Phillips AR

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Name Phillips AR,
Institution University of Auckland

School of Biological Sciences

Applied Surgery and Metabolism Laboratory

Address Thomas Building - 3 a

Symonds Street,

City Auckland
State/Province
Country New Zealand
Email c.tse@auckland.ac.nz
Weblink
O2k-Network Lab NZ Auckland Hickey AJ


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Publications

 PublishedReference
Chu 2016 World J Gastroenterol2016Chu MJ, Premkumar R, Hickey AJ, Jiang Y, Delahunt B, Phillips AR, Bartlett A (2016) Steatotic livers are susceptible to normothermic ischemia-reperfusion injury from mitochondrial Complex-I dysfunction. World J Gastroenterol 22:4673-84.
Chakraborty 2016 Pancreatology2016Chakraborty M, Hickey AJ, Petrov MS, Macdonald JR, Thompson N, Newby L, Sim D, Windsor JA, Phillips AR (2016) Mitochondrial dysfunction in peripheral blood mononuclear cells in early experimental and clinical acute pancreatitis. Pancreatology 16:739-47.
Chu 2015 Liver Transpl2015Chu MJ, Hickey AJ, Jiang Y, Petzer A, Bartlett AS, Phillips AR (2015) Mitochondrial dysfunction in steatotic rat livers occurs because a defect in complex I makes the liver susceptible to prolonged cold ischemia. Liver Transpl 21:396-407.
Chu 2014 PLoS One2014Chu MJ, Hickey AJ, Tagaloa S, Zhang L, Dare AJ, MacDonald JR, Yeong ML, Bartlett AS, Phillips AR (2014) Ob/ob mouse livers show decreased oxidative phosphorylation efficiencies and anaerobic capacities after cold ischemia. PLoS One 9:e100609.
Chu 2013 PLoS One2013Chu MJ, Phillips AR, Hosking AW, Macdonald JR, Bartlett AS, Hickey AJ (2013) Hepatic mitochondrial function analysis using needle liver biopsy samples. PLoS One 8:e79097.
Mittal 2011 HPB (Oxford)2011Mittal A, Hickey AJ, Chai CC, Loveday BP, Thompson N, Dare A, Delahunt B, Cooper GJ, Windsor JA, Phillips AR (2011) Early organ-specific mitochondrial dysfunction of jejunum and lung found in rats with experimental acute pancreatitis. HPB (Oxford) 13:332-41.
Hickey 2009 Am J Physiol Cell Physiol2009Hickey AJ, Chai CC, Choong SY, de Freitas Costa S, Skea GL, Phillips AR, Cooper GJ (2009) Impaired ATP turnover and ADP supply depress cardiac mitochondrial respiration and elevate superoxide in nonfailing spontaneously hypertensive rat hearts. Am J Physiol Cell Physiol 297:C766–74.

Abstracts

 PublishedReference
Power 2014 Abstract MiP20142014The hot heart: cardiac mitochondrial energetics during hyperthermia.