Acta neuropathologica. Supplementum最新文献

Immunologic models of acute and chronic inflammation. 急性和慢性炎症的免疫学模型。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-69094-5_1

B H Waksman

引用次数: 3

Cerebrovascular transport mechanisms. International Congress of Neuropathology, Vienna, September 5-10, 1982. 脑血管运输机制。国际神经病理学大会，维也纳，1982年9月5日至10日。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01

引用次数: 0

Virologic models of chronic relapsing demyelinating disease. 慢性复发性脱髓鞘病的病毒学模型。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-69094-5_4

R L Knobler, M Rodriguez, P W Lampert, M B Oldstone

{"title":"Virologic models of chronic relapsing demyelinating disease.","authors":"R L Knobler, M Rodriguez, P W Lampert, M B Oldstone","doi":"10.1007/978-3-642-69094-5_4","DOIUrl":"https://doi.org/10.1007/978-3-642-69094-5_4","url":null,"abstract":"The present report, compares two murine models of virus induced chronic relapsing demyelination. MHV-induced demyelination in the BALB/c mouse results from the direct virus mediated cytolysis of oligodendrocytes. Extensive remyelination by oligodendrocytes is noted. Recurrent demyelination occurs in small areas. Infectious virus persists and viral antigens are localized within oligodendrocytes and their processes. TMEV-induced demyelination in SJL/J mice is associated with perivascular inflammatory infiltrates and is diminished by immunosuppressive measures. Remyelination by oligodendrocytes is delayed and incomplete. Chronic demyelination is widespread and associated with perivascular inflammatory infiltrates. The virus persists and viral antigen is localized within oligodendrocytes. The findings indicate virus persistence in oligodendrocytes in both models. Demyelination follows the disintegration of infected oligodendrocytes. Virus replication in oligodendrocytes is responsible for cell lysis in the MHV model whereas immune mediated injury of infected oligodendrocytes is considered to play a role in the pathogenesis of demyelination in the TMEV model.","PeriodicalId":75397,"journal":{"name":"Acta neuropathologica. Supplementum","volume":"9 ","pages":"31-7"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17374627","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

Enzyme cytochemistry of the cerebral microvessel wall. 脑微血管壁的酶细胞化学。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-68970-3_3

G W Kreutzberg, L Tóth

引用次数: 21

Murine experimental allergic encephalomyelitis. 小鼠实验性过敏性脑脊髓炎。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-69094-5_5

D E McFarlin

引用次数: 4

Biochemical modulation of blood-brain barrier permeability. 血脑屏障通透性的生化调节。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-68970-3_5

A Gjedde, C Crone

{"title":"Biochemical modulation of blood-brain barrier permeability.","authors":"A Gjedde, C Crone","doi":"10.1007/978-3-642-68970-3_5","DOIUrl":"https://doi.org/10.1007/978-3-642-68970-3_5","url":null,"abstract":"Hydrophilic substrates necessary for brain function cross the capillary by facilitated diffusion. The facilitation has many features in common with enzyme-catalyzed reactions and is probably subserved by protein entities in the endothelial wall. The proteins act as receptors, recognizing substrate molecules, and as translocators, giving the molecules access to an aqueous path through the endothelium. These receptor-translocators can be saturated, and the transport is subject to competitive inhibition by substrate analogs. Thus, amino acids inhibit the transport of each other, and galactose can inhibit glucose transport in suckling rats. The proteins can be induced, as in the case of ketone transport in starvation, and repressed, as in the case of glucose transport in hyperglycemia. In rats with hyperglycemia for three weeks, the maximum glucose transport capacity of the blood-brain barrier decreased from 400 to 290 mumol/hg/min. An important result of the description is the understanding that rigid distinctions between the function of receptors, translocators, and enzymes is impossible. Understanding of the biochemical properties of facilitated diffusion may help explain a variety of symptoms in many 'inborn errors of metabolism'. This understanding has followed greater, recent insights into the general properties of the blood-brain barrier (45,46,47).","PeriodicalId":75397,"journal":{"name":"Acta neuropathologica. Supplementum","volume":"8 ","pages":"59-74"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17406324","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: 13

Revised pathophysiology on BBB damage: the edema as an ingeniously provided condition for cell motility and lesion repair. 修订血脑屏障损伤的病理生理学:水肿为细胞运动和损伤修复提供了巧妙的条件。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-68970-3_9

F Ikuta, Y Yoshida, E Ohama, K Oyanagi, S Takeda, K Yamazaki, K Watabe

{"title":"Revised pathophysiology on BBB damage: the edema as an ingeniously provided condition for cell motility and lesion repair.","authors":"F Ikuta, Y Yoshida, E Ohama, K Oyanagi, S Takeda, K Yamazaki, K Watabe","doi":"10.1007/978-3-642-68970-3_9","DOIUrl":"https://doi.org/10.1007/978-3-642-68970-3_9","url":null,"abstract":"Probably, the most important evidence concerning the breakdown of the BBB is a large inflow of hematogenous fluid into the extravascular spaces. Thus all parenchymal cell elements represent freely floating cells in this fluid medium called the edema fluid. These essential morphological alterations, such as extremely expanded extracellular space and freely floating cells within the fluid, were also observed in the developing normal fetal brain. Many neuroblasts were vigorously migrating in the fetal brain, as were the macrophages and reactive astrocytes in the edema fluid. Obviously, hematogenous cells and reactive astrocytes in the edematous lesion take part in its repair. Many astrocytes, GFAP positive, in the 3 or 4 day-old lesions, revealed mitosis. And in vitro, when we immersed these astrocytes in the protein and glucose rich medium, they demonstrated a remarkably changed morphology and were moved into the M and G1 phases, thus gaining the ability of cell motility. This was also true in the edema fluid. Brain edema is definitely a serious \"pathological\" condition. But it is also conceivable from a different biological aspect that as a result of BBB \"opening\", free extracellular space essential for cell motility and a source of their energy is ingeniously provided for these cells, and thus the lesion can be effectively repaired. The biological significance of the edema fluid was emphasized and stereotaxic morphology and cinematography, supporting the above evidence, have also been presented.","PeriodicalId":75397,"journal":{"name":"Acta neuropathologica. Supplementum","volume":"8 ","pages":"103-10"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17631604","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: 47

Etiology and pathogenesis of monophasic and relapsing inflammatory demyelination - human and experimental. 单纯性和复发性炎性脱髓鞘的病因和发病机制——人和实验。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-69094-5_3

H M Wisniewski, H Lassmann

引用次数: 12

Morphofunctional aspects of the normal and pathological blood-brain barrier. 正常和病理血脑屏障的形态功能方面。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-68970-3_1

J Cervós-Navarro, J Artigas, B J Mrsulja

引用次数: 43

Morphology of cerebral endothelium and astrocytes as determinants of the neuronal microenvironment. 脑内皮和星形胶质细胞形态作为神经元微环境的决定因素。

Acta neuropathologica. Supplementum Pub Date : 1983-01-01 DOI: 10.1007/978-3-642-68970-3_2

M W Brightman, K Zis, J Anders

{"title":"Morphology of cerebral endothelium and astrocytes as determinants of the neuronal microenvironment.","authors":"M W Brightman, K Zis, J Anders","doi":"10.1007/978-3-642-68970-3_2","DOIUrl":"https://doi.org/10.1007/978-3-642-68970-3_2","url":null,"abstract":"The morphological features of the blood-brain barrier to macro-molecules under normal and perturbed conditions are reviewed in the context of some recent investigations. The electric charge on molecules of horseradish peroxidase (HRP) affect its pinocytosis and intracellular fate which pertains to problems of distinguishing endocytosis from vesicular transport across endothelium. When the barrier is opened, the number of pits, vesicles and tubules increases. Such cerebral endothelium resembles normal endothelium of certain fish where numerous membrane invaginations do not signify vesicular or tubular transport. However, such transport has not been entirely ruled out in reactive endothelium. Another route of exudation during barrier opening may be via patent endothelial junctions, especially during intravascular infusion of hyperosmotic solutions. The permeability of the tight junctions, however, is not reflected unequivocally by its intramembranous structure. Although astrocytes do not provide a barrier to the extracellular flow of solutes, their ubiquity may enable them to modify the composition of perineuronal fluid. Their orthogonal arrays of intramembranous particles may be involved. The number of assemblies increases in astrocytes reacting to trauma and to the extracellular accumulation of lactate and CO2. The assemblies might thus participate in the transport of catabolites to and from extracellular fluid.","PeriodicalId":75397,"journal":{"name":"Acta neuropathologica. Supplementum","volume":"8 ","pages":"21-33"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17406322","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: 30