Perceived Contributors to Job Quality and Retention at Home Care Cooperatives

Uterine Fibroid Diagnosis by Race and Ethnicity in an Integrated Health Care System

An Evidence Map of the Women Veterans’ Health Literature, 2016 to 2023

Detection Bias in EHR-Based Research on Clinical Exposures and Dementia

Placental and Fetal In Utero Growth Among Fetuses With Congenital Heart Disease

Interpreting Blood Culture Results as Early Guidance for Infective Endocarditis

Maternal Disability and Emergency Department Use for Infants

Verdiperstat in Amyotrophic Lateral Sclerosis

Radiofrequency treatment for chronic knee pain in people with knee osteoarthritis

Feedback regulation of retinaldehyde reductase DHRS3 , a critical determinant of retinoic acid homeostasis

Retinoic acid is crucial for vertebrate embryogenesis, influencing anterior‐posterior patterning and organogenesis through its interaction with nuclear hormone receptors comprising heterodimers of retinoic acid receptors (RARα, β, or γ) and retinoid X receptors (RXRα, β, or γ). Tissue retinoic acid levels are tightly regulated since both its excess and deficiency are deleterious. Dehydrogenase/reductase 3 (DHRS3) plays a critical role in this regulation by converting retinaldehyde to retinol, preventing excessive retinoic acid formation. Mutations in DHRS3 can result in embryonic lethality and congenital defects. This study shows that mouse Dhrs3 expression is responsive to vitamin A status and is directly regulated by the RAR/RXR complex through cis ‐regulatory elements. This highlights a negative feedback mechanism that ensures retinoic acid homeostasis.