Supporting Direct Breastfeeding for a Tracheostomy-Dependent Extremely Premature Infant: A Case Study.

Introduction: The benefits of human milk for preterm infants are well documented. Complex medical conditions can limit the extremely premature infant's ability to breastfeed and to receive human milk directly, yet these vulnerable infants may benefit most from receiving it.

Main Issue: Extremely preterm infants are at risk for infections, digestive challenges, and chronic lung disease, and occasionally require a tracheostomy to facilitate weaning from mechanical ventilation.

Phosphorylation of activation function-1 regulates proteasome-dependent nuclear mobility and E6-associated protein ubiquitin ligase recruitment to the estrogen receptor beta.

The ubiquitin-proteasome pathway has been recognized as an important regulator in the hormonal response by estrogen receptor (ER) alpha, but its impact on ERbeta function is poorly characterized. In the current study, we investigated the role of the ubiquitin-proteasome pathway in regulating ERbeta activity and identified regulatory sites within the activation function (AF)-1 domain that modulate ERbeta ubiquitination and nuclear dynamics in a hormone-independent manner. Although both ERalpha and ERbeta were dependent on proteasome function for their maximal response to estrogen, they were regulated differently by proteasome inhibition in the absence of hormone, an effect shown to be dependent on their respective AF-1 domain.

Selective hormone-dependent repression of estrogen receptor beta by a p38-activated ErbB2/ErbB3 pathway.

Deregulated signaling of ErbB2 receptor tyrosine kinase is often associated with hormone resistance in estrogen receptor alpha (ERalpha)-positive breast cancers, establishing a relationship between ErbB2 and ERalpha pathways. Although ERalpha and ERbeta are expressed in many breast cancer cells, the response of ERbeta to ErbB2 signaling is less well defined. In the present study, we demonstrate that ERbeta activity can be modulated by ErbB2 signaling in ER-expressing breast cancer cells.