Food Allergen Labeling and Purchasing Habits in the United States and Canada.

BACKGROUND: Mandatory labeling of products with top allergens has improved food safety for consumers. Precautionary allergen labeling (PAL), such as "may contain" or "manufactured on shared equipment," are voluntarily placed by the food industry. OBJECTIVE: To establish knowledge of PAL and its impact on purchasing habits by food-allergic consumers in North America. METHODS: Food Allergy Research & Education and Food Allergy Canada surveyed consumers in the United States and Canada on purchasing habits of food products featuring different types of PAL. Associations between respondents' purchasing behaviors and individual characteristics were estimated using multiple logistic regression. RESULTS: Of 6684 participants, 84.3% (n = 5634) were caregivers of a food-allergic child and 22.4% had food allergy themselves. Seventy-one percent reported a history of experiencing a severe allergic reaction. Buying practices varied on the basis of PAL wording; 11% of respondents purchased food with "may contain" labeling, whereas 40% purchased food that used "manufactured in a facility that also processes." Twenty-nine percent of respondents were unaware that the law requires labeling of priority food allergens. Forty-six percent were either unsure or incorrectly believed that PAL is required by law. Thirty-seven percent of respondents thought PAL was based on the amount of allergen present. History of a severe allergic reaction decreased the odds of purchasing foods with PAL. CONCLUSIONS: Almost half of consumers falsely believed that PAL was required by law. Up to 40% surveyed consumers purchased products with PAL. Understanding of PAL is poor, and improved awareness and guidelines are needed to help food-allergic consumers purchase food safely.

Parents' perceptions of a patient portal for managing their child's chronic illness.

Through interviews, we sought to describe parents' perceptions of a patient portal for the management of their child's chronic illness. Parents perceive patient portals as beneficial, providing easier communication with care providers, convenience, a sense of control, reduced anxiety, and reassurance. Future research should aim to quantitate these benefits.

Nicotine induces resistance to chemotherapy in nasal epithelial cancer.

BACKGROUND: Epidemiological and clinical data implicate that in patients with cancer, continued smoking causes progression of cancer growth and resistance to therapy. The carcinogens possess the ability to block apoptosis, an important mechanism in the development of tumors and resistance to chemotherapy. We previously showed that nicotine enhances growth and proliferation in lung cancer. However, the effects of nicotine, a tobacco carcinogen that inhibits apoptosis, have not been studied before in nasal epithelial carcinoma (NC). In this study, we sought to determine the effects of nicotine on chemotherapy-induced apoptosis in human NC. METHODS: Primary human NC cells were grown per protocol, treated with combination chemotherapy, and the apoptosis was assessed by TUNEL (terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling) and DNA fragmentation assays. The regulation of mitogen-activated protein kinase (MAPK) and protein kinase B (AKT) signal transduction pathway was examined by real time quantitative polymerized chain reaction, and immunofluorescent staining assays. RESULTS: Combination chemotherapy with cisplatin (35 microM) plus etoposide (20 microM) caused a significant increase in NC apoptosis compared with single agent alone, and nicotine, in part, inhibited chemotherapy-induced apoptosis in NC. Furthermore, nicotine induced activation of AKT and MAPK pathways, while inhibition of MAPK using U0126 and AKT by phosphatidylinositol 3-kinase inhibitor, LY294002, in part, blocked the antiapoptotic effects of nicotine against cisplatin and etoposide-induced apoptosis in NC. CONCLUSION: Nicotine inhibits chemotherapy-induced apoptosis in NC via the AKT and MAPK-mediated signaling pathways. We speculate that nicotine may play a role in oncogenesis and resistance to cancer therapy in NC.

Nicotine induces resistance to chemotherapy by modulating mitochondrial signaling in lung cancer.

Continued smoking causes tumor progression and resistance to therapy in lung cancer. Carcinogens possess the ability to block apoptosis, and thus may induce development of cancers and resistance to therapy. Tobacco carcinogens have been studied widely; however, little is known about the agents that inhibit apoptosis, such as nicotine. We determine whether mitochondrial signaling mediates antiapoptotic effects of nicotine in lung cancer. A549 cells were exposed to nicotine (1 muM) followed by cisplatin (35 muM) plus etoposide (20 muM) for 24 hours. We found that nicotine prevented chemotherapy-induced apoptosis, improved cell survival, and caused modest increases in DNA synthesis. Inhibition of mitogen-activated protein kinase (MAPK) and Akt prevented the antiapoptotic effects of nicotine and decreased chemotherapy-induced apoptosis. Small interfering RNA MAPK kinase-1 blocked antiapoptotic effects of nicotine, whereas small interfering RNA MAPK kinase-2 blocked chemotherapy-induced apoptosis. Nicotine prevented chemotherapy-induced reduction in mitochondrial membrane potential and caspase-9 activation. Antiapoptotic effects of nicotine were blocked by mitochondrial anion channel inhibitor, 4,4'diisothiocyanatostilbene-2,2'disulfonic acid. Chemotherapy enhanced translocation of proapoptotic Bax to the mitochondria, whereas nicotine blocked these effects. Nicotine up-regulated Akt-mediated antiapoptotic X-linked inhibitor of apoptosis protein and phosphorylated proapoptotic Bcl2-antagonist of cell death. The A549-rho0 cells, which lack mitochondrial DNA, demonstrated partial resistance to chemotherapy-induced apoptosis, but blocked the antiapoptotic effects of nicotine. Accordingly, we provide evidence that nicotine modulates mitochondrial signaling and inhibits chemotherapy-induced apoptosis in lung cancer. The mitochondrial regulation of nicotine imposes an important mechanism that can critically impair the treatment of lung cancer, because many cancer-therapeutic agents induce apoptosis via the mitochondrial death pathway. Strategies aimed at understanding nicotine-mediated signaling may facilitate the development of improved therapies in lung cancer.