INT15284
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The results showed that all immunomodulatory drugs applied in clinically relevant doses affect both the gene (LGALS3) and protein expression level of galectin-3. | |||||||||||||||
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The results showed that all immunomodulatory drugs applied in clinically relevant doses affect both the gene (LGALS3) and protein expression level of galectin-3. | |||||||||||||||
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Previous studies of these genes, including markers of toxic stress, apoptosis, growth regulation and repair, were consistent with documented toxicologic responses to CCl4, where expression of components of cytochrome P450 and other metabolic enzymes (Cyp2C, Cyp3A18, Cyp3A9, SCS and Fmo1) were found to decrease, whereas certain genes involved in the inflammatory response and signal transduction were increased (CD44 and Lgals3) [7]. | |||||||||||||||
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Of the 15 inflammatory genes tested, 12 genes (C1-INH, CCR5, CD44, CHI3L1, HSPB1, JAK3, LGALS3, LGALS3BP, LAMA5, PEDF, STAT3, TIMP1) were reproducibly upregulated at 3 months (Figures 4 &5). | |||||||||||||||
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In the preliminary studies, intranasal administration was not useful for elevating IgE in Fischer rats. | |||||||||||||||
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A substantial part of the psychodermatological literature has focused on atopic forms of eczema, and many of the above referred hypotheses concerning possible explanatory factors for the association between anxiety and depression, and eczema presuppose the involvement of atopy (elevated levels of IgE, in addition to "atopic symptoms" [16]) as a part of the aetiological chain underlying this association. | |||||||||||||||
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The possible participation of diesel exhaust inhalation during the fetal period in the elevation of IgE against pollen in postnatal life was investigated.
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Elevation of IgE against Japanese pollen was detected in the rats exposed to total or filtered diesel exhaust from the 7th day of gestation until 3 days after birth (Total-C-C, Filtered-C-C). | |||||||||||||||
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The second objective was to determine which substances particulate matter or the gaseous phase present in diesel exhaust are responsible for the elevation of IgE. | |||||||||||||||
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The present study provides the first evidence that inhalation of diesel exhaust during the differentiation periods of the immune system accelerated the elevation of immunoglobulin E (IgE) against Japanese cedar pollen. | |||||||||||||||
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Regarding which substances were more responsible for insufficient development of the immune system and elevation of IgE, filtered-exhaust that included the gaseous phase and ultra fine particles measuring less than 0.05 ? | |||||||||||||||
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Inhalation of diesel exhaust during differentiation of the immune system accelerated the elevation of IgE against pollen.
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Northern blot analysis revealed a 4.5-fold increase of galectin-1 mRNA (p < 0.01) and a 3.8-fold increase of galectin-3 mRNA (p < 0.01) in CP samples compared with normal controls. | |||||||||||||||
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Up-regulation of galectin-1 in fibroblasts and galectin-3 in ductular complexes suggests a role of these lectins in tissue remodeling in CP. | |||||||||||||||
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Mast cells are involved in allergic reactions where they release numerous vasoactive and other mediators in response to IgE and antigen. | |||||||||||||||
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CP samples exhibited moderate to intense galectin-1 mRNA signals in fibroblasts, whereas galectin-3 mRNA signals were intense in the cells of ductular complexes and weak in the degenerating acinar cells. | |||||||||||||||
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The level of circulating IgE and precipitating anti-ovalbumin antibodies decreased in rats given 10 injections of enkephalins. | |||||||||||||||
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Some, such as galectin-1, may be employed as anti-inflammatory agents, while others, such as galectin-3, are evidently suitable targets for anti-inflammatory drugs. | |||||||||||||||
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Ligation of dorsal roots resulted in disappearance of lectin reactivity in the spinal cord and caused accumulation of lectin-positive material proximal to the ligature, indicating somatofugal transport of galactose-containing glycoconjugates. | |||||||||||||||
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Galectin-1 and galectin-3 in chronic pancreatitis. | |||||||||||||||
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