bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE BLOOD‐NERVE BARRIER AND RECONSTITUTION OF THE PERINEURIUM FOLLOWING NERVE GRAFTING
Authors: AHMED A. M. , WELLER R. O. 
Published: May 2008

The blood‐nerve barrier and reconstitution of the perineurium following nerve graftingSural nerve autografts were performed on intact rat sural nerves and on sural nerves excised proximal to the site of grafting. The effect of the presence or absence of regenerating axons upon reconstitution of the perineurium at the graft junctions and upon re‐establishment of the blood‐nerve barrier to horseradish peroxidase (HRP) were studied over the succeeding 3–24 weeks. Compartmentation of the nerve fascicle occurred at the graft junctions where the perineurium was damaged. Each compartment contained Schwann cells with or without axons and was surrounded by elongated fibroblast‐like cells which resembled perineurial cells in the longer surviving animals. It was concluded that, (a) compartments form in a nerve at the site of perineurial damage even in the absence of axons; (b) although compartmentation may be a mechanism for perineurial regeneration and reconstitution of the blood‐nerve barrier, blood vessels and the cell layers forming compartments at graft junctions remain permeable to HRP for at least 6 months; and (c) the intact perineurium around the distal stump of a denervated nerve is permeable to HRP but the endoneurial blood vessels are not.
FINE STRUCTURE OF MUSCLE IN HUuMAN DISUSE ATROPHY: SIGNIFICANCE OF PROXIMAL MUSCLE INVOLVEMENT IN MUSCLE DISORDERS*
Authors: DASTUR DARAB K. , GAGRAT BOMI M. , MANGHANI DAYA K. 
Published: May 2008

Abstracts Dastur D.K., Gagrat B.M. & Manghani D.K. (1979) Neuropathology and Applied Neurobiology5, 85–101Fine structure of muscle in human disuse atrophy: significance of proximal muscle involvement in muscle disordersThe universal occurrence of weakness of skeletal musculature on disuse, however produced, and the paucity of published reports on the fine structural changes in human disuse atrophy, prompted the present investigation. The quadriceps muscle of a leg immobilized in plaster cast (for fracture) and of the opposite non‐immobilized limb was biopsied in four adult males, after periods of immobilization from 50 to 75 days. These 8 muscle specimens were examined for histopathological changes, and muscle fibre diameters were measured by micrometry from paraffin sections. The histograms revealed a larger proportion of small fibres (<20 μm) and a smaller proportion of large fibres (> 40μm) in the immobilized limb compared to the opposite. Thus, light microscopy showed only atrophic changes. This was confirmed by elec‐tronmicroscopy, where atrophy of few to several muscle fibres was seen in the form of loss of myofibrils, collapse and folding of the basement membrane and prominence of glycogen or muscle nuclei. The atrophic change was more severe in the immobilized limbs, but it was also noticeable in all the non‐immobilized limbs. Degenerative changes, especially disorganization and breakdown of myofibrils, and fragmentation of plasma membrane, were also seen in occasional atrophied muscle fibres, again more frequently in the immobilized limb. Lipofuscin was often found accumulated in muscle fibres and occasionally in endothelial cells of intramuscular blood vessels; the latter showed prominent pinocytotic vesicles or thickened basement membrane. It is concluded that both atrophy and degeneration of fibres of proximal muscles can occur as non‐specific consequences of disuse of the limb in man, that degeneration is a later and more severe change, that muscles even of the non‐immobilized leg are subjected to disuse atrophy during bed‐rest, and that the proximal muscles in man seem to have a natural susceptibility to atrophy and degeneration in any muscular disorder.
BASAL MEMBRANE LABYRINTHS IN THE HEALING STAGES OF CHICK NUTRITIONAL ENCEPHALOPATHY
Authors: SANDBANK U. , BUBIS J. J. , BARTOV I. , DROR I. , BUDOWSKI P. , WOLMAN M. 
Published: May 2008

Basal membrane labyrinths in the healing stages of chick nutritional encephalopathyChicks were fed a diet rich in oxidized oil and deficient in a‐tocopherol. As soon as nutritional encephalopathy developed the animals were immediately put on to a normal diet, and kept alive for up to 166 days. Examination of the cerebellum showed multiple foci of healed encephalomalacia with EM appearance of basal membrane labyrinths between astroglial cells and around blood vessels. The possible origin of the basement membrane material in this condition was considered and compared with similar formations in normal animals, in CNS tumour explants, and after portacaval anastomosis as well as after spinal cord lesions.
A NOTE ON THE PLOIDY OF PURKINJE CELLS; SEX CHROMATIN IN FIELD VOLE (Microtus agrestis) AND MAN
Authors: LEWIS P. D. , EVANS D. J. 
Published: May 2008

A note on the ploidy of Purkinje cells: sex chromatin in field vole (Microtus agrestis) and manExamination of sex chromatin bodies in Purkinje cell nuclei suggests only a diploid chromosomal content: there is no increase in number or size above that seen in diploid cells.
TRANSPORT OF MICROPEROXIDASE ACROSS SEGMENTS OF CEREBRAL ARTERIOLES UNDER NORMAL CONDITIONS
Authors: WESTERGAARD E. 
Published: May 2008

Westergaard E. (1980) Neuropathology and Applied Neurobiology 6, 267–277Transport of microperidoxase across segments of cerebral arterioles under normal conditionsMicroperoxidase, injected intravenously into mice, was allowed to circulate in the blood stream for 1 min to 1 h. The amount of reaction product in the walls of cerebral arterioles was most pronounced after circulation of 40 mg peroxidase for one min, the maximum dose used. The peroxidase was transported across the endothelium in a few segments of cerebral arterioles, lying on the surface of the brain or restricted to regions of the brain parenchyma. Reaction product was observed in vesicles: 1 open to the vessel lumen, 2 freely situated in the cytoplasm of endothelial cells, and 3 open to the subendothelial basement membrane. The endothelial cells did not show leaky plasma membranes. Channels or chains of vesicles, simultaneously open to the vessel lumen and the subendothelial basement membrane, were not seen, nor were fenestrae found. Furthermore, reaction product never formed a continuous column from the first luminal to the first abluminal tight junctions between two adjacent endothelial cells. From these observations, it is suggested that vesicular transfer of intravenously injected microperoxidase may occur under normal conditions across the endothelium in segments of cerebral arterioles.
IMMUNOGENETIC STUDIES OF MULTIPLE SCLEROSIS PATIENTS IN CAITHNESS COUNTY, SCOTLAND
Authors: ROBERTSON P. , WARD P. , BROSTOFF J. , PACK S. , FESTENSTEIN H. , SACKS J. , ROSENBERG R. A. , PETERS E. , STENNING P. , ZABRISKIE J. B. 
Published: May 2008

Robertson P., Ward P., Brostoff J., Pack S., Festenstein H., Sacks J., Rosenberg R.A., Peters E., Stenning P. & Zabriskie J.B. (1980) Neuropathology and Applied Neurobiology 6, 299–305Immunogenetic studies of multiple sclerosis patients in Caithness County, ScotlandThe present report indicates that there is an increased frequency of HLA‐B7 in multiple sclerosis patients compared to unrelated controls and unaffected siblings. HLA‐A3 was not significantly increased. The increased frequency of certain HLA antigens was not reflected in increased titres of serum measles antibodies in this group. In contrast to our previous studies, there were only minimal differences in the cellular response to measles antigen in multiple sclerosis patients as compared to siblings and unrelated controls.
FURTHER STUDIES OF THE CENTRAL NERVOUS SYSTEM IN CANINE GIANT AXONAL NEUROPATHY
Authors: GRIFFITHS I. R. , DUNCAN I. D. , McCULLOCH M. , CARMICHAEL S. 
Published: May 2008

Griffiths I.R., Duncan I.D., McCulloch M. & Carmichael S. (1980) Neuropathology and Applied Neurobiology 6, 421–432Further studies of the central nervous system in canine giant axonal neuropathyThe CNS of three further cases of canine giant axonal neuropathy (GAN) were examined. The axonal swellings were present in the distal portions of the spinal long tracts and their terminations in the cerebellar vermis; in the distal optic pathways; the nuclei of the habenulo‐interpeduncular tract; certain thalamic relay nuclei and the cerebral cortex. The swellings were present both paranodally and internodally with the myelin sheath being attenuated or even absent. Excessive numbers of disordered 10 nm neurofilaments were the main constituent although mitochondria, membranous bodies, glycogen bodies and amorphous electron dense material also accumulated, particularly in the fasciculus gracilis. The neurotubules tended to form small sub‐axolemmal or intra‐axonal islands. Complex interdigitations of oligodendrog‐lia and axolemma were found in the affected areas. A small number of fibres in the rostral fasciculus gracilis showed marked proliferation of the smooth endoplasmic reticulum which may represent abortive attempts at regeneration. A small proportion of astrocytic processes were markedly enlarged with excessive whorling of the glial filaments. The accumulation of these various organelles in the non‐terminal axon in the absence of mechanical obstruction suggests a defect in axoplasmic transport which may result from an energy failure as suggested in toxic neuropathies. The significance and pathogenesis of the glial filamentous changes and those reported in other cells in human GAN is at present uncertain.
THE EFFECTS OF THYROIDECTOMY ON THE EXTRAOCULAR MUSCLES OF THE RAT: A HISTOCHEMICAL STUDY
Authors: VITA G. F. , MASTAGLIA F. L. 
Published: May 2008

VAccepted for publication ita G.F. & Mastaglia F.L. (1980) Neuropathology and Applied NeurobiologyThe effects of thyroidectomy on the extraocular muscles of the rat: a histochemical studyThe effects of thyroidectomy on the metabolic properties of the rat extraocular muscles have been studied using histochemical techniques. Six months after removal of the thyroid gland a significant increase in the proportion of Type 1 fibres was found in the central zone of the superior rectus (SR) and in the levator palpebrae superioris muscles, but not in the medial rectus (MR) or superior oblique (SO) muscles. Other changes included an increased proportion of Type 2a fibres and reduced proportions of Type 2a and 2b fibres in the central zone of the SR, and an increased proportion of type 2a, and a reduced proportion of Type 2a' fibres in the peripheral zone of the SR, MR and SO. In addition, there was a mild hypertrophy of Type 1 fibres in the MR, and a mild atrophy of Type 2 fibres in each of the muscles studied. The physiological significance of these findings is discussed.
HISTOCHEMICAL STUDY ON OXIDATIVE ENZYME ACTIVITY IN THE BRAIN, PARTICULARLY OF ASTROCYTES, IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: HANAKITA JUNYA , HAZAMA FUMITADA , AMANO SHIGERU , YAMADA EIJI , HANDA HAJIME 
Published: May 2008

Hanakita J., Hazama F., Amano S., Yamada E. & Handa H. (1980)Neuropathology and Applied Neurobiology 6, 471–482Histochemical study on oxidative enzyme activity in the brain, particularly of astrocytes, in spontaneously hypertensive ratsIn order to obtain indirect information concerning brain oedema or increased vascular permeability under hypertensive conditions, the enzyme responses of astrocytes in the brains of spontaneously hypertensive rats were histo‐chemically investigated. Reactions for oxidative enzymes, such as NADH2‐, NADPH2‐tetrazolium reductases and succinate dehydrogenase were performed on SHR brains of various ages. In the hypertensive rats, proliferation, hypertrophy and increased enzyme activity were observed in astrocytes, particularly in the white matter. This activation of astrocytes appeared at 12 13 weeks‐of‐age and increased with advancing age. These findings suggest that increased vascular permeability of the materials in the smaller molecules begins in the early stage of the development of hypertension before the breakdown of the blood‐brain barrier. Many degenerating astrocytes, showing clasmatodendritic changes, were observed in severely oedematous regions or around cystic foci in the white matter. The changes in astrocytic function seem to be related to the development of the parenchymal changes, particularly of the white matter in the chronic hypertensive state.
CORTICAL ORGANIZATION OF THE POSTERO‐MEDIAL BARREL‐SUBFIELD IN MICE AND ITS REORGANIZATION AFTER DESTRUCTION OF VIBRISSAL FOLLICLES AFTER BIRTH
Authors: PIDOUX B. , DIEBLER M. F. , SAVY CL. , FARKAS E. , VERLEY R. 
Published: May 2008

Pidoux B., Diebler M. F., Savy CL, Farkas E. & Verley R. 1980 Neuropathology and Applied Neurobiology 6, 93–107Cortical organization of the postero‐medial barrel‐subfield in mice and its reorganization after destruction of vibrissal follicles after birthThe postero‐medial barrel‐subfield (PMBSF) of the SI cortex of normal adult mice contains clusters of cells called ‘barrels’. Each barrel histochemically shows increased activity of succinate, lactate, and glucose‐6‐phosphate dehydrogenase and also GABA‐T activity. Some neuronal perikarya in the barrel walls show GABA‐T activity. Mitochondrial a‐GPDH and AChE show equal activities in the hollows and in the walls of the barrels. On this cortical vibrissa field, the contralateral and ipsilateral vibrissae project somatotopi‐cally in a way which coincides with the barrels. The mystacial vibrissae and the common fur of the muzzle project to different loci. The cortical surface area for the normal fur is 0–025 mm2, whereas the cortical vibrissal area is 10 mm2. In mice with lesioned whisker pads the succinate‐dehydrogenase activity of the IVth layer in the vibrissal area becomes a continuous sheet similar to the adjacent IVth layer, the thickness of the cortex is relatively preserved, and the total enzyme activities, biochemically assayed, are unchanged. These features can be explained by a functional substitution. In mice with whisker pads lesioned since birth, the vibrissal area can still be identified by the projections from ipsilateral vibrissae (undamaged side). This vibrissal area, and this alone, is found to be invaded by projections from the contralateral common fur of the muzzle. Experimental data suggest that the compensatory process may result from an invasion of the vibrissal area by a new set of ascending fibers, and not merely from axonal sprouting either at the periphery or at the cortical level.
AN INVESTIGATION OF THE INFLUENCE OF THE EXTRACELLULAR ENVIRONMENT ON THE REGENERATION OF THE NORMAL AND DYSTROPHIC MOUSE MUSCLEIN VITRO
Authors: WEST M. R. , PARSONS R. 
Published: May 2008

West M.R. & Parsons R. 1980 Neuropathology and Applied Neurobiology 6,181–194An investigation of the influence of the extracellular environment on the regeneration of the normal and dystrophic mouse muscle in vitroThe regenerative response of normal and dystrophic muscle cultured with fetal spinal cord has been investigated. Nearly all the normal muscle explants regenerated, but the dystrophic muscle gave a much more varied response as only 30% regenerated, and 38% showed total explant degradation with loss of all recognisable muscle elements. Forty‐five % of the dystrophic explants, produced ‘pseudostraps’ in which there was an apparent block of myoblast fusion. Cultures in which cellular contact between spinal cord tissue and the normal or dystrophic muscle was prevented showed less regeneration than when it was allowed. However, the incidence of regeneration in these cultures was much higher than when the muscle was cultured in isolation. Direct cellular contact between the cord and the muscle is, therefore, not necessary to initiate regeneration which is presumably mediated in these cultures by changes in the chemical environment. This is substantiated by the almost complete absence of regeneration in cultures of muscle alone, where the fibres were shown to be devoid of nuclei within 5 days. The experiments have shown that under our conditions, a myogenic defect is apparent in the dystrophic muscle. This does not exlude a possible neuronal involvement in the aetiology of the disease, although we have no evidence to support it.
OVINE CEROID‐LIPOFUSCINOSIS: A MODEL OF BATTEN'S DISEASE
Authors: JOLLY R. D. , JANMAAT A. , WEST D. M. , MORRISON I. 
Published: May 2008

Jolly R.D., Janmaat A., West D.M. & Morrison I. 1980 Neuropathology and Applied Neurobiology 6,195–209Ovine ceroid‐lipofuscinosis: a model of Batten's diseaseAn inherited neurological disease of sheep was characterized by the intracellular accumulation of autofiuorescent lipopigments in neurones and a wide variety of other cells within the body. The staining, fluorescent, ultrastruc‐tural and physical characteristics of the storage material were similar to those found in a heterogeneous group of storage diseases of children known as Batten's disease or the ceroid‐lipofuscinoses. The ovine disease did not exactly fit any of the main human entities, but had features in common with both the late infantile and juvenile forms. It was concluded that this was a useful model for studying the pathogenesis of this type of storage disease and for therapeutic trials. A flock of sheep is maintained for this purpose.
SOME RECENT ADVANCES IN THE CLINICAL ASPECTS OF MULTIPLE SCLEROSIS
Authors: TALLIS R. C. 
Published: May 2008

Tallis R.C. (1980) Neuropathology and Applied Neurobiology 6,325–335Annotation. Some recent advances in the clinical aspects of multiple sclerosis Recent work on the clinical aspects of multiple sclerosis is reviewed with particular regard to symptomatology: New approaches to clinical symptoms and the identification of more subtle impairments are illustrated by recent studies of visual function in M.S. patients; pathophysiology: It is now widely appreciated that the dysfunction observed in patients is not determined solely by histologically demonstrable demyelination. The function of the demye‐linated neuron is highly variable, being dependent upon factors which may change from day to day. Recent ideas about ‘neuro‐electric blocking factors’ and other factors that may influence demyelinated neurons and hence symptoms are discussed; diagnosis: tests on C.S.F., electro‐physiological and psychophysiological tests and computer tomography as aids to diagnosis and the controversy over ‘specific’ blood tests are reviewed; course and prognosis: Long term follow‐up studies confirm that, in a significant proportion of cases, the course of M.S. may be benign and have identified some early prognostic indices; Treatment: The results of trials of symptomatic (spinal cord stimulation) and would‐be curative therapies (such as dietary supplementation with poly‐unsaturated fatty acids and immunosuppression) are briefly discussed.
HISTOCHEMICAL AND ULTRASTRUCTURAL ANALYSIS OF THE MITOCHONDRIAL CHANGES IN A FAMILIAL MITOCHONDRIAL MYOPATHY
Authors: TASSIN S. , WALTER G. F. , BRUCHER J. M. , ROUSSEAU J. J. 
Published: May 2008

Tassin S., Walter G.F., Brucher J.M. & Rousseau J.J. (1980) Neuropathology and Applied Neurobiology 6, 337–347.Histochemical and ultrastructural analysis of the mitochondrial changes in a familial mitochondrial myopathyTwo familial cases of progressive external ophthalmoplegia with involvement of pharyngeal and distal muscles are presented. ‘Ragged‐red’ fibres were found in both cases. Excessive amounts of RNA, as evidenced by the acridine orange‐induced fluorescence, were noted in many muscle fibres, mostly in the ‘ragged‐red’ fibres. At the ultrastructural level, numerous mitochondrial changes with paracrystalline formations were noted. Those formations were observed in three forms and a three‐dimensional reconstruction is proposed which suggests that the paracrystalline formations consist of undulating parallel leaflets joined along the top of the undulations. Small transverse bridges between neighbouring cristae and between cristae and paracrystalline formations are also emphasized. All those mitochondrial abnormalities are thought to represent the morphological expression of a biochemical deficiency in the inner membrane. They are interpreted thus: firstly, the biochemical defect leads to a multiplication of the mitochondria with increase in their volume and proliferation of the cristae in order to improve energy production; secondly, bridges between the modified inner membranes induce attachment of the neighbouring cristae and result in paracrystalline formations.
ANNOTATION: AUTOMATED MICROSCOPY
Authors: ROSEN D. 
Published: May 2008

Rosen D. (1981) Neuropathology and Applied Neurobiology 7, 331–340 Annotation. Automated microscopyA number of automated microscopes are now commercially available. The principles of operation of such apparatus are briefly sketched and the main processes in the automation of picture acquisition and analysis are outlined. Examples are given of the automated examination of micrographs of nerves and muscles. The limitations of automated microscopy at the present time are stressed, but it is argued that the apparatus can be usefully employed for simple counting and sizing tasks while improved capabilities are being developed.
FUNCTIONAL ASPECTS AND PATHOGENETIC CONSIDERATIONS OF THE NEUROPATHY IN THE SPONTANEOUSLY DIABETIC BB‐WISTAR RAT
Authors: SIMA ANDERS A. F. , HAY KAZUKO 
Published: May 2008

Sima A.A.F. & Hay K. (1981) Neuropathology and Applied Neurobiology 7, 341–350Functional aspects and pathogenetic considerations of the neuropathy in the spontaneously diabetic BB‐Wistar ratElectrophysiological features were studied longitudinally in the spontaneously diabetic insulin‐dependent, BB‐Wistar rat. These were correlated in time with the state of the patency of the protective barriers in peripheral nerves. Motor nerve conduction velocity was significantly slowed only 3 weeks after the onset of the diabetes. When ultrastructural changes began, the maximal conduction velocity was further diminished. The amplitudes of evoked muscle potentials and distal latencies were significantly altered in diabetic rats. No change in the permeability of the blood‐nerve barrier could be demonstrated before, during or after the onset of the nerve conduction defect. The possible pathogenetic mechanisms are discussed and a possible mechanism is suggested, namely a reduced availability of energy to axons in diabetes.
COMPARISON BETWEEN THE EARLY CHANGES IN ISONIAZID INTOXICATION AND THE CHROMATOLYTIC RESPONSE TO NERVE LIGATION IN SPINAL GANGLION CELLS OF THE RAT
Authors: JONES H. B. , CAVANAGH J. B. 
Published: May 2008

Jones H.B. & Cavanagh J.B. (1981) Neuropathology and Applied Neurobiology 7, 489–501Comparison between the early changes in isoniazid intoxication and the chromatolytic response to nerve ligation in spinal ganglion cells of the ratThe early effects of acute isoniazid intoxication and the early responses of the neuron to axotomy have been compared in lumbar spinal ganglion cells in the rat. The cells were studied by light and electron microscopy during the 4 days after a single oral dose (2g/kg) of isoniazid and for four days after application of a tight ligature to the sciatic nerve at the level of the sciatic notch. After axotomy a greater proportion of cells showed changes visible by light and electron microscopy than after INH. Small dark neurons were affected more rapidly and more severely by both insults than the large light cells as evidenced principally by changes in their ribosomal organization. Large light cells showed little response to INH. The first response to axotomy was visible about 12 h after injury. The response to INH began 24 h after the single oral dose. The early cell responses to INH therefore apparently precede axon degeneration which is first seen 72 h later and are thus probably a direct toxic effect.