Physician
Rheumatology
Dr. Ralph C. Budd, MD
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Dr. Ralph C. Budd works in the field of Rheumatology. He researched medicine at Weill Cornell Medical College of Cornell University. Weill Cornell Medical College of Cornell University has a rank of 18 in research and a 49 in primary care He received 5 awards: "Regional Top Doctor", "CMS Meaningful Use Stage 1 Certification", "Elected Member", "Fellow" and "Fellow (FACR)". Ralph C. Budd is a published doctor and has 98 publications published. The lastest was: 'Lyme arthritis synovial gamma delta T cells respond to Borrelia burgdorferi lipoproteins and lipidated hexapeptides.' Ralph Budd accepts Medicare.
Publications
- γδ T Cells and dendritic cells in refractory Lyme Arthritis.
- IL-15 maintains T-Cell survival via S-nitrosylation-mediated inhibition of caspase-3.
- The Role of Sex Differences in Autophagy in the Heart During Coxsackievirus B3-Induced Myocarditis.
- The c-FLIPL cleavage product p43FLIP promotes activation of ERK, NF-κB, caspase-8 and T Cell survival.
- Interleukin-1 Receptor and Caspase-1 are Required for the Th17 Response in NO2-Promoted Allergic Airway Disease.
- Caspase-8 and FLIP regulate RIG-I/MDA5-induced innate immune host responses to picornaviruses.
- Proliferating ?? T Cells manifest high and spatially confined caspase-3 activity.
- Increased caspase activity primes human Lyme Arthritis synovial ?? T cells for proliferation and death.
- Redox-based regulation of apoptosis: S-glutathionylation as a regulatory mechanism to control Cell death.
- Reduced Immune Response to Borrelia burgdorferi in the Absence of {gamma}{delta} T Cells.
- Apoptosis regulators Fas and Bim synergistically control T-lymphocyte homeostatic proliferation.
- Regulation of apoptosis through cysteine oxidation: implications for fibrotic lung disease.
- Redox amplification of apoptosis by caspase-dependent cleavage of glutaredoxin 1 and S-glutathionylation of Fas.
- Activation of gamma delta T Cells by Borrelia burgdorferi is indirect via a TLR- and caspase-dependent pathway.
- Apoptosis regulators Fas and Bim cooperate in shutdown of Chronic immune responses and prevention of autoimmunity.
- Caspase-8 and c-FLIPL associate in lipid rafts with NF-kappaB adaptors during T Cell activation.
- The CD95 receptor: apoptosis revisited.
- Accumulation of NFAT mediates IL-2 expression in memory, but not naïve, CD4+ T Cells.
- Augmentation of proliferation of vascular smooth muscle Cells by plasminogen activator inhibitor type 1.
- Proteolytic regulation of nuclear factor of activated T (NFAT) c2 Cells and NFAT activity by caspase-3.
- Fas ligand deficiency impairs host inflammatory response against infection with the spirochete Borrelia burgdorferi.
- Lyme Arthritis synovial gammadelta T cells instruct dendritic cells via fas ligand.
- The death receptor Fas (CD95/APO-1) mediates the deletion of T lymphocytes undergoing homeostatic proliferation.
- Cellular FLIP long form augments caspase activity and death of T Cells through heterodimerization with and activation of caspase-8.
- Cellular FLIP (long form) regulates CD8+ T Cell activation through caspase-8-dependent NF-kappa B activation.
- Effector CD4+ T Cells generate intermediate caspase activity and cleavage of caspase-8 substrates.
- Inhibition of apoptosis and caspase-3 in vascular smooth muscle Cells by plasminogen activator inhibitor type-1.
- Cellular FLIP long form-transgenic mice manifest a Th2 cytokine bias and enhanced allergic airway inflammation.
- High expression of Fas ligand by synovial fluid-derived gamma delta T cells in Lyme Arthritis.
- The caspase 8 inhibitor c-FLIP(L) modulates T-Cell receptor-induced proliferation but not activation-induced Cell death of lymphocytes.
- Gammadelta T Cells promote a Th1 response during coxsackievirus B3 infection in vivo: role of Fas and Fas ligand.
- Expression level of c-FLIP versus Fas determines susceptibility to Fas ligand-induced Cell death in murine thymoma EL-4 Cells.
- Death receptors couple to both Cell proliferation and apoptosis.
- c-FLIP-Short Reduces Type I Interferon Production and Increases Viremia with Coxsackievirus B3.
- Serum amyloid A inhibits dendritic Cell apoptosis to induce glucocorticoid resistance in CD4(+) T Cells.
- Radioprotection by DNA ligands.
- Shared molecular markers of genetic predisposition to seropositive rheumatoid Arthritis.
- Diversity of cytokine synthesis and function of mouse CD4+ T Cells.
- A subset of memory CD4+ helper T lymphocytes identified by expression of Pgp-1.
- Introduction: lessons from the lpr mouse--T lymphocyte development.
- An overview of apoptosis.
- Parallels in T lymphocyte development between lpr and normal mice.
- T-Cell lineages, repertoire selection and tolerance induction.
- Activation-induced Cell death.
- Comment on "Essential Role of IL-17A in the formation of a mycobacterial infection-induced granuloma in the lung".
- Cultured Lyt-2- L3T4- T lymphocytes from normal thymus or lpr mice express a broad spectrum of cytolytic activity.
- Growth and differentiation in vitro of the accumulating Lyt-2-/L3T4- subset in lpr mice.
- The origin of CD4-CD8-TCR alpha beta+ thymocytes: a model based on T-Cell receptor avidity.
- Functional analysis of T Cell subsets from mice bearing the lpr gene.
- Developmentally regulated expression of T Cell receptor beta chain variable domains in immature thymocytes.
- Borrelia burgdorferi infection regulates CD1 expression in human Cells and tissues via IL1-β.
- MEK1 activation rescues Jurkat T Cells from Fas-induced apoptosis.
- Phosphorylation of FADD/MORT1 and Fas by kinases that associate with the membrane-proximal cytoplasmic domain of Fas.
- Delayed kinetics of T lymphocyte anergy and deletion in lpr mice.
- The caspase-8 inhibitor FLIP promotes activation of NF-kappaB and Erk signaling pathways.
- Accelerated programmed Cell death of MRL-lpr/lpr T lymphocytes.
- Pgp-1 (Ly 24) as a marker of murine memory T lymphocytes.
- Phenotypic identification of memory cytolytic T lymphocytes in a subset of Lyt-2+ Cells.
- Selectively increased production of interferon-gamma by subsets of Lyt-2+ and L3T4+ T Cells identified by expression of Pgp-1.
- Distinction of virgin and memory T lymphocytes. Stable acquisition of the Pgp-1 glycoprotein concomitant with antigenic stimulation.
- Expression of T-Cell receptors by functionally distinct subsets of immature adult thymocytes.
- CD2-CD4-CD8- lymph node T lymphocytes in MRL lpr/lpr mice are derived from a CD2+CD4+CD8+ thymic precursor.
- Transgene-encoded human CD2 acts in a dominant negative fashion to modify thymocyte selection signals in mice.
- Abnormal expression of T Cell receptor genes in Lyt-2- L3T4- lymphocytes of lpr mice: comparison with normal immature thymocytes.
- Co-stimulation via CD28 induces activation of a refractory subset of MRL-lpr/lpr T lymphocytes.
- Intact antigen receptor-mediated generation of inositol phosphates and increased intraCellular calcium in CD4 CD8 T lymphocytes from MRL lpr mice.
- Increased usage of V beta 2 and V beta 6 in rheumatoid synovial fluid T Cells.
- Down-modulation of CD2 delays deletion of superantigen-responsive T Cells.
- Abnormal regulation of the IL-2 promoter in lpr CD4-CD8- T lymphocytes results in constitutive expression of a novel nuclear factor of activated T Cells-binding factor.
- Elevated production of interferon-gamma and interleukin 4 by mature T Cells from autoimmune lpr mice correlates with Pgp-1 (CD44) expression.
- Anti-CD40L accelerates renal disease and adenopathy in MRL-lpr mice in parallel with decreased thymocyte apoptosis.
- CD2 expression on murine intestinal intraepithelial lymphocytes is bimodal and defines proliferative capacity.
- Spatial differences in active caspase-8 defines its role in T-Cell activation versus Cell death.
- Caspase activation is required for T Cell proliferation.
- A model for the origin of TCR-alphabeta+ CD4-CD8- B220+ Cells based on high affinity TCR signals.
- Apoptosis of Fashigh CD4+ synovial T cells by borrelia-reactive Fas-ligand(high) gamma delta T cells in Lyme Arthritis.
- Liver damage preferentially results from CD8(+) T Cells triggered by high affinity peptide antigens.
- Diversity of rheumatoid synovial tissue T Cells by T Cell receptor analysis. Oligoclonal expansion in interleukin-2-responsive Cells.
- T Cell lineages in the thymus of lpr/lpr mice. Evidence for parallel pathways of normal and abnormal T Cell development.
- Unstimulated rheumatoid synovial T-Cells have a consistent V beta gene bias when compared to peripheral blood T-Cells.
- JNK, but not MAPK, activation is associated with Fas-mediated apoptosis in human T Cells.
- Prominent T lymphocyte response to Borrelia burgdorferi from peripheral blood of unexposed donors.
- Decreased CD4-CD8- TCR-alpha beta + Cells in lpr/lpr mice lacking beta 2-microglobulin.
- Reversal of hyporesponsiveness in lpr CD4-CD8- T Cells is achieved by induction of Cell cycling and normalization of CD2 and p59fyn expression.
- A CD3- subset of CD4-8+ thymocytes: a rapidly cycling intermediate in the generation of CD4+8+ Cells.
- CD2 expression correlates with proliferative capacity of alpha beta + or gamma delta + CD4-CD8- T Cells in lpr mice.
- Biased T-cell antigen receptor repertoire in Lyme Arthritis.
- Reactive nitrogen species-induced Cell death requires Fas-dependent activation of c-Jun N-terminal kinase.
- Apoptosis in coxsackievirus B3-induced myocarditis and dilated cardiomyopathy.
- Lyme Arthritis synovial gamma delta T cells respond to Borrelia burgdorferi lipoproteins and lipidated hexapeptides.
- Liver damage by infiltrating CD8+ T Cells is Fas dependent.
- cFLIP regulation of lymphocyte activation and development.
- Reduced myocarditis following Coxsackievirus infection in Cellular FLICE inhibitory protein--long form-transgenic mice.
- Fas (CD95/APO-1) limits the expansion of T lymphocytes in an environment of limited T-Cell antigen receptor/MHC contacts.
- c-FLIP(S) reduces activation of caspase and NF-kappaB pathways and decreases T Cell survival.
- Morphological and cytochemical determination of Cell death by apoptosis.
- Attenuation of apoptosis and the eye of the beholder.
Schools
Joan Sanford I Weill Medical College Of Cornell University
Dartmouth Hitchcock
Procedures Preformed
- Joint Drainage
- Myofascial Trigger Point Injection
- Steroid Injection
- Trigger Point Injection
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Conditions Treated
- Ankylosing Vertebral Hyperostosis
- Arthritis
- Bursitis
- Carpal Tunnel Syndrome
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Doctors Specialties
- Rheumatology
Accepted Insurances
- Choice Plus POS II
- Blue Card PPO
- Cigna HMO
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- EBS-RMSCO
- First Health (Coventry Health Care) PPO
- Medicare MCR
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- United Healthcare
- Universal American
Awards
- Regional Top Doctor
- CMS Meaningful Use Stage 1 Certification
- Elected Member
- Fellow
- Fellow (FACR)
Education
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Dartmouth-Hitchcock Medical Center -
Weill Cornell Medical College of Cornell University
Drug Facts
| NPI NUMBER | 1609981315 | |
| NPPES Provider LastName | BUDD | |
| NPPES Provider FirstName | RALPH | |
| NPPES Provider ZIPCode | 054011473 | |
| NPPES Provider State | VT | |
| Specialty Description | Rheumatology | |
| Total Claim Count | 218.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1609981315 |
| Last Name Of The Provider | BUDD |
| First Name Of The Provider | RALPH |
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