-2 genome could hybridize subsequences of the mRNA of beta-globin and of type I interferons; (5) Conclusions Beyond viral protein production, COVID-19 might affect vital processes like host oxygen transport and immune response.Recently, a new coronavirus (SARS-CoV-2) was discovered in China. Due to its high level of contagion, it has already reached most countries, quickly becoming a pandemic. Although the most common symptoms are related to breathing problems, SARS-CoV-2 infections also affect the gastrointestinal tract culminating in inflammation and diarrhea. However, the mechanisms related to these enteric manifestations are still not well understood. Evidence shows that the SARS-CoV-2 binds to the angiotensin-converting enzyme receptor 2 (ACE2) in host cells as a viral invasion mechanism and can infect the lungs and the gut. Other viruses have already been linked to intestinal symptoms through binding to ACE2. In turn, this medical hypothesis article conjectures that the ACE2 downregulation caused by the SARS-CoV-2 internalization could lead to decreased activation of the mechanistic target of mTOR with increased autophagy and lead to intestinal dysbiosis, resulting in diarrhea. Besides that, dysbiosis can directly affect the respiratory system through the lungs. Although there are clues to other viruses that modulate the ACE2/gut/lungs axis, including the participation of autophagy and dysbiosis in the development of gastrointestinal symptoms, there is still no evidence of the ACE2/mTOR/autophagy pathway in SARS-CoV-2 infections. Thus, we propose that the new coronavirus causes a change in the intestinal microbiota, which culminates in a diarrheal process through the ACE2/mTOR/autophagy pathway into enterocytes. Our assumption is supported by premises that unregulated intestinal microbiota increases the susceptibility to other diseases and extra-intestinal manifestations, which can even cause remote damage in lungs. These putative connections lead us to suggest and encourage future studies aiming at assessing the aforementioned hypothesis and regulating dysbiosis caused by SARS-CoV-2 infection, in order to confirm the decrease in lung injuries and the improvement in the prognosis of the disease.The outbreak of coronavirus disease 2019 (COVID-19) requires urgent need for effective treatment. Severe COVID-19 is characterized by a cytokine storm syndrome with subsequent multiple organ failure (MOF) and acute respiratory distress syndrome (ARDS), which may lead to intensive care unit and increased risk of death. While awaiting a vaccine, targeting COVID-19-induced cytokine storm syndrome appears currently as the efficient strategy to reduce the mortality of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The stress-responsive enzyme, heme oxygenase-1 (HO-1) is largely known to protect against inflammatory response in animal models. HO-1 is induced by hemin, a well-tolerated molecule, used for decades in the treatment of acute intermittent porphyria. Experimental studies showed that hemin-induced HO-1 mitigates cytokine storm and lung injury in mouse models of sepsis and renal ischemia-reperfusion injury. Furthermore, HO-1 may also control numerous viral infections by inhibiting virus replication. In this context, we suggest the hypothesis that HO-1 cytoprotective pathway might be a promising target to control SARS-CoV-2 infection and mitigate COVID-19-induced cytokine storm and subsequent ARDS.Inflammation occurs when the material is implanted into the body. As one of the important immune cells in the regulation of inflammation, macrophages are able to remove pathogens and necrotic cells, and polarize to different phenotypes to regulate inflammatory response for tissue regeneration. Therefore, it is known that the sequential release of immunomodulatory cytokines from the surface of titanium (Ti) implants can regulate the polarization of macrophages and promote osseointegration of implants. In order to control the switch of macrophage phenotypes at desired time, we fabricated hydroxyapatite (HAp) nanotube arrays coating on Ti surface, by acid-etching, alkali-heating and HAp coating sequentially. Then we loaded the interleukin-4 (IL-4) encapsulated by poly (lactic-co-glycolic acid) (PLGA) on the bottom of the nanotube and the interferon-γ (IFN-γ) encapsulated by sodium hyaluronate (SH) on the top of the nanotube. click here Based on the physical and chemical properties of PLGA and SH and the spatial distribution of loaded cytokines, we hypothesized that the programmed release of IFN-γ and IL-4, which made the phenotypic transition of macrophages at a specific time, so as to regulate inflammation and promote osteogenic repair.
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