A5036645653- Multiple Sclerosis Research Studies
- Neurogenesis and neuroplasticity mechanisms
- Neuroinflammation and Neurodegeneration Mechanisms
- Nitric Oxide and Endothelin Effects
- Neurology and Historical Studies
- Systemic Lupus Erythematosus Research
- History of Medicine Studies
- RNA Research and Splicing
- Axon Guidance and Neuronal Signaling
- Genetic Neurodegenerative Diseases
- History of Medical Practice
- Systemic Sclerosis and Related Diseases
- Peripheral Neuropathies and Disorders
- Microtubule and mitosis dynamics
- Immunotherapy and Immune Responses
- Mitochondrial Function and Pathology
- MicroRNA in disease regulation
- RNA Interference and Gene Delivery
- Mast cells and histamine
- Wnt/β-catenin signaling in development and cancer
- Health, Environment, Cognitive Aging
- Hereditary Neurological Disorders
- Immunotoxicology and immune responses
- Salivary Gland Disorders and Functions
- Powdery Mildew Fungal Diseases
University of Illinois Chicago
2015-2025
University of Leeds
2017
Université de Montréal
2017
John B. Pierce Laboratory
2017
Jesse Brown VA Medical Center
2009-2016
University of Chicago
2001-2004
Université de Bordeaux
1993-2002
University of Bonn
2002
Wayne State University
1999
Institute of Neurological Sciences
1997
Under pathological conditions, microglia produce proinflammatory mediators which contribute to neurologic damage, and whose levels can be modulated by endogenous factors including neurotransmitters such as norepinephrine (NE). We investigated the ability of NE suppress microglial activation, in particular its effects on induction activity inducible form nitric oxide synthase (NOS2) possible role that IL-1β plays response. Rat cortical were stimulated with bacterial lipopolysaccharide (LPS)...
Extracellular vesicles (EVs) are membrane nanovesicles of diverse sizes secreted by different cell types and involved in intercellular communication. EVs shuttle proteins, nucleic acids, lipids that reflect their cellular origin could mediate biological function recipient cells. circulate fluids considered as potential biomarkers be used to analyze characterize disease development, course response treatment. exhibit specific distribution glycolipids organization, but little is known about...
Abstract Myelin repair is inhibited in multiple sclerosis (MS), ultimately leading to axonal damage and disability. We aimed understand the transcriptional mechanisms of regeneration primary human oligodendrocyte cultures isolated from white matter medically intractable epilepsy patients. Cultures at isolation contained 84% mature oligodendrocytes 16% progenitor cells (OPC). The two populations showed a protracted membranes expressing myelin proteins after 2–3 weeks culture, were kept...
Despite tremendous progress in characterizing the myriad cellular structures nervous system, a full appreciation of interdependent and intricate interactions between these is as yet unfulfilled. Indeed, few more so than interaction myelin internode its ensheathed axon. More half-century after ultrastructural characterization this axomyelin unit, we lack reliable understanding physiological properties, significance consequence pathobiological processes, means to gauge success or failure...
Multiple sclerosis (MS) is characterized by inflammation within the CNS. This inflammatory response associated with production of nitric oxide (NO) and NO-related species that nitrosylate thiols. We postulated MS patients would exhibit an antibody (Ab) directed against proteins containing S-nitrosocysteine (SNO-cysteine) showed anti-NO-cysteine Abs IgM isotype are in fact present sera some (Boullerne et al., 1995). report here presence a seemingly identical Ab SNO-cysteine acute model MS,...
Abstract : Nitric oxide (NO) produced in inflammatory lesions may play a major role the destruction of oligodendrocytes multiple sclerosis and experimental allergic encephalomyelitis. The transformed murine oligodendroglial line N20.1 is much more resistant than primary to killing by NO generator S ‐nitroso‐ N ‐acetyl‐DL‐penicillamine (SNAP). This observation prompted investigation mechanisms leading cell death cells comparison SNAP with another donor, sodium nitroprusside (SNP). We observed...
Active nitrogen species are overproduced in inflammatory brain lesions multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE). NO has been shown to mediate the death of oligodendrocytes (OLs), a primary target damage MS. To develop strategies protect OLs, we examined mechanisms cytotoxicity two donors, S-nitroso-N-acetyl-penicillamine (SNAP) sodium nitroprusside (SNP) on mature mouse OLs. Nitrosonium ion (NO+) rather than · mediates with both SNAP SNP, as by significant...
In EAE (experimental autoimmune encephalomyelitis), agonists of PPARs (peroxisome proliferator-activated receptors) provide clinical benefit and reduce damage. contrast with PPARγ, PPARδ are more effective when given at later stages increase myelin gene expression, suggesting effects on OL (oligodendrocyte) maturation. the present study we examined agonist GW0742 OPCs (OL progenitor cells), tested whether involve modulation BMPs (bone morphogenetic proteins). We show that mediated through...
We identified a family in which five siblings were diagnosed with multiple sclerosis (MS) or clinically isolated syndrome. Several women the maternal lineage have comorbidities typically associated Peutz Jeghers Syndrome, rare autosomal-dominant disease caused by mutations serine-threonine-kinase 11 (STK11) gene, encodes liver kinase B1. Sequence analysis of DNA from one sibling single-nucleotide polymorphism (SNP) within STK11 intron 5. This SNP (dbSNP ID: rs9282860) was TaqMan polymerase...
Abstract The most commonly used immunogen to induce experimental autoimmune encephalomyelitis is MOG 35‐55 , a 21‐residue peptide derived from myelin oligodendrocyte glycoprotein (MOG). In studies, mice exhibit chronic disease; however, in some studies show transient disease. One variable that not often controlled for the fraction of purified material, which can vary less than 50% over 90%, with remainder mass primarily comprised counter ion purification. We compared development clinical...
Abstract Liver kinase B1 (LKB1) is a ubiquitously expressed involved in the regulation of cell metabolism, growth, and inflammatory activation. We previously reported that single nucleotide polymorphism gene encoding LKB1 risk factor for multiple sclerosis (MS). Since astrocyte activation metabolic function have important roles regulating neuroinflammation neuropathology, we examined serine/threonine astrocytes chronic experimental autoimmune encephalomyelitis mouse model MS. To reduce LKB1,...
Currently, the genetic variants strongly associated with risk for Multiple Sclerosis (MS) are located in Major Histocompatibility Complex. This includes DRB1*15:01 and DRB1*15:03 alleles at HLA-DRB1 locus, latter restricted to African populations; DQB1*06:02 allele HLA-DQB1 locus which is high linkage disequilibrium (LD) DRB1*15:01; protective A*02:01 HLA-A locus. HLA identification facilitated by co-inherited ('tag') single nucleotide polymorphisms (SNPs); however, SNP validation not...