scholarly journals The Application of an Omentum Graft or Flap in Spinal Cord Injury

2021 ◽  
Vol 22 (15) ◽  
pp. 7930
Author(s):  
Li-Yu Fay ◽  
Yan-Ru Lin ◽  
Dann-Ying Liou ◽  
Chuan-Wen Chiu ◽  
Mei-Yin Yeh ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nerve Fibers ◽  
Omental Flap ◽  
Definitive Treatment ◽  
Injured Spinal Cord ◽  
Class Iii ◽  
Vascular Connection ◽  
Cord Injury ◽  
Omental Graft

Background: Spinal cord injury (SCI) causes a primary injury at the lesion site and triggers a secondary injury and prolonged inflammation. There has been no definitive treatment till now. Promoting angiogenesis is one of the most important strategies for functional recovery after SCI. The omentum, abundant in blood and lymph vessels, possesses the potent ability of tissue regeneration. Methods: The present work examines the efficacy of autologous omentum, either as a flap (with vascular connection intact) or graft (severed vascular connection), on spinal nerve regeneration. After contusive SCI in rats, a thin sheath of omentum was grafted to the injured spinal cord. Results: Omental graft improved behavior scores significantly from the 3rd to 6th week after injury (6th week, 5.5 ± 0.5 vs. 8.6 ± 1.3, p < 0.05). Furthermore, the reduction in cavity and the preservation of class III β-tubulin-positive nerve fibers in the injury area was noted. Next, the free omental flap was transposed to a completely transected SCI in rats through a pre-implanted tunnel. The flap remained vascularized and survived well several weeks after the operation. At 16 weeks post-treatment, SCI rats with omentum flap treatment displayed the preservation of significantly more nerve fibers (p < 0.05) and a reduced injured cavity, though locomotor scores were similar. Conclusions: Taken together, the findings of this study indicate that treatment with an omental graft or transposition of an omental flap on an injured spinal cord has a positive effect on nerve protection and tissue preservation in SCI rats. The current data highlight the importance of omentum in clinical applications.

scholarly journals White matter regeneration induced by aligned fibrin nanofiber hydrogel contributes to motor functional recovery in canine T12 spinal cord injury

2021 ◽  
Author(s):  
Zheng Cao ◽  
Weitao Man ◽  
Yuhui Xiong ◽  
Yi Guo ◽  
Shuhui Yang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Nerve Regeneration ◽  
Spinal Cord Injuries ◽  
Diffusion Tensor ◽  
Nerve Fibers ◽  
Functional Restoration ◽  
Large Animal ◽  
Cord Injury

Abstract A hierarchically aligned fibrin hydrogel (AFG) that possesses soft stiffness and aligned nanofiber structure has been successfully proven to facilitate neuroregeneration in vitro and in vivo. However, its potential in promoting nerve regeneration in large animal models that is critical for clinical translation has not been sufficiently specified. Here, the effects of AFG on directing neuroregeneration in canine hemisected T12 spinal cord injuries were explored. Histologically obvious white matter regeneration consisting of a large area of consecutive, compact, and aligned nerve fibers is induced by AFG, leading to a significant motor functional restoration. The canines with AFG implantation start to stand well with their defective legs from 3 to 4 weeks postoperatively and even effortlessly climb the steps from 7 to 8 weeks. Moreover, high-resolution multi-shot diffusion tensor imaging illustrates the spatiotemporal dynamics of nerve regeneration rapidly crossing the lesion within 4 weeks in the AFG group. Our findings indicate that AFG could be a potential therapeutic vehicle for spinal cord injury by inducing rapid white matter regeneration and restoring locomotion, pointing out its promising prospect in clinic practice.

scholarly journals Overexpression of Rictor in the injured spinal cord promotes functional recovery in a rat model of spinal cord injury

2020 ◽  
Vol 34 (5) ◽  
pp. 6984-6998
Author(s):  
Ningning Chen ◽  
Pengxiang Zhou ◽  
Xizhe Liu ◽  
Jiachun Li ◽  
Yong Wan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Rat Model ◽  
Injured Spinal Cord ◽  
Cord Injury

scholarly journals B-RAFV600E Inhibitor Dabrafenib Attenuates RIPK3-Mediated Necroptosis and Promotes Functional Recovery after Spinal Cord Injury

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1582 ◽  
Author(s):  
Takehiro Sugaya ◽  
Haruo Kanno ◽  
Michiharu Matsuda ◽  
Kyoichi Handa ◽  
Satoshi Tateda ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Tissue Damage ◽  
Neuroprotective Effect ◽  
Neural Tissue ◽  
Injured Spinal Cord ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Cord Injury

The receptor-interacting protein kinase 3 (RIPK3) is a key regulator of necroptosis and is involved in various pathologies of human diseases. We previously reported that RIPK3 expression is upregulated in various neural cells at the lesions and necroptosis contributed to secondary neural tissue damage after spinal cord injury (SCI). Interestingly, recent studies have shown that the B-RAFV600E inhibitor dabrafenib has a function to selectively inhibit RIPK3 and prevents necroptosis in various disease models. In the present study, using a mouse model of thoracic spinal cord contusion injury, we demonstrate that dabrafenib administration in the acute phase significantly inhibites RIPK3-mediated necroptosis in the injured spinal cord. The administration of dabrafenib attenuated secondary neural tissue damage, such as demyelination, neuronal loss, and axonal damage, following SCI. Importantly, the neuroprotective effect of dabrafenib dramatically improved the recovery of locomotor and sensory functions after SCI. Furthermore, the electrophysiological assessment of the injured spinal cord objectively confirmed that the functional recovery was enhanced by dabrafenib. These findings suggest that the B-RAFV600E inhibitor dabrafenib attenuates RIPK3-mediated necroptosis to provide a neuroprotective effect and promotes functional recovery after SCI. The administration of dabrafenib may be a novel therapeutic strategy for treating patients with SCI in the future.

Presence and significance of CD-95 (Fas/APO1) expression after spinal cord injury

2001 ◽  
Vol 94 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Mercedes Zurita ◽  
Jesús Vaquero ◽  
Isabel Zurita
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
Spinal Cord Tissue ◽  
Injured Spinal Cord ◽  
Content Type ◽  
Cord Injury ◽  
Positive Immunostaining ◽  
Fine Print

Object. A glycoprotein, CD95 (Fas/APO1) is widely considered to be implicated in the development of apoptosis in a number of tissues. Based on the hypothesis that apoptosis is related to cell death after spinal cord injury (SCI), the authors studied the presence and distribution of CD95 (Fas/APO1)-positive cells in injured spinal cord tissue for the purpose of determining the significance of this protein during the early phases of SCI. Methods. The presence and distribution of cells showing positive immunostaining for CD95 (Fas/APO1) were studied 1, 4, 8, 24, 48, and 72 hours and 1, 2, and 4 weeks after induction of experimental SCI in rats. Studies were conducted using a monoclonal antibody to the CD95 (Fas/APO1) protein. Positivity for CD95 (Fas/APO1) was observed in apoptotic cells, mainly in the gray matter, 1 hour after trauma, and the number of immunostained cells increased for the first 8 hours, at which time the protein was expressed in both gray and white matter. From 24 to 72 hours postinjury, the number of immunostained cells decreased in the gray matter, but increased in the white matter. From then on, there were fewer CD95 (Fas/APO1)-positive cells, but some cells in the white matter still exhibited positive immunostaining 1 and 2 weeks after injury. At 4 weeks, there remained no CD95 (Fas/APO1)-positive cells in injured spinal cord. Conclusions. These findings indicate that CD95 (Fas/APO1) is expressed after SCI, suggesting a role for this protein in the development of apoptosis after trauma and the possibility of a new therapeutic approach to SCI based on blocking the CD95 (Fas/APO1) system.

scholarly journals Spinal Cord Injury Induced Osteoporosis: Case Report and Current Literature

2021 ◽  
Vol 9 (2) ◽  
pp. 155-159
Author(s):  
Abdulai Bangura ◽  
Thomas Shuler ◽  
Lisa Wright ◽  
Anne Lake
Keyword(s):  
Bone Mineral Density ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Bone Loss ◽  
Bone Mineral ◽  
Treatment Plan ◽  
Treatment Options ◽  
Definitive Treatment ◽  
Mineral Density ◽  
Cord Injury

Background: Among the various etiologies of osteoporosis, spinal cord injury has a drastic progression of the disease, causing weekly bone loss. There is no definitive treatment for the prevention of osteoporosis in these individuals. This review illustrates the recent findings on the pathophysiology, treatment, and management of spinal cord injury-induced osteoporosis. Furthermore, we cover a case of a male patient who experienced severe bone loss after a spinal cord injury at the age of 21 years. The Case: We have a 57-year-old man with a history of AIS grade A spinal cord injury, level T11 with rod fixation from a motorcycle collision at age 21. His fracture history following the injury includes tibia, femur, and vertebral fractures. Bone mineral density imaging revealed notable T-scores ranging from -3.1 to -3.4 at the hip and femurs. Treatment plan consisted of teriparatide, dietary supplements, and physical therapy. Biomarkers from baseline to post one month of treatment revealed the following: procollagen type 1 N-terminal propeptide from 38 mcg/L to 70 mcg/L and C-terminal telopeptide from 209 pg/mL to 88 pg/mL, representing an increased bone formation and decreased bone resorption, respectively. After two years, bone mineral density T-scores improved to -2.7 on the left and the patient was capable of standing for the first time with the assistance of a standing frame. Conclusion: Our case exemplified the progression of the disease and treatment options. A basis for the derivation of future innovative therapies has been covered. Favorable treatments and management are described in the review.

scholarly journals In vivo conversion of rat astrocytes into neuronal cells through neural stem cells in injured spinal cord with a single zinc-finger transcription factor

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Masoumeh Zarei-Kheirabadi ◽  
Mahdi Hesaraki ◽  
Sahar Kiani ◽  
Hossein Baharvand
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Spinal Cord Injury ◽  
Neural Stem Cells ◽  
Rating Scale ◽  
Injured Spinal Cord ◽  
Functional Impairments ◽  
Cord Injury ◽  
Rat Astrocytes

Abstract Background Spinal cord injury (SCI) results in glial scar formation and irreversible neuronal loss, which finally leads to functional impairments and long-term disability. Our previous studies have demonstrated that the ectopic expression of Zfp521 reprograms fibroblasts and astrocytes into induced neural stem cells (iNSCs). However, it remains unclear whether treatment with Zfp521 also affects endogenous astrocytes, thus promoting further functional recovery following SCI. Methods Rat astrocytes were transdifferentiated into neural stem cells in vitro by ZFP521 or Sox2. Then, ZFP521 was applied to the spinal cord injury site of a rat. Transduction, real-time PCR, immunohistofluorescence, and function assessments were performed at 6 weeks post-transduction to evaluate improvement and in vivo lineage reprogramming of astrocytes. Results Here, we show that Zfp521 is more efficient in reprogramming cultured astrocytes compared with Sox2. In the injured spinal cord of an adult rat, resident astrocytes can be reprogrammed into neurons through a progenitor stage by Zfp521. Importantly, this treatment improves the functional abilities of the rats as evaluated by the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and further by calculation of its subscores. There was enhanced locomotor activity in the hind limbs, step length, toe spread, foot length, and paw area. In addition, motor evoked potential recordings demonstrated the functional integrity of the spinal cord. Conclusions These results have indicated that the generation of iNSCs or neurons from endogenous astrocytes by in situ reprogramming might be a potential strategy for SCI repair. Graphical abstract

Mannitol Reduces Spinal Cord Edema in Rats with Acute Traumatic Spinal Cord Injury

2020 ◽  
Vol 17 (6) ◽  
pp. 676-683
Author(s):  
Chao Zhang ◽  
Anming Hu ◽  
Yingli Jing ◽  
Degang Yang ◽  
Jianjun Li
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Red Blood Cells ◽  
Water Content ◽  
Blood Cells ◽  
Traumatic Spinal Cord Injury ◽  
Injured Spinal Cord ◽  
Cord Injury ◽  
Contrast Group ◽  
Spinal Cord Edema

Background: The research about anti-edema effects of mannitol on acute traumatic spinal cord injury (SCI) in rats is rare. Objective: This study aimed to explore the effect of mannitol on spinal cord edema after SCI in rats. Methods: Seventy-eight adult female rats were assigned to three groups randomly: a sham control group (n = 18), a contusion and normal saline contrast group (n=30), and a contusion and mannitol treatment group (n=30). We used the open-field test to estimate the functional recovery of rats weekly. Spinal cord water content was measured to determine the spinal cord edema. The ultrastructure features of the injured dorsolateral spinal cord were determined on the 7th day after SCI by HE staining. Results: The mannitol group had greatly improved Basso-Beattie-Bresnahan (BBB) scores when compared with the saline contrast group. The spinal cord water content was increased significantly after SCI, and there was no significant difference in the water content between the NaCl and mannitol groups 1 day after SCI. The water content at 3 and 7 days after SCI was significantly lower in the mannitol group than in the NaCl group (p < 0.05). Mannitol can reduce spinal cord edema by increasing the number of red blood cells in the injured spinal cord and decrease the ratio (dorsoventral diameter/ mediolateral diameter) of spinal cord 7 days post-SCI. Conclusion: Mannitol increases recovery of motor function in rats, reduces spinal cord edema and increases the number of red blood cells in the injured spinal cord, decreasing the ratio of spinal cord to reduce pressure.

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