bluuebunny/crossref_metadata_2025_split huggingface dataset:
RETARDED FETAL BRAIN DEVELOPMENT RESULTING FROM SEVERE DIETARY IODINE DEFICIENCY IN SHEEP
Authors: POTTER B. J. , MANO M. T. , BELLING G. B. , McINTOSH G. H. , HUA C. , CRAGG B. G. , MARSHALL J. , WELLBY M. L. , HETZEL B. S. 
Published: May 2008

Potter B.J., Mano M.T., Belling G.B., Mcintosh G.H., Hua C, Cragg B.G., Marshall J., Wellby M.L. & Hetzel B.S. 1982 Neuropathology and Applied Neurobiology 8, 303–313Retarded fetal brain development resulting from severe dietary iodine deficiency in sheepSheep have been used to study the effect of dietary iodine deficiency on the development of the fetal brain. Severe iodine deficiency caused reduction in fetal brain and body weights and in brain DNA and protein from 70 days gestation to parturition. The lowered brain weight and brain DNA at 70 days gestation indicates a reduced number of cells, probably due to slower neuroblast multiplication which normally occurs from 40–80 days in the sheep, and the reduction in DNA and protein after 80 days implies that the development of neuroglia could be slowed also in iodine deficiency. Morphological changes were observed in both the cerebral hemispheres and the cerebellum. In the cerebral hemispheres of the iodine‐deficient fetuses an increased density of neurons was apparent histologically in the motor cortex and visual cortex and in the CAI and CA4 areas of the hippocampus in comparison with controls. In the cerebellum there was delayed migration of cells from the external granular layer to the internal granular layer and increased density of Purkinje cells in the iodine‐deficient fetal brains. In addition, the molecular area was increased and the medullary area reduced in comparison with controls. These changes are indicative of delayed brain maturation. Evidence of fetal hypothyroidism was provided by low fetal thyroid iodine and plasma T4 values, thyroid hyperplasia from 70 days gestation, significant reduction in body weight at the same time as the brain retardation, and absence of wool growth and delayed skeletal maturation near parturition. It is apparent from the biochemical and histological changes observed during iodine deficiency that iodine is an essential element for normal fetal brain and physical development in the sheep.
VIRUS TITRES AND PERSISTENTLY RAISED WHITE CELL COUNTS IN CEREBROSPINAL FLUID IN MICE AFTER PERIPHERAL INFECTION WITH DEMYELINATING SEMLIKI FOREST VIRUS
Authors: PARSONS LINDA M. , WEBB H. E. 
Published: May 2008

Parsons L.M. & Webb H.E.1982Neuropathology and Applied Neurobiology 8, 395–401Virus titres and persistently raised white cell counts in cerebrospinal fluid in mice after peripheral infection with demyelinating Semliki Forest virusVirus titres and cell counts in the cerebrospinal fluid of mice have been examined following intraperitoneal inoculation of demyelinating Semliki Forest virus (SFV). Virus titres in cerebrospinal fluid were highest 2–4 days after infection and fell again after day 4, 48 h before reduction in brain titres. White cell counts were very low in the first 48 h and showed a steep rise from 4 days after infection to a peak on day 6. After day 8, cell numbers fell to a plateau level which was sustained up to day 61. The significance of these findings in relation to the pathogenesis of virus‐induced disease of the central nervous system is discussed.
IN‐SITU CHARACTERIZATION OF MONONUCLEAR CELL INFILTRATES IN LESIONS OF MULTIPLE SCLEROSIS
Authors: NYLAND HARALD , MÖRK SVERRE , MATRE ROALD 
Published: May 2008

Nyland H, Mork S & Matre R.1982Neuropathology and Applied Neurobiology 8, 403–411In‐situ characterization of mononuclear cell infiltrates in lesions of multiple sclerosisThe mononuclear cell infiltrates in autopsy material from brains and spinal cords of six patients with multiple sclerosis (MS) were characterized in situ. Receptors for sheep erythrocytes and anti‐T lymphocyte serum were used to identify T lymphocytes. Receptors for the activated third components of complement and for the Fc‐portion of IgG (Fey receptors) were used as markers for macrophages and lymphocytes. In acute and recent MS lesions, perivascular infiltrates of mononuclear cells were commonly found. Most cells were T lymphocytes. Some B lymphocytes were also demonstrated. The demyelinating lesions contained large numbers of lipid macrophages expressing Fey receptors. The lipid macrophages are probably derived from microglial cells. The chronic, demyelinated lesions contain a few mononuclear cells, mainly B lymphocytes and plasma cells.
ELECTRON MICROSCOPIC STUDY OF INTRANUCLEAR SPHERES OF BOUTEILLE TYPE‐III IN ASTROCYTES WITH SPECIAL REFERENCE TO LIVER CARCINOMA
Authors: GIBSON PETER H. 
Published: May 2008

Gibson P.H.1982
Neuropathology and Applied Neurobiology
8, 413 418Electron microscopic study of intranuclear spheres of Bouteille type‐Ill in astrocytes with special reference to liver carcinomaAstrocytic intranuclear spheres of Bouteille type‐Ill were studied with the electron microscope in the neocortex of 29 patients dying from various causes. The numbers of laminate whorls in these spheres in patients with carcinoma involving the liver were found statistically to be significantly more numerous than the whorls in the spheres of patients who did not have carcinoma of the liver. This second group included patients who were suffering from carcinoma of other organs or from cirrhosis of the liver. The frequency of cases with the spheres increased with age. The numbers of spheres found in people with liver carcinoma, carcinoma of other organs and cirrhosis were the same as the numbers found in people dying from other diseases. The possibility that the increase in numbers of whorls found in people with liver carcinoma was related to a raised metabolic activity of the astrocytes resulting from reduced catabolism of hormones or metabolites by the liver is briefly discussed.
THE DEVELOPMENT OF HUMAN FETAL DORSAL ROOT GANGLIA IN VITRO: THE FIRST 20 DAYS
Authors: CRAWFORD KATHRENE , ARMATI‐GULSON PATRICIA 
Published: May 2008

Crawford K. & Armati‐Gulson P. 1982 Neuropathology and Applied Neurobiology 8, 477–488The development of human fetal dorsal root ganglia in vitro: the first 20 daysHuman fetal dorsal root ganglia aged from 8 to 12 weeks post‐menstrual were grown in vitro for up to 20 days. Outgrowth of Schwann cells, axons and fibroblasts occurred after 4 h. By the 7th day in vitro Schwann cells enclosed bundles of axons and after 10 days some Schwann cells were seen to enclose individual axons. By the 20th day in vitro there was still a predominance of Schwann cells enclosing axonal bundles, but there were more individual axons ensheathed by three or four turns of Schwann cells. This arrangement mimics the early development in vivo of human dorsal root ganglia and provides the potential for an experimental system utilizing human nervous tissue rather than non‐human animal models.
THE EFFECT OF ETHANOL ON THE CELLULAR COMPOSITION OF THE CEREBELLUM
Authors: BORGES S. , LEWIS P. D. 
Published: May 2008

Borges S. & Lewis P.D. (1983) Neuropathology and Applied Neurobiology 9, 53–60The effect of ethanol on the cellular composition of the cerebellumPregnant Wistar rats were fed on a diet of food pellets and a 10% (v/v) solution of ethanol in water during pregnancy and up to 21 days postnatally. Control groups were given food pellets and water ad libitum. Areal analysis of the cerebellum of neonates showed a significant reduction of 9–7% to 12–4% in three selected lobules of the mid‐sagittal vermis. Although there were no significant decreases in the linear frequency and absolute number of Purkinje cells, all three lobules showed a small percentage decrease in the length of Purkinje cell layer. The total number of granule cells was significantly reduced in all three lobules, and the ratio of granule cells to Purkinje cells was reduced by between 8–6% and 13–6%, although not significantly. The pyknotic index in the external granular layer (but not in the internal granular layer) was significantly increased at 21 days, while mitotic activity was unchanged. The extent of the diminution in the cell number of the internal granular layer suggests that besides increased cell death there may be a disturbance of cell proliferation kinetics in the precursor pool of the external granular layer. Although it is known that high blood levels can cause death of Purkinje cells, the moderate alcohol blood levels attained in this study were insufficient to do so.
THE MORPHOLOGICAL EFFECTS OF LEAD ON THE DEVELOPING CENTRAL NERVOUS SYSTEM
Authors: WINDER C. , GARTEN L. L. , LEWIS P. D. 
Published: May 2008

Winder C, Garten L.L. & Lewis P.D. (1983) Neuropathology and Applied Neurobiology 9, 87–108The morphological effects of lead on the developing central nervous systemThe pathological changes found in the central nervous system of lead‐exposed humans and laboratory animals are reviewed. Data in man relate to relatively high exposure levels. In human childhood lead encephalopathy, which occurs with blood lead levels in the range 100–800 μg Pb/100 ml, oedema, vacuolation, haemorrhage and reactive glial changes appear to be secondary to microvascular lesions. No primary neuronal lesions have yet been clearly identified. Neurological signs and a pathological picture closely resembling that seen in human lead encephalopathy are obtained in young lead‐exposed rats with blood lead levels above 500 μg Pb/100 ml. Oedema and haemorrhage, cyst formation, reactive glial changes and nerve cell alterations are observed consequent to changes in capillary endothelial cells and basement membranes. High‐level lead exposure in rats also produces disturbances in myelinated axons and may affect neural network formation in the central nervous system. With intermediate lead levels (200–500 μg Pb/lOOml blood), vascular changes and their sequelae are not seen, but nutritional effects occur which may produce neuropathological changes. Data from recent studies on developing rats with low blood levels (up to 100 μg Pb/100 ml) appear to show effects of lead on maturing and differentiated nerve cell populations. The relevance of these changes to human subclinical lead intoxication remains to be seen. However, the overall correspondence of findings in lead‐poisoned man and rat would make further investigation in this area appear necessary.
ABNORMAL PERISOMATIC STRUCTURES IN NON‐PYRAMIDAL NEURONS IN THE CEREBRAL CORTEX IN DOWN'S SYNDROME
Authors: FABREGUES I. , FERRERf I. 
Published: May 2008

Fabregues I. & Ferrer I. (1983) Neuropathology and Applied Neurobiology 9, 165–170Abnormal perisomatic structures in non‐pyramidal neurons in the cerebral cortex in Down's syndromeAbnormal fine filopodium‐like and stubby perisomatic processes are reported in stellate neurons, bipolar neurons and neurons with double dendritic arborization in the cerebral cortex of two patients with Down's syndrome. These findings suggest a more generalized abnormality in the development of receptor structures in Down's syndrome
EVOLUTION OF THE INTRACELLULAR CHANGES IN NEURONS CAUSED BY TRIMETHYLTIN
Authors: BROWN A. W. , CAVANAGH J. B. , VERSCHOYLE R. D. , GYSBERS M. F. , JONES H. B. , ALDRLDGE W. N. 
Published: May 2008

Rats have been given a single dose of trimethyltin (10 mg/kg) and the intracellular events have been followed particularly in hippocampus, cerebral cortex, cerebellum and spinal ganglion cells. The earliest change visible occurs 12 h after this dose and is found to be dense membrane‐bound bodies, probably derived from branching tubulo‐vesicular smooth endoplasmic reticulum formations. These occur in close connection with rough endoplasmic reticulum and polyribosomes and appear also to have some association with the Golgi complex. At 24 h there is a general vacuolation of Golgi cisterns and SER membranes, and the membrane‐bound dense body formation is greatly increased. SER abnormalities are particularly conspicuous in Purkinje cells. In spinal ganglion cells, while vacuolation of Golgi cisterns is intense, dense bodies are inconspicuous and are replaced by increased autophagosomes, often of great complexity.By 48 h vacuolation of Golgi cisterns has waned, but accumulation of dense bodies and secondary lysosomes has steadily increased. In spinal ganglion cells autophagosomes only are increased as the Golgi vacuolation declines. At later times steady increases of lysosomal dense bodies is seen generally accompanied in hippocampal pyramidal cells and dentate fascia cells by abundant cell death.The suggestion is put forward that the Golgi complex may be the seat of the critical metabolic lesion and disturbances to protein transfer and protein synthesis follow. No explanation for the selective loss of hippocampal h1–5, (CA1‐CA4 except Sommer's sector) pyramidal cells and of small dentate fascia neurons can be derived from these conclusions.
EXPERIMENTAL BILATERAL CAROTID ARTERY OCCLUSION: A STUDY OF THE OPTIC NERVE IN THE RAT
Authors: TAKAMATSU J. , HIRANO A. , LEVY D. , HENKIND P. 
Published: May 2008

Experimental bilateral carotid artery occlusion: a study of the optic nerve in the ratThe presence of marked changes in the neural retina and retinal vessels of Long‐Evans pigmented rat following bilateral carotid ligation has been previously documented by serial ophthalmologic examinations. Light and electron microscopic studies of the optic nerve in this experimental animal model revealed advanced optic nerve atrophy in ten of twelve rats examined. There was no significant pathology in either the retina or optic nerve in the remaining two rats after carotid ligation or in the sham‐operated controls.
TWO TYPES OF BRAIN LESIONS IN WERNICKE'S ENCEPHALOPATHY
Authors: TORVIK> A. 
Published: May 2008

Torvik A. (1984) Neuropathology and Applied Neurobiology 11, 179–190Two types of brain lesions in Wernicke's encephalopathyAnalysis of 46 cases of Wernicke's encephalopathy showed that the pathological processes in the thalamus and inferior olives were clearly different from those in the mammillary bodies and the subependymal structures along the third and fourth ventricles and the aqueduct. The latter regions showed a progressive destruction of the neuropil with severe endothelial swelling and a definite sparing of the neurones. In the thalamus and inferior olives, by contrast, the reverse picture was found with neuronal disintegration, sparing of the neuropil, and a mild endothelial swelling. The disintegrating neurones in the thalamus and olives resembled those seen in anoxic necrosis. However, careful comparisons indicated a gradual drop out of the neurones in Wernicke's encephalopathy in contrast to the sudden and simultaneous affection of the neurones in anoxia. Furthermore, the nuclear structure of the affected neurones was better and longer preserved in the Wernicke lesions. The disintegrating neurones in Wernicke's disease were removed by neuronophagia and, in severe cases, the process led to a widespread neuronal loss in the thalamus and olives. The two types of histological processes largely paralleled each other in time and severity and it is suggested that they had the same aetiology.
ACRYLAMIDE‐INDUCED ASCENDING DEGENERATION OF LIGATED PERIPHERAL NERVE: EFFECT OF LIGATURE LOCATION
Authors: SHARER L. R. , LOWNDES H. E. 
Published: May 2008

AbstractSharer L. R. & Lowndes H. E. (1985) Neuropathology and Applied Neurobiology 11, 191–200Acrylamide‐induced ascending degeneration of ligated peripheral nerve: effect of ligature locationAcrylamide was administered to rats for 10 days (50 mg/kg/day) after ligation of either proximal (sciatic) or distal (posterior tibial) nerves. Morphologic evaluation of the nerves revealed severe degeneration 0–5 cm proximal to the ligature, with progressively less pronounced change at successively higher levels above the ligature, when compared with ligated non‐treated controls. Although severe degeneration of the nerves was observed in both proximal‐ and distal‐ligated groups of animals, the distal‐ligated group showed slightly more change (at 0–5 cm above the ligature), suggesting a minor effect of distance of the site of nerve injury from the nerve cell body.
2,5‐HEXANEDIONE AND ACRYLAMIDE PRODUCE REORGANIZATION OF MOTONEURON PERIKARYA
Authors: STERMAN A. B. , SPOSITO N. 
Published: May 2008

AbstractSterman A. B. & Sposito N. (1985) Neuropathology and Applied Neurobiology 11, 201–2122,5‐Hexanedione and acrylamide produce reorganization of motoneuron perikaryaDuring acrylamide and hexacarbon exposure few changes have been reported in motoneuron perikarya. In the present study, light microscopic examination of lumbar motoneurons from rats intoxicated with either 2,5‐hexanedione (2,5‐HD) or acrylamide showed relatively few nonspecific changes compared to controls. However, ultrastructural study of 2,5‐HD‐intoxicated perikarya revealed a range of cytological reorganization: nuclear eccentricity and capping, reduced numbers of large Nissl bodies, and mitochondrial hypertrophy and hyperplasia. In 2,5‐HD‐intoxicated perikarya, computer‐assisted stereologic analysis demonstrated a significant increase in the volume density of mitochondria, Ultra‐structurally, acrylamide‐intoxicated perikarya showed a marked reduction in the size of Nissl bodies. Stereologic analysis showed reductions in Nissl bodies, granular endoplasmic reticulum and Golgi complexes, and an increase in mitochondria. Taken together, these qualitative and morphometric changes, which were not obvious on light microscopic examination, imply significant reorganization of perikaryal metabolism.
PATHOGENESIS OF MOUSE SCRAPIE: DYNAMICS OF VACUOLATION IN BRAIN AND SPINAL CORD AFTER INTRAPERITONEAL INFECTION
Authors: COLE SHIRLEY , KIMBERLIN R. H. 
Published: May 2008

AbstractCole S. & Kimberlin R. H. (1984) Neuropathology and Applied Neurobiology 11, 213–227Pathogenesis of mouse scrapie: dynamics of vacuolation in brain and spinal cord after intraperitoneal infectionAt the late clinical stage of scrapie in mice, the severity and distribution of vacuolation in the brain (the lesion profile) is largely determined by the strain of agent and the genotype of the mouse: under controlled conditions, lesion profiles can be used to distinguish between scrapie strains. This paper describes the sequential development of lesions in brain at much earlier times and includes a study of spinal cord. Mice (CW) were infected intraperitoneally with 139A scrapie. Grey matter vacuolation first occurred in thoracic cord, developing later in lumbar and cervical cords, and then in various brain regions in a caudal to rostral sequence. This pattern closely matches the sequential spread of infection from mid‐thoracic cord to much of the CNS that was previously found in this scrapie model. Further studies of grey matter in spinal cord suggest that agent entered the mid‐thoracic region via sympathetic fibres. Vacuolation in white matter mirrored the grey matter pattern within an area but always occurred later. The severity of grey matter vacuolation in the four areas of the CNS where it developed early, reached plateau levels before the clinical stage of scrapie, but the severity was still increasing at the clinical stage in areas where vacuolation had started late. Hence the severity of lesions in a particular area may sometimes be limited by the time available for them to develop before the host dies. It appears that the distribution of vacuolation in this particular scrapie model is initially influenced by that of the infectious agent and only later does it reflect the distribution of vacuolation target areas shown by the characteristic lesion profile.
INTRACRANIAL MALIGNANT TERATOMA
Authors: DIENGDOH J. V. , BUXTON P. H. , FOY P. M. 
Published: May 2008

AbstractDiengdoh J. V., Buxton P. H. & Foy P. M. (1985) Neuropathology and Applied Neurobiology 11, 245–250Intracranial malignant teratomaA case of malignant teratoma arising near the third ventricle in an adult is reported. It represented a true teratoma containing elements of all three germ layers of which two, namely the mesenchymal and endodermal elements have undergone malignant change. It was characterized by rapid recurrences after two operations with death occurring shortly after the second operation.
CEROID‐LIPOFUSCINOSIS (BATTEN'S DISEASE): PATHOGENESIS OF BLINDNESS IN THE OVINE MODEL
Authors: MAYHEW I. G. , JOLLY R. D. , PICKETT B. T. , SLACK P. M. 
Published: May 2008

AbstractMayhew I. G., Jolly R. D., Pickett B. T. & Slack P. M. (1985) Neuropathology and Applied Neurobiology 11, 273–290Ceroid‐lipofuscinosis (Batten's disease): pathogenesis of blindness in the ovine modelBlindness is a feature of the group of storage diseases of children known as the ceroid‐lipofuscinoses. Sequential studies in the ovine model, which most resembles the juvenile form of human disease, showed clearly that blindness had two components, a central and a peripheral. Whereas the central component, attributable to neuronal death and atrophy of the cerebral cortex, was responsible for early loss of vision, retinal atrophy was also extremely advanced in terminal stages of the disease. The primary retinal change was one of dystrophy of photoreceptor outer segments which preceded degeneration and necrosis of the photoreceptors cells themselves. Electroretinography showed that there was a progressive loss of a‐ and b‐waves during the course of the disease, but this was preceded by a diminished c‐wave which was eventually replaced by a negative potential. However, the pigment epithelium remained functionally (azide responsive) and ultrastructurally intact throughout the study. Loss of brain weight with selective cerebral atrophy also correlated with abnormal behaviour and facial manoeuvres that were intrepreted as partial seizures that did not become generalized.
THE CONTUSION INDEX: A REAPPRAISAL IN HUMAN AND EXPERIMENTAL NON‐MISSILE HEAD INJURY
Authors: ADAMS J. H. , DOYLE D. , GRAHMA D. I. , LAWRENCE A. E. , McLELLAN D. R. , GENNARELLI T. A. , PASTUSZKO M. , SAKAMOTO T. 
Published: May 2008

AbstractAdams J. H., Doyle D., Graham D. I., Lawrence A. E., McLellan D. R., Gennarelli T. A., Pastuszko M. & Sakamoto T. (1985) Neuropathology and Applied Neurobiology 11, 299–308The contusion index: a reappraisal in human and experimental non‐missile head injuryA previously described method of quantifying cerebral contusions in man (the contusion index) caused by non‐missile head injury has been modified and applied to a larger series of cases, and used to assess contusions in experimental head injuries. The initial findings in man have been confirmed, viz. that contusions are most severe in the frontal and temporal lobes; that contusions may be entirely absent in a patient dying as a result of a head injury; that there is no correlation between the severity of contusions and the nature of the injury; that the concept of contrecoup must continue to be questioned; that contusions are more severe in patients who have a fracture of the skull in comparison to those who do not; that contusions are more severe in patients who do not experience a lucid interval than in those who do; and that contusions are less severe in patients with diffuse axonal injury than in those who do not have diffuse axonal injury. The distribution of contusions in subhuman primates is similar to that seen in man, and they occur more frequently with short duration than with long duration acceleration.