Abstracts
This guide gives markup examples of abstracts for members registering content by direct deposit of XML. Our web deposit form support abstracts.
Abstracts imported from JATS-formatted XML may be included in records deposited with us. A namespace prefix (jats:) must be used for the abstract and all child elements, and the namespace must be included in the schema declaration. MathML may be included in abstracts but must use a MathML-specific namespace prefix. Multiple abstracts may be included.
Abstracts may be registered for journal articles, books and book chapters, conference papers, posted content, dissertations, reports, and standards.
Abstracts schema declaration
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xmlns:mml="http://www.w3.org/1998/Math/MathML">
</person_name>
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<jats:abstract><jats:p>Acute and chronic lung inflammation is associated with numerous important disease pathologies including asthma, chronic obstructive pulmonary disease and silicosis. Lung fibroblasts are a novel and important target of anti-inflammatory therapy, as they orchestrate, respond to, and amplify inflammatory cascades and are the key cell in the pathogenesis of lung fibrosis. Peroxisome proliferator-activated receptor gamma (PPAR**<mml:math><mml:mi>**γ**</mml:mi></mml:math>**) ligands are small molecules that induce anti-inflammatory responses in a variety of tissues. Here, we report for the first time that PPAR**<mml:math><mml:mi>**γ**</mml:mi></mml:math>** ligands have potent anti-inflammatory effects on human lung fibroblasts. 2-cyano-3, 12-dioxoolean-1, 9-dien-28-oic acid (CDDO) and 15-deoxy-**<mml:math><mml:msup><mml:mi>**Δ**</mml:mi><mml:mrow><mml:mn>**12**</mml:mn><mml:mo>**,**</mml:mo><mml:mn>**14**</mml:mn></mml:mrow></mml:msup></mml:math>**-prostaglandin J<jats:sub>2</jats:sub> (15d-PGJ<jats:sub>2</jats:sub>) inhibit production of the inflammatory mediators interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), COX-2, and prostaglandin (PG)E<jats:sub>2</jats:sub> in primary human lung fibroblasts stimulated with either IL-1**<mml:math><mml:mi>**β**</mml:mi></mml:math>** or silica. The anti-inflammatory properties of these molecules are not blocked by the PPAR**<mml:math><mml:mi>**γ**</mml:mi></mml:math>** antagonist GW9662 and thus are largely PPAR**<mml:math><mml:mi>**γ**</mml:mi></mml:math>** independent. However, they are dependent on the presence of an electrophilic carbon. CDDO and 15d-PGJ<jats:sub>2</jats:sub>, but not rosiglitazone, inhibited NF-**<mml:math><mml:mi>**κ**</mml:mi></mml:math>**B activity. These results demonstrate that CDDO and 15d-PGJ<jats:sub>2</jats:sub> are potent attenuators of proinflammatory responses in lung fibroblasts and suggest that these molecules should be explored as the basis for novel, targeted anti-inflammatory therapies in the lung and other organs.</jats:p></jats:abstract>
<publication_date media_type="print">
<year>2000</year>
</publication_date>
