A. J. Cunningham
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Also affiliated: Ontario Institute for Cancer Research (1978–2004); Australian National University (1965–1977); Royal College of Surgeons in Ireland (1988–2001); University of Ottawa (1984); University of Toronto (1978–2004); Universität Ulm (2002); Cappagh National Orthopaedic Hospital (2001); University Hospital of Wales (2017); Cancer Institute (WIA) (1978); Beaumont Hospital (1988–2007); The Alfred Hospital (2014); Botsford Hospital (2007); Cork University Hospital (1992–2001); Princess Margaret Cancer Centre (1995–2001); Northern Health and Social Care Trust (2025); In-Q-Tel (2003); The Catholic University of Korea St. Vincent's Hospital (1985); St. Vincent's University Hospital (1985); Beaumont Hospital, Dearborn (2007); National Maternity Hospital (1989); Institute for Cancer Prevention (2002); University of Sunderland (2010–2012)
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Biography and Research Information
OverviewAI-generated summary
A. J. Cunningham's research has explored various aspects of immunology and medical interventions. Early work focused on methods for detecting single antibody-forming cells and investigating the mechanisms of immune tolerance in mice. More recent publications indicate a shift towards clinical research, including studies on the effects of psychological therapy on breast cancer patients, prediction of difficult tracheal intubation, and the impact of fenoldopam on renal function in surgical patients. Cunningham has also investigated the identification of tobacco-derived compounds in human pancreatic juice. With an h-index of 14 and over 1,500 citations, Cunningham has contributed to a publication record of 64 works. Collaborations include shared publications with Abdelrahman Y. Fouda, Carol Morris, and Piyanan Chuesiang.
Metrics
- h-index: 14
- Publications: 64
- Citations: 1,505
Selected Publications
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Myeloid HDAC3 deletion protects against traumatic optic injury (2026)
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HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis (2025)
Collaboration Network
Top Collaborators
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
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