Lung cancer is the leading cause of cancer death in the United States and worldwide. The higher mortality among patients with lung cancer is related to cases being diagnosed in late stage where treatment is limited. Urban and rural health outcomes are potentially influenced by differences in accessibility to health care services. We are unaware of existing research examining geographic differences in or factors related to lung cancer mortality in Florida. Therefore, this study aims to examine lung cancer mortality differences between urban and rural counties in Florida. We examined all 67 counties in Florida to investigate if a rural disparity exists in lung cancer mortality. We collected data from the National Cancer Institute (NCI) State Cancer Profile. We assigned urban and rural designation using the United States Census Bureau definition based on population density. We then used a t-test for unequal variances to compare the mean lung cancer mortality rate for the urban counties versus rural counties using Microsoft Excel. We used ArcGIS Pro software to create three maps: one showing urban and rural county designations, one showing lung cancer mortality, and a third bivariate map of urban and rural designations combined with age-adjusted lung cancer mortality rates together to examine the geographic distributions in Florida. We observed a mean age-adjusted lung cancer mortality of 62.7 per 100,000 for rural counties in Florida and a mean of 44.2 per 100,000 for urban counties which was significantly different using a t-test for unequal variances (p < 0.0001). The counties with the highest lung cancer mortality were grouped geographically in Florida’s Big Bend area. Overall, rural counties had a significantly higher average lung cancer mortality than the urban counties in Florida. Future research should examine factors affecting higher lung cancer mortality in rural counties such as screening locations and access to care.

Receptor-interacting protein 2 (RIP2) is a kinase which mediates signaling downstream of the bacterial peptidoglycan sensors Nucleotide-binding Oligomerization Domain (NOD) 1 and 2. Genetic loss or pharmaceutical inhibition of RIP2 has been shown to be beneficial in multiple inflammatory disease models with the effects largely attributed to reducing pro-inflammatory signaling downstream of peptidoglycan recognition. However, given the widespread expression of this kinase and its reported interactions with numerous other proteins, it is possible that RIP2 has many other unappreciated roles. In this work, we report the involvement of RIP2 in two novel pathways. First, we demonstrate a NOD2 dependent role for RIP2 in mediating ROS production downstream of FcƴR engagement. In these studies, we show that different members of the Src family kinases (SFKs) can promote RIP2 tyrosine phosphorylation and activation, providing a potential mechanism for such involvement. Second, we discover a novel role for RIP2 in the production of specialized pro-resolving lipid mediators (SPMs). SPMs are biologically active mediators which promote resolution by dampening the inflammatory immune response and enhancing the return to homeostasis. We show that NOD2 agonism leads to RIP2-dependent production of different SPMs in an in vivo murine peritonitis model. Using overexpression studies, we demonstrate that RIP2 promotes the modification and relocalization of various enzymes involved in SPM biosynthesis. Overall, our findings shed light on novel functional roles for NOD2 and RIP2 outside of peptidoglycan sensing. These data will have important implications for newly developing RIP2 targeted therapies by potentially determining the molecular basis for in vivo efficacy (or lack thereof) as well as elucidating a potential optimal therapeutic window for administration of such therapies for treatment of various inflammatory diseases.

This research provides ultrastructural information regarding pulmonary surfactant secretion from stimulation of adrenergic pathways to the lung via the stellate ganglion. This information will help clarify the important role of the sympathetic nervous system in surfactant disorders. It also provides insight into sympathetic mechanisms causing surfactant derangement in adult and infant respiratory distress syndromes (RDS). Basic cellular mechanisms of surfactant metabolism, including synthesis and packaging in lamellar bodies, were studied. Results shed light on these basic processes of lung cell function. The results of this study provide new avenues for studying a problem in health care that has long resisted advances, that of surfactant replacement therapy. It is expected that the results of this research, taken with information from other researches, will ultimately reduce the 50% mortality rate of the 150,000 patients annually suffering from RDS (Andreadis and Petty 1985).

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