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10.1016/j.mehy.2020.110117 http://scihub22266oqcxt.onion/10.1016/j.mehy.2020.110117 32721809!7367792!32721809     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Med+Hypotheses 2020 ; 143 (ä): 110117 Nephropedia Template TP {{tp|p=32721809|t=2020. Kawasaki-like disease in children with COVID-19: A hypothesis |pdf=|usr=}}{{32721809}} gab.com Text Kawasaki-like disease in children with COVID-19: A hypothesis JO: Med Hypotheses http://www.kidney.de/pget.php?&tw=1&pmid=32721809 #FOAvip With rapid spread of severe acute respiratory syndrome- corona virus-2 (SARS-COV-2) globally, some new aspects of the disease have been reported. Recently, it has been reported the incidence of Kawasaki-like disease among children with COVID-19. Since, children had been known to be less severely affected by the virus in part due to the higher concentration of Angiotensin converting enzyme (ACE)-2 receptor, this presentation has emerged concerns regarding the infection of children with SARS-COV2. ACE2 has anti-inflammatory, anti-fibrotic and anti-proliferative characteristics through converting angiotensin (Ag)-II to Ang (1-7). ACE2 receptor is downregulated by the SARS-COV through the spike protein of SARS-CoV (SARS-S) via a process that is tightly coupled with Tumor necrosis factor (TNF)-alpha production. TNF-alpha plays a key role in aneurysmal formation of coronary arteries in Kawasaki disease (KD). Affected children by COVID-19 with genetically-susceptible to KD might have genetically under-expression of ACE2 receptor that might further decrease the expression of ACE2 due to the downregulation of the receptor by the virus in these patients. It appears that TNF- alpha might be the cause and the consequence of the ACE2 receptor downregulation which results in arterial walls aneurysm. Conclusion: Genetically under-expression of ACE2 receptor in children with genetically-susceptible to KD who are infected with SARS-CoV-2 possibly further downregulates the ACE2 expression by TNF-alpha and leads to surge of inflammation including TNF-alpha and progression to Kawasaki-like disease. Twit Text FOAVip Kawasaki-like disease in children with COVID-19: A hypothesis ????Med Hypotheses http://www.kidney.de/pget.php?&tw=1&pmid=32721809 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32721809 #FOAvip English Wikipedia <ref>{{Cite pmid|32721809}}</ref> Kawasaki-like disease in children with COVID-19: A hypothesis #MMPMID32721809 Amirfakhryan H Med Hypotheses 2020[Oct]; 143 (ä): 110117 PMID32721809show ga With rapid spread of severe acute respiratory syndrome- corona virus-2 (SARS-COV-2) globally, some new aspects of the disease have been reported. Recently, it has been reported the incidence of Kawasaki-like disease among children with COVID-19. Since, children had been known to be less severely affected by the virus in part due to the higher concentration of Angiotensin converting enzyme (ACE)-2 receptor, this presentation has emerged concerns regarding the infection of children with SARS-COV2. ACE2 has anti-inflammatory, anti-fibrotic and anti-proliferative characteristics through converting angiotensin (Ag)-II to Ang (1-7). ACE2 receptor is downregulated by the SARS-COV through the spike protein of SARS-CoV (SARS-S) via a process that is tightly coupled with Tumor necrosis factor (TNF)-alpha production. TNF-alpha plays a key role in aneurysmal formation of coronary arteries in Kawasaki disease (KD). Affected children by COVID-19 with genetically-susceptible to KD might have genetically under-expression of ACE2 receptor that might further decrease the expression of ACE2 due to the downregulation of the receptor by the virus in these patients. It appears that TNF- alpha might be the cause and the consequence of the ACE2 receptor downregulation which results in arterial walls aneurysm. Conclusion: Genetically under-expression of ACE2 receptor in children with genetically-susceptible to KD who are infected with SARS-CoV-2 possibly further downregulates the ACE2 expression by TNF-alpha and leads to surge of inflammation including TNF-alpha and progression to Kawasaki-like disease. |*Models, Immunological[MESH] |*Pandemics[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Asia/epidemiology[MESH] |Betacoronavirus/*physiology[MESH] |COVID-19[MESH] |Child[MESH] |Coronary Vessels/immunology/pathology[MESH] |Coronavirus Infections/*complications/epidemiology/genetics[MESH] |Cytokine Release Syndrome/etiology[MESH] |Disease Progression[MESH] |Endothelium, Vascular/virology[MESH] |Genetic Predisposition to Disease[MESH] |Humans[MESH] |Inflammation[MESH] |Macrophage Activation[MESH] |Mucocutaneous Lymph Node Syndrome/epidemiology/*etiology/genetics/immunology[MESH] |Netherlands/epidemiology[MESH] |Peptidyl-Dipeptidase A/biosynthesis/genetics/physiology[MESH] |Pneumonia, Viral/*complications/epidemiology/genetics[MESH] |Receptors, Virus/biosynthesis/genetics/physiology[MESH] |SARS-CoV-2[MESH] |Seasons[MESH] |Spike Glycoprotein, Coronavirus/physiology[MESH] |Tumor Necrosis Factor-alpha/physiology[MESH]Kawasaki-like disease in children with COVID-19: A hypothesis (epmc).pdf DeepDyve Pubget Overpricing