EPolar-UNet: An edge-attending polar UNet for automatic medical image segmentation with small datasets.

BACKGROUND: Medical image segmentation is one of the most key steps in computer-aided clinical diagnosis, geometric characterization, measurement, image registration, and so forth. Convolutional neural networks especially UNet and its variants have been successfully used in many medical image segmentation tasks. However, the results are limited by the deficiency in extracting high resolution edge information because of the design of the skip connections in UNet and the need for large available datasets. PURPOSE: In this paper, we proposed an edge-attending polar UNet (EPolar-UNet), which was trained on the polar coordinate system instead of classic Cartesian coordinate system with an edge-attending construction in skip connection path. METHODS: EPolar-UNet extracted the location information from an eight-stacked hourglass network as the pole for polar transformation and extracted the boundary cues from an edge-attending UNet, which consisted of a deconvolution layer and a subtraction operation. RESULTS: We evaluated the performance of EPolar-UNet across three imaging modalities for different segmentation tasks: CVC-ClinicDB dataset for polyp, ISIC-2018 dataset for skin lesion, and our private ultrasound dataset for liver tumor segmentation. Our proposed model outperformed state-of-the-art models on all three datasets and needed only 30%-60% of training data compared with the benchmark UNet model to achieve similar performances for medical image segmentation tasks. CONCLUSIONS: We proposed an end-to-end EPolar-UNet for automatic medical image segmentation and showed good performance on small datasets, which was critical in the field of medical image segmentation.

A ROS-responsive loaded desferoxamine (DFO) hydrogel system for traumatic brain injury therapy.

Traumatic brain injury (TBI) produces excess iron, and increased iron accumulation in the brain leads to lipid peroxidation and reactive oxygen species (ROSs), which can exacerbate secondary damage and lead to disability and death. Therefore, inhibition of iron overload and oxidative stress has a significant role in the treatment of TBI. Functionalized hydrogels with iron overload inhibiting ability and of oxidative stress inhibiting ability will greatly contribute to the repair of TBI. Herein, an injectable, post-traumatic microenvironment-responsive, ROS-responsive hydrogel encapsulated with deferrioxamine mesylate (DFO) was developed. The hydrogel is rapidly formed via dynamic covalent bonding between phenylboronic acid grafted hyaluronic acid (HA-PBA) and polyvinyl alcohol (PVA), and phenylboronate bonds are used to respond to and reduce ROS levels in damaged brain tissue to promote neuronal recovery. The release of DFO from HA-PBA/PVA hydrogels in response to ROS further promotes neuronal regeneration and recovery by relieving iron overload and thus eradicating ROS. In the Feeney model of Sprague Dawley rats, HA-PBA/PVA/DFO hydrogel treatment significantly improved the behavior of TBI rats and reduced the area of brain contusion in rats. In addition, HA-PBA/PVA/DFO hydrogel significantly reduced iron overload to reduce ROS and could effectively promote post-traumatic neuronal recovery. Its effects were also explored, and notably, HA-PBA/PVA/DFO hydrogel can reduce iron overload as well as ROS, thus protecting neurons from death. Thus, this injectable, biocompatible and ROS-responsive drug-loaded hydrogel has great potential for the treatment of TBI. This work suggests a novel method for the treatment of secondary brain injury by inhibiting iron overload and the oxidative stress response after TBI.

Human neural stem cell secretome relieves endoplasmic reticulum stress-induced apoptosis and improves neuronal functions after traumatic brain injury in a rat model.

Neural stem cell secretome (NSC-S) plays an important role in neuroprotection and recovery. Studies have shown that endoplasmic reticulum stress (ER stress) is involved in the progression of traumatic brain injury (TBI) and is a crucial cause of secondary damage and neuronal death after brain injury. Whether NSC-S is engaged in ER stress and ER stress-mediated neuronal apoptosis post-TBI has not been investigated. In the study, the Feeney SD male rat model was established. The results showed that NSC-S treatment significantly improved the behavior of rats with TBI. In addition, NSC-S relieved ER stress in TBI rats and was observed by transmission electron microscopy and western blot. The specific mechanism was further elucidated that restoration was achieved by alleviating the PERK-eIF2α pathway and thus protecting neurons from apoptosis. Notably, the discovery of calumenin (CALU) in NSC-S by liquid chromatography-tandem mass spectrometry (LC-MS/MS/MS) may be related to the protective effect of NSC-S on ER stress in neurons. Also, the mechanism by which it functions may be related to ubiquitination. In summary, NSC-S improved prognosis and ER stress in TBI rats and might be a promising treatment for relieving TBI.