Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.21037/cdt-20-429 http://scihub22266oqcxt.onion/10.21037/cdt-20-429 32968645!7487391!32968645     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32968645&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cardiovasc+Diagn+Ther 2020 ; 10 (4): 892-897 Nephropedia Template TP {{tp|p=32968645|t=2020. Pulmonary vascular endothelial injury and acute pulmonary hypertension caused by COVID-19: the fundamental cause of refractory hypoxemia?|pdf=|usr=}}{{32968645}} gab.com Text Pulmonary vascular endothelial injury and acute pulmonary hypertension caused by COVID-19: the fundamental cause of refractory hypoxemia JO: Cardiovasc Diagn Ther http://www.kidney.de/pget.php?&tw=1&pmid=32968645 #FOAvip Coronavirus disease (COVID-19) is a severe infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that binds to the cells; angiotensin converting enzyme 2 (ACE2) receptor. In the first severe case of COVID-19 in Shenzhen city, we found that in addition to the typical clinical manifestations, our patient presented hemoptysis, refractory hypoxemia and pulmonary fibrosis-like changes on computed tomography (CT) involving alveoli and pulmonary interstitium in the early stage and acute pulmonary hypertension and right heart failure in the later stage, which were not completely justified by myocarditis, acute respiratory distress syndrome (ARDS), pulmonary fibrosis and high PEEP level. The lung compliance deterioration of this patient was not as serious as we expected, indicating classic ARDS was not existed. Simultaneously, the first autopsy report of COVID-19 in China showed normal-structured alveoli and massive thick excretion in the airway. Then, we speculated that the virus not only attacked alveolar epithelial cells, but also affected pulmonary vascular endothelial cells. Imbalance in the ACE2-RAAS- bradykinin axis and the cytokine storm could be an important mechanism leading to pathophysiological changes in pulmonary vascular and secondary refractory hypoxemia. Pulmonary vasculitis or capillaritis associated to immune damage and an inflammatory storm could exist in COVID-19 because of ground-glass opacities in the subpleural area, which are similar to connective tissue disease associated interstitial lung disease (CTD-ILD). Thus, this case elucidates new treatment measures for COVID-19. Twit Text FOAVip Pulmonary vascular endothelial injury and acute pulmonary hypertension caused by COVID-19: the fundamental cause of refractory hypoxemia ????Cardiovasc Diagn Ther http://www.kidney.de/pget.php?&tw=1&pmid=32968645 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32968645 #FOAvip English Wikipedia <ref>{{Cite pmid|32968645}}</ref> Pulmonary vascular endothelial injury and acute pulmonary hypertension caused by COVID-19: the fundamental cause of refractory hypoxemia? #MMPMID32968645 Wang X; Tu Y; Huang B; Li Y; Li Y; Zhang S; Lin Y; Huang L; Zhang W; Luo H Cardiovasc Diagn Ther 2020[Aug]; 10 (4): 892-897 PMID32968645show ga Coronavirus disease (COVID-19) is a severe infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that binds to the cells; angiotensin converting enzyme 2 (ACE2) receptor. In the first severe case of COVID-19 in Shenzhen city, we found that in addition to the typical clinical manifestations, our patient presented hemoptysis, refractory hypoxemia and pulmonary fibrosis-like changes on computed tomography (CT) involving alveoli and pulmonary interstitium in the early stage and acute pulmonary hypertension and right heart failure in the later stage, which were not completely justified by myocarditis, acute respiratory distress syndrome (ARDS), pulmonary fibrosis and high PEEP level. The lung compliance deterioration of this patient was not as serious as we expected, indicating classic ARDS was not existed. Simultaneously, the first autopsy report of COVID-19 in China showed normal-structured alveoli and massive thick excretion in the airway. Then, we speculated that the virus not only attacked alveolar epithelial cells, but also affected pulmonary vascular endothelial cells. Imbalance in the ACE2-RAAS- bradykinin axis and the cytokine storm could be an important mechanism leading to pathophysiological changes in pulmonary vascular and secondary refractory hypoxemia. Pulmonary vasculitis or capillaritis associated to immune damage and an inflammatory storm could exist in COVID-19 because of ground-glass opacities in the subpleural area, which are similar to connective tissue disease associated interstitial lung disease (CTD-ILD). Thus, this case elucidates new treatment measures for COVID-19. äPulmonary vascular endothelial injury and acute pulmonary hypertension(epmc).pdf DeepDyve Pubget Overpricing