bluuebunny/crossref_metadata_2025 huggingface dataset:
Low susceptibility of resident microglia to simian immunodeficiency virus replication during the early stages of infection
Authors: Boche D. , Gray F. , Chakrabarti L. , Hurtrel M. , Montagnier L. , Hurtrel B.
Published: May 2008

To assess the susceptibility of resident microglia to simian immunodeticiency virus (SIV) infection, we analysed the hrains of rhesus macaques after intracerebral (i.c.1 inoculation of the virus into the central region at 7 days, 1, 2 and 3 months post‐inoculation (p.i.). The brains of animals showed the same moderate neuro‐pathological changes in central, frontal and parietal regions of the brain. characterized by gliosis, microglial nodules, perivascular infiltrates and occasional white matter pallor and similar low numbers of infected cells detected by in situ hybridization. These results, showing that i.c. inoculation did not lead to preferential infection of brain tissue, even near the inoculation point at 7 days p.i., provide evidence for the low susceptibility of resident microglia to SIV replication during the early stages of infection.
Review: David Oppenheimer Memorial Lecture 1995: Some neuropathological aspects of Alzheimer's disease and its relevance to other disciplines*
Authors: Wisniewski H. M. , Wegiel J. , Kotula L.
Published: May 2008

Recent studies of diffuse Aβ plaques point to the neurons as a source of Aβ in diffuse plaques. The neuritic (primitive and classical) plaques appear to be the product of microglia and the myocytes are the source of amyloid deposits in the meningeal and cortical vessels. Dyshoric angiopathy is associated with deposits of amyloid by perivascular cells. Fibrillization of the neuron‐derived diffuse, thioflavine‐negative or benign plaques is poor or undetectable by current morphological methods including ultrastructural immunocytochemistry. It appears that fibrillization depends on the length of the Aβ peptides and on the presence of amyloid‐associated proteins. Four genes are now tightly linked with Alzheimer's disease (AD) and they are located on chromosomes 21, 19, 14 and 1. Therefore, AD should be considered a polyaetiological disease or syndrome. There are currently five transgenic mouse models overexpressing β‐APP. There is also a myocyte tissue culture model in which both soluble and fibrillized Aβ are found. The relationship between Aβ and neurofibrillary pathology is not clear and the current cascade hypothesis proposing that Aβ pathology drives the formulation of neurofibrillary tangles is being questioned. There is growing evidence that it is not the Aβ hypothesis, but the co‐existing Aβ neurofibrillary tangle pathology hypothesis which will be the basis for AD neuropathology.
Neurofibrillary tangles, but not Alzheimer‐type pathology, in a young boxer
Authors: Geddes J. F. , Vowles G. H. , Robinson S. F. D. , Sutcliffe J. C.
Published: May 2008

The chronic neurological sequelae of boxing are well described, but there have been few neuropathological studies of boxers dying early in their career. We report the case of a 23‐year‐old boxer, whose brain showed neurofibrillary tangles in all neocortical areas, but remarkable sparing of medial temporal lobe structures. These tangles, assumed to be the result of repetitive head injury, were the only detectable abnormality: none of the other changes previously described in the brains of retired boxers were seen. The distribution and features of the neuropathological findings in this case suggest that the mechanism of tangle formation induced by repetitive head trauma may be different from that in Alzheimer's disease.
mRNA for NGF and p75 in the central nervous system of rats affected by experimental allergic encephalomyelitis
Authors: Simone R. De , Micera A. , Tirassa P. , Aloe L.
Published: May 2008

R. De Simone, A. Micera, P. Tirassa and L. Aloe (1996) Neuropathology and Applied Neurobiology 22, 54‐59 mRNA for NGF and p75 in the central nervous system of rats affected by experimental allergic encephalomyelitis

In this study we measured the concentration of nerve growth factor (NGF) and the expression of NGF and the low affinity NGF‐receptor (NGF‐r) mRNA in the central nervous system (CNS) of rats affected by experimental allergic encephalomyelitis (EAE) during the acute phase of the disease. Significant levels of NGF protein were found in thalamus and cortex on day 13 postimmunization. Molecular analysis of the NGF gene expression and of its NGF‐r revealed that they were enhanced in several regions of the CNS of EAE rats when compared with untreated animals. These results suggest a functional link between local NGF synthesis and this autoimmune inflammatory disease.
Lectin histochemistry, ploidy level and proliferation indices in meningioma subtypes
Authors: Salmon I. , Cambyt I. , Remmelinck M. , Rombautt K. , Pasteels J.‐L , Brotchi J. , Kisssp R. , Danguy A.
Published: May 2008

I. Salmon, I. Camby, M. Remmelinck, K. Rombaut, J.‐L. Pasteels, J. Brotchi, R. Kiss and A. Danguy (1996) Neuropathology and Applied Neurobiology 22, 68–76

Lectin histochemistry, ploidy level and proliferation indices in meningioma subtypes

The glycohistochemical expression of binding sites for eight lectins is characterized in a series of 15 meningothelial, 10 fibroblastic and 15 transitional meningiomas. The correlation between lectin staining and either the proliferation index or ploidy level has also been investigated. The data show that the cytochemical binding of some lectins is of value in distinguishing between the different meningioma subgroups. For example, fibroblastic meningiomas express significantly higher amounts of wheat germ agglutinin (WGA) and Ulex europaeus agglutinin (UEA‐I) than the meningothelial sub‐type. Diploid tumours express a higher glycine maximus (SBA), Arachis hypogaea (PNA) and Phaseolus vulgaris leukoagglutinin (PHA‐L) binding than aneuploid tumours. These differences are probably due to the modification of post‐transcriptional glycosylation events linked to tumour ageing. The data also reveal that the increased binding of PHA‐L is inversely correlated with the proliferation indices of the tumours.
Glial cell transplanatation and remyelination of the central nervous system
Authors: Duncan I. D.
Published: May 2008

Glial cell transplantation has proved to be a powerful tool in the study of glial cell biology. The extent of myelination achieved by transplanting myelin‐producing cells into the CNS of myelin mutants, or into focal demyelinating lesions has raised hope that such a strategy may have therapeutic applications. Oligodendrocytes or Schwann cells could be used for repair. It is likely that the immature stages of the oligodendrocyte lineage have the best phenotypic characteristics for remyelination when transplanted, either as primary cells or as immortalized cells or cell lines. Prior culturing and growth factor treatment provides opportunities to expand cell populations before transplantation as dissociated cell preparations. Cell lines are attractive candidates for transplantation, but the risk of transformation must be monitored. The application of this technique to human myelin disorders may requier proof that migration, division and stable remyelination of axons by the tranplanted cells can occur in the presence of gliosis and inflammation.
Comparative in vivo and pathological analysis of the blood‐brain barrier in mouse telencephalic transplants
Authors: Isenmann S. , Brandner S. , Kühnet G. , Boner J. , Aguzzi A.
Published: May 2008

The post‐transplantation status of the blood‐brain barrier (BBB) is still a matter of debate. In an attempt to define BBB properties after neural transplantation in mice of a defined genetic background, we have used two exogenous markers (horseradish peroxidase and Evans blue), one endogenous marker (immunoglobulins), and in vivo contrast enhanced magnetic resonance imaging (MRI) and compared the results obtained with the different methods. With all four techniques employed, we found the BBB to be reconstituted in 67% of the grafts 3 weeks after grafting, and in more than 90% of all grafts 50 days after grafting. Horseradish peroxidase and contrast enhanced MRI were the most sensitive techniques, the latter offering the unique advantage of repetitive scanning of individual grafts. Our findings provide important information for transplantation studies in mouse models for neurodegenerative diseases.
Molecular analysis of the lissencephaly gene 1 (LIS‐1) in medulloblastomas
Authors: Koch A. , Tonnt J. , Kraus J. A. , Sörensen N. , Albrecht S. , Wiestler O. D. , Pietsch T.
Published: May 2008

A. Koch, J. Tonn, J. A. Kraus, N. Sörensen, S. Albrecht, 0. D. Wiestler and T. Pietsch (1996) Neuropathology and Applied Neurobiology22, 233–242
Immunocytochemically detectable metallothionein is expressed by astrocytes in the ischaemic human brain
Authors: Neal J. W. , Singhrao S. K. , Jasanit B. , Newman G. R.
Published: May 2008

Immunocytochemically detectable metallothionein is expressed by astrocytes in the ischaemic human brain

The metallothioneins in vitro are both effective free radical and transitional metal ion scavengers. For this reason we investigated the expression of this protein in the normal CNS and after ischaemia using a monoclonal anti‐metallothionein antibody to metallothionein isoforms I and II. Using immunohistochemistry and confocal laser scanning microscopy, we found anti‐GFAP and anti‐metallothionein were co‐localized in astrocytes at the edges of infarcts. Energy dispersive X‐ray micro‐analysis demonstrated high levels of copper and iron in the metallothionein positive reactive astrocytes. On the basis of the in vitro properties of these proteins, the functional importance of metallothionein in reactive astrocytes could be as a free radical scavenger and metal ion chelator.
Factors inducing mast cell accumulation in skeletal muscle
Authors: Lefaucheur J.‐P. , Gjata B. , Sebille A.
Published: May 2008

It has been suggested that mast cells contribute to the phenotype of dystrophinopathies, but the mechanisms of their recruitment into the skeletal muscle remain hypothetical. The aim of this study is to quantify the presence of mast cells in muscle during the cellular events of myofibre degeneration and regeneration. For this purpose, we compare the mast cell profile in dystrophin‐deficient mdx mice in which muscles exhibit spontaneous cycles of degeneration‐regeneration from 3 weeks of age, with that in Swiss mice in which muscles were injured either by ischaemia or by notexin injection. Notexin is an A2‐type phospholipase that rapidly disrupts myofibre plasma membranes, while ischaemia results in a slower process of degeneration. Both lesions are followed by a successful regeneration. In intact muscles, mast cell counts (mean±SEM/mm2) range from 1.8± 1 to 4.3 ± 1.6. The injection of notexin is far more potent in recruiting mast cells into damaged muscle than is ischaemia (118.5±13.0 vs 12.3 ± 1.8/mm2). Thus we conclude that the early disruption of the myofibre membrane could elicit mast cell accumulation in skeletal muscle. This may explain the elevated number of mast cells observed in mdx muscles, as dystrophin deficiency is thought to induce myofibre membrane leakage. On the other hand, mast cells are more numerous in muscles of young and adult mdx mice that are allowed to regenerate, than in muscles of older animals in which there is little regeneration and fibrosis develops. In injured muscles, the peak of mast cell number is at the onset of regeneration (by day 3 after notexin injection, and by day 11 after ischaemia), rather than during the phase of myofibre necrosis. Therefore, we suggest that the mast cells, through the effects of released mediators, could contribute to muscle regeneration.
The pathology of Charcot‐Marie‐Tooth disease and related disorders
Authors: Thomas P. K. , King R. H. M. , Small J. R. , Robertson A. M.
Published: May 2008

Approximately a quarter of a century ago, the disorders originally designated as Charcot‐Marie‐Tooth disease and Dejerine‐Sottas disease were shown by combined clinical, electrophysiological and nerve biopsy studies to be genetically complex. In pathological terms they could be broadly classified into demyelinating neuropathies and axonopathies. Advances in the molecular genetics of these disorders, particularly for those with a demyelinating basis, have recently produced substantial new insights. The identification of mutations in genes for myelin proteins has provided the opportunity for investigating the precise mechanisms of these neuropathies, including the use of spontaneous and genetically engineered animal models.
Plastic phenotype of human oligodendroglial tumour cells in vitro
Authors: Tenenbaum L. , Teugels E. , Dogusan Z. , Avellana‐Adalid V. , Hooghe‐Peters E. L.
Published: May 2008

Human oligodendroglioma cells cultured in serum‐supplemented media lose their oligodendrocytic antigenic markers and acquire astrocytic markers. However, after reimplantation in rodent brain, these cells re‐express oligodendrocytic markers. This switch in human oligodendroglioma cell phenotype could result from the interplay of different stimuli in vitro vs in vivo. The in vitro differentiation into astrocytes might result from non‐physiological culture conditions. It is shown that human oligodendroglioma cells behave in a way similar to that of rodent bipotential O–2 A progenitor cells which can be driven to differentiate into either oligodendrocytes or type 2‐astrocytes depending on the culture medium. Indeed, in serum‐supplemented medium, human oligodendroglioma cells proliferated and expressed the GFAP astrocytic marker. In chemically defined medium containing insulin, human oligodendroglioma cells were quiescent and expressed the 01 oligodendrocyte‐specific marker. In both media human oligodendroglioma cells expressed the A2B5 membrane marker as well as the SCIP transcription factor specific of 0–2 A cells, further confirming their oligodendrocytic origin. Replacement of insulin by platelet‐derived growth factor (PDGF) and basic fibroblast growth factor (PDGF), known to maintain 0–2 A progenitors in a proliferative state, stimulated DNA replication of human oligodendroglioma cells cultured in chemically defined medium.
Drainage of CSF through lymphatic pathways and arachnoid villi in sheep: measurement of 125l‐albumin clearance
Authors: Boulton M. , Yonung A. , Hay J. , Armstrong D. , Flessner M. , Schwartz M. , Johnston M.
Published: May 2008

We investigated lymphatic drainage pathways of the central nervous system in conscious sheep and quantified the clearance of a cerebrospinal fluid (CSF) tracer into lymph and blood. In the first group of studies, 125I‐HSA was injected into the lateral ventricles of the brain or into lumbar CSF and after 6 h, various lymph nodes and tissues were excised and counted for radioactivity. Multiple lymphatic drainage pathways of cranial CSF existed in the head and neck region defined by elevated 125I‐HSA in the retropharyngeal/cervical, thymic, pre‐auricular and submandibular nodes. Implicated in spinal CSF drainage were mainly the lumbar and intercostal nodes. In a second group of experiments, multiple cervical vessels and the thoracic duct were cannulated and lymph diverted from the animals. Transport of tracer through arachnoid villi was taken from recoveries in venous blood. Following intraventricular administration, the 6 h recoveries of 125I‐HSA in the lymph (sum of cervical and thoracic duct) and blood were 8.2%± 3.0 and 12.5%± 4.5 respectively and at 22 h, 25.1%± 6.9 and 20.8%± 4.1 respectively. When 125I‐HSA was injected into lumbar CSF, the 6 h recoveries of tracer in thoracic duct and blood were 11.6%± 2.7 and 16.3%± 3.7 respectively. Total lymph and blood recoveries were not significantly different in any experiment. We conclude that the clearance of 125I‐HSA from the CSF is almost equally distributed between lymphatic and arachnoid villi pathways.
Selective alterations in the cellular distribution of apolipoprotein E immunoreactivity following transient cerebral ischaemia in the rat
Authors: Horsburgh K. , Nicoll J. A. R.
Published: May 2008

The aim of this study was to examine the cellular localization and alterations of apolipoprotein E (apoE) following a transient ischaemic insult using immunohistochemistry. Transient cerebral ischaemia was induced in Wistar rats by occlusion of both carotid arteries with hypotension followed by reperfusion for 4 h (n = 5), 24 h (n = 5) or 72 h (n = 6). In sham‐operated animals (n=9), the carotids were not occluded. In this model, ischaemia for 15 min results in selective neuronal damage in the caudate nucleus and neocortex (24 h after reperfusion) and the hippocampal CA1 pyramidal cells (72 h after reperfusion) while there is minimal damage in other areas such as the CA3 hippocampal region. In sham animals, apoE immunoreactivity was confined to astrocytes and their processes. ApoE immunoreactivity was not altered at 4 h post‐ischaemic reperfusion. At 24 h reperfusion, intense apoE staining of the cytoplasm of astrocytes and neuropil within the caudate and neocortex was observed and at 72 h reperfusion apoE stained neuronal cell bodies within these regions. Within the CA1 region at 24 h reperfusion, there was increased immunoreactivity of the cytoplasm of astrocytes and the neuropil was more intensely stained compared with sham animals. At 72 h reperfusion, intense apoE staining of pyramidal cell bodies and dendrites was consistently observed in the CA1 region of the hippocampus. In contrast, at 72 h reperfusion, apoE staining of astrocytic processes was dramatically reduced in the CA1 region although GFAP staining indicated their preservation. The results demonstrate that following an ischaemic insult apoE is localized to degenerating neurons and their processes. This may indicate an inherent protective response of cells to injury. Alternatively, the results are consistent with the hypothesis that apoE is synthesized and released by astrocytes and taken up by neurons following injury.
Transcription factors in early development of the central nervous system
Authors: Scotting P. J. , Rex M.
Published: May 2008

In studies of the central nervous system (CNS) few areas have progressed faster than the study of transcription factors and their role in controlling gene expression during development. Evidence for the pivotal roles of these factors in the formation of the CNS is reviewed; from neural induction to the maturation of neurons and the specilication of cells according to their position within the CNS. In all of these processes, epigenetic factors affect the cells' developmental fate but it is transcription factors within the cells which function both to decode these incoming messages and then to effect changes in the expression of other genes. Soluble factors such as retinoic acid and the products of the Noggin and Sonic hedgehog genes induce changes in families of transcription factors such as the Hox, Sox. Pax and Pou gene products and these alter the expression of banks of downstream genes thereby controlling the developmental fate of those cells. Recent advances in understanding of the molecular events underlying normal neurogenesis might now lead to a clearer understanding of the molecular abnormalities underlying several developmetal disorder of the CNS.
Apoptosis in perinatal hypoxic‐ischaemic cerebral damage
Authors: Edwards A. D. , Mehmet H.
Published: May 2008

Perinatal hypoxia‐ischaemia induces a biphasic cerebral injury: the depletion in high energy phosphates during the insult returns to normal soon after resuscitation. However, some 8–15 h later a second phase of impaired energy metabolism begins, which is related to the severity of later neurodevelopmental impairment. Delayed injury differs from acute hypoxia‐ischaemia because intracellular acidosis does not occur. Apoptosis may be a mechanism of delayed cellular injury. Apoptotic cells and typical DNA fragmentation have been found after perinatal hypoxia‐ischaemia. In newborn piglets, fraction of apoptotic cells was directly related to the degree of high energy phosphate depletion during hypoxia‐ischaemia. Apoptosis may be interrupted: in piglets, brain cooling for 12 h following resuscitation reduced the fraction of apoptotic but not necrotic cells. These results have implications for both the understanding of cerebral injury and the use of hypothermia as a neural rescue strategy in the developing brain.
Developmental spectrum of the excitotoxic cascade induced by ibotenate: a model of hypoxic insults in fetuses and neonates
Authors: Gressens P. , Marret S. , Evrard P.
Published: May 2008

Ibotenate, a glutamatergic agonist, was used to study the spectrum of excitoxic disturbances at different ages of cerebral development. Cultures of whole mouse embryo were submitted to ibotenate at E8 for 20 h: during the phase of early premigratory differentiation; ibotenate did not induce any detectable histological lesion. During migration of supragranular neurons, newborn hamsters intracerebrally injected at P0 with ibotenate display neuronal migration disorders graded from nodular heterotopias to extensive laminar heterotopias mimicking some aspects of lissencephalic and double‐cortex syndromes. After completion of neuronal layer V, P0 mice injected with ibotenate exhibit laminar neuronal depopulation of layer V‐VIa mimicking human micro‐gyria. At P5 in mouse, after completion of neuronal migration of the cortical plate, ibotenate induces neuronal loss in all cortical layers and the formation of porencephalic cysts. This study emphasizes the dramatic role played by glutamate in brain development, in the occurrence of neuronal migration disorders in the cortex. and in grey and white matter damage.
Correlations between the morphology of diffuse and primitive β‐amyloid (Aβ) deposits and the frequency of associated cells in Down's syndrome
Authors: Armstrong R. A.
Published: May 2008

Correlations between the morphology of β‐amyloid (Aβ) deposits and the frequency with which they are associated with neurons and glial cells were studied in Down's syndrome. The diameter of diffuse deposits was positively correlated with the frequency of large (>25 μm) neuronal cell bodies in the isocortex and with glial cells in the hippocampus. Diameters of primitive deposits were positively correlated with glial cells in the hippocampus and with glial cells and neurons in the isocortex. Staining intensity was positively correlated with glial cells especially in the hippocampus. The data suggest that: (i) diffuse deposits develop from neurons and primitive deposits from glia; (ii) the size of Aβ deposits depends on the numbers of neurons and glia; (iii) glial cells are also involved in the conversion of Aβ to amyloid; and (iv) the increased density of primitive deposits in the hippocampus is determined by the high density of glial cells.
Cell‐adhesion molecules in human meningiomas: correlation with clinical and morphological data
Authors: Figarella‐Branger D. , Roche P. H. , Daniel L. , Dufour H. , Bianco N. , Pellissier J. F.
Published: May 2008

Integrins form a family of cell adhesion molecules. CD44 glycoproteins are found in a wide variety of isoforms; the most common, CD44s (standard) is widely distributed, and functions as an adhesion molecule. In this study, we have investigated immunohistochemically the distribution of some VLA integrins (α2, α5 and α6 chains of β1 integrins) and CD44s in 44 meningioma specimens and normal arachnoid villi. Meningiomas were of meningothelial (16), transitional (13) and fibroblastic (15) subtypes. There were 13 grade I, 19 grade II and 12 grade III (27%). Immunoprecipitates were quantified by image analysis and correlated with clinical (age, sex, location) and morphological data (histological subtypes and grades). VLA α5 chain was expressed by normal arachnoid villi (mainly cap cells) and by 42 out of 44 meningioma specimens. Expression was lower in fibroblastic meningiomas (P=0.02). VLA α2 and α6 chains were not observed in normal arachnoid villi. VLA α2 was expressed by 15 meningiomas, VLA α6 by 10. Interestingly, meningiomas expressing either VLA α2 or α6 were usually of grade III (P≤0.05). CD44s was found on various parts of arachnoid villi and in all meningiomas although expression was higher in meningothelial and transitional than in fibroblastic (P≤0.001). These results show that VLA α5 and CD44s are widely expressed by arachnoid villi and meningiomas, in contrast to VLA α2 and VLA α6. It was noted that high grade meningiomas (III) express VLA α2 and α6 suggesting that changes in integrin pattern expression are a feature of these meningiomas. Moreover, strong CD44s expression characterizes meningothelial and transitional meningiomas. Previous studies have shown that high NCAM expression is a feature of fibroblastic meningiomas whereas meningothelial and transitional meningiomas expressed mainly E‐Cadherin, and that polysialylated NCAM expression was restricted to high grade meningiomas. Taken together these features suggest that each cell adhesion molecule has a characteristic pattern of expression according to meningioma subtype and grade. No correlation was seen between integrins and CD44s expression and clinical data.
Selective damage to the cerebellar vermis in chronic alcoholism: a contribution from neurotoxicology to an old problem of selective vulnerability
Authors: Cavanagh J. B. , Holton J. L. , Nolan C. C.
Published: May 2008

J. B. Cavanagh, J. L. Holton and C. C. Nolan (1997) Neuropathology and Applied Neurobiology23, 355–363

Selective damage to the cerebellar vermis in chronic alcoholism: a contribution from neurotoxicology to an old problem of selective vulnerability

The curiously consistent localization of cerebellar cortical damage in chronic alcoholism is re‐evaluated in the light of selective damage, with a similar topography in the cerebellar vermal region, in superficial siderosis in man and in experimental animals exposed to certain toxic substances. Attention is drawn to the capacity for Purkinje cell dendrites and Bergmann glia to extract materials from the CSF, and to the close anatomical relationships of the susceptible lobules I‐II, IX and X to the roof of the IVth ventricle and to the cistern of the great cerebral veins. This restriction of damage to vermis and paravermis may reflect some compartmentalization of CSF flow within leptomeninges, consistently increasing exposure of these cerebellar surfaces to materials circulating in the CSF. In other circumstances when this pattern of damage is encountered it raises the question as to whether other environmental agents, gaining access to the CSF, may be similarly distributed.
Sub‐acute cerebellar degeneration with anti‐Yo autoantibodies: immunohistochemical analysis of the immune reaction in the central nervous system
Authors: Giometto B. , Marchiori* G. C. , Nicolao P. , Scaravilli T. , Lion A. , Bardin* P. G. , Tavolato B.
Published: May 2008

B. Giometto, G. C. Marchiori, P. Nicolao, T. Scaravilli, A. Lion, P. G. Bardin and B. Tavolato (1997) Neuropathology and Applied Neurobiology, 23, 468–474

Sub‐acute cerebellar degeneration without any anti‐Yo autoantibodies: immunomstochemical analysis of the immune reaction in the central nervous system

We report the pathological findings of a woman with a sub‐acute cerebellar syndrome who had undergone surgery 3 years before for endometrial carcinoma. Both serum and cerebrospinal fluid contained high titres of autoantibodies against the cytoplasm of Purkinje cells that recognized a band of 62 kDa on immunoblotting of neuronal extracted proteins (pattern anti‐Yo). No tumour was found despite a full range of gynaecological investigations; the neoplastic marker CA125 was slightly elevated and oligoclonal bands were detected in the cerebrospinal fluid. The patient died from acute myocardial infarction 4 months after developing this syndrome. At autopsy, no macroscopic evidence of tumour was obtained and the brain showed no abnormalities. On microscopic examination of the central nervous system diffuse degeneration of Purkinje cells could be seen throughout the cerebellum. Immunohistochemical analysis showed a CD8 lymphocyte infiltration in the cerebellum and cerebral cortex and diffuse microglial activation throughout the brain. These cells expressed high levels of MHC‐II antigens on their cell membranes. The serum autoantibodies reacted with the cytoplasm of the remaining Purkinje cells. The short interval between the onset of symptoms and death of the patient could explain the difference between our findings and those reported in the literature in which no inflammatory infiltrates were detected. The immunohistochemical findings as well as the inflammatory cerebrospinal fluid profile seen in our case seem to support the concept that in paraneoplastic cerebellar degeneration with anti‐Yo antibodies, an immune mediated mechanism is responsible for the damage to the cerebellum.
Expression of myogenic regulatory factors (MRFs) in human neuromuscular disorders
Authors: Olivé M. , Martinez‐Matos J. A. , Pirretas P. , Povedano M. , Navarro C. , Ferrer I.
Published: May 2008

M. Olivé, J. A. Martínez‐Matos, P. Pirretas, M. Povedano, C. Navarro and I. Ferrer (1997) Neuropathology and Applied Neurobiology 23, 475–482

Expression of myogenic regulatory factors (MRFs) in human neuromuscular disorders

Immunohistochemical studies using antibodies to myogenic regulatory factors (MRFs) Myo D, myogenin, myf‐5, and myf‐6, and transcription factors c‐Fos and c‐Jun, were performed on muscle biopsies from patients suffering from Duchenne and Becker muscular dystrophies, polymyositis, and denervation atrophy, to investigate whether expression of these factors occurs during degeneration and regeneration of adult muscle fibres. Strong Myo D, myogenin, myf‐5 and myf‐6 immunoreactivity was observed in the nuclei of small regenerating fibres and satellite cells, as revealed by double‐labelling immunohistochemistry with N‐CAM antibodies, in Duchenne and Becker muscular dystrophies and in polymyositis. This suggests that the myogenic programme is activated during regeneration of adult human muscle fibres. In addition, strong myf‐6 and c‐Jun immunoreactivity was found in the cytoplasm of some necrotic muscle fibres in patients with Duchenne and Becker muscular dystrophies and in patients with polymyositis. The latter findings suggest that strong cytoplasmic expression of myf‐6 and c‐Jun is related to the process of muscle fibre degeneration that occurs in these conditions. Increased Myo D, myogenin, myf‐5 and myf‐6 immunoreactivity was not observed in the nuclei of denervated muscle fibres, although strong c‐Fos and c‐Jun immunoreactivity was seen in the nuclei of denervated muscle fibres; this suggests that denervation triggers the expression of these transcription factors. Taken together, these observations demonstrate that MRFs and c‐Fos and c‐Jun are selectively expressed in different human muscular disorders.
Relationship between apolipoprotein E and the amyloid deposits and dystrophic neurites of Alzheimer's disease
Authors: Dickson T. C. , Saunders H. L. , Vickers J. C.
Published: May 2008

T. C. Dickson, H. L. Saunders and J. C. Vickers (1997) Neuropathology and Applied Neurobiology, 23, 483–491

Relationship between apolipoprotein E and the amyloid deposits and dystrophic neurites of Alzheimer's disease

Although the inheritance of certain apolipoprotein E (ApoE) alleles has been recognized as a genetic risk factor for Alzheimer's disease, the role of ApoE in the pathology underlying this disease is unclear. Several reports have emphasized the association of ApoE with either β‐amyloid plaque formation or the development of neurofibrillary pathology. Utilization of multiple label immunohistochemical methods enabled us to examine directly the localization of ApoE immunoreactivity relative to β‐ amyloid plaques, dystrophic neurites and neurofibrillary tangles. In Alzheimer's disease cases, β‐amyloid plaques showing high ApoE immunoreactivity were localized to layers II, III and V of the neocortex. In layer I, β‐amyloid plaques were unlabelled for ApoE relative to β‐amyloid. Dense core plaques labelled for β‐amyloid often had only the central portions labelled for ApoE. Conversely, ApoE labelled spherical structures within some plaques were not immunoreactive for β‐amyloid or dystrophic neurite markers. Unlike β‐amyloid labelled plaques, all ApoE immunoreactive plaques were associated with dystrophic neurites. In preclinical Alzheimer's disease cases, most plaques were double labelled for β‐amyloid and ApoE. ApoE did not label dystrophic neurites or the early stages of neurofibrillary tangle formation, indicating that ApoE may not be directly involved in neurofibrillary pathology. The specific presence of ApoE in plaques associated with dystrophic neurites in demented patients suggests that ApoE may contribute toward a higher degree of β‐ amyloid fibrillogenesis, enhancing the ability of certain plaques to cause damage to surrounding axons.
Significant loss of pyramidal neurons in the angular gyrus of patients with Huntington's disease
Authors: Macdonald V. , Halliday G.M. , Trent R.J. , McCusker E.A.
Published: May 2008

V. Macdonald, G.M. Halliday, R.J. Trent and E.A. McCusker (1997) Neuropathology and Applied Neurobiology 23, 492–495

Significant loss of pyramidal neurons in the angular gyrus of patients with Huntington's disease

The primary site of pathology in Huntington's disease (HD) is the caudate nucleus. However, cortical changes are also commonly reported. While many researchers have studied pathology in the frontal lobe, little attention has been paid to posterior cortical regions. The aim of this study is to examine pathology in the parietal lobe in patients with HD as it has specific projections to the caudate nucleus. Post‐mortem brain tissue was obtained from HD patients with both a positive family history and clinicopathological diagnosis (n=6; Vonsattel grades 2–4) as well as from neurologically normal controls (n=6). The angular gyrus of the parietal lobe was sampled and cellular quantification of SMI‐32 immunohistochemically detected pyramidal neurons performed. Cortical blocks were sectioned at 50 μm on a cryostat and stained immunohistochemically using antigen retrieval methods and peroxidase visualization. HD subjects had noticeable histological changes including smaller neurons and a disruption of cortical laminar pattern. Quantification using a point counting method to find the areal fraction of immunoreactive neurons revealed a severe loss of pyramidal neurons in the angular gyrus of HD subjects compared with controls (reduced on average to 55% of mean control values, P= 0.038 using the Mann–Whitney U‐test). This striking cortical pathology suggests that HD may preferentially target posterior cortical regions, particularly the angular gyrus which has a significant projection to the caudate nucleus in primates.
Microbially mediated carbonates in the Holocene deposits from Sarliève, a small ancient lake of the French Massif Central, testify to the evolution of a restricted environment
Authors: BRÉHÉRET JEAN‐GABRIEL , FOURMONT AGATHE , MACAIRE JEAN‐JACQUES , NÉGREL PHILIPPE
Published: May 2008

Both the mineralogy and facies of lacustrine bio‐induced carbonates are controlled largely by hydrological factors that are highly dependent upon climatic influence. As such they are useful tools in characterizing ancient lake environments. In this way, the study of the sedimentary record from the small ancient Sarliève Lake (Limagne, Massif Central, France) aims to reconstruct the hydrological evolution during the Holocene, using petrographical, mineralogical and geochemical analyses. The fine‐grained marls, mainly calcitic, display numerous layers rich in pristine Ca‐dolomite, with small amounts of aragonite, which are clearly autochthonous. As these minerals are rather unusual in the temperate climatic context of western Europe, the question arises about their forming conditions, and therefore that of the lacustrine environment. Ca‐dolomite prevails at the base of the sequence as a massive dolomicrite layer and, in the middle part, it builds up most of the numerous laminae closely associated with organic matter. Scanning electron microscope observations reveal the abundance of tiny crystals (tens to hundreds of nanometres) mainly organized as microspheres looking like cocci or bacilli. Such a facies is interpreted as resulting from the fossilization of benthic microbial communities by dolomite precipitation following organic matter consumption and extracellular polymeric substance degradation. These microbial dolomites were precipitated in a saline environment, as a consequence of excess evaporation from the system, as is also suggested by their positive ∂18O values. The facies sequence expresses the following evolution: (i) saline pan, i.e. endorheic stage with a perennial lowstand in lake level (Boreal to early Atlantic periods); (ii) large fluctuations in lake level with sporadic freshening of the system (Atlantic); (iii) open lake stage (sub‐boreal); and (iv) anthropogenic drainage (sub‐Atlantic).
A review of pesticide policies and regulations for urban amenity areas in seven European countries
Authors: KRISTOFFERSEN P , RASK A M , GRUNDY A C , FRANZEN I , KEMPENAAR C , RAISIO J , SCHROEDER H , SPIJKER J , VERSCHWELE A , ZARINA L
Published: May 2008

An analysis of the regulations of herbicide use for weed control in non‐agricultural/urban amenity areas, including actual pesticide use, was carried out as a joint survey of seven European countries: Denmark, Finland, Germany, Latvia, the Netherlands, Sweden and United Kingdom. Herbicides constitute the major part of the pesticides used in urban amenity areas. Herbicide use on hard surfaces is the largest in terms of volume and potential contamination of surface and groundwater. The aim of the study was to investigate the differences in political interest and public debate on the ‘use of pesticides in public urban amenity areas’, regulations within each country at national, regional and local levels, possible use of alternative weed control methods and the amounts of pesticides used on urban amenity areas. A comparative analysis revealed major differences in political interest, regulations and availability of statistics on pesticide use. Denmark, Sweden, the Netherlands and Germany have, or have had, a strong public and political interest for reducing the use of herbicides to control weeds in urban amenity areas and also have very strict regulations. The UK is currently undergoing a period of increasing awareness and strengthening regulation, while Latvia and Finland do not have specific regulations for weed control in urban amenity areas or on hard surfaces. Statistics on pesticide/herbicide use on urban amenity areas were only available in Denmark and the Netherlands. Developing this kind of information base reveals the differences in herbicide use, regulations and policies in European countries and may enhance the transfer of knowledge on sustainable weed control across countries.
Physiological and molecular bases of glyphosate resistance in Conyza bonariensis biotypes from Spain
Authors: DINELLI G , MAROTTI I , BONETTI A , CATIZONE P , URBANO J M , BARNES J
Published: May 2008

The physiological and molecular bases of glyphosate resistance in one susceptible (S) and four resistant (R) Conyza bonariensis biotypes (sampled in orchards from Andalusia, Spain) were investigated. Resistance index (RI) values of the four R biotypes ranged between 2.9 and 5.6. The main physiological difference between S and R biotypes was the dissimilar mobility of glyphosate in the whole plant. In R biotypes, the herbicide was translocated less from leaves to culm and root, and more from culm to leaves compared with the S biotype. The upward mobility of glyphosate via xylem suggests that the herbicide may be sequestered to the apoplast or the vacuole. The hypothesis of an insensitive 5‐enolpyruvylshikimate‐3‐phosphate synthase (EPSPS) was provisionally discarded on the basis of shikimate accumulation in R plant tissues after glyphosate treatment. At the molecular level, the relative abundance of EPSPS mRNA prior to glyphosate treatment was approximately double in two R biotypes compared with the S standard and the other R biotypes. Moreover, the two R biotypes having both no translocation and doubled EPSPS mRNA levels had also the highest RI. These results suggest that two factors may be related to glyphosate resistance in the R biotypes: (i) impaired translocation and (ii) high basal EPSPS transcript levels. The comparison between these findings and earlier results on glyphosate resistance mechanism in Conyza canadensis biotypes from the USA, suggests that similar agronomic factors (repeated application of glyphosate, no crop and herbicide rotation, no tillage) have selected similar traits on different genetic pools of the resistance‐prone Conyza genus.
Soil water availability affects green area and biomass growth of Cynodon dactylon
Authors: DE ABELLEYRA D , VERDÚ A M C , KRUK B C , SATORRE E H
Published: May 2008

Bermuda grass (Cynodon dactylon) is a stoloniferous and rhizomatous prostrate weed displaying high growth rates under non‐limiting conditions. Radiation has been considered the major factor affecting C. dactylon patch extension and biomass growth, but little is known about the influence of water availability on those processes. C. dactylon green area and biomass growth were analysed in response to different soil water conditions. Four experiments comprising eight drought treatments were carried out during 2 years at different dates, to generate a wide range of soil water and evaporative demand conditions. Significant reductions in weed green area and biomass growth were found between treatments when low soil water conditions were imposed. Reductions in green area were of greater magnitude than reductions in biomass, suggesting a higher effect of drought on green area increment. There were significant (P < 0.05) relationships between green area increment and cumulative incident radiation, although slopes [relative green area growth rates (RGAGR)] differed among treatments. A strong logistic relationship was found between RGAGR and the ratio of plant‐available soil water to potential evapotranspiration. The approach and parameters generated in this work can be used to predict C. dactylon growth changes under rain‐fed conditions.
A rare case of leishmaniasis recidiva cutis evolving for 31 years caused by Leishmania tropica
Authors: Stefanidou Maria P. , Antoniou Maria , Koutsopoulos Athanassios V. , Neofytou Yiannakis T. , Krasagakis Konstantinos , Krüger‐Krasagakis Sabine , Tselentis Yiannis , Tosca Adroniki D.
Published: May 2008

A 64‐year‐old woman presented with erythematous, infiltrative plaques with a central atrophic area on both zygomatic regions. Several yellow‐reddish papules were seen at the periphery of the plaques and showed an “apple‐jelly” color on diascopy (Fig. 1). No visceral involvement was detected.

Erythematous, infiltrative plaque with a central atrophic area

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The past medical history revealed that, at 3 years of age, she had developed an “Oriental sore” on both cheeks that healed with permanent scars. Thirty years later, she noticed an erythematous patch around the scars. She reported a hospital admission 22 years earlier for cutaneous leishmaniasis (CL); this was treated with pentavalent antimonial therapy for 10 days with partial improvement, when she refused further treatment. The lesions worsened in the summer and gradually became disfiguring, which prompted her to seek medical consultation.

Laboratory findings were normal. Leishmania antibody titers were negative. Tissue samples were obtained by biopsy from the border of the lesion for culture, polymerase chain reaction (PCR), and histopathologic examination. Histology revealed a dermal infiltrate with tuberculoid granulomas surrounded by lymphocytes, histiocytes, and some plasma cells, but no caseation necrosis. A few Leishmania organisms were found on careful searching (Fig. 2). Leishmania tropica was identified by culture and PCR.

(A) Granulomatous infiltrate intermingled with lymphocytes and histiocytes in the dermis (hematoxylin and eosin, ×40). (B) Granulomas lack caseation necrosis (hematoxylin and eosin, ×200). (C) Leishmania organisms in the cytoplasm of a giant cell (Giemsa stain, × 600)

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A diagnosis of leishmaniasis recidiva cutis (LRC) was made on the basis of the anamnestic data together with the clinical, histopathologic, biologic, and molecular findings. Complete regression was achieved with meglumine antimoniate (Glucantime) given intramuscularly (15 mg SbV/kg/day for 15 days) and cryosurgery with liquid nitrogen. No recurrence was noted during a 12‐month follow‐up period.
Concordant over‐expression of transcription factor Sp1 and vascular endothelial growth factor in extramammary Paget's disease
Authors: Chen Si‐Yuan , Takeuchi Satoshi , Moroi Yoichi , Hayashida Sayaka , Kido Makiko , Uchi Hiroshi , Takahara Masakazu , Uenotsuchi Takeshi , Tu Ya‐Ting , Urabe Kazunori , Furue Masutaka
Published: May 2008

Background  Specificity protein 1 (Sp1) is a transcription factor and shown to be a sequence‐specific DNA‐binding protein that activate a broad and diverse spectrum of mammalian gene, such as vascular endothelial growth factor (VEGF) gene. But the expression of Sp1 and VEGF has not previously been investigated in extramammary Paget's disease (EMPD).

Methods  To investigate the expression of Sp1 and VEGF proteins in EMPD and to assess their relationships and potential contribution to malignant transduction of EMPD, paraffin‐embedded EMPD specimens (35 tissue samples from 33 patients with primary EMPD, including two samples of metastatic lymph nodes from two patients) were subjected to immunohistochemical staining for Sp1 and VEGF.

Results  All of the 35 EMPD specimens, including all of six invasive EMPD and two metastatic lymph node specimens, showed strong nuclear positive staining for Sp1 and strong cytoplasmic positive staining for VEGF. The expression levels (% positive cells) of Sp1 and VEGF in EMPD were significantly higher than those of normal skin (NS). There was a significantly high correlation between expression levels of Sp1 and VEGF in EMPD.

Conclusions  The present study reveals that the concordant over‐expression of Sp1 and VEGF may play a pivotal role in the tumorigenesis and further malignant transduction of EMPD.
Impact of smoking on pemphigus
Authors: Valikhani Mahin , Kavusi Suzan , Chams‐Davatchi Cheyda , Hallaji Zahra , Esmaili Nafiseh , Ghandi Narges , Farahani Farzaneh , Lajevardi Vahide
Published: May 2008

Background  A positive history of smoking is less common in patients with pemphigus than in healthy subjects. The aim of this case–control study was to compare the remission rate and clinical locations involved in smokers and nonsmokers with pemphigus vulgaris.

Methods  Seventy patients with pemphigus vulgaris, treated with a uniform protocol, were enrolled. The sites of involvement, average time needed for disease control, and number of relapses were compared in smokers and nonsmokers. At the end of the first and second years of treatment, the rate of remission was compared in the two groups.

Results  Ten of the patients were current cigarette smokers, but the other 60 (85.7%) had no history of smoking. There was no difference in the rate of cutaneous or mucosal involvement between smokers and nonsmokers. The predominant subtype was the mucocutaneous type in both groups. Smokers with pemphigus vulgaris achieved partial remission more frequently than nonsmokers at the end of the first year of treatment. The number of patients in remission at the end of the second year of therapy was significantly higher for smokers with pemphigus than for nonsmokers. The main reason for disease activity in both groups was recurrence.

Conclusions  Cigarette smoking may not affect the rate of cutaneous or mucosal involvement in pemphigus; however, the data indicate that remission may be achieved sooner in pemphigus patients who smoke.