1020 Sansom Street
Thompson Building, Suite 239
Philadelphia, PA 19107
(215) 955-6844
(215) 923-6225 fax
Thompson Building, Suite 239
Philadelphia, PA 19107
(215) 955-6844
(215) 923-6225 fax
Most Recent Peer-reviewed Publications
- Effect of Iron Chelators on Methemoglobin and Thrombin Preconditioning
- Hemopexin decreases hemin accumulation and catabolism by neural cells
- Iron accumulation and neurotoxicity in cortical cultures treated with holotransferrin
- Increased striatal injury and behavioral deficits after intracerebral hemorrhage in hemopexin knockout mi Laboratory investigation
- Apotransferrin protects cortical neurons from hemoglobin toxicity
- Accelerated hemolysis and neurotoxicity in neuron-glia-blood clot co-cultures
- Iron regulatory protein-2 knockout increases perihematomal ferritin expression and cell viability after intracerebral hemorrhage
- Heme oxygenase-2 deletion causes endothelial cell activation marked by oxidative stress, inflammation, and angiogenesis
- Minocycline attenuates iron neurotoxicity in cortical cell cultures
- Increasing expression of H- or L-ferritin protects cortical astrocytes from hemin toxicity
- Heme oxygenase activity and hemoglobin neurotoxicity are attenuated by inhibitors of the MEK/ERK pathway
- Iron regulatory proteins increase neuronal vulnerability to hydrogen peroxide
- Exacerbated corneal inflammation and neovascularization in the HO-2 null mice is ameliorated by biliverdin
- Neurons lacking iron regulatory protein-2 are highly resistant to the toxicity of hemoglobin
- Hemoglobin neurotoxicity is attenuated by inhibitors of the protein kinase CK2 independent of heme oxygenase activity
- Carbon monoxide donors or heme oxygenase-1 (HO-1) overexpression blocks interleukin-18-mediated NF-κB-PTEN-dependent human cardiac endothelial cell death
- Time course of increased heme oxygenase activity and expression after experimental intracerebral hemorrhage: Correlation with oxidative injury
- Astrocyte-specific heme oxygenase-1 hyperexpression attenuates heme-mediated oxidative injury
- Interactions between NO, CO and an endothelium-derived hyperpolarizing factor (EDHF) in maintaining patency of the ductus arteriosus in the mouse
- H-ras Inhibits RhoA/ROCK Leading to a Decrease in the Basal Tone in the Internal Anal Sphincter