bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE CELLULAR ORIGIN OF LYSOSOMAL ENZYMES IN THE PLAQUE IN MULTIPLE SCLEROSIS.
Authors: ALLEN INGRID V. , GLOVER G. , McKEOWN STEPHANIE R. , McCORMICK D. 
Published: May 2008

The cellular origin of lysosomal enzymes in the plaque in multiple sclerosis. II. A histochemical study with combined demonstration of myelin and acid phosphatase.Existing techniques have been adapted and it has been possible to demonstrate acid phosphatase (APP) and myelin, lipid or astrocytic fibres in the same histological section. In normal controls APP was demonstrated in neurons, astrocytes, ependy‐ma including choroid plexus epithelium and in pericytes, but not in oligodendro‐cytes. In multiple sclerosis (MS), APP positive cells were found in the plaque, plaque edge and macroscopically normal white matter. Contrary to some previous reports, not only macrophages, but also astrocytes in the MS plaque were found to be APP positive, although the distribution of enzyme in these cells was predominantly diffuse, unlike the particulate distribution in normal astrocytes and other APP positive cells: the significance of this finding is discussed. It is concluded that astrocytes and macrophages are the main source of the elevated levels of APP found biochemically in MS and that in old plaques astrocytes make the major contribution.
TELLURIUM‐INDUCED NEUROPATHY: CORRELATIVE PHYSIOLOGICAL, MORPHOLOGICAL AND ELECTRON MICROPROBE STUDIES
Authors: DUCKETT S. , SAID G. , STRELETZ L. G. , WHITE R. G. , GALLE P. 
Published: May 2008

Tellurium‐induced neuropathy: correlative physiological, morphological and electron microprobe studiesElemental tellurium (Te) was included in the normal diet of 15–day‐old rats and every day thereafter for 35 days. Within 24 hours a segmental demyelination was seen in the sciatic nerve. On the 2nd day, Te was localized in the cytoplasm of the Schwann cells. On the 3rd day paralysis of the hind legs appeared which lasted 7–10 days. The paralysis then disappeared and demyelination ceased, although the rats were still ingesting Te. After one week there was also slight demyelination in the brachial plexus. Motor nerve conduction velocities were reduced below the normal control range, but only after the rats had taken Te for at least 7 days. This peripheral neuropathy can only be induced in the rat by Te ingestion between the 15th and 35th days of post‐natal life, not before or after this period of time.
THE FINE STRUCTURE OF THE CNS IN MULTIPLE SCLEROSIS.
Authors: KIRK J. 
Published: May 2008

The fine structure of the CNS in multiple sclerosis. II. Vesicular demyelina‐tion in an acute caseTubular vesicular and net‐like dissolution of myelin sheaths associated with complete demyelination and preservation of axons, is described in the brain, obtained within 4 h of death, from a patient who died with acute multiple sclerosis (MS). It was rare, being found in only three out of twenty‐three blocks examined, and was seen mainly in the partially demyelinated margin of an active plaque in the white matter. The possibility that post‐mortem autolytic changes or fixation artefact might have accounted for the appearances is considered, but is thought unlikely. The findings, though not specific would be expected if current theories invoking myelin‐directed ‘autoimmune’ mechanisms in MS pathogenesis are correct. However, other myelin‐directed mechanisms cannot be excluded on the basis of this evidence alone.
LATE RADIATION DAMAGE TO THE CENTRAL NERVOUS SYSTEM: A RADIOBIOLOGICAL INTERPRETATION
Authors: HOPEWELL J. W. 
Published: May 2008

Annotation. Late radiation damage to the central nervous system: a radiobiological interpretationThe evidence in support of the two opposing views as to the pathogenesis of late radiation damage to the central nervous system after therapeutic doses of radiation are briefly reviewed. Analysis of the radiation dose levels used by various investigators holding opposing views as to Pathogenesis of CNS lesions they reported, suggests that both groups of protagonists were in part correct. Both vascular and glial changes are important in the development of late radiation damage to the nervous system; the preponderance of one or the other type of cell damage depends upon the radiation dose. Vascular effects occur at lower dose levels but after a longer latent period than effects mediated through damage to neuroglia. Current radiobiological concepts and their possible importance in establishing the radiosensitivity of the central nervous system are discussed. The origins of both vascular and neuroglial cell mediated changes are discussed in terms of the reproductive loss of radiation damaged cells. This view is supported by some recent experimental findings. The radiobiological basis of some recently investigated treatment modalities aimed at improving the control of intracranial gliomata by radiotherapy are also considered.
MORPHOMETRIC STUDIES OF RAT GLIAL CELL ULTRASTRUCTURE AFTER UREASE‐INDUCED HYPERAMMONAEMIA
Authors: LAURSEN H. , DIEMER N. H. 
Published: May 2008

Morphometric studies of rat glial cell ultrastructure after urease‐induced hyperammonaemiaThe ultrastructure of astrocytes and oligodendrocytes was investigated in hyper‐ammonaemic rats injected daily with urease for 4 days. Glial cells were randomly photographed and magnified × 28 000. Cell and nuclear sizes were estimated by planimetry. and mitochondrial size and density were measured by image analysis. After 4 days of hyperammonaemia the astrocyte cytoplasmic area was increased by 46%. Mitochondrial area was increased by 20%, but after correction for cytoplasmic oedema the number and size of mitochondria were not significantly increased. The nuclear and cytoplasmic areas of oligodendrocytes were unchanged. The mitochondria of oligodendrocytes were small in the hyperammonaemic group and so was their percentage area to cytoplasmic area, but their numbers were unchanged. It, was concluded that hyperammonaemia induces astrocyte oedema and increases the astrocyte mitochondrial content. These findings support the assumption that the astrocytes are the active cells in the brain metabolism of ammonia. The decrease in oligodendrocyte mitochondrial content could be considered a point against an active function of oligodendrocyte mitochondria in ammonia metabolism in hyperammonaemia.
UPTAKE AND RETROGRADE AXONAL TRANSPORT OF HORSERADISH PEROXIDASE IN NORMAL AND AXOTOMIZED MOTOR NEURONS DURING POSTNATAL DEVELOPMENT
Authors: OLSSON T. , KRISTENSSON K. 
Published: May 2008

Olsson T. & Kristensson K. (1979) Neuropathology and Applied Neurobiology5, 377–387Abstract Uptake and retrograde axonal transport of horseradish peroxidase in normal and axotomized motor neurons during postnatal developmentThe axonal uptake and somatopetal transport of horseradish peroxidase (HRP) was studied during early postnatal development of facial neurons in mice and rats. HRP injected systemically or locally into the muscles of the vibrissae, diffused into the region of the immature neuromuscular junction and was incorporated into vesicles in the axon terminals on the first and third postnatal days, at a time when synaptic vesicles were already present. HRP later was found in the nerve cell bodies of the facial nucleus in the brain stem indicating a somatopetal transport of the tracer in axons. The response of facial neurons to nerve transection changed from rapid neuronal death to prolonged survival between the 6th and 10th postnatal day. HRP was transferred to nerve cell bodies after topical application to the proximal stump of transected facial nerves in rats 3 days‐of‐age. In the perikaryon it was localized to vesicles and vacuoles with no signs of leakage into the cytoplasm. In the light of our findings different hypotheses for the mechanism of the neuronal death in the immature animals are discussed.
EXPERIMENTAL OBSTRUCTIVE HYDROCEPHALUS IN THE RAT: A SCANNING ELECTRON MICROSCOPIC STUDY
Authors: COLLINS PATRICIA 
Published: May 2008

Experimental obstructive hydrocephalus in the rat: a scanning electron microscopic studyHydrocephalus was induced in 12‐day old rats by the cisternal infusion of a concentrated kaolin suspension. The animals were killed at day 20 and the ependymal lining of all the ventricles prepared for scanning electron microscopy. The dilation of the ventricles was moderate to gross in all cases. The ependyma of the lateral ventricles was similar in both control and experimental animals. Ependymal damage was present in six out of the twelve hydrocephalic rats. Two had fibres visible on the ependymal surface. Four had tears covered with small round cells, believed to be responsible for the repair of the ependyma. The third ventricle, cerebral aqueduct and fourth ventricle enlarged by incorporating folds of ependyma, present in control animals, into the ventricular walls. The circumventricular organs present in the third and fourth ventricles were not damaged by the dilation of the ventricles, even in severe hydrocephalus.
FOETAL BRAIN DEVELOPMENT IN THE SHEEP
Authors: McINTOSH G. H. , BAGHURST KATRINE I. , POTTER B. J. , HETZEL B. S. 
Published: May 2008

Abstracts McIntosh G.H., Baghurst K.I., Potter B.J.& HetzelB.S. (1979) Neuropathology and Applied Neurobiology5, 103–114Foetal brain development in the sheepThe pattern of normal foetal brain development has been described for the Merino sheep. Controlled flock matings were used and foetuses removed by hysterotomy at 40, 54, 67, 81, 90, 95, 109, 121, and 150 days of gestation. Lambs at 7 days after birth and adults were also studied. The CNS was dissected, separated and weighed as four segments—cerebral hemispheres, brain stem, cerebellum and spinal cord. Determinations of DNA, RNA, protein, cholesterol and water content were subsequently carried out on each segment. Brain weight increased from 0.264 g (40 days) to 52.74 g at 150 days. The ratio to body weight decreased from 6.7% (40 days) to 1.5% (150 days). DNA increased more rapidly from 40 to 90 days in the cerebral hemispheres and brain stem than in the cerebellum and spinal cord and this increase preceded the main increase in weight. Increases in cholesterol and decreases in water content were also more marked in the cerebral hemispheres and brain stem. Increase in brain weight occurred in two phases, one up to 90 days followed by a more rapid and larger increase after 90 days which continued to birth. These two phases appear to reflect an increase in neuroblast multiplication followed by neuroglial multiplication and myelination respectively. At birth, brain weight had reached 50% of adult size, the cerebral hemispheres 52% of adult size, the cerebellum 40% and spinal cord 40%. The relative maturity of the brain at birth justifies the classification of the sheep as a prenatal brain developer.
THE EFFECTS OF POSTNATAL LEAD EXPOSURE ON Purkinje cell DENDRITIC DEVELOPMENT IN THE RAT
Authors: McCONNELL P. , BERRY M. 
Published: May 2008

Abstracts McConnell P. & Berry M. (1979) Neuropathology and Applied Neurobiology5, 115–132The effects of postnatal lead exposure on Purkinje cell dendritic development in the ratRat pups, suckled by mothers maintained after parturition on a diet containing 4% lead acetate, were killed at 30 days and their cerebella examined. The blood lead was greatly increased in these animals (258.20 26.72 μg/100 ml) as compared with controls (4.75 ± 0.75 pμ/100 ml) and their mean body weight was reduced by 28%. Cerebellar weight, however, remained unchanged. Histologically the vermis showed vacuolation of the white matter and an increase in the size of Purkinje cell bodies. The total number of Purkinje and granule cells and their densities were unchanged except in animals with encephalopathy when these parameters were reduced. Network analysis of the dendritic trees of Purkinje cells indicated a 34.8% reduction in total dendritic length, due to reduction in total segment number and in the length of distal segments. Dendritic density and the frequency of trichotomous branching were unchanged by the experimental treatment. The density of dendritic spines over the periphery of the network was normal. The topology of the dendritic trees of Purkinje cells was abnormal in that branching patterns deviated from the normal pattern generated by random terminal growth. These results suggest that lead causes changes in Purkinje cell metabolism which reduce the rate of dendritic growth and cause abnormal branching. It remains to be determined whether these are direct effects or secondary to the vascular changes known to occur in the cerebellum during lead intoxication.
VASOACTIVE INTESTINAL POLYPEPTIDE IN THE PITUITARY PARS NERVOSA
Authors: NOORDEN SUSAN VAN , POLAK JULIA M. , BLOOM S. R. , BRYANT M. G. 
Published: May 2008

Abstracts Van Noorden S., Polak J.M., Bloom S.R. & Bryant M.G. (1979) Neuropathology and Applied Neurobiology 5, 149–153Vasoactive intestinal polypeptide in the pituitary pars nervosaVasoactive intestinal polypeptide (VIP) is a widely distributed neuropeptide which has recently been found in the hypothalamus and in hypothalamo‐hypophyseal portal blood. We have examined the pituitary of several mammalian species for the presence of VIP by immunocytochemistry and radioimmunoassay and report here that the pars nervosa contains a considerable quantity of VIP (100–250 fmol/ mg) which, in the dog, can be shown to be present in nerve fibres. It is possible that neurohypophyseal VIP may be a local releasing agent for vasopressin.
MULTIPLE SCLEROSIS: A QUANTITATIVE AND QUALITATIVE STUDY OF IMMUNOGLOBULIN‐CONTAINING CELLS IN THE CENTRAL NERVOUS SYSTEM
Authors: ESIRI MARGARET M. 
Published: May 2008

Multiple sclerosis: a quantitive and qualitative study of immunoglobu‐lin‐containing cells in the central nervous systemAutopsy material from the brains and spinal cords of twenty‐three patients with multiple sclerosis was examined with the immunoperoxidase (PAP) method to compare the distribution of immunoglobulin (Ig)‐containing cells in demyelinated plaques and normally myelinated tissue. Ig‐containing cells were much more numerous within plaques than outside them and were more common in recent than in old plaques. Most of the heavy chain present was IgG with small amounts also of IgA. More cells were demonstrated to contain light chains than heavy chains. It is suggested on the basis of the pattern of distribution of Ig‐containing cells that a stimulus to B‐cell proliferation and maturation resides within plaques.
FURTHER OBSERVATIONS ON PARTICULATE STRUCTURES IN SCRAPIE AFFECTED BRAIN
Authors: NARANG H. K. , CHANDLER R. L. , ANGER H. S. 
Published: May 2008

Further observations on particulate structures in scrapie affected brainA search procedure at the ultrastructural level revealed characteristic particulate structures in mice of two further laboratory stocks experimentally inoculated with scrapie. The structures represent a specific change related to scrapie disease; their relationship to the scrapie agent is discussed.
THE ASSOCIATION OF HYDROCEPHALUS AND ARNOLD‐CHIARI MALFORMATION WITH SPINA BIFIDA IN THE FETUS
Authors: BELL JEANNE E. , GORDON A. , MALONEY A. F. J. 
Published: May 2008

The association of hydrocephalus and Arnold‐Chiari malformation with spina bifida in the fetus.Twenty‐one fetuses with spina bifida and twenty apparently normal fetuses of between 14–23 weeks gestation were examined for the presence of hydrocephalus and Arnold‐Chiari malformation. Sacral, lumbo‐sacral, lumbar, thoraco‐lumbo‐sacral and thoraco‐lumbar lesions were found. Some were closed, some were open. The amount of neural tissue at the site of the lesion was very variable. In three cases, diastematomyelia was found. The heads of spina bifida fetuses were not enlarged. Hydrocephalus was found in eleven of them and the Arnold‐Chiari malformation in twelve. In nine fetuses the abnormalities co‐existed. Hydrocephalic brains showed depression of the tentorium, abnormalities in the corpus callosum and absence of the lateral fissure. The more cephalad and extensive the spinal lesion, the more likely it was to be accompanied by brain abnormalities. Isolated sacral defects were not associated either with hydrocephalus or with the Arnold‐Chiari malformation. Pathological changes in the brain occurred in the presence of both open and closed spinal lesions and were apparently unrelated to fetal age. No evidence was found as to the sequence in which these brain abnormalities appeared.
A COMPARATIVE QUANTITATIVE AND MORPHOLOGICAL STUDY OF AGEING IN THE MOUSE NEOSTRIATUM, INDUSIUM GRISEUM AND ANTERIOR COMMISSURE
Authors: STURROCK R. R. 
Published: May 2008

A comparative quantitive and morphological study of ageing in the mouse neostriatum, indusium griseum and anterior commissure R. R. SturrockThe glia: neuron ratio increased between 5 and 9 months in the neostriatum and indusium griseum and thereafter remained constant until 18 months‐of‐age. Between 18 and 22 months the glia:neuron ratio did not change in the neostriatum, but increased significantly in the indusium griseum due to a combination of a loss of neurons and an increase in glia. The 6–9 month rise was mainly due to an increase in the number of astrocytes in both regions although there was some increase in oligodendrocytes at this time. The increase in glia in the indusium griseum between 18 and 22 months was due to an increase in both astrocytes and microglia. In the anterior commissure, the pattern of glial change was almost identical in both limbs with oligodendrocytes increasing between 6 and 9 months then decreasing between 9 and 18 months. Astrocytes decreased between 6 and 18 months. Between 18 and 22 months oligodendrocytes and microglia both increased in number. There was a decrease in glioblasts in both limbs with age. The age at which lipofuscin appeared was different in each type of glial cell and in each region studied. Microglia contained lipofuscin at 6 months in all regions. Astrocytes first contained lipofuscin at 6 months in the neostriatum, at 9 months in the indusium griseum and at 15 months in the anterior commissure. Oligodendrocytes first contained lipofuscin at 12 months in the anterior commissure, at 18 months in the indusium griseum and at 18 months in the neostriatum. Ependy‐mal cells adjacent to the neostriatum contained lipofuscin and osmiophilic lipid at 6 months but by 12 months the latter had become much less osmiophilic. Foamy pericytes were found in all regions: from 6 months in the neostriatum; from 9 months in the indusium griseum and from 15 months in the anterior commissure. These contained lipid droplets, were only found adjacent to arterioles or venules, and were likely Ibrahim's neurolipomastocytes. The response of glia to ageing varies in different regions of grey matter, but is similar in two different regions of white matter. These age changes may be related to different levels of metabolic activity of glia in different parts of the brain.
ANAPLASTIC EPENDYMOMA OF THE SPINAL CORD
Authors: MØRK S. J. , RISBERG G. , KROGNESS K. 
Published: May 2008

Mork S.J., Risberg G. & Krogness K. (1980) Neuropathology and Applied Neurobiology 6, 307–311Anaplastic ependymoma of the spinal cordAn intraspinal ependymoma with cytological signs of malignancy and unusual further development was diagnosed in a 12‐year‐old boy. Only partial removal was possible and postoperative Co60 treatment was given. Ascending tumour growth was evident clinically in the spinal canal, and 3 months later signs of intracranial extension of the tumour developed. The patient died 6½ years after the onset. Autopsy showed an anaplastic ependymoma with extensive intraspinal and intracranial growth. No other neoplasms were found. There was extraspinal extension of tumour into the laminectomy scar, but no metastases.
ULTRASTRUCTURAL CHANGES OF MUSCLES DURING ATTACKS OF ADYNAMIA EPISODICA HEREDITARIA
Authors: WALTER G. F. , AUBOCK L. 
Published: May 2008

Walter G.F. & Auböck L. (1980) Neuropathology and Applied Neurobiology 6, 313–317Case report. Ultrastructural changes of muscles during attacks of adynamia episodica hereditariaIn an ultrastuctural study of biopsies of quadriceps femoris muscle from two patients during attacks of adynamia episodica hereditaria. Marked pinocy‐tosis along the sarcolemma and an interfibrillary oedema were observed, together with a ‘bamboo‐like’ shape of the myofibrils. Other non‐specific abnormalities were also found.
ANNOTATION: RECENT BIOCHEMICAL AND IMMUNOLOGICAL OBSERVATIONS IN MULTIPLE SCLEROSIS
Authors: CUZNER M. L. 
Published: May 2008

Cuzner M.L. (1980) Neuropathology and Applied Neurobiology 6, 405–414Annotation. Recent biochemical and immunological observations in multiple sclerosisAs there is evidence of early biochemical and histological changes in the normal‐appearing white matter in MS, which appear to be independent of or precede demyelination, the formation of plaques may be incidental to a more primary lesion. The finding of persistently increased levels of IgG in the CSF of patients with MS points to an ongoing immune reaction in the CNS, possibly against an infective agent; but virus‐specific antibodies account for only a small proportion of the IgG in the CSF. Furthermore, in vitro assays of T cell function suggest that there may be a regulator T cell defect in MS. Salk and colleagues (1980) have postulated that MS may be a disorder, attributable to multiple inducing agents, which is potentiated through deregulation of lymphocyte function.
THE EFFECT OF SUB‐DURAL NERVE TISSUE TRANSPLANTATION ON THE SPINAL CORD OF THE RAT
Authors: BLAKEMORE W. F. 
Published: May 2008

Blakemore W.F. (1980) Neuropathology and Applied Neurobiology 6, 433–447The effect of sub‐dural nerve transplantation on the spinal cord of the ratThe effects of sub‐dural transplantation of autologous sciatic nerve on the dorsal columns of the rat was investigated. Combinations of the following procedures were used: 1 local X‐irradiation with 4000 rad to suppress inherent remyelination activity; 2 small areas of primary demyelination induced by injection of lysolecithin or 6‐aminonicotinamide; 3 transplantation of untreated or freeze‐killed nerve, either teased or unteased. The lesions formed were examined for suppression of remyelination by local cells, remyelination by transplanted Schwann cells, deleterious effects of transplantation on the spinal cord, and the presence of suprapial nerve fibres. The following conclusions were drawn: 1 that 4000 rad of local X‐irradiation suppresses inherent remyelination by oligodendroglia and local Schwann cells even when transplanted freeze‐killed sciatic nerve is present; 2 that demyelinated axons can be remyelinated by Schwann cells from transplanted untreated nerve; 3 that the placing of peripheral nerve over the dorsal columns induces primary demyelination in both irradiated and non‐irradiated animals; 4 that the placing of peripheral nerve over demyelinated locally X‐irradiated spinal cord can lead to fibrous tissue invasion of the spinal cord and partial demyelination of the lateral and ventral columns; and 5 that transplantation of viable peripheral nerve onto the dorsal columns induces the formation of suprapial nerve fibres, which increase in number if demyelination or axonal damage is present in the dorsal columns. It seems probable, therefore, that elements in the peripheral nerve may exert trophic effects on dorsal column nerve fibres.