Impact of Nutritional Status on Total Brain Tissue Volumes in Preterm Infants.

Preterm infants bypass the crucial in utero period of brain development and are at increased risk of malnutrition. We aimed to determine if their nutritional status is associated with brain tissue volumes at term equivalent age (TEA), applying recently published malnutrition guidelines for preterm infants. We performed a single center retrospective chart review of 198 infants < 30 weeks' gestation between 2018 and 2021.

Comparing head ultrasounds and susceptibility-weighted imaging for the detection of low-grade hemorrhages in preterm infants.

Objective: Intraventricular hemorrhage (IVH) is a complication of prematurity. Grades III and IV IVH lead to significant morbidity, but mounting evidence shows low-grade IVH (grades I-II) may be associated with adverse sequelae. Head ultrasounds (HUS) are used to screen infants for IVH but may miss low-grade IVH.

Pharmacological correction of long QT-linked mutations in KCNH2 (hERG) increases the trafficking of Kv11.1 channels stored in the transitional endoplasmic reticulum.

KCNH2 encodes Kv11.1 and underlies the rapidly activating delayed rectifier K(+) current (IKr) in the heart. Loss-of-function KCNH2 mutations cause the type 2 long QT syndrome (LQT2), and most LQT2-linked missense mutations inhibit the trafficking of Kv11.

Trafficking-deficient hERG K⁺ channels linked to long QT syndrome are regulated by a microtubule-dependent quality control compartment in the ER.

The human ether-a-go-go related gene (hERG) encodes the voltage-gated K(+) channel that underlies the rapidly activating delayed-rectifier current in cardiac myocytes. hERG is synthesized in the endoplasmic reticulum (ER) as an "immature" N-linked glycoprotein and is terminally glycosylated in the Golgi apparatus. Most hERG missense mutations linked to long QT syndrome type 2 (LQT2) reduce the terminal glycosylation and functional expression.