Infiltrating macrophages are key to the development of seizures following virus infection. - Wikidata - thesis-toulmin - TriplyDB

Infiltrating macrophages are key to the development of seizures following virus infection.

Infiltrating macrophages are key to the development of seizures following virus infection.

http://www.wikidata.org/entity/Q36559966

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Neuroprotection mediated by inhibition of calpain during acute viral encephalitis Astrocyte galectin-9 potentiates microglial TNF secretion Pro-epileptogenic effects of viral-like inflammation in both mature and immature brains.Hippocampal TNFα Signaling Contributes to Seizure Generation in an Infection-Induced Mouse Model of Limbic Epilepsy.Three immune-mediated disease models induced by Theiler's virus: Multiple sclerosis, seizures and myocarditis.Picornavirus infection leading to immunosuppression.Berteroin present in cruciferous vegetables exerts potent anti-inflammatory properties in murine macrophages and mouse skin.Distinct kinetics of viral replication, T cell infiltration, and fibrosis in three phases of myocarditis following Theiler's virus infection.DA virus mutant H101 has altered CNS pathogenesis and causes immunosuppression.Evaluating an etiologically relevant platform for therapy development for temporal lobe epilepsy: effects of carbamazepine and valproic acid on acute seizures and chronic behavioral comorbidities in the Theiler's murine encephalomyelitis virus mouse Acthar gel treatment suppresses acute exacerbations in a murine model of relapsing-remitting multiple sclerosis.Neuropeptide Y Negatively Influences Monocyte Recruitment to the Central Nervous System during Retrovirus Infection.Does brain inflammation mediate pathological outcomes in epilepsy?Infections, inflammation and epilepsy The effects of diet on the severity of central nervous system disease: One part of lab-to-lab variability Neuronal Injury, Gliosis, and Glial Proliferation in Two Models of Temporal Lobe Epilepsy.IRF3 helps control acute TMEV infection through IL-6 expression but contributes to acute hippocampus damage following TMEV infection.Using sex differences in the developing brain to identify nodes of influence for seizure susceptibility and epileptogenesis.Disease modification in epilepsy: from animal models to clinical applications.Targeting specific cells in the brain with nanomedicines for CNS therapies Cytotoxic CD8+ T cell ablation enhances the capacity of regulatory T cells to delay viral elimination in Theiler's murine encephalomyelitis.Theiler's murine encephalomyelitis virus infection of SJL/J and C57BL/6J mice: Models for multiple sclerosis and epilepsy.T-bet, but not Gata3, overexpression is detrimental in a neurotropic viral infection.The influence of macrophage growth factors on Theiler's Murine Encephalomyelitis Virus (TMEV) infection and activation of macrophages.The role of peripheral interleukin-6 in the development of acute seizures following virus encephalitis.Complement Components Are Expressed by Infiltrating Macrophages/Activated Microglia Early Following Viral Infection.Tumor Necrosis Factor Alpha-Induced Recruitment of Inflammatory Mononuclear Cells Leads to Inflammation and Altered Brain Development in Murine Cytomegalovirus-Infected Newborn Mice.Previously diagnosed influenza infections and the risk of developing epilepsy.The West Nile virus-like flavivirus Koutango is highly virulent in mice due to delayed viral clearance and the induction of a poor neutralizing antibody response.Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infection.Mycophenolate mofetil prevents the delayed T cell response after pilocarpine-induced status epilepticus in mice.The immune response to picornavirus infection and the effect of immune manipulation on acute seizures.Diffusion Basis Spectrum and Diffusion Tensor Imaging Detect Hippocampal Inflammation and Dendritic Injury in a Virus-Induced Mouse Model of Epilepsy.Intact interleukin-10 receptor signaling protects from hippocampal damage elicited by experimental neurotropic virus infection of SJL mice.Chemokine receptors CCR2 and CX3CR1 regulate viral encephalitis-induced hippocampal damage but not seizures

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Infiltrating macrophages are key to the development of seizures following virus infection.

http://www.wikidata.org/entity/Q36559966

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

Infiltrating macrophages are k ...... res following virus infection.

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Infiltrating macrophages are k ...... res following virus infection.

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Infiltrating macrophages are k ...... res following virus infection.

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Infiltrating macrophages are k ...... res following virus infection.

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Infiltrating macrophages are k ...... res following virus infection.

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Infiltrating macrophages are k ...... res following virus infection.

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Journal of Virology

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Infiltrating macrophages are key to the development of seizures following virus infection

@en

P2093

Daniel J Doty

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Jane E Libbey

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Matthew F Cusick

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Robert S Fujinami

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P2860

Sensitive indicators of injury reveal hippocampal damage in C57BL/6J mice treated with kainic acid in the absence of tonic-clonic seizures

SPONTANEOUS ENCEPHALOMYELITIS OF MICE, A NEW VIRUS DISEASE

Location and distribution of virus antigen in the central nervous system of mice persistently infected with Theiler's virus

Modification of seizure activity by electrical stimulation. II. Motor seizure

Role of microglial-derived tumor necrosis factor in mediating CD14 transcription and nuclear factor kappa B activity in the brain during endotoxemia

Fate mapping analysis reveals that adult microglia derive from primitive macrophages

A role for leukocyte-endothelial adhesion mechanisms in epilepsy

Antagonism of peripheral inflammation reduces the severity of status epilepticus.

Voluntary exercise protects hippocampal neurons from trimethyltin injury: possible role of interleukin-6 to modulate tumor necrosis factor receptor-mediated neurotoxicity.

Role of dendritic cells in differential susceptibility to viral demyelinating disease.

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1849-1860

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10.1128/JVI.02747-12

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3

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87

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23236075

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