Neurodegeneration最新文献

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Neurochemical Studies of Alzheimer's Disease 阿尔茨海默病的神经化学研究
Neurodegeneration Pub Date : 1996-12-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0051
Alan M. Palmer
{"title":"Neurochemical Studies of Alzheimer's Disease","authors":"Alan M. Palmer","doi":"10.1006/neur.1996.0051","DOIUrl":"10.1006/neur.1996.0051","url":null,"abstract":"<div><p>Neurochemical studies of post-mortem human brain have made a major contribution to understanding the neuronal basis of neurodegenerative disease and formed the basis of rational therapies for such disorders. The application of this approach to the neurochemical pathology of Alzheimer's disease was pioneered by David Bowen. By combining assessment of post-mortem tissue (where the disease has usually run its full course) with tissue obtained ante-mortem (where the disease course is incomplete), it has been possible to (1) establish which neurones are lost in the disease, (2) determine which neurones are lost early in the course of the disease, and (3) discern which changes relate with the symptomatology of the disease. Thus, loss of cholinergic, noradrenergic and serotonergic innervation to the cortex occurs at an early stage, since markers of the neurones are lost in both post-mortem and ante-mortem tissue. By contrast, dopaminergic innervation remains intact and markers of cortical GABAergic interneurones are affected in post-mortem tissue only, suggesting that loss of GABAergic neurones occurs only at a late stage of the disease. Cholinergic markers and the number of pyramidal cell perikarya correlate with the severity of dementia, suggesting that loss of cholinergic and EAA neurones is the major contributor to the cognitive impairments of Alzheimer's disease. Loss of noradrenergic and serotonergic neurones probably contributes to the emergence of non-cognitive impairments in behaviour. Possible causes of selective neuronal loss are discussed.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 4","pages":"Pages 381-391"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 103
Glial Cell Derived Neurotrophic Factors and Alzheimer's Disease 神经胶质细胞源性神经营养因子与阿尔茨海默病
Neurodegeneration Pub Date : 1996-12-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0068
Ambrish J. Patel, Colin Wickenden, Angela Jen, H.A.Rohan de Silva
{"title":"Glial Cell Derived Neurotrophic Factors and Alzheimer's Disease","authors":"Ambrish J. Patel,&nbsp;Colin Wickenden,&nbsp;Angela Jen,&nbsp;H.A.Rohan de Silva","doi":"10.1006/neur.1996.0068","DOIUrl":"10.1006/neur.1996.0068","url":null,"abstract":"<div><p>In Alzheimer's disease the normal balance of metabolic pathways regulating trophic factors/cytokines is disrupted; local reduction may result in neurons being deprived of neurotrophic factors while an excess may initiate a cascade of interaction between glial cells and β-amyloid precursor protein metabolism thereby facilitating plaque formation. This paper briefly discusses the findings of our group on aspects ranging from cholinergic humoral and trophic factors to mechanisms underlying amyloidogenesis in Alzheimer's disease.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 4","pages":"Pages 489-496"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20066526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
Neurochemical Modulation of the Hippocampus in Learning, Remembering and Forgetting in Primates 灵长类动物学习、记忆和遗忘过程中海马体的神经化学调节
Neurodegeneration Pub Date : 1996-12-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0064
R.M. Ridley, J.A. Harder, H.F. Baker
{"title":"Neurochemical Modulation of the Hippocampus in Learning, Remembering and Forgetting in Primates","authors":"R.M. Ridley,&nbsp;J.A. Harder,&nbsp;H.F. Baker","doi":"10.1006/neur.1996.0064","DOIUrl":"10.1006/neur.1996.0064","url":null,"abstract":"<div><p>Information about the outside world is carried into the hippocampus by glutamatergic pyramidal cell pathways from the posterior association cortex via the subiculum. Processed information is carried away from the hippocampus by a reciprocal glutamatergic pathway back into posterior association cortex. These pathways are thought to be crucial for the acquisition of long term memories although it seems likely that memories are stored in cortex rather than within the hippocampus. The hippocampus is supported by functionally excitatory cholinergic modulation via fornical afferents and by functionally inhibitory serotonergic modulation specifically via 5HT<sub>1A</sub>receptors. Cholinergic modulation of the hippocampus is necessary for efficient acquisition of visuospatial tasks but not for retention of similar tasks first acquired prior to surgery. Cholinergic modulation of areas outside the hippocampus may contribute to the maintenance of memories and non-cholinergic efferents in the fornix may be required for retrieval of tasks first learnt when the hippocampus was intact. Impairments on acquisition of visuospatial tasks brought about by fornix transection can be ameliorated by direct stimulation of cholinergic receptors using pilocarpine or by blockade of the serotonergic inhibitory modulation of the hippocampus using the 5HT<sub>1A</sub>receptor antagonist, WAY100635, indicating an equal-but-opposite modulatory effect of these two neurotransmitters on hippocampal function.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 4","pages":"Pages 467-471"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0064","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20066522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
From Acetylcholine to Amyloid: Neurotransmitters and the Pathology of Alzheimer's Disease 从乙酰胆碱到淀粉样蛋白:神经递质和阿尔茨海默病的病理
Neurodegeneration Pub Date : 1996-12-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0066
Roger M. Nitsch
{"title":"From Acetylcholine to Amyloid: Neurotransmitters and the Pathology of Alzheimer's Disease","authors":"Roger M. Nitsch","doi":"10.1006/neur.1996.0066","DOIUrl":"10.1006/neur.1996.0066","url":null,"abstract":"<div><p>Brain amyloid deposits play a central role in the histopathology of Alzheimer's disease (AD), as evidenced by increased formation of amyloid β peptides (Aβ) in genetic forms of AD that are caused by mutations in the presenilin genes, or the amyloid β protein precursor (APP) gene. Neuronal deafferentation in AD brain may also be associated with accelerated Aβ formation, because APP processing is regulated by neuronal activity, presumably via several G protein-coupled neurotransmitter receptors. Subtype-selective agonists including muscarinic m1 receptor ligands may be useful for the pharmacological reduction of Aβ formation.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 4","pages":"Pages 477-482"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0066","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20066524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 69
Ganglioside Alterations in the Central and Peripheral Nervous Systems of Patients with Creutzfeldt-Jakob Disease 克雅氏病患者中枢和周围神经系统的神经节苷脂改变
Neurodegeneration Pub Date : 1996-12-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0045
Yoshio Ohtani , Yoichi Tamai , Yuko Ohnuki , Sadanori Miura
{"title":"Ganglioside Alterations in the Central and Peripheral Nervous Systems of Patients with Creutzfeldt-Jakob Disease","authors":"Yoshio Ohtani ,&nbsp;Yoichi Tamai ,&nbsp;Yuko Ohnuki ,&nbsp;Sadanori Miura","doi":"10.1006/neur.1996.0045","DOIUrl":"10.1006/neur.1996.0045","url":null,"abstract":"<div><p>We have examined the distribution and composition of gangliosides in central and peripheral nervous tissues from two patients with Creutzfeldt-Jakob disease (CJD). There were marked decreases in total ganglioside levels in CJD, with reductions in the cerebral cortex and cerebellum in the order of 20–30% and 50% of control values, respectively, though in spinal cord and sciatic nerve total gangliosides were not significantly altered. The percentage distribution of individual gangliosides was characterized by marked increases in GD3 and GD2, contrasting with severe decreases in GD1a, GD1b, GT1b and GQ1b; such changes were found throughout the patients' nervous tissues. An abnormal long-chain base composition was detected with the d20:1 component being decreased to less than 50% of control values, in the cerebrum, cerebellum and spinal cord. Changes in gangliosides occurred even in those tissues not severely affected neuropathogically. These ganglioside abnormalities are discussed in relationship to the pathogenesis of CJD.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 4","pages":"Pages 331-338"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 20
Quantification of Alzheimer-Type Neurofibrillary Lesions by Automated Image Analysis 阿尔茨海默病型神经原纤维病变的自动图像分析定量
Neurodegeneration Pub Date : 1996-09-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0033
Jeanette E. McKenzie , Gareth W. Roberts , M.Claire Royston
{"title":"Quantification of Alzheimer-Type Neurofibrillary Lesions by Automated Image Analysis","authors":"Jeanette E. McKenzie ,&nbsp;Gareth W. Roberts ,&nbsp;M.Claire Royston","doi":"10.1006/neur.1996.0033","DOIUrl":"10.1006/neur.1996.0033","url":null,"abstract":"<div><p>Neurofibrillary pathology is seen in a wide variety of disorders such as Alzheimer's disease (AD), progressive supranuclear palsy and the Parkinsonism-dementia amyotrophic lateral sclerosis complex of Guam. To assess the pathological importance of these lesions quantitative studies need to be undertaken. To date, most neuropathological studies have been based on qualitative, or at best semi-quantitative, data reporting the presence or absence of specific lesion types. To obtain such data traditionally involves laborious manual measurements, which rely heavily on the skill of the investigator and tend to have low inter- and intra-rater reliabilities. We have developed a novel analysis technique, using colour image analysis, which can accurately quantify the total amount of neurofibrillary damage present. Furthermore we have developed a set of mathematically defined morphological criteria to allow objective discrimination between the three types of neurofibrillary damage seen in the cortex immunostained with Alz–50. Use of this novel technique provides a reliable, rational means for the classification of neurofibrillary lesions.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 3","pages":"Pages 251-258"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19876054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Assessment of Functional Impairment Following Permanent Middle Cerebral Artery Occlusion in a Non-Human Primate Species 非人类灵长类动物永久性大脑中动脉闭塞后的功能损害评估
Neurodegeneration Pub Date : 1996-09-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0036
J.W.B. Marshall, R.M. Ridley
{"title":"Assessment of Functional Impairment Following Permanent Middle Cerebral Artery Occlusion in a Non-Human Primate Species","authors":"J.W.B. Marshall,&nbsp;R.M. Ridley","doi":"10.1006/neur.1996.0036","DOIUrl":"10.1006/neur.1996.0036","url":null,"abstract":"<div><p>The purpose of the present study was to examine and quantify the functional consequence of a focal cerebral ischaemic lesion in a primate species, the marmoset. Following craniotomy and retraction of the frontal and temporal lobes, the middle cerebral artery was permanently occluded by means of electrocoagulation. Three and eight weeks after surgery, various behavioural tests were used to give a quantifiable measure to the neurological deficits produced. These tests required the monkeys to reach into tubes for foodbits, retrieve rewards from the steps of two designs of «staircases», respond to one of two simultaneously presented rewarded tubes, remove adhesive labels attached to their feet, and respond to sensory stimuli. Unilateral motor impairment of the contralateral forelimb and neglect of contralateral tactile stimuli were seen in all subjects, and spatial neglect was also present in some monkeys. Subsequent histological analysis revealed unilateral cortical damage in all subjects with varying amounts of injury to the caudate and the putamen in some animals. These results demonstrate the potential for the use of this species in future investigations to examine the effect of neuroprotective treatment on functional outcome after a focal ischaemic insult.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 3","pages":"Pages 275-286"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19876057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 66
Region- and Neurotransmitter-dependent Species and Strain Differences in DSP–4–induced Monoamine Depletion in Rodents 区域和神经递质依赖的物种和品系差异在啮齿类动物中引起的单胺消耗
Neurodegeneration Pub Date : 1996-09-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0032
Francesco Fornai , Lucia Bassi , Maria Tilde Torracca , Maria Grazia Alessandrı̀ , Vera Scalori , Giovanni U. Corsini
{"title":"Region- and Neurotransmitter-dependent Species and Strain Differences in DSP–4–induced Monoamine Depletion in Rodents","authors":"Francesco Fornai ,&nbsp;Lucia Bassi ,&nbsp;Maria Tilde Torracca ,&nbsp;Maria Grazia Alessandrı̀ ,&nbsp;Vera Scalori ,&nbsp;Giovanni U. Corsini","doi":"10.1006/neur.1996.0032","DOIUrl":"10.1006/neur.1996.0032","url":null,"abstract":"<div><p>The neurotoxin N-(-2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) is commonly used as a chemical tool to induce selective denervation of noradrenergic terminals arising from the locus coeruleus and to study the molecular mechanisms underlying degeneration of central noradrenergic axons in rodents. Monoamine depletion in different rodent species after DSP-4 is generally assumed to occur with a similar pattern. To verify this assumption, in the present study we evaluated the different patterns of monoamine depletion produced by DSP-4 in different brain regions of two different strains of mice and rats 3, 7 and 14 days after DSP-4 administration. In this report, we show that there are evident species and strain differences concerning the pattern of norepinephrine depletion in various brain regions. Moreover, serotonin levels are fully preserved following DSP-4 in mice, whereas there is a significant serotonin decrease in specific brain regions after the same dose of DSP-4 in rats. Apart from disclosing species and strain variability among rodents in neurotoxin-induced monoamine depletion, these findings suggest that DSP-4 should be considered as a different neurotoxin, depending on the species and strain in which it is administered.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 3","pages":"Pages 241-249"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19876053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 66
Alteration in Brain Presenilin 1 mRNA Expression in Early Onset Familial Alzheimer's Disease 早发性家族性阿尔茨海默病中脑早老素1 mRNA表达的改变
Neurodegeneration Pub Date : 1996-09-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0029
Amanda J.L. Barton , Barry W. Crook , Eric H. Karran , Frank Brown , Deborah Dewar , David M.A. Mann , R.Carl A. Pearson , David I. Graham , John Hardy , Mike Hutton , Karen Duff , Alison M. Goate , Robert F. Clark , Gareth W. Roberts
{"title":"Alteration in Brain Presenilin 1 mRNA Expression in Early Onset Familial Alzheimer's Disease","authors":"Amanda J.L. Barton ,&nbsp;Barry W. Crook ,&nbsp;Eric H. Karran ,&nbsp;Frank Brown ,&nbsp;Deborah Dewar ,&nbsp;David M.A. Mann ,&nbsp;R.Carl A. Pearson ,&nbsp;David I. Graham ,&nbsp;John Hardy ,&nbsp;Mike Hutton ,&nbsp;Karen Duff ,&nbsp;Alison M. Goate ,&nbsp;Robert F. Clark ,&nbsp;Gareth W. Roberts","doi":"10.1006/neur.1996.0029","DOIUrl":"10.1006/neur.1996.0029","url":null,"abstract":"<div><p>The expression of the presenilin 1 (PS–1) gene has been investigated by<em>in situ</em>hybridization in early onset familial Alzheimer's disease (FAD), late onset Alzheimer's disease (AD) and normal control brain. Mutations in this gene are responsible for chromosome 14–linked FAD. We have found that presenilin 1 mRNA is present throughout the human brain with a distribution consistent with both a glial and neuronal localization. The<em>in situ</em>hybridization pattern was similar for the controls, the early onset FAD cases and the late onset AD cases. However, one of the two forms of the mRNA for PS–1, the long form (which contains a sequence encoding a four amino acid (VRSQ) insert at its 5′end) was significantly reduced in early onset FAD brain compared with late onset AD. We suggest that this long transcript may alter the normal pathway for processing of amyloid precursor protein, the protein which appears to be central in the pathogenesis of AD.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 3","pages":"Pages 213-218"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19874838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 12
Comparative Investigation of Neurofibrillary Damage in the Temporal Lobe in Alzheimer's Disease, Down's Syndrome and Dementia Pugilistica 阿尔茨海默病、唐氏综合征和拳击性痴呆颞叶神经原纤维损伤的比较研究
Neurodegeneration Pub Date : 1996-09-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0034
Jeanette E. McKenzie , Gareth W. Roberts , M.Claire Royston
{"title":"Comparative Investigation of Neurofibrillary Damage in the Temporal Lobe in Alzheimer's Disease, Down's Syndrome and Dementia Pugilistica","authors":"Jeanette E. McKenzie ,&nbsp;Gareth W. Roberts ,&nbsp;M.Claire Royston","doi":"10.1006/neur.1996.0034","DOIUrl":"10.1006/neur.1996.0034","url":null,"abstract":"<div><p>Neurofibrillary lesions such as neurofibrillary tangles, neurites and neuropil threads are used as neuropathological markers of Alzheimer's disease (AD). However these lesions are also seen in non-demented elderly cases as well as in several other disorders such as Down's syndrome (DS), dementia pugilistica (DP) and Parkinson's disease. Quantitative studies may therefore help in understanding the pathophysiological role of these lesions. Using a novel image analysis technique we have quantified the extent of neurofibrillary damage in AD, DS and DP. We have found that the extent of neurofibrillary change did not significantly differ beween AD and DS, though there were also strong parallels between AD and DP. We conclude that both genetic (as in DS) and environmental (as in DP) risk factors for AD-type pathology provide a similar pattern of neurofibrillary degeneration to that in AD itself suggesting that similar degenerative mechanisms might be triggered in all three conditions.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 3","pages":"Pages 259-264"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19876055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 23
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