Attending Cardiac Surgeon, Director of Cardiac Surgery, Appleton Heart Institute, Thedacare/Appleton Medical Center
Thoracic Surgery
Dr. Robert J. Ferrante, MD
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Robert Ferrante works in the field of Thoracic Surgery. He studied medicine at Rutgers New Jersey Medical School. Rutgers New Jersey Medical School is ranked 76/0 in Research/PrimaryCare. He over the years received 1 awards: "Fellow (FACS)". Robert J. Ferrante is also published. He has 101 publications published. The lastest publication: "Oxidative stress in Huntington''s disease.' He is registered with Medicare.
Publications
- Inhibition of mitochondrial protein import by mutant huntingtin.
- Melatonin inhibits the caspase-1/cytochrome c/caspase-3 cell death pathway, inhibits MT1 receptor loss and delays Disease progression in a mouse model of amyotrophic l...
- A novel method for detecting 7-methyl guanine reveals aberrant methylation levels in Huntington Disease.
- MAP Kinase Phosphatase 1 (MKP-1/DUSP1) Is Neuroprotective in Huntington's Disease via Additive Effects of JNK and p38 Inhibition.
- SCAMP5 links endoplasmic reticulum stress to the accumulation of expanded polyglutamine protein aggregates via endocytosis inhibition.
- Inhibitors of cytochrome c release with therapeutic potential for Huntington's Disease.
- Mitochondrial nuclear receptors and transcription factors: who's minding the cell?
- Neuroprotective effects of synaptic modulation in Huntington's Disease R6/2 mice.
- Conformation-sensitive antibodies against alzheimer amyloid-beta by immunization with a thioredoxin-constrained B-cell epitope peptide.
- ESET/SETDB1 gene expression and histone H3 (K9) trimethylation in Huntington's Disease.
- Role of cyclooxygenase-2 induction by transcription factor Sp1 and Sp3 in neuronal oxidative and DNA damage response.
- Sp1 is up-regulated in cellular and transgenic models of Huntington Disease, and its reduction is neuroprotective.
- Mice lacking alpha-synuclein are resistant to mitochondrial toxins.
- Mitochondrial cyclic AMP response element-binding protein (CREB) mediates mitochondrial gene expression and neuronal survival.
- Chronology of behavioral symptoms and neuropathological sequela in R6/2 Huntington's Disease transgenic mice.
- Antioxidants modulate mitochondrial PKA and increase CREB binding to D-loop DNA of the mitochondrial genome in neurons.
- Chemotherapy for the brain: the antitumor antibiotic mithramycin prolongs survival in a mouse model of Huntington's Disease.
- Anti-inflammatory treatment with acetylsalicylate or rofecoxib is not neuroprotective in Huntington's Disease transgenic mice.
- Translating therapies for Huntington's Disease from genetic animal models to clinical trials.
- Prophylactic creatine administration mediates neuroprotection in cerebral ischemia in mice.
- Minocycline inhibits caspase-independent and -dependent mitochondrial cell death pathways in models of Huntington's Disease.
- Sp1 and Sp3 are oxidative stress-inducible, antideath transcription factors in cortical neurons.
- Translational control of inducible nitric oxide synthase expression by arginine can explain the arginine paradox.
- Histone deacetylase inhibitors prevent oxidative neuronal death independent of expanded polyglutamine repeats via an Sp1-dependent pathway.
- Cdc42-interacting protein 4 binds to huntingtin: neuropathologic and biological evidence for a role in Huntington's Disease.
- Huntington's Disease of the endocrine pancreas: insulin deficiency and diabetes mellitus due to impaired insulin gene expression.
- Therapeutic effects of cystamine in a murine model of Huntington's Disease.
- Mice overexpressing 70-kDa heat shock protein show increased resistance to malonate and 3-nitropropionic acid.
- Therapeutic effects of coenzyme Q10 and remacemide in transgenic mouse models of Huntington's Disease.
- Cytochrome C and caspase-9 expression in Huntington's Disease.
- Pre-excimer laser and post-excimer laser refractive surgery measurements of scotopic pupil diameter using 2 pupillometers.
- Two-stage liver transplantation with temporary porto-middle hepatic vein shunt.
- Increased oxidative damage to DNA in a transgenic mouse model of Huntington's Disease.
- Lipoic acid improves survival in transgenic mouse models of Huntington''s Disease.
- Therapeutic efficacy of EGb761 (Gingko biloba extract) in a transgenic mouse model of amyotrophic lateral sclerosis.
- Dichloroacetate exerts therapeutic effects in transgenic mouse models of Huntington's Disease.
- Creatine increase survival and delays motor symptoms in a transgenic animal model of Huntington's Disease.
- Transgenic ALS mice show increased vulnerability to the mitochondrial toxins MPTP and 3-nitropropionic acid.
- The Gln-Ala repeat transcriptional activator CA150 interacts with huntingtin: neuropathologic and genetic evidence for a role in Huntington's Disease pathogenesis.
- Mice with a partial deficiency of manganese superoxide dismutase show increased vulnerability to the mitochondrial toxins malonate, 3-nitropropionic acid, and MPTP.
- Malonate and 3-nitropropionic acid neurotoxicity are reduced in transgenic mice expressing a caspase-1 dominant-negative mutant.
- Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington Disease.
- Neuroprotective effects of creatine in a transgenic mouse model of Huntington's Disease.
- Inhibition of neuronal nitric oxide synthase protects against MPTP toxicity.
- Nonlinear decrease over time in N-acetyl aspartate levels in the absence of neuronal loss and increases in glutamine and glucose in transgenic Huntington's Disease mice.
- Partial deficiency of manganese superoxide dismutase exacerbates a transgenic mouse model of amyotrophic lateral sclerosis.
- MPTP induces alpha-synuclein aggregation in the substantia nigra of baboons.
- Neurotoxicity and oxidative damage of beta amyloid 1-42 versus beta amyloid 1-40 in the mouse cerebral cortex.
- Mice deficient in cellular glutathione peroxidase show increased vulnerability to malonate, 3-nitropropionic acid, and 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine.
- Huntington aggregates may not predict neuronal death in Huntington's Disease.
- Tissue transglutaminase is increased in Huntington's Disease brain.
- Mice lacking cytosolic copper/zinc superoxide dismutase display a distinctive motor axonopathy.
- Near-infrared fluorescence spectroscopy detects Alzheimer's Disease in vitro.
- Neuronal nitric oxide synthase activation and peroxynitrite formation in ischemic stroke linked to neural damage.
- Creatine and cyclocreatine attenuate MPTP neurotoxicity.
- Transgenic mice expressing a dominant negative mutant interleukin-1beta converting enzyme show resistance to MPTP neurotoxicity.
- Increased nitrotyrosine immunoreactivity in substantia nigra neurons in MPTP treated baboons is blocked by inhibition of neuronal nitric oxide synthase.
- Nuclear and neuropil aggregates in Huntington's Disease: relationship to neuropathology.
- Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis.
- Oxidative stress is attenuated in mice overexpressing BCL-2.
- Oxidative stress in Huntington''s Disease.
- Increased vulnerability to 3-nitropropionic acid in an animal model of Huntington's Disease.
- Mice deficient in group IV cytosolic phospholipase A2 are resistant to MPTP neurotoxicity.
- Oral Dyskinesias and striatal lesions in rats after long-term co-treatment with haloperidol and 3-nitropropionic acid.
- The cellular and subcellular localization of huntingtin-associated protein 1 (HAP1): comparison with huntingtin in rat and human.
- A human HAP1 homologue. Cloning, expression, and interaction with huntingtin.
- Neuroprotective effects of creatine and cyclocreatine in animal models of Huntington's Disease.
- Increased 3-nitrotyrosine in both sporadic and familial amyotrophic lateral sclerosis.
- Evidence of increased oxidative damage in both sporadic and familial amyotrophic lateral sclerosis.
- Increased 3-nitrotyrosine and oxidative damage in mice with a human copper/zinc superoxide dismutase mutation.
- Mechanisms of reduced striatal NMDA excitotoxicity in type I nitric oxide synthase knock-out mice.
- Systemic administration of rotenone produces selective damage in the striatum and globus pallidus, but not in the substantia nigra.
- Time course of leukocyte adhesion to endothelium in ischemia-reperfusion.
- Inhibition of white blood cell adhesion at reperfusion decreases tissue damage in postischemic striated muscle.
- Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury.
- Chronic 3-nitropropionic acid treatment in baboons replicates the cognitive and motor deficits of Huntington's Disease.
- Blockade of neuronal nitric oxide synthase protects against excitotoxicity in vivo.
- Excitotoxin lesions in primates as a model for Huntington's Disease: histopathologic and neurochemical characterization.
- Age-dependent vulnerability of the striatum to the mitochondrial toxin 3-nitropropionic acid.
- Coagulation effects of cyclosporine in liver transplantation.
- Malonate produces striatal lesions by indirect NMDA receptor activation.
- A frequent ala 4 to val superoxide dismutase-1 mutation is associated with a rapidly progressive familial amyotrophic lateral sclerosis.
- 3-Acetylpyridine produces age-dependent excitotoxic lesions in rat striatum.
- Movement disorder following excitotoxin lesions in primates.
- Studies of hepatic warm ischemia in the obese Zucker rat.
- Substance P and substance P receptor histochemistry in human neurodegenerative Diseases.
- Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid.
- Chronic mitochondrial energy impairment produces selective striatal degeneration and abnormal choreiform movements in primates.
- 3-Nitropropionic acid neurotoxicity is attenuated in copper/zinc superoxide dismutase transgenic mice.
- Involvement of free radicals in excitotoxicity in vivo.
- Sparing of acetylcholinesterase-containing striatal neurons in Huntington''s Disease.
- Morphologic and histochemical characteristics of a spared subset of striatal neurons in Huntington's Disease.
- Selective sparing of a class of striatal neurons in Huntington's Disease.
- Tyrosine hydroxylase-like immunoreactivity is distributed in the matrix compartment of normal human and Huntington''s Disease striatum.
- Neuropeptide Y, somatostatin, and reduced nicotinamide adenine dinucleotide phosphate diaphorase in the human striatum: a combined immunocytochemical and enzyme histoc...
- Differential sparing of somatostatin-neuropeptide Y and cholinergic neurons following striatal excitotoxin lesions.
- Systemic approaches to modifying quinolinic acid striatal lesions in rats.
- Topography of enkephalin, substance P and acetylcholinesterase staining in Huntington''s Disease striatum.
- Botulinum A toxin for the treatment of spasmodic torticollis: dysphagia and regional toxin spread.
- Proliferative and degenerative changes in striatal spiny neurons in Huntington's Disease: a combined study using the section-Golgi method and calbindin D28k immunocyto...
Schools
UmdnjNew Jersey Medical School
UMDNJ New Jersey Med School
University Of Al Hospital
Procedures Preformed
- Ablation for Treatment of Cardiac Arrhythmias
- Aortic Repair, Open or Repair of Arterial Aneurysm, Open
- Cardiac Catheterization (incl. Coronary Angiography)
- Cardiac Myocardial Perfusion Imaging
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Conditions Treated
- Aneurysm and Dissection of Heart
- Angina and Acute Coronary Syndrome
- Aortic Aneurysm
- Aortic Dissection
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Doctors Specialties
- Cardiac Surgery
- Thoracic Surgery
Accepted Insurances
- Choice Plus POS II
- American Enterprise Group
- Anthem Blue Cross Blue Shield HMO
- Anthem Blue Cross Blue Shield PPO
- Blue Preferred Plus POS
- Blue Card PPO
- Blue Cross Blue Shield of Illinois PPO
- Blue Cross Accord
- CHAMPVA
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- Commercial Insurance Company
- Choice Care PPO
- Medicaid
- Medicare MCR
- MultiPlan PPO
- Pekin Insurance
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- United Healthcare
Awards
- Fellow (FACS)
Education
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University of Alabama Medical Center -
UMDNJ-New Jersey Medical School -
Rutgers New Jersey Medical School
Drug Facts
| NPI NUMBER | 1346226826 | |
| NPPES Provider LastName | FERRANTE | |
| NPPES Provider FirstName | ROBERT | |
| NPPES Provider ZIPCode | 549113454 | |
| NPPES Provider State | WI | |
| Specialty Description | Thoracic Surgery | |
| Total Claim Count | 80.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1346226826 |
| Last Name Of The Provider | FERRANTE |
| First Name Of The Provider | ROBERT |
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