Buprenorphine pharmacotherapy for the management of neonatal abstinence syndrome in methadone-exposed neonates.

We aimed to compare the outcomes of pharmacotherapy with either buprenorphine or methadone in infants treated for neonatal abstinence syndrome (NAS) secondary to intrauterine exposure to methadone. This is a multi-center, retrospective cohort study to assess length of treatment (LOT), hospital length of stay (LOS), and cumulative opioid exposure between infants treated with either methadone or buprenorphine for NAS secondary to in utero exposure to methadone. Infants delivered at a gestational age ≥35 weeks and a maternal history of opioid-use disorder and/or urine drug screen positive for methadone, and postnatal pharmacotherapy for NAS with either buprenorphine or methadone as first-line opioid replacement therapy, were eligible.

Comparison of Neonatal Abstinence Syndrome Treatment with Sublingual Buprenorphine versus Conventional Opioids.

Objective:  The objective of this study was to compare duration of opioid treatment and length of stay outcomes for neonatal abstinence syndrome (NAS) using sublingual buprenorphine versus traditional weaning with methadone or morphine.

Study Design:  This retrospective cohort analysis evaluated infants treated for NAS at a single community hospital from July 2013 through June 2017. A standardized weaning protocol was introduced in June 2015, allowing for treatment with sublingual buprenorphine regardless of type of intrauterine opioid exposure.

Nedd4-2-mediated ubiquitination facilitates processing of surfactant protein-C.

We previously proposed a model of surfactant protein (SP)-C biosynthesis in which internalization of the proprotein from the limiting membrane of the multivesicular body to internal vesicles represents a key step in the processing and secretion of SP-C. To test this hypothesis, alanine mutagenesis of the N-terminal propeptide of SP-C was performed. Adenoviruses encoding mutant proproteins were infected into type II cells isolated from Sftpc(-/-) mice, and media analyzed for secreted SP-C 24 hours after infection.

Partial SP-B deficiency perturbs lung function and causes air space abnormalities.

Surfactant protein B (SP-B) is required for function of newborn and adult lung, and partial deficiency has been associated with susceptibility to lung injury. In the present study, transgenic mice were produced in which expression of SP-B in type II epithelial cells was conditionally regulated. Concentrations of SP-B were maintained at 60-70% of that normally present in control.

Processing of pulmonary surfactant protein B by napsin and cathepsin H.

Surfactant protein B (SP-B) is an essential constituent of pulmonary surfactant. SP-B is synthesized in alveolar type II cells as a preproprotein and processed to the mature peptide by the cleavage of NH2- and COOH-terminal peptides. An aspartyl protease has been suggested to cleave the NH2-terminal propeptide resulting in a 25-kDa intermediate.

Maintenance of the mouse type II cell phenotype in vitro.

The purpose of this study was to identify culture conditions for maintenance of isolated mouse type II cells with intact surfactant protein (SP) and phospholipid production. Type II cells were isolated from 6-wk-old mice and cultured on Matrigel matrix-rat tail collagen (70:30 vol/vol) in bronchial epithelial cell growth medium minus hydrocortisone plus 5% charcoal-stripped FBS and 10 ng/ml keratinocyte growth factor. Under these conditions, type II cells actively produced surfactant phospholipids and proteins for at least 7 days.