bluuebunny/crossref_metadata_2025_split huggingface dataset:
CHANGES IN THE DISTRIBUTION OF HISTOCHEMICALLY LOCALIZED MERCURY IN THE CNS AND IN TISSUE LEVELS OF ORGANIC AND INORGANIC MERCURY DURING THE DEVELOPMENT OF INTOXICATION IN METHYLMERCURY TREATED RATS
Authors: HARGREAVES R. J. , FOSTER J. R. , PELLING D. , MOORHOUSE S. R. , GANGOLLI S. D. , ROWLAND I. R. 
Published: May 2008

AbstractHargreaves R. J., Foster J. R., Pelling D., Moorhouse S. R., Gangolli S. D. & Rowland I. R. (1985) Neuropathology and Applied Neurobiology 11, 383–401Changes in the distribution of histochemically localized mercury in the CNS and in tissue levels of organic and inorganic mercury during the development of intoxication in methylmercury treated ratsThe development of neurotoxicity in rats after exposure to methylmercuric chloride was monitored using behavioural indices. At selected time points the cellular localization of mercury and the relative amounts of organic and inorganic mercury were determined in several regions of the CNS, and in some non‐neural tissues. The CNS showed an affinity for organic mercury, the levels of inorganic mercury remaining low throughout symptomatic intoxication. Histopathological changes were not closely related to the regional tissue content of the organic or inorganic forms, nor to mercury localized histochemically at the cellular level. The stained deposits, which had focal cytoplasmic distribution, appeared in glial cells initially then in larger neurones as the intoxication progressed. These observations may represent changes in the mercury content of different cell types or reflect differences in the way that they handle a similar burden of mercury. A transitory accumulation of mercury in glial cells may be a factor contributing to the occurrence of a latent period and sequestration of mercury in cytoplasmic organelles may serve to protect some cell types from injury.
PROGRESSIVE AXONOPATHY: AN INHERITED NEUROPATHY OF BOXER DOGS. 2. THE NATURE AND DISTRIBUTION OF THE PATHOLOGICAL CHANGES
Authors: GRIFFITHS I. R. , McCULLOCH M. C. , ABRAHAMS S. 
Published: May 2008

AbstractGriffiths I. R., McCulloch M. C. & Abrahams S. (1985) Neuropathology and Applied Neurobiology 11, 431–446Progressive Axonopathy: an inherited neuropathy of boxer dogs. 2. The nature and distribution of the pathological changesThis report describes the neuropathology of progressive axonopathy (PA), an autosomal recessive inherited neuropathy of Boxer dogs, which affects CNS and PNS. The nerve roots contain numerous myelin bubbles and proximal paranodal axonal swellings containing vesicles, vesiculo‐tubular profiles and disorganized neurofilaments. The myelin sheath overlying such swellings is often attenuated. As the disease develops there are progressive changes in the myelin sheath with thinning at paranodal and internodal locations, loss of myelin from lengths of axon and the formation of short internodes with disproportionately thin sheaths. The abnormalities show a very definite selectivity for nerve roots and proximal nerves. Conversely, the frequency of degeneration and regeneration is greater distally except in the cervical ventral roots which contain numerous regenerating clusters. In the CNS numerous axonal spheroids are found in the lateral and ventral columns of the spinal cord and in various brain stem nuclei, particularly the superior olives, accessory cuneate nuclei and lateral lemniscus and its nucleus. Axonal degeneration which occurs mainly in the cord shows no obvious tract or proximal/distal selectivity. The optic pathways are also involved, predominantly adjacent to the chiasma. The autonomic nervous system is affected and distal limb muscles show varying, but usually minor, degrees of neurogenic atrophy. The condition, which has no obvious direct parallel in human or veterinary medicine, shows gross disturbances of axon‐glial interrelationships in both CNS and PNS.
TRANSMISSIBLE MINK ENCEPHALOPATHY (TME) IN CHINESE HAMSTERS: IDENTIFICATION OF TWO STRAINS OF TME AND COMPARISONS WITH SCRAPIE
Authors: KIMBERLIN R. H. , COLE SHIRLEY , WALKER CAROL A. 
Published: May 2008

AbstractKimberlin R. H., Cole S. & Walker C. A. (1986) Neuropathology and Applied Neurobiology 12, 197–206Transmissible mink encephalopathy (TME) in Chinese hamsters: identification of two strains of TME and comparisons with scrapieTME from a single source was transmitted by intracerebral injection to Chinese hamsters, producing clinical disease in all seven animals after incubation periods of over 600 days. The brain from each of the primary cases was used to establish separate intracerebral passage‐lines of TME and this led to the isolation of two different strains of agent, designated 333K and 333W. These strains were easily distinguished by the incubation periods they produced (about 130 and 230 days, respectively) under standard conditions of infection, and by the characteristic profiles of vacuolation seen in different regions of the brain. Comparisons were made with a strain of scrapie passaged in Chinese hamsters, designated 34W, which could be distinguished from both strains of TME. Nevertheless the properties of the scrapie and TME strains overlapped, with one of the TME strains (333K) resembling the 34W strain of scrapie in Chinese hamsters more closely than the other TME strain (333W). These similarities strengthen the view that TME and scrapie are caused by a similar type of infectious agent. The very large ‘species barrier effect’ on transmitting TME to Chinese hamsters was in marked contrast to the minimal effect seen with scrapie and an explanation for this is suggested. Two interesting pathological features of the study were (a) the severe loss of pyramidal cells produced in the hippocampus by the 34W strain of scrapie, and (b) the focal, symmetrical vacuolation of the thalamus caused by 333K TME.
THE EFFECTS ON FETAL BRAIN DEVELOPMENT IN THE RAT OF A SEVERELY IODINE DEFICIENT DIET DERIVED FROM AN ENDEMIC AREA: OBSERVATIONS ON THE FIRST GENERATION
Authors: JIANQUN LI , XIN WANG , YUQUIN YAN , KEWEI WANG , DAKAI QIN , ZHENFU XIN , JUN WEI 
Published: May 2008

The effects on fetal brain development in the rat of a severely iodine deficient diet derived from an endemic area: observations on the first generationRats were fed on a severely iodine deficient diet (iodine content 4.5 μg/100 g) similar to that being consumed by people living in a village with a high rate of endemic cretinism. After a period of 4 months, the thyroid and brain were studied in the adult and their fetuses at 16, 17, 18, 19 and 20 days of gestation, and in postnatal animals at 1, 5, 10, 20, 30 and 60 days of age. By comparison with a control group (diet with iodine content 54.7 μg/100 g) the experimental group showed marked goitres, a higher uptake of 125I by the thyroid, reduced serum T4, and reduction in brain weight. The cerebral and cerebellar histological findings showed that the density of brain cells had increased, and the mean neuron size was reduced. Furthermore, disappearance of the cerebellar EGL was delayed. These findings indicate that this animal model is likely to be suitable for the studies of endemic cretinism in man.
UNOCYTOCHEMICAL CHARACTERIZATION OF THE A15 A5 TRANSPLANTABLE BRAIN TUMOUR MODEL IN VIVO
Authors: SAGGU H. , PILKINGTON G. J. 
Published: May 2008

Immunocytochemical characterization of the A15 A5 transplantable brain tumour model in vivoA comparative immunocytochemical study was carried out on intracerebral and extracranial gliomas of the rat produced by intracerebral injection of low (10th) and high (40th) in vitro passages of neoplastic glial cells. The cells injected were a neoplastic astrocytic clone– A15 A5– derived from a mixed glioma induced transplacentally by N‐ethyl‐N‐nitrosourea (ENU) in a BD‐IX rat. An inverse relationship was seen between the expression of the astrocytic markers glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) at low and high passage: GFAP decreased with increasing passage while GS increased. The distribution of vimentin, the major cytoskeletal component of immature glia, was constant, irrespective of passage–a feature consistent with previous in vitro findings. The expression of laminin by both reactive and neoplastic astrocytes increased with increasing passage, while high magnification examination revealed the presence of the glycoprotein fibronectin on the cell‐surfaces of A15 A5‐derived tumour cells. Both neoplastic and reactive astrocytes expressed S‐100 protein with a higher proportion of positive cells in extracranial tumours. Occasional cells, probably actively phagocytozing populations of reactive astrocytes and macrophages, were positive for alpha‐1‐antitrypsin. None of the neoplastic cells expressed the oligodendrocyte marker carbonic anhydrase II. This immunocytochemical study supports previous morphological findings in differences in differentiation between the cells of tumours produced by high and low passage cells.
AN ULTRASTRUCTURAL ANALYSIS OF THE EFFECTS OF ACCUMULATION OF NEUROFIBRILLARY TANGLE IN PYRAMIDAL NEURONS OF THE CEREBRAL CORTEX IN ALZHEIMER'S DISEASE
Authors: SUMPTER P. Q. , MANN D. M. A. , DAVIES C. A. , YATES P. O. , SNOWDEN J. S. , NEARY D. 
Published: May 2008

An ultrastructural analysis of the effects of accumulation of neurofibrillary tangle in pyramidal neurons of the cerebral cortex in Alzheimer's diseaseQuantitative morphometric (stereological) methods have been used to assess the effects of accumulation of neurofibrillary material on the fine structure of pyramidal cells in biopsy specimens of temporal cortex from nine patients with Alzheimer's disease. When compared with non‐tangled cells from the same patients, tangled cells show an increase in total area of cytoplasm due to the accumulation of tangle and a reduction in the area of the nucleus; the area proportion of the cell body occupied by total cytoplasm, therefore, increases whereas that of the nucleus decreases. Within the total cytoplasm, nucleolar and mitochondrial areas are maintained, but that of lipofuscin is increased, though all are increased when expressed as a proportion of the useful cytoplasm alone (i.e. total cytoplasmic area minus area occupied by tangle). Measures of the amount of rough endoplasmic reticulum and ribosomes are decreased overall in tangled cells, though when related to useful cytoplasm alone such measures approach non‐tangled cell values. Measures of smooth endoplasmic reticulum are unaltered throughout. When related to the amount of tangle within cells it was found that the most heavily tangled cells retain 28% of useful cytoplasm, 72% of the nuclear area, 50% of the rough endoplasmic reticulum and 27% of ribosomes present within least tangled and non‐tangled cells. By contrast, mitochondrial area is maintained and that of lipofuscin increased. The capacity for protein synthesis in tangled cells appears, therefore, to be progressively decreased with accumulation of tangle, whereas that for oxidative metabolism is maintained and lysosomal activity, perhaps, increased. Neurofibrillary tangle formation and accumulation may, therefore, lead to the eventual death of neurons and be the major cause of nerve cell loss in Alzheimer's disease.
THE DEVELOPMENT OF THE HUMAN BLOOD‐BRAIN AND BLOOD‐CSF BARRIERS
Authors: MØLLGÅRD K. , SAUNDERS N. R. 
Published: May 2008

The development of the human blood‐brain and blood‐CSF barriersThe commonly held belief that the fetal blood‐brain and blood‐CSF barriers are immature is reviewed. Results obtained from carefully conducted experiments with horseradish peroxidase and optimal freeze‐fracturing suggest that the chick, rat and monkey brain barrier systems to proteins are tight from the earliest stages of development. Previous studies are reviewed in the light of new information on retrograde axonal transport, circumventricular organs, the proper use of horseradish peroxidase, freeze‐fracturing, immunocytochemistry and plasma protein gene expression in the developing human brain. Original data on the development of human brain barrier systems are included. Tight junctions between cerebral endothelial and choroid plexus epithelial cells form the morphological basis for these systems. CSF in the fetus contains a remarkably high concentration of protein in contrast to adult CSF which is characterized by a very low protein concentration. This has previously been interpreted as due to immaturity of barriers in the fetal brain. Tight junctions between cerebral endothelial cells and between choroid plexus epithelial cells have been investigated in human embryos and fetuses by freeze fracture and thin section electron microscopy. As soon as the choroid plexus and the brain capillaries differentiated they exhibited well formed tight junctions. These junctions were very complex at early stages of development. A new barrier consisting of ‘strap junctions’ was found in the developing germinal matrix. The very high concentration of protein in early human fetal CSF cannot be accounted for by a lack of tight junctions
PERIPHERAL NERVE REGENERATION THROUGH GRAFTS OF LIVING AND FREEZE‐DRIED CNS TISSUE
Authors: ANDERSON P. N. , TURMAINE M. 
Published: May 2008

Peripheral nerve regeneration through grafts of living and freeze‐dried CNS tissueThe ability of peripheral nerve fibres to regenerate through the central nervous system (CNS) extracellular matrix in the presence of CNS myelin debris was examined using living and freeze‐dried optic nerve grafts. The grafts were placed end‐to‐end with the proximal stumps of severed common peroneal nerves of inbred mice. Within a 4 week period, regenerating peripheral nervous system fibres were found in only two of 14 living grafts. However axons always grew into freeze‐dried grafts within one week, despite the presence of CNS myelin debris. The regenerating axons in freeze‐dried grafts were accompanied by Schwann cells and were initially found associated with the inner aspect of the glial basal lamina. Although the extracellular matrix of the freeze‐dried CNS tissue was subsequently reorganized by invading cells, it seems likely that neither the nature of the CNS extracellular matrix nor the presence of CNS myelin debris had a major inhibitory influence on peripheral nerve regeneration. It is suggested that the presence of living astrocytes covered by a basal lamina at the proximal end of the living optic nerve grafts may inhibit their penetration by regenerating axons.
ANTIGENIC EXPRESSION BY CELLS DERIVED FROM HUMAN GLIOMAS DOES NOT CORRELATE WITH MORPHOLOGICAL CLASSIFICATION
Authors: KENNEDY P. G. E. , WATKINS B. A. , THOMAS D. G. T. , NOBLE M. D. 
Published: May 2008

Antigenic expression by cells derived from human gliomas does not correlate with morphological classificationWe have found that cell populations derived from human gliomas can be divided into antigenic classes which are not predictable on the basis of standard morphological analysis and which, most frequently, do not support the lineage assignations of various tumours as determined by traditional neuropathological methods. For example, only 6/60 cultures derived from astrocytomas expressed glial fibrillary acidic protein (GFAP), an astrocyte specific marker, and all six of these cultures were derived from morphological categories which more frequently gave rise to populations which did not express GFAP. None of the seven oligodendrogliomas or four oligo‐astrocytomas examined expressed antigens specifically expressed by oligodendrocytes. Most tumour‐derived populations, from all classes of tumour and all grades of malignancy, expressed cell‐surface fibronectin, an extracellular matrix protein only rarely found on the surfaces of CNS macroglia; such cells did not express glial‐specific antigens (e.g., GFAP) in vitro. Investigation of antigen expression in tumour biopsies indicated that some tumours also consisted largely or wholly of cells which expressed fibronectin in situ. Fibronectin‐expressing cells were aneuploid and were not contact inhibited in their growth, indicating that they were transformed cells. We have also identified two previously unknown antigenic phenotypes among the gliomas.
1,3‐DINITROBENZENE‐INDUCED ENCEPHALOPATHY IN RATS
Authors: PHILBERT M. A. , NOLAN C. C. , CREMER J. E. , TUCKER D. , BROWN A. W. 
Published: May 2008

1,3‐Dinitrobenzene‐induced encephalopathy in ratsExposure to 1,3‐dinitrobenzene (1,3‐DNB) in humans induces methaemoglobinaemia, nausea and nervous symptoms. When given to conventional rats, twice‐daily oral doses of 10mgkg‐1 1,3‐DNB produce methaemoglobinaemia and frequently ataxia after four or five doses. In germ free rats given only a single oral dose of 20mgkg‐1, similar symptoms occur but are of more rapid onset. Light and electron microscope examinations reveal an acute thiamine deficiency‐like lesion in the brain stems of both ataxic and apparently normal rats. Bilaterally symmetrical vacuolated lesions involve cerebellar roof, vestibular and superior olivary nuclei and the inferior colliculi. Frequent petechial haemorrhages are associated with these lesions, the erythrocytes usually being limited to enlarged Virchow‐Robin spaces but sometimes spreading more widely. The primary cellular targets appear to be astrocytes, oligodendrocytes and vascular elements with secondary neuronal involvement. It is suggested that 1,3‐DNB interferes with intracellular redox mechanisms resulting in impaired glucose oxidation.
EPITHELIAL MEMBRANE ANTIGEN EXPRESSION IN EPENDYMOMAS
Authors: CRUZ–SANCHEZ F. F. , ROSSI M. L. , ESIRI M. M. , READING M. 
Published: May 2008

Epithelial membrane antigen expression in ependymomasTwenty–seven ependymomas were studied (18 ‘benign’ or low grade and nine ‘malignant’ or high grade) by means of a monoclonal antibody to epithelial membrane antigen (E29) and an antiserum to glial fibrillary acidic protein (GFAP). The E29 antibody reacted with ‘benign’ ependymomas but not with ‘malignant’ ones. Staining was located on the cell surface and especially that facing rosette lumina. Cells forming papillary structures and ependymal epithelium showed a similar distribution of staining. Glial fibrillary acidic protein (GFAP) reactivity was seen in all tumours, with a perivascular accentuation in ‘malignant’ ones. Staining occurred in the cytoplasm of scattered cells and in those forming papillary structures, ependymal epithelium and rosettes. Our results may have implications in relation to the cytogenesis of these tumours and may also be useful in the histological assessment of ‘benign’versus‘malignant’ ependymomas.
CORRELATION OF TRIPHENYLTETRAZOLIUM CHLORIDE PERFUSION STAINING WITH CONVENTIONAL NEUROHISTOLOGY IN THE DETECTION OF EARLY BRAIN ISCHAEMIA
Authors: PARK C. K. , MENDELOW A. D. , GRAHAM D. I. , McCULLOCH J. , TEASDALE G. M. 
Published: May 2008

Correlation of triphenyltetrazolium chloride perfusion staining with conventional neurohistology in the detection of early brain ischaemiaTriphenyltetrazolium chloride (TTC) has been used to detect experimental brain ischaemia but its accuracy has not been established fully, especially in models of early brain ischaemia. We have developed a technique that combines TTC–staining and perfusion–fixation with formalin in the same specimen.The left middle cerebral artery of 12 rats, anaesthetized with halothane were exposed via a subtemporal approach and occluded for 4 h. The animals were perfused transcardially with TTC (2%) and formalin (10%). The forebrain was sliced and the size of the ischaemic area, delineated by TTC, was measured. The brain slices were then processed for light microscopy, and the amount of ischaemic damage determined. The ischaemic volumes of the hemisphere and cortex assessed by TTC (127–4 ± 21–7 mm3 and 18–4 ± 30 mm3) were larger than the volumes measured by microscopy (104–3 ± 16–6 mm3 and 15–2 ± 3–6 mm3) but there was no statistical difference between them. Correlation of the ischaemic volumes in hemisphere and cortex between the two methods was good (r2= 0–9221, P < 001 and r2= 0–9243, P < 0001), but the correlation of the ischaemic areas at specific coronal planes was poor. The ischaemic volume of caudate nucleus measured by TTC (15–2 ± 3–6 mm3) was smaller than the volume assessed by microscopy (18–4 ± 3–0 mm3) and the correlation was poor (r2= 0–6650)It is concluded that TTC–staining provides only an approximation of the amount of early ischaemic brain damage subsequently identified by conventional light microscopy.
THE mdx MOUSE SKELETAL MUSCLE MYOPATHY: II. CONTRACTILE PROPERTIES
Authors: COULTON G. R. , CURTIN N. A. , MORGAN J. E. , PARTRIDGE T. A. 
Published: May 2008

The mdx mouse skeletal muscle myopathy: II. Contractile propertiesThe contractile properties of soleus muscles from mdx and control mice aged between 26 and 350 days were compared with those of muscles from similarly aged control mice. Mdx mice were in general heavier (their individual soleus muscles were also heavier), of greater cross–sectional area and greater standard length than age–matched controls. Isometric forces produced by soleus muscles from young mdx mice (≤ 100 days) were similar to controls, but were weaker when force was normalized for crosssectional area. Conversely, although the absolute isometric forces produced by older (>100 days) mdx muscles were greater than age–matched controls, when normalized for cross–sectional area they were similar. No differences were found between mdx and control muscles in terms of length–force or force–velocity relationships.Thus, young mdx control muscles produce similar absolute isometric force but mdx mouse muscles are larger. When muscle size is accounted for, in terms of cross–sectional area, younger mdx muscles are, therefore, weaker than controls. Inefficient contraction of young mdx muscles may result from lack of contractile fibres, physiological inefficiency of contractile fibres, or loss of tendon–fibre continuity during muscle fibre necrosis and regeneration. The striking supernormal size and strength of older mdx muscles reflects their considerable regenerative capacity; whether this is due to an increase in muscle fibre number rather than fibre hypertrophy remains unclear.
FOCAL DENDRITIC SWELLINGS IN PURKINJE CELLS IN MUCOPOLYSACCHARIDOSES TYPES I, II AND III. A GOLGI AND ULTRASTRUCTURAL STUDY
Authors: FERRER I. , CUSÍ V. , PINEDA M. , GALOFRÉ E. , VILA J. 
Published: May 2008

Focal dendritic swellings in Purkinje cells in mucopolysaccharidoses types I, II and IIIFocal dendritic swellings in secondary dendrites of Purkinje cells were observed in post–mortem samples of the cerebellum processed by the Golgi method from three patients affected by mucopolysaccharidoses (MPS) types I–H, II and III. These focal dendritic swellings exhibited smooth surfaces but secondary formation of spine–like appendages was absent; in contrast, terminal, spiny branchlets were preserved. Complementary electron–microscopical examination of these samples revealed that membranous cytoplasmic bodies and zebra–like inclusions accounted for the material stored in these focal swellings in MPS I–H and MPS II; in addition, granulomembranous cytosomes with fine, densely–packed membranous profiles were encountered in MPS III.Focal dendritic swellings in Purkinje cells may result in abnormal electrical activity, thus producing informational imbalance on the Purkinje cell dendritic arborization in human mucopolysaccharidoses.