bluuebunny/crossref_metadata_2025_split huggingface dataset:
ANNOTATION: NERVE CELL PROTEIN METABOLISM AND DEGENERATIVE DISEASE
Authors: MANN D. M. A. 
Published: May 2008

Mann D.M.A. (1982) Neuropathology and Applied Neurobiology 8, 161–176Annotation. Nerve cell protein metabolism and degenerative diseaseThe mechanisms and organelles through which control of protein synthesis within healthy nerve cells is governed are discussed, and the ways in which expression of these biochemical pathways can be related to cell morphology are described. The volumes of the nucleus and nucleolus, and the amount of RNA within the cell body, are all interrelated and seem to be set at genetically predetermined levels which normally match the neurones basal needs for replacement proteins in respect of the size of its' projection field. However, in situations of (induced) hyperactivity or cell damage, or in others where disease may lower nerve cell activity, the protein requirements change, and it is noted that these morphological features also alter in a direction appropriate to the need for greater or lesser amounts of protein. How these alterations in protein synthesis can provide information as to both the basic pathology, or even the pathogenesis, of degenerative disease of the nervous system is illustrated by reference to Alzheimer's disease and motor neurone disease.
THE EFFECTS OF CASTRATION ON THE SUBEPENDYMAL PLATE OF THE RAT
Authors: HOPKINS B. , HOPEWELL J. W. 
Published: May 2008

Hopkins B. & Hopewell J. W. (1982) Neuropathology and Applied Neurobiology 8, 189–195The effects of castration on the subependymal plate of the ratEarlier studies have shown that glial tumours, produced by the intracerebral implantation of chemical carcinogens, originate from the subependymal plate. In the present study the effects of castration on cell number and proliferation in the subependymal region has been investigated as such treatment has been shown to reduce the incidence of gliomata produced by an implanted carcinogen.An age‐related reduction in mitotic activity and nuclear density was found in the subependymal plate. Castration produced a consistent reduction in mitotic activity but the nuclear density was unchanged.The results suggest that the reduction in tumour incidence produced by castration cannot be explained simply on the basis of reduced proliferation in the population believed to be at risk and that other, as yet, undefined factors must be involved.In addition, it appeared that there was also no simple relationship between brain growth and cell proliferation in the subependymal plate.
THE DEVELOPMENT OF RETINITIS IN MICE WITH NONFATAL HERPES SIMPLEX ENCEPHALITIS
Authors: ANDERSON JANICE R. , FIELD H. J. 
Published: May 2008

Anderson J.R. & Field H.J. 1982 Neuropathology and Applied Neurobiology 8, 277–287The development of retinitis in mice with non‐fatal herpes simplex encephalitisA mutant strain of herpes simplex virus, type 1 (HSVl), selected for high resistance to acyclovir (ACV) was inoculated intracerebrally into mice. The mice survived with no obvious neurological signs but developed cataracts within 4–8 weeks of inoculation. Histological examination revealed only a mild encephalitis, but around 7 days after injection a florid, necrotizing, viral retinitis developed. There was almost simultaneous involvement of both eyes. Inflammatory cell infiltration and early myelin degeneration along the course of the optic nerve suggested cell to cell spread of virus to the retinal nerve cell bodies. Although virus could only be recovered from the eye in the early stages of retinitis, destruction of the neural retina was frequently complete and subsequently the optic nerves showed Wallerian type degeneration. Visible cataracts were a late complication, but changes in the lens were initiated during the phase of acute retinitis. This experiment shows that antiviral agents may induce mutant forms which cannot reproduce classical disease, but are capable of permissive infection in unexpected sites. Herpes retinitis is occasionally recognized as a complication of fatal HSV encephalitis in man. Theoretically, more effective treatment of encephalitis with nucleoside analogues, for example with acyclovir, could reveal the development of retinitis in survivors.
THE EARLY EVOLUTION OF NEUROFILAMENTOUS ACCUMULATIONS DUE TO 2,5‐HEXANEDIOL IN THE OPTIC PATHWAYS OF THE RAT
Authors: JONES H. B. , CAVANAGH J. B. 
Published: May 2008

Jones H.B. & Cavanagh J.B. 1982 Neuropathology and Applied Neurobiology 8, 289–301The early evolution of neurofilamentous accumulations due to 2,5‐hexanediol in the optic pathways of the ratRats were given 2,5‐hexanediol in their water for more than 5 weeks. The changes in the optic pathways were studied both qualitatively and quantitatively. Increase in 10‐nm filaments within axons was noticeable from 10 days onwards in the superior colliculus and in the brachium of the superior colliculus. From then onwards there was a steady increase in the number of affected axons, and their gross enlargement occurred. The proportion of affected fibres in the brachia was in fact few, but all fibres were of retinotectal origin. Less than half of those in the superior colliculus that were swollen were of retinal origin. Measurement of axon diameter versus myelin sheath thickness showed gross relative thinning of the latter. Axon degeneration did not occur but there was increasing ultrastructral evidence of impairment of transport of organelles both centrifugally and centripetally as the filamentous masses accumulated.
THE PATHOKINETICS OF ACRYLAMIDE INTOXICATION: A REASSESSMENT OF THE PROBLEM
Authors: CAVANAGH J. B. 
Published: May 2008

Cavanagh J.B. 1982 Neuropathology and Applied Neurobiology 8, 315–336The pathokinetics of acrylamide intoxication: a reassessment of the problemAcrylamide was given intraperitoneal^ to rats (30 mg/kg/day, five times/week) for 3 weeks, and the nervous and muscle tissues were examined by conventional methods over 5 weeks. Three striking cellular changes were observed. 1 Scattered degeneration of many Purkinje cells from 5 days onwards. 2 Widespread swelling and argyrophilia of nerve terminals from 10 days in both PNS and CNS. Motor and sensory endings were equally affected in all muscles examined. Synaptic and preterminal swelling also occurred in spinal cord, brain stem, and in certain cerebellar terminals. Degeneration occasionally followed this change, particularly in sensory nerve fibres, but not necessarily. 3 Chromatolysis in spinal ganglion cells and occasionally in anterior horn cells from 7 days onwards before the onset of axonal degeneration. This unique sequence of events is discussed in the light of the metabolic and other changes described by earlier authors.
ETHIDIUM BROMIDE INDUCED DEMYELINATION IN THE SPINAL CORD OF THE CAT
Authors: BLAKEMORE W. F. 
Published: May 2008

Blakemore W.F.1982 Neuropathology and Applied Neurobiology 8, 365–375Ethidium bromide induced demyelination in the spinal cord of the catSmall volumes of ethidium bromide were injected into the dorsal column of the spinal cord of cats. Oligodendrocytes and astrocytes showed morphological evidence of intoxication by ethidium bromide from 2 days after injection. However, apart from around the point of injection and the needle tract, demyelination did not occur until between 8 and 14 days. Both oligodendrocytes and astrocytes were absent from the demyelinated area at 14 days and all but a small number of demyelinated axons were remyelinated by Schwann cells. These cells first appeared in the lesion at 10 days, but axon association and myelination did not occur until 16 days. This model of experimental demyelination indicates once again that Schwann cell invasion of demyelinated areas in the CNS occurs if both oligodendrocytes and astrocytes are destroyed. None of the lesions in the present investigation were in continuity with root entry zones, indicating that this location is not a prerequisite for Schwann cell invasion of the CNS.
BASAL GANGLIA DEGENERATION, MYELIN ALTERATIONS, AND ENZYME INHIBITION INDUCED IN MICE BY THE PLANT TOXIN 3‐NITROPROPANOIC ACID
Authors: GOULD DANIEL H. , GUSTINE DAVID L. 
Published: May 2008

Gould D. H.&Gustine D. L.1982Neuropathology and Applied Neurobiology 8, 377–393Basal ganglia degeneration, myelin alterations, and enzyme inhibition induced in mice by the plant toxin 3‐nitropropanoic acidThe plant toxin, 3‐nitropropanoic acid, produced topographically and morphologically distinctive lesions in mice after daily intraperitoneal injections. In the lateral caudate‐putamen there were bilateral and symmetrical lesions consisting of marked swelling and pyknosis of individual cells and processes in otherwise unaffected tissue. The appearance of transitional forms and the usual post‐synaptic location of the swollen processes indicated that affected cells were neurons. A few mice exhibited a more diffuse spongy change in the lateral caudate‐putamen that caused major architectural changes. In the globus pallidus, entopeduncular nucleus, and anterior substantia nigra pars reticulata there was fine spongy change of the neuropil that spared cell bodies, and was primarily due to swelling of dendrites. A third lesion pattern in myelinated tracts of the midbrain, medulla, and spinal cord consisted of adaxonal, intramyelinic cleft formation. Succinate dehydrogenase activities assayed in frozen brain sections and in isolated mitochondria were markedly reduced in intoxicated mice.
ACTION OF PYRETHROID INSECTICIDES ON THE VERTEBRATE NERVOUS SYSTEM
Authors: VIJVERBERG HENK P. M. , BERCKEN JOEP VAN DEN 
Published: May 2008

Vijverberg H.P.M. & van den Bercken J.1982 Neuropathology and Applied Neurobiology8, 421–440Annotation. Action of pyrethroid insecticides on the vertebrate nervous systemThe neurotoxic action of the synthetic pyrethroid insecticides has received much interest in recent years, as the number of available pyrethroids and their practical applications have greatly increased. Although the majority of pyrethroids have a low oral toxicity to mammals, they may cause severe neurotoxic symptoms whenever they reach the nervous system in sufficient amount.The principal effect of pyrethroids in the vertebrate nervous system is to induce repetitive activity, particularly in the sensory nervous system. This repetitive activity originates from a prolongation of the transient increase in sodium permeability of the nerve membrane associated with excitation. Available evidence indicates that pyrethroids primarily interfere with the sodium channels in the nerve membrane. All active pyrethroids affect sodium channel gating in a similar manner, but marked differences in neurotoxic activity exist between the various pyrethroids, especially between ot‐cyano and non‐cyano compounds.
A CHANGE IN SUSCEPTIBILITY OF RAT CEREBELLAR PURKINJE CELLS TO DAMAGE BY ACETALDEHYDE DURING FETAL, NEONATAL AND ADULT LIFE
Authors: PHILLIPS S. C. , CRAGG B. G. 
Published: May 2008

Phillips S.C. & Cragg B.G. 1982 Neuropathology a id Applied Neurobiology 8, 455–463A change in susceptibility of rat cerebellar Purkinje cells to damage by acetaldehyde during fetal neonatal and adult lifeThe sensitivity of rat cerebellar Purkinje cells to acetaldehyde during fetal, neonatal or adult life has been assessed by histological techniques. A pregnant female rat was exposed to ethanol vapour during the last 2 weeks of gestation while metabolism of acetaldehyde was blocked by injections of disulfiram (200mg/kg) on days E14, E16, E18 and E20. Purkinje cells were counted in the offspring 5 days after birth. The number of Purkinje cells in lobes I and VIII were 52% and 42% less than age matched controls. Smaller reductions were found in lobes V and X. The weight of the cerebellum was reduced by 42%. Neonatal rats received disulfiram (40mg) on the second day after birth and were exposed to ethanol vapour during daylight hours on the third and fourth days. Purkinje cells were counted at 5 days after birth, and losses similar to those described above were found. The weight of the cerebellum was reduced by 47%. Adult male rats were exposed to ethanol vapour for 2 weeks and given disulfiram (200mg/kg) on every second day. No reduction in cerebellar weight or loss of Purkinje cells was detected. When the dura overlying the cerebellum in adult rats was superfused with acetaldehyde solutions for 1 h, a 1–6 M solution caused degeneration whereas a 0–68 M solution did not. Thus the combination of high blood ethanol and acetaldehyde levels is damaging to perinatal Purkinje cells, whereas adult cells are resistant. We found the same ranking of susceptibility with ethanol alone (Philips & Cragg, 1982a and it was surprising that the cell losses with acetaldehyde were only marginally greater than those with ethanol alone, in view of the greater neurotoxicity of acetaldehyde during acute exposure (Phillips, 1981.
THE EFFECTS OF ACRYLAMIDE ON β‐GLUCURONIDASE AND ACID PHOSPHATASE ACTIVITIES IN RAT SCIATIC NERVE ABOVE AND BELOW A LIGATURE
Authors: CAVANAGH J. B. , NOLAN C. C. 
Published: May 2008

Cavanagh J.B. & Nolan C.C. 1982 Neuropathology and Applied Neurobiology 8, 465–476The effects of acrylamide on β‐glucuronidase and acid phosphatase activities in rat sciatic nerve above and below a ligatureThe enzymes β‐glucuronidase and acid phosphatase have been assayed by histochemical and by fluorimetric methods above and below a tightly tied ligature on the rat sciatic nerve over the subsequent 10 days. These findings have been compared with similarly treated animals also given four daily doses of acrylamide (50 mg/kg). The following have been found:1 during this time, acrylamide at this dose causes slight increases in β‐glucuronidase in untied sciatic nerves, detectable both histochemically and fluorimetrically;2 below the ligature both enzyme activities were greatly increased and this was slightly reduced in the acrylamide‐dosed animals;3 there was a mild rise in β‐glucuronidase activity in the 10 cm above the ligature in undosed animals demonstrable both histochemically and fluorimetrically;4 that in the acrylamide‐dosed animals there was a marked rise in β‐glucuronidase activity both 10 cm and 20 cm above the ligature which was intensified at 7 days and at 10 days after dosing. This was demonstrated both histochemically and fluorimetrically.These results are discussed in the light of the known sheath cell and axonal responses to acrylamide intoxication.
A METHOD FOR DETERMINING TENTORIAL HERNIATION IN CLOSED‐HEAD INJURY FROM A QUANTITATIVE ESTIMATION OF CEREBRAL TRAUMA
Authors: GIBSON P. H. 
Published: May 2008

Gibson P.H. 1982 Neuropathology and Applied Neurobiology 8, 489–493A method for determining tentorial herniation in closed‐head injury from a quantitative estimation of cerebral traumaCerebral damage in 42 cases involving closed‐head injury was studied post mortem. The cases were divided into those that showed tentorial herniation and those that did not on the basis of the clinical histories and examination of the intact brains at autopsy. Damage seen histologically in coronal sections through the cerebral hemispheres and brain‐stem was recorded on diagrams. The area of damage was quantified by placing over the diagrams a cm2 grid. The numbers of squares with damage in, length of survival following the accident and the age of the cases were found by a ranking method to be statistically significantly different in herniated and non‐herniated cases. These three parameters were used in an empirically derived expression to give an index that was statistically significantly different for herniated and non‐herniated cases. The purpose of the index was to obtain an objective method of assessing the degree of tentorial herniation in brain‐stem damage resulting from herniation.
STRUCTURAL CHANGE IN MUSCLES OF THE DYSTROPHIC CHICKEN. I. QUANTITATIVE INDICES
Authors: PIZZEY J. A. , BARNARD E. A. 
Published: May 2008

Pizzey J.A. & Barnard E.A, (1983) Neuropathology and Applied Neurobiology 9, 21–38Structural change in muscles of the dystrophic chicken. I. quantitative indicesThe pectoral and posterior latissimus dorsi (PLD) muscles in the dystrophic chicken show many pathological changes. At 7 weeks of age, in a strain of these birds bred for early onset of this inherited disorder, physical weakness is established and these changes can be clearly assessed. Quantitative indices of these progressive changes were obtained by light and electron microscopic analyses; these indices cover fibre hypertrophy, fibre area variation, nuclei distribution, phagocytosis and satellite cell and fibroblast populations. The dystrophic pectoral muscle at 7 weeks is more severely affected than the PLD. In the former, there is an increase of peripheral myonuclei per fibre cross‐section of over 200%, a hypertrophy factor nearly 200‐fold greater than normal and longitudinal fibre splitting in 11% of the fibres. Many foci of degeneration are also present at this early stage. Although regenerating fibres are uncommon, an increased satellite cell population is observed. These indices provide a basis for assessing the effects of in vivo drug treatments, at the level of muscle structure.
PROCEEDINGS OF THE SIXTY‐THIRD MEETING OF THE BRITISH NEUROPATHOLOGICAL SOCIETY HELD AT CHURCHILL COLLEGE, CAMBRIDGE 15–16 JULY 1982
Authors: ADAMS PRESIDENT: J. HUME 
Published: May 2008

Craggs R. (introduced) & King R. H. M. (Royal Free Hospital School of Medicine, London NW3 2PF)King R. H. M. & Thomas P. K. (Royal Free Hospital School of Medicine, London NW3 2PF) Love S. (Institute of Neurology, Queen Square, WCIN 3BG)Jones H. B. (introduced) & Cavanagh J. B. (Institute of Neurology, London WCIN 3BG)Kemplay Sheila (introduced) & Cavanagh J. B. (Institute of Neurology, London WClN 3BG)Reske‐Nielsen E. & Daa Schroder H. (introduced) (Aarhus Kommunehospital, DK‐8000 Aarhus C, Denmark)Goebel H. H., Fidzianska A. (introduced) & Osborn M. (introduced) (University of Gottingen and Max Planck Institute for Biophysical Chemistry, D‐3400 Gottingen, FRG)Koppel H., Clarke S. (introduced) & Innocenti G. M. (introduced) (Institute of Anatomy, Lausanne, Switzerland)Anderson J. R. & Treip C. S. (Addenbrooke's Hospital Cambridge CB2 2QQ)Sapsford I. (introduced) & Weller R. O. (Southampton General Hospital,Reid H. (Department of Pathology, University of Manchester M13 9PT)Deane B. R., Greenwood J., (introduced) Lantos P. L. & Pratt O. E. (Institute of Psychiatry, London SE5 8AF)Ilgren E. B. (introduced) & Kaye A. (introduced) (Radcliffe Infirmary, Oxford OX2 6HE)Garson J. A., Coakham H. B., Harper E. I., Kemshead J. (all introduced) & Brownell Betty. (Brain Tumour Research Laboratory, Frenchay Hospital, Bristol. Imperial Cancer Research Fund, London)McLellan D. R., Adams J. H., Doyle D., Graham D. I, Kerr A. (introduced) & Murray L. S. (introduced) (Institute of Neurological Sciences, Glasgow G51 4TF)Harper C. G. (introduced) & Blumbergs P. C. (introduced) (Royal Perth Hospital, Western Australia and Institute of Medical and Veterinary Science, Adelaide, South Australia)Allsop D. (introduced), Landon M. (introduced) & Kidd M. (The Medical School, Nottingham NG7 2UH)Wilcock G. K. (introduced), Esiri M. M. & Bowen D. M. (introduced) (Radcliffe Infirmary Oxford OX2 6HE & Institute of Neurology, London WCIN 3BG)Mann D. M. A. & Yates P. O. (University of Manchester, Manchester M13 9PT)Esiri M. M. & Tomlinson A. H. (introduced) (Radcliffe Infirmary, Oxford OX2 6HE)Anderson J. R & Field H. J. (introduced) (Addenbrooke's Hospital, Cambridge CB2 2QQ and University of Cambridge, Cambridge)Kristensson K. Leestma J. (introduced), Norrby E. (introduced) & Orvell C. (introduced) (Karolinska Institute,Griffiths T. (introduced), Evans M. C. (introduced) & Meldrum B. S. (Institute of Psychiatry, London SE5 8AF)McConnell P. (introduced) & Berry M. (Medical School, Birmingham, B15 2TJ)Allen Y.S., RobertsG.W., Crow T.J. M. (Histochemistry Unit, Royal Postgraduate Medical School, London, W12 and Clinical Research Centre, Harrow, Middlesex)
STRUCTURAL CHANGE IN MUSCLES OF THE DYSTROPHIC CHICKEN. II. PROGRESSION OF THE HISTOPATHOLOGY IN THE PECTORALIS MUSCLE
Authors: PIZZEY J. A. , BARNARD E. A. 
Published: May 2008

Pizzey J.A.&Barnard E.A.(1983)Neuropathology and Applied Neurobiology 9, 149–164Structural change in muscles of the dystrophic chicken. II. Progression of the histopathology in the pectoralis muscleDystrophic (D) and normal (N) chicken pectoral muscle was analysed for histopathological differences from the embryo (day 20) through to the mature adult stage. A variety of indices of structural changes were used, to express the progression quantitatively. At the embryonic stage, fibroblast numbers (but not satellite cell numbers) are increased in D. D shows fibre hypertrophy discernable from about 4 days after hatching. Other abnormalities of fibre size and shape appear in D from about 2 weeks onwards. Nuclei numbers and location change characteristically in D, compared to N, from about 4 days, and these differences subsequently become very prominent. Fibre splitting and phagocytosis become significant in D from about 2 weeks onwards and increase noticeably thereafter. The later stages in D, with gross loss of muscle fibres, are also described, in the pectoral and posterior latissimus dorsi muscles. The analyses show that some of the structural changes in D precede the discernable difference in fibre type composition which develops between D and N. The changes in the muscle used provide a basis for assessing the effects of drug treatments at various stages, including the early post‐hatch period.
THE EFFECTS OF MULTIPLE SEQUENTIAL EPISODES OF DEMYELINATION IN THE SCIATIC NERVE OF THE MOUSE
Authors: HALL SUSAN M. 
Published: May 2008

The effects of multiple sequential episodes of demyelination in the sciatic nerve of the mouseIntraneural injections of lysophosphatidyl choline were used to examine the effects of multiple episodes of demyelination and repair in the sciatic nerves of adult mice. It was found that the early phases of repair, from initiation of myelinolysis to the appearance of promyelinated fibres, were achieved more rapidly in multiple‐injected nerves than in single‐injected nerves. However, this lead was temporary, since subsequent remyelination was delayed in the multiple‐injected nerves until several days after it had been established in most single‐demyelinated nerves. Cell‐mediated demyelination was seen in multiple‐injected nerves, but never in single‐injected nerves. The results are discussed in terms of a the contribution of supernumerary Schwann cells to the acute stage of the programme of cellular repair; and b the possibility that the ‘normal’ response to an injection of LPC in a nerve which has previously undergone several episodes of demyelination is exacerbated by a local and self‐limiting immune‐mediated reaction.
A CEREBELLAR ABNORMALITY IN THE MOUSE WITH MOTOR END‐PLATE DISEASE
Authors: BOAKES R. J. , HARRIS J. B. , DICK D.K. 
Published: May 2008

A cerebellar abnormality in the mouse with motor end‐plate diseaseThe murine mutant with motor end‐plate disease (med) exhibits a progressive weakness which is due to a functional denervation of skeletal muscle. It is inherited as an autosomal recessive trait and has two alleles. One of these is the jolting (medjo) mouse which also suffers from a disturbance of locomotion. Although the jolting animal was originally thought to suffer from a disorder of neuromuscular transmission, the organization of the peripheral nervous system is indistinguishable from normal and neuromuscular transmission is unimpaired. It is now clear that abnormalities in the cerebellum are responsible for the gait problems of the jolting mouse, and a preliminary morphological and neurophysiological examination of the mouse with motor end‐plate disease has shown that it also has cerebellar abnormalities. Axonal spheroids may be seen on cerebellar Purkinje cell axons in the med mouse, and the character of extra‐cellular recordings obtained from the Purkinje cells is abnormal.