Background: Spinal cord injury (SCI) is a severe condition that disrupts patients' physiological, mental, and social well-being state and exerts great financial burden on patients, their families and social healthcare system. This review intends to compile studies regarding epidemiological features of SCI in China.Methods: Searches were conducted on PubMed, EMBASE, Web of Science and Cochrane Library for relevant studies published through January, 2018. Studies reported methodological and epidemiological data were collected by two authors independently.Results: Seventeen studies met the inclusion criteria. Two studies reported incidence of SCI that is 60.6 in Beijing (2002) and 23.7 in Tianjin (2004–2008). All studies showed male had a larger percentage in SCI compared to female except Taiwan (2000–2003). The average male and female ratio was 3–4:1 in China and the highest male and female ratio was 5.74: 1 in Tianjin (2004–2007). Farmers, laborers and unemployed people accounted for more than half of the SCI patients in China. Fall was the primary causation with exception of Heilongjiang (2009–2013), Beijing (2001–2010), and Taiwan (2002–2003), where motor vehicle collision (MCVs) was the leading causation. Pulmonary infection, urinary tract infection and bedsore were common complications, accounting for approximately 70% of SCI patients in China.Conclusion: This review shows that epidemiological features of SCI are various in different regions in China and prevention should be implemented by regions. The number of patients with SCI result from fall and MCVs may become a main public health problem because population aging and economic developing in China. However, because all included studies were retrospective and lacking a register system in China, some data were incomplete and some cases may be left out, so the conclusion may not be generalizable to the other regions.
The Ras/Raf/ERK1/2 signaling pathway controls many cellular responses such as cell proliferation, migration, differentiation, and death. In the nervous system, emerging evidence also points to a death-promoting role for ERK1/2 in both in vitro and in vivo models of neuronal death. Recent studies have suggested that abnormal apoptosis in the central nervous system may be involved in the pathogenesis of autism. Two studies reported that both a microdeletion and microduplication on chromosome 16, which includes the MAPK3 gene that encodes ERK1, are associated with autism. In addition, our recent work showed that Ras/Raf/ERK1/2 signaling activities were significantly up-regulated in the frontal cortex of autistic individuals and in the BTBR murine model of autism. To further investigate how Ras/Raf/ERK1/2 up-regulation may lead to the development of autism, we developed a cellular model of Raf/ERK up-regulation by over-expressing c-Raf in cultured cortical neurons (CNs) and cerebellar granule cells (CGCs). We found that Raf/ERK up-regulation stimulates the migration of both CNs and CGCs, and impairs the formation of excitatory synapses in CNs. In addition, we found that Raf/ERK up-regulation inhibits the development of mature dendritic spines in CNs. Investigating the possible mechanisms through which Raf/ERK up-regulation affects excitatory synapse formation and dendritic spine development, we discovered that Raf/ERK up-regulation suppresses the development and maturation of CNs. Together, these results suggest that the up-regulation of the Raf/ERK signaling pathway may contribute to the pathogenesis of autism through both its impairment of cortical neuron development and causing neural circuit imbalances.
BackgroundAutism is a neurodevelopmental disorder characterized by impairments in social interaction, verbal communication and repetitive behaviors. To date the etiology of this disorder is poorly understood. Studies suggest that astrocytes play critical roles in neural plasticity by detecting neuronal activity and modulating neuronal networks. Recently, a number of studies suggested that an abnormal function of glia/astrocytes may be involved in the development of autism. However, there is yet no direct evidence showing how astrocytes develop in the brain of autistic individuals.MethodsStudy subjects include brain tissue from autistic subjects, BTBR T + tfJ (BTBR) and Neuroligin (NL)-3 knock-down mice. Western blot analysis, Immunohistochemistry and confocal microscopy studies have been used to examine the density and morphology of astrocytes, as well as Wnt and β-catenin protein expression.ResultsIn this study, we demonstrate that the astrocytes in autisitc subjects exhibit significantly reduced branching processes, total branching length and cell body sizes. We also detected an astrocytosis in the frontal cortex of autistic subjects. In addition, we found that the astrocytes in the brain of an NL3 knockdown mouse exhibited similar alterations to what we found in the autistic brain. Furthermore, we detected that both Wnt and β-catenin proteins are decreased in the frontal cortex of autistic subjects. Wnt/β-catenin pathway has been suggested to be involved in the regulation of astrocyte development.ConclusionsOur findings imply that defects in astrocytes could impair neuronal plasticity and partially contribute to the development of autistic-like behaviors in both humans and mice. The alteration of Wnt/β-catenin pathway in the brain of autistic subjects may contribute to the changes of astrocytes.
The present study aimed to investigate the role of microRNA (miR)-99b-5p in spinal cord injury (SCI). Reverse transcription-quantitative polymerase chain reaction demonstrated that, compared with control mice, the expression levels of miR-99b-5p were upregulated in the mouse spinal cord following SCI. Mechanistic target of rapamycin (mTOR) was predicted to be the possible target of miR-99b-5p according to TargetScan and microrna databases. Dual-luciferase reporter assay verified that miR-99b-5p was able to target mTOR. Furthermore, the results of an apoptosis analysis demonstrated that there were few apoptotic neurons in the control group, whereas SCI induced a significant increase in the number of apoptotic cells. Conversely, apoptosis was inhibited following transfection with a miR-99b-5p inhibitor. The effects of miR-99b-5p on neurite growth were also evaluated. The results of an immunofluorescence analysis indicated that neurite growth was normal in the control group, whereas SCI induced a reduction in neurite growth, which was rescued following transfection with a miR-99b-5p inhibitor. The protein expression levels of mTOR were detected in the three groups by western blotting. The results demonstrated that, compared with the control group, the protein expression levels of mTOR were significantly reduced in SCI neurons, whereas transfection with a miR-99b-5p inhibitor suppressed the SCI-induced reduction of mTOR. In conclusion, treatment with a miR-99b-5p inhibitor may attenuate SCI-induced harmful alterations in spinal cord neurons via the regulation of mTOR expression.
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