OBJECTIVE: To investigate the protective effect of tumor necrosis factor-alpha(TNF-alpha) on spinal motor neurons after peripheral nerve injury. METHODS: Twenty Wistar rats were divided into two groups, the right sciatic nerves of 20 Wistar rats were transected, the proximal stumps were inserted into a single blind silicone tube. 16 microliters of normal saline(NS) and TNF-alpha(30 U/ml) were injected into the silicone tubes. After 2 weeks, the 4th, 5th lumbar spinal cord were taken for examination. Enzyme histochemical technique and image analysis were used to show acetylcholinesterase(AChE) and nitric oxide synthase(NOS) activity of spinal motor neurons. RESULTS: The number of AChE and NOS staining neurons were 8.65 +/- 1.98 and 5.92 +/- 1.36 in the experimental group and 6.37 +/- 1.42 and 8.67 +/- 1.45 in the control group respectively, there were significant difference between the two groups(P lt; 0.01). CONCLUSION: It suggests that TNF-alpha has protective effect on motor neurons after peripheral nerve injury.
OBJECTIVE To study the protective effects of Schwann cell derived neurotrophic factor (SDNF) on motoneurons of spinal anterior horn from spinal root avulsion induced cell death. METHODS Twenty SD rats were made the animal model of C6.7 spinal root avulsion induced motoneuron degeneration, and SDNF was applied at the lesion site of spinal cord once a week. After three weeks, the C6.7 spinal region was dissected out for motoneuron count, morphological analysis and nitric oxide synthase (NOS) enzyme histochemistry. RESULTS 68.6% motoneurons of spinal anterior horn death were occurred after 3 weeks following surgery, the size of survivors was significantly atrophy and NOS positive neurons increased. However, in animals which received SDNF treatment, the death of motoneurons was significantly decreased, the atrophy of surviving motoneurons was prevented, and expression of NOS was inhibited. CONCLUSION SDNF can prevent the death of motoneurons following spinal root avulsion. Nitric oxide may play a role in these injury induced motoneuron death.
How to realize the control of limb movement and apply it to intelligent robot systems at the level of cerebellar cortical neurons is a hot topic in the fields of artificial intelligence and rehabilitation medicine. At present, the cerebellar model usually used is only for the purpose of controlling the effect, borrowing from the functional mode of the cerebellum, but it ignores the structural characteristics of the cerebellum. In fact, in addition to being used for controlling purposes, the cerebellar model should also have the interpretability of the control process and be able to analyze the consequences of cerebellar lesions. Therefore, it is necessary to establish a bionic cerebellar model which could better express the characteristics of the cerebellum. In this paper, the process that the cerebellum processes external input information and then generates control instructions at the neuron level was explored. By functionally segmenting the cerebellum into homogeneous structures, a novel bionic cerebellar motion control model incorporating all major cell types and connections was established. Simulation experiments and force feedback device control experiments show that the bionic cerebellar motion control model can achieve better control effect than the currently widely used cerebellar model articulation controller, which verifies the effectiveness of the bionic cerebellar motion control model. It has laid the foundation for real brain-like artificial intelligence control.
Objective To observe the structural changes of urinary center and the expression of Bcl-2 after conus medullaris injury in rats brain so as to explore the possible influence factors of degeneration in brain. Methods Thirty-six adult Sprague-Dawley rats were randomly divided into experimental group (n=30) and control group (n=6). In the experimental group, the conus medullaris injury model was established by cutting off the spinal nerve below L4, and no treatment was done in the control group. The modeling operations in the experimental group were successful, and 2 rats died at 3 months and 5 months after modeling operation respectively, which may be caused by renal failure or urinary tract infection. In the experimental group, 6, 6, 6, 5, and 5 rats were killed at 1 day, 1 week, and 1, 3, 6 months after operation respectively, and 1 rat was killed at each time point in the control group. The dorsolateral tissue of the pontine tegmentum was harvested to perform HE staining and Bcl-2 immunohistochemical SP staining. Results HE staining showed that there was no obvious difference between the experimental group and the control group at 1 day after operation, the neurons were densely packed, arranged neatly, and the nucleoli were clear; at 1 week, the space between the neurons in the experimental group were slightly widened; at 1 month, nucleus retraction in some neurons happened in the experimental group; at 3 and 6 months, the nuclei in the experimental group were more and more condensed, and even some cells disappeared. Bcl-2 immunohistochemical SP staining showed that the expression of Bcl-2 in the control group was weakly positive. The positive expression of Bcl-2 was found at 1 day after operation in the experimental group; the positive expression of Bcl-2 at 7 days after operation was significantly higher than that in the control group, and reached the peak; the positive expression of Bcl-2 decreased gradually at 1, 3, and 6 months after modeling operation, but it was still higher than that of the control group. Conclusion The urinary center appears structure degeneration and necrocytosis after conus medullaris injury in rats brain. The elevated expression of Bcl-2 may be associated with brain tissue repair and function remodeling.
摘要:目的:分析高胆红素血症新生儿血清神经元特异性烯醇化酶(NSE)含量和新生儿行为神经能力测评(Neonatal Behavioral Neurological Assessment,NBNA)的变化,探讨高胆红素血症新生儿血清NSE含量变化的临床意义。方法:应用放射免疫分析法分别测定60例高胆红素血症新生儿和20例对照组新生儿血清NSE含量,同步测定血清总胆红素(TSB),进行NBNA评分;高胆红素血症组早期干预后再次测定血清NSE含量。结果: 与对照组比较,高胆红素血症新生儿血清TSB、NSE含量显著升高,而NBNA评分明显降低,差异有显著性意义(Plt;0.01);对照组与高胆红素血症新生儿轻度增高、中度增高、重度增高四组两两比较(均Plt;0.05),存在显著性差异;血清NSE含量与NBNA评分呈明显负相关(r=-0628,Plt;0.01);高胆红素血症新生儿经早期干预治疗后,血清NSE含量均下降(Plt;0.05),差异有显著性。结论: 高胆红素血症可导致新生儿脑损伤,血清NSE含量可以作为脑损伤的监测指标。Abstract: Objective: To analyze levels of neuronspecific enolase(NSE)in serum and neonatal behavioral neurological assessment (NBNA), to study whether NSE in serum can be used as a tool for the early identification of brain damage in neonatal hyperbilirubinemia. Methods: Serum NSE level of 60 full term infants with hyperbilirubinemia and 20 cases as to control group were measured by radioimmunoassay; Also total serum bilirubin (TSB) and NBNA were detected. In the hyperbilirubinemia group,serum NSE level were measured second when TSB were less than 855 μmol/L(5 mg/dL). Results: Compared with control group,the levels of serum TSB、NSE of the hyperbilirubinemia group were significantly higher, but NBNA score was significantly lower. The levels of serum NSE was significantly negative related to NBNA score. In the hyperbilirubinemia group, serum NSE level were significantly lower after treatment. Conclusion: Hyperbilirubinemia in neonates can cause brain damage. Serum NSE level could work as monitoring indexes of this damage.
Physiological studies have revealed that rats perform spatial localization relying on grid cells and place cells in the entorhinal-hippocampal CA3 structure. The dynamic connection between the entorhinal-hippocampal structure and the prefrontal cortex is crucial for navigation. Based on these findings, this paper proposes a spatial navigation method based on the entorhinal-hippocampal-prefrontal information transmission circuit of the rat’s brain, with the aim of endowing the mobile robot with strong spatial navigation capability. Using the hippocampal CA3-prefrontal spatial navigation model as a foundation, this paper constructed a dynamic self-organizing model with the hippocampal CA1 place cells as the basic unit to optimize the navigation path. The path information was then fed back to the impulse neural network via hippocampal CA3 place cells and prefrontal cortex action neurons, improving the convergence speed of the model and helping to establish long-term memory of navigation habits. To verify the validity of the method, two-dimensional simulation experiments and three-dimensional simulation robot experiments were designed in this paper. The experimental results showed that the method presented in this paper not only surpassed other algorithms in terms of navigation efficiency and convergence speed, but also exhibited good adaptability to dynamic navigation tasks. Furthermore, our method can be effectively applied to mobile robots.
OBJECTIVE Following the delayed repair of peripheral nerve injury, the cell number of anterior horn of the spinal cord and its ultrastructural changes, motorneuron and its electrophysiological changes were investigated. METHODS In 16 rabbits the common peroneal nerves of both sides being transected one year later were divided into four groups randomly: the degeneration group and regeneration of 1, 3 and 5 months groups. Another 4 rabbits were used for control. All transected common peroneal nerves underwent epineural suture except for the degeneration group the electrophysiological examination was carried out at 1, 3 and 5 months postoperatively. Retrograde labelling of the anterior horn cells was demonstrated and the cells were observed under light and electronmicroscope. RESULTS 1. The number of labelled anterior horn cell in the spinal cord was 45% of the normal population after denervation for one year (P lt; 0.01). The number of labelled cells increased steadily from 48% to 57% and 68% of normal values at 1, 3 and 5 months following delayed nerve repair (P lt; 0.01). 2. The ultrastructure of the anterior horn cells of the recover gradually after repair. 3. With the progress of regeneration the latency become shortened, the conduction velocity was increased, the amplitude of action potential was increased. CONCLUSION Following delayed repair of injury of peripheral nerve, the morphology of anterior horn cells of spinal cord and electrophysiological display all revealed evidence of regeneration, thus the late repair of injury of peripheral nerve was valid.
Objective To summarize the clinical features of motor neuron disease ( MND) with main presentation of pulmonary hypertension, so as to improve the diagnosis.Methods A patientwithMND whose main presentation was pulmonary hypertension was analyzed retrospectively. Meanwhile related literatures were reviewed. Clinical data including symptoms, early signs, misdiagnosis causes, and necessary functional examination of respiratory muscle were collected. Results The symptoms of MND was slow-onset and insidious with gradual progression over time. History inquiring found that the symptoms of muscle wasting and physical debilitation emerged long time before the respiratory symptoms. Physical examination also revealed obvious sign of muscle atrophy. Conclusions MND with main presentation of pulmonary hypertension has been recognized insufficiently and often misdiagnosed as other pulmonary diseases. Detailed history taking, systematic physical examination, and convenient functional examination of respiratory muscle,can not only reduce misdiagnosis, but also avoid some expensive and traumatic process.
Objective To evaluate the diagnostic value of serum neuron specific enolase (NSE) in patients with small cell lung cancer. Methods We searched MEDLINE, EMBASE, The Cochrane Library and other databases (1966 to March 2007) to collect studies which evaluated the diagnostic value of NSE in patients with small cell lung cancer. The heterogeneity of included studies was tested by the Cochrane Collaboration’s software RevMan 4.2. The Summary Receiver Operating Characteristic (SROC) curve and meta-analyses were performed by MetaDisc. Results Fifteen studies involving 4221 patients (672 SCLC and 3549 NSCLC patients, all diagnosed by the gold standard) were included. Meta-analyses showed that the heterogeneity among studies was high (P=0.000 2, I2=66.1%), the pooled sensitivity was 0.67 (95%CI 0.64 to 0.71) and the pooled specificity was 0.91 (95%CI 0.90 to 0.92). Subgroup analyses indicated that 4 of the studies which used the reagent supplied by The Academy of Military Medical Sciences (P=0.33, I2=13.4%, AUC= 0.9672, SE=0.0393) and another 4 which used the reagent supplied by Roche (P=0.23, I2=29.9%, AUC=0.8311, SE=0.0836) had no heterogeneity. Conclusion NSE could be regarded as one of the reference tests in patients with small cell lung cancer, but more high quality trials are required.
Objective To study the method to inhibit perioperative internal mammary artery (IMA) spasm from the perspective of muscarinic receptor, and research the function of muscarinic cholinergic receptor subtypes of IMA. Methods IMA segments in vitro with intact endothelium were obtained from 30 patients who underwent coronary artery bypass grafting (CABG). According to muscarinic receptor antagonists of different concentrations， They were divided into control group (not using receptor antagonist), atropine group (nonselective M receptor antagonist), pirenzepine group (M1 receptor antagonist) and Methoctramine group(M2 receptor antagonist) by random number table. The effects of antagonists on vasodilatation were analyzed, Scott ratio was used to calculate affinity index (pD2) and Schild plot was used to count rivalry index (pA2). Results Acetylcholine (Ach)induced concentrationdependentrelaxation response of IMA segments with intact endothelium precontracted with potassium chloride (KCl). The pD2 was 6.92±0.05. The effects of atropine, pirenzepine and methoctramine on doseresponse curve induced by Ach with intact endothelium were all concentrationdependent. With the increase of the concentration of antagonists, the Achinduced doseresponse curves had a significant shift to right(Plt;0.05). Atropine, pirenzepine and Methoctramine competitively antagonized the reaction of vessel to Ach. The pA2 were 9.62±0.15,7.70±0.08 and 630±0.08, respectively. Conclusion The Achinduced relaxation response of IMA with intact endothelium is concentrationdependent. According to the affinity of different antagonist, IMA in Vitro Achinduced relaxation response is implemented by acting on nonneuronal muscarinic cholinergic M1 receptor subtype.