Professor, Medicine, University Massachusetts Medical School
Endocrinology
Dr. John P. Mordes, MD
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John Mordes practices Endocrinology. He attended Harvard Medical School. Harvard Medical School is a one of the best medicals schools. Harvard Medical School is ranked 1 in research and 12 in primary care medicine He received awards:"Meaningful Use Stage 1 Certification". John Mordes has written publications. He has 49 publications published with PubMed. The lastest paper is: 'Medications for weight loss.' He accepts Medicare payments and is listed with Medicare.gov.
Publications
- Medications for weight loss.
- Evaluation, Medical Therapy, and Course of Adult Persistent Hyperinsulinemic Hypoglycemia After Roux-en-Y Gastric Bypass Surgery: A Case Series.
- Diubiquitin (Ubd) is a susceptibility gene for virus-triggered autoimmune Diabetes in rats.
- Autoantigen-Induced Focusing Of Vβ13+ T-Cells Precedes Onset Of Autoimmune Diabetes In The Lew.1wr1 Rat.
- Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 Diabetes.
- Implications of using hemoglobin A1C for diagnosing Diabetes mellitus.
- Identification of a serum-induced transcriptional signature associated with type 1 Diabetes in the BioBreeding rat.
- Successful treatment of persistent hyperinsulinemic hypoglycemia With nifedipine in an adult patient.
- Infection with viruses from several families triggers autoimmune Diabetes in LEW*1WR1 rats: prevention of Diabetes by maternal immunization.
- A novel role for the centrosomal protein, pericentrin, in regulation of insulin secretory vesicle docking in mouse pancreatic beta-cells.
- Virus-induced autoimmune Diabetes in the LEW.1WR1 rat requires Iddm14 and a genetic locus proximal to the major histocompatibility complex.
- Analysis of the rat Iddm14 Diabetes susceptibility locus in multiple rat strains: identification of a susceptibility haplotype in the Tcrb-V locus.
- CHOP mediates endoplasmic reticulum stress-induced apoptosis in Gimap5-deficient T cells.
- Depletion of the programmed death-1 receptor completely reverses established clonal anergy in CD4(+) T lymphocytes via an interleukin-2-dependent mechanism.
- Type 1 IFN mediates cross-talk between innate and adaptive immunity that abrogates transplantation tolerance.
- A novel susceptibility locus on rat chromosome 8 affects spontaneous but not experimentally induced type 1 Diabetes.
- Refinement of the Iddm4 Diabetes susceptibility locus reveals TCRVbeta4 as a candidate gene.
- Development of new-generation HU-PBMC-NOD/SCID mice to study human islet alloreactivity.
- TLR9-signaling pathways are involved in Kilham rat virus-induced autoimmune Diabetes in the biobreeding Diabetes-resistant rat.
- A regulatory CD4+ T cell subset in the BB rat model of autoimmune Diabetes expresses neither CD25 nor Foxp3.
- ART2, a T cell surface mono-ADP-ribosyltransferase, generates extracellular poly(ADP-ribose).
- Costimulatory blockade induces hyporesponsiveness in T cells that recognize alloantigen via indirect antigen presentation.
- TLR agonists abrogate costimulation blockade-induced prolongation of skin allografts.
- LEW.1WR1 rats develop autoimmune Diabetes spontaneously and in response to environmental perturbation.
- The rat Diabetes susceptibility locus Iddm4 and at least one additional gene are required for autoimmune Diabetes induced by viral infection.
- TLR activation synergizes with Kilham rat virus infection to induce Diabetes in BBDR rats.
- Autoimmune Diabetes and resistance to xenograft transplantation tolerance in NOD mice.
- Early growth response gene-2, a zinc-finger transcription factor, is required for full induction of clonal anergy in CD4+ T cells.
- Evaluation of donor-specific transfusion sources: unique failure of bone marrow cells to induce prolonged skin allograft survival With anti-CD154 monoclonal antibody.
- Regulation of skin and islet allograft survival in mice treated With costimulation blockade is mediated by different CD4+ cell subsets and different mechanisms.
- Islet allograft survival induced by costimulation blockade in NOD mice is controlled by allelic variants of Idd3.
- Prolonged survival of neonatal porcine islet xenografts in mice treated With a donor-specific transfusion and anti-CD154 antibody.
- Deficiencies in gut NK cell number and function precede Diabetes onset in BB rats.
- Rat models of type 1 Diabetes: genetics, environment, and autoimmunity.
- Comparative mapping of rat Iddm4 to segments on HSA7 and MMU6.
- Islet cell autoimmunity and transplantation tolerance: two distinct mechanisms?
- Alloimmune injury and rejection of human skin grafts on human peripheral blood lymphocyte-reconstituted non-obese diabetic severe combined immunodeficient beta2-microg...
- Ian4 is required for mitochondrial integrity and T cell survival.
- Hematopoietic chimerism and central tolerance created by peripheral-tolerance induction Without myeloablative conditioning.
- Genetic separation of the transplantation tolerance and autoimmune phenoTypes in NOD mice.
- Induction of tolerance for islet transplantation for type 1 Diabetes.
- Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic mice.
- Infections that induce autoimmune Diabetes in BBDR rats modulate CD4+CD25+ T cell populations.
- Blockade of CD40-mediated signaling is sufficient for inducing islet but not skin transplantation tolerance.
- NOD congenic mice genetically protected from autoimmune Diabetes remain resistant to transplantation tolerance induction.
- The iddm4 locus segregates with Diabetes susceptibility in congenic WF.iddm4 rats.
- Viral abrogation of stem cell transplantation tolerance causes graft rejection and host death by different mechanisms.
- The Missing Heritability in T1D and Potential New Targets for Prevention.
Schools
Harvard Medical School
Mount Auburn Hospital
Peter Bent Brigham Hospital
University Mass Med Center
Conditions Treated
- Adrenal Incidentaloma
- Diabetes Type 1
- Diabetes Type 2
- Diabetes With Renal Manifestations
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Doctors Specialties
- Endocrinology
Accepted Insurances
Awards
- Meaningful Use Stage 1 Certification
Education
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University of Massachusetts -
Brigham and Women's Hospital -
Massachusetts General Hospital -
Harvard Medical School
Hospital
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UMass Memorial Medical Center
Drug Facts
| NPI NUMBER | 1760466031 | |
| NPPES Provider LastName | MORDES | |
| NPPES Provider FirstName | JOHN | |
| NPPES Provider ZIPCode | 016550002 | |
| NPPES Provider State | MA | |
| Specialty Description | Endocrinology | |
| Total Claim Count | 525.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1760466031 |
| Last Name Of The Provider | MORDES |
| First Name Of The Provider | JOHN |
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