1,721,092 research outputs found
INI879997 Supplemental Material3 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material3 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material5 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material5 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material6 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material6 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material4 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material4 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material2 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material2 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material1 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material1 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
The Abstruse Side of Type I Interferon Immunotherapy for COVID-19 Cases with Comorbidities
No full textThe Coronavirus Disease-2019 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has claimed 1.2 million people globally since December 2019. Although the host factors underpinning COVID-19 pathology are not fully understood, type I interferon (IFN-I) response is considered crucial for SARS-CoV-2 pathogenesis. Perturbations in IFN-I signaling and associated interferon-inducible genes (ISG) are among the primary disease severity indicators in COVID-19. Consequently, IFN-I therapy, either alone or in- combination with existing antiviral or anti-inflammatory drugs, is tested in many ongoing clinical trials to reduce COVID-19 mortality. Since signaling by the IFN-I family of molecules regulates host immune response to other infectious and non-infectious diseases, any imbalance in this family of cytokines would impact the clinical outcome of COVID-19, as well as other co-existing diseases. Therefore, it is imperative to evaluate the beneficial-versus-detrimental effects of IFN-I immunotherapy for COVID-19 patients with divergent disease severity and other co-existing conditions. This review article summarizes the role of IFN-I signaling in infectious and non-infectious diseases of humans. It highlights the precautionary measures to be considered before administering IFN-I to COVID-19 patients having other co-existing disorders. Finally, suggestions are proposed to improve IFN-I immunotherapy to COVID-19
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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