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actinomycin d/inflammation

Врската е зачувана во таблата со исечоци
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Enhancement of inflammation and histamine formation by actinomycin D.

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1. An inflammation model developed in other laboratories was used in this study. Mice given endotoxin intranasally developed lung inflammation which progresses in intensity for several days. Lung weight is a satisfactory measure of inflammation.2. In lungs of mice treated intranasally with

Mechanisms of anti-inflammatory action of dexamethasone: blockade by hydrocortisone mesylate and actinomycin D of the inhibitory effect of dexamethasone on leukocyte infiltration in inflammatory sites.

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The present study was designed to clarify molecular mechanisms underlying inhibitory effect of dexamethasone on leukocyte infiltration in the inflammatory site. For the assay of leukocyte infiltration, two or four blebs were made s.c. on the back of rats by injecting with 2% carboxymethyl cellulose

Blockade by anti-glucocorticoids, actinomycin D and cycloheximide of the anti-inflammatory action of some Kampohozai (Chinese traditional medicines) against serotonin.

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Blockade by anti-glucocorticoids, progesterone and 17 alpha-methyltestosterone, a messenger ribonucleic acid (m-RNA) synthesis inhibitor, actinomycin D, and a protein synthesis inhibitor, cycloheximide, of the anti-exudative action of five kinds of Kampohozai (Daisaikoto, Shosaikoto, Saikokeishito,

Actinomycin D peritonitis in rats: a tool for the study of early events in inflammation.

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The injection of 50 microgram i.p. of actinomycin D produces, in rats, a biphasic inflammatory reaction. The first short lasting phase (approximately 24 h) is characterized by the decrease of the peritoneal cells number, by the increase of the levels of both cAMP and cGMP in the peritoneal cells and

Characteristic features of actinomycin D-induced paw inflammation of the rat.

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Blockade by antiglucocorticoids, actinomycin D and cycloheximide of anti-inflammatory action of dexamethasone against bradykinin.

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Enhanced uptake of actinomycin D in cultured mammalian cells by the anti-inflammatory, non-steroid drug benzydamine.

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Transcription factors and inflammatory gene regulation : strategic approaches.

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In chronic inflammatory diseases, the expression of multiple genes, including those for cytokines, chemokines, adhesion molecules, receptors, and inflammatory enzymes, is often upregulated. The problem for many academic or industrial scientists is to elucidate the mechanisms behind this upregulation

[Retroperitoneal inflammatory fibrosarcoma; a case report].

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A 62-year-old man was admitted to our hospital complaining of lower abdominal mass and weight loss. Computed tomography and magnetic resonance imaging studies revealed a large tumor occupying the pelvis and expanding into inferior vena cava, which reached to the renal pedicle. Open biopsy was

Human bronchial and parenchymal fibroblasts display differences in basal inflammatory phenotype and response to IL-17A.

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Chronic inflammation, typified by increased expression of IL-17A, together with airway and parenchymal remodelling are features of chronic lung diseases. Emerging evidence suggests that phenotypic heterogeneity of repair and inflammatory capacities of fibroblasts may contribute to the differential

ApoA-1 Mimetic Peptide ELK-2A2K2E Decreases Inflammatory Factor Levels Through the ABCA1-JAK2-STAT3-TTP Axis in THP-1-Derived Macrophages.

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OBJECTIVE The aim of this study was to determine whether the apolipoprotein A-1 (apoA-1) mimetic peptide ELK-2A2K2E regulates inflammatory cytokine expression through activating the adenosine triphosphate-binding cassette transporter A1 (ABCA1)-janus kinase 2 (JAK2)-signal transducer and activator

AMP-activated protein kinase agonist N6-(3-hydroxyphenyl)adenosine protects against fulminant hepatitis by suppressing inflammation and apoptosis.

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Both AMP-activated protein kinase (AMPK) agonist and inhibitor have been reported to protect against fulminant hepatitis, implying that AMPK may play a complicated role in the development of fulminant hepatitis. In this study, we exploited whether the novel AMPK agonist N6-(3-hydroxyphenyl)adenosine

Different cellular effects of four anti-inflammatory eye drops on human corneal epithelial cells: independent in active components.

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OBJECTIVE To evaluate and compare the cellular effects of four commercially available anti-inflammatory eye drops and their active components on human corneal epithelial cells (HCECs) in vitro. METHODS The cellular effects of four eye drops (Bromfenac Sodium Hydrate Eye Drops, Pranoprofen Eye Drops,

Induction of ornithine decarboxylase in mouse tissues following the injection of mitogenic substances. Enhancement by actinomycin D.

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Experiments were carried out to study the mechanism of the induction of ornithine decarboxylase (ODC) in mouse tissues by the injection of a lipopolysaccharide (LPS). In addition to LPS, various mitogenic substances, such as concanavalin A, pokeweed mitogen, polyI:polyC and a phorbol diester,

Effects of ciclosporin and protein synthesis inhibitors on cutaneous inflammation in mouse skin.

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Ciclosporin is clinically effective in a variety of inflammatory skin diseases. We have therefore studied the effects of the drug on cutaneous inflammation in mice. Ciclosporin inhibited the inflammatory response to 12-O-tetradecanoylphorbol-13-acetate (TPA) and to the contact sensitising agent
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