21 results on '"Annie Gervais"'
Search Results
2. Acute Neuroinflammation Promotes Cell Responses to 1800 MHz GSM Electromagnetic Fields in the Rat Cerebral Cortex
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Julie Lameth, Annie Gervais, Catherine Colin, Philippe Lévêque, Thérèse M. Jay, Jean-Marc Edeline, Michel Mallat, Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute ( ICM ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -CHU Pitié-Salpêtrière [APHP]-Centre National de la Recherche Scientifique ( CNRS ), BIO-INGENIERIE ( XLIM-BIO-INGENIERIE ), XLIM ( XLIM ), Université de Limoges ( UNILIM ) -Centre National de la Recherche Scientifique ( CNRS ) -Université de Limoges ( UNILIM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut des Neurosciences de Paris-Saclay ( Neuro-PSI ), Université Paris-Sud - Paris 11 ( UP11 ) -Centre National de la Recherche Scientifique ( CNRS ), Centre de Psychiatrie et Neurosciences ( CPN - U894 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS), BIO-INGENIERIE (XLIM-BIO-INGENIERIE), XLIM (XLIM), Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS), Institut des Neurosciences Paris-Saclay (NeuroPSI), Université Paris-Sud - Paris 11 (UP11)-Centre National de la Recherche Scientifique (CNRS), Institut de psychiatrie et neurosciences (U894 / UMS 1266), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Centre de Psychiatrie et Neurosciences (U894), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-CHU Pitié-Salpêtrière [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)
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0301 basic medicine ,Lipopolysaccharides ,Male ,Neuroimmunomodulation ,[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology ,Interleukin-1beta ,Lipopolysaccharide ,Toxicology ,[ SDV.NEU.PC ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior ,03 medical and health sciences ,[ SDV.NEU.SC ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences ,0302 clinical medicine ,Neuroinflammation ,Animals ,RNA, Messenger ,Receptors, AMPA ,AMPA receptor ,Rats, Wistar ,Cerebral Cortex ,Inflammation ,Neurons ,[SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior ,General Neuroscience ,[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences ,Electromagnetic fields ,Disease Models, Animal ,030104 developmental biology ,Radiofrequency ,[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology ,Acute Disease ,NADPH Oxidase 2 ,Microglia ,Mobile phone ,030217 neurology & neurosurgery ,Cell Phone - Abstract
International audience; Mobile phone communications are conveyed by radiofrequency (RF) electromagnetic fields, including pulse-modulated global system for mobile communications (GSM)-1800 MHz, whose effects on the CNS affected by pathological states remain to be specified. Here, we investigated whether a 2-h head-only exposure to GSM-1800 MHz could impact on a neuroinflammatory reaction triggered by lipopolysaccharide (LPS) in 2-week-old or adult rats. We focused on the cerebral cortex in which the specific absorption rate (SAR) of RF averaged 2.9 W/kg. In developing rats, 24 h after GSM exposure, the levels of cortical interleukin-1ß (IL1ß) or NOX2 NADPH oxidase transcripts were reduced by 50 to 60%, in comparison with sham-exposed animals (SAR = 0), as assessed by RT-qPCR. Adult rats exposed to GSM also showed a 50% reduction in the level of IL1ß mRNA, but they differed from developing rats by the lack of NOX2 gene suppression and by displaying a significant growth response of microglial cell processes imaged in anti-Iba1-stained cortical sections. As neuroinflammation is often associated with changes in excitatory neurotransmission, we evaluated changes in expression and phosphorylation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the adult cerebral cortex by Western blot analyses. We found that GSM exposure decreased phosphorylation at two residues on the GluA1 AMPAR subunit (serine 831 and 845). The GSM-induced changes in gene expressions, microglia, and GluA1 phosphorylation did not persist 72 h after RF exposure and were not observed in the absence of LPS pretreatment. Together, our data provide evidence that GSM-1800 MHz can modulate CNS cell responses triggered by an acute neuroinflammatory state.
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- 2017
3. The NADPH oxidase Nox2 regulates VEGFR1/CSF-1R-mediated microglial chemotaxis and promotes early postnatal infiltration of phagocytes in the subventricular zone of the mouse cerebral cortex
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Aurélia Lelli, Catherine Colin, Peter Carmeliet, Michel Mallat, Karl-Heinz Krause, Cyril Chéret, Carmen Ruiz de Almodovar, Séverine Boillée, and Annie Gervais
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Macrophage colony-stimulating factor ,Phagocyte ,Subventricular zone ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,030304 developmental biology ,0303 health sciences ,NADPH oxidase ,biology ,Microglia ,urogenital system ,Chemotaxis ,Cell biology ,medicine.anatomical_structure ,nervous system ,Neurology ,chemistry ,Cerebral cortex ,Apocynin ,cardiovascular system ,biology.protein ,Neuroscience ,hormones, hormone substitutes, and hormone antagonists ,030217 neurology & neurosurgery ,circulatory and respiratory physiology - Abstract
The phagocyte NADPH oxidase Nox2 generates superoxide ions implicated in the elimination of microorganisms and the redox control of inflammatory signaling. However, the role of Nox2 in phagocyte functions unrelated to immunity or pathologies is unknown. During development, oriented cell migrations insure the timely recruitment and function of phagocytes in developing tissues. Here, we have addressed the role of Nox2 in the directional migration of microglial cells during development. We show that microglial Nox2 regulates the chemotaxis of purified microglia mediated by the colony stimulating factor-1 receptor (CSF-1R) and the vascular endothelial growth factor receptor-1 (VEGFR1). Stimulation of these receptors triggers activation of Nox2 at the leading edge of polarized cells. In the early postnatal stages of mouse brain development, Nox2 is activated in macrophages / microglial cells in the lateral ventricle or the adjacent subventricular zone (SVZ). Fluorescent microglia injected into the lateral ventricle infiltrate the dorso-caudal SVZ through a mechanism that is blocked by pretreatment of the injected cells with an irreversible Nox inhibitor. Infiltration of endogenous microglia into the caudal SVZ of the cerebral cortex is prevented by (1) Nox2 gene deficiency, (2) treatment with a Nox2 inhibitor (apocynin), and (3) invalidation of the VEGFR1 kinase. We conclude that phagocytes move out of the lateral ventricle soon after birth and infiltrate the cortical SVZ through a mechanism requiring microglial Nox2 and VEGFR1 activation. Nox2 therefore modulates the migration of microglia and their development.
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- 2013
4. Erratum to: Acute Neuroinflammation Promotes Cell Responses to 1800 MHz GSM Electromagnetic Fields in the rat Cerebral Cortex
- Author
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Philippe Lévêque, Catherine Colin, Michel Mallat, Julie Lameth, Jean-Marc Edeline, Annie Gervais, Thérèse M. Jay, Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), BIO-INGENIERIE (XLIM-BIO-INGENIERIE), XLIM (XLIM), Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS), Centre de Psychiatrie et Neurosciences (U894), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des Neurosciences Paris-Saclay (NeuroPSI), Université Paris-Sud - Paris 11 (UP11)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS), Institut de psychiatrie et neurosciences (U894 / UMS 1266), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-CHU Pitié-Salpêtrière [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)
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0301 basic medicine ,[SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior ,Microglia ,[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology ,General Neuroscience ,[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences ,AMPA receptor ,Neurotransmission ,Biology ,Toxicology ,Cell biology ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,medicine.anatomical_structure ,Cerebral cortex ,medicine ,Excitatory postsynaptic potential ,Phosphorylation ,Receptor ,Neuroscience ,030217 neurology & neurosurgery ,Neuroinflammation - Abstract
Mobile phone communications are conveyed by radiofrequency (RF) electromagnetic fields, including pulse-modulated global system for mobile communications (GSM)-1800 MHz, whose effects on the CNS affected by pathological states remain to be specified. Here, we investigated whether a 2-h head-only exposure to GSM-1800 MHz could impact on a neuroinflammatory reaction triggered by lipopolysaccharide (LPS) in 2-week-old or adult rats. We focused on the cerebral cortex in which the specific absorption rate (SAR) of RF averaged 2.9 W/kg. In developing rats, 24 h after GSM exposure, the levels of cortical interleukin-1s (IL1s) or NOX2 NADPH oxidase transcripts were reduced by 50 to 60%, in comparison with sham-exposed animals (SAR = 0), as assessed by RT-qPCR. Adult rats exposed to GSM also showed a 50% reduction in the level of IL1s mRNA, but they differed from developing rats by the lack of NOX2 gene suppression and by displaying a significant growth response of microglial cell processes imaged in anti-Iba1-stained cortical sections. As neuroinflammation is often associated with changes in excitatory neurotransmission, we evaluated changes in expression and phosphorylation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the adult cerebral cortex by Western blot analyses. We found that GSM exposure decreased phosphorylation at two residues on the GluA1 AMPAR subunit (serine 831 and 845). The GSM-induced changes in gene expressions, microglia, and GluA1 phosphorylation did not persist 72 h after RF exposure and were not observed in the absence of LPS pretreatment. Together, our data provide evidence that GSM-1800 MHz can modulate CNS cell responses triggered by an acute neuroinflammatory state.
- Published
- 2017
5. Atlastin-1, the dynamin-like GTPase responsible for spastic paraplegia SPG3A, remodels lipid membranes and may form tubules and vesicles in the endoplasmic reticulum
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Merle Ruberg, Annie Gervais, Marie-Paule Muriel, Aurélien Dauphin, Michito Namekawa, and Alexis Brice
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Dynamins ,GTPase ,Biology ,Endoplasmic Reticulum ,Microtubules ,Biochemistry ,Cell Line ,GTP Phosphohydrolases ,Membrane Lipids ,Cellular and Molecular Neuroscience ,symbols.namesake ,GTP-Binding Proteins ,Humans ,Dynamin ,Membrane tubulation ,Spastic Paraplegia, Hereditary ,Endoplasmic reticulum ,Vesicle ,Cytoplasmic Vesicles ,Membrane Proteins ,Golgi apparatus ,Transport protein ,Cell biology ,Vesicular transport protein ,Protein Transport ,symbols - Abstract
We examined the effects of wild-type and mutant atlastin-1 on vesicle transport in the endoplasmic reticulum (ER)-Golgi interface and vesicle budding from ER-derived microsomes using the temperature-sensitive reporter vesicular stomatitis virus glycoprotein (VSV-G), and the ability of purified atlastin-1 to form tubules or vesicles from protein-free phosphatidylserine liposomes. A GTPase domain mutation (T162P) altered the cellular distribution of the ER, but none of the mutations studied significantly affected transport from the ER to the Golgi apparatus. The mutations also had no significant effect on the incorporation of VSV-G into vesicles formed from ER microsomes. Atlastin-1, however, was also incorporated into microsome-derived vesicles, suggesting that it might be implicated in vesicle formation. Purified atlastin-1 transformed phosphatidylserine liposomes into branched tubules and polygonal networks of tubules and vesicles, an action inhibited by GDP and the synthetic dynamin inhibitor dynasore. The GTPase mutations T162P and R217C decreased but did not totally prevent this action; the C-terminal transmembrane domain mutation R495W was as active as the wild-type enzyme. Similar effects were observed in human embryonic kidney cells over-expressing mutant atlastin-1. We concluded that atlastin-1, like dynamin, might be implicated in membrane tubulation and vesiculation and participated in the formation as well as the function of the ER.
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- 2009
6. System Xc−and Apolipoprotein E Expressed by Microglia Have Opposite Effects on the Neurotoxicity of Amyloid-β Peptide 1–40
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Ina Hinners, Si Qin, Cyril Chéret, Catherine Colin, Annie Gervais, and Michel Mallat
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Male ,Apolipoprotein E ,Amino Acid Transport System y+ ,Cell Survival ,Amyloid beta ,Excitotoxicity ,Glutamic Acid ,Mice, Transgenic ,Cell Communication ,medicine.disease_cause ,Neuroprotection ,Mice ,Apolipoproteins E ,Alzheimer Disease ,medicine ,Amyloid precursor protein ,Animals ,Humans ,Senile plaques ,Rats, Wistar ,Cells, Cultured ,Mice, Knockout ,Neurons ,Amyloid beta-Peptides ,Cell Death ,biology ,Microglia ,General Neuroscience ,Neurotoxicity ,Articles ,medicine.disease ,Coculture Techniques ,Peptide Fragments ,Rats ,Cell biology ,Mice, Inbred C57BL ,medicine.anatomical_structure ,Gene Expression Regulation ,nervous system ,Biochemistry ,Nerve Degeneration ,biology.protein ,Female - Abstract
Because senile plaques in Alzheimer's disease (AD) contain reactive microglia in addition to potentially neurotoxic aggregates of amyloid-β (Aβ), we examined the influence of microglia on the viability of rodent neurons in culture exposed to aggregated Aβ 1–40. Microglia enhanced the toxicity of Aβ by releasing glutamate through the cystine-glutamate antiporter system Xc−. This may be relevant to Aβ toxicity in AD, because the system Xc−-specific xCT gene is expressed not only in cultured microglia but also in reactive microglia within or surrounding amyloid plaques in transgenic mice expressing mutant human amyloid precursor protein or in wild-type mice injected with Aβ. Inhibition of NMDA receptors or system Xc−prevented the microglia-enhanced neurotoxicity of Aβ but also unmasked a neuroprotective effect of microglia mediated by microglial secretion of apolipoprotein E (apoE) in the culture medium. Immunodepletion of apoE or targeted inactivation of the apoE gene in microglia abrogated neuroprotection by microglial conditioned medium, whereas supplementation by human apoE isoforms restored protection, which was potentiated by the presence of microglia-derived cofactors. These results suggest that inhibition of microglial system Xc−might be of therapeutic value in the treatment of AD. Its inhibition not only prevents glutamate excitotoxicity but also facilitates neuroprotection by apoE.
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- 2006
7. Microglia Promote the Death of Developing Purkinje Cells
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Nico van Rooijen, Catherine Colin, José L. Marín-Teva, Isabelle Dusart, Annie Gervais, Michel Mallat, Biologie des Interactions Neurones / Glie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Developpement Normal et Pathologique du Cerveau, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Molecular Cell Biology, VUmc, Institut National de la Santé et de la Recherche Médicale and grants from Ensemble contre le SIDA and from Electricité de France to M.M. and from the French Ministry of Research and Technology to M.M. and I.D. J.L.M. was supported by a Spanish Ministry o, and VU University medical center
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Nervous system ,Programmed cell death ,Cell Survival ,Neuroscience(all) ,Cell Respiration ,Purkinje cell ,Cell ,Presynaptic Terminals ,Synaptogenesis ,Apoptosis ,Cell Communication ,In Vitro Techniques ,Biology ,Antibodies ,Receptors, Tumor Necrosis Factor ,Cerebellar Cortex ,Mice ,Purkinje Cells ,medicine ,Animals ,Enzyme Inhibitors ,Mice, Knockout ,Microglia ,Caspase 3 ,General Neuroscience ,[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences ,Cell Differentiation ,Free Radical Scavengers ,Cell biology ,Mice, Inbred C57BL ,medicine.anatomical_structure ,nervous system ,Caspases ,Neuron death ,Neuroscience ,Signal Transduction - Abstract
The loss of neuronal cells, a prominent event in the development of the nervous system, involves regulated triggering of programmed cell death, followed by efficient removal of cell corpses. Professional phagocytes, such as microglia, contribute to the elimination of dead cells. Here we provide evidence that, in addition to their phagocytic activity, microglia promote the death of developing neurons engaged in synaptogenesis. In the developing mouse cerebellum, Purkinje cells die, and 60% of these neurons that already expressed activated caspase-3 were engulfed or contacted by spreading processes emitted by microglial cells. Apoptosis of Purkinje cells in cerebellar slices was strongly reduced by selective elimination of microglia. Superoxide ions produced by microglial respiratory bursts played a major role in this Purkinje cell death. Our study illustrates a mammalian form of engulfment-promoted cell death that links the execution of neuron death to the scavenging of dead cells.
- Published
- 2004
8. Regulation of Microglial Development: A Novel Role for Thyroid Hormone
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Catherine Colin, Flavia Regina Souza Lima, Vivaldo Moura Neto, Mireille Izembart, Michel Mallat, and Annie Gervais
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Thyroid Hormones ,endocrine system ,medicine.medical_specialty ,Cell Survival ,Cell ,Cell Count ,Biology ,Hyperthyroidism ,Hypothyroidism ,Pregnancy ,Methylthiouracil ,Internal medicine ,medicine ,Animals ,ARTICLE ,Rats, Wistar ,Receptor ,Cells, Cultured ,Receptors, Thyroid Hormone ,Thyroid hormone receptor ,Triiodothyronine ,Microglia ,Reverse Transcriptase Polymerase Chain Reaction ,General Neuroscience ,Thyroid ,Brain ,Rats ,Endocrinology ,medicine.anatomical_structure ,Prenatal Exposure Delayed Effects ,Forebrain ,Female ,Cell Division ,Iodine ,Hormone - Abstract
The postnatal development of rat microglia is marked by an important increase in the number of microglial cells and the growth of their ramified processes. We studied the role of thyroid hormone in microglial development. The distribution and morphology of microglial cells stained with isolectin B4 or monoclonal antibody ED1 were analyzed in cortical and subcortical forebrain regions of developing rats rendered hypothyroid by prenatal and postnatal treatment with methyl-thiouracil. Microglial processes were markedly less abundant in hypothyroid pups than in age-matched normal animals, from postnatal day 4 up to the end of the third postnatal week of life. A delay in process extension and a decrease in the density of microglial cell bodies, as shown by cell counts in the developing cingulate cortex of normal and hypothyroid animals, were responsible for these differences. Conversely, neonatal rat hyperthyroidism, induced by daily injections of 3,5,3'-triiodothyronine (T3), accelerated the extension of microglial processes and increased the density of cortical microglial cell bodies above physiological levels during the first postnatal week of life. Reverse transcription-PCR and immunological analyses indicated that cultured cortical ameboid microglial cells expressed the alpha1 and beta1 isoforms of nuclear thyroid hormone receptors. Consistent with the trophic and morphogenetic effects of thyroid hormone observed in situ, T3 favored the survival of cultured purified microglial cells and the growth of their processes. These results demonstrate that thyroid hormone promotes the growth and morphological differentiation of microglia during development.
- Published
- 2001
9. Frequency and relevance of IgM intrathecal synthesis in multiple sclerosis
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Annie Gervais, O. Gaillard, P. Lambin, F. Bricaire, E. Schuller, Jean Yves Delattre, J. Reboul, and O. Lyon-Caen
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business.industry ,Multiple sclerosis ,Central nervous system ,Intrathecal ,medicine.disease ,Dithiothreitol ,chemistry.chemical_compound ,Cerebrospinal fluid ,medicine.anatomical_structure ,Neurology ,chemistry ,Immunity ,Immunology ,medicine ,Neurology (clinical) ,Elisa method ,business ,CSF albumin - Abstract
Using a new ELISA method we have measured the IgM concentration in the serum and the cerebrospinal fluid CSF from 110 neurological patients. Among there, 41 had multiple sclerosis (MS), 48 other inflammatory diseases (OID), including 30 AIDS, and 21 non-inflammatory neurological diseases (NID). A highly significant correlation was established between results with native IgM and the dithiothreitol reduced IgM. An intrathecal synthesis (ITS) of IgM was detected using the CSF IgM/CSF albumin ratio, the IgM index and a quantitative formula in 33 patients: nine MS, 23 OID (including 18 AIDS) and one NID. The frequency of IgM ITS was 22% in MS patients, 48% in the OID (60% in AIDS) and 5% in the NID groups. This ITS was not impaired by an increase in serum IgM concentration or by a blood-CSF barrier damage. These facts confirm that intrathecal immunity is not a "steady-state" related to the general immunity but a specific response restricted to the central nervous system. Conversely, CSF IgM increase and IgM ITS were closely related (p < 10(-6) ). In addition, IgM ITS and IgG ITS were found to be highly correlated in OID, especially in AIDS patients: such correlation was not observed in the MS group. No significant correlations were observed between IgM ITS and any of the clinical parameters in MS patients. These results suggest the probable specificity of IgM ITS in MS patients.
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- 2013
10. Activation of ionotropic glutamate receptors reduces the production of transforming growth factor-ß2 by developing neurons
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Jacques Glowinski, Annie Gervais, Alexandre Dobbertin, and Michel Mallat
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Kainic acid ,General Neuroscience ,Glutamate receptor ,Kainate receptor ,AMPA receptor ,Cell biology ,chemistry.chemical_compound ,nervous system ,chemistry ,embryonic structures ,CNQX ,NMDA receptor ,Long-term depression ,Neuroscience ,Ionotropic effect - Abstract
Neuronal cultures derived from developing rat cerebral cortex were used to investigate the influence of glutamate receptors on the neuronal production of transforming growth factor-beta2 (TGFbeta2), a multifunctional cytokine that modulates neuronal and glial growth. Long-term exposure (48 h) of cortical neurons to selective antagonists of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors markedly increased TGFbeta2 levels in the culture medium. Conversely, treatment with NMDA or kainate reduced TGFbeta2 to levels below those in untreated cultures. The effect of kainate did not require NMDA receptor activity. Neuronal depolarization with K+ also reduced TGFbeta2 levels by opening voltage-gated L-type Ca2+ channels. Semi-quantitative RT-PCR measurements of neuronal TGFbeta2 mRNA showed that NMDA or AMPA/kainate receptor stimulation reduced TGFbeta2 mRNA levels. These results demonstrate that tonic activation of glutamate-gated cation channels downregulates neuronal expression of the TGFbeta2 gene and provide evidence for a novel mechanism whereby excitatory amino acids could influence the development of glial and neuronal lineages.
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- 2000
11. A Sensitive Time-Resolved Immunofluorometric Assay for the Measurement of Apolipoprotein B in Cerebrospinal Fluid. Application to Multiple Sclerosis and Other Neurological Diseases
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D. Meillet, Jean Yves Delattre, M. Bordas-Fonfrède, I. Osman, A. Legrand, E. Schuller, Annie Gervais, and O. Gaillard
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Adult ,Male ,medicine.medical_specialty ,Multiple Sclerosis ,Apolipoprotein B ,Microgram ,Fluoroimmunoassay ,education ,Clinical Biochemistry ,Central nervous system ,Sensitivity and Specificity ,Central nervous system disease ,chemistry.chemical_compound ,Cerebrospinal fluid ,Nephelometry and Turbidimetry ,Internal medicine ,medicine ,Humans ,Receptor ,Aged ,Apolipoproteins B ,biology ,Multiple sclerosis ,Biochemistry (medical) ,Reproducibility of Results ,General Medicine ,Middle Aged ,medicine.disease ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Low-density lipoprotein ,biology.protein ,Female ,lipids (amino acids, peptides, and proteins) ,Nervous System Diseases - Abstract
Although low density lipoprotein receptors have been described on oligodendrocytes, apolipoprotein B was thought to be absent or present in only very small amounts in cerebrospinal fluid (CSF). Several immunoassays have been used for the measurement of apolipoprotein B in serum. However, the majority of methods cannot be used to measure small amounts of apolipoprotein B in CSF. In this study, we describe a highly sensitive time resolved immunofluorometric assay (TR-IFMA) using europium as label (detection limit: 0.3 microgram/l). The reliability of the TR-IFMA for the measurement of apolipoprotein B was first studied in serum. Serum and CSF apolipoprotein B concentrations were then determined in subjects free of neurological disorders and in patients with multiple sclerosis. Local intrathecal apolipoprotein B synthesis was calculated. Although the high sensitivity of the TR-IFMA allowed low amounts of apolipoprotein B in CSF to be detected (0.11 +/- 0.06; 0.12 +/- 0.06 mg/l in controls and multiple sclerosis patients, respectively), no apolipoprotein B could be detected in CSF by electroimmunodiffusion. As suggested by the blood/CSF apolipoprotein B ratio (about 6000), no apolipoprotein B synthesis was observed by both using apolipoprotein B index and formula. This indicates its probable serum origin. Moreover, there was no difference between controls and multiple sclerosis patients in CSF, serum, blood/CSF, index, and local intrathecal apoliprotein B synthesis. Finally, these results suggest that the role of apolipoprotein B in lipid transport in the central nervous system may be questionable.
- Published
- 1995
12. Fibronectin in plasma and CSF: Evidence for its intrathecal synthesis
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Annie Gervais and E. Schuller
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Adult ,Male ,Pathology ,medicine.medical_specialty ,Immunology ,Intrathecal ,Cerebrospinal fluid ,Reference Values ,Internal medicine ,medicine ,Humans ,Immunology and Allergy ,Serum Albumin ,CSF albumin ,biology ,business.industry ,Mental Disorders ,Multiple sclerosis ,Middle Aged ,medicine.disease ,Fibronectins ,Peripheral ,Fibronectin ,Endocrinology ,Neurology ,biology.protein ,Female ,Neurology (clinical) ,Nervous System Diseases ,business - Abstract
A new methodology, using electroimmunodiffusion, has been described for the determination of fibronectin (Fn) in plasma and CSF. Fn was determined in the plasma of 35 normal subjects, and in the plasma and the CSF of 86 patients: 10 controls, 17 definite MS, 15 other inflammatory processes, 11 degenerative diseases, 13 peripheral neuropathies and 20 other neurological diseases. The normal mean was 354 ± 53 μg/ml in plasma, not influenced by sex or age, and in the CSF 2,3 ± 0,85 μg/ml. A significant increase of plasma Fn was observed in each of the patients-group. In the CSF an increase of Fn was observed predominantly in inflammatory processes but not in MS. An intrathecal synthesis of Fn was established in 24 76 patients, most often in inflammatory ( 9 15 ) processes but rarely ( 3 17 ) in MS. The intrathecal synthesis was suspected from the CSF Fn/CSF Albumin ratio and calculated using a formula derived from the principles previously described for IgG intrathecal synthesis. It represents the principal source of Fn increase in the CSF. In all inflammatory processes (including MS) the eventual influence of corticoids, immunosuppresive or anti-inflammatory drugs has not been established. The significance of the CSF Fn level in MS is discussed with regard to the recent demonstration of its presence within MS lesions and on macrophages in plaques.
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- 1991
13. Neurotoxic activation of microglia is promoted by a nox1-dependent NADPH oxidase
- Author
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Lahouari Amar, Karl-Heinz Krause, Jacques Mallet, Cyril Chéret, Philippe Ravassard, Aurélia Lelli, Ana Cumano, Catherine Colin, Annie Gervais, Michel Mallat, IFR des Neurosciences, Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Biologie des Interactions Neurones / Glie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Génétique moléculaire de la neurotransmission et des processus neurodégénératifs (LGMNPN), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Développement des Lymphocytes, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Biology of Ageing Laboratories, Université de Genève = University of Geneva (UNIGE), Vougny, Marie-Christine, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), and University of Geneva [Switzerland]
- Subjects
Lipopolysaccharides ,rac1 GTP-Binding Protein ,Male ,MESH: Membrane Glycoproteins ,MESH: rac GTP-Binding Proteins ,ddc:616.07 ,MESH: Neuropeptides ,MESH: Mice, Knockout ,MESH: Corpus Striatum ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Gliosis/enzymology/physiopathology ,NADH, NADPH Oxidoreductases ,MESH: Animals ,MESH: Proteins ,Gliosis ,MESH: NADPH Oxidase ,Mice, Knockout ,0303 health sciences ,NADPH oxidase ,Membrane Glycoproteins ,MESH: NADH, NADPH Oxidoreductases ,MESH: Oxidative Stress ,biology ,Microglia ,Superoxide ,Nitrites/metabolism ,General Neuroscience ,MESH: Nitrites ,NADPH Oxidase/genetics/metabolism ,MESH: Reactive Oxygen Species ,MESH: Gliosis ,Articles ,Cell biology ,rac GTP-Binding Proteins ,Nitric oxide synthase ,MESH: Microglia ,medicine.anatomical_structure ,Biochemistry ,NOX1 ,NADPH Oxidase 2 ,NADPH Oxidase 1 ,cardiovascular system ,Encephalitis ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Female ,Inflammation Mediators ,Zymosan/metabolism ,Rac GTP-Binding Proteins/genetics/metabolism ,MESH: Zymosan ,[SDV.IMM] Life Sciences [q-bio]/Immunology ,Neurotoxins ,MESH: Inflammation Mediators ,NADH, NADPH Oxidoreductases/genetics/metabolism ,Cytochrome b Group/genetics/metabolism ,Corpus Striatum/drug effects/enzymology/physiopathology ,Neurotoxins/pharmacology ,Microglia/drug effects/enzymology ,Nitric oxide ,03 medical and health sciences ,MESH: Mice, Inbred C57BL ,Reactive Oxygen Species/metabolism ,medicine ,MESH: Cytochrome b Group ,Animals ,Oxidative Stress/drug effects/physiology ,MESH: Mice ,Neuroinflammation ,Nitrites ,030304 developmental biology ,Adaptor Proteins, Signal Transducing ,MESH: Neurotoxins ,Encephalitis/enzymology/physiopathology ,Neuropeptides/genetics/metabolism ,Neuropeptides ,Zymosan ,NADPH Oxidases ,Proteins ,Proteins/genetics/metabolism ,Membrane Glycoproteins/genetics ,Cytochrome b Group ,Lipopolysaccharides/pharmacology ,Corpus Striatum ,MESH: Male ,Inflammation Mediators/pharmacology ,Mice, Inbred C57BL ,Oxidative Stress ,chemistry ,Apocynin ,biology.protein ,MESH: Encephalitis ,MESH: Lipopolysaccharides ,Reactive Oxygen Species ,MESH: Female ,030217 neurology & neurosurgery - Abstract
Reactive oxygen species (ROS) modulate intracellular signaling but are also responsible for neuronal damage in pathological states. Microglia, the resident CNS macrophages, are prominent sources of ROS through expression of the phagocyte oxidase which catalytic subunit Nox2 generates superoxide ion (O2·−). Here we show that microglia also express Nox1 and other components of nonphagocyte NADPH oxidases, including p22phox, NOXO1, NOXA1, and Rac1/2. The subcellular distribution and functions of Nox1 were determined by blocking Nox activity with diphenylene iodonium or apocynin, and by silencing theNox1gene in microglia purified from wild-type (WT) or Nox2-KO mice. [Nox1-p22phox] dimers localized in intracellular compartments are recruited to phagosome membranes during microglial phagocytosis of zymosan, and Nox1 produces O2·−in zymosan-loaded phagosomes. In microglia activated with lipopolysaccharide (LPS), Nox1 produces O2·−, which enhances cell expression of inducible nitric oxide synthase and secretion of interleukin-1β. Comparisons of microglia purified from WT, Nox2-KO, or Nox1-KO mice indicate that both Nox1 and Nox2 are required to optimize microglial production of nitric oxide. By injecting LPS in the striatum of WT and Nox1-KO mice, we show that Nox1 also enhances microglial production of cytotoxic nitrite species and promotes loss of presynaptic proteins in striatal neurons. These results demonstrate the functional expression of Nox1 in resident CNS phagocytes, which can promote production of neurotoxic compounds during neuroinflammation. Our study also shows that Nox1- and Nox2-dependent oxidases play distinct roles in microglial activation and that Nox1 is a possible target for the treatment of neuroinflammatory states.
- Published
- 2008
14. Apolipoprotein E and multiple sclerosis: a biochemical and genetic investigation
- Author
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Olivier Lyon-Caen, Olivier Gaillard, D. Meillet, E. Schuller, Bertrand Fontaine, E Plassart, Annie Gervais, and Jacques Delattre
- Subjects
Apolipoprotein E ,Adult ,Male ,medicine.medical_specialty ,Multiple Sclerosis ,Central nervous system disease ,chemistry.chemical_compound ,Myelin ,Cerebrospinal fluid ,Apolipoproteins E ,Internal medicine ,medicine ,Demyelinating disease ,Humans ,Fluorometry ,Amyotrophic lateral sclerosis ,Aged ,Polymorphism, Genetic ,Cholesterol ,business.industry ,Multiple sclerosis ,Osmolar Concentration ,Middle Aged ,medicine.disease ,Endocrinology ,medicine.anatomical_structure ,Neurology ,chemistry ,Immunology ,Immunologic Techniques ,lipids (amino acids, peptides, and proteins) ,Female ,Neurology (clinical) ,business - Abstract
Apolipoprotein E (apo E) is postulated to be a major lipid carrier protein in the brain involved in brain development and repair. Multiple sclerosis (MS) is a major demyelinating disease characterized by destruction of myelin and marked alteration of myelin cholesterol and lipid metabolism. We have determined serum and cerebrospinal fluid (CSF) apo E concentrations using an original time-resolved immunofluorometric assay and calculated intrathecal apo E concentration. Apo E concentrations were determined in 13 control subjects and 129 neurological patients: 34 definite MS patients, 25 with Guillain-Barre syndrome (GBS), 32 with amyotrophic lateral sclerosis (ALS) and 38 with other neurological diseases. Seven clinical parameters (sex, age, age at MS onset, duration of the disease, course, clinical status and disability score) were considered in MS patients. Significant (P < 0.01) decrease in CSF apo E was observed in MS, linked to a decrease in intrathecal apo E. The decreased CSF apo E concentration in MS patients occur independent of the apo E genotype. Apo E is considered as a neurotrophic factor in the brain. Any decrease in intrathecal apo E synthesis would thus contribute to progression of neurological diseases, such as MS.
- Published
- 1998
15. Apolipoprotein E polymorphism in multiple sclerosis
- Author
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Oliver Gaillard, E Plassart, Annie Gervais, J. Reboul, Bertrand Fontaine, and E. Schuller
- Subjects
Apolipoprotein E ,Adult ,Male ,030213 general clinical medicine ,medicine.medical_specialty ,Multiple Sclerosis ,Adolescent ,Clinical Biochemistry ,Population ,Central nervous system ,030209 endocrinology & metabolism ,Biology ,Central nervous system disease ,03 medical and health sciences ,chemistry.chemical_compound ,Myelin ,0302 clinical medicine ,Apolipoproteins E ,Internal medicine ,medicine ,Demyelinating disease ,Humans ,education ,Alleles ,Aged ,education.field_of_study ,Polymorphism, Genetic ,Cholesterol ,Multiple sclerosis ,General Medicine ,Middle Aged ,medicine.disease ,medicine.anatomical_structure ,Endocrinology ,Phenotype ,chemistry ,Case-Control Studies ,lipids (amino acids, peptides, and proteins) ,Female - Abstract
Apolipoprotein E (apo E) is a polymorphic plasma protein involved in cholesterol transport. Apo E is produced and secreted in the central nervous system by astrocytes. Following peripheral nerve injury in rats, the synthesis of apo E increases 250to 350-fold. A similar increase is observed in the central nervous system when the optic nerve and spinal cord are injured. It was suggested that apo E redistributes lipid, participates in cholesterol homeostasis in the brain and is implicated in the growth and repair of the nervous system. I Three common variants of apo E are present in the general human population, c2, d and fA coding for three isoforms (apo E2, apo E3, apo E4). These isoforms differ from each other by a single aminoacid substitution. The most frequent phenotype in the normal population is apo E3/ apo E3 and the two minor isoforms are associated with altered recognition of specific receptors. Recent genetic evidence suggests that inheritance of the c4 allele is associated with increased risk for sporadic and earlier onset of Alzheimer's disease (AD).2 In contrast, Rubinsztein found no influence of the apo E phenotype in a small group of patients with multiple sclerosis (MS).' MS is the major demyelinating disease. The increased higher incidence in women, the racial and familial clustering of MS cases and the high concordance rate in monozygotic twins (26%) compared with dizygotic twins (2'3%) and non twin siblings (1'9%), suggest that a genetic component influences susceptibility to MS. 4 We recently demonstrated that apo E concentrations in cerebrospinal fluid (CSF) and apo E intrathecal synthesis are decreased in MS patients. The reduction of CSF apo E levels may impair myelin repair and influence disease progression in MS patients.
- Published
- 1998
16. Intrathecal Synthesis of β2-Microglobulin and Lysozyme: Differential Markers of Nervous System Involvement in Patients Infected with Human Immunodeficiency Virus Type 1
- Author
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Annie Gervais, D. Meillet, E. Schuller, J Delattre, Marc Gentilini, Laurent Bélec, Nicole Celton, and J. Reboul
- Subjects
Adult ,Male ,Nervous system ,AIDS Dementia Complex ,education ,Clinical Biochemistry ,Central nervous system ,Immunoglobulins ,HIV Infections ,Biology ,Virus ,chemistry.chemical_compound ,Cerebrospinal fluid ,Central Nervous System Diseases ,Predictive Value of Tests ,Albumins ,medicine ,Humans ,Beta-2 microglobulin ,Multiple sclerosis ,Biochemistry (medical) ,Complement C4 ,General Medicine ,Middle Aged ,medicine.disease ,medicine.anatomical_structure ,Spinal Cord ,chemistry ,Immunology ,HIV-1 ,Female ,Muramidase ,Lysozyme ,beta 2-Microglobulin ,Meningitis ,Biomarkers - Abstract
beta 2-Microglobulin and lysozyme were determined in paired serum and cerebrospinal fluid samples from 137 patients, using immunofluorometry and ELISA, respectively. Of these patients, 54 were infected by human immunodeficiency virus type 1 (HIV1) (including 20 AIDS dementia patients), 73 were HIV1-seronegative with neurological diseases (meningitis (n = 10), multiple sclerosis (n = 29), other neurological diseases (n = 34)) and 10 were controls. Intrathecal synthesis of beta 2-microglobulin occurred in each group. Conversely, lysozyme intrathecal synthesis was found only in meningitis (10/10) and in HIV1-infection (24/54). A pathological increase in beta 2-microglobulin intrathecal synthesis (> or = 2 mg/l) was observed in 45 patients (34 HIV1-infected patients and 11 HIV1-seronegative patients with neurological diseases). Serum concentration and intrathecal synthesis of beta 2-microglobulin were correlated only in the 20 AIDS dementia patients. The cerebrospinal fluid beta 2-microglobulin and lysozyme concentrations were correlated in the 54 HIV1-infected patients only. Blood CD4 + T-cell count was correlated negatively with beta 2-microglobulin intrathecal synthesis but not with lysozyme intrathecal synthesis. These data suggest that in the absence of any central nervous system opportunistic process the increase of beta 2-microglobulin intrathecal synthesis (> or = 2 mg/l) may be a reliable marker of central nervous system involvement in HIV1-infected patients. Intrathecal synthesis of lysozyme was related principally to HIV1-encephalitis and central nervous system opportunistic processes.
- Published
- 1993
17. Apolipoprotein E intrathecal synthesis is decreased in multiple sclerosis
- Author
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D. Meillet, J. Delattre, O. Gaillard, Annie Gervais, E. Schuller, Olivier Lyon-Caen, and F. Bricaire
- Subjects
Apolipoprotein E ,Neurology ,business.industry ,Multiple sclerosis ,Immunology ,medicine ,Immunology and Allergy ,Neurology (clinical) ,Pharmacology ,medicine.disease ,business ,Intrathecal - Published
- 1994
18. Intrathecal synthesis of IgM in multiple sclerosis and in acquired immunodeficiency syndrome
- Author
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Annie Gervais, F. Bricaire, E. Schuller, J. Delattre, O. Gaillard, J. Reboul, Olivier Lyon-Caen, and P. Lambin
- Subjects
Neurology ,Acquired immunodeficiency syndrome (AIDS) ,business.industry ,Multiple sclerosis ,Immunology ,medicine ,Immunology and Allergy ,Neurology (clinical) ,medicine.disease ,business ,Intrathecal - Published
- 1994
19. Measurement of apolipoprotein B andlipoprotein (a) in human cerebrospinal spinal fluid. Application to multiple sclerosis
- Author
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E. Schuller, Annie Gervais, J. Delattre, D. Meillet, O. Gaillard, and J. Galli
- Subjects
Pathology ,medicine.medical_specialty ,Apolipoprotein B ,biology ,business.industry ,Multiple sclerosis ,Immunology ,medicine.disease ,Neurology ,medicine ,biology.protein ,Immunology and Allergy ,Neurology (clinical) ,business - Published
- 1994
20. Intrathecal synthesis of IgG subclasses in multiple sclerosis and in AIDS
- Author
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P. Lambin, P. Lebon, E. Defendini, M. Dubarry, Annie Gervais, M. Levy, and E. Schuller
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Neurology ,Acquired immunodeficiency syndrome (AIDS) ,business.industry ,Multiple sclerosis ,Immunology ,medicine ,Immunology and Allergy ,Neurology (clinical) ,Igg subclasses ,medicine.disease ,Intrathecal ,business - Published
- 1991
21. Intrathecal synthesis (ITS) of β2 microglobulin: A specific marker of neuro-aids?
- Author
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Annie Gervais, A. DevilleChabrolle, D. Meillet, L. Khalil, Marc Gentilini, J. Reboul, E. Schuller, and L. Bélec
- Subjects
Neurology ,Neuro aids ,business.industry ,Beta-2 microglobulin ,Immunology ,Immunology and Allergy ,Medicine ,Neurology (clinical) ,business ,Intrathecal - Published
- 1991
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