Professor, Pharmacology, Stony Brook University SOM

Internal Medicine

Arthur P. Grollman, MD works in the field of Internal Medicine. He studied medicine at Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is a one of the best medicals schools. Johns Hopkins University School of Medicine is ranked 3/29 in Research/PrimaryCare. He over the years received 1 awards: "Elected Member". Arthur P. Grollman is also published. He has 99 publications published. The lastest publication: "A dynamic checkpoint in oxidative lesion discrimination by formamidopyrimidine-DNA glycosylase.'

Publications

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• A dynamic checkpoint in oxidative lesion discrimination by formamidopyrimidine-DNA glycosylase.
• Chronic dietary exposure to aristolochic acid and kidney function in native farmers from a Croatian endemic area and Bosnian immigrants.
• Active destabilization of base pairs by a DNA glycosylase wedge initiates damage recognition.
• Aristolochic acid-induced apoptosis and G2 cell cycle arrest depends on ROS generation and MAP kinases activation.
• Formalin-Fixed Paraffin Embedded Tissue as a Source for Quantitation of Carcinogen DNA Adducts: Aristolochic Acid as a Prototype Carcinogen.
• Bioactivation of the human carcinogen aristolochic acid.
• Mutational signature of aristolochic Acid exposure as revealed by whole-exome sequencing.
• Human Formalin-Fixed Paraffin-Embedded Tissues: An Untapped Specimen for Biomonitoring of Carcinogen DNA Adducts by Mass Spectrometry.
• TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal.
• Aristolochic acid nephropathy: Harbinger of a global iatrogenic disease.
• A fluorescence-based analysis of aristolochic acid-derived DNA adducts.
• Biomonitoring of Aristolactam-DNA Adducts in Human Tissues Using Ultra-Performance Liquid Chromatography/Ion-Trap Mass Spectrometry.
• Lack of recognition by global-genome nucleotide excision repair accounts for the high mutagenicity and persistence of aristolactam-DNA adducts.
• Aristolactam-DNA adducts are a biomarker of environmental exposure to aristolochic acid.
• Energetic Preference of 8-oxoG Eversion Pathways in a DNA Glycosylase.
• TP53 Mutational signature for aristolochic acid: An environmental carcinogen.
• Detoxification of aristolochic acid I by O-demethylation: less nephrotoxicity and genotoxicity of aristolochic acid Ia in rodents.
• Cytochrome P450 1A2 detoxicates aristolochic acid in the mouse.
• Molecular mechanics parameters for the FapydG DNA lesion.
• Molecular simulations reveal a common binding mode for glycosylase binding of oxidatively damaged DNA lesions.
• Role of environmental toxins in endemic (Balkan) nephropathy. October 2006, Zagreb, Croatia.
• Limitations of "evidence-based indications" for herbs.
• Aristolochic acid and the etiology of endemic (Balkan) nephropathy.
• Selective toxicity of aristolochic acids I and II.
• Catalytic mechanism of Escherichia coli endonuclease VIII: roles of the intercalation loop and the zinc finger.
• Computational analysis of the mode of binding of 8-oxoguanine to formamidopyrimidine-DNA glycosylase.
• Science and government. Review for NCCAM is overdue.
• Quantitative determination of aristolochic acid-derived DNA adducts in rats using 32P-postlabeling/polyacrylamide gel electrophoresis analysis.
• Proteomic approach to identification of proteins reactive for abasic sites in DNA.
• Dynamic behavior of DNA base pairs containing 8-oxoguanine.
• Academic perspectives on dietary supplements use: the need for new guidelines.
• Substrate discrimination by formamidopyrimidine-DNA glycosylase: distinguishing interactions within the active site.
• Mutagenic potential of benzo[a]pyrene-derived DNA adducts positioned in codon 273 of the human P53 gene.
• Mechanism of frameshift (deletion) generated by acetylaminofluorene-derived DNA adducts in vitro.
• Mutagenic properties of 3-(deoxyguanosin-N2-yl)-2-acetylaminofluorene, a persistent acetylaminofluorene-derived DNA adduct in mammalian cells.
• Substrate discrimination by formamidopyrimidine-DNA glycosylase: a mutational analysis.
• The thermodynamics of template-directed DNA synthesis: base insertion and extension enthalpies.
• Ephedra-free is not danger-free.
• Identification of tamoxifen-DNA adducts in monkeys treated with tamoxifen.
• Structure of DNA polymerase beta with the mutagenic DNA lesion 8-oxodeoxyguanine reveals structural insights into its coding potential.
• Botanical medicines--the need for new regulations.
• Mutagenic events in Escherichia coli and mammalian cells generated in response to acetylaminofluorene-derived DNA adducts positioned in the Nar I restriction enzyme site.
• Combining structural and bioinformatics methods for the analysis of functionally important residues in DNA glycosylases.
• Structure of formamidopyrimidine-DNA glycosylase covalently complexed to DNA.
• Translesion synthesis by human DNA polymerase kappa on a DNA template containing a single stereoisomer of dG-(+)- or dG-(-)-anti-N(2)-BPDE (7,8-dihydroxy-anti-9,10-epo...
• Genotoxic mechanism for the major acrolein-derived deoxyguanosine adduct in human cells.
• Glutamate dehydrogenase requirement for apoptosis induced by aristolochic acid in renal tubular epithelial cells.
• Management of uremia.
• STEROID HORMONE THERAPY.
• ANTIHYPERTENSIVE AND PRESSOR AGENTS OF RENAL ORIGIN.
• THE PATHOGENESIS OF HYPERTENSIVE CARDIOVASCULAR DISEASE.
• CAUSATIVE MECHANISMS IN ESSENTIAL HYPERTENSION.
• DIURETICS.
• GLUCAGON DEFICIENCY AS A CAUSE OF HYPOGLYCEMIA.
• EXPERIMENTAL PERIARTERITIS NODOSA IN THE RAT.
• AUTOIMMUNE FACTORS ASSOCIATED WITH INFARCTION OF THE KIDNEY.
• PERSONALITY CHANGES, HEADACHES AND ATAXIA.
• THE DIAGNOSIS OF GOUT.
• PRESSOR ACTIVITY OF RENAL VENOUS BLOOD IN HYPERTENSION.
• Enzymes of the kidney of the normal and hypertensive rat.
• A simplified procedure for the routine determination of uric acid.
• HYPOGLYCEMIA.
• REMEDIABLE HYPERTENSION DUE TO UNILATERAL RENAL DISEASE: CORRELATION OF SPLIT RENAL-FUNCTION TESTS AND PRESSOR ASSAYS OF RENAL VENOUS BLOOD IN HYPERTENSIVE PATIENTS.
• Hypotension-inducing drugs and their relation to hypertension.
• The pathogenesis of adrenal regeneration hypertension.
• Mechanisms of arterial blood pressure variations.
• Parathyroid syndromes and calcium metabolism.
• The preparation of renal extracts effective in reducing blood pressure in experimental hypertension.
• Induction of renal hypertension in rats and dogs by potassium or choline deficiency.
• Present concepts of the mechanism of urine formation and of diuretic action.
• Clinical pharmacology of antihypertensive agents.
• Electron microscopy in experimental hypertension; glomerular changes in choline-deficiency-induced hypertension in the rat.
• Toxicity of urea and its role in the pathogenesis of uremia.
• Renal lesions in experimental hypertension; morphological changes in the kidney of rats rendered chronically hypertensive following a period of choline deficiency.
• A unitary concept of experimental and clinical hypertensive cardiovascular disease.
• The role of salt in health and disease.
• The role of cholesterol in the body.
• The respiratory function of the lungs in health and disease.
• The relationship of salt and diet to diastolic hypertension.
• Maintenance of the cardiovascular system in the aged.
• The teratogenic induction of hypertension.
• Renal function in hypertensive cardiovascular disease of rat.
• Induction of hypertension in the frog by bilateral nephrectomy.
• The use and abuse of drugs.
• PRESSOR ACTIVITY OF RENAL VENOUS EFFLUENT OF NORMAL AND HYPERTENSIVE RATS.
• General aspects of hypertension; past, present and future.
• The effect of medullectomy and corticectomy on renal excretory function in the rat.
• Localization of blood pressure regulating and erythropoietic functions in rat kidney.
• A study of hypertension in the rat induced by infarction of the kidney.
• Medical management of hypertension.
• Atherosclerosis in the chicken. Correlation of the arterial blood pressure and arterial changes in the chicken.
• Metabolic observations in essential hypertension: sodium, chloride, potassium, water and hormones.
• The evaluation of therapeutic procedures used in the management of essential hypertension.
• The direct action of squill on the kidney as compared to certain other digitalis bodies.
• Surgical treatment of hypertension.
• The pathogenesis and treatment of hypertensive cardiovascular disease.
• Salt and water metabolism.
• Diabetes mellitus; physiologic considerations.

Schools

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• Johns Hopkins University School of Medicine

Doctors Specialties

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• Internal Medicine

Accepted Insurances

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Awards

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• Elected Member

Education

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• Johns Hopkins University
• Johns Hopkins University School of Medicine

Hospital

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• Stony Brook University Medical Center

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