It's Not Just: Evaluation of a Media Campaign to Motivate Action Around Targeting of Menthol Tobacco in Black Communities.

Introduction: For more than 60 years, tobacco companies have aggressively marketed menthol tobacco products in Black communities. In 2021, New York State Department of Health-funded grantees launched a media campaign aimed toward civically engaged New York adults to educate and mobilize community action to prevent targeted marketing of menthol tobacco. This study examined audience reactions to the campaign and associations between campaign awareness and key outcomes. Methods: Following campaign implementation, we administered 2 online, cross-sectional surveys to 2,000 civically engaged New York adults to assess campaign awareness, audience reactions, and campaign-related attitudes and behaviors. We examined sociodemographic differences in audience reactions and assessed multivariate associations between campaign awareness and key outcomes. Results: Overall, 40% of respondents were aware of the campaign. Perceived advertisement (ad) effectiveness was higher among Black, Hispanic, and nonsmoking respondents and those aware of the campaign. Negative reactions to ads were higher at wave 1, among non-Hispanic White and male respondents, and among current smokers. Campaign awareness was positively associated with campaign-related beliefs. The association between campaign awareness and support for a menthol ban varied by survey wave and race, with positive associations at wave 2 and among non-Hispanic White respondents only. Among wave 2 respondents only, campaign awareness was positively associated with actions to reduce the targeting of menthol in Black communities. Conclusion: Media campaigns can play an important role in raising awareness of menthol tobacco product targeting in Black communities and building public support for local and statewide menthol restrictions that may be implemented before federal product standards are in place.

Association of Escherichia coli O157:H7 with necrotizing enterocolitis in a full-term infant.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency of the neonate. NEC is predominantly seen in premature infants; however, in rare instances it can affect full-term infants as well. Although the pathogenesis of NEC remains elusive, it is well established that bacterial colonization is required for development of this disease. In this report, we present a case of a full-term infant, who developed a very aggressive form of NEC and was found to have Escherichia coli (E. coli) O157:H7 both in stool and blood cultures. Unfortunately, despite aggressive surgical and intensive care management, this infant suffered pan-intestinal necrosis and expired. We were not able to establish the route of transmission. To our knowledge, this is the first report of the association of E. coli O157:H7 with NEC.

Fgf10 dosage is critical for the amplification of epithelial cell progenitors and for the formation of multiple mesenchymal lineages during lung development.

The key role played by Fgf10 during early lung development is clearly illustrated in Fgf10 knockout mice, which exhibit lung agenesis. However, Fgf10 is continuously expressed throughout lung development suggesting extended as well as additional roles for FGF10 at later stages of lung organogenesis. We previously reported that the enhancer trap Mlcv1v-nLacZ-24 transgenic mouse strain functions as a reporter for Fgf10 expression and displays decreased endogenous Fgf10 expression. In this paper, we have generated an allelic series to determine the impact of Fgf10 dosage on lung development. We report that 80% of the newborn Fgf10 hypomorphic mice die within 24 h of birth due to respiratory failure. These mutant mouse lungs display severe hypoplasia, dilation of the distal airways and large hemorrhagic areas. Epithelial differentiation and proliferation studies indicate a specific decrease in TTF1 and SP-B expressing cells correlating with reduced epithelial cell proliferation and associated with a decrease in activation of the canonical Wnt signaling in the epithelium. Analysis of vascular development shows a reduction in PECAM expression at E14.5, which is associated with a simplification of the vascular tree at E18.5. We also show a decrease in alpha-SMA expression in the respiratory airway suggesting defective smooth muscle cell formation. At the molecular level, these defects are associated with decrease in Vegfa and Pdgfa expression likely resulting from the decrease of the epithelial/mesenchymal ratio in the Fgf10 hypomorphic lungs. Thus, our results indicate that FGF10 plays a pivotal role in maintaining epithelial progenitor cell proliferation as well as coordinating alveolar smooth muscle cell formation and vascular development.

Nitric oxide decreases endothelin-1 secretion through the activation of soluble guanylate cyclase.

The use of exogenous nitric oxide (NO) has been shown to alter the regulation of other endothelially derived mediators of vascular tone, such as endothelin-1 (ET-1). However, the interaction between NO and ET-1 appears to be complex and remains incompletely understood. One of the major actions of NO is the activation of soluble guanylate cyclase (sGC) with the subsequent generation of cGMP. Therefore, we undertook this study to test the hypothesis that NO regulates ET-1 production via the activation of the sGC/cGMP pathway. The results obtained indicated that the exposure of primary cultures of 4-wk-old ovine pulmonary arterial endothelial cells (4-wk PAECs) to the long-acting NO donor DETA NONOate induced both a dose- and time-dependent decrease in secreted ET-1. This decrease in ET-1 secretion occurred in the absence of changes in endothelin-converting enzyme-1 or sGC expression but in conjunction with a decrease in prepro-ET-1 mRNA. The changes in ET-1 release were inversely proportional to the cellular cGMP content. Furthermore, the NO-independent activator of sGC, YC-1, or treatment with a cGMP analog also produced significant decreases in ET-1 secretion. Conversely, pretreatment with the sGC inhibitor ODQ blocked the NO-induced decrease in ET-1. Therefore, we conclude that exposure of 4-wk PAECs to exogenous NO decreases secreted ET-1 resulting from the activation of sGC and increased cGMP generation.

Inhaled prostacyclin for term infants with persistent pulmonary hypertension refractory to inhaled nitric oxide.

We report the use of inhaled prostacyclin (PGI(2)) in 4 neonates with persistent pulmonary hypertension and hypoxemia refractory to inhaled nitric oxide. Oxygenation rapidly improved after inhalation of PGI(2) in all infants. The condition of one infant subsequently deteriorated, and alveolar capillary dysplasia was found at autopsy. The surviving infants were discharged with normal oxygen saturations in room air.