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IL-1 Receptor Antagonist Treatment Aggravates Staphylococcal Septic Arthritis and Sepsis in Mice.RAGE Deficiency Impairs Bacterial Clearance in Murine Staphylococcal Sepsis, but Has No Significant Impact on Staphylococcal Septic ArthritisBoth anti-TNF and CTLA4 Ig treatments attenuate the disease severity of staphylococcal dermatitis in mice.Tissue Plasminogen Activator Coating on Implant Surfaces Reduces Staphylococcus aureus Biofilm Formation.Adenovirus assembly is impaired by BMI1-related histone deacetylase activity.Deficiency of the Complement Component 3 but Not Factor B Aggravates Staphylococcus aureus Septic Arthritis in Mice.Galectin-3 Is a Target for Proteases Involved in the Virulence of Staphylococcus aureus.CTLA4 Immunoglobulin but Not Anti-Tumor Necrosis Factor Therapy Promotes Staphylococcal Septic Arthritis in Mice.Glioma cell proliferation controlled by ERK activity-dependent surface expression of PDGFRALack of Receptor for Advanced Glycation End products leads to less severe staphylococcal skin infection but more skin abscesses and prolonged wound healing.Human skin commensals augment Staphylococcus aureus pathogenesisLinkage between endosomal escape of LNP-mRNA and loading into EVs for transport to other cellsThe YIN and YANG of lipoproteins in developing and preventing infectious arthritis by Staphylococcus aureus
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description
investigador
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researcher
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wetenschapper
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name
Manli Na
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Manli Na
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type
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Manli Na
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Manli Na
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Manli Na
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Manli Na
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P31
P496
0000-0002-7306-8941