Understanding HCBS utilization: The role of disability onset age and length of disability.

Background: Younger adults aging with and older adults aging into disability often need support to remain in their homes and communities. However, researchers and policymakers lack sufficient understanding of their differing needs for home and community-based services (HCBS), largely due to limitations in existing data.

Objectives: This study addresses this gap by exploring select HCBS utilization among adults with disability onset before age 60 and those with onset after age 60, focusing on how aging and disability intersect.

A divergent two-domain structure of the anti-Müllerian hormone prodomain.

TGFβ family ligands are synthesized as precursors consisting of an N-terminal prodomain and C-terminal growth factor (GF) signaling domain. After proteolytic processing, the prodomain typically remains noncovalently associated with the GF, sometimes forming a high-affinity latent procomplex that requires activation. For the TGFβ family ligand anti-Müllerian hormone (AMH), the prodomain maintains a high-affinity interaction with its GF that does not render it latent.

Human TRMT1 and TRMT1L paralogs ensure the proper modification state, stability, and function of tRNAs.

The tRNA methyltransferase 1 (TRMT1) enzyme catalyzes the N2,N2-dimethylguanosine (m2,2G) modification in tRNAs. Intriguingly, vertebrates encode an additional tRNA methyltransferase 1-like (TRMT1L) paralog. Here, we use a comprehensive tRNA sequencing approach to decipher targets of human TRMT1 and TRMT1L.

Children's views on outdoor advertising of unhealthy food and beverages near schools.

Children are often exposed to unhealthy outdoor food advertisements during the school commute. This exposure can have negative public health consequences given childhood weight gain has been linked to the marketing of energy-dense and nutrient-poor foods. This study aimed to explore schoolchildren's lived experiences and attitudes towards outdoor advertising surrounding their schools.

Mutation in leads to early motor dysfunction and widespread aberrant axon terminals in a beta-propeller protein associated neurodegeneration (BPAN) patient-inspired mouse model.

Beta-propeller Protein Associated Neurodegeneration (BPAN) is a devastating neurodevelopmental and neurodegenerative disease linked to variants in . Currently, there is no cure or disease altering treatment for this disease. This is, in part, due to a lack of insight into early phenotypes of BPAN progression and 's role in establishing and maintaining neurological function.