Objective To explore the effects of Neurogenesin 1 (Ng1) gene on functional recovery after spinal cord injury (SCI) and its mechanism. Methods Thirty-six rats (aging 4 months, weighing 230 g and being male or female), were randomly divided into two groups: experimental group (n=18) and control group (n=18). After spinal cord contusive injury at T10 level was made in all these rats using modified Allen’s method, Ng1 recombinant plasmid and blank plasmid were transfectedinto the damaged areas of exprimental group and control group respectively by Alzet pumps. At 1 day, 1 week, 2 weeks, 3 weeks, and 4 weeks after SCI, Basso-Beattle-Bresnahan (BBB) Rating Scale was used to observe the recovery of motor function. At 1 week after injury, the expressions of Ng1 mRNA and protein in injured spinal cord were detected by RT-PCR and Western blot techniques. And at 2 and 4 weeks, double immunofluorescence and histopathologic examinations were performed to study the prol iferation of the adult endogenous neural stem cells and pathological change after SCI. Results At 1-4 weeks after SCI, the BBB scores in the exprimental group was significantly higher than that in control group (P lt; 0.05), and at 4 weeks the BBB score of the experimental group (16.80 ± 1.79) was significantly higher than that of the control group (9.60 ± 1.67), (P lt; 0.01). RTPCR and Western blot showed that the mRNA and protein expressions of Ng1 were observed in the exprimental group and no expression was seen in the control group. Histologic observation showed that the morphology of spinal cord and neurons in the exprimental group was better than that in the control group and was close to the normal tissue. The mean number of Nestin+/ BrdU+ newborn endogenous neural stem cells in the exprimental group was significantly more than that in control group (P lt; 0.05). Conclusion Ng1 gene could promote the prol iferation of endogenous neural stem cells and protect the injured neurons, which enhances the repair of the motor function after SCI.
Objective To investigate the management of the soft tissue defect after the Achilles tendon repair. Methods From April 1996 to April 2006, 24 patients(17 males, 7 females; aged 16-59 years), who suffered from postoperative Achilles tendon exposure caused by local soft-tissue necrosis after the Achilles tendon repair, were treated and evaluated. Of the 24patients, 8 had an original open injury (machinecrush injury in 2 patients, heavy-object press injury in 3, motorcycle wheel crush injury in 3) and 16 patients had a closed injury (sports injury). In their treatment, the transferof the sural neurovascular flap was performed on 8 patients and the transfer ofthe saphenous neurovascular flap was performed on 3 patients. The secondary Achilles tendon repair was performed on 13 patients before the neurovascular flap transfer was performed. The time between the injury and the operation was 9-76 days, and the time between the Achilles tendon expousure and the operation was 3-65 days. Results All the flaps survived and the Achilles tendon exposure was well covered by the flaps of good texture. Eighteen patients followed up for 6 months to 24 months had no flap complication, and the two point discrimination of the flaps was 12-20 mm. The AOFASAnkleHindfoot Scale assessment revealed that 8 patients had an excellent result, 6 had a good result, 3 had a fair result, and just 1 had a poor result, with theexcellent and good results accounting for 77.8%. Sixteen patients (89%) were able toperform a tip-toe stance on their operative sides, and only 3 of them complained a loss of plantarflexion strength. However, 2 patients still could not perform the tip-toe stance. Conclusion The Achilles tendon repair, ifnot well performed, can result in the local soft-tissue necrosis and the subsequent Achilles tendon exposure. If those complications occur, the neurovascular flap transfer should be performed as soon as possible; if necessary, the secondary Achilles tendon repair should be performed, too.
Currently, approximately one-third of epilepsy patients exhibit resistance to anti-seizure medications (Anti-seizure medications, ASMs), which can only alleviate symptoms, but cannot completely cure the condition. Consequently, the development of new ASMs from an understanding of epilepsy pathogenesis has emerged as an urgent social issue. The role of neuroinflammation in various neurological diseases has garnered significant attention as a popular research topic both domestically and internationally. Numerous studies have corroborated the involvement of neuroinflammation in the onset and progression of epilepsy. The biological target, Translocator protein 18 kDa (TSPO), is considered as a marker of neuroinflammation and is intricately involved in the entire neuroinflammatory response. Investigating the function of TSPO in epilepsy neuroinflammation can potentially uncover new treatment targets. At present, the exact mechanism of TSPO in epilepsy neuroinflammation remains unclear, thus necessitating a comprehensive summary and overview. This article reviewed the advancements made in TSPO research within the realm of neuroinflammation and its role in epileptic neuroinflammation, aiming to contribute novel insights for the identification of related targets and pathways for epilepsy treatment.
Objective To investigate the possibility of theadipose tissue-derived stromal cells(ADSCs) to differentiate into the neuron-like cells and to explore a new cell source for the transplantation related to the central nervous system. Methods Adipose was digested by collagenase, cultured in the fetal bovine serum containing a medium. Trypse was used to digest the cells and the cell passage was performed. The 3rd to the 9th passage ADSCs were used to make an induction. Isobutylmethylxanthine, indomethacin, insulin, and dexamethasone were used to induce the ADSCs to differentiate into the neuron-like cells and adipocytes. Sudan black B and immunocytochemistry were used to identify the cells. Results A population of the ADSCs could be isolated from the adult human adipose tissue, they were processed to obtain a fibroblast-like population of the cells and could be maintained in vitro for an extendedperiod with the stable population doubling, and they were expanded as the undifferentiated cells in culture for more than 20 passages, which indicated their proliferative capacity. They expressed vimentin and nestin, and characteristics of the neuron precursor stem cells at an early stage of differentiation. And the majority of the ADSCs also expressed the neuron-specific enolase and βⅢ-tubulin, characteristics of the neurons. Isobutyl-methyxanthine, indomethacin, insulin, and dexamethasone induced 40%-50% of ADSCs to differentiate into adipocytes and 0.1%0.2% of ADSCs into neuron-like cells. The neuron-like cells had a complicated morphology of the neurons, and they exhibited a neuron phenotype, expressed nestin, vimentin, neuron-specific enolase and βⅢ-tubulin, but some neuron-like cells also expressed thesmooth muscle actin (SMA), and the characteristics of the smooth muscle cells; however, the neurons from the central nervous system were never reported to express this kind of protein. Therefore, the neuron-like cells from the ADSCs could be regarded as functional neurons. Conclusion Ourresults support the hypothesis that the adult adipose tissue contains the stem cells capable of differentiating into the neuron-like cells, and they can overcome their mesenchymal commitment, which represents an alternative autologous stemcell source for transplantation related to the central nervous system.
Age-related macular degeneration (AMD) is an age-related neurodegenerative eye disease characterized by degeneration and progressive death of retinal pigment epithelium (RPE) and photoreceptor cells. In recent years, as a new treatment for AMD, stem cell therapy has attracted wide attention in the field of AMD, and has become a current research hotspot. Although stem cell therapy carries risks such as increased incidence of cancer and immune rejection, it significantly promotes damaged photoreceptor cells and retinal cells by differentiating into RPE cells and other retinal cell types, as well as secreting neurotrophic factors and extracellular vesicles. In particular, the development of embryonic stem cell-derived RPE cells, its cryopreservation technology and the advancement of plasmid, adeno-associated virus, Sendai virus and other delivery technologies have laid a solid foundation for stem cell therapy of AMD. As a new method to prevent retinal damage and photoreceptor degeneration, stem cell neuroprotective therapy has shown great potential, and with the continuous maturity and improvement of these technologies, stem cell therapy is expected to provide new ideas for the prevention and treatment of AMD in the future.
ObjectiveTo analyze the causes of unrelieved epilepsy thoroughly in children with isolated focal cortical dysplasia (FCD) based on MRI.MethodsRetrospective analysis of MRI and clinical data of 21 children with isolated FCD during July 2014 to January 2018, which confirmed by pathology and unrelieved thoroughly after operation performed, the pathological types and MRI signs were analyzed, as well as the frequency of different MRI signs in FCD of each pathological type. Analyzed the possible factors of surgical failure.ResultsAmong the 21 cases, there were 15 males and 6 females, with an average age of (5.7±0.3) years and an average course of disease of (3.4±0.5) years.MRI signs of this part of the children were mainly manifested by blurred focal gray matter boundaries, abnormal cortical structure changes (thickening and/or thinning), transmantle signs (abnormal cone signals extending from subcortical white matter to the ventricle) and abnormal gray matter signals, which were similar to MRI signs of FCD with satisfactory postoperative epilepsy control. 17 cases (80.9%) appeared epileptic discharge after operation in the EEG monitoring area 2 weeks to 6 months, FCD type I and type Ⅱ accounted for 35.3%, 64.7% respectively. During intraoperative EEG monitoring, no epileptiform discharge was observed in the transmantle sign region in 6 cases, and the region was retained, and only the surrounding abnormal discharge cortex was removed, complete removal of the tansmantle sign and surrounding abnormal discharge area was performed in 2 cases, and different degrees of epileptic epilepsy were observed in both methods.ConclusionMRI signs of isolated FCD with unrelieved epilepsy after operation were nonspecific, there were still epilepsy of varying degrees after all epileptogenic lesions have been removed, the cause may be related to potential epileptic factors.
Objective To study the changes of blood flow of the already-compressed cauda equina under dynamic burden, high frequency stimulation (HFS) and increased additional compression, and to clarify the mechanism of neurogenic intermittent claudication. Methods Thirty SD rats were divided into 5 groups, 6 in each. All groups were operated with laminectomy of the fifth lumbar verfebra. One hour after the measurement of blood flow,in 4experimental groups, the silicon sheets were inserted into the spinal canal of L4 and L6 to cause double level compression of cauda equina by 30%. Two hours after onset of compression, no dynamic burden was introduced to the subjects of the experimental group 1. Only HFS was introduced to the subjects of the experimental group 2 for 6 minutes. Both HFS and increased additional compression were introduced to the subjects of the experimental group 3 for 6 minutes. While only increased additional compression was introduced to the subjects of the experimental group 4 for 6 minutes. The subjects of control group only underwent laminectomy of the fifth lumbar vertebra and HFS 6 minutes. The blood flow of cauda equina was measured with laser Doppler flowmeter. Results In the first 2 hours, there was no significant change of cauda equina blood flow in the control group. During the time of HFS, the blood flow increased significantly to 186.4%±31.5% of initial value (Plt;0.05). In the experimental group 1, there was no blood flow change during the period of dynamic burden（110.4％±7.5％，Pgt;0.05）. After introduction of dynamic burden, there was no blood flow changes in the experimental group 2 (111.6％±17.6％，Pgt;0.05). The blood flow in the experimental group 3 decreased to 65.3%±10.7% of initial value (Plt;0.05); and the blood flow in the experimental group 4 decreased to 60.1%±9.2% of initial value (Plt;0.01). There was no significant difference between the experimental groups 3 and 4 (Pgt;0.05). Conclusion The results above show that during the period of increased impulse transmission, double level compression of cauda equina may limit the increase of blood flow, which maycause relative ischemia. If there is increased additional compression along with increased impulse transmission, the blood flow will decrease significantly, which will cause absolute ischemia.
Objective To observe the ultrastructural characteristics of human retinal progenitor cells cultured in vitro. Methods Six 5-month-old human fetuses（12 eyes）without eye diseases were selected. Retinal progenitor cells from the retina of one eye of each fetus were cultured in vitro，and observed by transmission electronic microscopy（TEM）; while those from the other eye were directly observed by TEM. Results Abundant heterochromatin were found in the karyon of 5-month embryonic retinal neuroepithelial cells，and the figure of the karyons was irregular.A few scattered initial cells were seen in retinal neuroepithelial layer with large karyon，smooth surface，abundant euchromatin，and distinct nucleolus.The human retinal progenitor cells cultured in vitro had the same ultrastructural characteristics as the initial cells:with huge karyon which almost occupied the whole cell，little cytoplasm，distint nucleolus，abundant euchromatin，and little heterochromatin.The cells clung to each other in the neural globoid cell mass.The size of the outer cells was large，and karyokinesis could be found. Conclusion The cultured human retinal progenitor cells are provided with the same ultrastructure characteristics as the initial cells. (Chin J Ocul Fundus Dis, 2006, 22: 185-187)
Objective To separate each protein band from the nerve regeneration conditioned fluid(NRCF）and to study whether there are somenew and unknown neurotrophic factors in the protein bands with a relative molecular mass of 220×103. Methods The silicone nerve regenerationchambers were formed in the sciatic nerve of the 25 New Zealand rabbits (weight,1.8-2.5 kg), and NRCF was taken from it at 1 week after operation. The Nativepolyacrylamide gel electrophoresis (Native-PAGE) was used for separating the proteins from NRCF and detecting the relative molecular mass. The Western blot and ELISA were used to observe whether the protein bands ［220×103 (Band a), (20-40)×103(Band c)］ of NRCF could combine with the antibody of the known antibody of neurotrophic factor (NTF):nerve growth factor(NGF), glial cell-derived neurotrophic factor(GDNF), brainderived neurotrophic factor(BDNF), neurotrophin 3(NT-3)， NT-4, ciliang neurotrophic factor(CNTF). Results Separated by Native-PAGE, NRCF mainly contained two protein bands:Band a had a relative molecular mass about 220×103, and Band c had a relative molecular mass about (20-40)×103. Band a could not combine with the antibodies of the NGF, BDNF, CNTF, and NT-3, but could combine with the antibody of NT-4.Band c could combine with the antibodies of NGF, BDNF, CNTF and NT-3, but could not combine with the antibodies of NT-4 and GDNF. Conclusion The protein bands with a relative molecular mass of 220×103 have ber neurotropic and neurotrophic effects than the protein bands with a relative molecular mass of (20-40)×103, which contains NGF,CNTF, etc. NT-4 just has a weak or no effect on the sympathetic neurone. This indicates that there is a new NTF in the protein bands with a relative molecular mass of 220×103, which only combines with the antibody of NT-4.
Clinical trial, an important research method, plays a crucial role in the development of medicine. It provides important decision support for medical workers. Medical research proposal should be posted at clinical trial registries. Researchers should update original data and research results, which contributes to data sharing. Clinical trial registration can avoid repetitive research and make clinical trials more transparent and standardized. This paper briefly introduces the clinical trial registration, including the definition, the significance, the history, the scope of registration, the organization of registration, and some common problems in the process of registration. Taking the application of clinical trial registration in the field of neurological research as an example, the article describes the current application status of clinical trial registration and explores it’s value and deficiency in specific clinical research, to provoke the awareness on trial registration, which can help to improve the quality of clinical trials.