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Stress-mediated aggregation of disease-associated proteins in amyloid bodies.
Sci Rep
September 2023
Department of Molecular Biology and Biochemistry, Simon Fraser University, 8888 University Drive, €, BC, V5A 1S6, Canada.
The formation of protein aggregates is a hallmark of many neurodegenerative diseases and systemic amyloidoses. These disorders are associated with the fibrillation of a variety of proteins/peptides, which ultimately leads to cell toxicity and tissue damage. Understanding how amyloid aggregation occurs and developing compounds that impair this process is a major challenge in the health science community.
View Article and Find Full Text PDF[Screening of key genes and pathways of ischemic stroke and prediction of traditional Chinese medicines based on bioinformatics].
Zhongguo Zhong Yao Za Zhi
April 2021
Department of Neurology, Dongzhimen Hospital, Beijing University of Chinese Medicine Beijing 100700, China Institute for Brain Disorders, Beijing University of Chinese Medicine Bejing 100700, China.
The aim of this paper was to explore the key genes and pathogenesis of ischemic stroke(IS) by bioinformatics, and predict the potential traditional Chinese medicines for IS. Based on the gene-chip raw data set of GSE22255 from National Center of Biotechnology Information(NCBI), the article enrolled in 20 patients with ischemic stroke and 20 sex-and age-matched controls, and differentially expressed genes(DEGs) were screened based on R language software. The DAVID tool and R language software were used to perform gene ontology(GO) biological process enrichment analysis and Kyoto encyclopedia of genes and gnomes(KEGG) pathway enrichment analysis.
View Article and Find Full Text PDFIsolevuglandin adducts in disease.
Antioxid Redox Signal
June 2015
Department of Chemistry, Case Western Reserve University, Cleveland, Ohio.
Significance: A diverse family of lipid-derived levulinaldehydes, isolevuglandins (isoLGs), is produced by rearrangement of endoperoxide intermediates generated through both cyclooxygenase (COX) and free radical-induced cyclooxygenation of polyunsaturated fatty acids and their phospholipid esters. The formation and reactions of isoLGs with other biomolecules has been linked to alcoholic liver disease, Alzheimer's disease, age-related macular degeneration, atherosclerosis, cardiac arythmias, cancer, end-stage renal disease, glaucoma, inflammation of allergies and infection, mitochondrial dysfunction, multiple sclerosis, and thrombosis. This review chronicles progress in understanding the chemistry of isoLGs, detecting their production in vivo and understanding their biological consequences.
View Article and Find Full Text PDFWDR81 is necessary for purkinje and photoreceptor cell survival.
J Neurosci
April 2013
Department of Neurology, University of Chicago Center for Peripheral Neuropathy, University of Chicago, Chicago, Illinois 60637, USA.
The gene encoding the WD repeat-containing protein 81 (WDR81) has recently been described as the disease locus in a consanguineous family that suffers from cerebellar ataxia, mental retardation, and quadrupedal locomotion syndrome (CAMRQ2). Adult mice from the N-ethyl-N-nitrosourea-induced mutant mouse line nur5 display tremor and an abnormal gait, as well as Purkinje cell degeneration and photoreceptor cell loss. We have used polymorphic marker mapping to demonstrate that affected nur5 mice carry a missense mutation, L1349P, in the Wdr81 gene.
View Article and Find Full Text PDFImaging elevated brain arachidonic acid signaling in unanesthetized serotonin transporter (5-HTT)-deficient mice.
Neuropsychopharmacology
June 2009
Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Certain polymorphisms reduce serotonin (5-HT) reuptake transporter (5-HTT) function and increase susceptibility to psychiatric disorders. Heterozygous (5-HTT(+/-))-deficient mice, models for humans with these polymorphisms, have elevated brain 5-HT concentrations and behavioral abnormalities. As postsynaptic 5-HT(2A/2C) receptors are coupled to cytosolic phospholipase A(2) (cPLA(2)), which releases arachidonic acid (AA) from membrane phospholipid, 5-HTT-deficient mice may have altered brain AA signaling and metabolism.
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