Perinatal Nicotine Exposure Disrupts Hematopoietic Stem Cell Development and Elevates Influenza Susceptibility in Adulthood.

Tobacco use during pregnancy has many deleterious health consequences for not only the smoking mother, but also on the unborn fetus. Children of smoking mothers are reported to have higher frequency and severity of respiratory diseases later in life; however, the mechanisms driving this increased vulnerability are not clearly understood. One potential cause of increased disease susceptibility is an altered immune system, originating in epigenetically maladaptive hematopoietic stem cells (HSCs).

Integrating AI-powered text mining from PubTator into the manual curation workflow at the Comparative Toxicogenomics Database.

The Comparative Toxicogenomics Database (CTD) is a manually curated knowledge- and discovery-base that seeks to advance understanding about the relationship between environmental exposures and human health. CTD's manual curation process extracts from the biomedical literature molecular relationships between chemicals/drugs, genes/proteins, phenotypes, diseases, anatomical terms, and species. These relationships are organized in a highly systematic way in order to make them not only informative but also scientifically computational, enabling inferential hypotheses to be formed to address gaps in understanding.

Comparative Toxicogenomics Database's 20th anniversary: update 2025.

For 20 years, the Comparative Toxicogenomics Database (CTD; https://ctdbase.org) has provided high-quality, literature-based curated content describing how environmental chemicals affect human health. Today, CTD includes over 94 million toxicogenomic connections relating chemicals, genes/proteins, phenotypes, anatomical terms, diseases, comparative species, pathways and exposures.

An aberrant immune-epithelial progenitor niche drives viral lung sequelae.

The long-term physiological consequences of respiratory viral infections, particularly in the aftermath of the COVID-19 pandemic-termed post-acute sequelae of SARS-CoV-2 (PASC)-are rapidly evolving into a major public health concern. While the cellular and molecular aetiologies of these sequelae are poorly defined, increasing evidence implicates abnormal immune responses and/or impaired organ recovery after infection. However, the precise mechanisms that link these processes in the context of PASC remain unclear.

Transforming environmental health datasets from the comparative toxicogenomics database into chord diagrams to visualize molecular mechanisms.

In environmental health, the specific molecular mechanisms connecting a chemical exposure to an adverse endpoint are often unknown, reflecting knowledge gaps. At the public Comparative Toxicogenomics Database (CTD; https://ctdbase.org/), we integrate manually curated, literature-based interactions from CTD to compute four-unit blocks of information organized as a potential step-wise molecular mechanism, known as "CGPD-tetramers," wherein a chemical interacts with a gene product to trigger a phenotype which can be linked to a disease.