scispace - formally typeset
D

Di Qu

Researcher at Fudan University

Publications -  65
Citations -  3454

Di Qu is an academic researcher from Fudan University. The author has contributed to research in topics: Biofilm & Staphylococcus epidermidis. The author has an hindex of 22, co-authored 59 publications receiving 2510 citations. Previous affiliations of Di Qu include Chinese Academy of Sciences & Fudan University Shanghai Medical College.

Papers
More filters
Journal ArticleDOI

Role of autolysin-mediated DNA release in biofilm formation of Staphylococcus epidermidis

TL;DR: Evidence is presented that extracellular DNA is important for the initial phase of biofilm development by S. epidermidis on polystyrene or glass surfaces under static or hydrodynamic conditions, and that the ext racellular DNA promotes biofilm formation of the remaining population.
Journal ArticleDOI

Genome-based analysis of virulence genes in a non-biofilm-forming Staphylococcus epidermidis strain (ATCC 12228).

TL;DR: The complete genome of Staphylococcus epidermidis strain ATCC 12228, a non‐biofilm forming, non‐infection associated strain used for detection of residual antibiotics in food products, was sequenced and the ica operon coding for the enzymes synthesizing interbacterial cellular polysaccharide is missing.
Journal ArticleDOI

A genome-wide CRISPR screen identifies host factors that regulate SARS-CoV-2 entry.

TL;DR: In this paper, the authors performed a genome-wide CRISPR screen and identified several endosomal entry-specific regulators, including host factors regulating the surface expression of angiotensin-converting enzyme 2 (ACE2) for SARS-CoV-2.
Journal ArticleDOI

Decoy nanoparticles protect against COVID-19 by concurrently adsorbing viruses and inflammatory cytokines

TL;DR: A decoy nanoparticle is reported against COVID-19 through a powerful two-step neutralization approach: virus neutralization in the first step followed by cytokine neutralizationIn the second step, the nanodecoys efficiently bind and neutralize inflammatory cytokines including interleukin 6 (IL-6) and granulocyte−macrophage colony-stimulating factor (GM-CSF), and significantly suppress immune disorder and lung injury in an acute pneumonia mouse model.