Hillary Idogwu1, Magdalena Sokolska2, Pang Raymand 3, Saiful Islam4, Christopher Meehan 3, Adnan Avdic-Belltheus 3, Kathryn Marinello 3, Ingran Lingam 3, Tatenda Mutshiya 3, Alan Bainbridge 2, Nikki Robertson 3, David Thomas1, and Xavier Golay1
1Brain Repair and Rehabilitation, Institute of Neurology, UCL Queen Square Institute of Neurology, London, United Kingdom, 2Medical Physics and Biomedical Engineering, UCLH NHS Foundation Trust, London, United Kingdom, 3Neonatology, UCL EGA Institute for Women's Health, London, United Kingdom, 4UCL Queen Square Institute of Neurology, London, United Kingdom
1Brain Repair and Rehabilitation, Institute of Neurology, UCL Queen Square Institute of Neurology, London, United Kingdom, 2Medical Physics and Biomedical Engineering, UCLH NHS Foundation Trust, London, United Kingdom, 3Neonatology, UCL EGA Institute for Women's Health, London, United Kingdom, 4UCL Queen Square Institute of Neurology, London, United Kingdom
In this work, we hypothesised that the combination of CBF with BGT Lac/NAA would be more closely associated with quantitative cell death than either alone after HI or inflammation sensitized injury in a piglet model undergoing a variety of neuroprotective interventions.
Figure 1. Plots of correlation of 24h, 48h and average CBF with Cell death in BGT. (CBF = cerebral blood flow, BGT = basal ganglia thalamus)
Figure 2. Plots of correlation of 24h, 48h and average CBF with Iba1 ramification index in the cortex. Iba1 = ionized calcium binding adaptor molecule 1 (CBF = cerebral blood flow)