bluuebunny/crossref_metadata_2025_split huggingface dataset:
MYELINATION OF THE MOUSE CORPUS CALLOSUM
Authors: STURROCK R. R. 
Published: May 2008

Sturrock R. R. (1980) Neuropathology and Applied Neurobiology 6, 415–420Myelination of the mouse corpus callosumMyelination has been studied in the corpus callosum of the mouse brain between birth and 240 days‐of‐age. Myelin sheaths were first seen at 11 days. The most rapid phase of myelination occurred between 14 and 45 days when 13–5% of axons were myelinated, but myelination continued at a reduced rate up to 240 days when 28% of axons were myelinated. The mean diameter of unmyelinated axons was more or less constant throughout the study with an overall mean diameter of 0–25 ± 0–01 μn. Similarly myelinated axon diameter showed little variation with age with a mean diameter of 0–46 ± 001 μn. This suggests that in the corpus callosum axons do not increase in size until they begin to myelinate.
PERSISTENT MULTIPLICATION OF AXON‐ASSOCIATED CELLS IN THE SPINAL ROOTS OF DYSTROPHIC MICE
Authors: PERKINS C. S. , BRAY G. M. , AGUAYO A. J. 
Published: May 2008

Perkins C. S., Bray G. M. & Aguayo A. J. 1980 Neuropathology and Applied Neurobiology 6, 83–91Persistent multiplication of axon‐associated cells in the spinal roots of dystrophic miceAxons which lack Schwann cells characterize the spinal roots of dystrophic mice. In these nerves, two types of cells are associated with large axons– typical Schwann cells which ensheath and myelinate individual axons and ‘uncommitted’ cells which closely contact some axons but do not unsheath them normally. Although neonatal Schwann cell multiplication in dystrophic spinal roots is less than normal, the ‘uncommitted’ cells continue to multiply in adult animals. Thus, these cells are presumably responsive to the mitogenic stimulus of axons, but are unable to extend radially and longitudinally to form a myelin sheath. This disorder of axon‐sheath cell interactions could be due to an intrinsic abnormality of Schwann cells or a failure of the mechanisms whereby axons induce Schwann cell differentiation.
A MORPHOLOGICAL LIFESPAN STUDY OF NEUROLIPOMASTOCYTES IN VARIOUS REGIONS OF THE MOUSE FOREBRAIN
Authors: STURROCK R. R. 
Published: May 2008

Sturrock R.R. 1980 Neuropathology and Applied Neurobiology 6, 211–219A morphological lifespan study of neurolipomastocytes in various regions of the mouse forebrainThe neostriatum, indusium griseum and anterior commissure of the mouse brain were examined by semithin light microscopy and electron microscopy in an attempt to identify and follow the development of the cells named neurolipomastocytes by Ibrahim et al. 1979. These cells were first seen at 5 dayspost natum in the indusium griseum and in the leptomeninges adjacent to it. Neurolipomastocytes were always associated with arterioles or venules almost invariably at the site of vessel branching. Their major feature was the presence of round osmiophilic granules. In older animals their cytoplasm contained large quantities of foamy vesicles. This foamy cytoplasm was restricted to neurolipomastocytes and was not a feature of ageing capillary pericytes which showed little morphological evidence of ageing apart from the occasional lipofuscin body.
SPONGIFORM POLIOENCEPHALOMYELOPATHY CAUSED BY A MURINE RETROVIRUS. II. ULTRASTRUCTURAL LOCALIZATION OF VIRUS REPLICATION AND SPONGIFORM CHANGES IN THE CENTRAL NERVOUS SYSTEM
Authors: SWARZ J. R. , BROOKS B. R. , JOHNSON R. T. 
Published: May 2008

Swarz J.R., Brooks B.R. & Johnson R.T. (1981) Neuropathology and Applied Neurobiology 7, 365–380Spongiform polioencephalomyelopathy caused by a murine retrovirus. II. Ultrastructural localization of virus replication and spongiform changes in the central nervous systemThe development of murine retrovirus induced spongiform polioencephalomyelopathy was studied sequentially by electron microscopy. During the initial 30 days, viral infection of the central nervous system, as evidenced by viral budding from membranes, was limited to endothelial cells and pericytes. Viral particles were observed in the lumen of blood vessels, extracellular spaces and astrocytic endfeet surrounding blood vessels, but no morphological evidence of productive infection was found in astrocytes or neurons during early development of vacuolation. The earliest lesions in the neuropil consisted of swelling of astroglia followed by vacuolation, initially in axons and dendrites and later in neuronal and astrocytic soma, where vacuoles appeared to arise from dilated cisternae of the Golgi apparatus. Vacuoles contained only amorphous debris and fragments of membranes. Virions budding aberrantly into vacuoles were seen only in mice surviving beyond 35 days. Numerous reactive astrocytes were observed, but inflammatory cells were absent. The ultrastructural changes were remarkably similar to those described in scrapie, Kuru, and Creutzfeldt‐Jakob disease.
IMMUNOCYTOCHEMICAL STUDY OF P0 GLYCOPROTEIN, P1 AND P2 BASIC PROTEINS, AND MYELIN‐ASSOCIATED GLYCOPROTEIN (MAG) IN LESIONS OF IDIOPATHIC POLYNEURITIS
Authors: SCHOBER R. , ITOYAMA Y. , STERNBERGER NANCY H. , TRAPP B. D. , RICHARDSON E. P. , ASBURY A. K. , QUARLES R. H. , WEBSTER H. DEF. 
Published: May 2008

Schober R., Itoyama Y., Sternberger N.H., Trapp B.D., Richardson E.P., Asbury A.K., Quarles R.H. & Webster H. deF. (1981) Neuropathology and Applied Neurobiology 7, 421–434Immunocytochemical study of P0 glycoprotein, P1 and P2 basic proteins, and myelin‐associated glycoprotein (MAG) in lesions of idiopathic polyneuritisTo investigate the mechanism of myelin breakdown in idiopathic polyneuritis, paraffin and Epon sections of lesions were immunostained with antisera to four proteins in myelin sheaths. Three of these (P0, P2, and BP) are constituents of compact myelin whereas myelin‐associated glycoprotein (MAG) is restricted to membranes near Schwann cell cytoplasm in periaxonal and paranodal regions and in Schmidt‐Lanterman clefts. In early lesions, there were focal abnormalities in P2, P0, and BP immunostaining of paranodal and intemodal myelin. No single protein was affected selectively and lesions occurred in fibres of all sizes, not just in larger fibres selectively stained by P2 antiserum. Early changes in MAG immunostaining occurred only in regions where myelin immunostaining also was abnormal. More severe, later changes in the distribution of P0, P2, BP and MAG were consistent with the sequence of myelinated fibre alterations seen in segmental demyelination and Wallerian degeneration. In regenerating fibres, MAG antiserum stained periaxonal regions intensely; thin regenerating myelin sheaths were stained by P0 and BP antisera, but not by P2 antiserum. The results show that myelin sheath changes are identified more easily in immunostained sections than in conventional histological preparations. Our data also suggest that in idiopathic neuritis, myelin sheaths are the primary target and that the breakdown of myelin and its proteins is not secondary to Schwann cell damage.
EOSINOPHILIC FASCIITIS: AN ULTRASTRUCTURAL AND IMMUNOHISTOCHEMICAL STUDY OF THE INTERMEDIATE FILAMENT PROTEIN SKELETIN IN REGENERATING MUSCLE FIBRES
Authors: THORNELL L.‐E. , BJELLE A. 
Published: May 2008

Thornell L.‐E. & Bjelle A. (1981) Neuropathology and Applied Neurobiology 7, 435–449Eosinophilic fasciitis: an ultrastructural and immunohistochemical study of the intermediate filament protein skeletin in regenerating muscle fibresIn a case of eosinophilic fasciitis with pronounced muscle involvement non‐specific ultrastructural signs of degeneration were observed in areas of perifascicular atrophy. By combined immunohistochemical and electron microscopical techniques intermediate skeletin filaments were demonstrated. These filaments, when found in combination with nuclei with large nucleoli and an abundance of polyribosomes are a sign of regeneration of muscle fibres. This finding is a useful indicator in assessing the prognosis and therapy of muscle involvement in eosinophilic fasciitis.
MUSCLE FIBRE SIZE AND SHAPE IN DUCHENNE MUSCULAR DYSTROPHY
Authors: WATKINS S. C. , CULLEN M. J. 
Published: May 2008

Watkins S.C. & Cullen M.J. (1982) Neuropathology and Applied Neurobiology 8, 11–17Muscle fibre size and shape in Duchenne muscular dystrophyA method for measuring fibre area and shape which obviates variabilities inherent in diameter measuring techniques was applied to dystrophic and normal human muscle. It was seen that the mean fibre area in patients with Duchenne muscular dystrophy (DMD) increases with age at a greater rate than that of the controls until approximately 5 years‐of‐age, when it decreases rapidly. This is due to an increasing population of small regenerating, regenerated or split fibres. The shape of fibres was expressed as a form factor and it was seen that the fibres measured from DMD biopsies were less regular in shape than the controls due to constraints placed on the normal growth of regenerating fibres by the proliferation of connective tissue.
CHRONIC RELAPSING EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN THE GUINEA‐PIG: IN‐VITRO ANALYSIS OF MENINGEAL INFLAMMATORY CELLS
Authors: ALLSOPP GRETA , TURK J. L. 
Published: May 2008

Allsopp G. & Turk J. L. (1982) Neuropathology and Applied Neurobiology 8, 63–70Chronic relapsing experimental allergic encephalomyelitis in the guinea‐pig: in‐vitro analysis of meningeal inflammatory cellsInflammatory cells from the meninges of guinea‐pigs with chronic relapsing experimental allergic encephalomyelitis (CREAE) have been isolated and compared to a similar cell population obtained from guinea‐pigs with acute EAE. A mean of 6.2 × 106 cells were recovered from the brains of animals with CREAE while a similar number of cells (8.0 × 106) was obtained from animals with acute EAE. Only 5.3% of the cells from animals with CREAE were found to be phagocytic in contrast with 28% of the cells obtained from animals with acute EAE. The meningeal inflammatory cells from guinea‐pigs with CREAE did not respond, in the lymphocyte transformation test, to specific antigens or to mitogen. Peritoneal exudate cells (PECs) from these animals did, however, proliferate in the presence of tuberculin and of mitogen, but not with the brain antigen myelin basic protein (MBP). In contrast, the meningeal inflammatory cells from animals with acute EAE did respond to mitogen and PECs from the same animals responded to both the specific antigens and to the mitogen. The meningeal inflammatory cells and PECs from the guinea‐pigs with CREAE did, however, behave in a similar manner to similar cell populations obtained from guinea‐pigs fully protected against clinical signs of acute EAE.
FACTORS WHICH AFFECT THE FUSION OF ALLOGENEIC MUSCLE PRECURSOR CELLS IN VIVO
Authors: WATT DIANA J. 
Published: May 2008

Watt D.J. (1981) Neuropathology and Applied Neurobiology 8, 135–147Factors which affect the fusion of allogeneic muscle precursor cells in vivokeletal muscle allografts in mice have been used to study the factors which promote the fusion in vivo of muscle precursor cells derived from different strains of mice. Tolerance of host mice to allogeneic donor tissues has been induced either by the injection of donor spleen cells into newborn recipients, or by the irradiation and reconstitution, with donor bone marrow cells, of the haemopoietic system of the thymectomized recipient. The isoenzymes of glucose‐6‐phosphate isomerase (GPI) have been used as markers to distinguish the contribution of host and donor tissues to these allografts. In 174 of 204 such grafts evidence of both host and donor tissues was found. In 57 grafts which yielded a ‘hybrid’ isoenzyme of GPI, it was inferred that host and donor muscle cells had fused to form mosaic fibres. The following factors appear to influence the fusion of muscle precursor cells: a the presence within grafts of adequate numbers of precursor cells of both the host and the donor strains; b the particular strain‐combinations used; c the immunological state of the host.
IDPN NEUROPATHY IN THE CAT: COEXISTENCE OF PROXIMAL AND DISTAL AXONAL SWELLINGS
Authors: GRIFFIN JOHN W. , GOLD BRUCE G. , CORK LINDA C. , PRICE DONALD L. , LOWNDES HERBERT E. 
Published: May 2008

Griffin J.W., Gold B.G., Cork L.C., Price D.L. & Lowndes H.E. 1982 Neuropathology and Applied Neurobiology 8, 351–36IDPN neuropathy in the cat: coexistence of proximal and distal axonal swellingsAdministration of β, β'‐iminodipropionitrile (IDPN) to rodents has previously been shown to produce neurofilament‐filled axonal swellings in the proximal regions of motor and sensory nerve fibers. Because of the distinctive distribution of these swellings, IDPN has been classed as a proximal axonopathy and thereby distinguished from other disorders in which similar axonal swellings occur in the distal parts of the axon (distal axonopathies). This report describes the pathology in the peripheral nerves of cats which received intermittent injections of IDPN and calls attention to two previously undescribed pathological changes. First, in addition to the typical proximal swellings associated with IDPN, these animals developed numerous axonal swellings within the distal branches of the sciatic nerve. Distal swellings were present as early as 23 days after initiation of intoxication, indicating that they formed locally (rather than developing in the proximal axon and undergoing transport into the distal regions). The second finding was Wallerian‐like degeneration within the affected nerve branches.These changes in the distal sciatic nerve and its branches closely resembled the pathology of the distal axonopathies produced by agents such as the neurotoxic hexacarbons and carbon disulfide. The pathological similarities suggest that IDPN may share with these agents pathogenetic mechanisms to an extent not previously suspected.
THE ORGANIZATION OF ASTROCYTES IN ORGANOTYPIC MOUSE SPINAL CORD CULTURE: AN ELECTRON MICROSCOPE STUDY
Authors: KUSAKA H. , HIRANO A. , BORNSTEIN M. B. , RAINE C. S. 
Published: May 2008

The organization of astrocytes in organotypic mouse spinal cord culture: an electron microscope studyThe organization of astrocytes in myelinated culture of mouse spinal cord tissue was analysed ultrastructurally and compared with the pattern in vivo. Astrocyte cell bodies and their processes, connected by punctate adhesions and gap junctions, formed a continuous layer around the entire explant. Throughout the parenchyma, thin astrocytic processes penetrated the neuropil, separated neurons, and invested some synaptic complexes. Others formed flattened sheets and contacted directly with the basal surface of ependymal cells. In the absence of mesenchymal elements, astrocytes in vitro occasionally possessed fragments of basal lamina on the surface of the explant and around minute intercellular spaces. Except for an incomplete basal lamina, these findings indicate that astrocytes in vitro are organized in a manner essentially identical to the situation in vivo.
SOME HISTOCHEMICAL OBSERVATIONS ON INVASIVE CELLS IN A MYOPATHY INDUCED IN RATS WITH 5–HYDROXYTRYPTAMINE
Authors: CHRISTIE K. N. , MODI B. V. 
Published: May 2008

Some histochemical observations on invasive cells in a myopathy induced in rats with 5‐hydroxytryptamineThe enzyme cytochemistry and proportion of mononuclear cells exclusively present within degenerating muscle fibres of the soleus of rats 24 h after a single intraperitoneal injection of 5‐hydroxytryptamine (5‐HT) (10 mg/kg) were studied. The following enzymes displayed strong cytochemical activities within these cells: non‐specific esterase (against naphthol AS‐D acetate and a‐naphthylacetate), aminopeptidase (against leucine‐4‐methoxy‐2‐naphthylamide) and dipeptidyl peptidase 11. A peroxidatic activity was also present, but was found to arise from cytochrome oxidase in phagocytosed muscle mitochondria. The aminopeptidase activity in the monocytic cells increased by roughly 50% between 6 and 24 h after 5‐HT administration. Dipeptidyl peptidase II was found, by the use of appropriate inhibitors, to be present in both mononuclear cells and muscle fibres and may be implicated in degrading the basal lamina of muscle fibres, thereby permitting access to the mononuclear cells. The morphological, enzyme histochemical and electron microscopical evidence suggest that the cells which invade muscle fibres in the early stages of a myopathy induced by 5‐HT in rats are actively phagocytosing, mature macrophages.
GLYCOGEN CONTENT AND FRUCTOSE‐1, 6‐BIPHOSPHATASE ACTIVITY IN METHIONINE SULFOXIMINE EPILEPTOGENIC MOUSE BRAIN AND LIVER AFTER PROTEIN SYNTHESIS INHIBITION
Authors: HEVOR T. K. , DELORME P. , GAYET J. 
Published: May 2008

Glycogen content and fructose‐1, 6‐biphosphatase activity in methionine sulfoximine epileptogenic mouse brain and liver after protein synthesis inhibitionMice given intraperitoneal injections of methionine sulfoximine (MSO) (100 mg/kg body weight) showed tonic‐clonic seizures 7 to 8h later. The protein synthesis inhibitors actinomycin D and cycloheximide, when combined with MSO delayed the onset of seizures. Methionine completely abolished the convulsions and metyrapone delayed them for some hours. Twenty‐four h after the administration of the convulsant, the activity of the gluconeogenic enzyme, fructose‐1, 6‐biphosphatase (FBPase), and the glycogen content were determined in different areas of the brain. MSO induced an increase in both FBPase activity and glycogen content. These effects were antagonized by the inhibitors of protein synthesis. Metyrapone partly inhibited MSO‐induced increases of FBPase activity and glycogen content whereas methionine completely abolished them. MSO decreased glycogen content in liver but had no effect on blood glucose level 24 h after its administration. These findings suggested that in MSO epileptogenic brain, glycogen accumulation may proceed from an enhanced gluconeogenesis.
EFFECTS OF PRENATAL EXPOSURE TO ETHANOL ON THE MATURATION OF THE PYRAMIDAL NEURONS IN THE CEREBRAL CORTEX OF THE GUINEA‐PIG: A QUANTITATIVE GOLGI STUDY
Authors: FABREGUES I. , FERRER I. , GAIRI J. M. , CAHUANA A. , GINER P. 
Published: May 2008

AbstractFabregues I., Ferrer I., Gairi J. M., Cahuana A. & Giner P. (1985) Neuropathology and Applied Neurobiology 11, 291–298Effects of prenatal exposure to ethanol on the maturation of the pyramidal neurons in the cerebral cortex of the guinea‐pig: a quantitative golgi studyThe effects of chronic ethanol consumption during gestation on the development of layer V pyramidal cells was studied quantitatively in the somatosensory cerebral cortex of the newborn guinea‐pig. The spread of the basilar dendritic arborizations and counts of dendritic spines on the apical dendrite of neurons that had been processed with the rapid Golgi method were compared with those found in age‐matched controls receiving an isocaloric diet without alcohol. There were significant differences in the number of primary basilar dendrites (P < 005) and dendritic ramifications at a distance of 25 μM from the soma (P < 0.01) between the alcohol‐exposed and control animals. There also were significant differences in the number of dendritic spines on the apical dendrite (P < 0.001). This experimental model further illustrates developmental anomalies in the cerebral cortex following prenatal ethanol exposure.
PATHOLOGY OF CREUTZFELDT‐JAKOB DISEASE ASSOCIATED WITH PITUITARY‐DERIVED HUMAN GROWTH HORMONE ADMINISTRATION
Authors: WELLER R. O. , STEART P. V. , POWELL‐JACKSON J. D. 
Published: May 2008

AbstractWeller R. O., Steart P. V. & Powell‐Jackson J. D. (1986) Neuropathology and Applied Neurobiology 12, 117–129Pathology of Creutzfeldt‐Jacob disease associated with pituitary‐derived human growth hormone administrationThis report describes the pathological features in the brain of a 22 year old woman who died with Creutzfeldt‐Jakob disease 81/2 years after completing a 4 year course of injections of human growth hormone derived from cadaver pituitaries. Spongiform change was seen in the frontal cortex. There was gliosis and neuronal loss throughout the frontal cortex, basal ganglia, thalamus, peri‐aqueductal grey matter and tectum of the mid brain, pontine nuclei and dorsal medulla but no evidence of inflammation. Extensive atrophy and gliosis of the cerebellar cortex was present with widespread loss of neurons from the internal granular layer but relative sparing of Purkinje cells. Gliosis and atrophy of the mammillary bodies and gliosis of the hypothalamus may have been related to the previous surgical excision of a craniopharyngioma at the age of 21/2 years. The pattern of changes presented is comparable to that in other cases of Creutzfeldt‐Jakob disease including those previously reported after human growth hormone administration.
SCRAPIE: HOW MUCH DO WE REALLY UNDERSTAND?
Authors: KIMBERLIN R. H. 
Published: May 2008

AbstractKimberlin R. H. (1986) Neuropathology and Applied Neurobiology 12, 131–147Scrapie: how much do we really understand?Biological studies have produced convincing evidence for different scrapie strains, some of which undergo mutation. This argues strongly in favour of the infectious scrapie agent having a genome. The length of incubation period is influenced by the strain of agent but is also under strict host control. In mice, this control is exerted by a gene called Sine which affects the overall rate of agent replication in the CNS. After peripheral infection, invasion of the CNS from lymphoreticular sites of agent replication is a key step in pathogenesis. Evidence from one scrapie model indicates spread of infection along autonomic nerves to the thoracic spinal cord and then to other parts of the CNS. Other studies have shown that infection can spread in neurons. There are close relationships between the presence of replicating agent and the development of vacuolation, and also of cerebral amyloid when it occurs. We can, therefore, begin to understand the patterns of lesion development in the brain in terms of the targeting of infection and its replication at certain sites. Structures known as SAF (Scrapie Associated Fibrils) have been discovered in extracts of scrapie brain (but not uninfected brain) and a glycoprotein (PrP 27–30: SAF protein) is a major constituent of purified SAF. The glycoprotein is coded by a single gene which is present in several species and expressed in uninfected brain. The normal protein seems to be modified in scrapie infected brain so that it accumulates as SAF. The modified protein may also be deposited as extracellular amyloid because there appear to be common epitopes between SAF and scrapie amyloid. The biochemical nature of the scrapie agent remains in doubt and the association between infectivity and purified SAF may arise fortuitously from the fact that scrapie agent is ‘sticky’.
CEREBROVASCULAR AMYLOIDOSIS IN SCRAPIE‐AFFECTED SHEEP
Authors: GILMOUR J. S. , BRUCE M. E. , MACKELLAR A. 
Published: May 2008

AbstractGilmour J. S., Bruce M. E. & MacKellar A. (1985) Neuropathology and Applied Neurobiology 11, 173–183Cerebrovascular Amyloidosis in scrapie‐affected sheepCerebrovascular amyloidosis (CA) was found in the cerebral and cerebellar cortices in 11 of 20 sheep, of six different breeds, with naturally‐occurring scrapie. The occurrence of the lesion did not appear to be influenced by the age of the sheep. This was not seen in 20 brains from age‐and breed‐matched sheep with other conditions. Furthermore, it was not found in 20 sheep experimentally infected with scrapie by sub‐cutaneous inoculation, or in 22 sheep with natural scrapie in a closed breeding group, but it was present at low frequency in a production flock, closed apart from the introduction of rams. It is concluded that this lesion is strongly associated with sheep scrapie disease, but that its occurrence varies between different groups of scrapie sheep. A major source of this variation is likely to be the strain of the agent, though other factors may be involved as has been shown for cerebral amyloidosis in experimental mouse scrapie.