bluuebunny/crossref_metadata_2025_split huggingface dataset:
RETINOPATHY IN MICE WITH EXPERIMENTAL SCRAPIE
Authors: FOSTER J. D. , FRASER H. , BRUCE M. E. 
Published: May 2008

AbstractFoster J. D., Fraser H. & Bruce M. E. (1986) Neuropathology and Applied Neurobiology 12, 185–196Retinopathy in mice with experimental scrapieScrapie is a naturally occurring neurological disease of adult sheep and goats with an incubation period of several years. Some strains of the causal agent can infect laboratory mice in which the incubation period, as well as the severity and distribution of vacuolar degeneration in the brain, varies according to the strain of the agent and the genotype of the mouse. Retinopathy, involving the partial or complete loss of the photoreceptor layer, was observed in a number of murine scrapie models but was absent in others. The severity of retinopathy depended on both the strain of scrapie and the genotype of mouse used. Some scrapie strains (22C, 87A and 87V) produced minimal or no retinal pathology, others (ME7, 22A and 22L) produced changes in the retinae of only certain mouse genotypes, while the strains 79A and 139A produced degeneration of the photoreceptor layer in every mouse genotype investigated. The severity of retinopathy in the various models did not correlate with the overall intensity of vacuolar degeneration in the brain, with the severity of vacuolation in the centres in the brain controlling pupillary constriction, or with the incubation period.
EVIDENCE THAT TRANSMISSIBLE MINK ENCEPHALOPATHY AGENT IS BIOLOGICALLY INACTIVE IN MICE
Authors: TAYLOR D. M. , DICKINSON A. G. , FRASER H. , MARSH R. F. 
Published: May 2008

AbstractTaylor D. M., Dickinson A. G., Fraser H. & Marsh R. F. (1986) Neuropathology and Applied Neurobiology 12, 207–215Evidence that transmissible mink encephalopathy agent is biologically inactive in miceTransmissible mink encephalopathy (TME) is probably a form of the sheep disease, scrapie, introduced by accidentally feeding mink with scrapie‐infected sheep tissues. Although no successful transmissions of TME to mice have been achieved previous work has involved various limitations. To maximize the possibility of transmission, 176 mice, representing 14 different genotypes mostly not previously tested with TME, were injected with TME‐infected mink brain from three sources with different histories. No scrapie‐like disease was detected clinically or histologically in these mice or in a further 111 which were subsequently injected with brain or spleen material from 10 of the TME‐injected mice killed when senile. Furthermore, a series of experiments involving seven strains of scrapie, demonstrated that prior injection of mice with TME failed to affect the normal progress of scrapie infection indicating that TME agent had not occupied scrapie replication sites or otherwise influenced the pathogenesis of scrapie. The overall conclusion from these experiments is that TME is biologically inactive in mice. Although many strains of natural scrapie can be transmitted to laboratory mice, this has not been possible with all strains and it is concluded that one or more of such strains is likely to be the cause of TME in mink.
EFFECTS OF PRENATAL ETHANOL EXPOSURE ON PHYSICAL GROWTH, SENSORY REFLEX MATURATION AND BRAIN DEVELOPMENT IN THE RAT
Authors: LOPEZ‐TEJERO D. , FERRER I. , LLOBERA M. , HERRERA E. 
Published: May 2008

Effects of prenatal ethanol exposure on physical growths, sensory reflex maturation and brain development in the ratIn the offspring of ethanol‐treated rats during gestation (25% ethanol in drinking water) decreased litter size, increased postnatal mortality rate, reduced body weight and body size, delayed ear opening, eyelid opening and teeth eruption, retarded air righting reflex acquisition, impaired brain growth, reduced cortical thickness and delayed maturation of layer Vth's pyramidal neurons: (a) reduced basilar dendritic arborization and (b) decreased number of spines in the apical dendrite, were observed when compared with age‐matched controls fed with a standard diet. Minimal effects were found in the offspring of fibre‐treated rats during gestation (standard diet mixed with cellulose) in which the body weight was similar to that of controls, although both the calorific intake from food and the mother's weight gain during pregnancy were similar to those of the ethanol‐treated group. All these abnormal parameters became normal at the end of the first month of postnatal life, indicating recovery of these developmental defects produced by prenatal ethanol consumption.
DEGENERATIVE CHANGES IN RAT INTRASPINAL SCHWANN CELLS FOLLOWING TELLURIUM INTOXICATION
Authors: HAMMANG J. P. , DUNCAN I. D. , GILMORE S. A. 
Published: May 2008

Degenerative changes in rat intraspinal Schwann cells following tellurium intoxicationA diet containing 1.25% elemental tellurium (Te) when fed to rats in week 3 of life produces acute peripheral nervous system (PNS) demyelination. The purpose of this investigation was to determine whether Te has the same neurotoxic effect on Schwann cells and their associated myelin when located within the spinal cord. Schwann cells were induced into the CNS by irradiating the lumbosacral spinal cord of 3 day‐old rats with 4000 rads of soft X‐rays (Heard & Gilmore, 1980). At 22–28 days of age, a diet containing 1.25% Te was fed to half of these rats, and others were fed on rat chow alone. Non‐irradiated rats of the same age were divided into two similarly fed groups. At intervals from 2 to 15 days after the iniation of this diet, the rats were perfused and the irradiated portion of the cord, or comparable level in non‐irradiated rats, was trimmed and processed for light and electron microscopy and immunocytochemistry. All rats fed Te became paretic by 6–7 days, and diffuse demyelination with obvious degenerative changes in Schwann cells was seen in the nerve roots. Immunocytochemical localization of Schwann cells and peripheral myelin in the spinal cord was demonstrated using Po antiserum, and in these areas the reduction of astrocytes and their processes was shown using sections incubated with GFAP antiserum. In these areas, as in the roots, there was myelin lamellar separation, and many Schwann cells contained cytoplasmic vacuoles, hypertrophied lysosomal structures and myelin debris. Adjacent oligodendrocytes and CNS myelin were apparently unaffected, confirming a differential susceptibility of oligodendrocytes and Schwann cells. There were no Schwann cell abnormalities in the non Te‐fed irradiated rats. This experimental model provides a situation in which other neurotoxic compounds can be evaluated to compare their effects on CNS and PNS myelin in the same milieu.
RADIATION INDUCED DAMAGE IN THE CHOROID PLEXUS OF THE RAT BRAIN: A HISTOLOGICAL EVALUATION
Authors: CALVO W. , HOPEWELL J. W. , REINHOLD H. S. , YEUNG T. K. 
Published: May 2008

Early and late histological changes have been investigated in the choroid plexus after the local irradiation of the brain of rats with single doses of 17‐5‐25 Gy of X‐rays. Changes were seen in epithelial cells within 1 week of irradiation. This was characterized by vacuolation, blebbing and partial lysis of the cytoplasm. Oedema in the underlying connective tissue was also seen after 1 week. A marked reduction in the number of endothelial cells, lining the walls of blood vessels, was found after 12 weeks; the severity was dose related and increased with time after irradiation. Slight atrophy of the epithelium was seen after 12 weeks.The reduction in endothelial cell number was associated with an attempt at regeneration as indicated by endothelial nuclear enlargement, nuclear pairs or groups and by the appearance of mitotic figures. Evidence or epithelial regeneration was not seen until week 26.Interstitial fibrosis was seen from 26 weeks after irradiation with the severity being both dose and time related. These late fibrotic changes were associated with basal membrane thickening, degenerative changes in the tunica media of arterioles and the appearance of thrombi.These changes are compared and contrasted with those seen in other normal tissues after irradiation and are discussed in terms of their relevance to the development of late radiation damage to the central nervous system.This work forms part of the collaborative programme of the European Late Effects Project Group (EULEP) and was partly supported by the Radiation Protection Programme of the Commission of the European Communities, Contract Nos. B10‐C‐345‐80‐D and B10‐E‐490 UKH. The Research Institute, Churchill Hospital, is supported by a grant from the Cancer Research Campaign (CRC). The authors would like to thank Miss S. Messenger for her care of the animals and Mrs B. Schur for the excellent histological preparations.
THE PROGRESSION OF THE PATHOLOGICAL CHANGES OF ALZHEIMER'S DISEASE IN FRONTAL AND TEMPORAL NEOCORTEX EXAMINED BOTH AT BIOPSY AND AT AUTOPSY
Authors: MANN D. M. A. , MARCYNIUK B. , YATES P. O. , NEARY D. , SNOWDEN J. S. 
Published: May 2008

The progression of the pathological changes of Alzheimer's disease in frontal and temporal neocortex examined both at biopsy and at autopsyBrains were obtained at autopsy from five patients with Alzheimer's disease, each of whom had undergone diagnostic craniotomy 3–7 years previously. It was possible, therefore, to examine the number (density) and nucleolar volume of pyramidal nerve cells, and the density of senile plaques and neurofibrillary tangles within the cerebral cortex on two occasions during the progression of their illness, and to assess how these measures might have changed during the period between biopsy and death. In all five patients, at biopsy, the density and the nucleolar volume of pyramidal nerve cells was significantly less than controls and, in general, values for both these measures fell significantly further from biopsy to death. By contrast, in none of the five patients did senile plaque density consistently change from biopsy to death; neurofibrillary tangle density either did not change, or indeed sometimes decreased from biopsy to death. These data show that both the clinical and the pathological progression of Alzheimer's disease is marked by a continuing loss of pyramidal cells from frontal and temporal cortex, although the densities of plaques and tangles within the cortex do not, per se, correlate with the stage of the illness. The usefulness of measurement of plaque and tangle densities as pathological criteria by which the clinical and neurochemical deficits of Alzheimer's disease can be compared in different patients is clearly questionable.
IDENTIFICATION OF THE NORMAL MICROGLIAL POPULATION IN HUMAN AND RODENT NERVOUS TISSUE USING LECTIN–HISTOCHEMISTRY
Authors: SUZUKI H. , FRANZ H. , YAMAMOTO T. , IWASAKI Y. , KONNO H. 
Published: May 2008

Identification of the normal microglial population in human and rodent nervous tissue using lectin–histochemistryMistletoe iectin–1 (ML–1) and Ricinus communis agglutinin–120 (RCA–1) both possess D–galactose–specific surface–binding sites. They were used to selectively identify microglial populations in aldehyde–fixed normal brain tissue by lectin immunohistochemistry on paraffin and frozen sections. Mistletoe lectin–1 was superior to RCA–1 in labelling microglia in the rat brain, whereas RCA–1 labelled human microglia better than ML–1. Thus, RCA–1 and ML–1 supplement each other for identifying microglial in human and rodent central nervous system tissues. The high reproducibility of the results and the applicability of the technique to routine histology, using formalin–fixed tissue, should facilitate study of the histogenesis and role of microglia in the CNS.
INHERITED PRENATAL HYDROCEPHALUS IN THE H–Tx RAT: A MORPHOLOGICAL STUDY
Authors: JONES H. C. , BUCKNALL R. M. 
Published: May 2008

Inherited prenatal hydrocephalus in the H–Tx rat: a morphological studyThe H–Tx rat has inherited hydrocephalus which is present at birth. In order to investigate the onset and early stages of hydrocephalus, the heads of fetuses from 16 to 21 days gestation and at 1 day after birth, were serially sectioned using conventional wax histology. Lateral and third ventricle volumes were measured with a graphics tablet and microcomputer. Hydrocephalus was first detected at 18–20 days gestation by enlarged lateral ventricles and it was sometimes accompanied by a large third ventricle. Most hydrocephalics had a non–patent cerebral aqueduct between the third ventricle and the posterior collicular recess and the remainder (about 25%) had an aqueduct which was patent but with a smaller lumen than in non–hydrocephalic littermates. Some fetuses prior to 18 days gestation with normal lateral ventricles also had nonpatent aqueducts. Abnormal aqueducts were lined by ependymal cells which were ventrally displaced by thickening of the overlying midbrain; also the subcommissural organ was foreshortened. Infusion with fluorescent markers confirmed that the flow pathway through the aqueduct was obstructed in many hydrocephalic rats. It is concluded that the hydrocephalus may be the result of abnormal brain development in the midline region of the dorsal mesencephalon, leading to aqueduct closure.
PERSISTENT MERCURY IN NERVE CELLS 16 YEARS AFTER METALLIC MERCURY POISONING
Authors: HARGREAVES R. J. , EVANS J. G. , JANOTA I. , MAGOS L. , CAVANAGH J. B. 
Published: May 2008

Hargreaves R.J., Evans J. G., Janota I., Magos L. & Cavanagh J. B. (1988) Neuropathology and Applied Neurobiology 14, 443–452Persistent mercury in nerve cells 16 years after metallic mercury poisoningA male subject, after exposure to mercury metal at work in 1968, developed classical signs of mercurialism from which he made a slow clinical recovery. He subsequently developed psychoneurotic symptoms and became an alcoholic; he never returned to work and died in 1984. No histological changes relevant to mercury intoxication were found in the brain, but staining by Danscher & Schroeder's method for mercury showed many positively staining lysosomal dense bodies in a large proportion of nerve cells, and the presence of mercury was confirmed by elemental X–ray analysis. The mercury content of the brain was increased, much of it being present in colloidal form.
VARICOSITIES IN HUMAN FETAL SCIATIC NERVE FIBRES
Authors: TOMÉ F. M. S. , TEGNÉR R. , CHEVALLAY M. 
Published: May 2008

Tome F. M. S., Tegner R. & Chevallay M. (1988) Neuropathology and Applied Neurobiology 14, 495–504Varicosities in human fetal sciatic nerve fibresA morphological study performed on sciatic nerves from 10 fetuses aged 19 to 32 weeks revealed variations in axonal diameter along the length of the fibres but a uniform myelin sheath thickness. This gave the fibres a beaded appearance. The diameter of the axon in the varicosities was up to seven–times greater than that of the intervening axon. The varicosities were separated by distances up to 50 μm. Both myelinated and single unmyelinated fibres had varicosities. Neurofilaments and neurotubules were more densely packed in the axons between the varicosities. The absolute number of filaments and tubules per axon was similar in axons with equal numbers of myelin lamellae but with different diameters, as calculated from transverse sections. The varicosities were observed in all fetuses aged 19 to 24 weeks, but in only one of the two fetuses aged 28 weeks. They were not present in the 32 week fetus. They appear to be a characteristic morphological feature of nerve fibres during early fetal life and can be identified only in teased fibre preparations or in longitudinal sections of the nerve. Their presence explains the bimodal or markedly skewed distribution of myelinated fibre axon diameters that was seen in nerves from young fetuses. It also helps in understanding the discrepancies reported in size patterns between axon diameter and myelin thickness. It is possible that the varicosities may be partially artefactual but their occurrence may imply a particular vulnerability of fetal nerve fibres. Their production may be related to movements of the axoplasmic fluid which is abundant in young fetuses.
INCREASED DIAMETER OF DEMYELINATED AXONS IN CHRONIC MULTIPLE SCLEROSIS OF THE SPINAL CORD
Authors: SHINTAKU M. , HIRANO A. , LLENA J. F. 
Published: May 2008

Shintaku M., Hirano A. & Llena J. F. (1988) Neuropathology and Applied Neurobiology 14, 505–510Increased diameter of demyelinated axons in chronic multiple sclerosis of the spinal cordIn an autopsied case of chronic multiple sclerosis, many axons in some demyelinated plaques of the spinal cord had remarkably increased diameters and reduced argentophilia. The increase in axonal diameter extended for some distance and was restricted to the demyelinated areas. A review of 22 autopsy cases of chronic multiple sclerosis revealed similar findings in the plaques of the spinal cord in seven cases. They were also noted in the brain but much less frequently. On electron microscopy, the neurofilaments in these enlarged demyelinated axons were not closely packed but were separated by an increased amount of electron–lucent axoplasm. It is thought that this finding may be a manifestation of increased water content in the axoplasm secondary to increased permeability of the demyelinated axolemma.
ROSENTHAL FIBRES ARE BASED ON THE UBIQUITINATION OF GLIAL FILAMENTS
Authors: LOWE J. , MORRELL K. , LENNOX G. , LANDON M. , MAYER R. J. 
Published: May 2008

Rosenthal fibres are based on the ubiquitination of glial filamentsImmunocytochemical localization of the cell stress‐associated protein ubiquitin was performed on human lesions containing Rosenthal fibres. Ubiquitin was localized around the periphery of classical Rosenthal fibres but not in the amorphous central areas; the ubiquitin‐positive regions corresponded to the immunocytochemical localization of glial fibrillary acidic protein (GFAP). Compact bundles of GFAP in glial processes without a non‐staining core were also associated with ubiquitin, while loosely aggregated cellular GFAP was not. The relationship between compact bundles of GFAP and the amorphous osmiophilic central component of Rosenthal fibres has been uncertain. These data, however, show that the compact bundles of glial filaments are distinct from normal GFAP in being associated with ubiquitin. A role for ubiquitin in Rosenthal fibre formation is suggested. We propose that the term Rosenthal fibre be restricted to mean the hyaline amorphous core of these structures, while realizing that this is based on a wider abnormality of surrounding glial fibrillary acidic protein filaments.
THE CORRELATION OF ELECTRORETINOGRAPHIC AND HISTOPATHOLOGICAL FINDINGS IN THE EYES OF MICE INFECTED WITH THE 79A STRAIN OF SCRAPIE
Authors: CURTIS R. , FRASER H. , FOSTER J. D. , SCOTT J. R. 
Published: May 2008

The correlation of electroretinographic and histopathological findings in the eyes of mice infected with the 79A strain of scrapieRetinal degeneration was produced using the 79A strain of scrapie injected intracerebrally into mice of the MM inbred strain, and studied by electroretinography and light and electron microscopy during the preclinical and clinical phases of the disease. The changes in the electroretinogram (ERG), detectable in some mice at 118 days postinjection (d.p.i.), appeared to coincide with the earliest morphological evidence of photoreceptor damage. In the early stages there was a progressive reduction of b‐wave amplitude without marked loss of retinal sensitivity or significant change in a‐ and b‐wave peak implicit times. Extinction of the ERG, observed in half the mice examined at 144 d.p.i., approximated to a stage of the retinopathy in which the outer nuclear layer was reduced to about four rows of nuclei. Early morphological changes suggested that the primary lesion involved the integrity of the photoreceptor as a whole, the electrophysiological findings reflecting a primary loss of light sensitive tissue rather than impairment of the transduction mechanism or neurotransmission.
REPORTS OF MEETINGS
Authors: LUTHERT P. , PILKINGTON G. J. 
Published: May 2008

BLOOD–BRAIN BARRIER CLUB: FOURTH ANNUAL SYMPOSIUM, INSTITUTE OF PSYCHIATRY, LONDON 27 APRIL (1988)THE BRITISH GLIOMA GROUP: EIGHTH ANNUAL MEETING, UNIVERSITY OF SURREY, GUILDFORD 2728 JULY 1988
AN IMMUNOHISTOCHEMICAL CHARACTERIZATION OF THE PRIMITIVE AND MATURING NEUROEPITHELIAL COMPONENTS IN THE OTT–6050 TRANSPLANTABLE MOUSE TERATOMA
Authors: CACCAMO D. V. , KATSETOS C. D. , FRANKFURTER A. , COLLINS V. P. , VANDENBURG S. R. , HERMAN M. M. 
Published: May 2008

The neuroepithelial component of the OTT–6050 mouse teratoma has previously been characterized as an experimental system for the study of differentiation and cytologic maturation in embryonal tumours of the human central nervous system. A number of transplantable tumours composed of primitive stem cells and of a neuroepithelial component displaying a spectrum of differentiation were previously produced by centrifugal elutriation of the dissociated OTT–6050 teratoma. These tumours have provided a reproducible cell population that has permitted the study of both the early and later stages of neoplastic neurocytogenesis.The purpose of the present study was to detect, by immunohistochemistry, the earliest stages of neurocytogenesis in these tumours as shown by the expression of neuron–associated microtubule proteins. This was correlated to the appearance and localization of other markers associated with neuronal and glial differentiation. The primitive neuroepithelial structures resembling neural tubes (medulloepithelial rosettes) contained single or small groups of cells which reacted with the monoclonal antibody TUJl, specific for the neuron–associated class III β–tubulin isotype. Immature neuroblasts and maturing polar neurons also showed immunoreactivity with TUJl, whereas reactivity for microtubule–associated protein 2 (MAP2), tau, the 200 kilodalton isoform of neurofilament protein, neuron–specific enolase and synaptophysin was primarily seen in maturing neurons. By comparison, both medulloepithelial and ependymoblastic rosettes, neuroblasts and glial cells were immunopositive with monoclonal antibody TU27, which defines an antigenic site shared by most mammalian β–tubulin isotypes. Astroglia were reactive with antisera to glial fibrillary acidic and S–100 proteins, but not with monoclonal antibody (MAb) TUJ1, or with MAbs to the other neuron–associated cytoskeletal proteins, MAP2, tau and the 200 kilodalton subunit of neurofilament protein.Our findings suggest that (1) expression of the class III β–tubulin isotype is an early event during neoplastic neurocytogenesis, (2) this isotype is subsequently preserved in maturing neuronal populations, and (3) it is not present at detectable levels in stem cells or glial cells. The observation that morphologically undifferentiated neuroepithelial cells express a neuron–associated β–tubulin isotype signifies the value of examining tubulin isotype expression in the characterization of normal and neoplastic neuroepithelial differentiation.