Automated Brain Hemorrhage Classification and Volume Analysis

Brain hemorrhage is a serious and life-threatening condition. It cancause permanent and lifelong disability even when it is not fatal. The wordhemorrhage denotes leakage of blood within the brain and this leakage ofblood from capillaries causes stroke and adequate supply of oxygen to thebrain is hindered. Modern imaging methods such as computed tomography(CT) and magnetic resonance imaging (MRI) are employed to get an idearegarding the extent of the damage. An early diagnosis and treatment can savelives and limit the adverse effects of a brain hemorrhage. In this case, a deepneural network (DNN) is an effective choice for the early identification andclassification of brain hemorrhage for the timely recovery and treatment of anaffected person. In this paper, the proposed research work is divided into twonovel approaches, where, one for the classification and the other for volumecalculation of brain hemorrhage. Two different datasets are used for twodifferent techniques classification and volume. A novel algorithm is proposedto calculate the volume of hemorrhage using CT scan images. In the firstapproach, the ‘RSNA’ dataset is used to classify the brain hemorrhage typesusing transfer learning and achieved an accuracy of 93.77%. Furthermore,in the second approach, a novel algorithm has been proposed to calculate thevolume of brain hemorrhage and achieved tremendous results as 1035.91mm3and 9.25 cm3, using the PhysioNet CT scan tomography dataset.

Efficient Morphological Segmentation of Brain Hemorrhage Stroke Lesion Through MultiResUNet

Brain Hemorrhagic stroke is a serious malady that is caused by the drop in blood flow through the brain and causes the brain to malfunction.Precise segmentation of brain hemorrhage is crucial,so an enhanced segmentation is carried out in this research work.The brain image of various patients has taken using an MRI scanner by the utilization of T1,T2,and FLAIR sequence.This work aims to segment the Brain Hemorrhagic stroke using deep learning-based Multi-resolution UNet(multires UNet)through morphological operations.It is hard to precisely segment the brain lesions to extract the existing region of stroke.This crucial step is accomplished by this proposed MMU-Net methodology by precise segmentation of stroke lesions.The proposed method efficiently determines the hemorrhagic stroke with improved accuracy of 95%compared with the existing segmentation techniques such as U-net++,ResNet,Multires UNET and 3D-ResU-Net and also provides improved performance of 2D and 3D U-Net with an enhanced outcome.The performancemeasure of the proposed methodology acquires an improved accuracy,precision ratio,sensitivity,and specificity rate of 0.07%,0.04%,0.04%,and 0.05%in comparison to U-net,ResNet,Multires UNET and 3D-ResU-Net techniques respectively.

Toll-like receptor 4 as a possible therapeutic target for delayed brain injuries after aneurysmal subarachnoid hemorrhage

Neuroinflammation is a well-recognized consequence of subarachnoid hemorrhage（SAH）, and Toll-like receptor（TLR） 4 may be an important therapeutic target for post-SAH neuroinflammation. Of the TLR family members, TLR4 is expressed in various cell types in the central nervous system, and is unique in that it can signal through both the myeloid differentiation primary-response protein 88-dependent and the toll receptor associated activator of interferon-dependent cascades to coordinate the maximal inflammatory response. TLR4 can be activated by many endogenous ligands having damage-associated molecular patterns including heme and fibrinogen at the rupture of an intracranial aneurysm, and the resultant inflammatory reaction and thereby tissue damages may furthermore activate TLR4. It is widely accepted that the excreted products of TLR4 signaling alter neuronal functions. Previous studies have focused on the pathway through nuclear factor（NF）-κΒ signaling among TLR4 signaling pathways as to the development of early brain injury（EBI） such as neuronal apoptosis and blood-brain barrier disruption, and cerebral vasospasm. However, many findings suggest that both pathways via NF-κΒ and mitogen-activated protein kinases may be involved in EBI and cerebral vasospasm development. To overcome EBI and cerebral vasospasm is important to improve outcomes after SAH, because both EBI and vasopasm are responsible for delayed brain injuries or delayed cerebral ischemia, the most important preventable cause of poor outcomes after SAH. Increasing evidence has shown that TLR4 signaling plays an important role in SAH-induced brain injuries. Better understanding of the roles of TLR4 signaling in SAH will facilitate development of new treatments.

Changes in hemeoxygenase-1 and superoxide dismutase in the peri-hematomal brain tissues of rats following intracerebral hemorrhage

BACKGROUND: The mechanism of intracerebral hemorrhage (ICH)-induced hemorrhagic brain injury is very complicated, involving the position-occupying effect of cephalophyma, ischemic factors, the toxic effect of hematoma components, the destruction of blood-brain barrier, etc. The expression and effect of hemeoxygenase-1 (HO-1) in the cerebrovascular disease has been paid close attention. OBJECTIVE: To observe the expression of HO-1 and change of superoxide dismutase (SOD) in the peri-hematomal brain tissue of rats following ICH. DESIGN: Randomized controlled animal experiment. SETTING: Department of Neurology, Yijishan Hospital Affiliated to Wannan Medical College. MATERIALS: Forty healthy male SD rats, of clean grade, weighing from 250 to 300 g, were provided by Qinglongshan Animal Farm of Nanjing. The involved 40 rats were randomized into sham-operation group (n =5) and ICH group (n =35), and ICH group was divided into 7 subgroups with 5 rats in each: ICH 6, 12, 24, 48, 72, 100 and 168 hours groups. Rabbit anti-rat HO-1 immunohistochemial kit ( Boster Co., Ltd., Wuhan) and SOD kit (Jiancheng Bioengineering Institute, Nanjing)were used in this experiment. METHODS: This experiment was carried out in the Department of Neurology, Yijishan Hospital Affiliated to Wannan Medical College Between April and July 2005. In the ICH group: Autologous blood of rats was injected into the head of caudate nucleus to create ICH animal models. In the sham-operation group, the same amount of normal saline was injected into the head of caudate nucleus of rats. The brains of rats in each group were harvested at different time points. The hematoma-side brain tissue was cut open in the coronal plane taking hematomal region as center, and the posterior part was fixed with 100 g/L neutral formaldehyde. 100 mg brain tissue was taken from anterior part. The number of positive cells in HO-1 and SOD activity in peri-hematomal brain tissue at different time after ICH were detected by immunohistochemical method and xanthine oxidation method respectively. MAIN OUTCOME MEASURES: ① The expression of HO-1 in the peri-hematomal brain tissue of rats in two groups following ICH.② The expression of SOD activity in the peri-hematomal brain tissue of rats in two groups following ICH. RESULTS: ①The number of HO-1 positive cells in the peri-hematomal brain tissue of rats in two groups following ICH 6, 12, 24, 48, 72, 120 and 168 hours was (11.03±2.01),(16.47±2.98),(25.50±5.65),(51.57±7.05),(47.33±4.73),(26.57±5.12),(7.63±2.17) cells/high-fold visual field , respectively; The number of HO-1 positive cells in the ICH 12-120 hours groups was significantly higher than that of sham-operation group [(6.07±1.85)cells/high-fold visual field, P < 0.01]; The HO-1 positive cells were the most in the ICH 48 hours group and were still expressed a little in the ICH 168 hours group. ② The SOD in the brain tissue of rats at ICH 6, 12, 24, 48, 72, 120 and 168 hours was (404.46±8.14),(396.84±10.97),(387.74±5.32),(356.21±9.27),(307.95±10.15),(357.48±11.28) and (402.98±7.23) kNU/g, respectively; The SOD activity of ICH 12 to 120 hours groups was significantly lower than that of sham-operation group [(415.47±11.44) kNU/g,P < 0.01], and that of ICH 72 hours group was the lowest. There was no significant difference of SOD activity between ICH 168 hours group and sham-operation group (P > 0.05). CONCLUSION: Following ICH, the expression of HO-1 in peri-hematomal brain tissue of rats in two groups is obviously increased, but the antioxidant ability of brain tissue is decreased. The changes of both maybe play an important role in the formation of ICH-induced hemorrhagic brain injury.

Susceptibility-weighted imaging is suitable for evaluating signal strength in different brain regions of a rabbit model of acute hemorrhagic anemia

Acute hemorrhagic anemia can decrease blood flow and oxygen supply to brain, and affect its physiological function. While detecting changes in brain function in patients with acute hemorrhagic anemia is helpful for preventing neurological complications and evaluating therapeutic effects, clinical changes in the nervous systems of these patients have not received much attention. In part, this is because current techniques can only indirectly detect changes in brain function following onset of anemia, which leads to lags between real changes in brain function and their detection.

Maltol as a Novel Agent Protecting SH-SY5Y Cells Against Hemin-induced Ferroptosis

Ferroptosis triggered by hemin is regarded as a primary factor accounting for neuronal death secondary to intracerebral hemorrhage.Thus,compounds with inhibitory effect on hemin-induced ferroptosis might be potential medicines to prevent neuronal death caused by intracerebral hemorrhage.Herein,we investigate whether maltol could alleviate hemin-induced SH-SY5Y cell ferroptosis and its potential mechanisms.It is found that maltol effectively prevents hemin-induced SH-SY5Y cell ferroptosis via three pathways.The first one is inhibiting intracellular iron increase via preventing upregulation of transferrin receptor,the second one is alleviating lipid peroxidation via attenuating H_(2)O_(2) generation by NOX4 and promoting H_(2)O_(2) clearance by catalase,and the third one is to reduce peroxidized lipids via maintaining GPX4/GSH pathway.Therefore,maltol is a novel agent preventing hemin-induced SH-SY5Y cell ferroptosis.