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glutamic acid/inflammation
Врската е зачувана во таблата со исечоци
Страница 1 од 490 резултати
Human fibroblasts ubiquitously express glutamic acid decarboxylase 65 (GAD 65): possible effects of connective tissue inflammation on GAD antibody titer.
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BACKGROUND
Type 1 diabetes is caused by a destruction of pancreatic beta cells due to autoimmunity. Autoantibody against glutamic acid decarboxylase (GAD) 65 expressed in pancreatic beta cells is widely used as a predictive marker for pancreatic destruction. In this study, we hypothesized that if
Peripheral inflammation is associated with increased glutamic acid decarboxylase immunoreactivity in the rat spinal cord.
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We have examined the frequency and distribution of neuron profiles immunoreactive for glutamic acid decarboxylase, a biosynthetic enzyme for the putative inhibitory neurotransmitter, gamma aminobutyric acid, in the lumbar spinal cord of colchicine-treated rats with unilateral inflammation of a
Effects of a new anti-allergic agent: the magnesium salt of N-acetyl-aspartyl-glutamic acid on experimental allergic inflammation of the rabbit eye.
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We evaluated the efficacy of N-Acetyl-Aspartyl-Glutamic acid (magnesium salt) (NAAGA) eye-drops in preventing the conjunctival and uveal allergic inflammation induced by reverse passive Arthus reaction in the rabbit. The permeability of the blood-conjunctival and blood-aqueous barriers was
Design, synthesis and biological evaluation of glutamic acid derivatives as anti-oxidant and anti-inflammatory agents.
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A series of glutamic acid derivatives was synthesized and evaluated for their antioxidant activity and stability. We found several potent and stable glutamic acid derivatives. Among them, compound 12b exhibited good in vitro activity, chemical stability and cytotoxicity. A prototype compound 12b
Comparative study of in vitro inhibition of activation of the classical and alternative pathways of human complement by the magnesium and sodium salts of the anti-inflammatory peptide N-acetyl-aspartyl-glutamic acid (NAAGA).
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The inhibitory activity of the sodium salt of the anti-inflammatory peptide N-acetyl-aspartyl-glutamic acid (NAAGA) on activation of the classical and alternative pathways of human complement was compared with that of the clinically used magnesium salt of NAAGA (NAAGA-Mg). Sodium salt of NAAGA
Novel anti-inflammatory undecapeptides that contain anisolyated glutamic acid derivatives.
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In various animal models of tissue injury, corticotropin-releasing factor (CRF) and related peptides inhibit swelling, edema and loss of protein from the vascular compartment. To search for smaller peptide segments of CRF that might retain anti-inflammatory activity, the authors tested peptides
Poly-γ-glutamic acid attenuates angiogenesis and inflammation in experimental colitis.
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Poly-γ-glutamic acid (γ-PGA), naturally secreted from various strains of Bacillus, has anti-inflammatory activity. In inflammatory bowel disease (IBD), inflammation is promoted and sustained by angiogenesis; however, the role played by γ-PGA in this condition is unclear. Therefore, we evaluated
Cytoplasmic Localization of Proline, Glutamic Acid, Leucine-rich Protein 1 (PELP1) Induces Breast Epithelial Cell Migration through Up-regulation of Inhibitor of κB Kinase ϵ and Inflammatory Cross-talk with Macrophages.
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Cytoplasmic localization of proline, glutamic acid, leucine-rich protein 1 (PELP1) is observed in ∼40% of women with invasive breast cancer. In mouse models, PELP1 overexpression in the mammary gland leads to premalignant lesions and eventually mammary tumors. In preliminary clinical studies,
Macrophage response to chitosan/poly-(γ-glutamic acid) nanoparticles carrying an anti-inflammatory drug.
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The inflammatory response to biomaterials, traditionally viewed as detrimental, is nowadays considered essential for tissue repair/regeneration, being macrophages recognized as the key players in resolving inflammation. Here, the preparation of chitosan (Ch)/poly-(γ-glutamic acid) (γ-PGA)
Pro-inflammatory chitosan/poly(γ-glutamic acid) nanoparticles modulate human antigen-presenting cells phenotype and revert their pro-invasive capacity.
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Anticancer immune responses depend on efficient presentation of tumor antigens and co-stimulatory signals provided by antigen-presenting cells (APCs). However, it is described that immature dendritic cells (DCs) and macrophages at the tumor site may have an immunosuppressive profile, which limits
Bacillus-derived poly-γ-glutamic acid attenuates allergic airway inflammation through a Toll-like receptor-4-dependent pathway in a murine model of asthma.
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BACKGROUND
Asthma is an inflammatory disease of the airways that is mediated by Th2 responses. Poly-γ-glutamic acid (γ-PGA) is an extracellular polymeric compound that is synthesized by Bacillus cells. Previously, we found that γ-PGA promoted Th1 cell development in a manner dependent on
Anti-inflammatory Chitosan/Poly-γ-glutamic acid nanoparticles control inflammation while remodeling extracellular matrix in degenerated intervertebral disc.
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Intervertebral disc (IVD) degeneration is one of the most common causes of low back pain (LBP), the leading disorder in terms of years lived with disability. Inflammation can play a role in LPB, while impairs IVD regeneration. In spite of this, different inflammatory targets have been purposed in
Poly-gamma-glutamic acid from Bacillus subtilis upregulates pro-inflammatory cytokines while inhibiting NLRP3, NLRC4 and AIM2 inflammasome activation.
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Poly-gamma-glutamic acid (γ-PGA) is a natural, edible and non-toxic polymer synthesized by Bacillus subtilis and is suggested as a safe biomaterial for the use in hydrogels and vaccine adjuvants. However, the effect of γ-PGA on inflammasome activation has not yet been studied in macrophages.
Anti-glutamic Acid decarboxylase antibody associated limbic encephalitis in a child: expanding the spectrum of pediatric inflammatory brain diseases.
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Anti-glutamic acid decarboxylase directed antibodies are a rare cause of autoimmune limbic encephalitis that is relatively resistant to immunotherapy. Here we report a 15-year-old boy with nonparaneoplastic, anti-glutamic acid decarboxylase limbic encephalitis presenting with subacute headache,
Glutamic acid decarboxylase autoimmunity with brainstem, extrapyramidal, and spinal cord dysfunction.
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OBJECTIVE
To describe novel neurological manifestations associated with glutamic acid decarboxylase (GAD65) autoimmunity.
METHODS
This retrospective study (1987-2003) describes 62 patients Incidentally found to have a serum autoantibody that bound selectively to synapse-rich central nervous system
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