Bronchopulmonary Dysplasia.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease, associated with premature birth, that arises during the infantile period. It is an evolving disease process with an unchanged incidence due to advancements in neonatal care which allow for the survival of premature infants of lower gestational ages and birth weights. Currently, there are few effective interventions to prevent BPD. However, careful attention to BPD phenotypes and comprehensive care provided by an interdisciplinary team have improved care. Interventions early in the disease course hold promise for improving long-term survival and outcomes in adulthood for this high-risk population.

Posterior tracheopexy for preterm infants with severe bronchopulmonary dysplasia and severe tracheobronchomalacia: A case series.

We report a series of four patients with severe bronchopulmonary dysplasia (BPD) who underwent posterior tracheopexy for severe tracheomalacia (TM). While posterior tracheopexy is an established surgical treatment for TM associated with tracheoesophageal fistula, it has not been previously described in TM associated with BPD. There were no significant intraoperative or postoperative complications from the surgeries. Three of the four patients required tracheostomy and mechanical ventilation, which may reflect the degree of lung disease and other multisystem comorbidities in these patients. More investigation is needed to determine whether posterior tracheopexy is an effective surgical option for TM related to BPD.

SIRT1 inactivation evokes antitumor activities in NSCLC through the tumor suppressor p27.

UNLABELLED: P27(Kip1) (CDKN1B) regulates cellular proliferation and senescence, and p27(Kip1) deficiency in cancer is strongly correlated with poor prognosis of multiple cancer types. Understanding the mechanism of p27(Kip1) loss in cancer and the consequences of restoring p27(Kip1) levels is therefore critical for effective management during therapy. Here, SIRT1, a class III histone deacetylase (HDAC), is identified as an important regulator of p27(Kip1) expression. Mechanistically, SIRT1 reduces p27(Kip1) expression by decreasing p27(Kip1) protein stability through the ubiquitin-proteasome pathway. In addition, SIRT1 silencing suppresses non-small cell lung cancer (NSCLC) proliferation and induces senescence in a p27(Kip1)-dependent manner. Furthermore, SIRT1 silencing dramatically suppresses tumor formation and proliferation in two distinct NSCLC xenograft mouse models. Collectively, these data demonstrate that not only SIRT1 is an important regulator of p27(Kip1) but also SIRT inhibition induces senescence and antigrowth potential in lung cancer in vivo. IMPLICATIONS: SIRT1 is a key regulator of p27 protein levels and SIRT1 inhibition is a viable strategy for NSCLC therapy by means of p27 reactivation.