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Shuangqi Cai

Researcher at Guangxi Medical University

Publications -  12
Citations -  416

Shuangqi Cai is an academic researcher from Guangxi Medical University. The author has contributed to research in topics: Pseudomonas aeruginosa & Biofilm. The author has an hindex of 6, co-authored 10 publications receiving 257 citations.

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Baicalin inhibits biofilm formation, attenuates the quorum sensing-controlled virulence and enhances Pseudomonas aeruginosa clearance in a mouse peritoneal implant infection model.

TL;DR: Zhang et al. as mentioned in this paper demonstrated the ability of sub-minimum inhibitory concentrations (sub-MICs) of Baicalin, an active natural compound extracted from the traditional Chinese medicinal Scutellaria baicalensis, to inhibit the formation of Pseudomonas aeruginosa biofilms and enhance the bactericidal effects of various conventional antibiotics in vitro.
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Baicalein Inhibits Staphylococcus aureus Biofilm Formation and the Quorum Sensing System In Vitro

TL;DR: In this paper, the authors used a clinically isolated strain of Staphylococcus aureus 17546 (t037) for biofilm formation and evaluated its antibiofilm activity.
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The rapid in vivo evolution of Pseudomonas aeruginosa in ventilator-associated pneumonia patients leads to attenuated virulence

TL;DR: Analysis showed that positive selection dominantly shaped P. aeruginosa genomes during VAP infections and led to three convergent evolution events, including loss-of-function mutations of lasR and mpl, and a pyoverdine-deficient phenotype, suggesting the short-term in vivo evolution of P. Aero leads to attenuated virulence.
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The miRNA-149-5p/MyD88 axis is responsible for ursolic acid-mediated attenuation of the stemness and chemoresistance of non-small cell lung cancer cells

TL;DR: Results suggest that UA could attenuate the stemness and chemoresistance of NSCLC cells through targeting miR‐149‐5p/MyD88 axis.
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Circular RNA hsa_circ_0096157 contributes to cisplatin resistance by proliferation, cell cycle progression, and suppressing apoptosis of non-small-cell lung carcinoma cells.

TL;DR: Increased hsa_circ_0096157 expression contributed to DDP resistance in NSCLC cells by promoting cell proliferation, migration, invasion and cell cycle progression and inhibiting apoptosis.