Muscle-derived myostatin is a major endocrine driver of follicle-stimulating hormone synthesis.

Myostatin is a paracrine myokine that regulates muscle mass in a variety of species, including humans. In this work, we report a functional role for myostatin as an endocrine hormone that directly promotes pituitary follicle-stimulating hormone (FSH) synthesis and thereby ovarian function in mice. Previously, this FSH-stimulating role was attributed to other members of the transforming growth factor-β family, the activins.

Breastfeeding Journeys: Comparing Mothers' Experiences with Autistic and Neurotypical Infants.

Breastfeeding is a complex task that requires proficiency at several key developmental skills to feed successfully. It is unclear how Autism Spectrum Disorder (ASD) affects an infant's breastfeeding experience and conflicting reports exist on shortened breastfeeding duration in infants later diagnosed with ASD. The purpose of this study was to describe the experiences of mothers breastfeeding both their autistic and neurotypical children to better understand the differences in their breastfeeding experiences and maternal and infant factors that contributed to breastfeeding cessation in their autistic child.

Novel Dynamic Organ Storage System Enhances Liver Graft Function in a Porcine Donation After Circulatory Death Model.

Donation after circulatory death (DCD) livers face increased risks of critical complications when preserved with static cold storage (SCS). Although machine perfusion (MP) may mitigate these risks, its cost and logistical complexity limit widespread application. We developed the Dynamic Organ Storage System (DOSS), which delivers oxygenated perfusate at 10°C with minimal electrical power requirement and allows real-time effluent sampling in a portable cooler.

INF2 mutations cause kidney disease through a gain-of-function mechanism.

Heterozygosity for inverted formin-2 (INF2) mutations causes focal segmental glomerulosclerosis (FSGS) with or without Charcot-Marie-Tooth disease. A key question is whether the disease is caused by gain-of-function effects on INF2 or loss of function (haploinsufficiency). Despite established roles in multiple cellular processes, neither INF2 knockout mice nor mice with a disease-associated point mutation display an evident kidney or neurologic phenotype.