bluuebunny/crossref_metadata_2025_split huggingface dataset:
A HISTOCHEMICAL STUDY OF FIBRE TYPES IN RAT EXTRAOCULAR MUSCLES
Authors: VITA G. F. , MASTAGLIA F. L. , JOHNSON M. A. 
Published: May 2008

Vita G.F., Mastaglia F.L. & Johnson M.A. (1980) Neuropathology and Applied Neurobiology 6, 449–463A histochemical study of fibre types in rat extraocular musclesThe histochemical fibre type composition of the rat superior and medial rectus (SR and MR), superior oblique (SO) and levator palpebrae superioris (LPS) muscles was studied using the myofibrillar ATPase and NADH‐tetrazo‐lium reductase (NADH‐TR) techniques. In the SR, MR and SO a peripheral zone containing small fibres and a central zone containing both small and large fibres could be identified. Four fibre types were present in the central zone of these muscles and were categorised as Type 1, Type 2a, Type 2a', and Type 2b. Four fibre types were also identified in the peripheral zone–Type 1, Type 2a, Type 2a' and Type 2c. In the LPS Type 1, Type 2, Type 2a', Type 2b and Type 2c fibres were evenly intermixed without a zonal arrangement. The Type 1, Type 2a, Type 2b and Type 2c fibres correspond to accepted fibre types in the rat limb muscles. The Type 2a' and Type 2a' fibres were differentiated from the Type 2a fibres on the basis of size and pattern and intensity of staining with the NADH‐TR technique. The Type 2c fibres, which possess both acid‐stable and alkali‐stable myofibrillar ATPase, are considered to represent intermediate fibres in the process of transformation from Type 2 to Type 1, rather than fibres with a dual innervation as has been suggested in the past. The implications of these histochemical findings are considered in relationship to the physiology of individual motor units and to the function of the extraocular muscles.
VARIATION WITH AGE IN THE VOLUMES OF GREY AND WHITE MATTER IN THE CEREBRAL HEMISPHERES OF MAN: MEASUREMENTS WITH AN IMAGE ANALYSER
Authors: MILLER A. K. H. , ALSTON R. L. , CORSELLIS J. A. N. 
Published: May 2008

Miller A. K. H., Alston R. L. & Corsellis J. A. N. 1980 Neuropathology and Applied Neurology 6, 119–132Variation with age in the volumes of grey and white matter in the cerebral hemispheres of man: measurements with an image analyserThe total volumes and relative quantities of grey and white matter have been measured in sixty‐five normal male and sixty‐five normal female cerebral hemispheres. Fixed hemisphere volume was found to fall linearly at 35% per decade for men from 641 ml at the age of 20 to 463 ml at the age of 100. For women the decrease was 1–9% per decade from 531 ml at 20 years to 462 ml at 100 years. After correction for the effects of fixation and for the secular increase in brain size, it was concluded that mean hemisphere volume remained roughly constant between the ages of 20 and 50 years (558 ml for men, 474 ml for women). After the age of 50 the mean volume in both sexes fell at about 2% per decade. The ratio of the volumes of grey to white matter was the same for the two sexes at all ages. Its mean value was 1–3 at the age of 20, falling to 11 at the age of 50, then rising steadily to over 1–5 at 100 years. It is impossible in practice to correct these measurements for the effects of fixation or secular change. Fourteen hemispheres from thirteen elderly female dements were also measured. The total volume was 18% lower than for an age‐matched group of normals, but the ratio of grey to white matter was identical.
LYSOSOMAL HYDROLASES IN LONG TERM CULTURES OF HUMAN GLIOMAS: TOTAL ENZYME ACTIVITIES AND RATE OF EXTRACELLULAR ACCUMULATION
Authors: MCCORMICK D. , MAUNOURY R. , DELPECH B. 
Published: May 2008

McCormick D., Manoury R. & Delpech B. 1980 Neuropathology and Applied Neurobiology 6, 133–141Lysosomal hydrolases in long term cultures of human gliomas: total enzyme activities and rate of extracellular accumulationA number of investigations have suggested a fundamental role for lysosomal enzymes in growth control of normal cells and in the loss of growth control which occurs in neoplasia and in cell cultures transformed by oncogenic viruses. In this investigation total enzyme activities and rates of extracellular accumulation of enzyme were measured in long term cultures of gliomas and normal human astrocytes. Marked differences were found between the cultures with regard to total enzyme activity. Exocytosis rates of the enzymes also showed differences, with one group of tumours demonstrating low or intermediate rates and another smaller group with high rates. There was no positive correlation between the enzyme profile of the cultures and their tumorigenicity in nude mice.
FURTHER ULTRASTRUCTURAL OBSERVATIONS OF VIRUS MORPHOGENESIS AND MYELIN PATHOLOGY IN JHM VIRUS ENCEPHALOMYELITIS
Authors: FLEURY H. J. A. , SHEPPARD RACHEL D. , BORNSTEIN M. B. , RAINE C. S. 
Published: May 2008

Fleury H.J.A., Sheppard R.D., Bornstein M.B. & Raine C.S. 1980 Neuropathology and Applied Neurobiology 6,165–179Further ultrastructural observations of virus morphogenesis and myelin pathology in JHM virus encephalomyelitisGroups of 3, 17, and 28‐day‐old Swiss mice were inoculated intracerebrally with JHM virus, the neurotropic strain of mouse hepatitis virus (MHV), and studied serially by virologic and morphologic techniques. Beginning 2–5 days post‐inoculation, all groups of infected mice developed CNS lesions which were destructive in the 3‐day‐old group and demyelinative in the 17 and 28‐day‐old animals. Infectious virus could be isolated from the brain, spinal cord, and liver. Electron microscopy demonstrated the virus to be pantropic in the CNS with virions occurring within ependymal cells, astrocytes, neurons, oligodendrocytes, endothelial cells, and cell of haematogenous origin. Giant cell formation was a constant feature. In regions of demyelination, oligodendrocytes exhibited a propensity to proliferative aberrant membrane. Myelin degradation was accompanied by membrane vesiculation and by the stripping action of macrophages. The lesions were not due to CNS elements in the inoculum since in animals inoculated with normal CNS suspensions from appropriate age groups failed to show lesions. The morphogenesis of JHM virions was followed ultrastructurally as was the formation of syncytia in the different cell types. In addition to delineating virus morphogenesis and myelin pathology, the results underscore the pantropic nature of JHM virus in the CNS, the systemic nature of the infection, and that oligodendrocytes were the principal targets.
CYCLOLEUCINE ENCEPHALOPATHY
Authors: GRECO CLAUDIA M. , POWELL H. C. , GARRETT R. S. , LAMPERT P. W. 
Published: May 2008

Greco C. M., Powell H. C, Garrett R. S. & Lampert P. W. (1980) Neuropathology and Applied Neurobiology 6,349–360Cycloleucine encephalopathyCycloleucine, a non‐metabolizable amino acid analogue produces status spongiosus in cerebral white matter of rats and mice as well as a distinctive lesion of astrocytes. Its mechanisms of action include competition with natural amino acids from transport across the blood‐brain barrier leading to inhibition of entry of circulating amino acids into brain, interference with ribosomal RNA maturation, and blockage of transmethylation reactions, including the conversion of homocystine to methionine. Cycloleucine also affects the kidney, producing aminoaciduria. Electron microscopy of cerebral white matter reveals spongiform changes of myelin sheaths caused by separation of myelin lamellae along intraperiod lines and accumulation of whorls of filaments in astrocytes. The myelinopathy is dose related and its toxicity is cumulative due to its long half‐life in animals. The findings are discussed with reference to other spongiform myelinopathies, including status spongiosus observed in homocystinuria and other aminoacidurias.
PERIPHERAL NEUROPATHY IN MOUSE HEREDITARY DIABETES MELLITUS. II. ULTRASTRUCTURAL CORRELATES OF DEGENERATIVE AND REGENERATIVE CHANGES
Authors: CARSON K. A. , BOSSEN E. H. , HANKER J. S. 
Published: May 2008

Carson K.A., Bossen E.H. & Hanker J.S. (1980) Neuropathology and Applied Neurobiology 6,361–374Peripheral neuropathy in mouse hereditary diabetes mellitus. II. Ultrastructural correlates of degenerative and regenerative changesThe fine structural changes in some peripheral nerves and sensory ganglia from mice (C57BL/K & J, db/db) with an hereditary diabetic syndrome, similar to human maturity‐onset diabetes mellitus, were studied during development of the mild peripheral neuropathy. The abnormalities observed included axonal degeneration, disruption of myelin, accumulation of electron‐dense material in axons, satellite cells and Schwann cells, increased frequency of it granules of Reich in Schwann cells, enlarged mitochondria, and proliferated and thickened Schwann cell basal laminae. Distal hind limb nerves were most affected. Sensory ganglion neurons were normal except for occasional chro‐matolytic cells, so that nerve cell loss was not present in this peripheral neuropathy. Morphological indications of Schwann cell hyperplasia, hypertrophy, and axonal sprouting supported the contention that a continuous cycle of axonal degeneration and regeneration was occurring. The ultrastructural changes and accumulation of electron‐opaque, lipid material suggested that a defect in lipid metabolism, secondary to the diabetic condition, could be an important factor in the peripheral neuropathy in the diabetic mouse.
STUDY OF AXONAL DYSTROPHY. II. DYSTROPHY AND ATROPHY OF THE PRESYNAPTIC BOUTONS: A DUAL PATHOLOGY
Authors: FUJISAWA K. , SHIRAKI H. 
Published: May 2008

Fujisawa K. & Shiraki H. (1980) Neuropathology and Applied Neurobiology 6, 387–398Study of axonal dystrophy. II. Dystrophy and atrophy of the presynaptic boutons: a dual pathologyIn succession to the previous quantitative work, a qualitative study has been carried out on the nature of a dual pathology affecting presynaptic boutons in the posterior tract nuclei of ageing rats. Based on the morphology of dystrophic boutons in early stage, it is concluded that the initial and therefore essential characteristic of dystrophic process is an abnormal increase of normal axonal components within the presynaptic boutons, and that various abnormal substructures of spheroids hitherto reported in the literature are probably the result of their secondary metamorphosis. The dystrophic process within the posterior tract nuclei is a selective one, involving presynaptic boutons and preterminal axons only of the posterior tract fibres. Comparison of the frequency of early dystrophic boutons and of fully grown‐up spheroids indicates that a small percentage of boutons deriving from posterior tract fibres become dystrophic and of these dystrophic boutons only a small percentage again continue to develop unto large spheroids, throughout lifespan of the animals. On the other hand, in search of a morphological counterpart for the age‐related decrease of volume ratio of presynaptic boutons to the neuropil, some dubious atrophic changes were also found in presynaptic boutons, which could have been easily missed from observation if studied qualitatively alone. Accordingly, no less numerous boutons other than dystrophic ones are supposed to atrophy ‘independently’ and to disappear ‘silently’ during the same period. The dystrophic and the atrophic changes involve different boutons (of different or the same terminal axons) within the same gray matter. This dual pathology of boutons needs further elucidation of its neurocytopathological as well as neurobiological background in the future.
TOPOGRAPHY OF NEUROFIBRILLARY TANGLES AND GRANULOVACUOLES IN HIPPOCAMPI OF PATIENTS WITH DOWN'S SYNDROME: QUANTITATIVE COMPARISON WITH NORMAL AGEING AND ALZHEIMER'S DISEASE
Authors: BALL M. J. , NUTTALL K. 
Published: May 2008

Ball M. J. & Nuttall, K. (1981) Neuropathology and Applied Neurobiology 7, 13–20Topography of neurofibrillary tangles and granulovacuoles in hippocampi of patients with Down's syndrome: quantitative comparison with normal ageing and Alzheimer's diseaseAn XY pen recorder linked potentiometrically to a sampling stage microscope permitted the plotting of topographic ‘scattergrams’ to determine the precise cytoarchitectonic localization of neurofibrillary tangles and granulovacuo‐lar degeneration in hippocampal neurones of Down's syndrome adult brains. The area (and hence volume) of six cortical ‘zones’ surveyed was measured with a digitizer and programmable calculator. In decreasing magnitude of affliction, the rank order for neurofibrillary tangles was: entorhinal > subiculum > H1 > endplate > H2 > presubiculum. That for granulovacuolar change was: subiculum > H1 > H2 > endplate > entorhinal > presubiculum. These striking regional predispositions suggest that a common neurotransmitter deficit may underlie the local selectivity of such lesions in Down's syndrome brains; and the predilections' marked similarities to ranking orders, already noted both in normal aged subjects and especially in senile dements of the Alzheimer type, enhance the importance of the Down's syndrome neuraxis as a key to the puzzle of Alzheimer's dementia.
THE SUPRAHABENULAR RECESS IN THE RAT: A QUANTITATIVE STUDY OF CILIATED CELLS, SUPRAEPENDYMAL CELLS AND SOME SPECIFIC FEATURES OF SUPRAEPENDYMAL FIBRES
Authors: TULSI R. S. , DREOSTI I. E. 
Published: May 2008

Tulsi R.S. & Dreosti I.E. (1981) Neuropathology and Applied Neurobiology 7, 21–36The suprahabenular recess in the rat: a quantitative study of ciliated cells, supraependymal cells and some specific features ofsupraependy‐mal fibresUsing light microscopy, scanning and transmission electron microscopy, an extensive quantitative analysis of ciliated ependymal cells, supraependymal cells and supraependymal fibres in the suprahabenular recess of twenty‐two adult Wistar rats was carried out. In addition, six animals were used to determine the origin of supraependymal fibres and their relationship to ependyma. The findings were as follows: ciliated cells–mean 3–32 ± 0–26 per 1000 μm2 (range 0–10); supraependymal cells–5–91 ± 1–37 per recess (range 2–16). Average number of cilia per cell in different animals ranged from 31 to 33. Sex did not influence the density of ciliated ependyma or supraependymal cells. Evidence was obtained that some supraependymal fibres are closely associated with aberrant commissural fibres. The supraependymal fibres enter the suprahabenular recess and form gap junctions, and other types of junctions, with subjacent ependyma.
THE DEVELOPMENT OF BRAIN TUMOURS PRODUCED IN RATS BY THE INTRACEREBRAL INJECTION OF NEOPLASTIC GLIAL CELLS: A FINE STRUCTURAL STUDY*
Authors: DAVAKI PANAYOTA , LANTOS P. L. 
Published: May 2008

Davaki P. & Lantos P.L. (1981) Neuropathology and Applied Neurobiology 7,49–61The development of brain tumours produced in rats by the intracerebral injection of neoplastic glial cells: a fine structural studyTumours were produced by the intracerebral injection of a clone of glial cells derived from a glioma induced transplacentally by N‐ethyl‐N‐nitrosourea in a BD‐IX rat. The injection of 5 times 105 cells into the left frontal lobe resulted in a 100% incidence of tumours. To follow the development of the neoplasms, the brains were studied from 1 day to 4 weeks after injection. The tumours maintained their glial characters throughout, but their features changed with time. Ultrastructurally, they were pleomorphic: the proportion of fibrillary astrocytes, undifferentiated and intermediate cell types varied according to tumour size. When smaller (1 and 2 weeks), fibrillary astrocytes predominated, but when larger (3 and 4 weeks), the number of undifferentiated astrocytes considerably increased. A reproducible brain tumour model with a short latency has thus been established and characterized, which may be of use for chemo‐ and radiotherapeutic studies and for examining the mechanisms of cerebral oedema.
A LIGHT AND ELECTRON MICROSCOPIC HISTOCHEMICAL STUDY ON THE MECHANISM OF DFP‐INDUCED ACUTE AND SUBACUTE MYOPATHY
Authors: TÓTH L. , KARCSÚ SAROLTA , POBERAI MÁRIA , SÁVAY GY. 
Published: May 2008

Tóth L., Karcsú S., Poberai M. & Sávay Gy. (1981) Neuropathology and Applied Neurobiology 7, 399–410A light and electron microscopic histochemical study on the mechanism of DFP‐induced acute and subacute myopathyThe histochemical changes occuring in association with the development of acute and subacute myopathy have been studied in the rat diaphragm 30 min‐48 h after a single i.p. injection of 1–82 mg/kg of the irreversible cholinesterase inhibitor organophosphate, diisopropylfluorophosphate (DFP). In addition to a considerable inhibition of the AChE activity of the motor end‐plates, accumulation of ionic Ca2+ and an increase in neutral protease activity in the subjunctional sarcoplasm have been demonstrated. A temporal and causal relationship has been established between the histochemical changes and the development of the ultrastructural signs of myopathy.
COMPARATIVE MORPHOLOGY OF MEASLES VIRUS AND PARAMYXOVIRUS‐LIKE TUBULES IN MULTIPLE SCLEROSIS USING RUTHENIUM RED STAIN
Authors: NARANG H. K. 
Published: May 2008

Narang H.K. (1981) Neuropathology and Applied Neurobiology 7, 411–420 Comparative morphology of measles virus and paramyxovirus‐like tubules in multiple sclerosis using ruthenium red stainMorphology of intracytoplasmic nucleocapsid measles virus from mouse brain and tissue culture was studied with the use of ruthenium red by tilting and high resolution electron microscopy and compared with the paramyxovirus‐like tubules found in multiple sclerosis (MS). Both in vivo and in vitro the measles nucleo‐protein profiles were surrounded by ‘fuzzy’ material which could be resolved in a pentagon shape and this stained specifically with ruthenium red. The tubules found in MS appeared not to have a ‘fuzzy’ coat and also did not stain with ruthenium red. The main difference observed between infected tissue culture cells and mouse brain was that in the latter no alignment of measles nucleoprotein was observed under the cell membrane and no budding particles were seen. The virus could not be passed to mice or tissue culture from the infected mouse brain.
A QUANTITATIVE STUDY OF AGE‐RELATED CHANGES IN THE VASCULAR ARCHITECTURE OF THE RAT CEREBRAL CORTEX
Authors: WILKINSON J. H. , HOPEWELL J. W. , REINHOLD H. S. 
Published: May 2008

Wilkinson J.H., Hopewell J.W. & Reinhold H.S. (1981) Neuropathology and Applied Neurobiology 7, 451–462A quantitative study of age‐related changes in the vascular architecture of the rat cerebral cortexA quantitative study of age related changes in the vascular architecture of the rat cerebral cortex is described. A special vessel‐filling technique, which allowed the simultaneous fixation of the vasculature, aided the identification of the vessels in histological sections. Vascular parameters, which included the total number of vessel fragments, a blood volume and a vessel wall‐surface area index were obtained using a Quantimet 720 shape‐analysing computer. In animals aged 13–83 weeks, there was an increase in the above vascular parameters which could mainly be attributed to an increase in the number of vessels with a diameter > 8 μm. In very old rats, aged 124 weeks, the vascularity of the cerebral cortex was severely reduced. These changes, which are very similar to those reported in the ageing human cerebral cortex, may be explained by either direct or indirect effects on the cerebral vasculature. Possible mechanisms are discussed in relation to similar changes observed in the cerebral vasculature after several different insults.
THE EFFECT OF PROTECTING GUINEA‐PIGS AGAINST EAE ON THE MENINGEAL INFLAMMATORY CELL‐INFILTRATE
Authors: ALLSOPP GRETA , PARKER DARIEN , TURK J. L. 
Published: May 2008

Allsopp G., Parker D. & Turk J.L. (1981) Neuropathology and Applied Neurobiology 7, 477–487The effect of protecting guinea‐pigs against EAE on the meningeal inflammatory cell infiltrateGuinea‐pigs were found to be fully protected from the clinical signs of EAE when they were given spinal cord in FIA either 3, 7 or 14 days before immunization with spinal cord in FCA. If the animals were protected by the recruitment of suppressor cells then cyclophosphamide (CY) might break this protection. CY at 300 mg/kg) and 20 mg/kg was given either before the protective inoculum to try to eliminate suppressor cell precursors or before immunization to eliminate the suppressor cells themselves. No clinical signs of EAE developed in any of these groups of guinea‐pigs. It was found, however, that large numbers of meningeal inflammatory cells could be isolated from the brains of guinea‐pigs protected from EAE when the protective inoculum was given only 1 week before immunization. These cell numbers were further significantly increased by giving CY in addition to the protective inoculum. The meningeal inflammatory cells and peritoneal exudate cells (PECs) from guinea‐pigs protected against EAE were compared to those isolated from animals with acute EAE. These cells from guinea‐pigs with acute EAE responded, in the lymphocyte transformation test, to the mitogen. The PECs also responded to the brain antigen, myelin basic protein (MBP) and to tuberculin (PPD). The meningeal inflammatory cells did not respond to either antigen. The PECs from animals protected against EAE responded to mitogen and PPD, but not to MBP, but the meningeal inflammatory cells did not respond to antigen or mitogen. The percentage of T lymphocytes in the meningeal inflammatory infiltrates of protected and unprotected guinea‐pigs was similar, but that of phagocytic cells was significantly depressed in the inflammatory infiltrates of animals protected against EAE.
EFFECTS OF AGE ON CEREBRAL AMYLOID PLAQUES IN MURINE SCRAPIE
Authors: BRUCE MOIRA E. , FRASER H. 
Published: May 2008

Bruce M.E. & Fraser H. (1982) Neuropathology and Applied Neurobiology 8, 71–74Effects of age on cerebral amyloid plaques in murine scrapieThe frequency of cerebral amyloid plaques in murine scrapie was not influenced by the age of the mouse at injection in a study using several combinations of agent strain and mouse strain. In addition amyloid plaques were not seen in a series of extremely old uninfected mice.
A QUANTITATIVE STUDY OF VASCULAR PERMEABILITY TO HORSERADISH PEROXIDASE, AND THE SUBSEQUENT FATE OF THE TRACER, IN RAT BRAINS AFTER PORTOCAVAL ANASTOMOSIS
Authors: SUMNER B. E. H. 
Published: May 2008

Sumner B. E. H. (1982) Neuropathology and Applied Neurobiology 8, 117–133A quantitative study of vascular permeability to horseradish peroxidase, and the subsequent fate of the tracer, in rat brains after portocaval anastomosisLabelled blood vessel segments, exudation patches, and pericytic granular cells were counted in sections of rat brain which had been fixed and tested with DAB from 3 min to 24 h after intravenous injection of horseradish peroxidase (HRP).In normal rats, 3 min after injection, only 1% of the total blood vessel segments had walls penetrated by HRP, but in rats 14 days after portocaval anastomosis (PCA) 44% of the total segments had labelled walls, a frequency of 3033 permeable segments/mm3 of brain. In normal rats no exudation patches were found, but after PCA there were seven patches/mm3 of brain. Maximum vascular wall labelling and maximum exudation occurred in the cerebellum and medulla of the operated rats. Hardly any pericytic cells were labelled 3 min after injection.In operated rats 2 h after injection of HRP, labelled vascular walls were fewer and exudation had disappeared, but 204 pericytic cells/mm3 of brain contained HRP‐labelled granules, i.e. 60% of the total pericytes. Highest numbers were found in the most anterior section of the brain sample. Later after injection these numbers declined.It is suggested that most of the protein which leaked into the brain after PCA returned to the blood whence it came, but that some was captured and hydrolysed by the granular pericytes.