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10.3390/molecules26010101 http://scihub22266oqcxt.onion/10.3390/molecules26010101 33379366!7794754!33379366     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Molecules 2020 ; 26 (1): ä Nephropedia Template TP {{tp|p=33379366|t=2020. Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity |pdf=|usr=}}{{33379366}} gab.com Text Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity JO: Molecules http://www.kidney.de/pget.php?&tw=1&pmid=33379366 #FOAvip (1) Background: Nicotine is implicated in the SARS-COV-2 infection through activation of the alpha7-nAChR and over-expression of ACE2. Our objective was to clarify the role of nicotine in SARS-CoV-2 infection exploring its molecular and cellular activity. (2) Methods: HBEpC or si-mRNA-alpha7-HBEpC were treated for 1 h, 48 h or continuously with 10(-7) M nicotine, a concentration mimicking human exposure to a cigarette. Cell viability and proliferation were evaluated by trypan blue dye exclusion and cell counting, migration by cell migration assay, senescence by SA-beta-Gal activity, and anchorage-independent growth by cloning in soft agar. Expression of Ki67, p53/phospho-p53, VEGF, EGFR/pEGFR, phospho-p38, intracellular Ca(2+), ATP and EMT were evaluated by ELISA and/or Western blotting. (3) Results: nicotine induced through alpha7-nAChR (i) increase in cell viability, (ii) cell proliferation, (iii) Ki67 over-expression, (iv) phospho-p38 up-regulation, (v) EGFR/pEGFR over-expression, (vi) increase in basal Ca(2+) concentration, (vii) reduction of ATP production, (viii) decreased level of p53/phospho-p53, (ix) delayed senescence, (x) VEGF increase, (xi) EMT and consequent (xii) enhanced migration, and (xiii) ability to grow independently of the substrate. (4) Conclusions: Based on our results and on evidence showing that nicotine potentiates viral infection, it is likely that nicotine is involved in SARS-CoV-2 infection and severity. Twit Text FOAVip Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity ????Molecules http://www.kidney.de/pget.php?&tw=1&pmid=33379366 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33379366 #FOAvip English Wikipedia <ref>{{Cite pmid|33379366}}</ref> Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity #MMPMID33379366 Lupacchini L; Maggi F; Tomino C; De Dominicis C; Mollinari C; Fini M; Bonassi S; Merlo D; Russo P Molecules 2020[Dec]; 26 (1): ä PMID33379366show ga (1) Background: Nicotine is implicated in the SARS-COV-2 infection through activation of the alpha7-nAChR and over-expression of ACE2. Our objective was to clarify the role of nicotine in SARS-CoV-2 infection exploring its molecular and cellular activity. (2) Methods: HBEpC or si-mRNA-alpha7-HBEpC were treated for 1 h, 48 h or continuously with 10(-7) M nicotine, a concentration mimicking human exposure to a cigarette. Cell viability and proliferation were evaluated by trypan blue dye exclusion and cell counting, migration by cell migration assay, senescence by SA-beta-Gal activity, and anchorage-independent growth by cloning in soft agar. Expression of Ki67, p53/phospho-p53, VEGF, EGFR/pEGFR, phospho-p38, intracellular Ca(2+), ATP and EMT were evaluated by ELISA and/or Western blotting. (3) Results: nicotine induced through alpha7-nAChR (i) increase in cell viability, (ii) cell proliferation, (iii) Ki67 over-expression, (iv) phospho-p38 up-regulation, (v) EGFR/pEGFR over-expression, (vi) increase in basal Ca(2+) concentration, (vii) reduction of ATP production, (viii) decreased level of p53/phospho-p53, (ix) delayed senescence, (x) VEGF increase, (xi) EMT and consequent (xii) enhanced migration, and (xiii) ability to grow independently of the substrate. (4) Conclusions: Based on our results and on evidence showing that nicotine potentiates viral infection, it is likely that nicotine is involved in SARS-CoV-2 infection and severity. |Angiotensin-Converting Enzyme 2/metabolism[MESH] |COVID-19/*pathology/virology[MESH] |Cell Line[MESH] |Cell Movement/drug effects[MESH] |Cell Proliferation/drug effects[MESH] |Cell Survival/drug effects[MESH] |Epithelial Cells/*drug effects/virology[MESH] |Humans[MESH] |Nicotine/*adverse effects[MESH] |Receptors, Nicotinic/metabolism[MESH] |Respiratory System/*drug effects/virology[MESH] |SARS-CoV-2/pathogenicity[MESH] |Severity of Illness Index[MESH] |Signal Transduction/drug effects[MESH] |Smoking/adverse effects[MESH]Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS(epmc).pdf DeepDyve Pubget Overpricing