bluuebunny/crossref_metadata_2025_split huggingface dataset:
MYELIN OEDEMA, OPTIC NEUROPATHY AND RETINOPATHY IN EXPERIMENTALSTYPANDRA IMBRICATA TOXICOSIS
Authors: HUXTABLE C. R. , DORLING P. R. , SLATTER D. H. 
Published: May 2008

Huxtable C.R., Dorling P.R. & Slatter D.H. 1980 Neuropathology and Applied Neurobiology 6, 221–232Myelin oedema, optic neuropathy and retinopathy in experimental Stypandra imbricata toxicosisRats experimentally poisoned with the toxic plant Stypandra imbricata developed acute oedema of central and peripheral myelin and extensive axonal degeneration in the optic nerves. The oedema developed with vacuolation and splitting of myelin lamellae at the intraperiod line. Following recovery from acute intoxication, myelin oedema resolved after 6 to 12 weeks, but severe retinal degeneration and optic nerve atrophy remained. Morphological abnormalties in glial cells and axons were only found in the optic nerves. It was concluded that there is probably also a direct toxic effect on the axons of the optic nerve and the photoreceptor cells of the retina. The chemical nature of the toxin remains to be defined but the marked similarity of its toxic effects to those of hexachlorophene are noted.
PROCEEDINGS OF THE FIFTY‐EIGHTH MEETING OF THE BRITISH NEUROPATHOLOGICAL SOCIETY HELD AT THE NATIONAL HOSPITAL AND THE INSTITUTE OF NEUROLOGY, LONDON, 18–19 JANUARY 1980
Authors: TOMLINSON B. E. 
Published: May 2008

Allt G. & Ghabriel M.N. (introduced) (Middlesex Hospital Medical School, London WlP 6DB)Clifford‐Jones R.E. (introduced), Landon D.N. & McDonald W.I. (Institute of Neurology, London WC1N 3BG)Abrahams P.H. (introduced), Day A. (introduced) & Allt G. (The Middlesex Hospital Medical School, London W1P 6DPBruce M.E. & Dickinson A.G. (introduced) (ARC Animal Breeding Research Organisation, Edinburgh EH9 3JQ)Fraser H. & Bruce M.E. (ARC Animal Breeding Research Organisation, Edinburgh EH9 3JQ)Adams J.H., Graham D.I. (Department of Neuropathology, Institute of Neurological Sciences, Glasgow G51 4TF) & Gennarelli T.A. (introduced) (Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104)Hubbard B.M. & Anderson J.M. (Ninewells Hospital and Medical School, Dundee DD1 9SY)Averback P. (introduced) (Department of Pathology, University of Cambridge Cambridge CB2 1QP)Narang H.K. (Public Health Laboratory, Newcastle upon Tyne NE4 6BE)Sturrock R.R. (introduced) (Department of Anatomy, University of Dundee, Scotland)Jacobs J.M. & Duchen L.W. (Department of Neuropathology, Institute of Neurology London WC1N 3BG)Gomez S. (introduced) & Queiroz L.S. (introduced) (Institute of Neurology, London WC1N 3BG)Swash M., Schwartz M.S. (introduced) & Sar‐geant M.K. (introduced) (Department of Morbid Anatomy, The London Hospital, London El)Deane B.R. (introduced) & Lantos P.L. (The Middlesex Hospital Medical School, LondonCaine G. (introduced), Davis B.E. (introduced), Cox S. (introduced) & Weller R.O. (Department of Pathology (Neuropathology), University of Southampton S09 4XY)McCormick D. & Wallace I. (introduced) (Pathology Department, Queen's University, Belfast BT12 6BA)Scaravilli F., Teixeira F. (introduced) & Jacobs J.M. (Institute of Neurology, London, WC1N 3BG)Griffiths I.R., Duncan I.D., McCulloch M. (introduced) & Carmichael S. (introduced) (Department of Veterinary Surgery, University of Glasgow, G61 1QH)Blakemore W.F., Palmer A.C. & Patterson R.C. (introduced) (Department of Clinical Veterinary Medicine, Cambridge CB3 OES)Lewis P.D. & Carr J. (introduced) (Royal Postgraduate Medical School, London W12 OHS)Pratt O.E. (Institute of Psychiatry, London SE5 8AF)Tomkins C. (introduced), King R.H.M. & Thomas P.K. (Department of Neurological Science, Royal Free Hospital, London NW3 2QG)Woodhams P.L. (introduced) (MRC Developmental Neurobiology Unit, Institute of Neurology, London WC1N 2NS), Roberts G.W. (introduced) & Polak J.M. (Royal Postgraduate Medical School, London W12 OHS)Reid H. (Department of Pathology, University of Manchester M13 9PL)
THE MITOCHONDRIAL CONTENT OF ENDOTHELIAL CELLS AND THE BASEMENT MEMBRANE THICKNESS OF RAT BRAIN CAPILLARIES AFTER PORTOCAVAL ANASTOMOSIS
Authors: LAURSEN H. 
Published: May 2008

Laursen H. (1980) Neuropathology and Applied Neurobiology 6,375–386The mitochondrial content of endothelial cells and the basement membrane thickness of rat brain capillaries after portocaval anastomosisThe volume of mitochondria in brain capillary endothelium and the harmonic mean basement membrane thickness were estimated in rats after portocaval anastomosis for 10 days, 30 days and 10 weeks. The mitochondrial volume was from 5–73% to 7–64% of the endothelial volume. There was no difference between the control and experimental animals. The harmonic mean thickness of the basement membrane was calculated from orthogonal intercepts measured on a reciprocal logarithmic scale. This method leads to an approximately normal distribution of the measurements. The harmonic mean thickness was 57–8 nm in controls, 54–6 nm after 10 days, 63–2 nm after 30 days and 600 nm after 10 weeks portocaval anastomosis. The increase after 30 days was significantly different from the first two measurements. It is concluded that only a small increase in harmonic mean thickness of the basement membrane, and thereby an increase in diffusion resistance, have occurred after 30 days portocaval anastomosis.
THE DEVELOPMENT OF PERIVENTRICULAR LESIONS IN CHRONIC RELAPSING EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN GUINEA‐PIGS: A LIGHT AND SCANNING ELECTRON MICROSCOPIC STUDY
Authors: LASSMANN H. , KITZ K. , WISNIEWKSI H. M. 
Published: May 2008

Lassmann H., Kitz K. & Wiśniewski H.M. (1981) Neuropathology and Applied Neurobiology 7,1–11The development of periventricular lesions in chronic relapsing experimental allergic encephalomyelitis in guinea‐pigs: a light and scanning electron microscopic studyPeriventricular lesions in the centrum semiovale are the most frequent changes in the brain in chronic relapsing experimental encephalomyelitis in guinea‐pigs. They are generally distributed symmetrically at the lateral angle of the ventricular wall. The number of lesions and their size increases in anterior‐posterior direction. Typically periventricular lesions in the later chronic stages are similar to those in multiple sclerosis. Earlier lesions generally originate in the depth of the white matter and secondarily, by extension, reach the ventricular surface. Lesions developing at later stages after sensitization may also originate from the ventricular wall and extent into the centrum semiovale. In these latter, severe structural changes in the ventricular ependyma may generally be found. Increased intracranial pressure in these animals may be one of the possible mechanisms leading to the peculiar topographical distribution of the periventricular lesions.
NEUROFIBRILLARY PATHOLOGY AND PROTEIN SYNTHETIC CAPABILITY IN NERVE CELLS IN ALZHEIMER'S DISEASE
Authors: MANN D. M. A. , NEARY D. , YATES P. O. , LINCOLN J. , SNOWDEN J. S. , STANWORTH P. 
Published: May 2008

Mann D.M.A., Neary D., Yates, P.O., Lincoln J., Snowden J.S. & Stan‐worth P. (1981) Neuropathology and Applied Neurobiology 7, 37–47Neurofibrillary pathology and protein synthetic capability in nerve cells in Alzheimer's disease Nucleolar volume was measured in nerve cells of the temporal cortex in cases of Alzheimer's disease, obtained at both biopsy and autopsy. Measurements were made on those nerve cells containing neurofibrillary tangles and also on ones free of such changes. Results showed that nucleolar volume is significantly reduced, by at least 40%, in both tangle and non‐tangle bearing cells, in both biopsy and autopsy cases, when compared with corresponding values from appropriate control cases. Furthermore, in the autopsy cases, nerve cell nucleolar volume was reduced by a further 30% in tangle bearing cells compared to non‐tangle bearing neighbours. No such difference was noted in these cells in the biopsy cases. These findings imply that alterations in protein synthetic capability occur in nerve cells early in the course of Alzheimer's disease, and that this change is not, at least in these initial stages, related to accumulation of neurofibrillary material within the cell body, although later on such accumulation may result in added disruption of cell metabolism.
A SURVEY OF ETHYLNITROSOUREA‐INDUCED RAT GLIOMAS FOR THE PRESENCE OF TUMOUR REJECTION ANTIGENS EXPRESSED IN VIVO
Authors: SPENCE ALEX M. , PRIESTLEY GREGORY 
Published: May 2008

Spence A.M. & Priestley G. (1981) Neuropathology and Applied Neurobiology 7,63–75.A survey of ethylnitrosourea‐induced rat gliomas for the presence of tumour rejection antigens expressed in vivoTransplanted lines of seven F‐344 (Fischer) rat malignant gliomas induced transplacentally with ethylnitrosourea (ENU) were surveyed by in vivo im‐munoprotection assays for the presence of tumour rejection antigens. These gliomas were representative of commonplace histological types of human primary brain tumours and were analyzed in early transplantation passages. The classical tumour ligation method of immunizing animals was attempted with five glioma lines, but was found unusable in four of these because of a high incidence of local tumour recurrences and distant metastases. In most experiments the animals were immunized by repeated inoculations of heavily‐irradiated tumour cells. Two gliomas, a glioblastoma multiforme and a mixed astrocytoma‐ependymoma, demonstrated weak but statistically significant tumour rejection responses. Immunization with three other tumours, a mixed oligodendroglioma‐astrocytoma and two glioblastomas multiforme, led to enhanced outgrowth of the challenge cell inocula. Neither a rejection nor an enhancement response was observed in assays of the remaining two neoplasms, a glioblastoma multiforme and a mixed astrocytoma‐oligodendroglioma. Immunization with a 3‐methylcholanthrene‐induced urinary bladder carcinoma line, used as a control in assays of six gliomas, had no effect on the outgrowth of transplanted glioma cells. These results suggest that ENU‐induced malignant rat gliomas do not uniformly elicit strong tumour‐rejection responses in vivo.
THE DEVELOPMENT OF RAT DORSAL ROOT GANGLIA IN THREE EXPERIMENTAL MEDIA CONTAINING LANDRY‐GUILLAIN‐BARRÉ, ALCOHOLIC PERIPHERAL NEUROPATHY OR NORMAL ADULT SERA
Authors: ARMATI‐GULSON PATRICIA J. 
Published: May 2008

Armati‐Gulson P.J. (1981) Neuropathology and Applied Neurobiology 7, 351–363The development of rat dorsal root ganglia in three experimental media containing Landry‐Guillain‐Barré, alcoholic peripheral neuropathy or normal adult seraDevelopment of rat dorsal root ganglia in vitro mimics the development of rat dorsal root ganglia in vivo when grown in medium containing human cord serum. When serum from patients either in the acute phase of Landry‐Guillain‐Barré syndrome or with alcoholic peripheral neuropathy is substituted for human cord serum, maturation is inhibited. Development of fetal relationships occurs between the Schwann cells and axons and many axons become enclosed within the processes of a single Schwann cell. Formation of myelin does not occur. The substitution of normal adult blood for cord serum also inhibits maturation, but unlike development with neuropathic serum, the Schwann cells and axons do not become associated and myelination does not occur.
HEPATIC BETA GALACTOSIDASE AND FELINE GMI GANGLIOSIDOSIS
Authors: BARNES I. C. , KELLY D. F. , PENNOCK C. A. , RANDELL J. A. J. 
Published: May 2008

Barnes I.C., Kelly D.F., Pennock C.A. & Randell J.A.J. (1981) Neuropathology and Applied Neurobiology 7, 463–476Hepatic beta galactosidase and feline GMI gangliosidosisThis paper describes the clinical, morphological and biochemical features of three cats with a progressive neurological disorder. Clinical features were ataxia and progressive tremor. The morphological characteristics were those of a lysosomal storage disease affecting neurones of the central nervous system and autonomic ganglia; membranous cytoplasmic bodies were demonstrated by electron microscopy in cerebral neurones. Chemical analysis of brain from two of the cats revealed an increased content of total gangliosides, sialic acid and a specific increase in GMI ganglioside. Enzyme analysis of homogenates of leucocytes, spleen and brain showed less than 5% of normal 4‐methylumbelliferyl‐β galatosidase (4MU‐β gal) activity. In liver, activity was markedly reduced at pH values below 4.2, but there was considerable activity above this value. The properties of 4MU‐β gal in normal and diseased feline livers were investigated. Sephadex gel filtration of diseased liver homogenates showed an absence of two thermolabile ‘acid’ components, and reduced activity of a third thermostable ‘neutral’ component. The biochemical abnormalities found in the diseased cats are similar to those found in human juvenile GMI gangliosidosis (type 2).
ANNOTATION: THE CLASSIFICATION OF TUMOURS OF THE CENTRAL NERVOUS SYSTEM
Authors: BARNARD R. O. 
Published: May 2008

Barnard R.O. (1981) Neuropathology and Applied Neurobiology 8, 1–10 Annotation. The classification of tumours of the central nervous systemPresent day classification of CNS tumours is discussed in the light of the recent attempt by World Health Organization investigators to put forward a widely acceptable classification the use of which will facilitate communication between pathologists of different countries.
THE PATTERN OF RECOVERY OF AXONS IN THE NERVOUS SYSTEM OF RATS FOLLOWING 2,5‐HEXANEDIOL INTOXICATION: A QUESTION OF RHEOLOGY?
Authors: CAVANAGH J. B. 
Published: May 2008

Cavanagh J.B. (1982) Neuropathology and Applied Neurobiology 8, 19–34The pattern of recovery of axons in the nervous system of rats following 2,5‐hexanediol intoxication: a question of rheology?Rats have been dosed with 2, 5‐hexanediol for 48 days and then allowed to recover. The changes in the accumulations of neurofilamentous masses in various pathways in CNS and PNS have been followed by light microscopy over the subsequent 9 weeks. It was found that many CNS pathways allow the argyrophilic masses to pass to their terminals from whence they subsequently disappear, usually over 5–6 weeks. Little or no axonal degeneration is seen where this happens. The same occurs in many peripheral nerves, particularly cranial nerves. However, in many tracts in the spinal cord and in many axons in the longer peripheral nerves, filamentous masses remain and becomes associated with axon degeneration, and, in tracts, gliosis. The importance of paranodal constrictions at nodes of Ranvier which tend to be greater in larger diameter axons is emphasized as a likely mechanism for the axon degeneration which largely took place during the recovery period.
DEMYELINATION INDUCED IN MICE BY AVIRULENT SEMLIKI FOREST VIRUS. I. VIROLOGY AND EFFECTS ON OPTIC NERVE
Authors: ILLAVIA SHIRIN J. , WEBB H. E. , PATHAK SNEHLATA 
Published: May 2008

Illavia S.J., Webb H.E. & Pathak S. (1982) Neuropathology and Applied Neurobiology 8, 35–42Demyelination induced in mice by avirulent Semliki Forest virus. I. Virology and effects on optic nervewiss A2G mice were infected intraperitoneally with an avirulent strain of Semliki Forest virus. The virus titres in the optic nerves, retina and brain were estimated on post‐inoculation days 3 to 8. High titres of virus were obtained in the optic nerve, retina and brain. The optic nerves, retina and brain were studied by light microscopy up to post‐inoculation day 67. Electron microscope studies were carried out on the optic nerve on post‐inoculation days 11 and 14. Inflammatory, microcystic changes and demyelination seen in the optic nerve were similar to those found in the central nervous system.
DEMYELINATION INDUCED IN MICE BY AVIRULENT SEMLIKI FOREST VIRUS. II. AN ULTRASTRUCTURAL STUDY OF FOCAL DEMYELINATION IN THE BRAIN
Authors: KELLY W. R. , BLAKEMORE W. F. , JAGELMAN S. , WEBB H. E. 
Published: May 2008

Kelly W.R., Blakemore W.F., Jagelman S. & Webb H.E. (1982) Neuropathology and Applied Neurobiology 8, 43–53Demyelination induced in mice by avirulent Semliki Forest virus. II. An ultrastructural study of the focal demyelination in the brainFour‐week‐old mice were infected intraperitoneally with an avirulent strain A7(74) of Semliki Forest virus (SFV) and killed at 4, 10, 15, 21 and 29 days after inoculation. Focal demyelinating lesions were present by 10 days. These were usually accompanied by a mononuclear infiltrate which included lymphocytes possessing characteristic cytoplasmic projections. These latter extended deep into the cytoplasm of adjacent cells, which were usually astrocytes and macrophages. Other features of the focal lesions were expansion of the extracellular space and demyelination which appeared to be fragmentation or lysis rather than stripping of myelin by macrophages. Although healing occurred in some mice after 4 weeks, acute lesions were still found in others of the same age. It was concluded that the demyelination probably had an immunological basis, and interaction between elements of the immune system and glial cells was a factor which inhibited orderly remyelination of the relatively mild lesions resulting from this infection.
IMMUNOHISTOCHEMICAL STAINING OF SENILE PLAQUES
Authors: MANN D. M. A. , DAVIES J. S. , HAWKES J. , YATES P. O. 
Published: May 2008

Mann D.M.A., Davies J.S., Hawkes J. & Yates P.O. (1982) Neuropathology and Applied Neurobiology 8, 55–61Immunohistochemieal staining of senile plaquesImmunohistochemical staining of serum proteins, including immunoglobulins, was carried out on formalin‐fixed cerebral tissue from 24 autopsy cases (twenty dements, four controls) and fifteen biopsy cases (ten dements, five controls). Sixteen of the autopsy cases showed focal regions where there was staining of globulins and other serum proteins within senile plaque ‘cores’, nerve cell perikarya and astrocytes. This pattern of staining, generally, occurred either in relation to areas of cerebral infarction or in the neighbourhood of small arteries displaying arteriosclerotic changes. In tissue areas, distant from these vascular alterations, no staining occurred. Furthermore, none of the biopsy cases showed any such areas of staining. These findings indicate that the positive immunohistochemical reactions demonstrated within senile plaques (and other tissue components) are more likely to result from leakage of serum proteins, including immunoglobulins out of damaged vessels and into the brain parenchyma, rather than being indicative of the involvement of immunological mechanisms in the aetiology of plaques, as has been suggested by other workers.
HISTORICAL SURVEY THE CONCEPT OF A SENSORIMOTOR CORTEX: ITS LATER HISTORY DURING THE TWENTIETH CENTURY
Authors: MEYER ALFRED 
Published: May 2008

Meyer A. (1982) Neuropathology and Applied Neurobiology 8, 81–93Historical survey. The concept of a sensorimotor cortex: its later history during the twentieth centuryThis paper continues the historical review on the concept of a sensorimotor cortex into the twentieth century. Paul Flechsig was probably the first to accept this concept after the turn of the century. Like Munk, he believed in an almost reflex‐like unity between cortical sensory and motor function. With the help of his myelogenetic technique, Flechsig also demonstrated convincingly in the human brain that the two Rolandic convolutions receive a separate influx of thalamic afferents. Had this finding met with more attention, much experimental work by some of the distinguished later investigators might have proved to be unnecessary. Research has now reached a state when an early plausible explanation of the problem may be confidently expected.
CHANGES IN NERVOUS TISSUE IN BOVINE GENERALIZED GLYCOGENOSIS TYPE II
Authors: COOK R. D. , HOWELL J. McC. , DORLING P. R. , RICHARDS R. B. 
Published: May 2008

Cook R.D., Howell J. McC, Dorling P.R. & Richards R.B. (1981) Neuropathology and Applied Neurobiology 8, 95–107Changes in nervous tissue in bovine generalized glycogenosis type IIGeneralized Glycogenosis type II has been diagnosed in seven calves from a herd of cattle maintained at the Murdoch University Veterinary School Farm. The syndromes seen are equivalent to the infantile and childhood forms of the disease in humans. In the brain and spinal cord of the calves acid a‐glucosidase activity was depressed and glycogen deposition was markedly increased. Swelling, vacuolation and glycogen deposition was present in neurones of the central and autonomic nervous systems and retina, in glia and in Schwann cells and fibroblasts within peripheral nerves. The distribution was similar to that seen in human cases. The glycogen was both membrane bound and free within the cytoplasm. Changes similar to those seen in axonal dystrophy were present and some nerve fibres showed Wallerian degeneration. Evidence of nerve cell destruction and nerve cell loss were not seen and the predominant clinical signs were related to muscle weakness.
NEURONAL AND LYMPHOCYTIC POPULATIONS IN HUMAN TRIGEMINAL GANGLIA: IMPLICATIONS FOR AGEING AND FOR LATENT VIRUS
Authors: BALL M. J. , NUTTALL K. , WARREN K. G. 
Published: May 2008

Ball M. J., Nuttall K. & Warren K. G. (1982) Neuropathology and Applied Neurobiology 8, 177–187Neuronal and lymphocytic populations in human trigeminal ganglia: implications for ageing and for latent virusThe number of neurones and of lymphocytes was determined morphometrically in serial sections of trigeminal ganglia harvested at autopsy from 64 human subjects dying at ages 2 months to 81 years. The nerve cell population varied from 20159 to 156 702 with a mean of 80 638 /ganglion and was unaffected by increasing age. The degree of lymphocytic infiltration, which was prominent and ubiquitous, also did not correlate with the subjects' age. There was no significant correlation between neuronal and lymphocyte counts. The inflammatory cells present throughout life apparently are unassociated with any detrimental effect upon the sensory neurones, and may represent a histopathological marker either of reactivating herpes virus or of virus maintained in a latent state within the Gasserian ganglia of man.
THE MITOCHONDRIAL DISORDERS: PATHOGENESIS AND AETIOLOGICAL CLASSIFICATION
Authors: TASSIN S. , BRUCHER J. M. 
Published: May 2008

Tassin S. & Brucher J. M. 1982 Neuropathology and Applied Neurobiology 8, 251–263Annotation. The mitochondrial disorders: pathogenesis and aetiological classificationMitochondrial myopathies form a heterogeneous group of muscular diseases characterized by the presence of morphological mitochondrial abnormalities. These abnormalities are interpreted as the stereotyped morphological expression of a cellular energy deficiency. They represent a compensatory mechanism destined to increase ATP production. On this pathogenetic basis, an aetiological classification for the mitochondrial myopathies is proposed. The consequences of this hypothesis on the meaning of the morphological abnormalities, notably the changes in the amount of glycogen and lipids associated with mitochondrial alterations, are analysed.