ABSTRACT
<p><b>PURPOSE</b>To investigate the in vitro effect of short interfering RNAs (siRNAs) against Nogo receptor (NgR) on neurite outgrowth under an inhibitory substrate of central nervous system (CNS) myelin.</p><p><b>METHODS</b>Three siRNA sequences against NgR were designed and transfected into cerebellar granule cells (CGCs) to screen for the most effcient sequence of NgR siRNA by using reverse transcription polymerase chain reaction (RT-PCR) and immunofluorescence staining. NgR siRNA sequence 1 was found the most efficient which was then transfected into the CGCs grown on CNS myelin substrate to observe its disinhibition for neurite outgrowth.</p><p><b>RESULTS</b>Compared with the scrambled control sequence of siRNA, the NgR siRNA sequence 1 significantly decreased NgR mRNA level at 24 h and 48 h (p <0.05), which was recovered by 96 h after transfection. NgR immunoreactivity was also markedly reduced at 24 and 48 h after the transfection of siRNA sequence 1 compared with that before transfection (p<0.05). The NgR immunoreactivity was recovered after 72 h post-transfection. Moreover, the neurite outgrowth on the myelin substrate was greatly improved within 72 h after the transfection with siRNA sequence 1 compared with the scrambled sequence-transfected group or non-transfected group (p<0.05).</p><p><b>CONCLUSION</b>siRNA-mediated knockdown of NgR expression contributes to neurite outgrowth in vitro.</p>
Subject(s)
Animals , Rats , Cells, Cultured , Myelin Sheath , Physiology , Neuronal Outgrowth , Physiology , Nogo Receptor 1 , Genetics , Physiology , RNA, Small Interfering , Rats, Sprague-DawleyABSTRACT
Objective To discuss the frequent etiology of spontaneous sub-cortical hemorrhage and its diag- nosis.Methods The clinical materials of 79 cases of spontaneous sub-cortical hemorrhage were analyzed.Results 56% of the hemorrhage was caused by arterial-venous malformation.48% of the hemorrhage was caused by occult AVM.Conclusion AVM is the most frequent etiology of spontaneous sub-cortical hemorrhage.CTA plays a special role in its diagnosis.
ABSTRACT
<p><b>BACKGROUND</b>Schwannoma is the tumor arising mainly from the cranial and spinal nerves. Bilateral vestibular schwannoma is the hallmark of neurofibromatosis type 2 (NF2). The NF2 gene has been cloned with comprehensive analysis of its mutations in schwannoma. However, most studies focused on vestibular schwannoma. There are differences in proliferation of tumor cell and ultrastructure between vestibular and spinal schwannomas. It is unknown whether genetic alterations in vestibular schwannoma are different from those in non-vestibular schwannoma. We analyzed the loss of heterozygosity (LOH) on chromosome 22 in patients with sporadic schwannoma including vestibular and spinal schwannomas and correlated this genetic alteration with tumor proliferation.</p><p><b>METHODS</b>In 54 unrelated patients without clinical NF1 or NF2, 36 patients had sporadic vestibular schwannoma, and 18 dorsal spinal root schwannoma. Four highly polymorphic linkage to NF2 gene microsatellite DNA markers (D22S264, D22S268, D22S280, CRYB2) were used to analyze LOH. The proliferative index was evaluated by Ki-67 and proliferative cell nuclear antigen (PCNA) immunostaining. Student's t test was used to analyze the difference of the proliferative index between schwannoma with LOH and that without LOH. The difference of the frequency of LOH in vestibular and spinal schwannomas was investigated by the chi-square test.</p><p><b>RESULTS</b>Twenty-three schwannomas (42.6%, 23/54) showed allele loss. The frequency of LOH in vestibular schwannoma was significantly higher than that in spinal schwannoma (chi2 = 5.14, P < 0.05). The proliferative index of schwannoma with LOH was significantly higher than that without LOH (tki-67 = 2.97, P = 0.0045; tPCNA = 2.93, P = 0.0051).</p><p><b>CONCLUSIONS</b>LOH on chromosome 22 is a frequent event in the tumorigenesis of sporadic schwannoma. And, there is a correlation between LOH on chromosome 22 and proliferative activity in schwannoma. The frequency of LOH in vestibular schwannoma is significantly different from that in spinal schwannoma.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Cell Proliferation , Chromosomes, Human, Pair 22 , Genes, Neurofibromatosis 2 , Loss of Heterozygosity , Neurilemmoma , Genetics , Pathology , Neuroma, Acoustic , Genetics , Spinal Cord Neoplasms , Genetics , Spinal Nerve RootsABSTRACT
<p><b>OBJECTIVE</b>To determine the effect of arousal methods for prolonged coma of 175 patients with severe traumatic brain injury and related factors.</p><p><b>METHODS</b>There were 175 cases with persistent coma longer than 1 month after severe traumatic brain injury. Coma lasted 1-12 months. Arousal procedures included hyperbaric oxygen, physical therapy and arousal drugs.</p><p><b>RESULTS</b>In the 175 prolonged coma patients 110 got recovery of consciousness; in 118 cases with coma of 1-3 months, 86 cases recovered consciousness (72.9%); in 42 cases with coma of 4-6 months, 20 cases recovered consciousness (47.6); and in 15 cases with coma of longer than 6 months, only 4 cases recovered consciousness (26.7%). The recovery of consciousness depended on patient's primary brain stem damage, cerebral hernia, GCS score, and age.</p><p><b>CONCLUSIONS</b>Application of appropriate arousal procedures improves recovery of consciousness in patients with prolonged coma.</p>
Subject(s)
Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Brain Injuries , Therapeutics , Coma, Post-Head Injury , Therapeutics , Glasgow Coma Scale , Recovery of Function , Treatment OutcomeABSTRACT
Objective To investigate neuroprotective effect of AM-36 on secondary brain injury following traumatic brain injury(TBI)in rats.Methods A total of 38 male Sprague-Dawley rats were divided into an experimental group,a control group and a sham operation group,then sustained to moder- ate TBI.AM-36(0.1 ml/100 g)was administered intraperitoneally in the experimental group and isoton- ic saline solution was administered intraperitoneally in the control and the sham operation groups at 30 mi- nutes,24 and 48 hours after TBI,respectively.The brain water content was determined at 24 hours after TBI.Rats were sacrificed by decapitation at 24 hours or one week after TBI for observing histological changes in peripheral cortex,thalamus and hippocampus by means of Hematoxylin and Eosin staining and Fluoro-Jade(F-J)staining.Results The brain water content of bilateral hemispheres 24 hours after TBI in the experimental group was significantly decreased,compared to that of the control group.Histo- logical examination revealed less degenerating neurons(F-J positive neurons)in the cortex,thalamus, CAI and CA3 of the hippocampus in AM-36 treated rats 24 hours and one week after injury(P＜0.05). Conclusion Systemic administration of AM-36 at the early stage after TBI can decrease brain water content and exert neuroprotective effect on TBI.F-J staining can be used for histopathologic quantitation of neuronal damage,for it can accurately exhibit pathologic changes following TBI induced by fluid per- cussion.