bluuebunny/crossref_metadata_2025_split huggingface dataset:
INHIBITION OF CEREBELLAR DENDRITE DEVELOPMENT IN NEONATAL THYROID DEFICIENCY
Authors: BROWN W. J. , VERITY M. A. , SMITH R. L. 
Published: May 2008

Inhibition of cerebellar dendrite development in neonatal thyroid deficiencyThyroid hormone deficiency was induced in neonatal rats by propylthiouracil. Serum thyroxine levels were assayed and thyroid tissue was examined to assess the clinical condition. At 8, 14, 20, 30 and 42 days after birth, age‐matched controls and hypothyroid animals were killed by perfusion. Nissl stains, Golgi preparations, and electron microscopy were done on the cortex of Lobules IX and X of the developing cerebellum. Measurements of the molecular layer revealed that at 8 days, controls are slightly but significantly wider, but at 20 days the difference is much greater and remains so even at 42 days. Golgi studies show deceleration and distortion of development of the Purkinje cell dendritic tree in the abnormal rats. Spine counts of the spiny branchlets on these dendrites show the same incidence per linear micrometer as the age‐matched controls, but linear measurements of the branchlets show that the deficient animals have shorter branchlets and regions where spines are absent. Electron microscopy shows that if a spine does develop, it appears similar in control and hypothyroid animals at comparable ages. The effect of the abnormal Purkinje cell dendritic arborization on synaptogenesis in the molecular layer is discussed.
ACUTE EFFECTS OF TRIETHYL TIN ON THE RAT MYELIN SHEATH
Authors: JACOBS JEAN M. , CREMER JILL E. , CAVANAGH J. B. 
Published: May 2008

Acute effects of triethyl tin on the rat myelin sheathTriethyl tin, when given intravenously to the rat, produces intramyelin vacuoles in 2 h after 10 mg/kg and 1 h after 20 mg/kg. No preceding changes occur in astro‐cytes, oligodendrocytes, or extracellular space. The vacuoles appear to begin in the outer lamellae of the sheath and may move with time inwards towards the axon. They occupy only a sector of the sheath, at least during the first few hours. Fibres of all sizes are equally affected. It is suggested that this substance acts directly on the membrane of the oligodendroglial myelin. No effects were found on retinal rod cells or peripheral myelin.
IMMUNOFLUORESCENCE DEMONSTRATES THE DISTRIBUTION OF ACTIN, MYOSIN AND INTERMEDIATE FILAMENTS IN CULTURED NEUROBLASTOMA CELLS
Authors: SOTELO J. , TOH B. H. , YILDIZ A. , OSUNG O. , HOLBOROW E. J. 
Published: May 2008

Immunofluorescence demonstrates the distribution of actin, myosin and intermediate filaments in cultured neuroblastoma cellsMonolayers of cultured neuroblastoma cells were examined for immunofluorescent reactivity with antibodies directed against actin, myosin or intermediate filaments. In well spread cells, antibody to intermediate filaments stained an intricate cyto‐plasmic network which extended as filament bundles into cell processes; in poorly spread or rounded cells, the antibody stained thick juxtanuclear filament bundles. By contrast, antibodies to actin or myosin reacted with microspikes and with axonal growth cones. The different topographical distribution of actin, myosin and intermediate filaments suggests that while actin and myosin may have roles in axon elongation, intermediate filaments may function as an internal cytoskeleton as well as in axoplasmic transport. The different distribution of intermediate filaments in well spread compared with rounded cells suggests that the cell makes its filaments prior to axon development and that the filaments subsequently unwind and migrate into the cell processes to form the axon skeleton.
PAIRED HELICAL FILAMENTS IN RAT SPINAL GANGLIA FOLLOWING CHRONIC ALCOHOL ADMINISTRATION: AN ELECTRON MICROSCOPIC INVESTIGATION*
Authors: VOLK B. 
Published: May 2008

Volk B. 1980Neuropathology and Applied Neurobiology6, 143–153Paired helical filaments in rat spinal ganglia following chronic alcohol administration: an electron microscopic investigationYouang Wistar rats were given a 15% (v/v) ethanol solutionad libitumfor at least 6 months, spinal ganglia (C6–7 and Ll‐2) in some of the experimental animals showed paired helical filaments. These curvilinear profiles consisted of 10 nm filaments with the twist every 35nm. There was also an increase in granular material and in nematosomes. Whether these features may be caused by an impaired cerebral protein biosynthesis is discussed.
PATHOLOGY OF DISULFIRAM NEUROPATHY
Authors: BOULDIN T. W. , HALL C. D. , KRIGMAN M. R. 
Published: May 2008

Bouldin T.W., Hall CD & Krigman M.R.1980 Neuropathology and Applied Neurobiology 6, 155–160Case report. Pathology of disulfiram neuropathyThe pathological changes in a sural nerve biopsy from a 42‐year‐old woman with disulfiram‐induced peripheral neuropathy were assessed by quantitative light microscopy, electron microscopy, and the study of teased nerve fibres. The nerve had a marked loss of myelinated fibres; of the remaining myelinated fibres some were undergoing Wallerian‐type axonal degeneration. Large myelinated fibres were preferentially involved. Primary demyelination, remyelination, and evidence of regeneration were not present. Because of the marked differences between the pathological findings in disulfiram neuropathy and carbon disulfide neuropathy, it is concluded that carbon disulfide is not responsible for the neurotoxic effect of disulfiram.
EFFECTS OF DEXAMETHASONE ON FIBRE SUBTYPES IN RAT MUSCLE
Authors: LIVINGSTONE I. , JOHNSON M. A. , MASTAGLIA F. L. 
Published: May 2008

Livingstone I., Johnson M.A. & Mastaglia F.L. (1981) Neuropathology and Applied Neurobiology 7, 381–398Effects of dexamethasone on fibre subtypes in rat muscleThe extent to which dexamethasone treatment produced atrophy of fast‐twitch (EDL) and slow‐twitch (SOL) muscles in the rat was investigated. The mean weight of steroid‐treated EDL muscles was decreased as compared to normal, whereas SOL muscles from normal and dexamethasone‐treated animals showed no significant difference. Muscle fibre diameters also showed comparatively minor changes in SOL, which consists of Type 1 (slow oxidative) and Type 2A (fast oxidative/glycolytic) fibres. Rat EDL contains, in addition to Type 1 and Type 2A fibres, two sub‐populations of fast glycolytic fibres (Types 2B and 2B'). These fibre types showed the most severe degree of atrophy both after dexamethasone treatment and after denervation. The mean ratio of the weights of denervated to innervated EDL muscles was lower in steroid‐treated rats than in normal animals suggesting that the atrophy produced by steroid treatment in conjunction with denervation was more than simply additive. Analysis of the proportions of histochemical fibre types in SOL and EDL showed that dexamethasone treatment produced no major alterations in the fibre type constitution of these muscles. However, further histochemical studies showed that there was relatively severe impairment of myophosphorylase activity in Type 2B' (fast glycolytic) fibres as compared to other fibre types; conversely Type 1 fibres frequently contained increased myophosphorylase. Levels of β‐hydroxybutyrate dehydrogenase were low in both normal and steroid‐treated EDL but high in SOL which also showed higher general oxidative activity. It is suggested that the particular susceptibility of fast glycolytic fibres to atrophy as a result of steroid treatment may be linked to: 1 the relatively severe reduction of myophosphorylase activity in these fibres and 2 their comparative inability to utilize alternative energy sources, especially substrates derived from free fatty acids.
PATHOGENICITY OF A POLIOMYELITIS‐LIKE DISEASE IN MONKEYS INFECTED ORALLY WITH ENTEROVIRUS 71: A MODEL FOR HUMAN INFECTION
Authors: HASHIMOTO ISAO , HAGIWARA AKIO 
Published: May 2008

Hashimoto I. & Hagiwara A. (1982) Neuropathology and Applied Neurobiology 8, 149–156Pathogenicity of a poliomyelitis‐like disease in monkeys infected orally with enterovirus 71: a model for human infectionTen cynomolgus monkeys were given enterovirus 71 (E71) by mouth. Clinically, only one monkey showed weakness of the lower extremities. Histopathologically, vascular lesions of variable intensity, perivascular cuffing, degeneration and necrosis of the neurons and neuronophagia were observed in the CNS of 7 monkeys. E71 was recovered from the CNS and specific immunofluorescence was detected in the neurons and in associated macrophages in the CNS. Serum neutralizing antibody titres rose from 14 to 21 days. These monkeys are as susceptible to E71 infection by the oral route as by the subcutaneous route as previously shown, and its neuronal virulence was confirmed by its producing CNS lesions after oral infection. The orally infected monkey with E71 appears to provide an excellent model for infection by this agent in man.
THE ROLE OF GLUTAMINE SYNTHETASE IN THE DIAGNOSIS OF CEREBRAL TUMOURS
Authors: PILKINGTON G. J. , LANTOS P. L. 
Published: May 2008

Pilkington G.L. & Lantos P.L. (1982) Neuropathology and Applied Neurobiology 8, 227–236The role of glutamine synthetase in the diagnosis of cerebral tumoursGlutamine synthetase (GS) was studied in a range of human brain tumours and compared with results obtained by staining for glial fibrillary acidic protein (GFAP) using the indirect immunoperoxidase and peroxidase‐anti‐peroxidase methods. All astrocytomas showed positive staining with GS, the degree of which was related to the extent of differentiation and the amount of cytoplasm of the constituent cells. Ependymomas were only weakly positive, although a dense GFAP reaction was detected around blood vessels; possibly due to the presence of astrocyte foot processes. Medulloblastomas showed signs of astrocytic differentiation by the presence of clusters of positively staining cells amongst undifferentiated neoplastic cells. Oligodendrocytomas and meningiomas were generally negative apart from occasional astrocytes within the former neoplasms. GS and GFAP staining corresponded in virtually all cases; however, GS demonstrated poorly‐fibrillated cells better than GFAP, but did not show cell processes so clearly. Although GS appears to be cell‐specific in the central nervous system for normal, reactive and neoplastic astrocytes, it is not organ‐specific and therefore also stains cells of other tissues, e.g. liver. GS offers a practical alternative to GFAP as an astrocyte specific marker in human cerebral tumours and may be of diagnostic value in cases where poorly‐differentiated astrocytic tumours have been found negative to conventional histological stains for glial fibres or demonstrate a weak positive reaction to GFAP.
A CHANGE IN SUSCEPTIBILITY OF RAT CEREBELLAR PURKINJE CELLS TO DAMAGE BY ALCOHOL DURING FETAL, NEONATAL AND ADULT LIFE
Authors: PHILLIPS S. C. , CRAGG B. G. 
Published: May 2008

Phillips S.C. & Cragg B.G.1982 Neuropathology and Applied Neurobiology 8, 441–454A change in susceptibility of rat cerebellar Purkinje cells to damage by alcohol during fetal, neonatal and adult lifeThe sensitivity of rat cerebellar Purkinje cells to ethanol exposure during fetal, neonatal or adult life was assessed by histological techniques. Pregnant female rats were exposed to ethanol vapour during the last 2 weeks of gestation. Purkinje cells were counted 5 days after the pups were born. The number of Purkinje cells in lobe VIII was reduced by 45%, and the linear density of Purkinje cells in lobe I was 47% less than in controls not exposed to ethanol. Smaller reductions were found in other lobes. The weight of the cerebellum was reduced by 34%. Neonatal rats were exposed to ethanol vapour briefly during daylight hours on the third and fourth days after birth. Purkinje cells were counted on the fifth day after birth, and losses similar to those described above were found, with additional significant reductions of cell numbers in lobe I and of Purkinje cell density in lobe VIII. The weight of the cerebellum was reduced by only 4%. Adult male rats were exposed to ethanol vapour for 3 weeks and no Purkinje cell losses were subsequently found. The dura overlying the cerebellum of separate adult male rats was superfused with 100% ethanol for 1 h and no abnormalities were detected with electron microscopy in the exposed cortex 6 days later. It is remarkable that the brief neonatal treatment caused a more widespread loss of Purkinje cells than the 10 days of exposure to ethanol in utero, whereas the Purkinje cells present in adult animals show a great resistance to ethanol. The neonatal period seems to be a time of high susceptibility of Purkinje cells to ethanol.
CRYSTALLINE AGGREGATES OF PROTEIN‐GLYCOGEN COMPLEXES (ALIAS ‘VIRUS‐LIKE PARTICLES’) IN SKELETAL MUSCLE: REPORT OF A CASE AND REVIEW OF THE LITERATURE
Authors: PALMUCCI L. , ANZIL A. P. , LUH S. 
Published: May 2008

Palmucci L., Anzil A.P. & Luh S. (1983) Neuropathology and Applied Neurobiology 9, 61–71Crystalline aggregates of protein‐glycogen complexes (alias ‘viruslike particles’) in skeletal muscle: report of a case and review of the literatureCrystalline arrays of so‐called ‘virus‐like particles’ were found in postmortem samples of skeletal muscle obtained from an 11‐month‐old female infant. In a large number of skeletal muscle fibres crystalline inclusions were abundant, variously configurated and positively stained with a cytochemical method for polysaccharides. A battery of enzymatic tests, including some with diastase and a‐amylase, was, however, entirely non‐contributory. A muscle biopsy studied 5 months before death had disclosed no crystalline inclusions of any kind. The literature concerning similar cases of ‘virus‐like particles’, crystalline glycogen aggregates or protein‐glycogen complexes in muscle is reviewed. Possible reasons underlying the aggregation of protein‐glycogen complexes into crystalline arrays are discussed.
A QUANTITATIVE METHOD FOR COMPARING THE DISTRIBUTION OF CEREBRAL TRAUMA IN CLOSED‐HEAD INJURIES WITH AND WITHOUT TENTORIAL HERNIATION
Authors: GIBSON P. H. 
Published: May 2008

Gibson P. H. (1983)Neuropathology and Applied Neurobiology9, 135–148A quantitative method for comparing the distribution of cerebral trauma in closed‐head injuries with and without tentorial herniationDamage to the cerebral and cerebellar hemispheres and brain‐stem was investigated in forty‐seven cases of closed‐head injury of which twenty‐four had undergone tentorial herniation. The damage was assessed by eye in coronal sections as well as microscopically using celloidin and paraffin techniques. All cases had damage to the hemispheres and brain‐stem. The types and positions of the damage were plotted on charts and quantified by using a cm2grid system. The quantity of the haemorrhage and ischaemia in the hemispheres was found by Student'st‐test to be statistically greater (P< 0001) for cases which had herniated. Haemorrhage and ischaemia were most frequently seen on the ventral aspect of the hemispheres and particularly the frontal lobes. The distribution of the haemorrhage and ischaemia was the same for both the herniated and non‐herniated brains. In a subsample of sixteen cases statistically significant differences were found using they2test for the positions of brain‐stem damageper sein herniated and non‐herniated brains. In a second subsample of thirty‐two cases a statistical difference in the position of haemorrhage was also found. The greatest damage to the brain‐stem was medial and rostral in herniated brains and paralateral and rostral but extending further caudally in non‐herniated brains. The variation in quantity of the five types of damage with length of survival was compared for herniated and non‐herniated brains.
ADRENOLEUKODYSTROPHY: CLINICAL, PATHOLOGICAL AND BIOCHEMICAL FINDINGS IN TWO BROTHERS WITH THE ONSET OF CEREBRAL DISEASE IN ADULT LIFE
Authors: ESIRI M. M. , HYMAN M. , HORTON L. , LINDENBAUM R. H. 
Published: May 2008

Adrenoleukodystrophy: clinical, pathological and biochemical findings in two brothers with the onset of cerebral disease in adult lifeTwo brothers are described in whom adrenoleukodystrophy (ALD) presented as progressive cerebral degeneration in early adult life. Diagnosis during the life of one brother was based on cerebral biopsy appearances. At autopsy there was a leucodystrophy and an additional myelopathy in both cases. Biochemical studies carried out on the propositi and other family members revealed characteristic abnormalities of ALD in the propositi and two, as yet clinically unaffected, adult brothers, and abnormalities characteristic of the heterozygous state in their mother. Neither of the clinically affected brothers showed clinical features of hypoadrenalism and these cases emphasize the importance of considering the diagnosis of ALD in adult males with leucodystrophy even in the absence of overt adrenal insufficiency.
GLYCOGEN PARTICLES IN METHIONINE SULFOXIMINE EPILEPTOGENIC RODENT BRAIN AND LIVER AFTER THE ADMINISTRATION OF METHIONINE AND ACTINOMYCIN D
Authors: DELORME P. , HEVOR T. K. 
Published: May 2008

Glycogen particles in methionine sulfoximine epileptogenic rodent brain and liver after the administration of methionine and actinomycin DRats and mice were submitted either to the convulsant methionine sulfoximine (MSO) alone or to MSO combined with actinomycin D or methionine respectively. Twenty‐four hours after the intraperitoneal administration of these compounds, the animals were killed and tissue samples were prepared for electron microscopy. Methionine sulfoximine induced ‘grand mal’ type seizures which were abolished by methionine. In saline controls, glycogen was as β particles located in the cytoplasm of astrocytes, i.e. in perikarya and processes. Liver glycogen was as perinuclear masses of a and β particles or as αparticles scattered in all the cytoplasm. When the rodents were treated with MSO, glycogen was as α and β particles which invaded all areas of the astrocyte cytoplasm, this increase being tremendous in perivascular end feet. Actinomycin D slowed down the accumulation of glycogen particles while methionine completely abolished it. In any case, glycogen particles were confined to the astrocytes and were never seen in other types of cells. In liver, MSO induced an important decrease or a complete disappearance of glycogen particles. When the convulsant was combined with actinomycin D or with methionine, the figures looked like those of controls. These results have been discussed in relation to the mechanism of glycogenesis in central nervous system of rodents submitted to MSO.
AGE‐RELATED VARIATIONS IN THE NEURON CONTENT OF THE CEREBRAL CORTEX IN SENILE DEMENTIA OF ALZHEIMER TYPE
Authors: HUBBARD B. M. , ANDERSON J. M. 
Published: May 2008

AbstractHubbard B. M. & Anderson J. M. (1985) Neuropathology and Applied Neurobiology, 11, 369–382Age‐related variations in the neuron content of the cerebral cortex in senile dementia of Alzheimer typeThe cell content of the cerebral cortex in senile dementia of Alzheimer type has been examined using a stereological method which combines gross cortical measurements and microscopical observations to give volumetric data on cells and neuropil. In the neocortex only the large (> 12 µm diameter) neuron fraction was found to be abnormal; the volume of these cells was reduced in most patients aged less than 80 years, but was not usually abnormal for age in older cases. Smaller neurons and glial cells showed no consistent change from normal values. Neuropil was diminished in both age groups, so that patients over 80 years of age tended to show cerebral atrophy without neocortical neuron loss. By contrast to the neocortex, the subiculum of the hippocampus consistently showed pathological neuron loss in both age groups.
A MORPHOMETRIC STUDY OF THE MICROVASCULATURE OF A RAT GLIOMA
Authors: LUTHERT P. J. , LANTOS P. L. 
Published: May 2008

AbstractLuthert P. J. & Lantos P. L. (1985) Neuropathology and Applied Neurobiology, 11, 461–473A morphometric study of the microvasculature of a rat gliomaIntracerebral tumours were produced in BD IX rats by the inoculation of neoplastic astrocytes. Following perfusion‐fixation, 10 firw sections were stained with toluidine‐blue and photographed so as to construct photomontages embracing deep tumour, tumour edge and surrounding brain. Thirteen montages from 9 tumours were studied. Successive 200 mm samples were analysed with a digitizing tablet and, for each sample the following were measured (a) the number of vascular profiles per unit area, (b) the mean vessel circumference and diameter and (c) the approximate fractions of the sample occupied by tumour and necrosis. Towards the tumour centre, vascular density dropped to 20% of that for normal cortex but vessel size more than doubled. The surface area fraction of the vessels reached a maximum at the tumour edge.These results provide not only an anatomical framework for both a variety of physiological studies and for the investigation of angiogenesis in this system but also have pharmacokinetic implications for the treatment of brain tumours.
CALCIFICATION IN THE HUMAN CHOROID PLEXUS, MENINGIOMAS AND PINEAL GLAND
Authors: ALCOLADO J. C. , MOORE I. E. , WELLER R. O. 
Published: May 2008

Calcification in the human choroid plexus, meningiomas and pineal glandCalcification in the stroma of adult telencephalic choroid plexus was studied of 20 postmortem brains and one biopsy by light microscopy, transmission and scanning electron microscopy and compared with calcification in psammoma bodies in normal arachnoid, five spinal meningiomas and in calcospherites of six pineal glands. Fifteen fetal and newborn choroid plexuses were also examined by light microscopy. Calcium deposition was observed in the subepithelial regions of the adult choroid plexus, in the walls of blood vessels but was mostly seen in spherical psammona bodies. Collagen whorls 20–60 μm in diameter and surrounded by arachnoid cells, were observed in the stroma of the choroid plexus; calcium, phosphorous and iron were deposited in the collagen whorls to form psammoma bodies. Matrix vesicles and spicules resembling hydroxyapatite were associated with the arachnoid cells surrounding the collagen whorls and with the collagen fibres within the whorls. The dense amorphous calcified core of each psammoma body was surrounded by an outer coating of entwined collagen fibres readily visible by scanning electron microscopy. Similar psammoma bodies were occasionally observed in normal arachnoid. Psammoma bodies in meningiomas resembled those in the choroid plexus stroma. Calcospherites in the pineal differed from psammoma bodies; they were lobulated, more irregular in shape and did not have a collagen base. The results of this study suggest that psammoma bodies in the choroid plexus, as in meningiomas, form by a process of dystrophic calcification associated with arachnoid cells and collagen fibres. The presence of iron in the choroid plexus psammoma bodies may be a result of haemorrhage into the stroma. The mechanism of calcification in pineal remains unclear.