Barbara McDermott

Research output

Research output per year 1992 1994 1996 1997 1998 2000 2001 2002 2004 2006 2007 2011 2020

• 44 Article
• 30 Meeting abstract
• 21 Abstract
• 9 Conference contribution

Research output per year

Research output per year

Search results

• 2016

  Glucagon-like peptide-1 based therapies as a novel approach for chronic heart failure

  Grieve, D., Robinson, E., Tate, M., Green, B. & McDermott, B., 30 May 2016, (Accepted).

  Research output: Contribution to conference › Abstract › peer-review

  • Combination Therapy 100%
  • Heart Failure 100%
  • Glucagon Like Peptide 1 100%
  • Glucagon-Like Peptide-1 100%
  • Diabetes Mellitus 80%

• Glucagon-like peptide-1 based therapies as a novel approach for chronic heart failure

  Grieve, D., Robinson, E., Tate, M., Green, B. & McDermott, B., 06 Feb 2016, (Accepted).

  Research output: Contribution to conference › Abstract

  • Combination Therapy 100%
  • Heart Failure 100%
  • Glucagon Like Peptide 1 100%
  • Glucagon-Like Peptide-1 100%
  • Diabetes Mellitus 80%
• 2015

  Exendin-4 Attenuates Experimental Diabetic Cardiomyopathy via Direct Actions on Inflammation

  Tate, M., Robinson, E., McDermott, B. J. & Grieve, D. J., May 2015.

  Research output: Contribution to conference › Abstract
• 2014

  Glucagon-like peptide-1 protects against adverse post-myocardial infarction remodeling via specific actions on inflammation and the extracellular matrix

  Robinson, E., Tate, M., McDermott, B., Green, B. D. & Grieve, D. J., Sept 2014, (Unpublished).

  Research output: Contribution to conference › Abstract › peer-review
• 2013

  Exendin-4 attenuates the development of experimental diabetic cardiomyopathy via specific actions on the extracellular matrix

  Tate, M., Robinson, E., McDermott, B. & Grieve, D., 2013, p. S6-S7. 2 p.

  Research output: Contribution to conference › Abstract › peer-review

• Glucagon-like peptide-1 improves cardiac function and protects against cardiac remodeling after myocardial infarction via specific actions on the extracellular matrix

  Robinson, E., Cassidy, R., Tate, M., McDermott, B., Green, B. & Grieve, D., 2013, p. S110-S111. 2 p.

  Research output: Contribution to conference › Abstract › peer-review
• 2012

  Cross-talk between NADPH oxidases and peroxisome proliferator-activated receptor-α differentially regulates left ventricular hypertrophy via specific activation of key signalling pathways.

  Harvey, A., Robinson, E., McDermott, B. & Grieve, D., 2012, p. S174. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Glucagon-like peptide-1 protects against cardiac dysfunction and extracellular matrix remodelling in experimental diabetes.

  Tate, M., Robinson, E., McDermott, B. & Grieve, D., 2012, p. A1. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Investigation of mechanisms underlying the interaction between Nox2 NADPH oxidase and PPAR-α in left ventricular hypertrophy.

  Harvey, A., Robinson, E., Simpson, D., McDermott, B. & Grieve, D., 2012, p. A2. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Modulation of oxidative stress induced apoptosis and autophagy in cardiomyocytes by intermedin.

  McCarthy, C., Zhao, Y., McKeag, P., Treggiari, D., McLaughlin, D., Colhoun, L., Grieve, D. & McDermott, B., 2012, p. A9-A10. 2 p.

  Research output: Contribution to conference › Abstract › peer-review
• 2011

  Does interaction between Peroxisome proliferator-activated receptor-α and NADPH oxidases play an important role in regulating pressure-overload cardiac hypertrophy?

  Harvey, A., Robinson, E., McDermott, B. & Grieve, D., 2011, p. e8. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Glucagon-like peptide-1 protects against cardiac remodeling after myocardial infarction via specific actions on the extracellular matrix.

  Robinson, E., Cassidy, R., McDermott, B., Green, B. & Grieve, D., 2011, p. e8. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Identification of an inherent mechanism of NADPH oxidase signalling in doxorubicin cardiotoxicity.

  McLaughlin, D., P, M., K, D., McVicar, C., Grieve, D. & McDermott, B., 2011, p. e8. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Mechanism of NADPH oxidase and downstream signalling in response to doxorubicin in cardiac myocytes.

  McLaughlin, D., P, M., K, D., McVicar, C., Grieve, D. & McDermott, B., 2011.

  Research output: Contribution to conference › Abstract › peer-review

• Modulation of extracellular matrix remodeling contributes to the protective effects of glucagon-like peptide-1 after myocardial infarction.

  Robinson, E., Cassidy, R., McDermott, B., Green, B. & Grieve, D., 2011, p. S41. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Peroxisome proliferator-activated receptor-α and NADPH oxidases interact to play an important regulatory role in pressure-overload cardiac hypertrophy.

  Harvey, A., Robinson, E., McDermott, B. & Grieve, D., 2011, p. S18. 1 p.

  Research output: Contribution to conference › Abstract › peer-review
• 2003

  ETA receptor-mediated contractile function is depressed in left ventricular cardiomyocyte hypertrophy and the response does not alter following transition to decompensated heart failure

  Kelso, E., Beadnell, G., Bell, D., Nicholls, P. & McDermott, B., 01 Jul 2003, p. 1. 1 p.

  Research output: Contribution to conference › Abstract › peer-review
• 2002

  Alterations in ETB receptor characteristics during development of hypertension-induced cardiomyocyte hypertrophy are prevented by bosentan

  Beadnell, G., Kelso, E., Bell, D., Nicholls, P. & McDermott, B., 01 Jul 2002, p. 1. 1 p.

  Research output: Contribution to conference › Abstract › peer-review
• 2001

  Altered ETB receptor-mediated signalling in ventricular cardiomyocytes in response to pressure overload

  Lee, G., Bell, D. & McDermott, B., 01 Aug 2001, p. 1. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• Contractile response to endothelin-1 is unaltered in response to pressure overload in the spontaneously hypertensive rat

  Argent, C., Bell, D., Kelso, E. & McDermott, B., 01 Sept 2001, p. 1. 1 p.

  Research output: Contribution to conference › Abstract › peer-review

• ETB receptor mediated cardiomyocyte hypertrophy in the spontaneously hypertensive rat

  Lee, G., Bell, D. & McDermott, B., 01 Sept 2001, p. 1. 1 p.

  Research output: Contribution to conference › Abstract › peer-review