Fan Responses to Virtual Reality Sport Sponsorship Activations: The Influence of Presence on Emotion and Attitude Formation

Considering the massive financial investment into sport sponsorship and the growth of the industry, it is important for managers to understand the strategic implications of their partnership decisions. This is even more essential in the current marketing landscape where advertising clutter and limited attention spans are rampant. Consequentially, experiential marketing has emerged to combat these challenges and provide consumers with unique and memorable experiences. Further, virtual reality (VR) has surfaced as a possible experiential marketing tool in that it has the capabilities of simulating one’s presence in a virtual environment: potentially creating those unique and memorable experiences. With sponsorship activation transitioning into an online environment further accelerated by the COVID-19 pandemic, the capabilities of virtual reality make it an attractive option to sport marketers. Presently, this technology is being applied without a clear purpose due to the newness of the platform and the lack of research and understanding regarding its true value. Thus, it is critical to examine how media modes, such as VR, may affect the impact of sponsorship messaging. In exploring sponsorship activation specifically, this study aimed to examine the use of 360-degree video and virtual reality as activation components, and if traditional non-immersive (phone, tablet, laptop, or desktop) and immersive (virtual reality) technologies differ in terms of their influence on important sponsor outcomes such as eliciting emotions and influencing attitudes. This study employed a survey design to compare responses between two groups. The first group experienced a 360-degree sport sponsorship activation video using non-immersive media while the second group experienced the same video in VR. A total of 114 responses were collected (57 in each group). Responses were then analyzed using two-way independent sample t-tests to find any statistically significant differences. Results showed that non-immersive respondents reported higher ratings of arousal compared to immersive respondents. Notably, there was a clear desire for 360-degree activation content from all users regardless of media mode. This study serves as a preliminary basis of valuation for virtual reality technology as it applies to sponsorship activation

Regional differences driving organic matter and trace metal signatures reflected in temperate reef bivalve communities on the South Island, New Zealand.

Increases in anthropogenic activity along coastal zones has led to an influx of terrestrial particulate matter containing high levels of nutrients and contaminants to coastal ecosystems. In order to manage these detrimental impacts, it is imperative that we understand the factors that drive the spatial variation in pollutants at both regional and local scales. Bivalves are key marine players in the processing of organic matter providing a link between benthic, pelagic, and terrestrial habitats. To this effect, bivalves are recognized as sentinel organisms in evaluating marine ecosystem function as well as detecting pollutants associated with land-based inputs. Therefore, changes to the basal organic matter source pools supporting these species will result in inherent changes in organic matter sources supporting species further up the food chain. Comparisons between Marlborough Sounds, Tasman Bay, and Fiordland on New Zealand’s South Island, provide a unique study system containing gradients in anthropogenic impacts influencing the uptake of organic matter and accumulation of pollutants in bivalves. The present study aimed to identify the influence of anthropogenic stressors in driving organic matter flux and trace element concentrations within bivalve communities in Marlborough Sounds, Tasman Bay, and Fiordland. We evaluated direct interactions between catchment modifications and salmon farming on feeding strategies, organic matter source pools, and trace element signatures of five individual bivalve species. We established that feeding strategies reveal interspecific differences among sites, while intraspecific differences are reflective of small-scale differences in organic matter resource pools. Further, organic matter source pools shaped by catchment modification and salmon farms revealed the observed differences in proportions of macroalgae supporting primary consumers. Lower proportions of organic matter were correlated with a high degree of catchment modification. Salmon farms influenced nutrient delivery to the surrounding benthos to all subtidal species. However, the intertidal (Mytilus galloprovincialis) was uninfluenced. Spatial difference in trace element concentrations tracked through basal organic matter source pools revealed the influence of catchment modification on the transmission of trace elements into bivalves. Further, aquaculture systems influenced the use of alternate basal organic matter sources (macroalgae versus phytoplankton) which were coincident with trace metal concentrations reflected in sediment-dwelling species. Lastly, as mercury concentrations have not been well resolved for commercially important bivalves in South Island fisheries, using current mercury analysis methodology, we reported baseline mercury concentrations. Further, we illustrated the influence of catchment modification from forestry on spatial variability in mercury concentrations. The contrast of the relatively developed catchments surrounding Marlborough Sounds and Tasman Bay with Fiordland’s relatively pristine forested catchment provides an important test of the links between anthropogenic activity and the contaminant loads reflected in coastal bivalves. Monitoring these coastal bivalves provided essential insight into the movement of particulate organic matter throughout food webs and their implications for ecosystem health

Quantum Entanglement of Identical Particles

We consider entanglement in a system of fixed number of identical particles. Since any operation should be symmetrized over all the identical particles and there is the precondition that the spatial wave functions overlap, the meaning of identical-particle entanglement is fundamentally different from that of distinguishable particles. The identical-particle counterpart of the Schmidt basis is shown to be the single-particle basis in which the one-particle reduced density matrix is diagonal. But it does not play a special role in the issue of entanglement, which depends on the single-particle basis chosen. The nonfactorization due to (anti)symmetrization is naturally excluded by using the (anti)symmetrized basis or, equivalently, the particle number representation. The natural degrees of freedom in quantifying the identical-particle entanglement in a chosen single-particle basis are occupation numbers of different single particle basis states. The entanglement between effectively distinguishable spins is shown to be a special case of the occupation-number entanglement.Comment: 5 pages, revtex4. A sentence is improve

A Pilot Study of Urokinase-Type Plasminogen Activator (uPA) Overexpression in the Brush Cytology of Patients with Malignant Pancreatic or Biliary Strictures

We have previously demonstrated that uPA is overexpressed in pancreatic tumors. In an attempt to diagnose these tumors earlier, we sought to determine whether uPA could be identified in endoscopic retrograde cholangiopancreatography obtained brushings in patients with malignant pancreatic and biliary strictures. Secondarily, uPA was measured in the serum of this patient population. uPA overexpression was identified in the cytologic tissue in 8 of 11 patients (72.7%). Serum analysis demonstrated a 2-fold higher concentration of uPA in the pancreaticobiliary cancer patients (1.27 versus 0.56 ng/mL; P = .0182). Also, uPA overexpression correlated with serum levels (P < .0001). This study confirms that uPA can be detected in the ERCP cytologically obtained tissue and is frequently present in a higher concentration in the serum of pancreaticobiliary cancer patients. A larger sample size will be required to address its value as a sensitive marker for the diagnosis of pancreatic or biliary cancers

Incidence, mechanism and prognostic value of activated AKT in pancreas cancer

When activated, the serine/threonine kinase AKT mediates an antiapoptotic signal implicated in chemoresistance of various cancers. The mechanism(s) of AKT activation are unknown, though overexpression of HER-2/neu has been implicated in breast cancer. Therefore, we determined the incidence of activated AKT in human pancreatic cancer, whether HER-2/neu is involved in AKT activation, and if AKT activation is associated with biologic behaviour. HER-2/neu expression and AKT activation were examined in seven pancreatic cancer cell lines by Western blotting. The in vitro effect of HER-2/neu inhibition on AKT activation was similarly determined. Finally, 78 pancreatic cancer specimens were examined for AKT activation and HER-2/neu overexpression, and correlated with the clinical prognostic variable of histologic grade. HER-2/neu was overexpressed in two of seven cell lines; these two cell lines demonstrated the highest level of AKT activation. Inhibition of HER-2/neu reduced AKT activation in vitro. AKT was activated in 46 out of 78 (59%) of the pancreatic cancers; HER-2/neu overexpression correlated with AKT activation (P=0.015). Furthermore, AKT activation was correlated with higher histologic tumour grade (P=0.047). Thus, it is concluded that AKT is frequently activated in pancreatic cancer; this antiapoptotic signal may be mediated by HER-2/neu overexpression. AKT activation is associated with tumour grade, an important prognostic factor

Epidermal growth factor induces HCCR expression via PI3K/Akt/mTOR signaling in PANC-1 pancreatic cancer cells

<p>Abstract</p> <p>Background</p> <p>Human cervical cancer oncoprotein 1 (HCCR-1), reported as a negative regulator of p53, is over-expressed in a variety of human cancers. However, it is yet unknown whether HCCR-1 plays any role in pancreatic cancer development. The aim of this study was to investigate the effect of epidermal growth factor on the expression of HCCR in pancreatic cancer cells, and to explore if PI3K/Akt/mTOR signaling pathway mediated this expression.</p> <p>Methods</p> <p>A polyclonal antibody against HCCR protein was raised by immunizing Balb/c mice with the purified recombinant protein pMBPc-HCCR. Tissue samples were constructed on a tissue chip, and the expression of HCCR was investigated by immunohistochemistry assay and Western blotting. Pancreatic cell line, PANC-1 cells were stably transfected with plasmids containing sense-HCCR-1 fragment and HCCR siRNA fragment. MTT and transwell assay were used to investigate the proliferation and invasion of stable tansfectants. The specific inhibitor of PI3K and mTOR was used to see if PI3K/mTOR signal transduction was involved in the induction of HCCR gene expression. A Luciferase assay was used to see if Akt can enhance the HCCR promoter activity.</p> <p>Results</p> <p>HCCR was up-regulated in pancreatic tumor tissues (mean Allred score 4.51 ± 1.549 <it>vs</it>. 2.87 ± 2.193, P < 0.01), especially with high expression in poorly differentiated pancreatic cancer. The growth of cells decreased in HCCR-1 siRNA transfected cells compared with vector transfectants. The number of invasion cells was significantly lower in HCCR-1 siRNA transfected cells (24.4 ± 9.9) than that in vector transfectants (49.1 ± 15.4). Treatment of PANC-1 cells with epidermal growth factor increased HCCR protein level in a dose- and time-dependent manner. However, application of LY294002 and rapamycin caused a dramatic reduction of epidermal growth factor-induced HCCR expression. Over-expression of exogenous constitutively active Akt increased the HCCR promoter activity; in contrast, dominant negative Akt decreased the promoter activity.</p> <p>Conclusions</p> <p>EGF-induced HCCR-1 over-expression is mediated by PI3K/AKT/mTOR signaling which plays a pivotal role in pancreatic tumor progression, suggesting that HCCR-1 could be a potential target for cancer therapeutics.</p

Serum CA 19-9 as a Marker of Resectability and Survival in Patients with Potentially Resectable Pancreatic Cancer Treated with Neoadjuvant Chemoradiation

Purpose The role of carbohydrate antigen (CA) 19-9 in the evaluation of patients with resectable pancreatic cancer treated with neoadjuvant therapy prior to planned surgical resection is unknown. We evaluated CA 19-9 as a marker of therapeutic response, completion of therapy, and survival in patients enrolled on two recently reported clinical trials. Patients and Methods We analyzed patients with radiographically resectable adenocarcinoma of the head/uncinate process treated on two phase II trials of neoadjuvant chemoradiation. Patients without evidence of disease progression following chemoradiation underwent pancreaticoduodenectomy (PD). CA 19-9 was evaluated in patients with a normal bilirubin level. Results We enrolled 174 patients, and 119 (68%) completed all therapy including PD. Pretreatment CA 19-9 <37 U/ml had a positive predictive value (PPV) for completing PD of 86% but a negative predictive value (NPV) of 33%. Among patients without evidence of disease at last follow-up, the highest pretreatment CA 19-9 was 1,125 U/ml. Restaging CA 19-9 <61 U/ml had a PPV of 93% and a NPV of 28% for completing PD among resectable patients. The area under the receiver-operating characteristics curve of pretreatment and restaging CA 19-9 levels for completing PD was 0.59 and 0.74, respectively. We identified no association between change in CA 19-9 and histopathologic response (P = 0.74). Conclusions Although the PPV of CA 19-9 for completing neoadjuvant therapy and undergoing PD was high, its clinical utility was compromised by a low NPV. Decision-making for patients with resectable PC should remain based on clinical assessment and radiographic staging.PublishedN/

Unified Semi-Classical Description of Intrinsic Spin-Hall Effect in Spintronic, Optical, and Graphene Systems

A semi-classical description of the intrinsic spin-Hall effect (SHE) is presented which is relevant for a wide class of systems. A heuristic model for the SHE is developed, starting with a fully quantum mechanical treatment, from which we construct an intuitive expression for the spin-Hall current and conductivity. Our method makes transparent the physical mechanism which drives the effect, and unifies the SHE across several spintronic and optical systems. Finally, we propose an analogous effect in bilayer graphene.Comment: 5 pages, 2 figures, 1 tabl

Targeting p110gamma in gastrointestinal cancers: attack on multiple fronts

Phosphoinositide 3-kinases (PI3Ks) regulate several cellular functions that are critical for cancer progression and development, including cell survival, proliferation and migration. Three classes of PI3Ks exist with the class I PI3K encompassing four isoforms of the catalytic subunit known as p110α, p110β, p110γ, and p110δ. Although for many years attention has been mainly focused on p110α recent evidence supports the conclusion that p110β, p110γ, and p110δ can also have a role in cancer. Amongst these, accumulating evidence now indicates that p110γ is involved in several cellular processes associated with cancer and indeed this specific isoform has emerged as a novel important player in cancer progression. Studies from our laboratory have identified a specific overexpression of p110γ in human pancreatic ductal adenocarcinoma (PDAC) and in hepatocellular carcinoma (HCC) tissues compared to their normal counterparts.Our data have further established that selective inhibition of p110γ is able to block PDAC and HCC cell proliferation, strongly suggesting that pharmacological inhibition of this enzyme can directly affect growth of these tumors. Furthermore, increasing evidence suggests that p110γ plays also a key role in the interactions between cancer cells and tumor microenvironment and in particular in tumor-associated immune response. It has also been reported that p110γ can regulate invasion of myeloid cells into tumors and tumor angiogenesis. Finally p110γ has also been directly involved in regulation of cancer cell migration. Taken together these data indicate that p110γ plays multiple roles in regulation of several processes that are critical for tumor progression and metastasis. This review will discuss the role of p110γ in gastrointestinal tumor development and progression and how targeting this enzyme might represent a way to target very aggressive tumors such as pancreatic and liver cancer on multiple fronts

Resveratrol Inhibits Growth of Orthotopic Pancreatic Tumors through Activation of FOXO Transcription Factors

BACKGROUND: The forkhead transcription factors of the O class (FOXO) play a direct role in cellular proliferation, oxidative stress response, and tumorigenesis. The objectives of this study were to examine whether FOXOs regulate antitumor activities of resveratrol in pancreatic cancer cells in vitro and in vivo. METHODOLOGY/PRINCIPAL FINDINGS: Pancreatic cancer cell lines were treated with resveratrol. Cell viability, colony formation, apoptosis and cell cycle were measured by XTT, soft agar, TUNEL and flow cytometry assays, respectively. FOXO nuclear translocation, DNA binding and transcriptional activities were measured by fluorescence technique, gelshift and luciferase assay, respectively. Mice were orthotopically implanted with PANC1 cells and orally gavaged with resveratrol. The components of PI3K and ERK pathways, FOXOs and their target gene expressions were measured by the Western blot analysis. Resveratrol inhibited cell viability and colony formations, and induced apoptosis through caspase-3 activation in four pancreatic cancer cell lines (PANC-1, MIA PaCa-2, Hs766T, and AsPC-1). Resveratrol induced cell cycle arrest by up-regulating the expression of p21/CIP1, p27/KIP1 and inhibiting the expression of cyclin D1. Resveratrol induced apoptosis by up-regulating Bim and activating caspase-3. Resveratrol inhibited phosphorylation of FOXOs, and enhanced their nuclear translocation, FOXO-DNA binding and transcriptional activities. The inhibition of PI3K/AKT and MEK/ERK pathways induced FOXO transcriptional activity and apoptosis. Furthermore, deletion of FOXO genes abrogated resveratrol-induced cell cycle arrest and apoptosis. Finally, resveratrol-treated mice showed significant inhibition in tumor growth which was associated with reduced phosphorylation of ERK, PI3K, AKT, FOXO1 and FOXO3a, and induction of apoptosis and FOXO target genes. CONCLUSIONS: These data suggest that inhibition of ERK and AKT pathways act together to activate FOXO transcription factors which are involved in resveratrol-mediated pancreatic tumor growth suppression