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| 1 | Nature brings new avenues to the therapy of central nervous system diseases——an overview of possible treatments derived from natural products显示文摘Natural products(NPs), including traditional Chinese medicine(TCM), have been long and widely used in the prevention and treatment of central nervous system(CNS) diseases by virtue of their abundant sources, diverse structures, and novel activities.In this review article, we intend to summarize and discuss the situation or status of the clinical employments or trials of the NPs and their derivatives with CNS activities. NPs that have been extensively studied in preclinical research in recent years are also included. The compounds presented in this review are classified according to their indications and followed by details such as natural sources, possible biological mechanisms, and development status, while a considerable proportion of them are found in TCM. In addition, some drug combinations with synergistic effects are also mentioned. According to their impressive therapeutic effects and novel chemical structures, NPs are not only effective therapeutic remedies in clinic, but also lead compounds for structural modification, which indicate that nature brings new avenues to the therapy of CNS diseases. | Junchi Zhang Yang He Xiangrui Jiang Hualiang Jiang Jingshan Shen | 2019 | Science China(Life Sciences)2019，62，10： | 30 |
| 2 | Mitophagy links oxidative stress conditions and neurodegenerative diseases显示文摘Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases. | Ulfuara Shefa Na Young Jeong In Ok Song Hyung-Joo Chung Dokyoung Kim Junyang Jung Youngbuhm Huh | 2019 | Neural Regeneration Research2019，14，5： | 21 |
| 3 | Hepatic encephalopathy:An approach to its multiple pathophysiological features显示文摘Hepatic encephalopathy(HE)is a neuropsychiatric complex syndrome,ranging from subtle behavioral abnormalities to deep coma and death.Hepatic encephalopathy emerges as the major complication of acute or chronic liver failure.Multiplicity of factors are involved in its pathophysiology,such as central and neuromuscular neurotransmission disorder,alterations in sleep patterns and cognition,changes in energy metabolism leading to cell injury,an oxidative/nitrosative state and a neuroinflammatory condition.Moreover,in acute HE,a condition of imminent threat of death is present due to a deleterious astrocyte swelling.In chronic HE,changes in calcium signaling,mitochondrial membrane potential and long term potential expression,N-methyl-D-aspartate-cGMP and peripheral benzodiazepine receptors alterations,and changes in the mRNA and protein expression and redistribution in the cerebral blood flow can be observed.The main molecule indicated as responsible for all these changes in HE is ammonia.There is no doubt that ammonia,a neurotoxic molecule,triggers or at least facilitates most of these changes.Ammonia plasma levels are increased two-to three-fold in patients with mild to moderate cirrhotic HE and up to ten-fold in patients with acute liver failure. Hepatic and inter-organ trafficking of ammonia and its metabolite,glutamine(GLN),lead to hyperammonemic conditions.Removal of hepatic ammonia is a differentiated work that includes the hepatocyte,through the urea cycle,converting ammonia into GLN via glutamine synthetase.Under pathological conditions,such as liver damage or liver blood bypass,the ammonia plasma level starts to rise and the risk of HE developing is high. Knowledge of the pathophysiology of HE is rapidly expanding and identification of focally localized triggers has led the development of new possibilities for HE to be considered.This editorial will focus on issues where, to the best of our knowledge,more research is needed in order to clarify,at least partially,controversial topics. | Juan Carlos Perazzo Silvina Tallis Amalia Delfante Pablo Andrés Souto Abraham Lemberg Francisco Xavier Eizayaga Salvador Romay | 2012 | World Journal of Hepatology2012，4，3： | 16 |
| 4 | Neurotherapeutic potential of erythropoietin after ischemic injury of the central nervous system显示文摘Erythropoietin (EPO) is one of the most successful biopharmaceuticals in history and is used for treating anemia of different origins. However, it became clear that EPO could also work in a neuroprotective, antiapoptotic, antioxidative, angiogenetic and neurotropic way. It causes stimulation of cells to delay cell apoptosis, especially in the central nervous system. In rodent models of focal cerebral ischemia, EPO showed an impressive reduction of infarct size by 30% and improvement of neurobehavioral outcome by nearly 40%. A large animal model dealing with ischemia and reperfusion of the spinal cord showed that EPO could reduce the risk of spinal cord injury significantly. In addition, some clinical studies tested whether EPO works in real live clinical settings. One of the most promising studies showed the innocuousness and improvements in follow-up, outcome scales and in infarct size, of EPO-use in humans suffering from ischemic stroke. Another study ended unfortunately in a negative outcome and an increased overall death rate in the EPO group. The most possible reason was the involvement of patients undergoing simultaneously systemic thrombolysis with recombinant tissue plasminogen activator. An experimental study on rats demonstrated that administration of EPO might exacerbate tissue plasminogen activator-induced brain hemorrhage without reducing the ischemic brain damage. This case shows clearly how useful animal models can be to check negative side effects of a treatment before going into clinical trials. Other groups looked in human trials at the effects of EPO on the outcome after ischemic stroke, relation to circulating endothelial progerdtor cells, aneurysmal subarachnoid hemorrhage, traumatic brain injury, hemoglobin transfusion thresholds and elective first-time coronary artery bypass surgery. Most of the results were pos-让ive, but are based mostly on small group sizes. However, some of the most neglected facts when focusing on experimental setups of ischemia of the central nervous system are issues like age and comorbidities. It might be extremely worthy to consider these points for future projects, because EPO might influence all these factors. | Florian Simon Nicolaos Floros Wiebke Ibing Hubert Schelzig Artis Knapsis | 2019 | Neural Regeneration Research2019，14，8： | 15 |
| 5 | WJSC 6^(th) Anniversary Special Issues(2):Mesenchymal stem cells Progress of mesenchymal stem cell therapy for neural and retinal diseases显示文摘Complex circuitry and limited regenerative power make central nervous system(CNS)disorders the most challenging and difficult for functional repair.With elusive disease mechanisms,traditional surgical and medical interventions merely slow down the progression of the neurodegenerative diseases.However,the number of neurons still diminishes in many patients.Recently,stem cell therapy has been proposed as a viable option.Mesenchymal stem cells(MSCs),a widely-studied human adult stem cell population,have been discovered for more than 20 years.MSCs have been found all over the body and can be conveniently obtained from different accessible tissues:bone marrow,blood,and adipose and dental tissue.MSCs have high proliferative and differentiation abilities,providing an inexhaustible source of neurons and glia for cell replacement therapy.Moreover,MSCs also show neuroprotective effects without any genetic modification or reprogramming.In addition,the extraordinary immunomodulatory properties of MSCs enable autologous and heterologous transplantation.These qualities heighten the clinical applicability of MSCs when dealing with the pathologies of CNS disorders.Here,we summarize the latest progress of MSC experimental research as well as human clinical trials for neural and retinal diseases.This review article will focus on multiple sclerosis,spinal cord injury,autism,glaucoma,retinitis pigmentosa and age-related macular degeneration. | Tsz Kin Ng Veronica R Fortino Daniel Pelaez Herman S Cheung | 2014 | World Journal of Stem Cells2014，6，2： | 13 |
| 6 | Effects of miR-219/miR-338 on microglia and astrocyte behaviors and astrocyte-oligodendrocyte precursor cell interactions显示文摘MiR-219 and miR-338(miR-219/miR-338)are oligodendrocyte-specific microRNAs.The overexpression of these miRs in oligodendrocyte precursor cells promotes their differentiation and maturation into oligodendrocytes,which may enhance axonal remyelination after nerve injuries in the central nervous system(CNS).As such,the delivery of miR-219/miR-338 to the CNS to promote oligodendrocyte precursor cell differentiation,maturation and myelination could be a promising approach for nerve repair.However,nerve injuries in the CNS also involve other cell types,such as microglia and astrocytes.Herein,we investigated the effects of miR-219/miR-338 treatment on microglia and astrocytes in vitro and in vivo.We found that miR-219/miR-338 diminished microglial expression of pro-inflammatory cytokines and suppressed astrocyte activation.In addition,we showed that miR-219/miR-338 enhanced oligodendrocyte precursor cell differentiation and maturation in a scratch assay paradigm that re-created a nerve injury condition in vitro.Collectively,our results suggest miR-219/miR-338 as a promising treatment for axonal remyelination in the CNS following nerve injuries.All experimental procedures were approved by the Institutional Animal Care and Use Committee(IACUC),Nanyang Technological University(approval No.A0309 and A0333)on April 27,2016 and October 8,2016. | Lan Huong Nguyen William Ong Kai Wang Mingfeng Wang Dean Nizetic Sing Yian Chew | 2020 | Neural Regeneration Research2020，15，4： | 11 |
| 7 | Rhombencephalitis caused by Listeria monocytogenes with hydrocephalus and intracranial hemorrhage:A case report and review of the literature显示文摘BACKGROUND Listeria monocytogenes(L. monocytogenes), a Gram-positive facultatively intracellular bacterium, is the causative agent of human listeriosis. Listeria infection is usually found in immunocompromised patients, including elderly people, pregnant women, and newborns, whereas it is rare in healthy people. L.monocytogenes may cause meningitis, meningoencephalitis, and some very rare and severe complications, such as hydrocephalus and intracranial hemorrhage,which cause high mortality and morbidity worldwide. Up to now, reports on hydrocephalus and intracranial hemorrhage due to L. monocytogenes are few.CASE SUMMARY We herein report a case of rhombencephalitis caused by L. monocytogenes in a 29-year-old man. He was admitted to the hospital with a 2-d history of headache and fever. He consumed unpasteurized cooked beef two days before appearance.His medical history included type 2 diabetes mellitus, and contaminated beef intake 2 d before onset. Cerebrospinal fluid analysis revealed Gram-positive rod infection, and blood culture was positive for L. monocytogenes. Magnetic resonance imaging findings suggested rhombencephalitis and hydrocephalus.Treatment was started empirically and then modified according to the blood culture results. Repeated CT images were suggestive of intracranial hemorrhage.Although the patient underwent aggressive external ventricular drainage, he died of a continuing deterioration of intracranial conditions.CONCLUSION Hydrocephalus, intracranial hemorrhage, and inappropriate antimicrobial treatment are the determinations of unfavorable outcomes. | Jing-Jing Liang Xiao-Yan He Hong Ye | 2019 | World Journal of Clinical Cases2019，7，4： | 9 |
| 8 | Taking central nervous system regenerative therapies to the clinic: curing rodents versus nonhuman primates versus humans显示文摘The central nervous system is known to have limited regenerative capacity.Not only does this halt the human body’s reparative processes after central nervous system lesions,but it also impedes the establishment of effective and safe therapeutic options for such patients.Despite the high prevalence of stroke and spinal cord injury in the general population,these conditions remain incurable and place a heavy burden on patients’families and on society more broadly.Neuroregeneration and neural engineering are diverse biomedical fields that attempt reparative treatments,utilizing stem cells-based strategies,biologically active molecules,nanotechnology,exosomes and highly tunable biodegradable systems(e.g.,certain hydrogels).Although there are studies demonstrating promising preclinical results,safe clinical translation has not yet been accomplished.A key gap in clinical translation is the absence of an ideal animal or ex vivo model that can perfectly simulate the human microenvironment,and also correspond to all the complex pathophysiological and neuroanatomical factors that affect functional outcomes in humans after central nervous system injury.Such an ideal model does not currently exist,but it seems that the nonhuman primate model is uniquely qualified for this role,given its close resemblance to humans.This review considers some regenerative therapies for central nervous system repair that hold promise for future clinical translation.In addition,it attempts to uncover some of the main reasons why clinical translation might fail without the implementation of nonhuman primate models in the research pipeline. | Magdalini Tsintou Kyriakos Dalamagkas Nikos Makris | 2020 | Neural Regeneration Research2020，15，3： | 7 |
| 9 | Trans-synaptic Neural Circuit-Tracing with Neurotropic Viruses显示文摘A central objective in deciphering the nervous system in health and disease is to define the connections of neurons. The propensity of neurotropic viruses to spread among synaptically-linked neurons makes them ideal for mapping neural circuits. So far, several classes of viral neuronal tracers have become available and provide a powerful toolbox for delineating neural networks. In this paper, we review the recent developments of neurotropic viral tracers and highlight their unique properties in revealing patterns of neuronal connections. | Jiamin Li Taian Liu Yun Dong Kunio Kondoh Zhonghua Lu | 2019 | Neuroscience Bulletin2019，35，5： | 7 |
| 10 | Extracellular vesicles in the diagnosis and treatment of central nervous system diseases显示文摘Extracellular vesicles,including exosomes and microvesicles,play a fundamental role in the activity of the nervous system,participating in signal transmission between neurons and providing the interaction of central nervous system with all body systems.In many neurodegenerative diseases,neurons pack toxic substances into vesicles and release them into the extracellular space,which leads to the spread of misfolded neurotoxic proteins.The contents of neuron-derived extracellular vesicles may indicate pathological changes in the central nervous system,and the analysis of extracellular vesicle molecular content contributes to the development of non-invasive methods for the diagnosis of many central nervous system diseases.Extracellular vesicles of neuronal origin can be isolated from various biological fluids due to their ability to cross the blood-brain barrier.Today,the diagnostic potential of almost all toxic proteins involved in nervous system disease pathogenesis,specificallyα-synuclein,tau protein,superoxide dismutase 1,FUS,leucine-rich repeat kinase 2,as well as some synaptic proteins,has been well evidenced.Special attention is paid to extracellular RNAs mostly associated with extracellular vesicles,which are important in the onset and development of many neurodegenerative diseases.Depending on parental cell type,extracellular vesicles may have different therapeutic properties,including neuroprotective,regenerative,and anti-inflammatory.Due to nano size,biosafety,ability to cross the blood-brain barrier,possibility of targeted delivery and the lack of an immune response,extracellular vesicles are a promising vehicle for the delivery of therapeutic substances for the treatment of neurodegenerative diseases and drug delivery to the brain.This review describes modern approaches of diagnosis and treatment of central nervous system diseases using extracellular vesicles. | Alisa A.Shaimardanova Valeriya V.Solovyeva Daria S.Chulpanova Victoria James Kristina V.Kitaeva Albert A.Rizvanov | 2020 | Neural Regeneration Research2020，15，4： | 7 |
| 11 | Characteristics and advantages of adeno-associated virus vector-mediated gene therapy for neurodegenerative diseases显示文摘Common neurodegenerative diseases of the central nervous system are characterized by progressive damage to the function of neurons, even leading to the permanent loss of function. Gene therapy via gene replacement or gene correction provides the potential for transformative therapies to delay or possibly stop further progression of the neurodegenerative disease in affected patients. Adeno-associated virus has been the vector of choice in recent clinical trials of therapies for neurodegenerative diseases due to its safety and efficiency in mediating gene transfer to the central nervous system. This review aims to discuss and summarize the progress and clinical applications of adeno-associated virus in neurodegenerative disease in central nervous system. Results from some clinical trials and successful cases of central neurodegenerative diseases deserve further study and exploration. | Yuan Qu Yi Liu Ahmed Fayyaz Noor Johnathan Tran Rui Li | 2019 | Neural Regeneration Research2019，14，6： | 6 |
| 12 | Transitions of the Understanding and Definition of Primary Glaucoma显示文摘Objective:In previous decades,glaucoma has been primarily attributed to elevated intraocular pressure (IOP),but this has gradually been replaced by the development of optic neuropathy as the central concept of glaucoma in developed countries.However,there still remain strong controversies in the definition of glaucoma in China.In this current review,we are going to discuss these controversies and elaborate on the historical transitions of the definition of glaucoma both in China and developed countries.Furthermore,we will briefly describe the 'ocular-cranial pressure gradient'theory and discuss the relationship between glaucoma and degenerative diseases of the central nervous system (CNS)in order to show the complex pathogenesis of glaucoma and the importance for the modification to the definition of glaucoma. Data Sources:We performed a comprehensive search in both PubMed and SinoMed using the following keywords:(a)'primary glaucoma'and 'guideline,'(b)'ocular-cranial pressure gradient,'and (c)'glaucoma,''Alzheimer's disease,'and 'Parkinson's disease.' The literature search included the related articles with no restrictions on publication date. Study Selection:The primary references were Chinese and English articles including (a)original guidelines and expert consensuses of primary glaucoma,(b)reviews focusing on the differences between various versions of these guidelines and consensuses,and (c)papers about ocular-cranial pressure gradient theory and the relationship between glaucoma and CNS degenerative diseases. Results:The definitions and classifications of both primary open-angle glaucoma and primary angle-closure glaucoma differ between Chinese glaucoma consensuses and international primary glaucoma guidelines.Chinese definitions and classifications put more emphasis on the IOP,while international guidelines put more emphasis on the presence of optic neuropathy.The ocular-cranial pressure gradient theory and the research on the relationship between glaucoma and CNS degenerative diseases have provided new directions for exploring the pathogenesis of glaucoma. Conclusions:As regards the definition and classification of primary glaucoma,we find that there are still some discrepancies between Chinese expert consensuses and international guidelines.Glaucoma is a disease with complex etiologies,while its common characteristic is a specific optic neuropathy.The current definition and understanding of glaucoma is an ongoing and evolving process,reflecting our latest available evidence on its pathogenesis.Chinese ophthalmology community may need to update our guidelines,accommodating these latest developments. | Si-An Liu Zhen-Ni Zhao Nan-Nan Sun Ying Han Jeremy Chen Zhi-Gang Fan | 2018 | Chinese Medical Journal2018，，23： | 6 |
| 13 | Alteration of the microRNA expression profile and identification of miRNA/mRNA negative regulation pairs in neural tube defects显示文摘MicroRNAs (miRNAs) are small, noncoding transcripts, and ~22 nucleotides long, which belong to a class of endogenous small regulatory RNA molecules that target mRNAs and trigger either translational suppression or mRNA degradation [1–3]. Several studies have shown that miRNAs play crucial roles in neurogenesis and development of nervous system [4,5] and have distinct expression patterns within the developing brain and central nervous system (CNS)[6]. Abnormal expression of miRNAs has also been reported in dysregulated neural tube (NT) development including NT defects (NTDs)[7,8]. To date, however, all NTD-related miRNA profiles were obtained from different microarray platforms, which always contain limited probes, and the data obtained are less precise in quantitative analysis. No quantitatively profiled global miRNA expression in mouse NTD fetuses has been characterized so far. To gain further insight of the possible roles of miRNAs in NTDs, we used deep sequencing to carry out a comprehensive survey of miRNA expression in all-trans retinoic acid (RA)-induced NTD mouse fetuses collected from three different embryonic time points (E8.5, E9.5, and E10.5). This study is the first, to our knowledge, to report the deep sequencing miRNA profile, which defined unique gene expression signatures of a range of miRNAs and their potential regulatory networks in response to RA stress and the development of NTDs in mouse model. | Juan Zhang Lihong Yang Juan Yu Qiaoyan Yang Jianbing Mu Jun Xie | 2019 | Acta Biochimica et Biophysica Sinica2019，51，7： | 6 |
| 14 | Progress in the Treatment of Fungal Infections of the Central Nervous System显示文摘HThe incidence of fungal infections of the central nervous system(CNS) has gradually increased in recent years. Intracranial fungal infection can be classified as diffuse and focal infections. The clinical manifestations of these infections include fever and cranial pressure caused by meningitis or meningoencephalitis, and focal neurological defects caused by lesions in the intracranial space. Diagnosing fungal infections of the CNS requires the comprehensive analysis of the patient's medical history, epidemiology, underlying disease, clinical manifestation, imaging manifestations, and various laboratory test results. The identification of fungal bodies or structures in brain tissue or cerebrospinal fluid specimens is the golden standard of diagnosis. The principles for the treatment of the fungal infections of the CNS are the effective control of pathogenic risk factors, use of effective antifungal drugs, and the active implementation of surgical intervention for fungal abscesses and granuloma. In the meantime, new diagnoses and treatments should be actively explored to improve the prognosis of patients. | Xuemei Li Xiaoxia Li | 2017 | 国际感染病学(电子版)2017，6，2： | 5 |
| 15 | 中枢神经系统运动障碍的诊断和处理显示文摘运动障碍(dyskinesia)是一种不自主运动,出现兼有肌张力障碍和舞蹈症的不自主动作,伴主动随意运动减少.目前,国内对之还没有恰当和统一的翻译,为避免与大概念的运动障碍(movement disorder)相区别,习惯于将帕金森病(pd)患者的dyskinesia翻译为'异动症',而其他情况下的dyskinesia则翻译为'运动障碍',如'迟发性运动障碍'和'发作性运动障碍'. | 王坚 | 2010 | 神经病学与神经康复学杂志2010，7，3： | 5 |
| 16 | 多发性硬化的病因和发病机制研究进展显示文摘多发性硬化(multiple sclerosis,ms)是一种中枢神经系统(central nervous system,cns)慢性炎性脱髓鞘疾病,临床上症状体征多样,病程反复,多见于青中年,女性是男性的2~3倍.早在15世纪就出现了可疑为ms病例的记载,19世纪30年代人们开始逐步认识这一疾病,提出了初步的临床诊断标准,但是直到目前ms具体的病因和发病机制尚不完全明确.近30年来ms已成为世界范围内的研究热点.经过大量系统深入的研究,目前ms被认为是一种由基因、病毒感染、环境等多种因素相互作用导致的自身免疫性疾病. | 戴永强 胡学强 | 2010 | 中国处方药2010，9，11： | 4 |
| 17 | Comparison and Correlation of Magnetic Resonance Imaging and Clinical Severity in Nonhuman Immunodeficiency Virus Patients with Cryptococcal Infection of Central Nervous System显示文摘Background:The incidence of cryptococcal meningitis among immunocompetent patients increases,especially in China and imaging plays an important role.The current study was to find the correlation between magnetic resonance imaging (MRI)manifestation and clinical severity in nonhuman immunodeficiency virus patients with cryptococcal infection of central nervous system (CNS). Methods:A total of 65 patients with CNS cryptococcal infection from August 2014 to October 2016 were retrospectively included in this study.All the patients had MRI data and clinical data.The patients were divided into two groups according to whether the patients were confirmed with identifiable underlying disease.Comparison and correlation of MRI and clinical data in both groups were investigated using independent sample t-test,Chi-square test,Mann-Whitney test and Spearman rank correlation analysis. Results:In all 65 patients,41 cases (41/65,63.1%;Group 1)had normal immunity and 24 cases (24/65,36.9%;Group 2)had at least one identifiable underlying disease.Fever,higher percentage of neutrophil (NEUT)in white blood cell (WBC),and increased cell number of cerebral spinal fluid (CSF)were much common in patients with underlying disease (Group 1 vs.Group 2:Fever:21/41 vs.21/24,x^2 =8.715,P =0.003;NEUT in WBC:73.15%vs.79.60%,Z=-2.370,P =0.018;cell number of CSF:19 vs.200,Z=-4.298,P <0.001;respectively).Compared to the patients with normal immunity,the lesions are more common in the basal ganglia among patients with identifiable underlying disease (Group 1 vs.Group 2:20/41 vs.20/24,x^2 =7.636,P =0.006).The number of the involved brain areas in patients with identifiable underlying disease were well correlated with the number of cells and pressure of CSF (r =-0.472,P =0.031,r =0.779,P =0.039;respectively). Conclusions:With the increased number of the involved brain areas in patients with identifiable underlying disease,the body has lower immunity against the organism which might result in higher intracranial pressure and more severe clinical status. | Xue-Qin Li Shuang Xia Jian-Song Ji Yong-Hua Tang Mei-Zhu Zheng Yong-Mei Li Fei Shan Zhi-Yan Lu Jian Wang Jin-Kang Liu Hui-Juan Zhang Yu-Xin Shi Hong-Jun Li | 2018 | Chinese Medical Journal2018，，24： | 3 |
| 18 | Study on development and localization of CTGF-immunoreactive cells in central nervous system of rats显示文摘Objective:To studythedevelopmentof connectivetissuegrowthfactor(CTGF)immunoreactivecellsin the centralnervoussystem(CNS)of E8-P300rats.Methods:Immunocytochemistrywasemployedinourstudy.Re sults:No CTGF-immunoreactivecellsweredetectedintheCNSof ratsduringprenatalstages.A fewof CTGF-positivecellswere detectedin theearlypostnatalstage.However,thepositivecellsincreasedgraduallyin laterstages.CTGF-immunoreac-tivecellswidelydistributedin theCNSof ratsin thefirst30to60dayspostnatally,andthedensityof immunoreactive productswasthehighestinthesedays.Thenumberandstainingintensityof CTGF-positivecellsdecreasedandtheirarea of distributiondiminishedgraduallywithage.Thepositivecellsincludedneuronsmainlylocated inthecingulatecortex,striatum,hippocampus,hypothalamusandcerebellum,andastrocytesinwhitematterof thespinalcordandependymal cellsof thebrain.Mostof CTGF-immunoreactivecellswerequitebiginsizewitha longprocess.Conclusion:CTGF-im-munoreactivecellswerefoundintheCNSof rats,andtheirnumbersandpositivesignaldecreasedwiththeage. | 苏炳银 蔡文琴 张成岗 | 2001 | Journal of Medical Colleges of PLA(China)2001，16，3： | 3 |
| 19 | Dendritic shrinkage after injury: a cellular killer or a necessity for axonal regeneration?显示文摘Dendrites form an essential component of the neuronal circuit have been largely overlooked in regenerative research. Nevertheless, subtle changes in the dendritic arbors of neurons are one of the first stages of various neurodegenerative diseases, leading to dysfunctional neuronal networks and ultimately cellular death. Maintaining dendrites is therefore considered an essential neuroprotective strategy. This mini-review aims to discuss an intriguing hypothesis, which postulates that dendritic shrinkage is an important stimulant to boost axonal regeneration, and thus that preserving dendrites might not be the ideal therapeutic method to regain a full functional network upon central nervous system damage. Indeed, our study in zebrafish, a versatile animal model with robust regenerative capacity recently unraveled that dendritic retraction is evoked prior to axonal regrowth after optic nerve injury. Strikingly, inhibiting dendritic pruning upon damage perturbed axonal regeneration. This constraining effect of dendrites on axonal regrowth has sporadically been proposed in literature, as summarized in this short narrative. In addition, the review discusses a plausible underlying mechanism for the observed antagonistic axon-dendrite interplay, which is based on energy restriction inside neurons. Axonal injury indeed leads to a high local energy demand in which efficient axonal energy supply is fundamental to ensure regrowth. At the same time, axonal lesion is known to induce m让ochondrial depolarization, causing energy depletion in the axonal compartment of damaged neurons. Mitochondria, however, become mostly stationary after development, which has been proposed as a potential underlying reason for the low regenerative capacity of adult mammals. Per contra, upon reduced neuronal activity, mitochondrial mobility enhances. In this view, dendritic shrinkage after axonal injury in zebrafish could result in less synaptic input and hence, a release of mitochondria within the soma-dendrite compartment that then translocate to the axonal growth cone to stimulate axonal regeneration. If this hypothesis proofs to be correct, i.e. dendritic remodeling serving as fuel for axonal regeneration, we envision a major shift in the research focus within the neuroregenerative field and in the potential uncovering of various novel therapeutic targets. | An Beckers Lieve Moons | 2019 | Neural Regeneration Research2019，14，8： | 2 |
| 20 | Central Nervous System Toxicity of Sodium Nitroprusside in Treatment of Patients with Aortic Dissection显示文摘This study examined the sodium nitroprusside (SNP) toxicity to central nervous system (CNS) in treatment of patients with aortic dissection (AD). The medical records of 191 AD patients who were admitted to Tongji Hospital, China, from Jan. 1998 to Feb. 2009 were retrospectively analyzed. There were 140 cases of hypertension (73.3%) and 13 cases of Marfan syndrome (6.8%) among the 191 AD patients. A total of 157 patients were given SNP treatment. The toxic reactions of CNS occurred in 18 subjects (11.5%). Most of the adverse reactions occurred on the fifth day following SNP injection. SNP infusion rate was significantly higher in patients who developed CNS toxicity. It was suggested that systemic hypertension is the most common predisposing factor for AD. The combination of SNP with a β-receptor blocker is a medical therapy commonly used in patients with AD. Cyanide and thio-cyanate toxicity from SNP treatment is always the consequence of prolonged drug infusion or relatively high dose administration. | 黄雪渊 侯凌波 唐家荣 张艳梅 陈复琼 汪道文 | 2012 | Journal of Huazhong University of Science and Technology(Medical Sciences)2012，32，6： | 2 |
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