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JOURNAL/nrgr/04.03/01300535-202503000-00028/figure1/v/2024-06-17T092413Z/r/image-tiff Spinal cord injury necessitates effective rehabilitation strategies, with exercise therapies showing promise in promoting recovery. This study investigated the impact of rehabilitation exercise on functional recovery and morphological changes following thoracic contusive spinal cord injury. After a 7-day recovery period after spinal cord injury, mice were assigned to either a trained group (10 weeks of voluntary running wheel or forced treadmill exercise) or an untrained group. Bi-weekly assessments revealed that the exercise-trained group, particularly the voluntary wheel exercise subgroup, displayed significantly improved locomotor recovery, more plasticity of dopaminergic and serotonin modulation compared with the untrained group. Additionally, exercise interventions led to gait pattern restoration and enhanced transcranial magnetic motor-evoked potentials. Despite consistent injury areas across groups, exercise training promoted terminal innervation of descending axons. In summary, voluntary wheel exercise shows promise for enhancing outcomes after thoracic contusive spinal cord injury, emphasizing the role of exercise modality in promoting recovery and morphological changes in spinal cord injuries. Our findings will influence future strategies for rehabilitation exercises, restoring functional movement after spinal cord injury.
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JOURNAL/nrgr/04.03/01300535-202505000-00029/figure1/v/2024-07-28T173839Z/r/image-tiff Schwann cell transplantation is considered one of the most promising cell-based therapy to repair injured spinal cord due to its unique growth-promoting and myelin-forming properties. A the Food and Drug Administration-approved Phase I clinical trial has been conducted to evaluate the safety of transplanted human autologous Schwann cells to treat patients with spinal cord injury. A major challenge for Schwann cell transplantation is that grafted Schwann cells are confined within the lesion cavity, and they do not migrate into the host environment due to the inhibitory barrier formed by injury-induced glial scar, thus limiting axonal reentry into the host spinal cord. Here we introduce a combinatorial strategy by suppressing the inhibitory extracellular environment with injection of lentivirus-mediated transfection of chondroitinase ABC gene at the rostral and caudal borders of the lesion site and simultaneously leveraging the repair capacity of transplanted Schwann cells in adult rats following a mid-thoracic contusive spinal cord injury. We report that when the glial scar was degraded by chondroitinase ABC at the rostral and caudal lesion borders, Schwann cells migrated for considerable distances in both rostral and caudal directions. Such Schwann cell migration led to enhanced axonal regrowth, including the serotonergic and dopaminergic axons originating from supraspinal regions, and promoted recovery of locomotor and urinary bladder functions. Importantly, the Schwann cell survival and axonal regrowth persisted up to 6 months after the injury, even when treatment was delayed for 3 months to mimic chronic spinal cord injury. These findings collectively show promising evidence for a combinatorial strategy with chondroitinase ABC and Schwann cells in promoting remodeling and recovery of function following spinal cord injury.
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JOURNAL/nrgr/04.03/01300535-202412000-00032/figure1/v/2024-04-08T165401Z/r/image-tiff For patients with chronic spinal cord injury, the conventional treatment is rehabilitation and treatment of spinal cord injury complications such as urinary tract infection, pressure sores, osteoporosis, and deep vein thrombosis. Surgery is rarely performed on spinal cord injury in the chronic phase, and few treatments have been proven effective in chronic spinal cord injury patients. Development of effective therapies for chronic spinal cord injury patients is needed. We conducted a randomized controlled clinical trial in patients with chronic complete thoracic spinal cord injury to compare intensive rehabilitation (weight-bearing walking training) alone with surgical intervention plus intensive rehabilitation. This clinical trial was registered at ClinicalTrials.gov (NCT02663310). The goal of surgical intervention was spinal cord detethering, restoration of cerebrospinal fluid flow, and elimination of residual spinal cord compression. We found that surgical intervention plus weight-bearing walking training was associated with a higher incidence of American Spinal Injury Association Impairment Scale improvement, reduced spasticity, and more rapid bowel and bladder functional recovery than weight-bearing walking training alone. Overall, the surgical procedures and intensive rehabilitation were safe. American Spinal Injury Association Impairment Scale improvement was more common in T7-T11 injuries than in T2-T6 injuries. Surgery combined with rehabilitation appears to have a role in treatment of chronic spinal cord injury patients.
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Spinal cord injury (SCI) often leads to neuronal loss, axonal degeneration, and behavioral dysfunction. We recently show that in vivo reprogramming of NG2 glia produces new neurons, reduces glial scaring, and ultimately leads to improved function after SCI. By examining endogenous neurons, we here unexpectedly uncover that NG2 glia reprogramming also induces robust axonal regeneration of the corticospinal tract and serotonergic neurons. Such reprogramming-induced axonal regeneration may contribute to the reconstruction of neural networks essential for behavioral recovery.
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Tissue damage resulting from a spinal cord injury (SCI) is primarily driven by a robust neuroimmune/neuroinflammatory response. This intricate process is mainly governed by a multitude of cytokines and cell surface proteins in the central nervous system (CNS). However, the critical components of the neuroimmune/neuroinflammatory response during SCI are still not well-defined. In this study, we investigated the impact of CD1d, an MHC class I-like molecule mostly known for presenting lipid antigens to natural killer T (NKT) cells and regulating immune/inflammatory responses, on neuroimmune/neuroinflammatory responses induced by SCI. We observed an increased expression of CD1d on various cell types within the spinal cord, including microglia/macrophages, oligodendrocytes (ODCs), and endothelial cells (DCs), but not on neurons or astrocytes post-SCI. In comparison to wildtype (WT) mice, a T10 contusive SCI in CD1d knockout (CD1dKO or Cd1d -/- ) mice resulted in markedly reduced proinflammatory cytokine release, microglia/macrophage activation and proliferation. Following SCI, the levels of inflammatory cytokines and activation/proliferation of microglia/macrophages were dramatically reduced, while anti-inflammatory cytokines such as IL-4 and growth factors like VEGF were substantially increased in the spinal cord tissues of CD1dKO mice when compared to WT mice. In the post-acute phase of SCI (day 7 post-SCI), CD1dKO mice had a significantly higher frequency of tissue-repairing macrophages, but not other types of immune cells, in the injured spinal cord tissues compared to WT mice. Moreover, CD1d-deficiency protected spinal cord neuronal cells and tissue, promoting functional recovery after a SCI. However, the neuroinflammation in WT mouse spinal cords was independent of the canonical CD1d/NKT cell axis. Finally, treatment of injured mice with a CD1d-specific monoclonal antibody significantly enhanced neuroprotection and improved functional recovery. Therefore, CD1d promotes the proinflammatory response following a SCI and represents a potential therapeutic target for spinal cord repair. Significance Statement: The cell surface molecule, CD1d, is known to be recognized by cells of the immune system. To our knowledge, this is the first observation that the CD1d molecule significantly contributes to neuroinflammation following a spinal cord injury (SCI) in a manner independent of the CD1d/NKT cell axis. This is important, because this work reveals CD1d as a potential therapeutic target following an acute SCI for which there are currently no effective treatments.
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Spinal cord injury (SCI) often leads to neuronal loss, axonal degeneration and behavioral dysfunction. We recently show that in vivo reprogramming of NG2 glia produces new neurons, reduces glial scaring, and ultimately leads to improved function after SCI. By examining endogenous neurons, we here unexpectedly uncover that NG2 glia reprogramming also induces robust axonal regeneration of the corticospinal tract and serotonergic neurons. Such reprogramming-induced axonal regeneration may contribute to the reconstruction of neural networks essential for behavioral recovery.
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Rarely, penetrating injuries to the spinal cord result from wooden objects, creating unique challenges to mitigate neurological injury and high rates of infection and foreign body reactions. We report a man who sustained a penetrating cervical spinal cord injury from a sharpened stick. While initially tetraparetic, he rapidly recovered function. The risks of neurological deterioration during surgical removal made the patient reluctant to consent to surgery despite the impalement of the spinal cord. A repeat MRI on day 3 showed an extension of edema indicating progressive inflammation. On the 7th day after injury, fever and paresthesias occurred with a large increase in serum inflammatory indicators, and the patient agreed to undergo surgical removal of the wooden object. We discuss the management nuances related to wood, the longitudinal evolution of MRI findings, infection risk, surgical risk mitigation and technique, an inflammatory marker profile, long-term recovery, and the surprisingly minimal neurological deficits associated with low-velocity midline spinal cord injuries. The patient had an excellent clinical outcome. The main lessons are that a wooden penetrating central nervous system injury has a high risk for infection, and that surgical removal from the spinal cord should be performed soon after injury and under direct visualization.
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The aim of this study was to analyze the carbon sink effect under natural vegetation restoration and the influence of changes in vegetation community characteristics on ecosystem carbon density in ecologically fragile areas of the Loess Plateau. In this study, the changes in carbon sequestration of a vegetation-soil system under eight successional stages[slope cropland, abandoned cropland for 10 years, abandoned cropland for 20 years, Sophora davidii (Franch.) Skeels., Betula platyphylla Suk., Pinus tabulaeformis Carr., Quercus wutaishanic Mary+P. tabulaeformis Carr mixed forests, and Q. wutaishanic Mary] in Ziwuling area over 150 restoration periods were investigated using the common method of spatial and temporal substitution. This study also discussed the relationship between changes in vegetation community characteristics and vegetation-soil system carbon density. The results showed that the community coverage of the investigated vegetation fluctuated from 85% in the slope cropland stage to 100% in the arbor stage. The number of species, Margalef index, Shannon-Wiener index, Pielou index, and Simpson index initially increased rapidly, then declined slowly until becoming stable, and reached a peak in the middle of the succession (B. platyphylla Suk.). The biomass and carbon density of vegetation components (above-ground biomass, below-ground roots, and litter) increased exponentially during the succession, i.e., increased slowly before B. platyphylla Suk. but increased significantly in B. platyphylla Suk. and P. tabulaeformis Carr.(P<0.05). The biomass and carbon density reached the maximum values of 27858.08 g·m-2 and 13232.51 g·m-2, respectively, in Q. wutaishanic Mary+P. tabulaeformis Carr mixed forests and tended to be stable in the late succession stage. Soil organic carbon density showed a power function relationship with vegetation restoration, with the greatest increase in the stages of abandoned cropland for 10 years and B. platyphylla, but no significant changes in the subsequent stages (P>0.05). In the early succession stage, the carbon density of the farmland ecosystem was the lowest (4395.70 g·m-2), whereas the other seven stages increased by 55.54%, 40.37%, 69.96%, 202.48%, 326.35%, 357.43%, and 351.07%, respectively, compared with the farmland ecosystem. Community coverage, Margalef index, Shannon-Wiener index, above-ground biomass, root biomass, and litter biomass were significantly positively correlated with vegetation-soil system carbon density (P<0.05). The carbon sink effect of long-term natural restoration in Ziwuling Region was significant, and the carbon density of the vegetation-soil system under interspecific competition tended to be stable in the late succession stage. Dynamic changes in the vegetation community structure and plant diversity during the succession process increased vegetation carbon density and soil carbon density. This study helps to clarify the carbon sink effect of natural vegetation restoration in ecologically fragile areas of the Loess Plateau and provides a theoretical basis for promoting natural forest conservation and achieving carbon neutrality.
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Secuestro de Carbono , Ecosistema , Carbono/análisis , Suelo/química , Bosques , ChinaRESUMEN
Autophagy contributes to bone homeostasis and development under physiological conditions. Although previous studies have demonstrated the induction of the autophagy machinery by endogenous glucocorticoids (GCs), the precise mechanisms involved have not yet been clarified. The current study aimed to explore the effect of a low dose of GC (10-8 M dexamethasone, Dex) on autophagy in mouse embryonic osteoblastic precursor cells (MC3T3-E1 cells) and the potential mechanisms. The results showed that 10-8 M Dex induced significant time-dependent increases in the expression and activation of serum- and glucocorticoid-induced kinase-1 (SGK1) in MC3T3-E1 cells and that these effects were accompanied by increased cell viability and decreased apoptosis. The autophagy inhibitor 3-MA significantly inhibited Dex-mediated promotion of viability. Moreover, Dex increased LC3II and Beclin-1 levels and decreased SQSTM/p62 levels in a time-dependent manner, and these effects were attenuated by pretreatment with 3-MA. Transfection of Dex-treated MC3T3-E1 cells with shRNA-SGK1 resulted in a significant reduction in cell viability and an increase in apoptosis. 3-MA further exacerbated these effects of SGK1 inhibition. Knocking down SGK1 before Dex exposure significantly reduced the phosphorylated forkhead box O3a (p-FOXO3a)/FOXO3 ratio, suppressed LC3II and Beclin-1 levels, and increased SQSTM/p62 levels in MC3T3-E1 cells, and these effects were amplified by 3-MA. In conclusion, the results revealed that low-dose GC treatment increased osteoblast viability by activating autophagy via the SGK1/FOXO3a pathway.
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Dexametasona , Glucocorticoides , Animales , Ratones , Glucocorticoides/farmacología , Glucocorticoides/metabolismo , Dexametasona/farmacología , Beclina-1/metabolismo , Línea Celular , Transducción de Señal , Autofagia , Osteoblastos/metabolismo , ApoptosisRESUMEN
Alterations in phospholipids have long been associated with spinal cord injury (SCI). However, their specific roles and signaling cascades in mediating cell death and tissue repair remain unclear. Here we investigated whether alterations of cardiolipin (CL), a family of mitochondrion-specific phospholipids, play a crucial role in mitochondrial dysfunction and neuronal death following SCI. Lipidomic analysis was used to determine the profile of CL alteration in the adult rat spinal cord following a moderate contusive SCI at the 10th thoracic (T10) level. Cellular, molecular, and genetic assessments were performed to determine whether CL alterations mediate mitochondrial dysfunction and neuronal death after SCI, and, if so, whether reversing CL alteration leads to neuroprotection after SCI. Using lipidomic analysis, we uncovered CL alterations at an early stage of SCI. Over 50 distinct CL species were identified, of which 50% showed significantly decreased abundance after SCI. The decreased CL species contained mainly polyunsaturated fatty acids that are highly susceptible to peroxidation. In parallel, 4-HNE, a lipid peroxidation marker, significantly increased after SCI. We found that mitochondrial oxidative stress not only induced CL oxidation, but also resulted in CL loss by activating cPLA2 to hydrolyze CL. CL alterations induced mitochondrial dysfunction and neuronal death. Remarkably, pharmacologic inhibition of CL alterations with XJB-5-131, a novel mitochondria-targeted electron and reactive oxygen species scavenger, reduced cell death, tissue damage and ameliorated motor deficits after SCI in adult rats. These findings suggest that CL alteration could be a novel mechanism that mediates injury-induced neuronal death, and a potential therapeutic target for ameliorating secondary SCI.
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Cardiolipinas , Traumatismos de la Médula Espinal , Ratas , Animales , Cardiolipinas/metabolismo , Médula Espinal/metabolismo , Traumatismos de la Médula Espinal/metabolismo , Muerte Celular , Mitocondrias/metabolismo , Fosfolípidos/metabolismo , HomeostasisRESUMEN
Since 1999, the "Grain for Green" Program has been extensively implemented in the Loess Plateau region. This measure has largely been of concern not only for its contribution to soil erosion reduction but also for its effects on carbon sequestration. The aim of this study was to assess the carbon sequestration characteristics of different restored vegetation types in areas with severe soil erosion on the Loess Plateau and to compare the effects of restoration age and slope direction on the vegetation carbon sequestration. To evaluate the carbon density and composition characteristics of different ecosystem types, six typical vegetation types (including farmland, grassland, Hippophae rhamnoides Linn., Caragana korshinskii Kom., Robinia pseudoacacia L., and Populus davidiana Dode.) were selected in the Loess Hilly Region, i.e., Wuqi County and Zhidan County in Northern Shaanxi province, which is a typical area for the implementation of artificial vegetation restoration. The results showed that:â vegetation restoration in the semi-arid loess region had a profound impact on carbon sequestration. The carbon density of different vegetations, as well as different vegetation components including above-ground vegetation, below-ground roots, and litter, shared the same pattern as tree>scrub>grassland>farmland. The 0-40 cm soil layer of the farmland showed the lowest soil organic carbon density (1355.5 g·m-2), compared to which those of grassland, H. rhamnoides Linn., C. korshinskii Kom., R. pseudoacacia L., and P. davidiana Dode. were higher by 91.4%, 125.2%, 144.0%, 124.5%, and 232.6%, respectively. â¡ It was common in grassland, H. rhamnoides Linn., C. korshinskii Kom., and P. davidiana Dode. for the carbon density of different vegetation components as well as soil organic carbon density of different soil layers (0-5, 5-20, and 20-40 cm) to generally show an increasing trend with increased restoration age. ⢠Slope direction had a significant impact on the vegetation carbon density only for H. rhamnoides Linn., C. korshinskii Kom., R. pseudoacacia L., and P. davidiana Dode., while showing the contrary for farmland and grassland. Soil organic carbon densities for sunny slopes were significantly lower than those for shaded slopes by 22.9%, 34.3%, 75.8%, 49.1%, 22.4%, and 69.4%, respectively, for farmland, grassland, H. rhamnoides Linn., C. korshinskii Kom., R. pseudoacacia L., and P. davidiana Dode. ⣠Ecosystem carbon density varied significantly for different ecosystem types, among which farmland showed the lowest (2022.1 g·m-2), and grassland, H. rhamnoides Linn., C. korshinskii Kom., R. pseudoacacia L., and P. davidiana Dode. showed values higher by 48.7%, 152.8%, 125.1%, 166.3%, and 530.7%, respectively. The carbon density of each ecosystem component showed a pattern as follows:soil layer>above-ground vegetation layer>root layer>litter layer. Soil organic carbon constituted the main part of the ecosystem carbon density and accounted for 67.0%, 86.3%, 59.7%, 72.7%, and 56.5%, respectively, for farmland, grassland, H. rhamnoides Linn., C. korshinskii Kom., and R. pseudoacacia L. These results can provide an essential basis for scientific management of ecosystem carbon pools and promote ecological environment management on the Loess Plateau.
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Secuestro de Carbono , Suelo , Carbono , Ecosistema , ÁrbolesRESUMEN
BACKGROUND: 7,8-Dihydroxyflavone (DHF) mimicks the physiological action of brain-derived neurotrophic factor (BDNF). Since local BDNF delivery to the injured spinal cord enhanced diaphragmatic respiratory function, we aimed to ascertain whether DHF might have similar beneficial effects after Brown-Sequard Syndrome in a rat model of spinal cord lateral hemisection (HX) at the 9th thoracic (T9) vertebral level. METHODS: Three sets of adult female rats were included: sham+vehicle group, T9HX+vehicle group and T9HX+DHF group. On the day of surgery, HX+DHF group received DHF (5 mg/kg) while HX+vehicle group received vehicle. Neurobehavioral function, morphology of motor neurons innervating the tibialis anterior muscle and the transmission in descending motor pathways were evaluated. RESULTS: Adult female rats received T9 HX had paralysis and loss of proprioception on the same side as the injury and loss of pain and temperature on the opposite side. We found that, in this model of Brown-Sequard syndrome, reduced cord dendritic arbor complexity, reduced cord motoneuron numbers, enlarged cord lesion volumes, reduced motor evoked potentials, and cord astrogliosis and microgliosis were noted after T9HX. All of the above-mentioned disorders showed recovery by Day 28 after surgery. Therapy with DHF significantly accelerated the electrophysiological, histological and functional recovery in these T9HX animals. CONCLUSIONS: Our data provide a biological basis for DHF as a neurotherapeutic agent to improve recovery after a Brown-Sequard syndrome. Such an effect may be mediated by synaptic plasticity and glia-mediated inflammation in the spared lumbar motoneuron pools to a T9HX.
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Síndrome de Brown-Séquard , Traumatismos de la Médula Espinal , Animales , Factor Neurotrófico Derivado del Encéfalo/metabolismo , Síndrome de Brown-Séquard/tratamiento farmacológico , Femenino , Flavonas , Ratas , Médula Espinal/metabolismo , Traumatismos de la Médula Espinal/complicaciones , Traumatismos de la Médula Espinal/tratamiento farmacológico , Traumatismos de la Médula Espinal/patologíaRESUMEN
Recovery from spinal cord injury (SCI) and other central nervous system (CNS) trauma is hampered by limits on axonal regeneration in the CNS. Regeneration is restricted by the lack of neuron-intrinsic regenerative capacity and by the repressive microenvironment confronting damaged axons. To address this challenge, we have developed a therapeutic strategy that co-targets kinases involved in both extrinsic and intrinsic regulatory pathways. Prior work identified a kinase inhibitor (RO48) with advantageous polypharmacology (co-inhibition of targets including ROCK2 and S6K1), which promoted CNS axon growth in vitro and corticospinal tract (CST) sprouting in a mouse pyramidotomy model. We now show that RO48 promotes neurite growth from sensory neurons and a variety of CNS neurons in vitro, and promotes CST sprouting and/or regeneration in multiple mouse models of spinal cord injury. Notably, these in vivo effects of RO48 were seen in several independent experimental series performed in distinct laboratories at different times. Finally, in a cervical dorsal hemisection model, RO48 not only promoted growth of CST axons beyond the lesion, but also improved behavioral recovery in the rotarod, gridwalk, and pellet retrieval tasks. Our results provide strong evidence for RO48 as an effective compound to promote axon growth and regeneration. Further, they point to strategies for increasing robustness of interventions in pre-clinical models.
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Axones , Traumatismos de la Médula Espinal , Animales , Axones/patología , Modelos Animales de Enfermedad , Ratones , Regeneración Nerviosa/fisiología , Neuronas/metabolismo , Tractos Piramidales/patología , Recuperación de la Función/fisiología , Médula Espinal/patología , Traumatismos de la Médula Espinal/patologíaRESUMEN
Understanding the reorganization of neural circuits spared after spinal cord injury in the motor cortex and spinal cord would provide insights for developing therapeutics. Using optogenetic mapping, we demonstrated a transhemispheric recruitment of neural circuits in the contralateral cortical M1/M2 area to improve the impaired forelimb function after a cervical 5 right-sided hemisection in mice, a model mimicking the human Brown-Séquard syndrome. This cortical reorganization can be elicited by a selective cortical optogenetic neuromodulation paradigm. Areas of whisker, jaw, and neck, together with the rostral forelimb area, on the motor cortex ipsilateral to the lesion were engaged to control the ipsilesional forelimb in both stimulation and nonstimulation groups 8 weeks following injury. However, significant functional benefits were only seen in the stimulation group. Using anterograde tracing, we further revealed a robust sprouting of the intact corticospinal tract in the spinal cord of those animals receiving optogenetic stimulation. The intraspinal corticospinal axonal sprouting correlated with the forelimb functional recovery. Thus, specific neuromodulation of the cortical neural circuits induced massive neural reorganization both in the motor cortex and spinal cord, constructing an alternative motor pathway in restoring impaired forelimb function.
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Corteza Motora , Traumatismos de la Médula Espinal , Animales , Miembro Anterior , Ratones , Corteza Motora/patología , Corteza Motora/fisiología , Tractos Piramidales/patología , Tractos Piramidales/fisiología , Recuperación de la Función/fisiología , Traumatismos de la Médula Espinal/patología , Traumatismos de la Médula Espinal/terapiaRESUMEN
PURPOSE: To analyse the effect of restoration and tooth tissue stress distribution under different occlusal preparation thickness, based on three-dimensional finite element modal of the mandibular second molar with root canal therapy and endocrown restorations. METHODS: A mandibular second molar was scanned by cone-beam CT (CBCT) and a three-dimensional finite element model with endocrown restortions was establishedï¼ Three kinds of endocrown restorations materials with different elastic modulus (glass ceramic, lithium disilicate ceramic and zirconia), and three types of occluscal thickness (1, 2 and 3 mm) were adopted. With a 200 N force loaded vertically and obliquely, the distribution and magnitude of stress in the tooth tissue and endocrown restorations were investigated by three-dimensional finite element analysisï¼ RESULTS: The restoration and tooth tissue maximum stress values were increased firstly and then decreased with the increasing of occlusal thickness; the base material maximum stress values were decreased with the increasing of occlusal thickness; the maximum stress values of tooth tissue and base material were increased with the increasing of restoration material's Young's modulus. Compared to the loading in vertical direction, the maximum stress values were increased with loading in oblique direction. CONCLUSIONS: It's beneficial for tooth tissue to reduce the stress concentration under 2mm thickness. The stress on endocrown will be more concentrated with the increasing of restoration material's Young's modulus.
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Materiales Dentales , Porcelana Dental , Análisis de Elementos Finitos , Análisis del Estrés Dental , Diente Molar/diagnóstico por imagen , Tratamiento del Conducto Radicular , Ensayo de MaterialesRESUMEN
PURPOSE: To investigate the effect of special oral care mode on periodontal health of adolescent orthodontic patients. METHODS: From January 2019 to January 2020, one hundred adolescent orthodontic patients who received treatment in our hospital were randomly divided into experimental group and control group according to the principle of completely random number table, with 50 cases in each group. Patients in the control group were given routine oral care, while those in the experimental group were given special oral care; three months later, the periodontal health status of the two groups were compared using SPSS 21.0 software package. RESULTS: There was no significant difference in PLI and GI between the two groups before treatment (Pï¼0.05). After treatment, PLI and GI in the experimental group were significantly lower than those in the control group(Pï¼0.01). There was no significance difference in SBI and EDI before treatment between the two groups(Pï¼0.05). After treatment, SBI and EDI in the experimental group were significantly lower than those in the control group(Pï¼0.01). There was no significant difference in the scores of periodontal health knowledge before treatment between the two groups(Pï¼0.05). After treatment, the scores of the two groups were significantly increased(Pï¼0.01), and the scores of the experimental group were significantly higher than those of the control group (Pï¼0.01). The patients' satisfaction in the experimental group was significantly higher than that in the control group (90.00% vs 72.00%, P=0.022). CONCLUSIONS: Special oral care mode can significantly improve periodontal health status of adolescent orthodontic patients.
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Satisfacción del Paciente , Humanos , Adolescente , Índice Periodontal , Índice de Placa DentalRESUMEN
Propriospinal neurons (PSNs) play a crucial role in motor control and sensory processing and contribute to plastic reorganization of spinal circuits responsible for recovery from spinal cord injury (SCI). Due to their scattered distribution and various intersegmental projection patterns, it is challenging to dissect the function of PSNs within the neuronal network. New genetically encoded tools, particularly cell-type-specific transgene expression methods using recombinant viral vectors combined with other genetic, pharmacologic, and optogenetic approaches, have enormous potential for visualizing PSNs in the neuronal circuits and monitoring and manipulating their activity. Furthermore, recombinant viral tools have been utilized to promote the intrinsic regenerative capacities of PSNs, towards manipulating the 'hostile' microenvironment for improving functional regeneration of PSNs. Here we summarize the latest development in this fast-moving field and provide a perspective for using this technology to dissect PSN physiological role in contributing to recovery of function after SCI.
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Técnicas de Transferencia de Gen , Plasticidad Neuronal , Neuronas , Propiocepción , Traumatismos de la Médula Espinal/fisiopatología , Traumatismos de la Médula Espinal/terapia , Médula Espinal/fisiopatología , Animales , Vectores Genéticos , Humanos , Red Nerviosa/fisiopatología , Regeneración Nerviosa , Vías Nerviosas/fisiopatología , Traumatismos de la Médula Espinal/genéticaRESUMEN
The benefits of transplanting cultured Schwann cells (SCs) for the treatment of spinal cord injury (SCI) have been systematically investigated in experimental animals since the early 1990s. Importantly, human SC (hSC) transplantation for SCI has advanced to clinical testing and safety has been established via clinical trials conducted in the USA and abroad. However, multiple barriers must be overcome to enable accessible and effective treatments for SCI patients. This review presents available information on hSC transplantation for SCI with the intention to uncover gaps in our knowledge and discuss areas for future development. To this end, we introduce the historical progression of the work that supports existing and prospective clinical initiatives and explain the reasons for the choice of hSCs while also addressing their limitations as cell therapy products. A search of the relevant literature revealed that rat SCs have served as a preclinical model of reference since the onset of investigations, and that hSC transplants are relatively understudied, possibly due to the sophisticated resources and expertise needed for the traditional processing of hSC cultures from human nerves. In turn, we reason that additional experimentation and a reexamination of the available data are needed to understand the therapeutic value of hSC transplants taking into consideration that the manufacturing of the hSCs themselves may require further development for extended uses in basic research and clinical settings.
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Mitochondria supply adenosine triphosphate (ATP) essential for neuronal survival and regeneration. Brain injury and ischemia trigger acute mitochondrial damage and a local energy crisis, leading to degeneration. Boosting local ATP supply in injured axons is thus critical to meet increased energy demand during nerve repair and regeneration in adult brains, where mitochondria remain largely stationary. Here, we elucidate an intrinsic energetic repair signaling axis that boosts axonal energy supply by reprogramming mitochondrial trafficking and anchoring in response to acute injury-ischemic stress in mature neurons and adult brains. P21-activated kinase 5 (PAK5) is a brain mitochondrial kinase with declined expression in mature neurons. PAK5 synthesis and signaling is spatiotemporally activated within axons in response to ischemic stress and axonal injury. PAK5 signaling remobilizes and replaces damaged mitochondria via the phosphorylation switch that turns off the axonal mitochondrial anchor syntaphilin. Injury-ischemic insults trigger AKT growth signaling that activates PAK5 and boosts local energy supply, thus protecting axon survival and facilitating regeneration in in vitro and in vivo models. Our study reveals an axonal mitochondrial signaling axis that responds to injury and ischemia by remobilizing damaged mitochondria for replacement, thereby maintaining local energy supply to support central nervous system (CNS) survival and regeneration.