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Study highlights the crucial role of iNOS, whose activity is required for the anti-fibrotic properties of mesenchymal stem cells in experimental systemic sclerosis, with a special emphasis on NO-related anti-oxidant functions.
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The findings indicate that elderly mice were more susceptible to T. cruzi infection, which was potentially related to an attenuated response to antigenic stimulation, inhibition of iNOS gene expression and NO production, and antagonistic upregulation of arginase-1 gene expression and activity, which created favorable conditions for heart parasitism and myocarditis development.
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Studied role of leptin, iNOS and tenascin C in development of adipose tissue inflammation, extracellular matrix remodeling, and fibrosis in leptin knockout obese mice.
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this paper shows that NOS2 enhances the survival of mice during Salmonella Typhimurium infection-induced sepsis by increasing reactive oxygen species, inflammatory cytokines and recruitment of neutrophils to the peritoneal cavity
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High INOS expression is associated with sepsis.
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iNOS-derived NO during the late phase of sepsis caused vasodilation-induced hypothermia and a lethal hypodynamic state.
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study enables us to conclude that beta-cell stress is aggravated by the incapability of STAT5B to induce Nos2 resulting in HO accumulation and the ensuing oxidative stress enhances beta-cell damage.
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Nitrated POPC showed anti-inflammatory potential, as assessed by the inhibition of inducible nitric oxide synthase (iNOS) expression in RAW 264.7 macrophages activated by the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS) in a well-described in vitro model of inflammation
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these data show a role for iNOS-produced reactive oxygen species in maintaining homeostasis of the gut microbiota
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Results suggest that dopaminergic modulation of striatal function is altered in the iNOS KO mice. These alterations may be related to the decreased expression and activation of astrocytes and microglia in the iNOS KO mice. In conclusion, the phenotype profile of iNOS mutant mice corroborates iNOS constitutive function.
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The role of miR-294 and miR-721 in the regulation of NOS2 expression during Leishmania replication in infected macrophages pointing these miRNAs as potential new targets for drug development.
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Our results uncover the molecular mechanism behind the constricted regulation of Nos2 expression and open new therapeutic opportunities based on epigenetic activities of caspase-1 against infectious and inflammatory diseases.
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Data suggest that, in biocatalytic cycle of iNos, deferred ET (electron tunneling) from substrate or undue ET from/to cofactor leads to side products. These studies involved quantum mechanics, DFT (Density Functional Theory), thermodynamics, nondynamical electron correlation, and molecular modeling.
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iNOS-derived nitric oxide plays a role in telogen elongation under the inflammatory conditions associated with diabetes in mice.
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IFN-gamma-iNOS axis are an essential pathway in the pathogenesis of arenavirus hemorrhagic fever.
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tibias of botulin A toxin-treated and tail-suspended mice, which featured unloading and decreased bone mass, showed higher expression of IL-1beta, Lcn2 and Nos2, suggesting their pathophysiologic involvement in endothelial cell-osteoblast crosstalk.
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The studies established a potential link between leptin and adipocyte insulin responsiveness in an NOS2 dependent manner.
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Results demonstrate that TLR2 signal plays an important role in the regulation of iNOS expression after C. sinensis infection. TLR2 signal is also beneficial to limiting worm growth and development and contributing to the susceptibility to C. sinensis in which the iNOS/NO reactions possibly participate.
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Influence of 1mM MbetaCD on the fenoterol-driven changes in both contractility and NO level was strongly attenuated by inhibition of Gi-protein (pertussis toxin), Akt (Akt 1/2 kinase inhibitor) or NO-synthase (L-NAME)..Obtained results suggest that slight cholesterol depletion upregulates Gi-protein/Akt/NO-synthase signaling that attenuates the positive inotropic response to b2-adrenergic stimulation
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Diphenyleneiodonium selectively interacts with heme protein of iNOS, inhibiting nitric oxide production.