Peer crowd-based targeting in E-cigarette advertisements: a qualitative study to inform counter-marketing.

BACKGROUND:Cigarette lifestyle marketing with psychographic targeting has been well documented, but few studies address non-cigarette tobacco products. This study examined how young adults respond to e-cigarette advertisements featuring diverse peer crowds - peer groups with shared identities and lifestyles - to inform tobacco counter-marketing design. METHODS:Fifty-nine young adult tobacco users in California participated in interviews and viewed four to five e-cigarette advertisements that featured characters from various peer crowd groups. For each participant, half of the advertisements they viewed showed characters from the same peer crowd as their own, and the other half of the advertisements featured characters from a different peer crowd. Advertisements were presented in random order. Questions probed what types of cues are noticed in the advertisements, and whether and how much participants liked or disliked the advertisements. RESULTS:Results suggest that participants liked and provided richer descriptions of characters and social situations in the advertisements featuring their own peer crowd more than the advertisements featuring a different peer crowd. Mismatching age or device type was also noted: participants reported advertisements showing older adults were not intended for them. Participants who used larger vaporizers tended to dislike cigalike advertisements even if they featured a matching peer crowd. CONCLUSION:Peer crowd and lifestyle cues, age and device type are all salient features of e-cigarette advertising for young adults. Similarly, educational campaigns about e-cigarettes should employ peer crowd-based targeting to engage young adults, though messages should be carefully tested to ensure authentic and realistic portrayals

Access to health services in Western Newfoundland, Canada: Issues, barriers and recommendations emerging from a community-engaged research project

Research indicates that people living in rural and remote areas of Canada face challenges to accessing health services. This article reports on a community-engaged research project conducted by investigators at Memorial University of Newfoundland in collaboration with the Rural Secretariat Regional Councils and Regional Partnership Planners for the Corner Brook–Rocky Harbour and Stephenville–Port aux Basques Rural Secretariat Regions of Newfoundland and Labrador. The aim of this research was to gather information on barriers to accessing health services, to identify solutions to health services’ access issues and to inform policy advice to government on enhancing access to health services. Data was collected through: (1) targeted distribution of a survey to communities throughout the region, and (2) informal ‘kitchen table’ discussions to discuss health services’ access issues. A total of 1049 surveys were collected and 10 kitchen table discussions were held. Overall, the main barriers to care listed in the survey included long wait times, services not available in the area and services not available at time required. Other barriers noted by survey respondents included transportation problems, financial concerns, no medical insurance coverage, distance to travel and weather conditions. Some respondents reported poorer access to maternal/child health and breast and cervical screening services and a lack of access to general practitioners, pharmacy services, dentists and nurse practitioners. Recommendations that emerged from this research included improving the recruitment of rural physicians, exploring the use of nurse practitioners, assisting individuals with travel costs,  developing specialist outreach services, increasing use of telehealth services and initiating additional rural and remote health research.Keywords: rural, remote, healthcare, health services, social determinants of healt

“Creating What I Think I should Be Doing”: Contradictions and Learning of College Job Changers

This roundtable, and the study it is based on, outlines how non-faculty staff at a small college described their own workplace learning after a “significant” job change (as defined by the participant)

Inefficiency of classically simulating linear optical quantum computing with Fock-state inputs

Aaronson and Arkhipov recently used computational complexity theory to argue that classical computers very likely cannot efficiently simulate linear, multimode, quantum-optical interferometers with arbitrary Fock-state inputs [Aaronson and Arkhipov, Theory Comput. 9, 143 (2013)]. Here we present an elementary argument that utilizes only techniques from quantum optics. We explicitly construct the Hilbert space for such an interferometer and show that its dimension scales exponentially with all the physical resources. We also show in a simple example just how the Schr\"odinger and Heisenberg pictures of quantum theory, while mathematically equivalent, are not in general computationally equivalent. Finally, we conclude our argument by comparing the symmetry requirements of multiparticle bosonic to fermionic interferometers and, using simple physical reasoning, connect the nonsimulatability of the bosonic device to the complexity of computing the permanent of a large matrix.Comment: 7 pages, 1 figure Published in PRA Phys. Rev. A 89, 022328 (2014

Tumor-Associated Macrophages Suppress the Cytotoxic Activity of Antimitotic Agents.

Antimitotic agents, including Taxol, disrupt microtubule dynamics and cause a protracted mitotic arrest and subsequent cell death. Despite the broad utility of these drugs in breast cancer and other tumor types, clinical response remains variable. Tumor-associated macrophages (TAMs) suppress the duration of Taxol-induced mitotic arrest in breast cancer cells and promote earlier mitotic slippage. This correlates with a decrease in the phosphorylated form of histone H2AX (γH2AX), decreased p53 activation, and reduced cancer cell death in interphase. TAMs promote cancer cell viability following mitotic slippage in a manner sensitive to MAPK/ERK kinase (MEK) inhibition. Acute depletion of major histocompatibility complex class II low (MHCIIlo) TAMs increased Taxol-induced DNA damage and apoptosis in cancer cells, leading to greater efficacy in intervention trials. MEK inhibition blocked the protective capacity of TAMs and phenocopied the effects of TAM depletion on Taxol treatment. TAMs suppress the cytotoxic effects of Taxol, in part through cell non-autonomous modulation of mitotic arrest in cancer cells, and targeting TAM-cancer cell interactions potentiates Taxol efficacy

ARPES Study of X-Point Band Overlaps in LaB6_6 and SmB6_6 - Contrast to SrB6_6 and EuB6_6

In contrast to our recent finding of an X-point band gap in divalent hexaborides, we report here that angle resolved photoemission spectroscopy (ARPES) data shows that the gap is absent for trivalent LaB$_6$ and is absent or nearly so for mixed valent SmB$_6$. This finding demonstrates a nontrivial evolution of the band structure from divalent to trivalent hexaborides.Comment: submitted to SCES '0

Stories of Active Teaching: Embedding Civic Engagement in our Practice

How do we move beyond the well-worn path of information discovery and evaluation in our instruction? Join librarians and archivists from Western University and Huron University College, as we share stories that explore teaching civic engagement as an IL learning outcome

Loss of androgen signaling in mesenchymal sonic hedgehog responsive cells diminishes prostate development, growth, and regeneration.

Prostate embryonic development, pubertal and adult growth, maintenance, and regeneration are regulated through androgen signaling-mediated mesenchymal-epithelial interactions. Specifically, the essential role of mesenchymal androgen signaling in the development of prostate epithelium has been observed for over 30 years. However, the identity of the mesenchymal cells responsible for this paracrine regulation and related mechanisms are still unknown. Here, we provide the first demonstration of an indispensable role of the androgen receptor (AR) in sonic hedgehog (SHH) responsive Gli1-expressing cells, in regulating prostate development, growth, and regeneration. Selective deletion of AR expression in Gli1-expressing cells during embryogenesis disrupts prostatic budding and impairs prostate development and formation. Tissue recombination assays showed that urogenital mesenchyme (UGM) containing AR-deficient mesenchymal Gli1-expressing cells combined with wildtype urogenital epithelium (UGE) failed to develop normal prostate tissue in the presence of androgens, revealing the decisive role of AR in mesenchymal SHH responsive cells in prostate development. Prepubescent deletion of AR expression in Gli1-expressing cells resulted in severe impairment of androgen-induced prostate growth and regeneration. RNA-sequencing analysis showed significant alterations in signaling pathways related to prostate development, stem cells, and organ morphogenesis in AR-deficient Gli1-expressing cells. Among these altered pathways, the transforming growth factor β1 (TGFβ1) pathway was up-regulated in AR-deficient Gli1-expressing cells. We further demonstrated the activation of TGFβ1 signaling in AR-deleted prostatic Gli1-expressing cells, which inhibits prostate epithelium growth through paracrine regulation. These data demonstrate a novel role of the AR in the Gli1-expressing cellular niche for regulating prostatic cell fate, morphogenesis, and renewal, and elucidate the mechanism by which mesenchymal androgen-signaling through SHH-responsive cells elicits the growth and regeneration of prostate epithelium

CD39 activity correlates with stage and inhibits platelet reactivity in chronic lymphocytic leukemia

<p>Abstract</p> <p>Background</p> <p>Chronic lymphocytic leukemia (CLL) is characterized by accumulation of mature appearing lymphocytes and is rarely complicated by thrombosis. One possible explanation for the paucity of thrombotic events in these patients may be the presence of the ecto-nucleotidase CD39/NTDPase-1 on the surface of the malignant cells in CLL. CD39 is the major promoter of platelet inhibition <it>in vivo </it>via its metabolism of ADP to AMP. We hypothesize that if CD39 is observed on CLL cells, then patients with CLL may be relatively protected against platelet aggregation and recruitment and that CD39 may have other effects on CLL, including modulation of the disease, via its metabolism of ATP.</p> <p>Methods</p> <p>Normal and malignant lymphocytes were isolated from whole blood from patients with CLL and healthy volunteers. Enzyme activity was measured via radio-TLC assay and expression via FACS. Semi-quantititative RT-PCR for CD39 splice variants and platelet function tests were performed on several samples.</p> <p>Results</p> <p>Functional assays demonstrated that ADPase and ATPase activities were much higher in CLL cells than in total lymphocytes from the normal population on a per cell basis (p-value < 0.00001). CD39 activity was elevated in stage 0–2 CLL compared to stage 3–4 (p < 0.01). FACS of lymphocytes demonstrated CD39 expression on > 90% of normal and malignant B-lymphocytes and ~8% of normal T-lymphocytes. RT-PCR showed increased full length CD39 and splice variant 1.5, but decreased variant 1.3 in CLL cells. Platelet function tests showed inhibition of platelet activation and recruitment to ADP by CLL cells.</p> <p>Conclusion</p> <p>CD39 is expressed and active on CLL cells. Enzyme activity is higher in earlier stages of CLL and decreased enzyme activity may be associated with worsening disease. These results suggest that CD39 may play a role in the pathogenesis of malignancy and protect CLL patients from thrombotic events.</p