Neonatal hyperoxia abrogates the circadian protection from influenza infection in recovered adults.

RNA profiles from lungs of mice exposed to intermittent hypoxia shared similarity with gene expression changes in human lung from patients with pulmonary diseases, including pulmonary hypertension, COPD, and asthma.

Cellular stress in a disease-relevant cell type uncovers novel genetic effects on gene expression, which is likely relevant for disease.

Knocking out Folliculin (FLCN) in human renal epithelial cells activates STAT1/2-mediated gene expression, independent of interferon, uncovering a tissue-specific process potentially relevant in the cancer syndrome Birt-Hogg-Dubé (BHD).

Hypothetical battles between animals can be used to interest the general public in biology.

PDK1 serves as a critical role for intrinsically promoting T follicular helper cell differentiation and effector functions via controlling expression level of TCF1.

The immune effector Drosomycin buffers stress signaling in hypertrophic salivary glands to inhibit their disintegration, detection by the cellular immune response, and promotes further overgrowth.

The causal link between capillary amyloid‑β accumulation in the brain and cerebrovascular dysfunction, previously established in the Tg‑SwDI mouse model, is to be mitigated and remains to be fully uncovered.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.

Cellular immunological and biochemical analyses reveal how decoy IL-1RII is induced by human CD4⁺ T cells upon TCR-stimulation and regulates the Th17-Treg balance by modulating IL-1β responsiveness in IL-1RI⁺ cells.