Professor, Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School
Gastroenterology
Dr. John T. Lamont, MD
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John T. Lamont, MD is an expert in the field of Gastroenterology. He graduated from University of Rochester School of Medicine and Dentistry. He over the years received 1 awards: "Fellow (AGAF)". John T. Lamont, MD is a published doctor. He published 82 publications, including: 'Participation of reactive oxygen metabolites in Clostridium difficile toxin A-induced enteritis in rats.' Doctor John T. Lamont, MD is registered with Medicare and accepts Medicare payments.
Publications
- Clostridium difficile Infection: A Worldwide Disease.
- Overview of Clostridium difficile infection: implications for China.
- Fecal Transplantation for Recurrent Clostridium difficile Infection in Older Adults: A Review.
- The insect peptide, coprisin, prevents Clostridium difficile-mediated acute inflammation and mucosal damage through selective antimicrobial activity.
- Clostridium difficile toxin A decreases acetylation of tubulin, leading to microtubule depolymerization through activation of histone deacetylase 6, and this mediates ...
- Asymptomatic colonization by Clostridium difficile in infants: implications for Disease in later life.
- Recurrent clostridium difficile.
- Treatment of Clostridium difficile-associated Disease.
- Clostridium difficile--more difficult than ever.
- Clostridium difficile diarrhea: pathogenesis, epidemiology, and treatment.
- Clostridium difficile Colitis: epidemiology, pathophysiology, and treatment.
- Inactivation of Clostridium difficile cytotoxin by the neutrophil myeloperoxidase System.
- Pathophysiology, diagnosis and treatment of Clostridium difficile infection.
- Summary of Clostridium difficile workshop and symposium, 4-5 May 1995, Tours and Paris, France.
- Editorial: not so nosocomial anymore: the growing threat of community-acquired Clostridium difficile.
- Theodore E. Woodward Award. How bacterial enterotoxins work: insights from in vivo studies.
- Therapeutic implications of Clostridium difficile toxin during relapse of chronic inflammatory bowel Disease.
- Association of Clostridium difficile toxin with symptomatic relapse of chronic inflammatory bowel Disease.
- Counterimmunoelectrophoresis vs. cytotoxicity assay for the detection of Clostridium difficile toxin.
- Acute stress causes mucin release from rat colon: role of corticotropin releasing factor and mast cells.
- Clostridium difficile infection.
- Intravenous immunoglobulin therapy for severe Clostridium difficile Colitis.
- Experimental clindamycin-associated Colitis in rabbits. Evidence of toxin-mediated mucosal damage.
- Pathogenesis and clinical manifestations of Clostridium difficile diarrhea and Colitis.
- Clostridium difficile-associated diarrhea and Colitis: pathogenesis and therapy.
- Diagnostic tests for Clostridium difficile diarrhoea and Colitis: past, present and future.
- Clostridium difficile Colitis and diarrhea.
- Clostridium difficile cytotoxin inhibits protein synthesis in fibroblasts and Intestinal mucosa.
- Differential effects of Clostridium difficile toxins A and B on rabbit ileum.
- Clostridium difficile toxin B activates calcium influx required for actin disassembly during cytotoxicity.
- Treatment with intravenously administered gamma globulin of chronic relapsing Colitis induced by Clostridium difficile toxin.
- Clostridium difficile toxin B disrupts the barrier function of T84 monolayers.
- Effect of purified Clostridium difficile toxins on Intestinal smooth muscle. II. Toxin B.
- Effects of purified Clostridium difficile toxin A in the small intestine of the rat in vivo.
- Clostridium difficile toxin A-induced microVascular dysfunction. Role of histamine.
- Saccharomyces boulardii inhibits Clostridium difficile toxin A binding and enterotoxicity in rat ileum.
- Characterization of rabbit ileal receptors for Clostridium difficile toxin A. Evidence for a receptor-coupled G protein.
- Clostridium difficile toxin A stimulates intracellular calcium release and chemotactic response in human granulocytes.
- Effect of purified Clostridium difficile toxins on Intestinal smooth muscle. I. Toxin A.
- Bacteroides fragilis toxin 2 damages human colonic mucosa in vitro.
- Saccharomyces boulardii protease inhibits Clostridium difficile toxin A effects in the rat ileum.
- Rabbit sucrase-isomaltase contains a functional Intestinal receptor for Clostridium difficile toxin A.
- Diminished Clostridium difficile toxin A sensitivity in newborn rabbit ileum is associated with decreased toxin A receptor.
- CP-96,345, a substance P antagonist, inhibits rat Intestinal responses to Clostridium difficile toxin A but not cholera toxin.
- Comparative study of Clostridium difficile toxin A and cholera toxin in rabbit ileum.
- Clostridium difficile toxin A perturbs cytoskeletal structure and tight junction permeability of cultured human Intestinal epithelial monolayers.
- Clostridium difficile toxin A causes early damage to mitochondria in cultured cells.
- Mechanism of lovastatin-induced apoptosis in Intestinal epithelial cells.
- IL-8 release and neutrophil activation by Clostridium difficile toxin-exposed human monocytes.
- Purification and properties of Clostridium difficile cytotoxin B.
- Anti-Clostridium difficile bovine immunoglobulin concentrate inhibits cytotoxicity and enterotoxicity of C. difficile toxins.
- Survival of anti-Clostridium difficile bovine immunoglobulin concentrate in the human gastroIntestinal tract.
- C. difficile toxin A increases Intestinal permeability and induces Cl- secretion.
- Microbes and microbial toxins: paradigms for microbial-mucosal interactions II. The integrated response of the intestine to Clostridium difficile toxins.
- IL-11 inhibits Clostridium difficile toxin A enterotoxicity in rat ileum.
- Saccharomyces boulardii protease inhibits the effects of Clostridium difficile toxins A and B in human colonic mucosa.
- Macrophage-dependent stimulation of T cell-depleted spleen cells by Clostridium difficile toxin A and calcium ionophore.
- Bovine immunoglobulin concentrate-clostridium difficile retains C difficile toxin neutralising activity after passage through the human stomach and small intestine.
- A human antibody binds to alpha-galactose receptors and mimics the effects of Clostridium difficile toxin A in rat colon.
- Human colonic aspirates containing immunoglobulin A antibody to Clostridium difficile toxin A inhibit toxin A-receptor binding.
- Nitric oxide inhibits rat Intestinal secretion by Clostridium difficile toxin A but not Vibrio cholerae enterotoxin.
- Neuronal involvement in the Intestinal effects of Clostridium difficile toxin A and Vibrio cholerae enterotoxin in rat ileum.
- A receptor decoy inhibits the enterotoxic effects of Clostridium difficile toxin A in rat ileum.
- Epidermal growth factor attenuates Clostridium difficile toxin A- and B-induced damage of human colonic mucosa.
- Participation of reactive oxygen metabolites in Clostridium difficile toxin A-induced Enteritis in rats.
- Neutrophil recruitment in Clostridium difficile toxin A Enteritis in the rabbit.
- Clostridium difficile toxin A stimulates macrophage-inflammatory protein-2 production in rat Intestinal epithelial cells.
- Ketotifen inhibits Clostridium difficile toxin A-induced Enteritis in rat ileum.
- Involvement of Ras-related Rho proteins in the mechanisms of action of Clostridium difficile toxin A and toxin B.
- Clostridium difficile toxin B is more potent than toxin A in damaging human colonic epithelium in vitro.
- Clostridium difficile toxin A triggers human colonocyte IL-8 release via mitochondrial oxygen radical generation.
- Saccharomyces boulardii stimulates Intestinal immunoglobulin A immune response to Clostridium difficile toxin A in mice.
- Protein kinase C signaling regulates ZO-1 translocation and increased paracellular flux of T84 colonocytes exposed to Clostridium difficile toxin A.
- Clostridium difficile toxin B activates the EGF receptor and the ERK/MAP kinase pathway in human colonocytes.
- gp96 is a human colonocyte plasma membrane binding protein for Clostridium difficile toxin A.
- Protective role of HSP72 against Clostridium difficile toxin A-induced Intestinal epithelial cell dysfunction.
- p38 MAP kinase activation by Clostridium difficile toxin A mediates monocyte necrosis, IL-8 production, and Enteritis.
- Clostridium difficile toxin A-induced colonocyte apoptosis involves p53-dependent p21(WAF1/CIP1) induction via p38 mitogen-activated protein kinase.
- Inflammation and apoptosis in Clostridium difficile Enteritis is mediated by PGE2 up-regulation of Fas ligand.
- Clostridium difficile toxin A regulates inducible cyclooxygenase-2 and prostaglandin E2 synthesis in colonocytes via reactive oxygen species and activation of p38 MAPK.
- Clostridium difficile toxin A binds colonocyte Src causing dephosphorylation of focal adhesion kinase and paxillin.
Schools
University Of Rochester School Of Medicine and Dentistry
UCLA Med Center
Massachusetts General Hospital
Procedures Preformed
- Endoscopy (Esophagus, Stomach, Small Intestine)
Conditions Treated
- Abdominal Pain
- Anemia
- Benign Neoplasm of the Digestive System
- Cholecystitis and Gallstones
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Doctors Specialties
- Gastroenterology
Accepted Insurances
Awards
- Fellow (AGAF)
Education
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Massachusetts General Hospital -
UCLA Medical Center -
University of Rochester School of Medicine and Dentistry
Hospital
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Beth Israel Deaconess Medical Center
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