The Relationship between Various Measures of Perinatal Quality.

Objective: To examine the correlations between pairs of maternal, infant, and maternal-infant dyad quality measures to provide a comprehensive assessment of perinatal care.

Study Design: In a retrospective cohort study using birth and fetal death certificates linked to hospital discharge data from Michigan, Oregon, Pennsylvania, and South Carolina (2016-2018), we examined correlations between pairs of maternal, infant, and maternal-infant dyad quality measures. Maternal quality measures included nulliparous term singleton vertex (NTSV) cesarean birth, non-transfusion severe maternal morbidity (SMM), and a composite maternal outcome.

An integrated, multidisciplinary management team intervention to improve patient-centeredness, HIV, and maternal-child outcomes in Lesotho: formative research on participatory implementation strategies.

Background: Reducing perinatal HIV transmission and optimizing maternal and child health (MCH) outcomes in high HIV prevalence settings is an urgent, but complex, priority. Extant interventions over-emphasize individual-level provider and patient behaviors, and neglect critical health systems-level changes. The 'Integrated Management Team to Improve Maternal-Child Outcomes (IMPROVE)' study implemented a three-part, patient-centered, health-systems-level intervention to improve MCH and HIV outcomes in Lesotho.

Multifunctional Roles of Sec13 Paralogues in the Euglenozoan .

Secretory cargos are exported from the ER via COPII coated vesicles that have an inner matrix of Sec23/Sec24 heterotetramers and an outer cage of Sec13/Sec31 heterotetramers. In addition to COPII, Sec13 is part of the nuclear pore complex (NPC) and the regulatory SEA/GATOR complex in eukaryotes, which typically have one Sec13 orthologue. The kinetoplastid parasite has two paralogues: TbSec13.

Dilated cardiomyopathy-associated skeletal muscle actin (ACTA1) mutation R256H disrupts actin structure and function and causes cardiomyocyte hypocontractility.

Skeletal muscle actin (ACTA1) mutations are a prevalent cause of skeletal myopathies consistent with ACTA1's high expression in skeletal muscle. Rare de novo mutations in ACTA1 associated with combined cardiac and skeletal myopathies have been reported, but ACTA1 represents only ~20% of the total actin pool in cardiomyocytes, making its role in cardiomyopathy controversial. Here we demonstrate how a mutation in an actin isoform expressed at low levels in cardiomyocytes can cause cardiomyopathy by focusing on a unique ACTA1 variant, R256H.