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Image Search Results
Journal: BMC Microbiology
Article Title: A genomic analysis of Mycobacterium immunogenum strain CD11_6 and its potential role in the activation of T cells against Mycobacterium tuberculosis
doi: 10.1186/s12866-019-1421-y
Figure Lengend Snippet: Representation of common membrane proteins in all organisms
Article Snippet: 9. , Fig. 033285: Conserved
Techniques: Membrane
Journal: Annals of diagnostic pathology
Article Title: The differential immune response in mild versus fatal SARS-CoV2 infection.
doi: 10.1016/j.anndiagpath.2022.152032
Figure Lengend Snippet: Fig. 1. Viral findings in mild versus severe SARS-CoV2 infection. The control lungs showed no viral protein or RNA (panel A) whereas the lung tissue from someone who died of COVID-19 showed high viral RNA (panel B) and the spike protein subunit 2 (panel C) in the same alveolar wall distribution. Similarly, note the absence of the viral spike protein in the uninfected nasopharynx swab (panel D) and the strong signal for spike subunit 1 (panel E) and spike subunit 2 proteins (panel F) in glandular cells from a person with mild disease. NP – nasopharyngeal, NL – normal control, and the signal is brown due to DAB with hematoxylin counterstain. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Article Snippet:
Techniques: Infection, Control
Journal: Annals of diagnostic pathology
Article Title: The differential immune response in mild versus fatal SARS-CoV2 infection.
doi: 10.1016/j.anndiagpath.2022.152032
Figure Lengend Snippet: Fig. 2. Immune response in mild versus fatal SARS-CoV2 infection. The figure shows a graphic representation of the fold changes from baseline in the naso pharyngeal swabs positive for SARS-CoV2 (blue columns) as well as the lung tissues from fatal COVID-19 that either had very high copy SARS-CoV2 (orange columns) or were not associated with SARS-CoV2 infec tion (gray columns). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Article Snippet:
Techniques: Infection
Journal: Annals of diagnostic pathology
Article Title: The differential immune response in mild versus fatal SARS-CoV2 infection.
doi: 10.1016/j.anndiagpath.2022.152032
Figure Lengend Snippet: Fig. 4. In situ demonstration of the clotting and complement activation in the fatal COVID-19 lungs. Note the absence of complement component 6 in the normal lung (panel A) as well as the lung from a fatal COVID-19 case that did not contain detectable SARS-CoV2 RNA (panel B). Panel C shows that the signal for complement component 6 in the COVID-19 lung tissue associated with high SARS-CoV2 copy number localizes only to the alveolar septa (arrows) which also shows a strong signal for fibrinogen (panel D); no signal is evident in the small vessels (oval). Panel E shows the lack of signal for CD41 in the normal lung controls. In comparison, note the CD41+ platelet aggregates in the small vessels in a lung from a person who died of COVID-19 associated with high viral copy number (panel F) as well as from the same lung that was not associated with SARS-CoV2 infection (panel G). However, note that the CD41 signal localizes only to the alveolar septa in the lung with high copy SARS-CoV2 (arrow, panel F). Co-localization of CD41 (fluorescent red) with SARS-CoV2 RNA (fluorescent green) documents that CD41 strongly co-expressed with the viral RNA in the lung samples with high copy viral RNA (seen as fluorescent yellow, panel H). NL – normal control, and the signal in panels A–D is brown due to DAB and fast red in panels E–G with hematoxylin counterstain. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Article Snippet:
Techniques: In Situ, Coagulation, Activation Assay, Comparison, Infection, Control
Journal: Annals of diagnostic pathology
Article Title: The differential immune response in mild versus fatal SARS-CoV2 infection.
doi: 10.1016/j.anndiagpath.2022.152032
Figure Lengend Snippet: Fig. 3. In situ demonstration of the immune response in mild versus fatal SARS-CoV2 infection. Note the absence of a CD3 response in the uninfected nasopharynx swab (panel A) and the strong infiltration by these cells in an infected swab from a person with mild disease (panel B). Similarly, the control nasopharynx sample shows no PDL1 expression (panel C) whereas the infected nasopharynx shows a strong PDL1 response (panel D). Note that the lung from a fatal COVID-19 case not associated with viral infection did show a strong CD8 response (panel E) whereas this lung tissue from someone who died of COVID-19 that was strongly positive for SARS-CoV2 did not show a CD8 response (panel F). The control lungs showed a very weak PDL1 signal (panel G) whereas the COVID-19 lungs with high viral copy number did show strong PDL1 expression (panel H). NP – nasopharyngeal, NL – normal control, and the signal is brown due to DAB with hematoxylin counterstain. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Article Snippet:
Techniques: In Situ, Infection, Control, Expressing
Journal: Annals of diagnostic pathology
Article Title: The differential immune response in mild versus fatal SARS-CoV2 infection.
doi: 10.1016/j.anndiagpath.2022.152032
Figure Lengend Snippet: Fig. 6. H&E findings of mild versus fatal SARS-CoV2 infection. Panels A–C compare the cytologic findings in the normal nasopharynx (panel A) and mild infection (panel B); note that the glandular cells show degenerative changes that is highlighted with the EMA immunohistochemistry test (panel C). Panels D–F show suc cessively high magnifications in a lung from a person who died of COVID-19 in which viral RNA was not evident; note the presence of extensive organizing pneumonia with scattered chronic inflammatory infiltrates. Panels G-I show successively high magnifications in a lung from a person who died of COVID-19 with high copy viral RNA; note the diffuse alveolar damage characterized by hyaline membrane formation, hemorrhage, and destruction of lining pneumocytes.
Article Snippet:
Techniques: Infection, Immunohistochemistry, Membrane