Search

Acquiring High Resolution (HR) Magnetic Resonance (MR) images requires the patient to remain still for long periods of time, which causes patient discomfort and increases the probability of motion induced image artifacts. A possible solution is to acquire low resolution (LR) images and to process them with the Super Resolution Generative Adversarial Network (SRGAN) to create an HR version. Acquiring LR images requires a lower scan time than acquiring HR images, which allows for higher patient comfort and scanner throughput. This work applies SRGAN to MR images of the prostate to improve the in-plane resolution by factors of 4 and 8. The term 'super resolution' in the context of this paper defines the post processing enhancement of medical images as opposed to 'high resolution' which defines native image resolution acquired during the MR acquisition phase. We also compare the SRGAN to three other models: SRCNN, SRResNet, and Sparse Representation. While the SRGAN results do not have the best Peak Signal to Noise Ratio (PSNR) or Structural Similarity (SSIM) metrics, they are the visually most similar to the original HR images, as portrayed by the Mean Opinion Score (MOS) results., Comment: International Conference on Machine Learning Applications, 6 pages, 5 figures, 2 tables

Increased permeability of the blood-brain barrier (BBB) is important in neurological disorders. Neuroinflammation is associated with increased BBB breakdown and brain injury. Tumor necrosis factor-a (TNF-a) is involved in BBB injury and edema formation through a mechanism involving matrix metalloproteinase (MMP) upregulation. There is emerging evidence indicating that cyclooxygenase (COX) inhibition limits BBB disruption following ischemic stroke and bacterial meningitis, but the mechanisms involved are not known. We used intracerebral injection of TNF-a to study the effect of COX inhibition on TNF-a-induced BBB breakdown, MMP expression/activity and oxidative stress. BBB disruption was evaluated by the uptake of 14C-sucrose into the brain and by magnetic resonance imaging (MRI) utilizing Gd-DTPA as a paramagnetic contrast agent. Using selective inhibitors of each COX isoform, we found that COX-1 activity is more important than COX-2 in BBB opening. TNF-a induced a significant upregulation of gelatinase B (MMP-9), stromelysin-1 (MMP-3) and COX-2. In addition, TNF-a significantly depleted glutathione as compared to saline. Indomethacin (10 mg/kg; i.p.), an inhibitor of COX-1 and COX-2, reduced BBB damage at 24 h. Indomethacin significantly attenuated MMP-9 and MMP-3 expression and activation, and prevented the loss of endogenous radical scavenging capacity following intracerebral injection of TNF-a. Our results show for the first time that BBB disruption during neuroinflammation can be significantly reduced by administration of COX inhibitors. Modulation of COX in brain injury by COX inhibitors or agents modulating prostaglandin E2 formation/signaling may be useful in clinical settings associated with BBB disruption.