English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The identification of small molecules that target specific  CFTR  variants has ushered in a new era of treatment for cystic fibrosis (CF), yet optimal, individualized treatment of CF will require identification and targeting of disease modifiers. Here we use genome-wide association analysis to identify genetic modifiers of CF lung disease, the primary cause of mortality. Meta-analysis of 6,365 CF patients identifies five loci that display significant association with variation in lung disease. Regions on chr3q29 ( MUC4/MUC20; P =3.3 × 10 −11 ), chr5p15.3 ( SLC9A3; P =6.8 × 10 −12 ), chr6p21.3 (HLA Class II ; P =1.2 × 10 −8 ) and chrXq22-q23  (AGTR2/SLC6A14; P =1.8 × 10 −9 ) contain genes of high biological relevance to CF pathophysiology. The fifth locus, on chr11p12-p13 ( EHF/APIP; P =1.9 × 10 −10 ), was previously shown to be associated with lung disease. These results provide new insights into potential targets for modulating lung disease severity in CF.

Genome-wide association meta-analysis identifies five modifier loci of lung disease severity in cystic fibrosis