Professor, Neurology, University of Texas Medical School, Houston
Neurology
Dr. Staley A. Brod, MD
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Staley Brod is an expert in the field of Neurology. He graduated from University of Toledo College of Medicine. Staley Brod is also a published doctor. He has 49 paper published. The most recent paper is: Ingested interferon alpha suppresses type I diabetes in non-obese diabetic mice. He is registered with Medicare and accepts Medicare payments.
Publications
- Ingested (oral) tocilizumab inhibits EAE.
- Contrast enhanced MR venography with gadofosveset trisodium: Evaluation of the intracranial and extracranial venous system.
- Chronic cerebrospinal venous insufficiency: masked multimodal imaging assessment.
- Ingested (oral) thyrotropin releasing factor (TRH) inhibits EAE.
- Chronic cerebrospinal venous insufficiency: Case-control neurosonography results.
- Variable results after rituximab in neuromyelitis Optica.
- Oral ACTH (H.P. Acthar(®)Gel) inhibits IL-1 and IL-17 secretion in humans.
- Ingested (oral) SST inhibits EAE.
- Effect of ingested interferon-alpha on beta-cell function in children with new-onset type 1 diabetes.
- Ingested (oral) SIRS peptide 1-21 suppresses type 1 diabetes in NOD mice.
- Ingested (oral) IFN-alpha represses TNF-alpha mRNA in relapsing-remitting Multiple sclerosis.
- Ingested type I interferon: a potential treatment for autoimmunity.
- Ingested type I interferon: state of the art as treatment for autoimmunity.
- Idiopathic CSF pleocytosis in relapsing polychondritis.
- Antigen-driven peripheral immune tolerance. Suppression of organ-specific autoimmune diseases by oral administration of autoantigens.
- CTLA-4 and CD28 mRNA are coexpressed in most T cells after activation. Expression of CTLA-4 and CD28 mRNA does not correlate with the pattern of lymphokine production.
- Bio-equivalence of IM and SQ H.P. Acthar Gel.
- Ingested (oral) SIRS peptide 1-21 inhibits acute EAE by inducing Th2-like cytokines.
- Ingested (oral) alpha-MSH inhibits acute EAE.
- IM interferon beta-1a delays definite Multiple sclerosis 5 years after a first demyelinating event.
- Ingested (oral) ACTH inhibits EAE.
- Ingested IFN-alpha preserves residual beta cell function in type 1 diabetes.
- Autoimmunity is a type I interferon-deficiency syndrome corrected by ingested type I IFN via the GALT system.
- Ingested IFN-alpha: results of a pilot study in relapsing-remitting MS.
- Modification of acute experimental autoimmune encephalomyelitis in the Lewis rat by oral administration of type 1 interferons.
- Interferon-beta 1b treatment decreases tumor necrosis factor-alpha and increases interleukin-6 production in Multiple sclerosis.
- Oral administration of human or murine interferon alpha suppresses relapses and modifies adoptive transfer in experimental autoimmune encephalomyelitis.
- Oral administration of type I interferon modulates the course of experimental allergic Neuritis.
- Suppression of relapsing experimental autoimmune encephalomyelitis in the SJL/J mouse by oral administration of type I interferons.
- Oral administration of IFN-alpha is superior to subcutaneous administration of IFN-alpha in the suppression of chronic relapsing experimental autoimmune encephalomyeli...
- Ingested interferon alpha induces Mx mRNA.
- Combination therapy with glatiramer acetate (copolymer-1) and a type I interferon (IFN-alpha) does not improve experimental autoimmune encephalomyelitis.
- Adoptive transfer from interferon-alpha-fed mice is associated with inhibition of active experimental autoimmune encephalomyelitis by decreasing recipient tumor necros...
- Ingested IFN-alpha has biological effects in humans with relapsing-remitting Multiple sclerosis.
- Ingested interferon alpha suppresses type I diabetes in non-obese diabetic mice.
- IFN-beta 1b treatment of relapsing Multiple sclerosis has no effect on CD3-induced inflammatory or counterregulatory anti-inflammatory cytokine secretion ex vivo after...
- Ingested interferon-alpha prevents allograft islet transplant rejection.
- Defective CD3 mediated proliferation and LPS responsiveness in Multiple sclerosis.
- Increased in vitro induced CD4+ and CD8+ T cell IFN-gamma and CD4+ T cell IL-10 production in stable relapsing Multiple sclerosis.
- Unregulated inflammation shortens human functional longevity.
- Decreased CD3-mediated interferon-gamma production in relapsing-remitting Multiple sclerosis.
- Hypothesis: Multiple sclerosis is a type I interferon deficiency syndrome.
- Gut response. Therapy with ingested immunomodulatory proteins.
- Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin antigens: IV. Suppression of chronic relapsing disease in the Lewis rat and s...
- Common T-cell receptor V beta usage in oligoclonal T lymphocytes derived from cerebrospinal fluid and blood of patients with Multiple sclerosis.
- Restricted T cell expression of IL-2/IFN-gamma mRNA in human inflammatory disease.
- Multiple sclerosis: clinical presentation, diagnosis and treatment.
- Treatment of autoimmune diseases by oral tolerance to autoantigens.
Schools
University of Toledo College of Medicine
Med College Of Ohio Hospital
Procedures Preformed
- EEG (Electroencephalogram)
Conditions Treated
- Ataxia
- Dementia
- Dystonia
- Multiple Sclerosis (MS)
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Doctors Specialties
- Neurology
Accepted Insurances
Education
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Yale-New Haven Hospital -
University of Toledo College of Medicine
Drug Facts
| NPI NUMBER | 1740217322 | |
| NPPES Provider LastName | BROD | |
| NPPES Provider FirstName | STALEY | |
| NPPES Provider ZIPCode | 770303000 | |
| NPPES Provider State | TX | |
| Specialty Description | Neurology | |
| Total Claim Count | 589.0 | |
| Distinct Opioid Count | 1.0 | |
| Opioid Claim Count | 25.0 | |
| Percent Opioid Claims | 4.24 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1740217322 |
| Last Name Of The Provider | BROD |
| First Name Of The Provider | STALEY |
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