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

Background  A multidirectional relationship has been demonstrated between myocardial infarction (MI) and depression. However, the causal genetic factors and molecular mechanisms underlying this interaction remain unclear. The main purpose of this study was to identify potential candidate genes for the interaction between the two diseases.    Methods  Using a bioinformatics approach and existing gene expression data in the biomedical discovery support system (BITOLA), we defined the starting concept X as “Myocardial Infarction” and end concept Z as “Major Depressive Disorder” or “Depressive disorder”. All intermediate concepts relevant to the “Gene or Gene Product” for MI and depression were searched. Gene expression data and tissue-specific expression of potential candidate genes were evaluated using the Human eFP (electronic Fluorescent Pictograph) Browser, and intermediate concepts were filtered by manual inspection.    Results  Our analysis identified 128 genes common to both the “MI” and “depression” text mining concepts. Twenty-three of the 128 genes were selected as intermediates for this study, 9 of which passed the manual filtering step. Among the 9 genes,  LCAT ,  CD4 ,  SERPINA1 ,  IL6 , and  PPBP  failed to pass the follow-up filter in the Human eFP Browser, due to their low levels in the heart tissue. Finally, four genes ( GNB3 ,  CNR1 ,  MTHFR , and  NCAM1 ) remained.    Conclusions   GNB3 ,  CNR1 ,  MTHFR , and  NCAM1  are putative new candidate genes that may influence the interactions between MI and depression, and may represent potential targets for therapeutic intervention.

Using literature-based discovery to identify candidate genes for the interaction between myocardial infarction and depression