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Institution

University of Alabama

EducationTuscaloosa, Alabama, United States
About: University of Alabama is a education organization based out in Tuscaloosa, Alabama, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 27323 authors who have published 48609 publications receiving 1565337 citations. The organization is also known as: Alabama & Bama.


Papers
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Journal ArticleDOI
TL;DR: The authors used responses from a survey of marketing professionals in a structural equation model linking antecedents and consequences of two dimensions of personal moral philosophies (idealism and relativism) and perceived moral intensity (PMI).
Abstract: This study uses responses from a survey of marketing professionals in a structural equation model linking antecedents and consequences of two dimensions of personal moral philosophies (idealism and relativism) and perceived moral intensity (PMI). Mixed support is found for hypothesized effects of gender, religiosity, education, experience, salary, and corporate ethical values on idealism and relativism. Idealism increases and relativism decreases PMI in four ethical scenarios. PMI increases perceptions of ethical problems, which reduce intentions to act unethically. The study tests whether relationships between variables, revealing that PMI has direct as well as indirect effects on intentions. Intentions are also influenced by gender: women have more ethical intentions than men, on average, and this effect is not mediated by other variables in the model.

417 citations

Journal ArticleDOI
TL;DR: It is reported that LNO2 is a potent endogenous ligand for peroxisome proliferator-activated receptor γ (PPARγ) that acts within physiological concentration ranges and reveals that NO-mediated cell signaling reactions can be transduced by fatty acid nitration products and PPAR-dependent gene expression.
Abstract: Nitroalkene derivatives of linoleic acid (nitrolinoleic acid, LNO2) are formed via nitric oxide-dependent oxidative inflammatory reactions and are found at concentrations of ≈500 nM in the blood of healthy individuals. We report that LNO2 is a potent endogenous ligand for peroxisome proliferator-activated receptor γ (PPARγ; Ki ≈133 nM) that acts within physiological concentration ranges. This nuclear hormone receptor (PPARγ) regulates glucose homeostasis, lipid metabolism, and inflammation. PPARγ ligand activity is specific for LNO2 and not mediated by LNO2 decay products, NO donors, linoleic acid (LA), or oxidized LA. LNO2 is a significantly more robust PPARγ ligand than other reported endogenous PPARγ ligands, including lysophosphatidic acid (16:0 and 18:1), 15-deoxy-Δ12,14-PGJ2, conjugated LA and azelaoyl-phosphocholine. LNO2 activation of PPARγ via CV-1 cell luciferase reporter gene expression analysis revealed a ligand activity that rivals or exceeds synthetic PPARγ agonists such as rosiglitazone and ciglitazone, is coactivated by 9 cis-retinoic acid and is inhibited by the PPARγ antagonist GW9662. LNO2 induces PPARγ-dependent macrophage CD-36 expression, adipocyte differentiation, and glucose uptake also at a potency rivaling thiazolidinediones. These observations reveal that NO-mediated cell signaling reactions can be transduced by fatty acid nitration products and PPAR-dependent gene expression.

417 citations

Journal ArticleDOI
01 Nov 2006-Brain
TL;DR: In this paper, the role of TLR4 in the amyloidogenesis in vivo, determined the amounts of cerebral Abeta in Alzheimer's disease mouse models with different genotypes of TLRs using three distinct methods.
Abstract: Deposits of amyloid beta-protein (Abeta) in neuritic plaques and cerebral vessels are a pathological hallmark of Alzheimer's disease. Fibrillar Abeta deposits are closely associated with inflammatory responses such as activated microglia in brain with this disease. Increasing lines of evidence support the hypothesis that activated microglia, innate immune cells in the CNS, play a pivotal role in the progression of the disease: either clearing Abeta deposits by phagocytic activity or releasing cytotoxic substances and pro-inflammatory cytokines. Toll-like receptors (TLRs) are a family of pattern-recognition receptors in the innate immune system. Exogenous and endogenous TLR ligands activate microglia. To investigate the role of TLR4 in the amyloidogenesis in vivo, we determined the amounts of cerebral Abeta in Alzheimer's disease mouse models with different genotypes of TLR4 using three distinct methods. We show that mouse models (Mo/Hu APPswe PS1dE9 mice) homozygous for a destructive mutation of TLR4 (Tlr(Lps-d)/Tlr(Lps-d)) had increases in diffuse and fibrillar Abeta deposits by immunocytochemistry, fibrillar Abeta deposits by thioflavine-S staining and buffer-soluble and insoluble Abeta by ELISA in the cerebrum, as compared with TLR4 wild-type mouse models. Although the differences in these parameters were less significant, mouse models heterozygous for the mutation (Tlr(Lps-d)/) showed co-dominant phenotypes. Consistent with these observations in vivo, cultured microglia derived from Tlr(Lps-d)/Tlr(Lps-d) mice failed to show an increase in Abeta uptake after stimulation with a TLR4 ligand but not with a TLR9 ligand in vitro. Furthermore, activation of microglia (BV-2 cell) with a TLR2, TLR4 or TLR9 ligand, markedly boosted ingestion of Abeta in vitro. These results suggest that TLR signalling pathway(s) may be involved in clearance of Abeta-deposits in the brain and that TLRs can be a therapeutic target for Alzheimer's disease.

417 citations

Journal ArticleDOI
TL;DR: Current information on the biochemical properties, biosynthesis, and tissue distribution of Type I, II, and III collagens is summarized with special reference to possible unique functional roles fulfilled by each of thesecollagens.
Abstract: In recent years it has become evident that genetic polymorphism is dramatically expressed in the structural protein, collagen. Current information on the biochemical properties, biosynthesis, and tissue distribution of Type I, II, and III collagens is summarized with special reference to possible unique functional roles fulfilled by each of these collagens.

416 citations

Journal ArticleDOI
TL;DR: The COVID-19 spike binding site to the cell-surface receptor (Glucose Regulated Protein 78 (GRP78) is predicted using combined molecular modeling docking and structural bioinformatics and sequence and structural alignments show that four regions have sequence and physicochemical similarities to the cyclic Pep42.

416 citations


Authors

Showing all 27508 results

NameH-indexPapersCitations
Jasvinder A. Singh1762382223370
Hongfang Liu1662356156290
Ian J. Deary1661795114161
Yongsun Kim1562588145619
Dong-Chul Son138137098686
Simon C. Watkins13595068358
Kenichi Hatakeyama1341731102438
Conor Henderson133138788725
Peter R Hobson133159094257
Tulika Bose132128588895
Helen F Heath132118589466
James Rohlf131121589436
Panos A Razis130128790704
David B. Allison12983669697
Eduardo Marbán12957949586
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202372
2022358
20212,705
20202,759
20192,602
20182,411