References of "Neuropathology & Applied Neurobiology"
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See detailExpression pattern of synaptic vesicle protein 2 (SV2) isoforms in patients with temporal lobe epilepsy and hippocampal sclerosis
CREVECOEUR, Julie ULg; Kaminski, RM; Rogister, Bernard ULg et al

in Neuropathology & Applied Neurobiology (2014), 40(2), 191-204

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See detailThe in vitro influences of neurotensin on the motility characteristics of human U373 glioblastoma cells
Servotte, S.; Camby, I.; Debeir, O. et al

in Neuropathology & Applied Neurobiology (2006), 32(6), 575-584

Astrocytic tumours are associated with dismal prognoses due to their pronounced ability to diffusely invade the brain parenchyma. Various neuropeptides, including gastrin, are able to modulate tumour ... [more ▼]

Astrocytic tumours are associated with dismal prognoses due to their pronounced ability to diffusely invade the brain parenchyma. Various neuropeptides, including gastrin, are able to modulate tumour astrocyte migration. While neurotensin has been shown to influence the proliferation of glioma cells and the migratory ability of a large set of other cell types, its role in glioma cell migration has never been investigated. Neurotensin-induced modifications to the motility features of human U373 glioblastoma cells therefore constitute the topic of the present study. We evidenced that three subtypes of neurotensin receptors (NTR1, NTR2 and NTR3) are expressed in U373 glioblastoma cells, at least as far as their mRNAs are concerned. Treating U373 tumour cells with 10 nM neurotensin markedly modified the morphological patterns of these cells and also profoundly altered the organization of their actin cytoskeletons. Pull-down assays revealed that neurotensin induced the activation in U373 cells of both Rac1 and Cdc42 but not RhoA. Scratch wound assays evidenced that neurotensin (0.1 and 10 nM) very significantly inhibited wound colonization by U373 cells cultured in the absence of serum. In addition, quantitative phase-contrast videomicroscopy analyses showed that neurotensin decreases the motility levels of U373 glioblastoma cells when these cells are cultured on plastic. In sharp contrast, neurotensin stimulates the motility of U373 cells when they are cultured on laminin, which is a pro-adhesive extracellular matrix component ubiquitously secreted by glioma cells. Our data thus strongly suggest that, in addition to gastrin, neurotensin is a neuropeptide capable of modulating tumour astrocyte migration into the brain parenchyma. [less ▲]

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See detailComparative study of commercially available anti-alpha-synuclein antibodies.
Croisier, E.; MRes, D Elfant; Deprez, Manuel ULg et al

in Neuropathology & Applied Neurobiology (2006), 32(3), 351-6

Immunohistochemistry for alpha-synuclein has become the histological technique of choice for the diagnosis for Parkinson's disease, Dementia with Lewy bodies and Multiple System Atrophy (http://www.ICDNS ... [more ▼]

Immunohistochemistry for alpha-synuclein has become the histological technique of choice for the diagnosis for Parkinson's disease, Dementia with Lewy bodies and Multiple System Atrophy (http://www.ICDNS.org). Nevertheless, no standardised protocol has been proposed. We have reviewed 242 of the 270 studies published until June 2005 that mentioned immunohistochemistry for anti-alpha synuclein on human tissue and we found that only 75 (31%) used commercial antibodies. We also noted that protocols, particularly dilution and antigen unmasking, varied between studies, even when the same antibody was employed. In order to establish a standardised protocol for alpha-synuclein immunohistochemistry, which can be applied in diagnostic neuropathology we tested seven commercial monoclonal antibodies in brains of subjects with Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, multiple sclerosis with incidental Lewy bodies and aged-matched normal brain and determined for each antibody the best suited protocol for antigen unmasking. We evaluated the intensity of immunolabelling in Lewy bodies, neuropil threads, dendrites, pre-synaptic terminals, granular cytoplasmic positivity, peri-axonal positivity, glial inclusions and non-specific immunolabelling. Although our results showed that all the antibodies detected alpha-synuclein inclusions, differences were noted between antibodies, particularly with regard to the detection of glial inclusions. From our study, the best antibodies of the seven tested appeared to be those directed against amino acids 116-131 and 15-123 and we suggest them to be used in routine diagnostic practice for alpha-synucleinopathies. [less ▲]

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See detailMacrophage migration inhibitory factor (MIF) expression in human glioblastomas correlates with vascular endothelial growth factor (VEGF) expression
Munaut, Carine ULg; Boniver, Jacques ULg; Foidart, Jean-Michel ULg et al

in Neuropathology & Applied Neurobiology (2002), 28(6), 452-460

Macrophage migration inhibitory factor (MIF) is a peptide released upon hypothalamo-pituitary stimulation that acts as a potent endogenous antagonist of the glucocorticoid inhibition of acute inflammatory ... [more ▼]

Macrophage migration inhibitory factor (MIF) is a peptide released upon hypothalamo-pituitary stimulation that acts as a potent endogenous antagonist of the glucocorticoid inhibition of acute inflammatory response and subsequent antigen-specific response. MIF also sustains tumour growth as it promotes angiogenesis, overcomes p53-mediated cell growth arrest and inhibits tumour-specific immune responses. Using quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry, we studied MIF expression in 35 human glioblastomas and two normal brains. We compared these results with the expression of vascular endothelial growth factor (VEGF), the most potent angiogenic factor in glioblastomas. We detected MIF in normal cortical neurons and glial cells. All glioblastomas were positive for MIF mRNA with expression levels similar to or higher than those of normal brain. MIF immunoreactivity was seen mainly in tumour cells and less frequently in hyperplastic endothelial cells. The expressions of MIF and VEGF mRNA were strongly correlated (P < 0.0001). Our results demonstrate the expression of MIF in human glioblastomas, and indicate a close relationship with VEGF expression. This is of particular interest given the potential modulation of MIF by glucocorticosteroids. [less ▲]

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See detailHistoenzymology of the developing rat spinal cord.
Schoenen, Jean ULg

in Neuropathology & Applied Neurobiology (1978), 4(1), 37-46

Using histochemical methods the activity of acetycholinesterase, acid phosphatase and various dehydrogenases was investigated in the developing rat spinal cord. At the ninth embryonic day (E9) only the ... [more ▼]

Using histochemical methods the activity of acetycholinesterase, acid phosphatase and various dehydrogenases was investigated in the developing rat spinal cord. At the ninth embryonic day (E9) only the activity of the lactate dehydrogenase slow-moving isoenzymes was prominent in spinal neurons. Between E13 and E15 an increase was observed in the activity of most of the dehydrogenases and of acid phosphatase in motoneurons and posterior root ganglion cells. Between E15 and E17 acetylcholinesterase activity increased markedly. On E17 and E20, this enzyme was also detectable in anterior and posterior roots and in neurons of the intermediate grey matter. On E20, although all grey matter neurons were cytologically fully differentiated, their enzymatic content was found to be still incomplete. The prominent acid phosphatase reaction within laminae I and II, which is characteristic of the adult rat, was absent in the fetal spinal cord. These findings indicate that the spinal cord metabolism is predominantly anaerobic during the first two-thirds of gestation. The histoenzymological maturation of grey-matter neurons is delayed in comparison to their cytological differentiation. Furthermore, the ontogenesis of motoneuronal acetylcholinesterase activity correlates well with the development of motor activities in the rat fetus. [less ▲]

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