Professor of Emergency Medicine, Thomas Jefferson University
Emergency Medicine
Dr. Raymond F. Regan, MD
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Raymond Regan works in the field of Emergency Medicine. He studied medicine at Columbia University College of Physicians & Surgeons. Columbia University College of Physicians & Surgeons is a top medical college. Columbia University College of Physicians & Surgeons is ranked 8/52 in Research/PrimaryCare. Doctor Raymond F. Regan, MD is a published physician. He has 75 papers published. The most current publication "Extracellular reduced glutathione increases neuronal vulnerability to combined chemical hypoxia and glucose deprivation." He accepts Medicare payments and is listed with Medicare.gov.
Publications
- Astrocyte overexpression of heme oxygenase-1 improves outcome after intracerebral hemorrhage.
- Solid microparticles based on chitosan or methyl-beta-cyclodextrin: a first formulative approach to increase the nose-to-brain transport of deferoxamine mesylate.
- Targeting heme oxygenase after intracerebral hemorrhage.
- Delayed cutaneous wound closure in HO-2 deficient mice despite normal HO-1 expression.
- Curcumin-induced heme oxygenase-1 expression prevents H2O2-induced cell death in wild type and heme oxygenase-2 knockout adipose-derived mesenchymal stem cells.
- Neuroprotective effect of heme oxygenase-2 knockout in the blood injection model of intracerebral hemorrhage.
- Systemic Hemin Therapy Attenuates Blood-Brain Barrier Disruption after Intracerebral Hemorrhage.
- Hemin uptake and release by neurons and glia.
- A Rapid Fluorescent Method to Quantify Neuronal Loss after Experimental Intracerebral Hemorrhage.
- Effect of Iron Chelators on Methemoglobin and Thrombin Preconditioning.
- Hemopexin decreases hemin accumulation and catabolism by neural cells.
- Hemoglobin-based oxygen carriers: current status and future directions.
- Nitric oxide recombination to double mutants of myoglobin: role of ligand diffusion in a fluctuating heme pocket.
- Ligand diffusion in the distal heme pocket of myoglobin. A primary determinant of geminate rebinding.
- Glutamate neurotoxicity in spinal cord cell culture.
- Ligand binding and conformation change in the dimeric hemoglobin of the clam Scapharca inaequivalvis.
- Structural and functional effects of apolar mutations of the distal valine in myoglobin.
- cDNA cloning of a human dishevelled DVL-3 gene, mapping to 3q27, and expression in human breast and colon carcinomas.
- The unique heme-heme interactions of the homodimeric Scapharca inaequivalvis hemoglobin as probed in the protein reconstituted with unnatural 2,4 heme derivatives.
- Interactions between NO, CO and an endothelium-derived hyperpolarizing factor (EDHF) in maintaining patency of the ductus arteriosus in the mouse.
- Ligand binding in a hierarchy of globin complexes. The hexagonal bilayer hemoglobin of Lumbricus terrestris and its heme-containing subunits.
- Assessment of hemoglobin-dependent neurotoxicity: alpha-alpha crosslinked hemoglobin.
- Ultrastructure of excitotoxic neuronal death in murine cortical culture.
- Ferritin induction protects cortical astrocytes from heme-mediated oxidative injury.
- Neurotoxicity of hemoglobin in cortical cell culture.
- NMDA neurotoxicity in murine cortical cell cultures is not attenuated by hemoglobin or inhibition of nitric oxide synthesis.
- Potentiation of excitotoxic injury by high concentrations of extracellular reduced glutathione.
- The effect of NMDA, AMPA/kainate, and calcium channel antagonists on traumatic cortical neuronal injury in culture.
- Extracellular reduced glutathione increases neuronal vulnerability to combined chemical hypoxia and glucose deprivation.
- Hemoglobin potentiates excitotoxic injury in cortical cell culture.
- Magnesium deprivation decreases cellular reduced glutathione and causes oxidative neuronal death in murine cortical cultures.
- The vulnerability of spinal cord neurons to excitotoxic injury: comparison with cortical neurons.
- Traumatic neuronal injury in cortical cell culture is attenuated by 21-aminosteroids.
- Heme oxygenase-1 induction protects murine cortical astrocytes from hemoglobin toxicity.
- Exacerbated corneal inflammation and neovascularization in the HO-2 null mice is ameliorated by biliverdin.
- Estrogens attenuate neuronal injury due to hemoglobin, chemical hypoxia, and excitatory amino acids in murine cortical cultures.
- The effect of magnesium on oxidative neuronal injury in vitro.
- Toxic effect of hemoglobin on spinal cord neurons in culture.
- Activation of extracellular signal-regulated kinases potentiates hemin toxicity in astrocyte cultures.
- Iron accumulation and neurotoxicity in cortical cultures treated with holotransferrin.
- Increased striatal injury and behavioral deficits after intracerebral hemorrhage in hemopexin knockout mice.
- 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.
- Hemoglobin neurotoxicity is attenuated by inhibitors of the protein kinase CK2 independent of heme oxygenase activity.
- Iron regulatory proteins increase neuronal vulnerability to hydrogen peroxide.
- Neurons lacking iron regulatory protein-2 are highly resistant to the toxicity of hemoglobin.
- Carbon monoxide donors or heme oxygenase-1 (HO-1) overexpression blocks interleukin-18-mediated NF-kappaB-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.
- H-ras inhibits RhoA/ROCK leading to a decrease in the basal tone in the internal anal sphincter.
- Attenuation of oxidative injury after induction of experimental intracerebral hemorrhage in heme oxygenase-2 knockout mice.
- Heme oxygenase-2 is a critical determinant for execution of an acute inflammatory and reparative response.
- Effect of heme oxygenase-1 on the vulnerability of astrocytes and neurons to hemoglobin.
- HO-2 provides endogenous protection against oxidative stress and apoptosis caused by TNF-alpha in cerebral vascular endothelial cells.
- Heme oxygenase-2 deficiency contributes to diabetes-mediated increase in superoxide anion and renal dysfunction.
- Inhibition of the ERK/MAP kinase pathway attenuates heme oxygenase-1 expression and heme-mediated neuronal injury.
- Glutamate induces oxidative stress and apoptosis in cerebral vascular endothelial cells: contributions of HO-1 and HO-2 to cytoprotection.
- Nitric oxide not carbon monoxide mediates nonadrenergic noncholinergic relaxation in the murine internal anal sphincter.
- Cultured astrocytes from heme oxygenase-1 knockout mice are more vulnerable to heme-mediated oxidative injury.
- Increasing expression of heme oxygenase-1 by proteasome inhibition protects astrocytes from heme-mediated oxidative injury.
- The oxidative neurotoxicity of clioquinol.
- Effect of targeted deletion of the heme oxygenase-2 gene on hemoglobin toxicity in the striatum.
- Adenoviral transfer of the heme oxygenase-1 gene protects striatal astrocytes from heme-mediated oxidative injury.
- Heme oxygenase-2 gene deletion attenuates oxidative stress in neurons exposed to extracellular hemin.
- The neurotoxic effect of sickle cell hemoglobin.
- Heme oxygenase-2 gene deletion increases astrocyte vulnerability to hemin.
- Heme oxygenase-2 knockout neurons are less vulnerable to hemoglobin toxicity.
- Hemin induces an iron-dependent, oxidative injury to human neuron-like cells.
- Delayed treatment of hemoglobin neurotoxicity.
Schools
Columbia University College of Physicians And Surgeons
Deaconess Hospital
UCLA Med Center
Doctors Specialties
- Emergency Medicine
- Internal Medicine
Accepted Insurances
- Aetna
- Personal Choice PPO
- Regional Pref Network EPO
- Regional Pref Network HMO
- Regional Pref Network HMO+
- Regional Pref Network POS+
- Regional Pref Network PPO
- Blue Cross Blue Shield
- Cigna
- Commercial Insurance Company
- CoreSource
- Coventry Health America PPO
- First Health (Coventry Health Care) PPO
- Golden Rule
- Harvard Pilgrim Health Care PPO
- HealthPartners
- Humana
- Keystone Health Plan East HMO
- Medicare MCR
- MultiPlan PPO
- PHCS Network PPO
- QualCare HMO
- QualCare PPO
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- United Healthcare
Education
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Stanford University -
UCLA Medical Center -
Beth Israel Deaconess Medical Center -
Columbia University College of Physicians & Surgeons
Hospital
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Thomas Jefferson University Hospital
Drug Facts
| NPI NUMBER | 1659394575 | |
| NPPES Provider LastName | REGAN | |
| NPPES Provider FirstName | RAYMOND | |
| NPPES Provider ZIPCode | 19107 | |
| NPPES Provider State | PA | |
| Specialty Description | Emergency Medicine | |
| Total Claim Count | 27.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1659394575 |
| Last Name Of The Provider | REGAN |
| First Name Of The Provider | RAYMOND |
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