This year, metadata development is one of our key priorities and we’re making a start with the release of version 5.4.0 of our input schema with some long-awaited changes. This is the first in what will be a series of metadata schema updates.
What is in this update?
Publication typing for citations
This is fairly simple; we’ve added a ‘type’ attribute to the citations members supply. This means you can identify a journal article citation as a journal article, but more importantly, you can identify a dataset, software, blog post, or other citation that may not have an identifier assigned to it. This makes it easier for the many thousands of metadata users to connect these citations to identifiers. We know many publishers, particularly journal publishers, do collect this information already and will consider making this change to deposit citation types with their records.
Every year we release metadata for the full corpus of records registered with us, which can be downloaded for free in a single compressed file. This is one way in which we fulfil our mission to make metadata freely and widely available. By including the metadata of over 165 million research outputs from over 20,000 members worldwide and making them available in a standard format, we streamline access to metadata about scholarly objects such as journal articles, books, conference papers, preprints, research grants, standards, datasets, reports, blogs, and more.
Today, we’re delighted to let you know that Crossref members can now use ROR IDs to identify funders in any place where you currently use Funder IDs in your metadata. Funder IDs remain available, but this change allows publishers, service providers, and funders to streamline workflows and introduce efficiencies by using a single open identifier for both researcher affiliations and funding organizations.
As you probably know, the Research Organization Registry (ROR) is a global, community-led, carefully curated registry of open persistent identifiers for research organisations, including funding organisations. It’s a joint initiative led by the California Digital Library, Datacite and Crossref launched in 2019 that fulfills the long-standing need for an open organisation identifier.
We began our Global Equitable Membership (GEM) Program to provide greater membership equitability and accessibility to organizations in the world’s least economically advantaged countries. Eligibility for the program is based on a member’s country; our list of countries is predominantly based on the International Development Association (IDA). Eligible members pay no membership or content registration fees. The list undergoes periodic reviews, as countries may be added or removed over time as economic situations change.
This guide gives markup examples of abstracts for members registering content by direct deposit of XML. Our helper tools support the registration of 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.
</person_name></contributors><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_datemedia_type="print"><year>2000</year></publication_date>
