Haichao Wang

Globin attenuates the innate immune response to endotoxin.

HMGB-1, a DNA-binding protein with cytokine activity, induces brain TNF and IL-6 production, and mediates anorexia and taste aversion.

Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation.

Activation of gene expression in human neutrophils by high mobility group box 1 protein.

IFN-gamma induces high mobility group box 1 protein release partly through a TNF-dependent mechanism.

HMGB1 as a cytokine and therapeutic target.

Structural basis for the proinflammatory cytokine activity of high mobility group box 1.

Further characterization of high mobility group box 1 (HMGB1) as a proinflammatory cytokine: central nervous system effects.

Reversing established sepsis with antagonists of endogenous high-mobility group box 1.

Lipid unites disparate syndromes of sepsis.

Extracellular HMGB1 as a proinflammatory cytokine.

Recombinant HMGB1 with cytokine-stimulating activity.

Bench to bedside: HMGB1-a novel proinflammatory cytokine and potential therapeutic target for septic patients in the emergency department.

Pathogenic role of HMGB1 in SARS?

Bacterial endotoxin stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanisms.

Cholinergic agonists inhibit HMGB1 release and improve survival in experimental sepsis.

Suppression of HMGB1 release by stearoyl lysophosphatidylcholine:an additional mechanism for its therapeutic effects in experimental sepsis.

Adrenomedullin and its binding protein attenuate the proinflammatory response after hemorrhage.

The cytokine activity of HMGB1.

Suppressor alphabeta T lymphocytes control innate resistance to endotoxic shock.

Interferon-gamma inhibition attenuates lethality after cecal ligation and puncture in rats: implication of high mobility group box-1.

More tea for septic patients?--Green tea may reduce endotoxin-induced release of high mobility group box 1 and other pro-inflammatory cytokines.

The aqueous extract of a popular herbal nutrient supplement, Angelica sinensis, protects mice against lethal endotoxemia and sepsis.

Role of HMGB1 in cardiovascular diseases.

Potential role of high mobility group box 1 in viral infectious diseases.

Elevated high-mobility group box 1 levels in patients with cerebral and myocardial ischemia.

Role of HMGB1 in apoptosis-mediated sepsis lethality.

HMGB1 signals through toll-like receptor (TLR) 4 and TLR2.

Hydrogen peroxide stimulates macrophages and monocytes to actively release HMGB1.

A cardiovascular drug rescues mice from lethal sepsis by selectively attenuating a late-acting proinflammatory mediator, high mobility group box 1.

HMGB1 as a potential therapeutic target.

Nuclear heat shock protein 72 as a negative regulator of oxidative stress (hydrogen peroxide)-induced HMGB1 cytoplasmic translocation and release.

A novel role for HMGB1 in TLR9-mediated inflammatory responses to CpG-DNA.

The anti-inflammatory effects of heat shock protein 72 involve inhibition of high-mobility-group box 1 release and proinflammatory function in macrophages.

Adrenomedullin and adrenomedullin binding protein-1 prevent acute lung injury after gut ischemia-reperfusion.

Transcutaneous vagus nerve stimulation reduces serum high mobility group box 1 levels and improves survival in murine sepsis.

A major ingredient of green tea rescues mice from lethal sepsis partly by inhibiting HMGB1.

Alveolar macrophage suppression in sepsis is associated with high mobility group box 1 transmigration.

[Serum level of HMGB1 in patients with hepatitis B and its clinical significance].

A pilot study to detect high mobility group box 1 and heat shock protein 72 in cerebrospinal fluid of pediatric patients with meningitis.

[The expression of fetuin-A and its pathological significance in fulminant hepatic failure in mice].

Hyperglycemia aggravates endotoxin-induced high mobility group box 1 protein release: yet another reason not to be too sweet.

PACAP inhibit the release and cytokine activity of HMGB1 and improve the survival during lethal endotoxemia.

Splenectomy protects against sepsis lethality and reduces serum HMGB1 levels.

Therapeutic potential of HMGB1-targeting agents in sepsis.

Caging a Beast in the Inflammation Arena: Use of Chinese Medicinal Herbs to Inhibit a Late Mediator of Lethal Sepsis, HMGB1.

Ethyl pyruvate improves survival in awake hemorrhage.

Quercetin prevents LPS-induced high-mobility group box 1 release and proinflammatory function.

Novel HMGB1-inhibiting therapeutic agents for experimental sepsis.

Orexigenic hormone ghrelin ameliorates gut barrier dysfunction in sepsis in rats.

Spermine protects mice against lethal sepsis partly by attenuating surrogate inflammatory markers.

High-mobility group box 1 protein induces tissue factor expression in vascular endothelial cells via activation of NF-kappaB and Egr-1.

Immature dendritic cell-derived exosomes rescue septic animals via milk fat globule epidermal growth factor-factor VIII [corrected].

High mobility group box 1 protein as a potential drug target for infection- and injury-elicited inflammation.

Peripheral administration of fetuin-A attenuates early cerebral ischemic injury in rats.

[Effect of HMGB1 on human hepatoma cell line-HepG2 proliferation].

A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release.

A hepatic protein, fetuin-A, occupies a protective role in lethal systemic inflammation.

EGCG stimulates autophagy and reduces cytoplasmic HMGB1 levels in endotoxin-stimulated macrophages.

HMGB1 cytoplasmic translocation in patients with acute liver failure.

Peripheral administration of human adrenomedullin and its binding protein attenuates stroke-induced apoptosis and brain injury in rats.

Recombinant human MFG-E8 attenuates cerebral ischemic injury: its role in anti-inflammation and anti-apoptosis.

Anti-Inflammatory Role of Fetuin-A in Injury and Infection.

Inhibition of HMGB1 Enhances Bacterial Clearance and Protects against P. aeruginosa Pneumonia in Cystic Fibrosis.

Exposure of perfluorononanoic acid suppresses the hepatic insulin signal pathway and increases serum glucose in rats.