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Hector R. Wong

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  373
Citations -  18607

Hector R. Wong is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Sepsis & Septic shock. The author has an hindex of 72, co-authored 363 publications receiving 15495 citations. Previous affiliations of Hector R. Wong include University of Pittsburgh & University of Texas Medical Branch.

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Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children

Scott L. Weiss, +53 more
TL;DR: A large cohort of international experts was able to achieve consensus regarding many recommendations for the best care of children with sepsis, acknowledging that most aspects of care had relatively low quality of evidence resulting in the frequent issuance of weak recommendations.
Journal ArticleDOI

Surviving sepsis campaign international guidelines for the management of septic shock and sepsis-associated organ dysfunction in children

Scott L. Weiss, +54 more
TL;DR: A large cohort of international experts was able to achieve consensus regarding many recommendations for the best care of children with sepsis, acknowledging that most aspects of care had relatively low quality of evidence resulting in the frequent issuance of weak recommendations.
Journal ArticleDOI

Serum neutrophil gelatinase-associated lipocalin (NGAL) as a marker of acute kidney injury in critically ill children with septic shock.

TL;DR: Serum NGAL is a highly sensitive but nonspecific predictor of acute kidney injury in critically ill children with septic shock and further validation of serum NGAL as a biomarker of acute kidneys injury in this population is warranted.
Journal Article

Peroxynitrite-mediated DNA strand breakage activates poly-adenosine diphosphate ribosyl synthetase and causes cellular energy depletion in macrophages stimulated with bacterial lipopolysaccharide

TL;DR: The data suggest that inflammatory cell injury involved DNA strand breakage and PARS, triggering an energy-consuming, futile repair cycle leading to cellular energy depletion, and inhibition of PARS may improve cellular energy homeostasis in patho-physiologic conditions associated with peroxynitrite generation.
Journal ArticleDOI

Melatonin inhibits expression of the inducible isoform of nitric oxide synthase in murine macrophages: role of inhibition of NFκB activation

TL;DR: It is concluded that melatonin inhibits NO production in immunostimulated macrophages mainly by inhibiting the expression of iNOS, which may contribute to the anti‐inflammatory effects of this pineal secretory product.