Brain-computer interface is a communication system that connects the brain with computer (or other devices) but is not dependent on the normal output of the brain (i.e., peripheral nerve and muscle). Electro-oculogram is a dominant artifact which has a significant negative influence on further analysis of real electroencephalography data. This paper presented a data adaptive technique for artifact suppression and brain wave extraction from electroencephalography signals to detect regional brain activities. Empirical mode decomposition based adaptive thresholding approach was employed here to suppress the electro-oculogram artifact. Fractional Gaussian noise was used to determine the threshold level derived from the analysis data without any training. The purified electroencephalography signal was composed of the brain waves also called rhythmic components which represent the brain activities. The rhythmic components were extracted from each electroencephalography channel using adaptive wiener filter with the original scale. The regional brain activities were mapped on the basis of the spatial distribution of rhythmic components, and the results showed that different regions of the brain are activated in response to different stimuli. This research analyzed the activities of a single rhythmic component, alpha with respect to different motor imaginations. The experimental results showed that the proposed method is very efficient in artifact suppression and identifying individual motor imagery based on the activities of alpha component.
(1) Electroencephalography is a convenient tool used to monitor brain activities and for psychophysiological research. Electro-oculogram is a dominant artifact which has a significant negative influence on further analysis of real electroencephalography data. The perfect separation of electro-oculogram artifact from the raw electroencephalography data is a crucial step for the application of brain-computer interface.
(2) A novel data adaptive filtering technique is introduced to suppress the electro-oculogram artifact without any loss of original electroencephalography data. Different frequency filtering-based approaches are already proposed to remove the artifacts. Such types of filtering destroy electroencephalography information and hence decrease the performance in brain computer interface applications. The proposed energy based adaptive thresholding method performs electro-oculogram removal without any training phase.
(3) A Wiener filter based approach is developed to separate the alpha rhythm which potentially represents brain activity. Thus the Wiener filter based adaptive filtering enhances the detection rate of brain activity.
(4) The topographic brain map is derived to monitor the spatial activities of the alpha wave yielding the classification of different motor imaginations.
Ideal tissue-engineered scaffold materials regulate proliferation, apoptosis and differentiation of cells seeded on them by regulating gene expression. In this study, aligned and randomly oriented collagen nanofiber scaffolds were prepared using electronic spinning technology. Their diameters and appearance reached the standards of tissue-engineered nanometer scaffolds. The nanofiber scaffolds were characterized by a high swelling ratio, high porosity and good mechanical properties. The proliferation of spinal cord-derived neural stem cells on novel nanofiber scaffolds was obviously enhanced. The proportions of cells in the S and G2/M phases noticeably increased. Moreover, the proliferation rate of neural stem cells on the aligned collagen nanofiber scaffolds was high. The expression levels of cyclin D1 and cyclin-dependent kinase 2 were increased. Bcl-2 expression was significantly increased, but Bax and caspase-3 gene expressions were obviously decreased. There was no significant difference in the differentiation of neural stem cells into neurons on aligned and randomly oriented collagen nanofiber scaffolds. These results indicate that novel nanofiber scaffolds could promote the proliferation of spinal cord-derived neural stem cells and inhibit apoptosis without inducing differentiation. Nanofiber scaffolds regulate apoptosis and proliferation in neural stem cells by altering gene expression.
(1) Electronic spinning technology was used to obtain randomly oriented nanofiber membranes and aligned nanofiber membranes. The aligned and randomly oriented collagen nanometer scaffolds were shown to alter the biological behaviors of neural stem cells and induce changes in gene expression.
(2) The effects of the aligned nanofiber membranes on promoting neural stem cell proliferation and on inhibiting apoptosis of neural stem cells were better than those of the randomly oriented nanofiber membranes. Aligned and randomly oriented collagen nanometer scaffolds did not significantly induce apoptosis or differentiation in stem cells.
(3) Aligned and randomly oriented collagen nanometer scaffolds regulated the expression of apoptosis and cell cycle genes in neural stem cells.
The motor relearning program can significantly improve various functional disturbance induced by ischemic cerebrovascular diseases. However, its mechanism of action remains poorly understood. In injured brain tissues, glial fibrillary acidic protein and neurofilament protein changes can reflect the condition of injured neurons and astrocytes, while vascular endothelial growth factor and basic fibroblast growth factor changes can indicate angiogenesis. In the present study, we induced ischemic brain injury in the rhesus macaque by electrocoagulation of the M1 segment of the right middle cerebral artery. The motor relearning program was conducted for 60 days from the third day after model establishment. Immunohistochemistry and single-photon emission CT showed that the numbers of glial fibrillary acidic protein-, neurofilament protein-, vascular endothelial growth factor-and basic fibroblast growth factor-positive cells were significantly increased in the infarcted side compared with the contralateral hemisphere following the motor relearning program. Moreover, cerebral blood flow in the infarcted side was significantly improved. The clinical rating scale for stroke was used to assess neurological function changes in the rhesus macaque following the motor relearning program. Results showed that motor function was improved, and problems with consciousness, self-care ability and balance function were significantly ameliorated. These findings indicate that the motor relearning program significantly promoted neuronal regeneration, repair and angiogenesis in the surroundings of the infarcted hemisphere, and improve neurological function in the rhesus macaque following brain ischemia.
(1) We established a brain ischemia model in the rhesus macaque, as they exhibit more similar properties in inheritance and physiology compared with rodents.
(2) We examined the influence of a motor relearning program on neurological function and expression of glial fibrillary acidic protein, neurofilament protein, vascular endothelial growth factor and basic fibroblast growth factor in brain regions surrounding the ischemic region.
(3) The motor relearning program significantly promoted neuronal repair, regeneration and angiogenesis, and improved neurological function of the rhesus macaque after brain ischemia.
Increasing evidence has revealed that the activation of the JNK pathway participates in apoptosis of nerve cells and neurological function recovery after traumatic brain injury. However, which genes in the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in cell apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1, 3, 5, 14 and 28 days post injury.
These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.
(1) The downregulation of JNK3 expression in the peripheral area of the injured cerebral cortex in the early stages of traumatic brain injury may be associated with apoptosis of nerve cells. However, JNK1 and JNK2 expression remained unchanged.
(2) Changes in JNK3 expression in rats with traumatic brain injury correlated well with nerve cell apoptosis and neurological function changes.
(3) More apoptotic nerve cells were found at early stages when compared with late stage traumatic brain injury, which may be related to the induction of neural regeneration and repair and inhibition of cell apoptosis.
(4) JNK3 is involved in nerve cell apoptosis, neurological function recovery and neural regeneration.
We report on a stroke patient who showed delayed gait recovery between 8 and 11 months after the onset of intracerebral hemorrhage. This 32-year-old female patient underwent craniotomy and drainage for right intracerebral hemorrhage due to rupture of an arteriovenous malformation. Brain MR images revealed a large leukomalactic lesion in the right fronto-parietal cortex. Diffusion tensor tractography at 8 months after onset revealed that the right corticospinal tract was severely injured. At this time, the patient could not stand or walk despite undergoing rehabilitation from 2 months after onset. It was believed that severe spasticity of the left leg and right ankle was largely responsible, and thus, antispastic drugs, antispastic procedures (alcohol neurolysis of the motor branch of the tibial nerve and an intramuscular alcohol wash of both tibialis posterior muscles) and physical therapy were tried to control the spasticity. These measures relieved the severe spasticity, with the result that the patient was able to stand at 3 months. In addition, the improvements in sensorimotor function, visuospatial function, and cognition also seemed to contribute to gait recovery. As a result, she gained the ability to walk independently on even floor with a left ankle foot orthosis at 11 months after onset. This case illustrates that clinicians should attempt to find the cause of gait inability and to initiate intensive rehabilitation in stroke patients who cannot walk at 3-6 months after onset.
(1) This case report describes a stroke patient who demonstrated delayed gait recovery between 8 and 11 months after the onset of intracerebral hemorrhage.
(2) Severe spasticity of the lower extremity seemed to be largely responsible for gait inability in this patient.
(3) Clinicians should find the cause of gait inability and initiate intensive rehabilitation in stroke patients.
Vitamin D plays an important role in maintaining normal bone metabolism. Recent studies have suggested that vitamin D influences many other physiological processes, including muscle function, cardiovascular homeostasis, nerve function, and immune response. Furthermore, accumulated evidence suggests that vitamin D also mediates the immune system response to infection. Critical neurosurgical patients have higher infection and mortality rates. To correlate vitamin D deficiency to the immunological status of neurosurgical intensive care unit patients, we detected serum vitamin D level in 15 patients with clinically suspected infection and 10 patients with confirmed infection. Serum level of 25-hydroxyvitamin D, the primary circulating form of vitamin D, was significantly decreased in patients with suspected or confirmed infection after a 2-week neurosurgical intensive care unit hospitalization, while serum level of 1,25-dihydroxyvitamin D, the active form of vitamin D, was significantly decreased in patients after a 4-week neurosurgical intensive care unit hospitalization. These findings suggest that vitamin D deficiency is linked to the immunological status of neurosurgical intensive care unit patients and vitamin D supplementation can improve patient's immunological status.
(1) Vitamin D deficiency was correlated to the immunological status of neurosurgical intensive care unit patients.
(2) Serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were significantly decreased in patients with clinically suspected infection and confirmed infection after 2- and 4-week neurosurgical intensive care unit hospitalization.
(3) Vitamin D supplementation can help improve the immunological status of patients in the neurosurgical intensive care unit.
The miniature pig is an optimal animal model for studying nervous system disease because of its physiologic and pathologic features. However, the rete mirabile composed of arteries and veins at the skull base limits their application as a model of ischemic stroke by middle cerebral artery occlusion. The present study investigated the possibility of establishing an ischemic stroke model in the miniature pig by blocking the skull base retia with sodium alginate microspheres. Three Bama miniature pigs were used. Using the monitor of C-arm X-ray machine, sodium alginate microspheres (100-300 μm), a novel embolic material, were injected through the femoral artery, aortic arch, common carotid artery, ascending pharyngeal artery and the retia. Results were evaluated using carotid arteriography, MRI, behavior observation and histology. The unilateral rete mirabile was completely blocked, resulting in disturbance in blood supply to the basal ganglia, astasia of the right hind limb and salivation. MRI and hematoxylin-eosin staining showed an evident infarction focus in the basal ganglia. These findings indicate that sodium alginate microspheres are a suitable embolic material for blocking the skull base retia in miniature pigs to establish an ischemic stroke models.
(1) Miniature pigs can survive for a long period of time, are cost-effective and controllable. Thus, they are regarded as excellent models for studying nervous system diseases.
(2) The rete mirabile composed of arteries and veins at the skull base limits their application as an ischemic stroke model by middle cerebral artery occlusion.
(3) Sodium alginate microspheres can occlude the skull base retia of miniature pigs to establish ischemic stroke models.
(4) This method challenges the concept that the swine cannot be used to establish models of ischemic cerebrovascular diseases.
The scavenger receptor class B type I gene can protect against atherosclerosis; a mononucleotide polymorphism is associated with differences in blood lipid metabolism, postprandial serum lipid levels, insulin resistance, coronary artery disease and familial hyperlipidemia. In this study, the scavenger receptor class B type I gene exon 1 G4A gene polymorphism in atherosclerotic cerebral infarction patients, cerebral hemorrhage patients and normal controls was detected using the polymerase chain reaction-restriction fragment length polymorphism method. The results showed that the GA + AA genotype frequency of scavenger receptor class B type I gene G4A in atherosclerotic cerebral infarction patients was similar to that in cerebral hemorrhage patients and normal controls; however, the A allele frequency was significantly lower than that in normal controls. The serum level of high-density lipoprotein cholesterol in patients with the scavenger receptor class B type I gene G4A GA + AA genotype was significantly higher, while the serum level of low-density lipoprotein cholesterol was significantly lower than that in patients with the GG genotype, in both the atherosclerotic cerebral infarction and cerebral hemorrhage groups. The serum level of high-density lipoprotein cholesterol in patients with the scavenger receptor class B type I gene G4A GA + AA genotype was significantly higher, while the serum levels of low-density lipoprotein cholesterol and total cholesterol were significantly lower than those in normal controls with the GG genotype. Our experimental results suggest that the G4A polymorphism of the scavenger receptor class B type I gene is a possible predisposing risk factor for atherosclerotic cerebral infarction, and that it has no association with cerebral hemorrhage in the Han population in Hunan province of China. The A allele is possibly associated with the metabolism of high-density and low-density lipoprotein cholesterol.
(1) The scavenger receptor class B type I gene exon 1 G4A polymorphism locus may be associated with atherosclerotic cerebral infarction in the Han population from Hunan province of China, while it has no association with cerebral hemorrhage.
(2) When the scavenger receptor class B type I gene exon 1 G4A polymorphism mutates from G to A, leading to amino acid changes, changes in the structure of the protein may affect its functions and accordingly affect scavenger receptor class B type I gene expression. This impacts lipid metabolism and participates in the development of atherosclerosis, ultimately resulting in atherosclerotic cerebral infarction.
(3) Scavenger receptor class B type I gene may influence high-density and low-density lipoprotein metabolism, thus affecting the development of diseases relevant to atherosclerosis.
Lipopolysaccharide stimulates Toll-like receptor 4 on immune cells to produce immune mediators. Toll-like receptor 4 is also expressed by non-immune cells, which can be stimulated by lipopolysaccharide. However, whether Toll-like receptor 4 is expressed by primary cultured hippocampal neurons and its specific role in lipopolysaccharide-induced neuroinflammation is currently undefined. In this study, Toll-like receptor 4 antibody blocking was used to analyze the Toll-like receptor 4 signaling pathway and changes in inflammation of lipopolysaccharide stimulated hippocampal neurons. Immunofluorescence showed that Toll-like receptor 4 protein was mainly located in the membrane of hippocampal neurons. Quantitative reverse transcription-PCR and western blot assay showed that after stimulation of lipopolysaccharide, the mRNA and protein levels of Toll-like receptor 4 and the mRNA levels of interleukin-1β and tumor necrosis factor-α were significantly increased. In addition, there was increased phosphorylation and degradation of kappa B α inhibitor in the cytosol and increased nuclear factor-κB p65 expression in the nuclei. Pretreatment with Toll-like receptor 4 antibody could almost completely block this increase. These experimental findings indicate that lipopolysaccharide participates in neuroinflammation by stimulating Toll-like receptor 4/nuclear factor-κB pathway in hippocampal neurons, which may be both “passive victims” and “activators” of neuroinflammation.
(1) Lipopolysaccharide can activate the signaling pathway of nuclear factor-kappa B through Toll-like receptor 4 in rat hippocampal neurons, thus inducing neuroinflammation.
(2) Neurons may be both “passive victims” and “activators” of neuroinflammation.
We propose a method of reliable tracking orientation and flexible step size fiber tracking. A new directional strategy was defined to select one optimal tracking orientation from each directional set, which was based on the single-tensor model and the two-tensor model. The directional set of planar voxels contained three tracking directions: two from the two-tensor model and one from the single-tensor model. The directional set of linear voxels contained only one principal vector. In addition, a flexible step size, rather than fixable step sizes, was implemented to improve the accuracy of fiber tracking. We used two sets of human data to assess the performance of our method; one was from a healthy volunteer and the other from a patient with low-grade glioma. Results verified that our method was superior to the single-tensor Fiber Assignment by Continuous Tracking and the two-tensor eXtended Streamline Tractography for showing detailed images of fiber bundles.
(1) There is no gold standard to verify brain fiber tracking. There are several diffusion tensor fiber imaging methods including the linear method, probabilistic method, and the energy minimization method. Branching of fiber bundles and high accuracy fiber tracking are important in neuroimaging studies, for which the linear method is extensively used. The multiple-tensor model for solving the problem of branching is also becoming increasingly popular.
(2) We propose a novel linear method that can reveal more real fiber bundles compared with single-tensor Fiber Assignment by Continuous Tracking and two-tensor eXtended Streamline Tractography, and which was consistent with the anatomical structure. Our method used a tracking orientation choice and a flexible step size to ensure the reliability of tracking.
(3) We used human data to compare tracking outcomes of reliable tracking orientation and flexible step size fiber tracking with single-tensor Fiber Assignment by Continuous Tracking and two-tensor extended Streamline Tractography in a healthy volunteer and a patient with low-grade glioma.
(4) We qualitatively and quantitatively assessed the advantages and disadvantages of our method, single-tensor Fiber Assignment by Continuous Tracking, and two-tensor eXtended Streamline Tractography.
(5) Our method was superior to the single-tensor Fiber Assignment by Continuous Tracking and the two-tensor eXtended Streamline Tractography for detailed visualization of fiber bundles.