Faculty Directory

Jay Kramer

Jay Kramer

Associate Research Professor of Biochemistry and Molecular Medicine
Associate Research Professor of Medicine (Secondary)

Office Phone: 202-994-3539
Email: Email
Department: Biochemistry and Molecular Medicine

Education

  • BA, Northeastern University, 1976
  • MS, Lehigh University, 1979
  • PhD, Lehigh University, 1982

Research

Mechanism(s) through which dietary Mg-restricted diets mediate a pro-inflammatory/oxidative condition in rodent models, with emphasis on dietary threshold levels; The impact of dietary Mg-restricted diets on rat hearts subjected to ischemia / reperfusion (I/R) stress; Investigate the neuropeptide release mechanism exhibited by postischemic rat hearts as well as normally-perfused rat hearts exposed to varying perfusate Mg concentrations; The influence of chronic AZT treatment on tissue iron content in normal and Mg-restricted rodents; Assess the altered cardiotoxic effects of doxorubicin during iron overload and Mg-deficiency in rodents using echocardiography; The involvement of endogenous iron redistribution as a mechanism to explain the beneficial effects of pre-conditioning on post-ischemically-stressed hearts; Determine the exogenous iron threshold level which predisposes hearts to I/R stress; Assess the acute and chronic antioxidant effects of d-propranolol and its analogs on I/R hearts from iron-loaded rats; and Use echocardiography to investigate the potential benefits of: d-propranolol treatment during iron overload in rodents; neurokinin-1 (substance P) receptor blockade during diet- or EGFR inhibitor-induced Mg deficiency in rodents; and Mg-supplementation during chronic exposure to potentially toxic HAART drugs in rodents.

Publications

View publications by this faculty member from January 1, 2013 - present

Mak, I.-T, Kramer, J.H., Chmielinska, J.J, Spurney, C.F., Weglicki, W.B. The EGFR TKI, erlotinib, causes hypomagnesemia, oxidative stress and cardiac dysfunction: attenuation by substance P-receptor blockade. J. Cardiovasc. Pharmacol. In Press. 2014.

Mak, I.-T, Kramer, J.H., Chmielinska, J.J, Spurney, C.F., Weglicki, W.B. The EGFR TKI, erlotinib, causes hypomagnesemia, oxidative stress and cardiac dysfunction: attenuation by substance P-receptor blockade. J. Cardiovasc. Pharmacol. In Press. 2014.

McCaffrey, T.A., Tziros, C., Lewis, J., Katz, R., Siegel, R., Weglicki,W., Kramer, J., Mak, I-T., Toma, I.,Chen, L., Benas, E., Lowitt, A., Rao, S., Witkins, L., Lian, Y., Lai, Y.,Yang, Z., Fu, S.W. Genomic Profiling Reveals the Potential Role of TCL1A and MDR1 Deficiency in Chemotherapy-Induced Cardiotoxicity. Int. J. Biol. Sci. 9(4):350-360, 2013.

Mak, I.-T, Kramer, J.H., Chen X., Chmielinska, J.J, Spurney, C.F., Weglicki, W.B. Mg-supplementation Attenuates Ritonavir-induced Hyperlipidemia, Oxidative Stress and Cardiac Dysfunction in Rats. Am. J. Physiol. Regul. Integr. Comp. Physiol. 305: R1102–R1111, 2013.

McCaffrey, T.A., Tziros, C., Lewis, J., Katz, R., Siegel, R.,Weglicki,W., Kramer, J., Mak, I-T., Toma, I., Chen, L., Benas, E., Lowitt, A., Rao, S., Witkins, L., Lian, Y., Lai, Y.,Yang, Z., Fu, S.W. Genomic Profiling Reveals the Potential Role of TCL1A and MDR1 Deficiency in Chemotherapy-Induced Cardiotoxicity. International Journal of Biological Sciences, In Press, 2013.

Kramer J.H., Spurney, C.F., Iantorno, M., Tziros, C., Chmielinska, J.J., Mak I-T., Weglicki W.B. D-propranolol protects against oxidative stress and progressive cardiac dysfunction in Fe-overloaded rats. Can. J. Physiol. Pharmacol. 90(9):1257-68, 2012.

Weglicki, W.B., Kramer, J.H., Spurney, C.F., Chmielinska, J.J., Mak, I.T. The EGFR tyrosine kinase inhibitor tyrphostin AG-1478 causes hypomagnesemia and cardiac dysfunction. Can. J. Physiol. Pharmacol. 90(8):1145-9, 2012.

Mak, I.-T, Chmielinska, J.J, Kramer, J.H., Spurney, C.F., Weglicki, W.B. Loss Of Neutral Endopeptidase Activity Contributes To Neutrophil Activation And Cardiac Dysfunction During Chronic Hypomagnesemia: Substance P-Receptor Blockade Affords Protection. Exp. Clin. Cardiol. 16(4):121-124, 2011.

Weglicki, W.B., Chmielinska, J.J., Kramer, J.H., Mak, I-Tong. Cardiovascular and intestinal responses to oxidative and nitrosative stress during prolonged magnesium deficiency. Am. J. Med. Scis. 342(2):125-128, 2011.

Weglicki, W.B., Mak, I.-T., Chmielinska, J.J., Tejero-Taldo, M.I., Komarov, A., Kramer, J.H. The role of Magnesium Deficiency in Cardiovascular and Intestinal Inflammation. Magnes. Res. 23(4):1-8, 2010.

Mak, I. T., Chmielinska, J.J., Kramer, J.H., Weglicki. W.B. AZT-Induced Cardiovascular Toxicity - Attenuation by Mg-Supplementation. Cardiovascular Toxicol. 9:78-85, 2009.

Kramer, J.H., Spurney, C., Iantorno, M., Tziros, C., Mak, I-T., Tejero-Taldo, M.I., Chmielinska, J.J., Komarov, A.M., Weglicki, W.B. Neurogenic inflammation and cardiac dysfunction due to hypomagnesemia in a rodent model. Am. J. Med. Sci., 338:22-27, 2009.

Mak, I.T., Kramer, J.H., Chmielinska, J.J., Khalid, H., Landgraf, K., Weglicki, W.B. Inhibition of Neutral endopeptidase potentiates neutrophil activation during Mg-deficiency in the rat. Inflammation Research 57:300-305, 2008.

Kramer JH, Murthi SB, Wise RM, Mak IT, Weglicki WB. Antioxidant and lysosomotropic properties of acute d-propranolol underlies its cardioprotection of postischemic hearts from moderate iron-overloaded rats. Exp. Biol. Med. 231:473-484, 2006

Tejero-Taldo, M.I., Kramer, J.H., Mak, I-Tong, Komarov, A.M., Chmielinska, J.J., Weglicki, W.B. The nerve-heart connection in the pro-oxidant response to Mg-deficiency. Heart Failure Reviews 11:35-44, 2006.

Kramer, J.H. , Mak, I. T., Phillips, T.M., and Weglicki, W.B. Dietary Mg-intake influence circulating pro-inflammatory neuropeptide levels and loss of myocardial tolerance to postischemic stress Exp. Biol. Med. 228:665-673, 2003.

Additional publications published before January 1, 2013 may be available within Himmelfarb Library's database.

Industry Relationships and Collaborations

This faculty member (or a member of their immediate family) has reported a financial interest with the healthcare related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.

  • None