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    25 April 2014, Volume 9 Issue 8 Previous Issue    Next Issue
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    Spinal Cord Contusion
    Gong Ju, Jian Wang, Yazhou Wang, Xianghui Zhao
    2014, 9 (8):  789-794.  doi: 10.4103/1673-5374.131591
    Abstract ( 302 )   PDF (640KB) ( 873 )   Save

    Spinal cord injury is a major cause of disability with devastating neurological outcomes and limited therapeutic opportunities, even though there are thousands of publications on spinal cord injury annually. There are two major types of spinal cord injury, transaction of the spinal cord and spinal cord contusion. Both can theoretically be treated, but there is no well documented treatment in human being. As for spinal cord contusion, we have developed an operation with fabulous result.

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    The clinical rehabilitation of spine and spinal cord disorders: detection and evaluation using SPECT/CT
    Max J. Scheyerer, Clément M.L.Werner, Patrick Veit-Haibach
    2014, 9 (8):  795-797.  doi: 10.4103/1673-5374.131593
    Abstract ( 247 )   PDF (1027KB) ( 1053 )   Save

    Spine-related disorders are caused by several factors including (1) spinal nerve/visceral nerve stimulation by perivertebral aseptic inflammation, (2) spinal nerve/visceral nerve compression by injured periverterbal soft tissue, dislocated perivertebral small joint, and proliferative/degenerative tissue and, (3) secondary damage to the spinal cord, peripheral nerve, vessels and autonomic nerve, which further stimulate nerve root sheath and surrounding pain-carrying nerve fibers. Dr. Max J. Scheyerer from University Medical Center, in Germany showed that SPECT/CT can be helpful for some aspects by introducing a metabolical dimension to the classical way of morphology-based diagnostic.

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    Adipose-derived mesenchymal stem cell transplantation promotes adult neurogenesis in the brains of Alzheimer’s disease mice
    Yufang Yan, Tuo Ma, Kai Gong, Qiang Ao, Xiufang Zhang, Yandao Gong
    2014, 9 (8):  798-805.  doi: 10.4103/1673-5374.131596
    Abstract ( 328 )   PDF (849KB) ( 1459 )   Save

    In the present study, we transplanted adipose-derived mesenchymal stem cells into the hippocampi of APP/PS1 transgenic Alzheimer’s disease model mice. Immunofluorescence staining revealed that the number of newly generated (BrdU+) cells in the subgranular zone of the dentate gyrus in the hippocampus was significantly higher in Alzheimer’s disease mice after adipose-derived mesenchymal stem cell transplantation, and there was also a significant increase in the number of BrdU+/DCX+ neuroblasts in these animals. Adipose-derived mesenchymal stem cell transplantation enhanced neurogenic activity in the subventricular zone as well. Furthermore, adipose-derived mesenchymal stem cell transplantation reduced oxidative stress and alleviated cognitive impairment in the mice. Based on these findings, we propose that adipose-derived mesenchymal stem cell transplantation enhances endogenous neurogenesis in both the subgranular and subventricular zones in APP/PS1 transgenic Alzheimer’s disease mice, thereby facilitating functional recovery.

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    Bone marrow mesenchymal stem cells with Nogo-66 receptor gene silencing for repair of spinal cord injury
    Zhiyuan Li, Zhanxiu Zhang, Lili Zhao, Hui Li, Suxia Wang, Yong Shen
    2014, 9 (8):  806-814.  doi: 10.4103/1673-5374.131595
    Abstract ( 215 )   PDF (1850KB) ( 978 )   Save

    We hypothesized that RNA interference to silence Nogo-66 receptor gene expression in bone marrow mesenchymal stem cells before transplantation might further improve neurological function in rats with spinal cord transection injury. After 2 weeks, the number of neurons and BrdU-positive cells in the Nogo-66 receptor gene silencing group was higher than in the bone marrow mesenchymal stem cell group, and significantly greater compared with the model          group. After 4 weeks, behavioral performance was significantly enhanced in the model group. After 8 weeks, the number of horseradish peroxidase-labeled nerve fibers was higher in the Nogo-66 receptor gene silencing group than in the bone marrow mesenchymal stem cell group, and significantly higher than in the model group. The newly formed nerve fibers and myelinated nerve fibers were detectable in the central transverse plane section in the bone marrow mesenchymal stem cell group and in the Nogo-66 receptor gene silencing group.

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    Upregulation of Nogo receptor expression induces apoptosis of retinal ganglion cells in diabetic rats
    Xuezheng Liu, Zhongfu Zuo, Wanpeng Liu, Zhiyun Wang, Yang Hou, Yunjie Fu, Yuzhi Han
    2014, 9 (8):  815-820.  doi: 10.4103/1673-5374.131597
    Abstract ( 201 )   PDF (1464KB) ( 826 )   Save

    The Nogo receptor is an essential factor for neuronal apoptosis, but the changes in Nogo receptor expression in the retina and the effects of the Nogo receptor on retinal ganglion cell apoptosis in diabetes mellitus remain unclear. We found that Nogo receptor expression was mainly visible in retinal ganglion cells of a rat model of diabetes mellitus induced by streptozotocin. At 12 weeks after onset of diabetes mellitus, Nogo receptor and Rho kinase expression significantly increased in the retina, and retinal ganglion cell apoptosis was apparent. When RNA interference was used to suppress Nogo receptor expression in rat retina, Rho kinase expression was obviously inhibited, and retinal ganglion cell apoptosis was evidently reduced in rats with diabetes mellitus. These results indicate that upregulation of Nogo receptor expression is an important mechanism of retinal ganglion cell apoptosis in rats with diabetes mellitus.

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    Potential risk of mitomycin C at high concentrations on peripheral nerve structure
    Tao Sui, Jinhong Zhang, Shihao Du, Changhui Su, Jun Que, Xiaojian Cao
    2014, 9 (8):  821-827.  doi: 10.4103/1673-5374.131598
    Abstract ( 193 )   PDF (1706KB) ( 1034 )   Save

    Although the local application of mitomycin C may prevent epidural adhesion after laminectomy, mitomycin C can induce neurotoxicity in optic and acoustic nerves at high concentrations. To determine the safe concentration range for mitomycin C, cotton pads soaked with mitomycin C at different concentrations (0.1, 0.3, 0.5, and 0.7 mg/mL) were immediately applied for 5 minutes to the operation area of rats that had undergone laminectomy at L1. Rat sciatic nerves, instead of dorsal nerves, were used in this study. The results showed that mitomycin C at 0.1–0.5 mg/mL did not damage the structure and function of the sciatic nerve, while at 0.7 mg/mL, mitomycin C significantly reduced the thickness of the sciatic nerve myelin sheath compared with lower concentrations, though no functional change was found. These experimental findings indicate that the local application of mitomycin C at low concentrations is safe to prevent scar adhesion following laminectomy, but that mitomycin C at high concentrations (> 0.7 mg/mL) has potential safety risks to peripheral nerve structures.

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    miR-21 promotes the differentiation of hair follicle-derived neural crest stem cells into Schwann cells
    Yuxin Ni, Kaizhi Zhang, Xuejuan Liu, Tingting Yang, Baixiang Wang, Li Fu, Lan A, Yanmin Zhou
    2014, 9 (8):  828-836.  doi: 10.4103/1673-5374.131599
    Abstract ( 322 )   PDF (1182KB) ( 1290 )   Save

    Hair follicle-derived neural crest stem cells can be induced to differentiate into Schwann cells in vivo and in vitro. However, the underlying regulatory mechanism during cell differentiation remains poorly understood. This study isolated neural crest stem cells from human hair follicles and induced them to differentiate into Schwann cells. Quantitative RT-PCR showed that microRNA (miR)-21 expression was gradually increased during the differentiation of neural crest stem cells into Schwann cells. After transfection with the miR-21 agonist (agomir-21), the differentiation capacity of neural crest stem cells was enhanced. By contrast, after transfection with the miR-21 antagonist (antagomir-21), the differentiation capacity was attenuated. Further study results showed that SOX-2 was an effective target of miR-21. Without compromising SOX2 mRNA expression, miR-21 can down-regulate SOX protein expression by binding to the 3′-UTR of miR-21 mRNA. Knocking out the SOX2 gene from the neural crest stem cells significantly reversed the antagomir-21 inhibition of neural crest stem cells differentiating into Schwann cells. The results suggest that miR-21 expression was increased during the differentiation of neural crest stem cells into Schwann cells and miR-21 promoted the differentiation through down-regulating SOX protein expression by binding to the 3′-UTR of SOX2 mRNA.

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    Apoptosis is an obstacle to the differentiation of adipose-derived stromal cells into astrocytes
    Xiaodong Yuan, Qiaoyu Sun, Ya Ou, Shujuan Wang, Wenli Zhang, Hongliang Deng, Xiaoying Wu, Lili Zhang
    2014, 9 (8):  837-844.  doi: 10.4103/1673-5374.131600
    Abstract ( 243 )   PDF (2556KB) ( 1079 )   Save

    Previous studies have demonstrated that nerve cells differentiated from adipose-derived stromal cells after chemical induction have reduced viability; however, the underlying mechanisms remained unclear. In this study, we induced the differentiation of adult adipose-derived stromal cells into astrocytes using chemical induction. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry showed that, with increasing induction time, the apoptotic rate gradually increased, and the number of living cells gradually decreased. Immunohistochemical staining demonstrated that the number of glial fibrillary acidic protein-, caspase-3- and caspase-9-positive cells gradually increased with increasing induction time. Transmission electron microscopy revealed typical signs of apoptosis after differentiation. Taken together, our results indicate that caspase-dependent apoptosis is an obstacle to the differentiation of adipose-derived stromal cells into astrocytes. Inhibiting apoptosis may be an important strategy for increasing the efficiency of induction.

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    Citalopram increases the differentiation efficacy of bone marrow mesenchymal stem cells into neuronal-like cells
    Javad Verdi, Seyed Abdolreza Mortazavi-Tabatabaei, Shiva Sharif,Hadi Verdi, Alireza Shoae-Hassani
    2014, 9 (8):  845-850.  doi: 10.4103/1673-5374.131601
    Abstract ( 295 )   PDF (965KB) ( 949 )   Save

    Several studies have demonstrated that selective serotonin reuptake inhibitor antidepressants can promote neuronal cell proliferation and enhance neuroplasticity both in vitro and in vivo. It is hypothesized that citalopram, a selective serotonin reuptake inhibitor, can promote the neuronal differentiation of adult bone marrow mesenchymal stem cells. Citalopram strongly enhanced neuronal characteristics of the cells derived from bone marrow mesenchymal stem cells. The rate of cell death was decreased in citalopram-treated bone marrow mesenchymal stem cells than in control cells in neurobasal medium. In addition, the cumulative population doubling level of the citalopram-treated cells was significantly increased compared to that of control cells. Also BrdU incorporation was elevated in citalopram-treated cells. These findings suggest that citalopram can improve the neuronal-like cell differentiation of bone marrow mesenchymal stem cells by increasing cell proliferation and survival while maintaining their neuronal characteristics.

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    Fusion protein of single-chain variable domain fragments for treatment of myasthenia gravis
    Fangfang Li, Fanping Meng, Quanxin Jin, Changyuan Sun, Yingxin Li, Honghua Li, Songzhu Jin
    2014, 9 (8):  851-856.  doi: 10.4103/1673-5374.131611
    Abstract ( 225 )   PDF (484KB) ( 1063 )   Save

    Single-chain variable domain fragment (scFv) 637 is an antigen-specific scFv of myasthenia gravis. In this study, scFv and human serum albumin genes were conjugated and the fusion protein was expressed in Pichia pastoris. The affinity of scFv-human serum albumin fusion protein to bind to acetylcholine receptor at the neuromuscular junction of human intercostal muscles was detected by immunofluorescence staining. The ability of the fusion protein to block myasthenia gravis patient sera binding to acetylcholine receptors and its stability in healthy serum were measured by competitive ELISA. The results showed that the inhibition rate was 2.0–77.4%, and the stability of fusion protein in static healthy sera was about 3 days. This approach suggests the scFv-human serum albumin is a potential candidate for specific immunosuppressive therapy of myasthenia gravis.

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    Similar effects of substance P on learning and memory function between hippocampus and striatal marginal division
    Yan Yu, Changchun Zeng, Siyun Shu, Xuemei Liu, Chuhua Li
    2014, 9 (8):  857-863.  doi: 10.4103/1673-5374.131603
    Abstract ( 218 )   PDF (730KB) ( 1665 )   Save

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    The synthetic thyroid hormone, levothyroxine, protects cholinergic neurons in the hippocampus of naturally aged mice
    Ailing Fu, Rumei Zhou, Xingran Xu
    2014, 9 (8):  864-871.  doi: 10.4103/1673-5374.131602
    Abstract ( 268 )   PDF (973KB) ( 1298 )   Save

    The thyroid hormones, triiodothyronine and thyroxine, play important roles in cognitive function during the mammalian lifespan. However, thyroid hormones have not yet been used as a therapeutic agent for normal age-related cognitive deficits. In this study, CD-1 mice (aged 24 months) were intraperitoneally injected with levothyroxine (L-T4; 1.6 μg/kg per day) for 3 consecutive months. Our findings revealed a significant improvement in hippocampal cytoskeletal rearrangement of actin and an increase in serum hormone levels of L-T4-treated aged mice. Furthermore, the survival rate of these mice was dramatically increased from 60% to 93.3%. The Morris water maze task indicated that L-T4 restored impaired spatial memory in aged mice. Furthermore, level of choline acetyltransferase, acetylcholine, and superoxide dismutase were increased in these mice, thus suggesting that a possible mechanism by which L-T4 reversed cognitive impairment was caused by increased activity of these markers. Overall, supplement of low-dosage L-T4 may be a potential therapeutic strategy for normal age-related cognitive deficits.

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    Nasal mucosal inhalation of amyloid-beta peptide 3–10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1–42)
    Tongzi Jiang, Wanshu Guo, Sha Sha, Xiaona Xing, Rong Guo, Yunpeng Cao
    2014, 9 (8):  872-877.  doi: 10.4103/1673-5374.131605
    Abstract ( 261 )   PDF (358KB) ( 728 )   Save

    Three-month-old Alzheimer’s disease model transgenic mice were immunized with Aβ1–42, Plp-Adenovirus [Ad]-X-CMV-(Aβ3–10)10-CpG [AdCpG-(Aβ3–10)10] or AdCpG virus fluid via nasal mucosal inhalation, respectively. ELISA analysis of serum showed Aβ42 antibody titers were significantly increased in mice immunized with Aβ1–42 and AdCpG-(Aβ3–10)10. Concanavalin A and AdCpG-(Aβ3–10)10 stimulation significantly increased the number of proliferating spleen cells cultured from AdCpG(Aβ3–10)10 and Aβ42 groups compared with the control group. In the AdCpG(Aβ3–10)10 group, levels of interleukin (IL)-4 and IL-10 were increased, while those of IL-2 and interferon-γ were decreased. In the Aβ42 group, levels of IL-4, IL-10, IL-2 and interferon-γ were all increased. Experimental findings indicate that AdCpG-(Aβ3–10)10 vaccine can produce strong T helper 2 (Th2) humoral immune responses in addition to the production of Aβ42 antibody. The cellular immunologic response was weak and avoided Aβ1–42-mediated cytotoxicity.

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    Regulatory effects of anandamide on intracellular Ca2+ concentration increase in trigeminal ganglion neurons
    Yi Zhang, Hong Xie, Gang Lei, Fen Li, Jianping Pan, Changjin Liu, Zhiguo Liu, Lieju Liu, Xuehong Cao
    2014, 9 (8):  878-887.  doi: 10.4103/1673-5374.131607
    Abstract ( 246 )   PDF (1792KB) ( 1000 )   Save

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    Virtual reality interface devices in the reorganization of neural networks in the brain of patients with neurological diseases
    Valeska Gatica-Rojas, Guillermo Méndez-Rebolledo
    2014, 9 (8):  888-896.  doi: 10.4103/1673-5374.131612
    Abstract ( 205 )   PDF (464KB) ( 2020 )   Save

    Two key characteristics of all virtual reality applications are interaction and immersion. Systemic interaction is achieved through a variety of multisensory channels (hearing, sight, touch, and     smell), permitting the user to interact with the virtual world in real time. Immersion is the degree to which a person can feel wrapped in the virtual world through a defined interface. Virtual reality interface devices such as the Nintendo® Wii and its peripheral nunchuks-balance board, head mounted displays and joystick allow interaction and immersion in unreal environments created from computer software. Virtual environments are highly interactive, generating great activation of visual, vestibular and proprioceptive systems during the execution of a video game. In addition, they are entertaining and safe for the user. Recently, incorporating therapeutic purposes in virtual reality interface devices has allowed them to be used for the rehabilitation of neurological patients, e.g., balance training in older adults and dynamic stability in healthy participants. The improvements observed in neurological diseases (chronic stroke and cerebral palsy) have been                shown by changes in the reorganization of neural networks in patients’ brain, along with better hand function and other skills, contributing to their quality of life. The data generated by such studies could substantially contribute to physical rehabilitation strategies.

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