The Use of Substances Other Than Nicotine in Electronic Cigarettes Among College Students.

INTRODUCTION: Electronic cigarettes (e-cigarettes) have grown in popularity, especially among youth and young adults. Although e-cigarettes were originally intended to vaporize a liquid mixture containing nicotine, there appears to be an increasing trend in other substance use in e-cigarettes (OSUE). MATERIALS AND METHODS: Cross-sectional data from 1542 undergraduate college student e-cigarette users from a large Midwestern university were collected via online survey to assess prevalence of e-cigarette use, reasons for use, perceived harm, and prevalence and predictors of OSUE. RESULTS: Nearly 7% (6.94%) reported using an e-cigarette to vaporize and inhale a substance other than nicotine. Current tobacco cigarette smokers were significantly more likely to report OSUE (51.0%) as compared with never (33.7%) and former (15.4%) smokers. Among respondents reporting OSUE, the primary reason for e-cigarette use was "safer than cigarettes" (21.7%), followed by "experimentation" (18.9%) and "friends use" (17.0%). Most (77.9%) reported using cannabis or some derivative of cannabis in an e-cigarette. Binomial logistic regression found that women were less likely to report OSUE by a factor of 0.60, former tobacco cigarette smokers as compared with never smokers were more likely to report OSUE by a factor of 1.87, and e-cigarette users who reported using e-cigarettes for "cool or trendy" reasons were more likely to report OSUE by a factor of 2.89. DISCUSSION: Little is known regarding the health effects of cannabis and cannabis derivatives delivered through e-cigarettes. Concern may also be warranted regarding the potential dangers of this young population using substances more dangerous than cannabis in e-cigarettes. Knowledge is limited regarding the public health impact of vaping cannabis or other illicit substances among college student populations. This study stresses the need for continued research regarding the vaping of cannabis and other illicit substances among college students.

Incidental finding of tracheal bronchus complicating the anesthetic management of a left video-assisted thoracoscopic procedure.

Congenital abnormalities of the large airways are uncommon, but may occasionally pose significant difficulties for anesthesiologists. The tracheal bronchus is an anatomical variant in which an accessory bronchus originates directly from the trachea rather than distal to the carina, as a takeoff from the right mainstem bronchus. Anesthesiologists should be aware of this uncommon anomaly, its different variants, and its management in order to successfully establish one lung ventilation (OLV) for surgical isolation. In this article, we report the challenges encountered in establishing OLV in a patient with a previously undiagnosed aberrant right upper lobe bronchus arising directly from the trachea.

Egr-1 antisense oligonucleotides inhibit hypoxia-induced proliferation of pulmonary artery adventitial fibroblasts.

In most mammalian species, chronic exposure to hypoxia leads to pulmonary hypertension and vascular remodeling. The adventitial fibroblast, because of its ability to proliferate in response to hypoxia, is thought to be a critical cell in the remodeling process. However, the transcription factors driving hypoxia-induced fibroblast proliferation have yet to be elucidated. The early growth response-1 (Egr-1) transcription factor has been shown to be upregulated by hypoxia in pulmonary artery adventitial fibroblasts. We therefore hypothesized that Egr-1 is directly involved in hypoxia-induced adventitial fibroblast proliferation. Immunohistochemical analysis of in vivo lung tissue from animals exposed to chronic hypoxia revealed increased expression of Egr-1 in the pulmonary artery fibroblasts vs. expression shown in normoxic controls. In fibroblasts cultured from chronically hypoxic animals, exposure to 1% oxygen upregulated Egr-1 protein and cell proliferation. To evaluate the role of Egr-1 in hypoxia-induced proliferation, we employed an Egr-1 antisense strategy. Addition of antisense Egr-1 oligonucleotides, but not sense oligonucleotides, attenuated the hypoxia-induced upregulation of Egr-1 protein and reduced hypoxia-induced DNA synthesis by 50%. Cell proliferation was also significantly inhibited by the addition of antisense Egr-1 oligonucleotides but not the sense oligonucleotides. In addition, hypoxia-induced upregulations of cyclin D and epidermal growth factor receptor were attenuated by Egr-1 antisense oligonucleotides. We conclude that Egr-1 protein expression is very sensitive to upregulation by hypoxia in pulmonary artery adventitial fibroblasts and that it plays an important role in the autonomous growth phenotype induced by hypoxia in these cells.

Extracellular ATP-induced proliferation of adventitial fibroblasts requires phosphoinositide 3-kinase, Akt, mammalian target of rapamycin, and p70 S6 kinase signaling pathways.

Extracellular nucleotides are increasingly recognized as important regulators of growth in a variety of cell types. Recent studies have demonstrated that extracellular ATP is a potent inducer of fibroblast growth acting, at least in part, through an ERK1/2-dependent signaling pathway. However, the contributions of additional signaling pathways to extracellular ATP-mediated cell proliferation have not been defined. By using both pharmacologic and genetic approaches, we found that in addition to ERK1/2, phosphatidylinositol 3-kinase (PI3K), Akt, mammalian target of rapamycin (mTOR), and p70 S6K-dependent signaling pathways are required for ATP-induced proliferation of adventitial fibroblasts. We found that extracellular ATP acting in part through G(i) proteins increased PI3K activity in a time-dependent manner and transient phosphorylation of Akt. This PI3K pathway is not involved in ATP-induced activation of ERK1/2, implying activation of independent parallel signaling pathways by ATP. Extracellular ATP induced dramatic increases in mTOR and p70 S6K phosphorylation. This activation of the mTOR/p70 S6 kinase (p70 S6K) pathway in response to ATP is because of independent contributions of PI3K/Akt and ERK1/2 pathways, which converge on the level of p70 S6K. ATP-dependent activation of mTOR and p70 S6K also requires additional signaling inputs perhaps from pathways operating through Galpha or Gbetagamma subunits. Collectively, our data demonstrate that ATP-induced adventitial fibroblast proliferation requires activation and interaction of multiple signaling pathways such as PI3K, Akt, mTOR, p70 S6K, and ERK1/2 and provide evidence for purinergic regulation of the protein translational pathways related to cell proliferation.