@misc{martin_adler_macchione_akley_mckane_2005, title={Culture system for mouse tracheal epithelial cells}, volume={6,933,149}, number={2005 Aug. 23}, publisher={Washington, DC: U.S. Patent and Trademark Office}, author={Martin, L. D. and Adler, K. B. and Macchione, M. and Akley, N. J. and McKane, S. A.}, year={2005} }
 @article{lankford_macchione_crews_mckane_akley_martin_2005, title={Modeling the airway epithelium in allergic asthma: Interleukin-13-induced effects in differentiated murine tracheal epithelial cells}, volume={41}, number={7}, journal={In Vitro Cellular & Developmental Biology. Animal}, author={Lankford, S. M. and Macchione, M. and Crews, A. L. and McKane, S. A. and Akley, N. J. and Martin, L. D.}, year={2005}, pages={217–224} }
 @article{little_dean_young_mckane_martin_jones_blikslager_2003, title={PI3K signaling is required for prostaglandin-induced  mucosal recovery in ischemia-injured porcine ileum}, volume={284}, ISSN={0193-1857 1522-1547}, url={http://dx.doi.org/10.1152/ajpgi.00121.2002}, DOI={10.1152/ajpgi.00121.2002}, abstractNote={ We have previously shown that PGE2 and PGI2 induce recovery of transepithelial resistance (TER) in ischemia-injured porcine ileal mucosa, associated with initial increases in Cl−secretion. We believe that the latter generates an osmotic gradient that stimulates resealing of tight junctions. Because of evidence implicating phosphatidylinositol 3-kinase (PI3K) in regulating tight junction assembly, we postulated that this signaling pathway is involved in PG-induced mucosal recovery. Porcine ileum was subjected to 45 min of ischemia, after which TER was monitored for a 180-min recovery period. Endogenous PG production was inhibited with indomethacin (5 μM). PGE2 (1 μM) and PGI2(1 μM) stimulated recovery of TER, which was inhibited by serosal application of the osmotic agent urea (300 mosmol/kgH2O). The PI3K inhibitor wortmannin (10 nM) blocked recovery of TER in response to PGs or mucosal urea. Immunofluorescence imaging of recovering epithelium revealed that PGs restored occludin and zonula occludens-1 distribution to interepithelial junctions, and this pattern was disrupted by pretreatment with wortmannin. These experiments suggest that PGs stimulate recovery of paracellular resistance via a mechanism involving transepithelial osmotic gradients and PI3K-dependent restoration of tight junction protein distribution. }, number={1}, journal={American Journal of Physiology-Gastrointestinal and Liver Physiology}, publisher={American Physiological Society}, author={Little, Dianne and Dean, Rebecca A. and Young, Karen M. and McKane, Shaun A. and Martin, Linda D. and Jones, Samuel L. and Blikslager, Anthony T.}, year={2003}, month={Jan}, pages={G46–G56} }
 @article{booth_newcomb_mckane_crews_adler_bonner_martin_2003, title={Proliferation of the airway epithelium in asthma - Are inflammatory cells required?}, volume={123}, ISSN={["0012-3692"]}, DOI={10.1378/chest.123.3_suppl.384S}, abstractNote={Asthma is associated with a T helper type 2 phenotype in which interleukin (IL)-4, IL-5, and IL-13 predominate. In addition, the long-term presence of these inflammatory mediators is thought to lead to airway structural changes that are collectively referred to as airway remodeling. Data from our laboratory, and those of others, have suggested a role for IL-13 in the development of mucous cell hyperplasia that is associated with such remodeling. Others also have suggested a role for inflammatory cells such as neutrophils in mediating this process. Using normal human bronchial epithelial (NHBE) cells differentiated in vitro, we have shown recently that IL-13 (10 ng/mL for 24 h) induces the proliferation of NHBE cells via a mechanism that is dependent on the IL-13-induced release of transforming growth factor (TGF)-α by the epithelial cells. This epithelium-derived TGF-α then acts in an autocrine/paracrine manner to bind the epidermal growth factor receptor (EGFR) on these NHBE cells, enhancing proliferation. Specifically, soluble TGF-α is released by NHBE cells in response to IL-13 exposure (1 h), and the immunohistochemical analysis of cells exposed to IL-13 (after 1 and 4 h) has revealed a lack of membrane-bound TGF-α when compared to control cells. The IL-13-induced proliferative response can be blocked in a concentration-dependent manner by AG1478 (0.1, 1, and 5 μg/mL), which is a specific inhibitor of EGFR tyrosine kinase activity, and is eliminated by neutralizing TGF-α antibodies, while control antibodies (ie, anti-platelet-derived growth factor, epidermal growth factor [EGF], and heparin-binding EGF) have no effect.}, number={3}, journal={CHEST}, author={Booth, BW and Newcomb, DC and McKane, SA and Crews, AL and Adler, KB and Bonner, JC and Martin, LD}, year={2003}, month={Mar}, pages={384S–385S} }
 @article{anderson_frampton_mckeand_hodges_1992, title={TISSUE-CULTURE SHOOT AND ROOT-SYSTEM EFFECTS ON FIELD PERFORMANCE OF LOBLOLLY-PINE}, volume={22}, ISSN={["0045-5067"]}, DOI={10.1139/x92-007}, abstractNote={ To study differences in growth between loblolly pine (Pinustaeda L.) tissue-culture plantlets and seedlings, shoot systems of plantlets and seedlings were grafted onto plantlet and seedling root systems. After three growing seasons, plantlet root systems accounted for 0.3 m of height growth loss and 1.0 cm of loss in basal diameter, while plantlet shoot systems accounted for 0.6 m of height growth loss and 1.4 cm of loss in basal diameter. The mature-appearing morphology of plantlet shoots was due to the shoot system of plantlets and not to the indirect effect of the plantlet root system. }, number={1}, journal={CANADIAN JOURNAL OF FOREST RESEARCH-REVUE CANADIENNE DE RECHERCHE FORESTIERE}, author={ANDERSON, AB and FRAMPTON, LJ and MCKEAND, SE and HODGES, JF}, year={1992}, month={Jan}, pages={56–61} }