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• genetics, genomics and molecular biology
• infectious disease and the immune system
• cell and developmental biology/regenerative medicine
• neuroscience and mental health

• Paediatrics

• Haematology
• Hospice and palliative medicine
• Immunology
• Neonatology
• Psychiatry
• Radiology

Our research group aims to delineate perinatal and early neonatal inflammatory responses in health and disease. We have established longitudinal cohorts of infants with neonatal encephalopathy and preterm infants as well as neonatal controls in order to explore the role of early inflammatory changes and developmental and neuroimaging outcomes. We have studied the role of activated monocytes and neutrophils in neonatal diseases and the use of immunomodulatory agents such as vitamin d, vitamin a, melatonin, DMOG and activated protein c. We aim to understand the role of systemic inflammatory responses and neonatal multi organ outcome and the effect on childhood disorders and neurodevelopment. We are developing organ-specific biomarkers of longer term outcome and immunomodulation in vitro. Finally we are involved in the development of international clinical guidelines for neonatal sepsis and neonatal encephalopathy to implement to the results of he research.

Neonatal brain injury has multifactorial aetiology and causes significant neurological morbidity such as cerebral palsy. Therapeutic hypothermia (TH) is the only treatment available in term infants with neonatal encephalopathy (NE) but morbidity and mortality rates remain high with 50% of treated infants still having adverse outcomes. There is an urgent need for adjunctive therapies to improve neurodevelopmental outcomes. There is a narrow therapeutic window to activate neuroprotective therapies during the timeframe of the ischaemic reperfusion injury in NE. New biomarker identification will help to determine aetiology of NE and identify infants who will benefit from adjunctive therapies during this time period. Ischaemia reperfusion (IR) injury occurs when a hypoxic tissue is reperfused rapidly in NE. Oxidative damage, cellular apoptosis and atypical immune responses are generated through the production of mitochondrial oxygen species (ROS) in IR injury. ROS are produced at abnormally high levels during IR injury. Exploring this immune activation is crucial in the development of new treatments targeting ischaemic reperfusion injury. Preventing the accumulation of succinate, which is produced at high levels in persistent inflammation, via addition of malonate, a reversible inhibitor of succinate dehydrogenase will be explored as a therapy in IR injury alongside exploring other intermediates of the Kreb?s cycle as potential inhibitors of persistent inflammation. Babies with NE and control babies will be recruited across the 4 largest Maternity Hospitals in Ireland and cord blood and neonatal blood and urine samples analysed for markers of inflammation. MRI, clinical and neurodevelopmental outcome will be correlated with these results as well as multiorgan dysfunction, which occurs as a result of NE. The neurodevelopmental outcome will be assessed with clinical assessment and standardised developmental scoring systems.