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Weihua Cui

Researcher at University of Texas Medical Branch

Publications -  13
Citations -  418

Weihua Cui is an academic researcher from University of Texas Medical Branch. The author has contributed to research in topics: Burn injury & Dendritic cell. The author has an hindex of 9, co-authored 13 publications receiving 359 citations. Previous affiliations of Weihua Cui include Shriners Hospitals for Children - Galveston.

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Enhancement of Dendritic Cell Production by Fms-Like Tyrosine Kinase-3 Ligand Increases the Resistance of Mice to a Burn Wound Infection

TL;DR: It is indicated that Flt3L can increase the resistance of mice to a P. aeruginosa burn wound infection through both stimulation of dendritic cell production and enhancement of dendedritic cell function.
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Dendritic cells modulate burn wound healing by enhancing early proliferation

TL;DR: It is concluded that DCs play an important role in the acceleration of early wound healing events, likely by secreting factors that trigger the proliferation of cells that mediate wound healing.
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H2S, a Bacterial Defense Mechanism against the Host Immune Response.

TL;DR: It is found that inhibition of bacterial H2S production can increase the susceptibility of both bacterial species to rapid killing by immune cells and can improve bacterial clearance after severe burn, an injury that increases susceptibility to opportunistic infections.
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Prophylactic Treatment with Fms-Like Tyrosine Kinase-3 Ligand after Burn Injury Enhances Global Immune Responses to Infection

TL;DR: Test the hypothesis that Flt3L administration after burn injury decreases susceptibility to wound infections by enhancing global immune cell activation and suggests that dendritic cell enhancement by FlT3L treatments after burn injuries protects against opportunistic infections through promotion of local and systemic immune responses to infection.
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Endotoxin priming improves clearance of Pseudomonas aeruginosa in wild-type and interleukin-10 knockout mice.

TL;DR: Induction of LPS tolerance enhanced systemic clearance of Pseudomonas aeruginosa and that this effect was augmented by neutralization of IL-10, which reversed the endotoxin-tolerant state.