Currently, about one-third of patients with anti-epilepsy drug or resective surgery continue to have sezure, the mechanism remin unknown. Up to date, the main target for presurgical evaluation is to determene the EZ and SOZ. Since the early nineties of the last century network theory was introduct into neurology, provide new insights into understanding the onset, propagation and termination. Focal seizure can impact the function of whole brain, but the abnormal pattern is differet to generalized seizure. Brain network is a conception of mathematics. According to the epilepsy, network node and hub are related to the treatment. Graphy theory and connectivity are main algorithms. Understanding the mechanism of epilepsy deeply, since study the theory of epilepsy network, can improve the planning of surgery, resection epileptogenesis zone, seizure onset zone and abnormal node of hub simultaneously, increase the effect of resectiv surgery and predict the surgery outcome. Eventually, develop new drugs for correct the abnormal network and increase the effect. Nowadays, there are many algorithms for the brain network. Cooperative study by the clinicans and biophysicists instituted standard and extensively applied algorithms is the precondition of widely used clinically.
Objective To investigate the changes in the expression level of bone morphogenetic protein 2 (BMP2) in the bone callus of rats with femoral fracture and brain injury to explore the effect of the brain injury on the fracture healing and to explore the related mechanism. Methods Thirty-two 12 week old SD rats weighing 368±25 g were randomly divided into 4 groups of 8 rats in each. The rats in Group A had a femoral fracture and a brain injury for 1 week; the rats in Group B had a femoral fracture but without brain injury for 1 week; the rats in Group C had a fracture and a brain injury for 2 weeks; and the rats in Group D had a fracture but without brain injury for 2 weeks. Thus, Groups A and C were used as the femoral fracture and brain injury models, and Groups B and D as the pure femoral fracture models for the controlled study. After the X-ray films were taken, the bone callus was obtained 1 week and 2 weeks after operation, respectively. Then, the bone callus growth and its histology were examined with theHE staining, the expression and changes in the level of BMP-2 were examined with the immunohistochemical staining, and the level of BMP-2 mRNA was measured with the RT-PCR. Results The X-ray films showed that less bone callus formation was found in Group A, and the fracture line in Group B was clearer than that in Group A. There was a greater amount of callus in Group C, and the fracture line was blurred. Only a little bone callus formation was found in Group D. The HE staining indicated that more fibroblasts and early-stage chondrocytes were found in Group A; some fibroblasts in the fracture interspace and fewer early-stage chondrocytes in Group B; some newly-formed trabecular bone at the end of the fracture in Group C; but no trabecular bone formation in Group D. The immunohistochemical staining indicated that the positive expression of BMP2 was b in the cytoplasms of the fibroblasts, the mesenchymal cells, the vascular endothelial cells, the early-stage chondrocytes, and the osteoblasts. The number of the positive cells was greater in Group A than in Group B, with a higher color intensity. The number of the positive cells was greater in Group C than in Group D, with a higher color intensity. The percentages of the cells positive for BMP-2 in the callus were greater in Groups A and C (0.762%±0.052%，0.756%±0.079%)than in Groups B and D (0.702%±0.052%，0.672%±0.044%) at the same time point, ith a statistically significant difference (Plt;0.05). The RT-PCR analysis showed that the expression of BMP-2 mRNA in the callus in Groups A-D was decreased in sequence. There was a significantly higher level of the expression in Groups A and C(1.07±0.13，0.78±0.11) than in Groups B and D(0.91±0.12，0.61±0.08) at the same time point (Plt;0.05). Conclusion The brain injury can promote the fracture healing process, which is probably related to an increase in the expression level of BMP-2 after the brain injury.
Objective To observe the expression of related proteins of retina after subretinal implantation with inactive chips.Methods A total of 27 healthy adult New Zealand white rabbits were randomly divided into three groups: operation group (12 rabbits) in which the rabbits were implanted with inactive chips into the interspace beneath retina;shamoperation group (12 rabbits) in which the rabbits were implanted with inactive chips into the interspace beneath retina which was taken out immediately;the control group (3 rabbits). Animals were sacrified for immunohistological study 7,15,30 and 60 days after surgery.The rabbits in control group group were sacrified for immunohistological study after bred for 30 days.The expressions of glial fibrillary acidic protein (GFAP) and brain derived neurotrophic facor (BDNF) were observed.Results In operation group, the outer nulear layer of retina thinned, and the cells in the inner nulear layer was disorganized 7,15,and 30 days after the surgery;glial cells proliferated 60 days after surgery; the positive expression of BDNF and GFAP was more than that in the shamoperation and control group.In shamoperation group, the positive expression of BDNF and GFAP was more than that in the control group.No obvious difference of expression of BDNF and GFAP between each time point groups was found.Conclusions The expression of neroprotective related proteins increased after subretinal implantation with inactive chips suggests that limited neuroprotective effects might be led by the implantation.
Objective To investigate development and perspectives of brain death donation and transplantation. Methods The related literatures about the research of brain dead donors were reviewed. Results Brain death effects hemodynamic stability， hormonal changes， neuroimmunologic effects，and unleashes a cascade of inflammatory events， which may affect quality of graft， graft survival， and patient outcome. Moreover， the exact mechanism linked to brain death is incompletely understood. Conclusions The pathological physiology changes of brain dead donors has important impact on graft outcomes. However， subsequent work remains to be done.
Repeated transcranial magnetic stimulation (rTMS) is one of the commonly used brain stimulation techniques. In order to investigate the effects of rTMS on the excitability of different types of neurons, this study is conducted to investigate the effects of rTMS on the cognitive function of mice and the excitability of hippocampal glutaminergic neurons and gamma-aminobutyric neurons from the perspective of electrophysiology. In this study, mice were randomly divided into glutaminergic control group, glutaminergic magnetic stimulation group, gamma-aminobutyric acid energy control group, and gamma-aminobutyric acid magnetic stimulation group. The four groups of mice were injected with adeno-associated virus to label two types of neurons and were implanted optical fiber. The stimulation groups received 14 days of stimulation and the control groups received 14 days of pseudo-stimulation. The fluorescence intensity of calcium ions in mice was recorded by optical fiber system. Behavioral experiments were conducted to explore the changes of cognitive function in mice. The patch-clamp system was used to detect the changes of neuronal action potential characteristics. The results showed that rTMS significantly improved the cognitive function of mice, increased the amplitude of calcium fluorescence of glutamergic neurons and gamma-aminobutyric neurons in the hippocampus, and enhanced the action potential related indexes of glutamergic neurons and gamma-aminobutyric neurons. The results suggest that rTMS can improve the cognitive ability of mice by enhancing the excitability of hippocampal glutaminergic neurons and gamma-aminobutyric neurons.
Objective To set up and to evaluate an acute closed brain injury model in rats. Methods The acute closed brain injury was produced in rats by using an impactor consisting of a stand, a guide tube, a weight and a footplate. Ninetysix SD rats were divided into a control group(n＝32, no impact), a mild injury group(n＝32, impact once at force level of 400 g·cm) and a severe injury group(n＝32, impact once at force level of 800 g·cm) to elucidate the physiological responses, the pathophysiological changes and brain edema after brain injury at different injury levels. Results In the mild injury group and the severe injury group, a sudden rise or reduction of blood pressure, deep and fast breath apnea, and pain reflects inhibition were observed. The responses were more obvious in the severe injury group than in the mild injury group. The water content of the brain increased after 6 hours of injury. The pathological contusion and edema of brain were noted or above the impact force level of 800 g·cm. When the impact force rose to or over 1200g·cm, the animals died of persistent apnea mostly. Conclusion Although the established closed brain injury model with different biomechanical mechanisms as the clinical brain injury, it is in conformity with pathological changes and pathophysiological characteristics of acute clinical brain injury, it can be utilized extensively because of its convenient and practice.
ObjectiveTo investigate the protective effects of carboxymethylated chitosan (CMCS) on oxidative stress induced apoptosis of Schwann cells (SCs), and the expressions of brain derived neurotrophic factor (BDNF) and gl ial cell line derived neurotrophic factor (GDNF) in oxidative stress induced SCs. MethodsTwenty-four 3-5 days old Sprague Dawley rats (weighing 25-30 g, male or female) were involved in this study. The bilateral sciatic nerves of rats were harvested and SCs were isolated and cultured in vitro. The purity of SCs was identified by immunofluorescence staining of S-100. SCs were treated with different concentrations of hydrogen peroxide (H2O2, 0.01, 0.10, and 1.00 mmol/L) for 3, 6, 12, and 24 hours to establ ish the apoptotic model. The cell counting kit 8 (CCK-8) and flow cytometry analysis were used to detect the cell viabil ity and apoptosis induced by H2O2, and the optimal concentration and time for the apoptotic model of SCs were determined. The 2nd passage SCs were divided into 5 groups and were treated with PBS (control), with 1.00 mmol/L H2O2, with 1.00 mmol/L H2O2+50 μg/mL CMCS, with 1.00 mmol/L H2O2+100 μg/mL CMCS, and with 1.00 mmol/L H2O2+200 μg/mL CMCS, respectively. After cultured for 24 hours, the cell viabil ity was assessed by CCK-8, cell apoptosis was detected by flow cytometry analysis, the expressions of mRNA and protein of BDNF and GDNF were detected by real-time quantitative PCR and Western blot. ResultsThe immunofluorescence staining of S-100 indicated the positive rate was more than 95%. CCK-8 and flow cytometry results showed that H2O2 can inhibit the proliferation of SCs and induce the SCs apoptosis with dose dependent manner, the effect was the most significant at 1.00 mmol/L H2O2 for 24 hours; after addition of CMCS, SCs exhibited the increased proliferation and decreased apoptosis in a dose dependent manner. Real-time quantitative PCR and Western blot analysis showed that 1.00 mmol/L H2O2 can significantly inhibit BDNF and GDNF expression in SCs when compared with control group (P<0.05), 50-200 μg/mL CMCS can reverse the oxidative stress-induced BDNF and GDNF expression in SCs in a dose dependent manner, showing significant difference compared with control group and 1.00 mmol/L H2O2 induced group (P<0.05). There were significant differences among different CMCS treated groups (P<0.05). ConclusionCMCS has the protective stress on oxidative stress induced apoptosis of SCs, and may promote the BDNF and GDNF expressions of neurotrophic factors in oxidative stress induced SCs.
ObjectiveTo explore the correlation between urinary disorders and imaging changes of cerebral small vessel diseases (CSVDs) in community-dwelling populations.MethodsA cross-sectional analysis was conducted on participants enrolled in the Shunyi study from June 2013 to April 2016. Eligible participants were community-dwelling populations aged ≥35 years with interpretable magnetic resonance imaging scans and no history of stroke or urinary system diseases. Data on demographic characteristics, vascular risk factors, cognitive functions, and urinary disorders (including any form of urinary disorders, incontinence, daytime urination frequency, and nocturnal urination frequency) were collected. Imaging changes including white matter hyperintensities (WMHs), lacunes, cerebral microbleeds (CMBs), perivascular spaces (PVSs), and brain volume were measured using 3 T magnetic resonance imaging. Logistic regression model analysis was performed to identify the potential correlations between urinary disorders and imaging markers of CSVD.ResultsA total of 916 participants (with a mean age of 57.4 years; 36.2% were males) were finally enrolled in this study based on the enrollment criteria. CSVD imaging changes of WMHs, lacunes, CMBs, PVSs or brain volume were not associated with any form of urinary disorders in multivariable models (P>0.05). CSVD imaging changes were not associated with presence of urinary incontinence (P>0.05). In terms of urinary frequency, the CSVD imaging changes were not related to nocturnal urinary frequency (P>0.05). However, lower brain volume was correlated with daytime urination frequency [3-5 vs. <3 times per day: odds ratio (OR)=2.520, 95% confidence interval (CI) (1.278, 4.972), P=0.008; >5 vs. <3 times per day: OR=3.115, 95%CI (1.317, 7.372), P=0.010].ConclusionBrain atrophy may affect daytime urination frequency in community-dwelling populations.
Speech expression is an important high-level cognitive behavior of human beings. The realization of this behavior is closely related to human brain activity. Both true speech expression and speech imagination can activate part of the same brain area. Therefore, speech imagery becomes a new paradigm of brain-computer interaction. Brain-computer interface (BCI) based on speech imagery has the advantages of spontaneous generation, no training, and friendliness to subjects, so it has attracted the attention of many scholars. However, this interactive technology is not mature in the design of experimental paradigms and the choice of imagination materials, and there are many issues that need to be discussed urgently. Therefore, in response to these problems, this article first expounds the neural mechanism of speech imagery. Then, by reviewing the previous BCI research of speech imagery, the mainstream methods and core technologies of experimental paradigm, imagination materials, data processing and so on are systematically analyzed. Finally, the key problems and main challenges that restrict the development of this type of BCI are discussed. And the future development and application perspective of the speech imaginary BCI system are prospected.
Objective To assess the results of Fluoro Jade-c (FJC) staining in brain injury after deep hypothermia circulatory arrest (DHCA). Methods First, animal model of DHCA were established. We performed DHCA on six Chinese experimental minipigs and made sure all the pigs were alive after operation. Second, pathological examination was carried out on the brain tissues of these animals. After FJC staining, we respectively took out the positive and negative tissueparts and performed Hematoxylineosin (HE) staining, Nissl staining and Terminal deoxynucleotidyl Transferase BiotindUTP Nick End Labeling (TUNEL). Finally, the results of FJC was compared with TUNEL, Nissl staining, HE staining, to verify the accuracy and reliability of FJC in assessing brain injury after DHCA. Results Postoperative FJC staining discovered positive disease focuses on the experimental pigs. The comparative results of FJC were consistent with TUNEL (Kappa=0.526, Plt;0.01), Nissl staining (Kappa=0.555, Plt;0.01) and HE staining (Kappa=0.491, Plt;0.01). However, FJC staining image was much clearer and easier in identifying brain injury. Conclusion FJC is a reliable and convenient method to assess brain injury after DHCA.