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Nilova, Vera I. "Typological Model of the Basso Ostinato in Carl Nielsen’s Fifth Symphony." Music Scholarship / Problemy Muzykal'noj Nauki, no. 2 (2021): 232–42. http://dx.doi.org/10.33779/2587-6341.2021.2.232-242.
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Fana, Girma, Diriba Tadese, Hiwot Sebsibe, and Ramesh P. S. Verma. "Multi-Environment Trial Analysis of Food Barley in Ethiopia Using AMMI and GGE Biplot Methods." Journal of Plant Breeding and Genetics 6, no. 3 (December 26, 2018): 75–85. http://dx.doi.org/10.33687/pbg.006.03.2579.
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Food barley released varieties were tested in 2012 for performance across major environments in Ethiopia consisting of 12 varieties Diribe, Tilla, Abbay, Biftu, Defo, Dinsho, Mulu, Setegn, Misiratch, Basso, Mezezo and local checks over six locations Gergera, Estayish, Shambu, Arjo, Robe and Sinana. The objective was to determine genotype by environment interaction using AMMI and GGE biplot, compare the two models for identifying the adaptable and stable genotypes. Sinana was identified as the high yielding environment and MULU the high yielding variety with mean yields of 3466.31 and 3137.67 kg/ha, respectively. The mean yield at Estayish was lower (1535 kg/ha) than other environments whereas lower yield (2212.16 kg/ha) was also obtained from the variety DINSHO. The AMMI analysis of Variance indicated that 47% of the total sum of squares is attributed to the Environmental effect, 8% to the genotypic effect and 25% to the interaction. The first three principal components of the GEI explained 81% of the variation. Genotypes Basso, Biftu and Setegn were the most stable whereas Diribe was unstable. Variety Mulu was identified as the winner genotype by AMMI model whereas Diribe was identified as the winner by the GGE model. GGE model better explains the which-won-where scenario and hence preferred to AMMI model. The discriminating and representative view of the GGE biplot depicted that Sinana and Shambu are discriminating environments whereas Sinana, Estayish and Gergera are representative environments. Therefore, Sinana is the ideal environment for discriminating genotypes and representing other environments for selecting ideal genotypes.
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Swartz, Karin R., Nicole N. Scheff, Kelly N. Roberts, and Dominic B. Fee. "Exacerbation of spinal cord injury due to static compression occurring early after onset." Journal of Neurosurgery: Spine 11, no. 5 (November 2009): 570–74. http://dx.doi.org/10.3171/2009.5.spine08588.
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Object The authors used a rat model to assess spinal cord compression following an incomplete spinal cord injury (SCI). Methods Incomplete SCI was created in the thoracic spinal cord in a novel application of a rodent spinal cord compression model. A moderate impaction force was applied instantaneously to the spinal cord and was followed by 0 seconds, 10 seconds, 30 seconds, or 5 minutes of continued compression (termed “dwell”). The different groups were assessed by behavioral testing with the Basso, Beattie, Bresnahan locomotor rating scale, and with histological injury quantification and morphometrical analysis. Results Compression after the SCI resulted in worsened Basso, Beattie, Bresnahan scale scores; however, the duration of compression was not significant. Compression did not significantly affect the percentage of spared total tissue, percent spared total white matter, or percent spared total gray matter. Percent spared tissue at the epicenter of injury was statistically worsened by compression but not in a time-dependent manner. Conclusions The authors' results suggest that spinal cord compression after the initial injury is an additional mechanism by which SCI worsens, and that the mechanism of this injury occurs rapidly. These data, however, do not support duration of compression as a significant variable.
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Aoki, Masanori, Haruhiko Kishima, Kazuhiro Yoshimura, Masahiro Ishihara, Masaki Ueno, Katsuhiko Hata, Toshihide Yamashita, Koichi Iwatsuki, and Toshiki Yoshimine. "Limited functional recovery in rats with complete spinal cord injury after transplantation of whole-layer olfactory mucosa." Journal of Neurosurgery: Spine 12, no. 2 (February 2010): 122–30. http://dx.doi.org/10.3171/2009.9.spine09233.
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Object The olfactory mucosa (OM) consists of 2 layers, the epithelium and the lamina propria. Attempts have been made to restore motor function in rat models of spinal cord injury (SCI) by transplanting olfactory ensheathing cells from the lamina propria, but there has been no attempt to transplant the OM in animal models. To investigate the potential of the OM to restore motor function, the authors developed a rat model of SCI and delayed transplantation of syngenic OM. Methods Two weeks after complete transection of the spinal cord at the T-10 level in Wistar rats, pieces of syngenic whole-layer OM were transplanted into the lesion. Rats that underwent respiratory mucosa transplantation were used as controls. The authors evaluated the locomotor activity according to the Basso-Beattie-Bresnahan scale for 8 weeks after transplantation. Obtained spinal cords were analyzed histologically. Results The OM transplantation rats showed significantly greater hindlimb locomotor recovery than the respiratory mucosa–transplanted rats. However, the recovery was limited according to the Basso-Beattie-Bresnahan scale. In the histological examination, the serotonergic raphespinal tract was regenerated. The pseudocyst cavity volume in the vicinity of the SCI lesion correlated negatively with the functional recovery. Conclusions Transplantation of whole-layer OM in rats contributes to functional recovery from SCI, but the effect is limited. In addition to OM transplantation, other means would be necessary for better outcomes in clinical situations.
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Hendrix, Sven, Selien Sanchez, Elissia Ventriglia, and Stefanie Lemmens. "HDAC8 Inhibition Reduces Lesional Iba-1+ Cell Infiltration after Spinal Cord Injury without Effects on Functional Recovery." International Journal of Molecular Sciences 21, no. 12 (June 25, 2020): 4539. http://dx.doi.org/10.3390/ijms21124539.
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Pan-histone deacetylase (HDAC) inhibition with valproic acid (VPA) has beneficial effects after spinal cord injury (SCI), although with side effects. We focused on specific HDAC8 inhibition, because it is known to reduce anti-inflammatory mediators produced by macrophages (Mφ). We hypothesized that HDAC8 inhibition improves functional recovery after SCI by reducing pro-inflammatory classically activated Mφ. Specific HDAC8 inhibition with PCI-34051 reduced the numbers of perilesional Mφ as measured by histological analyses, but did not improve functional recovery (Basso Mouse Scale). We could not reproduce the published improvement of functional recovery described in contusion SCI models using VPA in our T-cut hemisection SCI model. The presence of spared fibers might be the underlying reason for the conflicting data in different SCI models.
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Legos, Jeffrey J., Kurt R. Gritman, Ronald F. Tuma, and William F. Young. "Coadministration of Methylprednisolone with Hypertonic Saline Solution Improves Overall Neurological Function and Survival Rates in a Chronic Model of Spinal Cord Injury." Neurosurgery 49, no. 6 (December 1, 2001): 1427–33. http://dx.doi.org/10.1097/00006123-200112000-00022.
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ABSTRACT OBJECTIVE We previously demonstrated that administration of 7.5% hypertonic saline (HS) significantly improved spinal cord blood flow and neurological outcomes after spinal cord injury. The aim of this study was to determine whether hypertonicity would enhance the effects of methylprednisolone (MP), further improving neurological function. METHODS Rat spinal cords were compressed for 10 minutes with 50 g of weight, and neurological function was assessed for 28 days, using the Basso-Beattie-Bresnahan locomotor rating scale. The control group received an intravenous injection of isotonic saline (IS) (5 ml/kg). Group 1 received an intravenous injection of 7.5% HS (5 ml/kg). Group 2 received an intravenous injection of MP (30 mg/kg) and IS (5 ml/kg). Group 3 received an intravenous injection of MP (30 mg/kg) administered with 7.5% HS (5 ml/kg). RESULTS At 24 hours after spinal cord injury, the combination of MP plus HS provided significant (P < 0.01) neurological improvements, compared with all other treatment groups. At 10 days after injury, the animals that had received MP plus HS exhibited significantly (P < 0.01) higher Basso-Beattie-Bresnahan scores, compared with the MP plus IS and control groups. The median survival time was significantly (P < 0.01) increased for the MP plus HS group (28 d), compared with the MP plus IS group (16 d). Because of the dramatic decrease in survival rates at 28 days after injury, there was a significant (P < 0.01) difference in neurological function only between the MP plus HS group and the control group. CONCLUSION The results indicate that the administration of HS may enhance the delivery of MP and prevent immunosuppression, leading to improvements in overall neurological function and survival rates after spinal cord injury.
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Lei, Fei, Wen He, Xinggui Tian, Qingzhong Zhou, Lipeng Zheng, Jianping Kang, Yueming Song, and Daxiong Feng. "GSK-3 Inhibitor Promotes Neuronal Cell Regeneration and Functional Recovery in a Rat Model of Spinal Cord Injury." BioMed Research International 2019 (August 4, 2019): 1–8. http://dx.doi.org/10.1155/2019/9628065.
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The reparative process following spinal cord injury (SCI) is extremely complicated. Cells in the microenvironment express multiple inhibitory factors that affect axonal regeneration over a prolonged period of time. The axon growth inhibitory factor glycogen synthase kinase-3 (GSK-3) is an important factor during these processes. TDZD-8 (4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione) is the most effective and specific non-ATP-competitive inhibitor of GSK-3. Here, we show that administering TDZD-8 after SCI was associated with significantly inhibited neuronal apoptosis, upregulated GAP-43 expression, increased density of cortical spinal tract fibers around areas of injury, and increased Basso, Beattie, and Bresnahan (BBB) scores in the lower limbs. These findings support the notion that GSK-3 inhibitors promote neuronal cell regeneration and lower limb functional recovery.
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Schicatano, Edward J., Michele A. Basso, and Craig Evinger. "Animal Model Explains the Origins of the Cranial Dystonia Benign Essential Blepharospasm." Journal of Neurophysiology 77, no. 5 (May 1, 1997): 2842–46. http://dx.doi.org/10.1152/jn.1997.77.5.2842.
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Schicatano, Edward J., Michele A. Basso, and Craig Evinger. Animal model explains the origins of the cranial dystonia benign essential blepharospasm. J. Neurophysiol. 77: 2842–2846, 1997. The current study demonstrates that combining two mild alterations to the rat trigeminal reflex blink system reproduces the symptoms of benign essential blepharospasm, a cranial dystonia characterized by uncontrollable spasms of blinking. The first modification, a small striatal dopamine depletion, reduces the tonic inhibition of trigeminal reflex blink circuits. The second alteration, a slight weakening of the lid-closing orbicularis oculi muscle, begins an adaptive increase in the drive on trigeminal sensory-motor blink circuits that initiates blepharospasm. By themselves, neither of these modifications causes spasms of lid closure, but combined, they induce bilateral forceful blinking and spasms of lid closure. A two-factor model based on these rodent experiments may explain the development of benign essential blepharospasm in humans. The first factor, a subclinical loss of striatal dopamine, creates a permissive environment within the trigeminal blink circuits. The second factor, an external ophthalmic insult, precipitates benign essential blepharospasm. This two-factor model may also be applicable to the genesis of other cranial dystonias.
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Gao, Kai, Guannan Wang, Yansong Wang, Donghe Han, Jing Bi, Yajiang Yuan, Tianchen Yao, Zhanghui Wan, Haihong Li, and Xifan Mei. "Neuroprotective Effect of Simvastatin via Inducing the Autophagy on Spinal Cord Injury in the Rat Model." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/260161.
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Simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, is invariably used to treat cardiovascular diseases. Simvastatin has been recently demonstrated to have a neuroprotective effect in nervous system diseases. The present study aimed to further verify the neuroprotection and molecular mechanism of simvastatin on rats after spinal cord injury (SCI). The expression of Beclin-1 and LC3-B was evidently enhanced at postoperation days 3 and 5, respectively. However, the reduction of the mTOR protein and ribosomal protein S6 kinase p70 subtype (p70S6K) phosphorylation level occurred at the same time after SCI. Simvastatin significantly increased the expression of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). Meanwhile, immunofluorescence results indicated that the expression of chondroitin sulfate proteoglycan (CSPG) and caspase-3 protein was obviously reduced by simvastatin. Furthermore, Nissl staining and Basso, Beattie, and Bresnahan (BBB) scores showed that the quantity and function of motor neurons were visibly preserved by simvastatin after SCI. The findings of this study showed that simvastatin induced autophagy by inhibiting the mTOR signaling pathway and contributed to neuroprotection after SCI.
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Šulla, I., V. Balik, J. Petrovičová, V. Almášiová, K. Holovská, and Z. Oroszová. "Rat Spinal Cord Injury Experimental Model." Folia Veterinaria 60, no. 2 (June 1, 2016): 41–46. http://dx.doi.org/10.1515/fv-2016-0017.
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Abstract Spinal cord injuries (SCI) with their tragic consequences belong to the most serious pathological conditions. That is why they have stimulated basic research workers, as well as health care practitioners, to search for an effective treatment for decades. Animal experimental models have been essential in these efforts. We have jointly decided to test and standardize one of the spinal cord injury compression models in rats. Twentythree adult female Wistar rats weighing 250-320 g were utilized. Employing general anaesthesia along with a mixture of sevoflurane with O2, 2 rats (sham controls) had their vertebral arch of either Th8 or Th9 vertebra removed (laminectomy). The other 21 experimental rats with similar laminectomies were divided into 3 subgroups (n = 7) which received compression impact forces of 30, 40 or 50 g (subgroups-1, -2, and -3, respectively) applied on their exposed spinal medulla for 15 minutes. All rats were observed for 28 days after the experimental procedure and their motor functions were assessed by the Basso, Beattie, Bresnahan (BBB) test 6 hours, 7, 21 and 28 days after the simulated SCI. All 23 rats survived the surgical procedures. The control rats were without any neurological deficits. There were, in every experimental subgroup, 1 or 2 rats with extreme BBB scores. So the rats with the maximum and minimum BBB values were excluded. Then, the results acquired in the residual 5 rats in each group were averaged and statistically analysed by the Tukey multiple comparisons test. Statistically significant intersubgroup differences were found at all survival times equal to or longer than 7 post SCI days. The goal of the SCI experiment was to generate a reproducible and reliable, submaximal spinal cord trauma model. The statistical analyses demonstrated that this objective was best achieved in the subgroup-2 with the 40 g compression.
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Mao, Xiaojie, Zhiyang Jiang, Chaohong Shi, Junjun Lu, and Gaofeng Rao. "Eriodictyol attenuates spinal cord injury by activating Nrf2/HO-1 pathway and inhibiting NF-κB pathway." Tropical Journal of Pharmaceutical Research 19, no. 8 (November 18, 2020): 1611–17. http://dx.doi.org/10.4314/tjpr.v19i8.7.
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Purpose: To investigate the effect of eriodictyol on spinal cord injury (SCI) and its underlying mechanism of action.Methods: Thirty Sprague-Dawley rats were assigned to sham, SCI, and eriodictyol-treated groups (SCI + Eri; 10, 20, and 50 mg/kg). Moderate spinal cord contusion injury was induced to model SCI. Locomotor recovery was assessed based on Basso, Beattie, and Bresnahan (BBB) score. Pain wasevaluated by paw withdrawal threshold (PWT) and latency (PWL), and spinal cord water content was measured. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) expression were determined by enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase quantitative polymerase chain reaction (RT-qPCR). Immunoassay was used to determine malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-PX) levels while Western blotting was employed to evaluate nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor-kappa B (NF-κB), and phosphorylated NF-κB (p-NF-κB) levels.Results: Eriodictyol elevated BBB score, PWT, and PWL in SCI rats but reduced spinal cord water content (p < 0.05). Eriodictyol treatment down-regulated TNF-α, IL-1β, IL-6, and MDA, whereas SOD, GSH, and GSH-PX levels were elevated (p < 0.05). Eriodictyol administration increased Nrf2 and HO-1 levels but reduced p-NF-κB/NF-κB.Conclusion: This study provides a potential therapy to promote long-term functional recovery following SCI.
Keywords: Spinal cord injury, Eriodictyol, Nrf2/HO-1 pathway, NF-κB signaling pathway, Polymerase chain reaction, Basso, Beattie and Bresnahan score
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Zheng, Weipeng, Fangtian Xu, Haoyi Chen, Ning Wang, Wende Xiao, YingJie Liang, and Shifeng Wen. "Time course of diffusion tensor imaging metrics in the chronic spinal cord compression rat model." Acta Radiologica 60, no. 5 (August 24, 2018): 653–62. http://dx.doi.org/10.1177/0284185118795335.
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Background Diffusion tensor imaging (DTI) provides information about water molecule diffusion in spinal cord. Purpose This study was aimed to investigate DTI changes in the different stages of compressive spinal cord induced by water-absorbing material implantation. Material and Methods The spinal cord compression was administered over the fourth cervical vertebral level in rat. Rat models were divided into five subgroups according to compression stages: sham group, group A: three-day compression rat models; group B: 12-day compression rat models; group C: 20-day compression rat models; group D: 60-day compression rat models. DTI including fractional anisotropy (FA) and apparent diffusion coefficient (ADC) in the compressive spinal cord were collected. The relationship between the Basso, Beattie, and Bresnahan (BBB) scores and DTI metrics was further explored. Results Compared with the sham group, BBB scoring of rat model showed a decreased tendency from group A ( P < 0.05) to group B ( P < 0.05). Then the motor function of rat model hindlimbs was recovered in some degree from group C ( P < 0.05) to group D ( P < 0.05) but had significant motor defects when compared with the normal level ( P < 0.05). The DTI metrics results revealed that chronic spinal cord compression resulted in lower FA value and higher ADC value at the compressive spinal cord level assessed at all four time-points ( P < 0.05). DTI metrics also showed a close correlation with motor function ( P < 0.05). Conclusion DTI is an optimal pre-clinical imaging tool to reflect locomotor performance and pathological status of compressive spinal cord epicenter in chronic spinal cord compression rat model.
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Mantha, Ajay, Federico G. Legnani, Carlos A. Bagley, Gary L. Gallia, Ira Garonzik, Gustavo Pradilla, Eric Amundson, Betty M. Tyler, Henry Brem, and Ziya L. Gokaslan. "A novel rat model for the study of intraosseous metastatic spine cancer." Journal of Neurosurgery: Spine 2, no. 3 (March 2005): 303–7. http://dx.doi.org/10.3171/spi.2005.2.3.0303.
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Object. Although metastatic spinal disease constitutes a significant percentage of all spinal column tumors, an accessible and reproducible animal model has not been reported. In this study the authors describe the technique for creating an intraosseous spinal tumor model in rats and present a functional and histological analysis. Methods. Eighteen female Fischer 344 rats were randomized into two groups. Group 1 animals underwent a transabdominal exposure and implantation of CRL-1666 breast adenocarcinoma into the L-6 vertebral body (VB). Animals in Group 2 underwent a sham operation. Hindlimb function was tested daily by using the Basso-Beattie-Bresnahan scale. Sixteen days after tumor implantation, animals were killed and their spines were removed for histological assessment. Statistical analysis was performed using the Wilcoxon signed-rank test. By Day 15 functional analysis showed a significant decrease in motor function in Group 1 animals (median functional score 2 of 21) compared with Group 2 rats (median functional score 21 of 21) (p = 0.0217). The onset of paraparesis in Group 1 occurred within 14 to 16 days of surgery. Histopathological analysis showed tumor proliferation through the VB and into the spinal canal, with marked osteolytic activity and spinal cord compression. Conclusions. Analysis of these findings demonstrates the consistency of tumor growth in this model and validates the utility of functional testing for onset of paresis. This new rat model allows for the preclinical evaluation of novel therapeutic treatments for patients harboring metastatic spine disease.
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Krupa, Petr, Katerina Stepankova, Jessica CF Kwok, James W. Fawcett, Veronika Cimermanova, Pavla Jendelova, and Lucia Machova Urdzikova. "New Model of Ventral Spinal Cord Lesion Induced by Balloon Compression in Rats." Biomedicines 8, no. 11 (November 5, 2020): 477. http://dx.doi.org/10.3390/biomedicines8110477.
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Despite the variety of experimental models of spinal cord injury (SCI) currently used, the model of the ventral compression cord injury, which is commonly seen in humans, is very limited. Ventral balloon compression injury reflects the common anatomical mechanism of a human lesion and has the advantage of grading the injury severity by controlling the inflated volume of the balloon. In this study, ventral compression of the SCI was performed by the anterior epidural placement of the balloon of a 2F Fogarty’s catheter, via laminectomy, at the level of T10. The balloon was rapidly inflated with 10 or 15 μL of saline and rested in situ for 5 min. The severity of the lesion was assessed by behavioral and immunohistochemical tests. Compression with the volume of 15 μL resulted in severe motor and sensory deficits represented by the complete inability to move across a horizontal ladder, a final Basso, Beattie and Bresnahan (BBB) score of 7.4 and a decreased withdrawal time in the plantar test (11.6 s). Histology and immunohistochemistry revealed a significant loss of white and gray matter with a loss of motoneuron, and an increased size of astrogliosis. An inflation volume of 10 μL resulted in a mild transient deficit. There are no other balloon compression models of ventral spinal cord injury. This study provided and validated a novel, easily replicable model of the ventral compression SCI, introduced by an inflated balloon of Fogarty´s catheter. For a severe incomplete deficit, an inflated volume should be maintained at 15 μL.
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Li, Dingding, Guannan Wang, Donghe Han, Jing Bi, Chenyuan Li, Hongyu Wang, Zhiyuan Liu, et al. "MP Resulting in Autophagic Cell Death of Microglia through Zinc Changes against Spinal Cord Injury." BioMed Research International 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/6090316.
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Methylprednisolone pulse therapy (MPPT), as a public recognized therapy of spinal cord injury (SCI), is doubted recently, and the exact mechanism of MP on SCI is unclear. This study sought to investigate the exact effect of MP on SCI. We examined the effect of MP in a model of SCI in vivo and an LPS induced model in vitro. We found that administration of MP produced an increase in the Basso, Beattie, and Bresnahan scores and motor neurons counts of injured rats. Besides the number of activated microglia was apparently reduced by MP in vivo, and Beclin-1 dependent autophagic cell death of microglia was induced by MP in LPS induced model. At the same time, MP increases cellular zinc concentration and level of ZIP8, and TPEN could revert effect of MP on autophagic cell death of microglia. Finally, we have found that MP could inhibit NF-κβin LPS induced model. These results show that the MP could result in autophagic cell death of microglia, which mainly depends on increasing cellular labile zinc, and may be associated with inhibition of NF-κβ, and that MP can produce neuroprotective effect in SCI.
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Falavigna, Asdrubal, Guilherme Finger, Cesar Sebben, Pedro Guarise da Silva, Lucas Piccoli Conzati, and Manuela Peletti-Figueiro. "Motor and histological findings in a model of sci: comparison between posterior and lateral clips." Coluna/Columna 13, no. 4 (December 2014): 318–21. http://dx.doi.org/10.1590/s1808-18512014130400474.
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Objective: To evaluate the locomotor and histological impact on the spinal cord comparing lateral and posterior clip placement. Method: Randomized experimental trial. Twenty female Wistar rats, weighing between 250 and 300 grams and aged 12-14 weeks were randomized in two groups according to the placement of the clip: lateral group (N=10) and posterior group (N=10). After exposing the thoracic segment of the spine (T8-T10), a laminectomy was performed at the T9 level under microscopic view. The spinal cord injury was made using a 5 mm long aneurysm clip with a closing pressure of 50 grams. Locomotor behavior was evaluated by the Basso, Beattie and Bresnahan scale in days 1, 7, 14, 21, and 28 after surgery. The area of injury was assessed by histological analysis and measured by a software. Results: The histological evaluation showed a larger mean area of 4.8±1mm² of lesion (P=0.03) in the lateral group when compared with the posterior group mean area of 2.3±2mm². There was no significant difference between lateral and posterior groups with respect to locomotor scores from day 1 to 28 (P=0.361). Conclusion: The lesion area observed in the spinal cord histology after lateral placement of a clip was significantly bigger than in the posterior placement. The motor evaluation showed similar BBB scores regardless of the type of clamping method.
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Han, Donghe, Shurui Chen, Shiqiang Fang, Shiqiong Liu, Meihua Jin, Zhanpeng Guo, Yajiang Yuan, Yansong Wang, Chang Liu, and Xifan Mei. "The Neuroprotective Effects of Muscle-Derived Stem Cells via Brain-Derived Neurotrophic Factor in Spinal Cord Injury Model." BioMed Research International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/1972608.
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Muscle-derived stem cells (MDSCs) possess multipotent differentiation and self-renewal capacities; however, the effects and mechanism in neuron injury remain unclear. The aim of this study was to investigate the effects of MDSCs on neuron secondary injury, oxidative stress-induced apoptosis. An in vivo study showed the Basso, Beattie, and Bresnahan (BBB) score and number of neurons significantly increased after MDSCs’ transplantation in spinal cord injury (SCI) rats. An in vitro study demonstrated that MDSCs attenuated neuron apoptosis, and the expression of antioxidants was upregulated as well as the ratio of Bcl-2 and Bax in the MNT (MDSCs cocultured with injured neurons) group compared with the NT (injured neurons) group. Both LC3II/LC3I andβ-catenin were enhanced in the MNT group, while XAV939 (aβ-catenin inhibitor) decreased the expression of nuclear erythroid-related factor 2 (Nrf2) and LC3II/LC3I. Moreover, MDSCs became NSE- (neuron-specific enolase-) positive neuron-like cells with brain-derived neurotrophic factor (BDNF) treatment. The correlation analysis indicated that there was a significant relation between the level of BDNF and neuron injury. These findings suggest that MDSCs may protect the spinal cord from injury by inhibiting apoptosis and replacing injured neurons, and the increased BDNF andβ-catenin could contribute to MDSCs’ effects.
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Aksoy, Yunus, Henrique S. Basso, and Ron P. Smith. "Medium-Run Implications of Changing Demographic Structures for the Macro-Economy." National Institute Economic Review 241 (August 2017): R58—R64. http://dx.doi.org/10.1177/002795011724100114.
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While there may be an important, but transitory, cyclical component in the poor performance of the past decade, we will emphasise the secular forces: the impact of demographic structure and innovation. We draw on the empirical and theoretical work reported in Aksoy, Basso, Smith and Grasl (2015), ABSG, about the impact of changes in demographic structure on macroeconomic outcomes. This suggests that changes in age profile not only have significant implications for savings, investment, real interest rates and growth but also for innovation. The size of the effects seems plausible. For instance, if in 2015 the UK had the 1970 age structure, it would have added 0.68 percentage points to the long-run annual growth rate. The model suggests that the population ageing predicted for the next decades will tend to reduce output growth and real interest rates across OECD countries.
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Zhang, Lijian, Xiaoqing Zhuang, Yao Chen, and Hechun Xia. "Intravenous transplantation of olfactory bulb ensheathing cells for a spinal cord hemisection injury rat model." Cell Transplantation 28, no. 12 (October 30, 2019): 1585–602. http://dx.doi.org/10.1177/0963689719883842.
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Cellular transplantation strategies utilizing intraspinal or intrathecal olfactory ensheathing cells (OECs) have been reported as beneficial for spinal cord injury (SCI). However, there are many disadvantages of these methods, including additional trauma to the spinal cord parenchyma and technical challenges. Therefore, we investigated the feasibility and potential benefits of intravenous transplantation of OECs in a rat hemisection SCI model. OECs derived from olfactory bulb tissue were labeled with quantum dots (QDs), and their biodistribution after intravenous transplantation was tracked using a fluorescence imaging system. Accumulation of the transplanted OECs was observed in the injured spinal cord within 10 min, peaked at seven days after cell transplantation, and decreased gradually thereafter. This time window corresponded to the blood–spinal cord barrier (BSCB) opening time, which was quantitated with the Evans blue leakage assay. Using immunohistochemistry, we examined neuronal growth (GAP-43), remyelination (MBP), and microglia (Iba-1) reactions at the lesion site. Motor function recovery was also measured using a classic open field test (Basso, Beattie and Bresnahan score). Compared with the group injected only with QDs, the rats that received OEC transplantation exhibited a prominent reduction in inflammatory responses, increased neurogenesis and remyelination, and significant improvement in motor function. We suggest that intravenous injection could also be an effective method for delivering OECs and improving functional outcomes after SCI. Moreover, the time course of BSCB disruption provides a clinically relevant therapeutic window for cell-based intervention.
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Song, Rachel B., D. Michele Basso, Ronaldo C. da Costa, Lesley C. Fisher, Xiaokui Mo, and Sarah A. Moore. "Adaptation of the Basso–Beattie–Bresnahan locomotor rating scale for use in a clinical model of spinal cord injury in dogs." Journal of Neuroscience Methods 268 (August 2016): 117–24. http://dx.doi.org/10.1016/j.jneumeth.2016.04.023.
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Basso, Antonella, and Stefania Funari. "A three-system approach that integrates DEA, BSC, and AHP for museum evaluation." Decisions in Economics and Finance 43, no. 2 (September 22, 2020): 413–41. http://dx.doi.org/10.1007/s10203-020-00298-4.
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AbstractThis paper proposes to measure the museums performance with a model that combines the Data Envelopment Analysis (DEA) and Balanced Scorecard (BSC) methodologies with a third method, the analytic hierarchy process (AHP), which is often used to support decision making. Starting from the two-stage DEA–BSC model of Basso et al. (Omega Int J Manag Sci 81:67–84, 2018), which integrates DEA and BSC, we explore the advantages to consider also the AHP methodology, with the aim to include the judgement of some museums’ experts on the relative importance of the BSC perspectives in the performance evaluation model. A first approach uses directly the AHP priorities derived from the judgements expressed by the museums’ experts interviewed to determine the weights to aggregate the four BSC performance scores into an overall performance indicator. A second approach uses the judgments of the museums’ experts indirectly to introduce proper restrictions on the output weights of the second-stage DEA model. With this approach, we overcome the problem arising from the dispersion of the preferences within the group of experts, that may heavily affects the first approach. Both approaches proposed in this contribution are applied to the case study of the municipal museums of Venice.
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Sun, Zhonglei, Yingfu Liu, Xianbin Kong, Renjie Wang, Yunqiang Xu, Chongzhi Shang, Jingrui Huo, et al. "Exendin-4 Plays a Protective Role in a Rat Model of Spinal Cord Injury Through SERCA2." Cellular Physiology and Biochemistry 47, no. 2 (2018): 617–29. http://dx.doi.org/10.1159/000490017.
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Background/Aims: Current therapies for spinal cord injury (SCI) have limited efficacy, and identifying a therapeutic target is a pressing need. Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) plays an important role in regulating calcium homeostasis, which has been shown to inhibit apoptosis. Exendin-4 has been shown to inhibit the apoptosis of nerve cells in SCI, which can also improve SERCA2 expression. In this study, we sought to determine whether exendin-4 plays a protective role in a rat model of SCI via SERCA2. Methods: To investigate the effects of exendin-4 on SCI, a rat model of SCI was induced by a modified version of Allen’s method. Spinal cord tissue sections from rats and western blot analysis were used to examine SERCA2 expression after treatment with the long-acting glucagon-like peptide 1 receptor exendin-4 or the SERCA2 antagonist 5(6)-carboxyfluorescein diacetate N-succinimidyl ester (CE). Locomotor function was evaluated using the Basso Beattie Bresnahan locomotor rating scale and slanting board test. Results: Cell apoptosis was increased with CE treatment and decreased with exendin-4 treatment. Upregulation of SERCA2 in female rats with SCI resulted in an improvement of motor function scores and histological changes. Conclusion: These findings suggest that exendin-4 plays a protective role in a rat model of SCI through SERCA2 via inhibition of apoptosis. Existing drugs targeting SERCA2 may be an effective therapeutic strategy for the treatment of SCI.
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Wiseman, Diana Barrett, Andrew T. Dailey, David Lundin, Jiegang Zhou, Adam Lipson, Alexis Falicov, and Christopher I. Shaffrey. "Magnesium efficacy in a rat spinal cord injury model." Journal of Neurosurgery: Spine 10, no. 4 (April 2009): 308–14. http://dx.doi.org/10.3171/spi.2009.10.4.308.
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Object Magnesium has been shown to have neuroprotective properties in short-term spinal cord injury (SCI) studies. The authors evaluated the efficacy of magnesium, methylprednisolone, and magnesium plus methylprednisolone in a rat SCI model. Methods A moderate-to-severe SCI was produced at T9–10 in rats, which then received saline, magnesium, methylprednisolone, or magnesium plus methylprednisolone within 10 minutes of injury. The Basso-Beattie-Bresnahan (BBB) motor score was evaluated weekly, beginning on postinjury Day 1. After 4 weeks, the rats' spinal cords were evaluated histologically to determine myelin index and gross white matter sparing. A second experiment was conducted to evaluate the effect of delayed administration (8, 12, or 24 hours postinjury) of magnesium on recovery. Results The mean BBB scores at 4 weeks showed that rats in which magnesium was administered (BBB Score 6.9 ± 3.9) recovered better than controls (4.2 ± 2.0, p < 0.01). Insufficient numbers of animals receiving methylprednisolone were available for analysis because of severe weight loss. The rats given magnesium within 8 hours of injury had better motor recovery at 4 weeks than control animals (13.8 ± 3.7 vs 8.6 ± 5.1, p < 0.01) or animals in which magnesium was administered at 12 or 24 hours after injury (p < 0.01). Steroids (30.2%), magnesium (32.3%), and a combination of these (42.3%) had a significant effect on white matter sparing (p < 0.05), but the effect was not synergistic (p > 0.8). Neither steroids nor magnesium had a significant effect on the myelin index (p > 0.1). Conclusions The rats receiving magnesium had significantly better BBB motor scores and white matter sparing 4 weeks after moderate-to-severe SCI than control animals. In addition, the groups given steroids only or magnesium and steroids had improved white matter sparing, although the limited numbers of animals reaching the study end point makes it difficult to draw firm conclusions about the utility of steroids in this model. The optimal timing of magnesium administration appears to be within 8 hours of injury.
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Bagley, Carlos A., Markus J. Bookland, Jonathan A. Pindrik, Tolga Ozmen, Ziya L. Gokaslan, and Timothy F. Witham. "Local delivery of OncoGel delays paresis in rat metastatic spinal tumor model." Journal of Neurosurgery: Spine 7, no. 2 (August 2007): 194–98. http://dx.doi.org/10.3171/spi-07/08/194.
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Object. Spinal column metastatic disease clinically affects thousands of cancer patients every year. Local chemotherapy represents a new option in the treatment of metastatic disease of the spine. Despite the clinical impact of metastatic spine disease, the literature currently lacks an accurate animal model for the effective dosing of local chemotherapeutic agents within the vertebral column. Methods. Female Fischer 344 rats, weighing 150 to 200 g each, were used in this study. After induction of anesthesia, a transabdominal approach to the ventral vertebral body of L-6 was performed. A small hole was drilled and 5 μL of ReGel (blank polymer), OncoGel (paclitaxel and ReGel) 1.5%, OncoGel 3.0%, or OncoGel 6.0% were immediately injected to determine drug toxicity. Based on these results, efficacy studies were performed by intratumoral injection of 5 μL of ReGel, OncoGel 3.0%, and OncoGel 6.0% on Day 6 in a CRL-1666 breast adenocarcinoma metastatic spine tumor model. Hind limb function was tested pre- and postoperatively using the Basso-Beattie-Bresnahan rating scale. Histological analysis of the spinal cord and vertebral column was performed when the animal died or was killed. Results. There were no signs of toxicity observed in association with any of the agents under study. No increased benefit was seen in the blank polymer group compared with the control group (tumor only). OncoGel 3.0% and OncoGel 6.0% were effective in delaying the onset of paralysis in the respective study groups. Conclusions. These findings demonstrate the potential benefit of OncoGel in cases of subtotal resections of metastatic spinal column tumors. OncoGel 6.0% is the most efficacious drug concentration and offers the best therapeutic option in this experimental model. These results provide promise for the development of local chemotherapeutic means to treat spinal metastases.
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Belotti, Vitor Novelini, David Ferreira Lopes Santos, and Leonardo Fernando Cruz Basso. "Metodologia de avaliação do risco em investimentos de inovação." Revista de Administração da UFSM 12, no. 5 (December 30, 2019): 953. http://dx.doi.org/10.5902/1983465924401.
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The aim of this research is to analyze a theoretical method for measuring the business risk of investments in innovation proposed by Basso and Kimura (2010). The bases of the conceptual model relate the risk of investments in innovation at the firm level to the risk of the sector. In an analogous way, this study measures the sectorial risk of the different Brazilian industries with the added risk of investments in innovation, and then shows the risks of the companies listed on B3 (the São Paulo Stock Exchange) that exhibited all the necessary information for the model. This is an exploratory study with a quantitative approach, based on descriptive statistical methods and the proposed empirical model. The materials that support the research were taken from the five available editions of the Technological Innovation Survey – PINTEC (2000, 2003, 2005, 2008 and 2011) and from the standardized financial statements of the selected companies. The results of the research confirmed the possibility of using the proposed methodology, with the use of weighted factors that – in this study – were guided by the Brazil Innovation Index. Thus, it was possible to measure the level of risk of each sector of Brazilian industry and of 85 companies.
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Wei, Jinsong, Jiafeng Wang, Yulan Zhou, Shouquan Yan, Keshen Li, and Hongsheng Lin. "MicroRNA-146a Contributes to SCI Recovery via Regulating TRAF6 and IRAK1 Expression." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/4013487.
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MicroRNA-146a participates in spinal cord injury (SCI) recovery. Until recently, how miRNA-146a participates in SCI remained unclear. In this study, we tried to explore the roles of miRNA-146a in the recovery of SCI using a rat model. The expression of the probable target genes of miRNA-146a (including IRAK1 and TARF6) as well as proinflammation cytokines were measured until 7 days after surgery in the three groups (sham group, SCI group, and miRNA-146a antagomir injection group). Also, the animals’ motivations were estimated using Basso Beattie Bresnahan (BBB) during the whole experiment. A luciferase assay was performed to demonstrate that miRNA-146a could directly target the mRNAs of IRAK1 and TRAF6. Our experiments indicate that miRNA-146a inhibits proinflammatory cytokine secretion by suppressing IRAK1 and TRAF6 expression in the SCI model. In contrast, miRNA-146a may be upregulated by inflammatory mediators via the IRAK1/TRAF6 pathway in the spinal cord. As a negative feedback element, miRNA-146a could make sure that the expression of IRAK1- and TRAF6-mediated genes was under tight control. Thus, miRNA-146a may serve as a novel therapeutic target for SCI interventions.
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Carta, Mauro Giovanni, Piero Coppo, Mario Antonio Reda, Maria Carolina Hardoy, and Bernardo Carpiniello. "Depression and social change. From transcultural psychiatry to a constructivist model." Epidemiologia e Psichiatria Sociale 10, no. 1 (March 2001): 46–58. http://dx.doi.org/10.1017/s1121189x00008538.
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RIASSUNTOSulla base di precedenti studi del nostro gruppo i cui risultati verranno sintetizzati, il lavoro avanza alcune ipotesi sull'evoluzione della sintomatologia depressiva e sul possibile incremento del rischio depressivo legato alle modificazioni sociali. Vengono esaminati i disturbi dell'umore in emigrati senegalesi ed i fattori protettivi quali uno stretto supporto sociale che sembrano determinare un basso rischio in queste popolazioni. Verrà analizzata l'ipotesi che l'“occidentalizzazione”, intesa come la perdita a livello individuale dello stile di vita tradizionale, delle abitudini lavorative, dei valori culturalmente determinati, della lingua, a favore delle attitudini influenzate dalla cultura occidentale, possa rappresentare un fattore di rischio per i disturbi depressivi, almeno nelle espressioni cliniche comuni nei contesti occidentali. Precedenti ricerche del nostro gruppo, sembrano infatti indicare la presenza di quadri depressivi in popolazioni scarsamente occidentalizzate quali i nomadi Peul o i contadini Dogon del Sub-Sahara, ma, in questo contesto, tuttavia, i sintomi depressivi, peraltro rari, appaiono secondari a disturbi somatici gravi, tranne che in individui scolarizzati. Le ricerche rilevano due distinte e contrapposte modalità di espressione clinica che vengono definite rispettivamente “occidentale” o della “colpa” e “tradizionale” o della “dislocazione dal gruppo”. Ulteriori indagini condotte in aree in rapida trasformazione sembrano indicare che i fattori ambientali possano influenzare l'evoluzione dei sintomi depressivi dall'una all'altra forma e modificare la soglia di scatenamento di schemi emotivo comportamentali depressivi. E' supposto che le perturbazioni dell'assetto sociale rendano adattive attitudini alia “iperesponsabilizzazione compulsiva”, una serie di convinzioni profonde che possono essere considerate allo stesso tempo come un prodotto dell'“occidentalizzazione” e come fattore di rischio depressivo. Gli individui dotati di tali caratteristiche di base, attraverso opportunità di vita offerte dal cambiamento sociale maturerebbero sistemi complessi e innovativi di interpretazione della realtà, di attribuzione della causalità e del controllo degli eventi, di vivere le emozioni. A partire da tale modello viene proposta una ridiscussione del concetto di soglia e una chiave di lettura della trasformazione della fenomenologia depressiva, se si ipotizza che i nuovi sistemi organizzativi della conoscenza, pur capaci di rispondere alle esigenze emergenti, espongano ad una maggiore vulnerability depressiva.
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Yao, Rubin, Lirong Ren, Shiyong Wang, Ming Zhang, and Kaishun Yang. "Euxanthone inhibits traumatic spinal cord injury via anti-oxidative stress and suppression of p38 and PI3K/Akt signaling pathway in a rat model." Translational Neuroscience 12, no. 1 (January 1, 2021): 114–26. http://dx.doi.org/10.1515/tnsci-2021-0012.
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Abstract Background Owing to neurite promoting, antioxidant and anti-inflammatory effects of Euxanthone (Eux), the investigation was aimed to probe the neuroprotective efficacy of Eux against traumatic spinal cord injury (t-SCI) in rats and whether Eux can improve neuropathic function in t-SCI. Method Sprague-Dawley (SD) rats were randomized in – Sham, t-SCI, Eux30, and Eux60 (t-SCI + 30 and 60 mg/kg respectively). Animals with compression force-induced t-SCI were subjected to estimation of locomotor functions. Spinal cord water content and Evans blue (EB) effusion were determined for quantifying edema and intactness of the spinal cord. Oxidative stress and immunochemical markers were quantified by ELISA and western blotting. Results Findings revealed that Eux60 group animals had greater Basso, Beattie, and Bresnahan (BBB) and (incline plane test) IPT score indicating improved locomotor functions. There was a reduction in the spinal edema and water content after Eux treatment, together with lowering of oxidative stress markers. The expression of IL-6, IL-12, IL-1β, caspase-3, RANKL, TLR4, NF-κB, p-38, PI3K, and Akt in spinal cord tissues of t-SCI-induced rats was lowered after Eux treatment. Conclusion Overall, the investigation advocates that Eux attenuates t-SCI and associated inflammation, oxidative damage, and resulting apoptosis via modulation of TLR4/NF-κB/p38 and PI3K/Akt signaling cascade.
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Wang, WeiHeng, Xiaodong Huang, Jian Li, Aijun Sun, Jiangming Yu, Ning Xie, YanHai Xi, and Xiaojian Ye. "Methane Suppresses Microglial Activation Related to Oxidative, Inflammatory, and Apoptotic Injury during Spinal Cord Injury in Rats." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/2190897.
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Objective. We investigated the hypothesis that methane-rich saline (MS) can be used to repair spinal cord injury (SCI) in a rat model through suppressing microglial activation related to oxidative, inflammatory, and apoptotic injury.Methods. MS was injected intraperitoneally in rats after SCI. Hematoxylin-eosin (HE) staining, oxidative stress, inflammatory parameters, and cell apoptosis were detected 72 h after SCI to determine the optimal dose. Then, we investigated the protective mechanisms and the long-term effects of MS on SCI. HE and microglial activation were observed. Neurological function was evaluated by the Basso, Beattie, and Bresnahan (BBB) scale.Results. MS can significantly decrease infarct area and inhibit oxidative stress, inflammation, and cell apoptosis 72 h following SCI. The MS protective effect at a dose of 20 ml/kg was better. Moreover, MS can significantly suppress microglial activation related to oxidative and inflammatory injury after SCI and improve hind limb neurological function.Conclusion. MS could repair SCI and reduce the release of oxidative stress, inflammatory cytokines, and cell apoptosis produced by activated microglia. MS provides a novel and promising strategy for the treatment of SCI.
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Li, Yi-Fan, Tie Li, Da-Wei Zhang, Hui Xue, Dong Chen, Chen Li, and Fu-Chun Wang. "The Comprehensive Therapy of Electroacupuncture Promotes Regeneration of Nerve Fibers and Motor Function Recovery in Rats after Spinal Cord Injury." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/7568697.
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The present study aimed to evaluate the role of the combination treatment of methylprednisolone (MP) and electroacupuncture (EA) in regeneration of nerve fibers and functional recovery in rats with spinal cord injury (SCI). Female Wistar rats were used for an SCI model by using a weight-drop hammer at levels T10 (spinal cord segment corresponding to the 10th thoracic vertebra). Four groups received different treatments for the study: SCI control, MP, MP and EA, and Sham. The growth of nerve fibers was examined by counting fluorescein positive nerve fibers. The motor functional recovery was evaluated by Basso, Beattie, Bresnahan (BBB) score, and electrophysiology analysis. We found that, compared to MP groups, there were more well-oriented and paralleled fluorescein positive nerve fibers in MP and EA group. Both latencies and amplitudes of the Motor Evoked Potential (MEP) in the combination therapy of MP and EA were higher than MP group. Additionally, recovered hindlimb movements were sustained in most rats in the MP and EA group. Our study indicated that combination therapies could become a powerful treatment for SCI in rats.
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Zhang, Hao, Alexander Younsi, Guoli Zheng, Mohamed Tail, Anna-Kathrin Harms, Judith Roth, Maryam Hatami, Thomas Skutella, Andreas Unterberg, and Klaus Zweckberger. "Sonic Hedgehog modulates the inflammatory response and improves functional recovery after spinal cord injury in a thoracic contusion–compression model." European Spine Journal 30, no. 6 (March 11, 2021): 1509–20. http://dx.doi.org/10.1007/s00586-021-06796-2.
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Abstract Purpose The Sonic Hedgehog (Shh) pathway has been associated with a protective role after injury to the central nervous system (CNS). We, therefore, investigated the effects of intrathecal Shh-administration in the subacute phase after thoracic spinal cord injury (SCI) on secondary injury processes in rats. Methods Twenty-one Wistar rats were subjected to thoracic clip-contusion/compression SCI at T9. Animals were randomized into three treatment groups (Shh, Vehicle, Sham). Seven days after SCI, osmotic pumps were implanted for seven-day continuous intrathecal administration of Shh. Basso, Beattie and Bresnahan (BBB) score, Gridwalk test and bodyweight were weekly assessed. Animals were sacrificed six weeks after SCI and immunohistological analyses were conducted. The results were compared between groups and statistical analysis was performed (p < 0.05 was considered significant). Results The intrathecal administration of Shh led to significantly increased polarization of macrophages toward the anti-inflammatory M2-phenotype, significantly decreased T-lymphocytic invasion and significantly reduced resident microglia six weeks after the injury. Reactive astrogliosis was also significantly reduced while changes in size of the posttraumatic cyst as well as the overall macrophagic infiltration, although reduced, remained insignificant. Finally, with the administration of Shh, gain of bodyweight (216.6 ± 3.65 g vs. 230.4 ± 5.477 g; p = 0.0111) and BBB score (8.2 ± 0.2 vs. 5.9 ± 0.7 points; p = 0.0365) were significantly improved compared to untreated animals six weeks after SCI as well. Conclusion Intrathecal Shh-administration showed neuroprotective effects with attenuated neuroinflammation, reduced astrogliosis and improved functional recovery six weeks after severe contusion/compression SCI.
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Tan, Hongpei, Yongxiang Tang, Jian Li, Tingting He, Ming Zhou, and Shuo Hu. "Prognosis Evaluation Using 18F-Alfatide II PET in a Rat Model of Spinal Cord Injury Treated With Estrogen." Molecular Imaging 19 (January 1, 2020): 153601212090919. http://dx.doi.org/10.1177/1536012120909199.
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Spinal cord injury (SCI) leads to severe dysfunction below injured segment and poses a great pressure to the individual and society. In this study, we applied 18F-alfatide II positron emission tomography/computed tomography (PET/CT) to monitor angiogenesis in an SCI model after estrogen (E2) treatment, as well as to evaluate the prognosis in a noninvasive manner. The SCI model was established with male rats and the rats were randomly divided into E2-treated group (SCI + E2) and E2-untreated group (SCI). Sham group was also used as control (Sham). The angiogenesis after SCI was monitored by 18F-alfatide II PET/CT and verified by immunofluorescence of CD31 and CD61. We also evaluated the level of E2 and growth-associated protein 43 (GAP43) by enzyme-linked immunosorbent assay. Finally, Basso, Beattie, and Bresnahan (BBB) scores were determined to evaluate the exercise capacity of the rats in all 3 groups. Our results showed that the BBB score of SCI + E2 group was significantly different from that of SCI group ( P < .05) and Sham group ( P < .01). The uptake of 18F-alfatide II was positively correlated with the expression level of GAP43, both of which reached the peak at day 7 after injury. CD31 and CD61 immunostaining further verified increased angiogenesis in E2-treated SCI lesions. We concluded that 18F-alfatide II PET/CT can monitor the angiogenesis status after SCI in vivo and it may help clinician predict the progression of patients with SCI. This may benefit the study of vascular repair after SCI and provide a tool for evaluation of SCI treatment in clinical practices.
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Povysheva, Tatyana, Maksim Shmarov, Denis Logunov, Boris Naroditsky, Ilya Shulman, Sergey Ogurcov, Pavel Kolesnikov, Rustem Islamov, and Yuri Chelyshev. "Post–spinal cord injury astrocyte-mediated functional recovery in rats after intraspinal injection of the recombinant adenoviral vectors Ad5-VEGF and Ad5-ANG." Journal of Neurosurgery: Spine 27, no. 1 (July 2017): 105–15. http://dx.doi.org/10.3171/2016.9.spine15959.
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OBJECTIVEThe most actively explored therapeutic strategy for overcoming spinal cord injury (SCI) is the delivery of genes encoding molecules that stimulate regeneration. In a mouse model of amyotrophic lateral sclerosis and in preliminary clinical trials in patients with amyotrophic lateral sclerosis, the combined administration of recombinant adenoviral vectors (Ad5-VEGF+Ad5-ANG) encoding the neurotrophic/angiogenic factors vascular endothelial growth factor (VEGF) and angiogenin (ANG) was found to slow the development of neurological deficits. These results suggest that there may be positive effects of this combination of genes in posttraumatic spinal cord regeneration. The objective of the present study was to determine the effects of Ad5-VEGF+Ad5-ANG combination therapy on motor function recovery and reactivity of astrocytes in a rat model of SCI.METHODSSpinal cord injury was induced in adult Wistar rats by the weight-drop method. Rats (n = 51) were divided into 2 groups: the experimental group (Ad5-VEGF+Ad5-ANG) and the control group (Ad5-GFP [green fluorescent protein]). Recovery of motor function was assessed using the Basso, Beattie, and Bresnahan scale. The duration and intensity of infectivity and gene expression from the injected vectors were assessed by immunofluorescent detection of GFP. Reactivity of glial cells was assessed by changes in the number of immunopositive cells expressing glial fibrillary acidic protein (GFAP), S100β, aquaporin 4 (AQP4), oligodendrocyte transcription factor 2, and chondroitin sulfate proteoglycan 4. The level of S100β mRNA expression in the spinal cord was estimated by real-time polymerase chain reaction.RESULTSPartial recovery of motor function was observed 30 days after surgery in both groups. However, Basso, Beattie, and Bresnahan scores were 35.9% higher in the Ad5-VEGF+Ad5-ANG group compared with the control group. Specific GFP signal was observed at distances of up to 5 mm in the rostral and caudal directions from the points of injection. A 1.5 to 2.0–fold increase in the number of GFAP+, S100β+, and AQP4+ cells was observed in the white and gray matter at a distance of up to 5 mm from the center of the lesion site in the caudal and rostral directions. At 30 days after injury, a 2-fold increase in S100β transcripts was observed in the Ad5-VEGF+Ad5-ANG group compared with the control group.CONCLUSIONSIntraspinal injection of recombinant adenoviral vectors encoding VEGF and ANG stimulates functional recovery after traumatic SCI. The increased number of S100β+ astrocytes induced by this approach may be a beneficial factor for maintaining the survival and function of neurons. Therefore, gene therapy with Ad5-VEGF+Ad5-ANG vectors is an effective therapeutic method for SCI treatment.
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Choi, Byung Hyune, Yoon Ha, Xian Huang, So Ra Park, Joonho Chung, Dong Keun Hyun, Hyeonseon Park, Hyung Chun Park, Sung Wan Kim, and Minhyung Lee. "Hypoxia-inducible expression of vascular endothelial growth factor for the treatment of spinal cord injury in a rat model." Journal of Neurosurgery: Spine 7, no. 1 (July 2007): 54–60. http://dx.doi.org/10.3171/spi-07/07/054.
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Object Vascular endothelial growth factor (VEGF) has been investigated as a therapy for many disorders and injuries involving ischemia. In this report, we constructed and evaluated a hypoxia-inducible VEGF expression system as a treatment for spinal cord injury (SCI). Methods The hypoxia-inducible VEGF plasmid was constructed using the erythropoietin (Epo) enhancer with the Simian virus 40 (SV40) promoter (pEpo-SV-VEGF) or the RTP801 promoter (pRTP801-VEGF). The expression of VEGF in vitro was evaluated after transfection into N2A cells. The plasmids were then injected into rat spinal cords with contusion injuries. The expression of VEGF in vivo was measured using reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Locomotor recovery in the rats was evaluated using the Basso, Beattie and Bresnahan (BBB) scale for locomotor analysis. Results In vitro transfection showed that pEpo-SV-VEGF or pRTP801-VEGF induced VEGF expression under hypoxic conditions, whereas pSV-VEGF did not. The VEGF level was higher in the pEpo-SV-VEGF and pRTP801-VEGF groups than in the control group. The VEGF expression was detected in neurons and astrocytes of the spinal cord. Locomotor recovery was improved in the pEpo-SV-VEGF and pRTP801-VEGF groups, and BBB scores were higher than in the control group. Staining using terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling showed that the number of apoptotic cells decreased in the plasmid-injected groups compared with the control group, and significant differences were observed between the hypoxia-responsive groups and the pSV-VEGF group. Conclusions These results suggest that the hypoxia-inducible VEGF expression system may be useful for gene therapy of SCI.
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Li, Ci, Guangjun Jiao, Wenliang Wu, Hongliang Wang, Shanwu Ren, Lu Zhang, Hongming Zhou, Haichun Liu, and Yunzhen Chen. "Exosomes from Bone Marrow Mesenchymal Stem Cells Inhibit Neuronal Apoptosis and Promote Motor Function Recovery via the Wnt/β-catenin Signaling Pathway." Cell Transplantation 28, no. 11 (August 19, 2019): 1373–83. http://dx.doi.org/10.1177/0963689719870999.
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Severe spinal cord injury (SCI) is caused by external mechanical injury, resulting in unrecoverable neurological injury. Recent studies have shown that exosomes derived from bone marrow mesenchymal stem cells (BMSCs-Exos) might be valuable paracrine molecules in the treatment of SCI. In this study, we designed SCI models in vivo and in vitro and then investigated the possible mechanism of successful repair by BMSCs-Exos. In vivo, we established one Sham group and two SCI model groups. The Basso, Beattie, Bresnahan (BBB) scores showed that BMSCs-Exos could effectively promote the recovery of spinal cord function. The results of the Nissl staining, immunohistochemistry, and TUNEL/NeuN/DAPI double staining showed that BMSCs-Exos inhibited neuronal apoptosis. Western blot analysis showed that the protein expression level of Bcl-2 was significantly increased in the BMSCs-Exos group compared with the PBS group, while the protein expression levels of Bax, cleaved caspase-3, and cleaved caspase-9 were significantly decreased. The results of western bolt and qRT-PCR demonstrated that BMSCs-Exos could activate the Wnt/β-catenin signaling pathway effectively. In vitro, we found that inhibition of the Wnt/β-catenin signaling pathway could promote neuronal apoptosis following lipopolysaccharide (LPS) induction. These results demonstrated that BMSCs-Exos may be a promising therapeutic for SCI by activating the Wnt/β-catenin signaling pathway.
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Marufa, Siti Ainun, Tsung-Hsun Hsieh, Jian-Chiun Liou, Hsin-Yung Chen, and Chih-Wei Peng. "Neuromodulatory effects of repetitive transcranial magnetic stimulation on neural plasticity and motor functions in rats with an incomplete spinal cord injury: A preliminary study." PLOS ONE 16, no. 6 (June 4, 2021): e0252965. http://dx.doi.org/10.1371/journal.pone.0252965.
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We investigated the effects of intermittent theta-burst stimulation (iTBS) on locomotor function, motor plasticity, and axonal regeneration in an animal model of incomplete spinal cord injury (SCI). Aneurysm clips with different compression forces were applied extradurally around the spinal cord at T10. Motor plasticity was evaluated by examining the motor evoked potentials (MEPs). Long-term iTBS treatment was given at the post-SCI 5th week and continued for 2 weeks (5 consecutive days/week). Time-course changes in locomotor function and the axonal regeneration level were measured by the Basso Beattie Bresnahan (BBB) scale, and growth-associated protein (GAP)-43 expression was detected in brain and spinal cord tissues. iTBS-induced potentiation was reduced at post-1-week SCI lesion and had recovered by 4 weeks post-SCI lesion, except in the severe group. Multiple sessions of iTBS treatment enhanced the motor plasticity in all SCI rats. The locomotor function revealed no significant changes between pre- and post-iTBS treatment in SCI rats. The GAP-43 expression level in the spinal cord increased following 2 weeks of iTBS treatment compared to the sham-treatment group. This preclinical model may provide a translational platform to further investigate therapeutic mechanisms of transcranial magnetic stimulation and enhance the possibility of the potential use of TMS with the iTBS scheme for treating SCIs.
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Tetreault, Lindsay A., Mary P. Zhu, Jefferson R. Wilson, Spyridon K. Karadimas, and Michael G. Fehlings. "The Impact of Riluzole on Neurobehavioral Outcomes in Preclinical Models of Traumatic and Nontraumatic Spinal Cord Injury: Results From a Systematic Review of the Literature." Global Spine Journal 10, no. 2 (May 12, 2019): 216–29. http://dx.doi.org/10.1177/2192568219835516.
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Study Design: Systematic review. Objective: To evaluate the impact of riluzole on neurobehavioral outcomes in preclinical models of nontraumatic and traumatic spinal cord injury (SCI). Methods: An extensive search of the literature was conducted in Medline, EMBASE, and Medline in Process. Studies were included if they evaluated the impact of riluzole on neurobehavioral outcomes in preclinical models of nontraumatic and traumatic SCI. Extensive data were extracted from relevant studies, including sample characteristics, injury model, outcomes assessed, timing of evaluation, and main results. The SYRCLE checklist was used to assess various sources of bias. Results: The search yielded a total of 3180 unique citations. A total of 16 studies were deemed relevant and were summarized in this review. Sample sizes ranged from 14 to 90, and injury models included traumatic SCI (n = 9), degenerative cervical myelopathy (n = 2), and spinal cord-ischemia (n = 5). The most commonly assessed outcome measures were BBB (Basso, Beattie, Besnahan) locomotor score and von Frey filament testing. In general, rats treated with riluzole exhibited significantly higher BBB locomotor scores than controls. Furthermore, riluzole significantly increased withdrawal thresholds to innocuous stimuli and tail flick latency following application of radiant heat stimuli. Finally, rats treated with riluzole achieved superior results on many components of gait assessment. Conclusion: In preclinical models of traumatic and nontraumatic SCI, riluzole significantly improves locomotor scores, gait function, and neuropathic pain. This review provides the background information necessary to interpret the results of clinical trials on the impact of riluzole in traumatic and nontraumatic SCI.
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Zhang, Zifeng, Zheng Huang, Hao Dai, Licheng Wei, Songtao Sun, and Feng Gao. "Therapeutic Efficacy of E-64-d, a Selective Calpain Inhibitor, in Experimental Acute Spinal Cord Injury." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/134242.
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This study aims to investigate the therapeutic effect of calpain inhibitor E-64-d on SCI and to find a new approach to treat SCI. When an SCI rat model was established, it was immediately administered with E-64-d. RT-PCR and Western blotting were used to determine the protein and mRNA levels of calpain 1 and 68-kD NFP. TUNEL staining and NeuN labeling were performed to analyze neuronal apoptosis in the lesion. Immunohistochemistry assay was carried out to observe the expressions of calpain 1 and GFAP. Cyclooxygenase-2 activity was measured to show the immune response status. Locomotor function was evaluated by inclined plane test and Basso, Beattie, and Bresnahan locomotor rating scale. The results showed that calpain 1 was activated after SCI occurred. Treatment with E-64-d decreased expressions of calpain 1 and GFAP, alleviated neuronal apoptosis, inhibited cyclooxygenase-2 activity, and resulted in the promoted locomotor function. Furthermore, combination of E-64-d and MP had better efficacy than did E-64-d or MP alone. E-64-d is expected to be applied to treat SCI, and its alliance with MP may provide a valid strategy for SCI therapy.
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Lee, Ji Yeoun, Shin Won Kim, Saet Pyoul Kim, Hyeonjin Kim, Jung-Eun Cheon, Seung-Ki Kim, Sun Ha Paek, Dachling Pang, and Kyu-Chang Wang. "A rat model of chronic syringomyelia induced by epidural compression of the lumbar spinal cord." Journal of Neurosurgery: Spine 27, no. 4 (October 2017): 458–67. http://dx.doi.org/10.3171/2016.9.spine16188.
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OBJECTIVEThere has been no established animal model of syringomyelia associated with lumbosacral spinal lipoma. The research on the pathophysiology of syringomyelia has been focused on Chiari malformation, trauma, and inflammation. To understand the pathophysiology of syringomyelia associated with occult spinal dysraphism, a novel animal model of syringomyelia induced by chronic mechanical compression of the lumbar spinal cord was created.METHODSThe model was made by epidural injection of highly concentrated paste-like kaolin solution through windows created by partial laminectomy of L-1 and L-5 vertebrae. Behavioral outcome in terms of motor (Basso-Beattie-Bresnahan score) and urinary function was assessed serially for 12 weeks. Magnetic resonance images were obtained in some animals to confirm the formation of a syrinx and to monitor changes in its size. Immunohistochemical studies, including analysis for glial fibrillary acidic protein, NeuN, CC1, ED-1, and caspase-3, were done.RESULTSBy 12 weeks after the epidural compression procedure, syringomyelia formation was confirmed in 85% of the rats (34 of 40) on histology and/or MRI. The syrinx cavities were found rostral to the epidural compression. Motor deficit of varying degrees was seen immediately after the procedure in 28% of the rats (11 of 40). In 13 rats (33%), lower urinary tract dysfunction was seen. Motor deficit improved by 5 weeks after the procedure, whereas urinary dysfunction mostly improved by 2 weeks. Five rats (13%, 5 of 40) died 1 month postoperatively or later, and 3 of the 5 had developed urinary tract infection. At 12 weeks after the operation, IHC showed no inflammatory process, demyelination, or accelerated apoptosis in the spinal cords surrounding the syrinx cavities, similar to sham-operated animals.CONCLUSIONSA novel experimental model for syringomyelia by epidural compression of the lumbar spinal cord has been created. The authors hope that it will serve as an important research tool to elucidate the pathogenesis of this type of syringomyelia, as well as the CSF hydrodynamics of the lumbar spinal cord.
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Orbach, Yair. "Parametric analysis of the Bass model." Innovative Marketing 12, no. 1 (April 27, 2016): 29–40. http://dx.doi.org/10.21511/im.12(1).2016.03.
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In this research, the authors explore the influence of the Bass model p, q parameters values on diffusion patterns and map p, q Euclidean space regions accordingly. The boundaries of four different sub-regions are classified and defined, in the region where both p, q are positive, according to the number of inflection point and peak of the non-cumulative sales curve. The researchers extend the p, q range beyond the common positive value restriction to regions where either p or q is negative. The case of negative p, which represents barriers to initial adoption, leads us to redefine the motivation for seeding, where seeding is essential to start the market rather than just for accelerating the diffusion. The case of negative q, caused by a declining motivation to adopt as the number of adopters increases, leads us to cases where the saturation of the market is at partial coverage rather than the usual full coverage at the long run. The authors develop a solution to the special case of p + q = 0, where the Bass solution cannot be used. Some differences are highlighted between the discrete time and continuous time flavors of the Bass model and the implication on the mapping. The distortion is presented, caused by the transition between continuous and discrete time forms, as a function of p, q values in the various regions
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Bi, Yunlong, Xi Chen, Yang Cao, Deshui Yu, Jia’ai Zhao, Yu Jing, and Gang Lv. "Nuclear Heme Oxidase-1 Inhibits Endoplasmic Reticulum Stress-Mediated Apoptosis after Spinal Cord Injury." BioMed Research International 2020 (August 3, 2020): 1–8. http://dx.doi.org/10.1155/2020/7576063.
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The treatment goal for spinal cord injury (SCI) is to repair neurites and suppress cellular apoptosis. This study is to investigate the effects of nuclear heme oxidase-1 (HO-1) on the acute spinal cord injury and the related mechanisms. The rat model of the SCI was established. On day 7, before model establishment, the adenovirus vector carrying nuclear HO-1 (Ad-GFP-HO-1CΔ23) was injected into the animals into the tenth thoracic spine (T10) segment by the intrathecal injection. Starting from after the model establishment to day 28, the recovery of motor function was assessed by the Basso-Beattie-Bresnahan (BBB) scoring method. Immunofluorescence was performed to detect the expression patterns of nuclear and cytoplasmic proteins. HE and Nissl staining methods were used to evaluate the structural damage and the number of surviving neurons near the injured area. The TUNEL method was conducted to evaluate the apoptotic degree. Protein expression levels were detected with the Western blot analysis. The BBB assay scores in the nuclear HO-1 group were significantly higher than the blank and adenovirus control groups. Moreover, compared to the blank and adenovirus control groups, the neuronal apoptosis in the nuclear HO-1 group was significantly alleviated. Furthermore, the expression levels of the endoplasmic reticulum stress-related proteins, i.e., CHOP, GRP78, and caspase-12, were significantly decreased in the nuclear HO-1 group. Nuclear HO-1 significantly improves the SCI, promotes the functional recovery, inhibits the endoplasmic reticulum stress, and alleviates the apoptotic process after SCI.
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Hsu, Wesley, I.-Mei Siu, Gustavo Pradilla, Ziya L. Gokaslan, George I. Jallo, and Gary L. Gallia. "Animal model of intramedullary spinal cord glioma using human glioblastoma multiforme neurospheres." Journal of Neurosurgery: Spine 16, no. 3 (March 2012): 315–19. http://dx.doi.org/10.3171/2011.11.spine11492.
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Object Advances in the diagnosis and management of patients with spinal cord tumors have been limited because of the rarity of the disease and the limitations of current animal models for spinal cord glioma. The ideal spinal cord tumor model would possess a number of characteristics, including the use of human glioma cells that capture the growth pattern and local invasive nature of their human counterpart. In this study, the authors' goal was to develop a novel spinal cord tumor model using a human neurosphere cell line. Methods Eighteen female athymic rats were randomized into 3 experimental groups. Animals in the first group (6 rats) received a 3-ml intramedullary injection containing DMEM and were used as controls. Animals in the second group (6 rats) received a 3-ml intramedullary injection containing 100,000 glioblastoma multiforme (GBM) neurosphere cells in 3 ml DMEM. Animals in the third group (6 rats) received a 3-ml intramedullary injection containing 9L gliosarcoma cells in 3 ml DMEM. Functional testing of hindlimb strength was assessed using the Basso-Beattie-Bresnahan (BBB) scale. Once the functional BBB score of an animal was less than or equal to 5 (slight movement of 2 joints and extensive movement of the third), euthanasia was performed. Results Animals in the GBM neurosphere group had a mean survival of 33.3 ± 2.0 days, which was approximately twice as long as animals in the 9L gliosarcoma group (16.3 ± 2.3 days). There was a significant difference between survival of the GBM neurosphere and 9L gliosarcoma groups (p < 0.001). None of the control animals died (p < 0.001 for GBM neurosphere group vs controls and 9L vs controls). Histopathological examination of the rats injected with 9L gliosarcoma revealed that all animals developed highly cellular, well-circumscribed lesions causing compression of the surrounding tissue, with minimal invasion of the surrounding gray and white matter. Histopathological examination of animals injected with GBM neurospheres revealed that all animals developed infiltrative lesions with a high degree of white and gray matter invasion along with areas of necrosis. Conclusions The authors have established a novel animal model of spinal cord glioma using neurospheres derived from human GBM. When injected into the spinal cords of athymic nude rats, neurospheres gave rise to infiltrative, actively proliferating tumors that were histologically identical to spinal cord glioma in humans. On the basis of their results, the authors conclude that this is a reproducible animal model of high-grade spinal cord glioma based on a human GBM neurosphere line. This model represents an improvement over other models using nonhuman glioma cell lines. Novel therapeutic strategies can be readily evaluated using this model.
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Wu, Ling-ling, Xiao-ming Pan, Hao-hao Chen, Xiao-yan Fu, Jinzhan Jiang, and Ming-xing Ding. "Repairing and Analgesic Effects of Umbilical Cord Mesenchymal Stem Cell Transplantation in Mice with Spinal Cord Injury." BioMed Research International 2020 (April 6, 2020): 1–10. http://dx.doi.org/10.1155/2020/7650354.
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Transplantation of human umbilical cord mesenchymal stem cells (hUC-MSCs) into spinal cord injury (SCI) may alleviate neuropathic pain and promote functional recovery. The underlying mechanism likely involves activation of glial cells and regulation of inflammatory factors but requires further validation. SCI was induced in 16 ICR mice using an SCI compression model, followed by injection of lentiviral vector-mediated green fluorescent protein- (GFP-) labeled hUC-MSCs 1 week later. Behavioral tests, histological evaluation, and inflammatory factor detection were performed in the treatment (SCI+hUC-MSCs) and model (SCI) groups. Histological evaluation revealed GFP expression in the spinal cord tissue of the treatment group, implying that the injected MSCs successfully migrated to the SCI. The Basso, Beattie, and Bresnahan (BBB) scores showed that motor function gradually recovered over time in both groups, but recovery speed was significantly higher in the treatment group than in the model group. The pain threshold in mice decreased after SCI but gradually increased over time owing to the self-repair function of the body. The corresponding pain threshold of the treatment group was significantly higher than that of the model group, indicating the therapeutic and analgesic effects of hUC-MSCs. Expression of IL-6 and TNF-α in the spinal cord tissue of the treated group decreased, whereas glial cell line-derived neurotrophic factor (GDNF) expression along with ED1 expression increased compared with those in the model group, suggesting that SCI activated ED1 inflammatory macrophages/microglia, which were subsequently reduced by hUC-MSC transplantation. hUC-MSCs are speculated to enhance the repair of the injured spinal cord tissue and exert an analgesic effect by reducing the secretion of inflammatory factors IL-6 and TNF-α and upregulating the expression of GDNF.
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Chen, Gang, Yimin Liang, Fanghu Chen, Haifeng Wang, and Guoming Zhu. "The effect of lithium chloride on the motor function of spinal cord injury–controlled rat and the relevant mechanism." European Journal of Inflammation 17 (January 2019): 205873921985285. http://dx.doi.org/10.1177/2058739219852855.
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The objective of this study is to discuss the effect and mechanism of lithium chloride on the rehabilitation of locomotion post spinal cord injury (SCI) by observing the effect of lithium chloride on the expression of the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) pathway. In total, 36 Sprague-Dawley (SD) rats were randomly divided into the sham operation group (n = 12), model group (n = 12), and lithium chloride group (n = 12). The sham operation group underwent laminectomy, while for the model group and the lithium chloride group with the NYU spinal cord impactor the SCI model was established. Basso, Beattie, and Bresnahan (BBB) score was used to evaluate locomotion after administration for 1, 3, 5, and 7 days, and the tissues were gathered for Nissl staining, transmission electron microscopy, immunofluorescence, and Western blot. With a statistical difference ( P < 0.05) on the 3rd day and significant difference ( P < 0.01) on the 5th day post administration, a higher BBB score was observed in the lithium chloride group indicating that lithium chloride improved the locomotion function after SCI. A better structure and morphology of neuron were observed by Nissl staining in the lithium chloride group. Lithium chloride promoted BDNF secretion from neurons in the spinal cord anterior horn with a significant difference compared to the model group ( P < 0.01). Compared with the model group, lithium chloride significantly promoted the expression of BDNF protein and phosphorylated TrkB protein ( P < 0.05), but no difference in the expression of TrkB was detected. Lithium chloride can alleviate the locomotion function after SCI with a mechanism that it can promote BDNF secretion from neurons in the spinal cord anterior horn and phosphorylation of TrkB to upregulate the BDNF/TrkB pathway supporting survival of neurons and regeneration and remyelination of axons.
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Li, Ke, Juntong Liu, Liangyu Song, Wei Lv, Xi Tian, Zhigang Li, and Suhua Shi. "Effect of Electroacupuncture Treatment at Dazhui (GV14) and Mingmen (GV4) Modulates the PI3K/AKT/mTOR Signaling Pathway in Rats after Spinal Cord Injury." Neural Plasticity 2020 (January 21, 2020): 1–13. http://dx.doi.org/10.1155/2020/5474608.
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Electroacupuncture (EA) is widely recognized as clinical treatment of spinal cord injury (SCI). The purpose of this study is to elucidate whether and how the PI3K/AKT/mTOR signaling pathway plays any role in EA treating SCI. Rats were randomly divided into four equal groups: Control Group, Sham-operation Group, Model Group, and EA Group, then further randomly divided into the following subgroups: 1-day (n=12), 1-day rapamycin (n=6), 14-day (n=18), and 28-day (n=18). A rat model of SCI was established by a modified Allen’s weight-drop method. In the EA Group, rats were stimulated on Dazhui (GV14) and Mingmen (GV4) for 20 min by sterilized stainless steel needles. In the EA Group, the Basso, Beattie, and Bresnahan locomotor rating scale showed obvious improved locomotor function, and hematoxylin-eosin staining and magnetic resonance imaging showed that the histological morphology change of injured spinal cord tissue was obviously alleviated. Also, blocking spinal mTOR by injection of rapamycin showed that mTOR existed in the injured spinal cord, and EA could significantly activate mTOR in SCI rats. And immunohistochemistry and western blot analysis on the PI3K/AKT/mTOR signaling pathway showed that levels of PI3K, AKT, mTOR, and p70S6K in the injured spinal cord tissue were greatly increased in the EA Group, while the levels of PTEN and caspase 3 were decreased. The present study suggests that EA could affect cell growth, apoptosis, and autophagy through the PI3K/AKT/mTOR signaling pathway.
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Tang, Wen-jing, Deng-lei Ma, Cui-cui Yang, Li Zhang, Ya-li Li, Lan Zhang, and Lin Li. "Cornel Iridoid Glycoside Improves Locomotor Impairment and Decreases Spinal Cord Damage in Rats." BioMed Research International 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/6725381.
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Purpose. This study was to investigate the effects of cornel iridoid glycoside (CIG) on spinal cord injury (SCI) in rats. Methods. The thoracic cord (at T9) of rats was injured by clip compression for 30 sec. Locomotor function was assessed using the Basso, Beattie, and Bresnahan (BBB) rating scale. Neuroanatomic stereological parameters as well as Nogo-A, p75 neurotrophin receptor (p75NTR), and ROCKII expression were measured by histological processing, immunohistochemistry, and stereological analyses. The axons passing through the lesion site were detected by BDA tracing. Results. Intragastric administration of CIG (60 and 180 mg/kg) improved the locomotor impairment at 10, 17, 24, and 31 days post-injury (dpi) compared with untreated SCI model rats. CIG treatment decreased the volume of the lesion epicenter (LEp) and increased the volume of spared tissue and the number of surviving neurons in the injured spinal cord at 31 dpi. CIG promoted the growth of BDA-positive axons and their passage through the lesion site and decreased the expression of Nogo-A, p75NTR, and ROCKII both in and around the LEp. Conclusion. CIG improved the locomotor impairment, decreased tissue damage, and downregulated the myelin-associated inhibition signaling pathway in SCI rats. The results suggest that CIG may be beneficial for SCI therapy.
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Lin, Fangqi, Baokun Zhang, Qiang Shi, Jiaming Liang, Xin Wang, Xiaofeng Lian, and Jianguang Xu. "The Conditioned Medium of Lactobacillus rhamnoides GG Regulates Microglia/Macrophage Polarization and Improves Functional Recovery after Spinal Cord Injury in Rats." BioMed Research International 2021 (July 10, 2021): 1–13. http://dx.doi.org/10.1155/2021/3376496.
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Lactobacillus rhamnoides, a human intestinal colonizer, can act through various pathways to induce microglia/macrophages to produce cytokines and to polarize microglia/macrophages to different phenotypes to reduce the inflammatory response. In this article, we evaluated the treatment potential of the Lactobacillus rhamnoides GG conditioned medium (LGG-CM) in rat model with SCI (acute spinal cord injury), including functional, neurophysiological, and histological outcomes and the underlying neuroprotective mechanisms. In our experiment, LGG-CM (30 mg/kg) was injected directly into the injury site in rats immediately after SCI. Measured by the BBB scale (Basso, Beattie, and Bresnahan locomotor rating scale) and inclined plane test, rats in the LGG-CM-treated group showed better locomotor scores. Moreover, compared to the vehicle treatment group, LGG-CM increased the mRNA level of the M2 marker (CD206), and decreased that of the M1 marker (iNOS). Western blot assays showed that LGG-CM-treated SCI rats had a higher grayscale ratio of p65 and a lower ratio of p-IκBα/IκBα. Our study shows that local injection of LGG-CM after acute SCI can inhibit inflammatory responses and improve motor function recovery. These effects may be related with the inhibition to the NF-κB (The nuclear factor-kappa B) signal pathway which leads to M2 microglia/macrophage polarization.
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Yoon, Hyung Ho, Hyang Ju Lee, Joongkee Min, Jeong Hoon Kim, Jin Hoon Park, Ji Hyun Kim, Seong Who Kim, Heuiran Lee, and Sang Ryong Jeon. "Optimal Ratio of Wnt3a Expression in Human Mesenchymal Stem Cells Promotes Axonal Regeneration in Spinal Cord Injured Rat Model." Journal of Korean Neurosurgical Society 64, no. 5 (September 1, 2021): 705–15. http://dx.doi.org/10.3340/jkns.2021.0003.
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Objective : Through our previous clinical trials, the demonstrated therapeutic effects of MSC in chronic spinal cord injury (SCI) were found to be not sufficient. Therefore, the need to develop stem cell agent with enhanced efficacy is increased. We transplanted enhanced Wnt3asecreting human mesenchymal stem cells (hMSC) into injured spines at 6 weeks after SCI to improve axonal regeneration in a rat model of chronic SCI. We hypothesized that enhanced Wnt3a protein expression could augment neuro-regeneration after SCI.Methods : Thirty-six Sprague-Dawley rats were injured using an Infinite Horizon (IH) impactor at the T9–10 vertebrae and separated into five groups : 1) phosphate-buffered saline injection (injury only group, n=7); 2) hMSC transplantation (MSC, n=7); 3) hMSC transfected with pLenti vector (without Wnt3a gene) transplantation (pLenti-MSC, n=7); 4) hMSC transfected with Wnt3a gene transplantation (Wnt3a-MSC, n=7); and 5) hMSC transfected with enhanced Wnt3a gene (1.7 fold Wnt3a mRNA expression) transplantation (1.7 Wnt3a-MSC, n=8). Six weeks after SCI, each 5×105 cells/15 µL at 2 points were injected using stereotactic and microsyringe pump. To evaluate functional recovery from SCI, rats underwent Basso-Beattie-Bresnahan (BBB) locomotor test on the first, second, and third days post-injury and then weekly for 14 weeks. Axonal regeneration was assessed using growth-associated protein 43 (GAP43), microtubule-associated protein 2 (MAP2), and neurofilament (NF) immunostaining.Results : Fourteen weeks after injury (8 weeks after transplantation), BBB score of the 1.7 Wnt3a-MSC group (15.0±0.28) was significantly higher than that of the injury only (10.0±0.48), MSC (12.57±0.48), pLenti-MSC (12.42±0.48), and Wnt3a-MSC (13.71±0.61) groups (p<0.05). Immunostaining revealed increased expression of axonal regeneration markers GAP43, MAP2, and NF in the Wnt3a-MSC and 1.7 Wnt3a-MSC groups.Conclusion : Our results showed that enhanced gene expression of Wnt3a in hMSC can potentiate axonal regeneration and improve functional recovery in a rat model of chronic SCI.
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Zhao, Jiagui, Likui Wang, and Yuanhai Li. "Electroacupuncture Alleviates the Inflammatory Response via Effects on M1 and M2 Macrophages after Spinal Cord Injury." Acupuncture in Medicine 35, no. 3 (June 2017): 224–30. http://dx.doi.org/10.1136/acupmed-2016-011107.
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Background Macrophages/microglia are important effector cells at the site of spinal cord injury (SCI). M1-type macrophages facilitate innate immunity to remove foreign microbes and wound debris from the injury site. M2-type macrophages exhibit tissue repair properties and attenuate production of pro-inflammatory cytokines. Regulation of the polarisation of M1/M2 macrophages may affect the inflammatory response in SCI and may be related to neurotrophin-3 (NT-3). Electroacupuncture (EA) at GV acupuncture points can be used as an adjuvant therapy for SCI. Aim To investigate the effects of EA on Basso, Beattie and Bresnahan (BBB) functional evaluation and inflammatory cytokines (tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and IL-10), and on the proportions of M1/M2 macrophages, and to provide a greater understanding of the mechanisms underlying the potential clinical treatment of SCI. Methods A rat SCI model was induced by spinal segment transection at T10 in 16 Sprague-Dawley rats. A further eight rats were included as a Control group. Ten surviving SCI model rats were divided into two groups (n=5 each): an SCI group that remained untreated; and an SCI+EA group that received EA at GV6 and GV9. Results EA improved BBB scores, inhibited the proportion of M1 macrophages and TNF-α, IL-1β and IL-6 levels, and downregulated the M1 marker CD86. By contrast, EA enhanced IL-10, the proportion of M2 macrophages and upregulated the M2 marker CD206 and NT-3 expression. Conclusions EA had a positive impact on SCI model rats. This may be related to the neuroprotective effect of NT-3, which may increase the polarisation of M2 microglia/macrophages.
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Zhong, Xueren, Yongzheng Bao, Qiang Wu, Xinhua Xi, Wengang Zhu, Sanmei Chen, and Junjian Liao. "Long noncoding RNA XIST knockdown relieves the injury of microglia cells after spinal cord injury by sponging miR-219-5p." Open Medicine 16, no. 1 (January 1, 2021): 1090–100. http://dx.doi.org/10.1515/med-2021-0292.
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Abstract Long noncoding RNAs have been demonstrated to play crucial roles in the pathogenesis of spinal cord injury (SCI). In this study, we aimed to explore the roles and underlying mechanisms of lncRNA X-inactive specific transcript (XIST) in SCI progression. SCI mice model was constructed and evaluated by the Basso–Beattie–Bresnahan method. The SCI cell model was constructed by treating BV2 cells with lipopolysaccharide (LPS). The levels of XIST and miR-219-5p were determined by the reverse transcription quantitative polymerase chain reaction. The concentrations of inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Protein levels were measured via western blot assay. Cell viability and apoptosis were evaluated by cell counting kit-8 assay and flow cytometry analysis, respectively. The relationship between XIST and miR-219-5p was analyzed by online tool starBase, dual-luciferase reporter assay, and RNA immunoprecipitation assay. As a result, the XIST level was enhanced and the miR-219-5p level was declined in the SCI mice model. XIST was also upregulated in LPS-induced BV2 cells. LPS treatment restrained BV2 cell viability and accelerated apoptosis and inflammatory response. XIST knockdown effectively weakened LPS-induced BV2 cell injury. miR-219-5p was identified as a target of XIST. Moreover, inhibition of miR-219-5p restored the impacts of XIST knockdown on cell viability, apoptosis, and inflammation in LPS-treated BV2 cells. In addition, LPS-induced XIST promoted the activation of the nuclear factor-κB (NF-κB) pathway by sponging miR-219-5p. In conclusion, XIST silencing promoted microglial cell viability and repressed apoptosis and inflammation by sponging miR-219-5p, thus promoting the recovery of SCI.