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10.1007/s11481-021-10012-9 http://scihub22266oqcxt.onion/10.1007/s11481-021-10012-9 34757528!8579188!34757528     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34757528&cmd=llinks): Failed to open stream: HTTP request failed! 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Network Meta-analysis on the Changes of Amyloid Precursor Protein Expression Following SARS-CoV-2 Infection |pdf=|usr=}}{{34757528}} gab.com Text Network Meta-analysis on the Changes of Amyloid Precursor Protein Expression Following SARS-CoV-2 Infection JO: J Neuroimmune Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=34757528 #FOAvip SARS-CoV-2 infection begins with the attachment of its spike (S) protein to angiotensin-converting enzyme-2 (ACE2) followed by complex host immune responses with cardiovascular and neurological implications. Our meta-analyses used QIAGEN Ingenuity Pathway Analysis (IPA) and Knowledge Base (QKB) to investigate how the expression of amyloid precursor protein (APP) was modulated by attachment of SARS-CoV-2 S protein in the brain microvascular endothelial cells (BMVECs) and during COVID-19 in progress. Published 80 host response genes reported to be modulated in BMVECs following SARS-CoV-2 S protein binding were used to identify key canonical pathways and intermediate molecules mediating the regulation of APP production following the attachment of S protein to endothelial cells. This revealed that the attachment of SARS-CoV-2 S protein may inhibit APP expression in the BMVECs. Our results shed light on the molecular mechanisms by which SARS-CoV-2 infection may potentiate the incidence of stroke by inhibiting the production of APP in the BMVECs. We also analyzed molecules associated with COVID-19, which revealed six upstream regulators, TNF, IFNG, STAT1, IL1beta, IL6, and STAT3. The upstream regulators mediate the increased production of APP via intermediators, with eleven regulated by all six upstream regulators. These COVID-19 upstream regulators increased APP expression with a statistically significant Z-score of 3.705 (p value = 0.000211). These findings have revealed molecular mechanisms by which COVID-19 disease may lead to long-term neurological manifestations resulting from the elevated APP expression in line with immune response in the host. Altogether, our study revealed two distinct scenarios which may have differential impact on APP expression. Twit Text FOAVip Network Meta-analysis on the Changes of Amyloid Precursor Protein Expression Following SARS-CoV-2 Infection ????J Neuroimmune Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=34757528 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34757528 #FOAvip English Wikipedia <ref>{{Cite pmid|34757528}}</ref> Network Meta-analysis on the Changes of Amyloid Precursor Protein Expression Following SARS-CoV-2 Infection #MMPMID34757528 Camacho RC; Alabed S; Zhou H; Chang SL J Neuroimmune Pharmacol 2021[Dec]; 16 (4): 756-769 PMID34757528show ga SARS-CoV-2 infection begins with the attachment of its spike (S) protein to angiotensin-converting enzyme-2 (ACE2) followed by complex host immune responses with cardiovascular and neurological implications. Our meta-analyses used QIAGEN Ingenuity Pathway Analysis (IPA) and Knowledge Base (QKB) to investigate how the expression of amyloid precursor protein (APP) was modulated by attachment of SARS-CoV-2 S protein in the brain microvascular endothelial cells (BMVECs) and during COVID-19 in progress. Published 80 host response genes reported to be modulated in BMVECs following SARS-CoV-2 S protein binding were used to identify key canonical pathways and intermediate molecules mediating the regulation of APP production following the attachment of S protein to endothelial cells. This revealed that the attachment of SARS-CoV-2 S protein may inhibit APP expression in the BMVECs. Our results shed light on the molecular mechanisms by which SARS-CoV-2 infection may potentiate the incidence of stroke by inhibiting the production of APP in the BMVECs. We also analyzed molecules associated with COVID-19, which revealed six upstream regulators, TNF, IFNG, STAT1, IL1beta, IL6, and STAT3. The upstream regulators mediate the increased production of APP via intermediators, with eleven regulated by all six upstream regulators. These COVID-19 upstream regulators increased APP expression with a statistically significant Z-score of 3.705 (p value = 0.000211). These findings have revealed molecular mechanisms by which COVID-19 disease may lead to long-term neurological manifestations resulting from the elevated APP expression in line with immune response in the host. Altogether, our study revealed two distinct scenarios which may have differential impact on APP expression. |*COVID-19/metabolism[MESH] |Amyloid beta-Protein Precursor/*metabolism[MESH] |Endothelial Cells/*metabolism/virology[MESH] |Humans[MESH] |Network Meta-Analysis[MESH] |SARS-CoV-2[MESH]Network Meta-analysis on the Changes of Amyloid Precursor Protein Expr(epmc).pdf DeepDyve Pubget Overpricing