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Objective To evaluate the value of electrospun polymethyl methacrylate (PMMA) nanofibers with different topological structures as scaffolds for growth of Schwann cells (SCs).Methods Electrospun PMMA nanofibers with random or aligned topological structures were fabricated and measured with biocompatibility.Lentivirus-transfected green fluorescent protein was used as the reporting gene to monitor form and growth manner of SCs on different substrates and dependency of cell body and process with fiber structure,with PMMA thin films served as the control.Results Electrospun PMMA nanofibers revealed good biocompatibility and could exert contact guidance to the growth of SCs.Topological structures of the electrospun nanofibers influenced cell morphology.SCs were aligned with the orientation of substrate fibers and form longer cell process when growing on aligned nanofibers (P ＜0.01).Primary SCs preferred to follow the cue of aligned nanofibers compared to random fibers.Conclusion Aligned electrospun PMMA nanofibers have the potentiality as transplantable scaffolds for loading SCs after neural injury.
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<p><b>OBJECTIVE</b>To evaluate the impact of the topographic features of electrospun polymethylmethacrylate (PMMA) nanofibers on growth pattern of primary rat astrocytes.</p><p><b>METHODS</b>Rat astrocytes were cultured on fabricated random and aligned electrospun nanofibers. Using PMMA film as the control, the cells were transfected with a lentivirus harboring GFP gene to reveal the cell growth pattern on different substrates.</p><p><b>RESULTS</b>oth random and aligned electrospun PMMA nanofibers could support the growth of rat astrocytes, but the topographic features of the fibers significantly affected their growth pattern. On aligned nanofibers, astrocytes extended long cell processes along the direction of the substrate fibers, and on random fibers the astrocytes formed shorter processes. On merged images of GFP expressions and substrate fibers, the cell processes of the astrocytes were shown to adhere to and elongate along the fibers both on random and aligned nanofibers.</p><p><b>CONCLUSION</b>The topographic features of PMMA nanofibers can significantly influence the growth pattern of primary rat astrocytes. Aligned electrospun nanofibers has the potential to serve as scaffold material for reducing glia scar formation after spinal cord injury.</p>
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Animals , Rats , Astrocytes , Cell Biology , Cells, Cultured , Nanofibers , Polymethyl Methacrylate , Tissue Engineering , Tissue ScaffoldsABSTRACT
The knowledge absence of neurosurgical regional anatomy is the major shortcoming which makes seven-year program medical students feel difficult in studying neurosurgical special course.The reasons for this phenomenon include the limited teaching time for basic medical course and the continuous progress in the field of neurological anatomy.The teacher should make good use of clinical resources to carry on the additional teaching of neurosurgical regional anatony.The detailed plans include small-class teaching and individual case analysis using the data of neuroimaging and angiography of the brain and spinal cord.All these measures are intend to let the students grasp of the basic knowledge clinical neurosurgery during the internship and make the smooth transition from interns to doctors,providing references for other department.
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Taking microneurosurgery approach and applied surgical anatomy training as the core and combining theoretical teaching and perioperative training as the main contents , training program achieved significant effect among specialty degree neurosurgery postgraduates. In order to further improve the quality of training, it is proposed to set up micro-neurosurgery training center and more complete train-ing system based on micro-neurosurgery contents thus to improve clinical ability of specialty degree neuro-surgery postgraduates.
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Objective To investigate the effects of peroxisome proliferator-activated receptor gamma (PPARγ) agonist pioglitazone on delayed neuronal death,apoptosis of neurocytes,and expression of intercellular adhesion molecule-1 ( ICAM-1 ) following traumatic brain injury (TBI) in rats.MethodsThirty-six Sprague-Dawley rats were randomized into sham injury group,control group and pioglitazone treatment group,with 12 rats in each group.TBI model was established by modified Feeney method.Treatment grouP received intragastric administration of pioglitazone at a dosage of 10 mg/kg,and the sham injury group and the control group were lavaged with isometric 0.2％ dimethyl sulphoxide.Paraffin sections of brain tissues collected at 48 hours after TBI were employed to observe delayed neuronal death,apoptosis of neurocytes and expression of ICAM-1 by Nissl staining,TUNEL staining and immunochemistry respectively.Results( 1 ) Cell loss rate of Nissl body in the treatment group [ ( 38.59 ± 1.97 ) ％ ]was significantly lower than that of the control group [ (51.25 ± 4.01 ) ％ ] ( P ＜ 0.05 ),but was higher than that of the sham injury group [ (8.65 ± 1.23 ) ％ ] ( P ＜ 0.01 ).(2) The number of apoptotic neurocytes of the treatment group (31.67 ± 4.76) was significantly lower than that of the control group (45.33 ± 4.68 ) ( P ＜ 0.05),but was higher than that of the sham injury group ( 16.83 ± 2.04 ) ( P ＜ 0.01 ).(3) The mean optical degree of ICAM-1 positive expression of the treatment group (0.26 ± 0.04) was significantly lower than that of the control group (0.31 ± 0.04) ( P ＜ 0.05 ),but was higher than that of the sham injury group (0.10 ± 0.02 ) ( P ＜ 0.01 ).ConclusionsThe PPARγagonist pioglitazone can reduce the apoptosis of neurocytes and protect neurons after TBI.Meanwhile,its suppression of ICAM-1 expression is probably a mechanism of the suppression of inflammatory reaction and neural protection.
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Objective Aim to explore the effect of hyperglycemia on the expression of glucose transporter 1 (GLUT-1)in rats at the acute phase of traumatic brain injury.Methods Adult male SD rats were randomly divided into 3 groups: normal control group, traumatic brain injury group and insulin treated group.The blood glucose concentration of the rats was measured before and after injury.The expression of GLUT-1 gene and protein in the injured and uninjured cortex was detected by reverse transcription polymerase chain reaction (RT-PCR) and western-blot.The apoptosis in the injured and uninjured cortex were detected by TUNEL staining.Results The blood glucose concentration increased markedly in traumatic brain injury group.The expression of GLUT-1 gene and protein in the injured cortex decreased in both the traumatic brain injury group and the insulin treated group.In contrast, the expression of GLUT-1 gene and protein significantly increased at 12 h, 24 h, 48 h, 72 h after injury in the insulin treated group compared with control(P＜0.01).The number of apoptotic cells in the insulin treated group were significantly larger than that in the traumatic brain injury group at each time point(P＜0.01).However, The number of apoptotic cell death remained unchange in the uninjured cortex in each group(P＞0.05).Conclusions The hyperglycemia after traumatic brain injury may increase the apoptotic cells in the injured brain through decreasing the expression of GLUT-1.
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Objective To study the changes of apoptosis in brain after traumatic injury(TBI)treated with exogenous vascular endothelial growth factor(VEGF)gene therapy in oder to find out the role of exogenous VEGF gene in protectiog brain tissue.Method The injurea cerebral cortex from the rat models of brain with traumatic injury was injected with adenovirus(adenovirus,Ad)as the carrier of VEGF-165 gene(Ad-VEGF-165 Gene).RT-PCR and Western blot were used to detect the expression of VEGF mRNA and VEGF protein in the brain 6 h,24 h,3 d,7 d and 14 d after injury,and apoptosis in the injured location of brain was also detected by TUNEL successively after Ad-VECF-165 gene therapy.Results With exogenous Ad-VEGF-165 applied to the locally injured brain tissue after injury,VEGF mRNA and VEGF protein showed consistent expression and their expressions were significantly higher than those in trauma group and vehicle control group.Compared with the trauma group.the apoptosis in the gene therapy group 24 h,3 d and 7 d after injury presented a.significant reduction,and had close relationship with VEGF.(Control group:4.17±0.73;TBI group,24 h:47.18±6.01,3 d:79.44±11.23;TBI+VEGF group.24 h:28.72±5.31,3 d:54.18±7.66;P＜0.05).Conclusions The exogenous VEGF gene therapy administered to have protective effects on the local brain tissue in rats with traumatic injury in a certain time.
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BACKGROUND: At present, traditional modalities of neuroimaging, such as CT and MRI, is very limited in the diagnosis and severity estimation of diffuse axonal injury (DAI).OBJECTIVE: To investigate the value of proton magnetic resonance spectroscopy (1HMRS) in the diagnosis and prognosis of DAI.DESIGN, TIME AND SETTING: Prospective clinical controlled observation. The study was performed at the Department of Neurosurgery, and Department of Radiology, First Affiliated Hospital of Chongqing Medical University between October 2002 and September 2007.PARTICIPANTS: A total of 63 subjects with traumatic brain injury were enrolled and divided into DAI group (n=27) and non-DAI group (n=36) according to the result of MRI. In addition, 20 healthy persons were served as control group.METHODS: Demographic and clinical data were recorded on admission and neuroimaging examinations including fluid attenuated inversion recovery were carried on according to carefully designed procedures, in addition, 1HMRS was performed and the data were analyzed in combination with clinical condition.MAIN OUTCOME MEASURES: The ratios of N-acetyl aspartate (NAA)/creatine (Cr) and creatine phosphate (Cr), Choline compound (Cho)/Cr, myoinositol (mlNs)/Cr, and glutamic acid (GIx)/Cr at genu and splenium of corpus cellosum, and basal ganglia were quantified using 1HMRS.RESULTS: Compared with control and non-DAI groups, DAI group had decreased NAA/Cr and increased Cho/Cr at genu and splenium of corpus callosum, and basal ganglia (P < 0.05- 0.01), as well as increased mlNs/Cr and Glx/Cr at genu and splenium of corpus cellosum (P < 0.05). Non-DAI group also showed decreased NAA/Cr at splenium and increased Cho/Cr at genu of corpus callosum compared with control group (P < 0.01), but the change degree was less than DAI group. A positive correlation between Cho/Cr at genu of corpus callosum and the peded of primary unconsciousness was identified in DAI group (r=0.824, P < 0.01). CONCLUSION: The 1HMRS indexes at genu and splenium of corpus callosum, and basal ganglia could serve as effective indexes for the diagnosis of DAI. The Cho/Cr could well reflect histological changes following injury and act as sensitive index to predict clinical injury.
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Objective To investigate the expression of apoptosis-related proteins in rat cerebral cortex following traumatic brain injuries(TBI)and discuss the role of oxygen free radical-mitochondria signal pathway in Edaravone treating TBI.Methods A total of 180 male adult Sprague-Dawley rats were randomly divided into TBI group,Edaravone treatment group and control group.Each group was divided into six subgroups at 1,3,6,24,48 and 72 hours after TBI.Edaravone treatment group was injected with Edaravone(10 mg/kg)and the other two groups injected with the same volume of 0.9%normal saline.The pathological change in the rat cortex following TBI was observed with HE staining.At different time points,the expressions of Cytc,Bcl-2 and Bax in rat cortex as well as cell apoptosis and MDA change were observed by means of immunohistechemistry,TUNEL and TAB.Results HE staining showed scattered degenerated and necrotic neurous in cerebral cortex six hours after neuron injury,which peaked at 24 hours.Compared with control group,intermediate product MDA of free radical was increased six hours after TBI and peaked at 48 hours in Edaravone treatment group,which was lower than TBI group especially at 24,48 and 72 hours(P＜0.05).Compared with control group,the immunity reaction of Cytc positive cells inereased at six hours and peaked at 24 hours in TBI group,with statistical difference at 3,6,24,48 and 72 hours(P＜0.05).Compared with TBI group,the immunity reaction of Cyte positive cells was decreased obviously at 24,48 and 72 hours in Edaravone treatment group.Hyperexcitability of Bcl-2 after TBI reached peak at 3 hours and decreased gradually.But the expression of Bax was increased gradually after TBI and peaked at 48 hours,when Bax/Bcl-2 reached peak too.Folowing TBI,TUNEL positive cells increased gradually and reached peak at 48 hours,with mainly type Ⅰ TUNEL cells before 24 hours and typeⅡTUNEL cells after 24 hours.Conclusions There exist necrosis and apoptosis of nerve cells in cortex after TBI,especially apoptosis.Oxygen free radical mitochondria is one of the signal transduction pathways of nerve cell apoptosis following TBI.Edaravone exerts certain therapeutic effect on TBI.
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BACKGROUND: Applying naloxone in acute brain injury can sustain the cerebral perfusion pressure(CPP), alleviate the cerebral edema and prevent the secondary brain damage to a certain degree. But the dosage and the administration of naloxone in clinical practices vary substantially according to the literatures.OBJECTIVE: To investigate the effect of different doses of naloxone on the changes in the absolute power values of electroencephalography(EEG) in acute brain injury, and study the protective effects of naloxone at different doses.DESIGN: Case-control study based on patients.SETTING: Neurosugery department of a hospital affiliated to a university PARTICIPANTS: From January 2002 to April 2003, at the Intensive Care Unit(ICU) of theNeurosugery Department of the First Hospital Affiliated to the Chongqin Medical University, 86 patients with moderate or severe acute closed brain injury were selected. Of all the patients, 59 were male and 27 were female, aged between 18 - 65.METHODS: According to the degree of injury graded by Glasgow Coma Scale(GCS), the 86 patients bearing acute brain injury were divided into 3 groups: GCS 3 - 5 group, GCS 6 - 8 group and GCS 9 - 12 group. Each group contained a naloxone treatment group and a matched control group. The naloxone treatment group consisted of a low-dose naloxone subgroup and a large-dose naloxone subgroup. The changes in the total power value of EEG before treatment and at the time of 30 minutes, 1, 2, 24, 48, 72 and 120 hours after treatment were measured respectively using quantitative EEG monitor.MAIN OUTCOME MEASURES: The changes in the total power value of the patients' EEG before and after treatment were observed and recorded.RESULTS: The difference between the total power of EEG of the GCS 9 - 12naloxone treatment group 1 hour after a naloxone treatment and that of the matched control group was statistically significant(P ＜ 0.05); The same comparison between the low-dose and the large-dose naloxone subgroups within the GCS 9 - 12 naloxone treatment group yielded no significant difference. In the GCS 6 - 8 naloxone treatment group, the difference between the total power of EEG 1 hour after a naloxone treatment and that of the matched control group was statistically significant, and the large dose subgroup was more significant than the low-dose group. In the GCS 3 - 5 naloxone treatment group, no significant difference between the total power of EEG of the naloxone group and that of the control group could be observed.CONCLUSION: The low-dose naloxone treatment is helpful enough on the intervention for moderate brain injury, and the large-dose naloxone treatment is better than the low-dose on severe brain injury. For the patients with exceptionally severe brain injury, both the two treatments are proved to have no therapeutic effects.
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0.05).Conclusion The variety of ECoG on patients with intracranial tumors undergone surgery is helpful to prognosticate postoperative early epilepsy.
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Objective To investigate the changes of region cerebral homodynamic and cerebral vascular autoregulation in traumatic brain injury(TBI) by dynamic CT perfusion(CTP) imaging in rat.Methods Forty-five SD rats underwent CTP,including 10 control rats and 35 TBI rats,on 1,6,24 h,and day 3,7,14,21 after TBI.The region of interest(ROI) was located near traumatic area within 2 mm and mirror area of relative brain hemisphere.False color pictures and dynamic rCBF,rCBV,MTT and PS were obtained in different time.Pathological examination was also done.Results The rCBF,rCBV on 1 h after TBI was lower than that of control group,and significantly higher on 6-24 h after TBI.They reached the peak on day 3.PS had a similar change compared with rCBF,rCBV,but a longer duration.MTT showed to moderate changes except an isolated tide on 3 days after TBI.The rCBF on mirror area of relative brain hemisphere was almost stable except 3 days after TBI,which was lower than that of control group.Meanwhile,the rCBV on mirror area of relative brain hemisphere was normal.Conclusion CTP is an advanced technique to investigate the changes of region cerebral homodynamic and cerebral vascular autoregulation in TBI.The early hypoperfusion and next hyperperfusion around traumatic areas after TBI suggest that the dysfunction of cerebral vascular autoregulation should be committed to the change of homodynamic in TBI.
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Objective To observe the protective effect of recombinant plasmid pCDNA3.1(+)/Ngb during focal cerebral ischemia in rat brain.Methods Fifty-four male Wistar rats were randomly divided into three groups:normal saline(NS)control group,plasmid control group,and recombinant neuroglobulin group.NS,plasmid pCDNA3.1(+)and recombinant plasmid pCDNA3.1(+)/Ngb were respectively injected into two sites of the rat cerebra1 cortex 24 hours before induction of neocortical focal ischemia by occlusion of the right middle cerebral artery for 24 hours.The condition of local ischemic damage,expression of bcl-2 and the apoptosis in neural cells were confirmed by staining with 2% 2.3.5-triphenyltetrazolium chloride,in-site cell apoptosis detection,indirect immunofluorescent staining and Western blotting,respectively.Results The extent of cerebral infarction tissue and the apoptosis cells in the pCDNA3.1(+)/Ngb group were significantly reduced than those in other control groups(P
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Objective To investigate the inhibition effect of pituitary tumor transforming gene(PTTG) antisense oligodeoxynucleotide(ASODN) on C6 glioblastoma in rats.Methods The C6 glioma cells were injected into the right caudate nucleus.PTTG-ASODN of 8 or 16 ?g/ml was injected into the tumor-affected area with stereotactic technique immediately,at 1st and 2nd week after inoculation of C6 cells.Three weeks after C6 cell inoculation,all rats were killed and the tumors were excised,then tumor volume was calculated and pathologically analysed,and immunohistochemical statining for GFAP, PCNA ang PTTG was performed.Results PTTG-ASODN could suppress the proliferation of C6 glioblastoma in a dose-and time-dependent manner.The inhibition effect was better when large-dose PTTG-ASODN was repeatedly used for glioblastoma as early as possible.Conclusion PTTG-ASODN can suppress the proliferation of glioblastoma,which may become a new strategy of gene therapy for glioblastoma.
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Objective To study the difference of the peripheral blood lymphocyte gene expression in the glioblastoma patients and the normal subjects by the gene chip engineering technique. Methods The human gene expression spectrum chip containing 13 824 cDNA was used to detect the gene expression in the peripheral blood lymphocytes of 23 glioblastoma patients and 40 normal persons. The lymphocyte mRNA in the glioblastoma patients and healthy subjects was withdrawn. The cDNA probe with the different fluorescein was made by reverse transcription. The probe and the chip were hybridized. The fluorescence intensity was scanned and digitized,and gene expression was compared between the two groups. Results The peripheral blood lymphocytes in the glioblastoma patients had 96 genes to present the difference expression with that of normal subjects,including 25 upregulated genes and 71 downregulated genes. Conclusion The gene expression in the peripheral blood lymphocytes of glioblastoma patients and normal subjects exists difference. The lymphocyte DNA union,the abnormal function of transcription and signal conduction are the possible reasons for the different immune function between the glioblastoma patients and the healthy subjects.
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The neurosurgery clinical practice is difficult and important for most undergraduate. The reasons come not only from the development of neurosurgical science,but from shortage of contents in basic peviod,so in clinical education the re-teaching of basic neurosurgical knowledge is important. Teachers should make full use of clinical resources to fulfill this teaching aim and the emphasis should be neuroanatomy and neurophysiology.
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Objective To explore specific risk factors in the early seizures after acute moderate and severe head injuries and understand incidence of nonconvulsive status epilepticus (NCSE) under coma. Methods Eighty-six patients with acute moderate and severe head injuries were monitored with video-electroencephalogram (video-EEG) for one week. Results (1) Of all, 7 cases (8.14%) had clinical seizures and 6 (6.98%) NCSE. (2) In patients with severe head injuries especially intracranial hemorrhage, post-traumatic seizures especially NCSE were more likely to occur, with no significant difference in sex and age. Conclusions Severe and critical head injuries and intracranial hemorrhage are specific risk factors for early post-traumatic seizures, especially NCSE. After brain injury, EEG should be used to evaluate traumatic coma even if clinical seizure does not appear.
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<p><b>OBJECTIVE</b>To investigate the effect of moderate hypothermia on responses of axonal cytoskeleton to axonal injury in the acute stage of injury.</p><p><b>METHODS</b>Of fifteen adult guinea pigs, twelve animals were subjected to stretch injury to the right optic nerves and divided into the normothermic group (n = 6) in which the animal's core temperature was maintained at 36.0-37.5 degrees C and the hypothermia group (n = 6) in which the core temperature was reduced to 32.0-32.5 degrees C after stretch injury. Remaining three animals sustained no injury to the right optic nerves and served as control group. Half of injured animals (n = 3) of either normothermic group or hypothermic group were killed at either 2 hours or 4 hours after injury. The ultrastructural changes of axonal cytoskeleton of the right optic nerve fibers from the animals were examined under a transmission electron microscope and analyzed by quantitative analysis with a computer image analysis system.</p><p><b>RESULTS</b>At 2 hours after stretch injury, there was a significant reduction in the mean number of microtubules (P < 0.001), and a significant increase in the mean intermicrotubule spacing (P < 0.05 or P < 0.01) in axons of all sizes in normothermic animals. The mean number of neurofilaments also decreased statistically (P < 0.01) in large and medium subgroups of axons in the same experimental group at 2 hours. By 4 hours, the large subgroup of axons in normothermic animals still demonstrated a significant decline in the mean number of microtubules (P < 0.01) and an increase in the mean intermicrotubule spacing (P < 0.05), while the medium and small subgroups of axons displayed a significant increase in the mean number of neurofilaments (P < 0.05) and reduction in the mean interneurofilament spacing (P < 0.05). On the contrary, either the mean number of microtubules and the mean intermicrotubule spacing, or the mean number of neurofilaments and interneurofilament spacing in axons of all sizes in hypothermic stretch-injured animals was not significant different from the mean values of sham-operated animals.</p><p><b>CONCLUSIONS</b>Posttraumatic moderate hypothermia induced immediately after axonal injury results in substantial protection of axonal cytoskeleton and ameliorates axonal damage.</p>
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Animals , Male , Axons , Pathology , Culture Techniques , Diffuse Axonal Injury , Pathology , Therapeutics , Disease Models, Animal , Guinea Pigs , Hypothermia, Induced , Methods , Microscopy, Electron , Optic Nerve , Pathology , Optic Nerve Injuries , Therapeutics , Probability , Random Allocation , Reference ValuesABSTRACT
Attentions have been paid to teaching Nepal students in English in our university,and many problems need to be analyzed and solved.Selection and application of appropriate teaching material,sufficient preparation before class and applying nimble teaching style have received satisfactory results.
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Objective To set up an animal model with severe head injury that is similar to clinical condition and treated with mild hypothermia. Methods A total of 120 SD rats were randomly divided into eight groups (n=15 in each group), ie, before cooling, cooling 6, 12, 24, 48, 72, 96 and 120 hours groups. The model was induced by dropping a object of 60 g from a height of 50 cm onto the epidura and treated with mild hypothermia (32-34℃). Blood pressure and ECG were observed and serum K+, Na+ and Mg 2+levels measured. The change of neuron microstructure in rat cerebral traumatic tissue of every group was observed by transmission electron microscope (TEM). Results Animal mortality increased but serum K+ and Mg 2+levels gradually decreased with the treating time lasting. Serum Na+ showed insignificant change. Bradytachycardia occurred in one rat of 72 hours group, two of 96 hours group and two of 120 hours group. TEM showed that the rat’s encephaledema presented gradual relief trend during mild hypothermia treatment. There was one rat in 96 hours group and one in 120 hours group with diffuse tubuli renales necrosis. Conclusion The established model is in conformity with the characteristics of vital sign, serum electrolyte and cerebral microstructure of clinical severe head injury treated with mild hypothermia.