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.

suck abstract from ncbi


10.1038/s41586-021-03569-1

http://scihub22266oqcxt.onion/10.1038/s41586-021-03569-1
suck pdf from google scholar
33915568!8814825!33915568
unlimited free pdf from europmc33915568    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi

pmid33915568
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • A molecular single-cell lung atlas of lethal COVID-19 #MMPMID33915568
  • Melms JC; Biermann J; Huang H; Wang Y; Nair A; Tagore S; Katsyv I; Rendeiro AF; Amin AD; Schapiro D; Frangieh CJ; Luoma AM; Filliol A; Fang Y; Ravichandran H; Clausi MG; Alba GA; Rogava M; Chen SW; Ho P; Montoro DT; Kornberg AE; Han AS; Bakhoum MF; Anandasabapathy N; Suarez-Farinas M; Bakhoum SF; Bram Y; Borczuk A; Guo XV; Lefkowitch JH; Marboe C; Lagana SM; Del Portillo A; Tsai EJ; Zorn E; Markowitz GS; Schwabe RF; Schwartz RE; Elemento O; Saqi A; Hibshoosh H; Que J; Izar B
  • Nature 2021[Jul]; 595 (7865): 114-119 PMID33915568show ga
  • Respiratory failure is the leading cause of death in patients with severe SARS-CoV-2 infection(1,2), but the host response at the lung tissue level is poorly understood. Here we performed single-nucleus RNA sequencing of about 116,000 nuclei from the lungs of nineteen individuals who died of COVID-19 and underwent rapid autopsy and seven control individuals. Integrated analyses identified substantial alterations in cellular composition, transcriptional cell states, and cell-to-cell interactions, thereby providing insight into the biology of lethal COVID-19. The lungs from individuals with COVID-19 were highly inflamed, with dense infiltration of aberrantly activated monocyte-derived macrophages and alveolar macrophages, but had impaired T cell responses. Monocyte/macrophage-derived interleukin-1beta and epithelial cell-derived interleukin-6 were unique features of SARS-CoV-2 infection compared to other viral and bacterial causes of pneumonia. Alveolar type 2 cells adopted an inflammation-associated transient progenitor cell state and failed to undergo full transition into alveolar type 1 cells, resulting in impaired lung regeneration. Furthermore, we identified expansion of recently described CTHRC1(+) pathological fibroblasts(3) contributing to rapidly ensuing pulmonary fibrosis in COVID-19. Inference of protein activity and ligand-receptor interactions identified putative drug targets to disrupt deleterious circuits. This atlas enables the dissection of lethal COVID-19, may inform our understanding of long-term complications of COVID-19 survivors, and provides an important resource for therapeutic development.
  • |*Single-Cell Analysis[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |Alveolar Epithelial Cells/pathology/virology[MESH]
  • |Atlases as Topic[MESH]
  • |Autopsy[MESH]
  • |COVID-19/immunology/*pathology/*virology[MESH]
  • |Case-Control Studies[MESH]
  • |Female[MESH]
  • |Fibroblasts/pathology[MESH]
  • |Fibrosis/pathology/virology[MESH]
  • |Humans[MESH]
  • |Inflammation/pathology/virology[MESH]
  • |Lung/*pathology[MESH]
  • |Macrophages, Alveolar/pathology/virology[MESH]
  • |Macrophages/pathology/virology[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Plasma Cells/immunology[MESH]
  • |SARS-CoV-2/*pathogenicity[MESH]
  • |T-Lymphocytes/immunology[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    114 7865.595 2021