Implicit memory and consumer choice: the mediating role of brand familiarity

Two experiments investigated the influence of implicit memory on consumer choice for brands with varying levels of familiarity. Priming was measured using a consideration-choice task, developed by Coates, Butler and Berry (2004). Experiment 1 employed a coupon-rating task at encoding that required participants to meaningfully process individual brand names, to assess whether priming could affect participants' final (preferred) choices for familiar brands. Experiment 2 used this same method to assess the impact of implicit memory on consideration and choice for unknown and leader brands, presented in conjunction with familiar competitors. Significant priming was obtained in both experiments, and was shown to directly influence final choice in the case of familiar and highly familiar leader brands. Moreover, it was shown that a single prior exposure could lead participants to consider buying an unknown, and indeed fictitious, brand. Copyright (c) 2006 John Wiley & Sons, Ltd.

Putting the emotion back: exploring the role of emotion in disengagement

This chapter explores the nature of disengagement and the role played by emotions and in doing so will disentangle the overlapping theories and definitions of both engagement and disengagement. The research that forms the basis for the chapter comes from two related studies exploring engagement and disengagement in 10 large UK public and private sector organisations. Both studies used an interpretive approach involving 75 managers and employees. The chapter suggests the that emotions play a mediating role in the process of disengagement and the emotional reaction involved provides a distinction to being ‘not engaged’. It highlights the confusion that different approaches bring to distinguishing engagement and disengagement from other job attitudes.

Self-construals, Symbolic and Hedonic Preferences, and Actual Purchase Behavior

The study explores the influence of the independent and interdependent self-construals on actual purchase behavior and the mediating role of consumer preferences for symbolic and hedonic meanings. Data were collected through a survey of about 1,000 respondents. Results indicate that independent consumers draw on the self/hedonic- and status-symbolic resources of clothing in the construction and expression of their identities. Regarding the interdependent consumers, they show no interest in clothing affiliation and status symbolism. The degree of preference for status-symbolic meaning mediates all effects of the independent and interdependent self-construals on actual purchase behavior; self-expressive/hedonic preferences mediate two of the three effects of the independent self on actual purchase behavior when accounting for suppression effects, whereas the expected mediation of preference for affiliation meaning is not supported.

Toward a view of complementarity trust and policy influence effects of corporate social responsibility and corporate political activity

The extant literature argues that nonmarket strategies can establish, sustain, or enhance a firm’s competitive advantage. Less clear is how and why effective nonmarket strategies influence a firm’s competitiveness. Moreover, the extant literature tends to examine the two building blocks of nonmarket strategy—corporate social responsibility (CSR) and corporate political activity (CPA)—separately. In this article, we extend trust to the nonmarket environment. We analyze how CSR and CPA complement each other to create strong trust between firms and the polity, and how they consequently influence government policy. We show the mediating role of trust in policy influence, and argue that CSR and CPA should be aligned for the successful influence of salient government policy.

The role of voltage gated T-type Ca2+ channel isoforms in mediating "capacitative" Ca2+ entry in cancer cells

The mechanism by which Ca2+ enters electrically non-excitable cells is unclear. The sensitivity of the Ca2+ entry pathway in electrically non-excitable cells to inhibition by extracellular Ni2+ was used to direct the synthesis of a library of simple, novel compounds. These novel compounds inhibit Ca2+ entry into and, consequently, proliferation of several cancer cell lines. They showed stereoselective inhibition of proliferation and Ca2+ influx with identical stereoselective inhibition of heterologously expressed Cav3.2 isoform of T-type Ca2+ channels. Proliferation of human embryonic kidney (HEK)293 cells transfected with the Cav3.2 Ca2+ channel was also blocked. Cancer cell lines sensitive to our compounds express message for the Cav3.2 T-type Ca2+ channel isoform, its delta25B splice variant, or both, while a cell line resistant to our compounds does not. These observations raise the possibility that clinically useful drugs can be designed based upon the ability to block these Ca2+ channels.

The role of the melanocortin 3 receptor in mediating the effects of gamma-MSH peptides on the adrenal

The pro-opiomelanocortin (POMC)-derived peptides, pro-gamma-MSH (16K fragment), and Lys-gamma(3)-MSH, have been shown to potentiate the steroidogenic action of corticotrophin (ACTH) on the adrenal cortex. Using a continuously perfused adrenal cell column system, we have tested the hypothesis that gamma-MSH peptides exert their effect through the Melanocortin 3 Receptor (MC3-R), since this is the only known receptor to have high affinity for gamma-MSH peptides and has been suggested to be expressed in the rat adrenal. To investigate this hypothesis we tested whether the MC3-R agonist MTII and antagonist SHU9119 could mimic or block the actions of pro-gamma-MSH. We found that MTII could not mimic, and SHU9119 could not block pro-gamma-MSH mediated potentiation of ACTH-induced steroidogenesis. These results suggest that the MC3-R is not involved in mediating the potentiation effect, adding further evidence to the argument that another melanocortin receptor exists.

Role of Nrf2 in the regulation of CD36 and stress protein expression in murine macrophages - Activation by oxidatively modified LDL and 4-hydroxynonenal

CD36 is an important scavenger receptor mediating uptake of oxidized low- density lipoproteins ( oxLDLs) and plays a key role in foam cell formation and the pathogenesis of atherosclerosis. We report the first evidence that the transcription factor Nrf2 is expressed in vascular smooth muscle cells, and demonstrate that oxLDLs cause nuclear accumulation of Nrf2 in murine macrophages, resulting in the activation of genes encoding CD36 and the stress proteins A170, heme oxygenase- 1 ( HO- 1), and peroxiredoxin I ( Prx I). 4- Hydroxy- 2- nonenal ( HNE), derived from lipid peroxidation, was one of the most effective activators of Nrf2. Using Nrf2- deficient macrophages, we established that Nrf2 partially regulates CD36 expression in response to oxLDLs, HNE, or the electrophilic agent diethylmaleate. In murine aortic smooth muscle cells, expressing negligible levels of CD36, both moderately and highly oxidized LDL caused only limited Nrf2 translocation and negligible increases in A170, HO- 1, and Prx I expression. However, treatment of smooth muscle cells with HNE significantly enhanced nuclear accumulation of Nrf2 and increased A170, HO- 1, and Prx I protein levels. Because PPAR-gamma can be activated by oxLDLs and controls expression of CD36 in macrophages, our results implicate Nrf2 as a second important transcription factor involved in the induction of the scavenger receptor CD36 and antioxidant stress genes in atherosclerosis.

Oocyte-mediated suppression of follicle-stimulating hormone- and insulin-like growth factor-induced secretion of steroids and inhibin-related proteins by bovine granulosa cells in vitro: Possible role of transforming growth factor alpha

The objective was to investigate the potential role of the oocyte in modulating proliferation and basal, FSH-induced and insulin-like growth factor (IGF)-induced secretion of inhibin A (inh A), activin A (act A), follistatin (FS), estradiol (E-2), and progesterone (P-4) by mural bovine granulosa cells. Cells from 4- to 6-mm follicles were cultured in serum-free medium containing insulin and androstenedione, and the effects of ovine FSH and IGF analogue (LR3-IGF-1) were tested alone and in the presence of denuded bovine oocytes (2, 8, or 20 per well). Medium was changed every 48 h, cultures were terminated after 144 h, and viable cell number was determined. Results are based on combined data from four independent cultures and are presented for the last time period only when responses were maximal. Both FSH and IGF increased (P < 0.001) secretion of inh A, act A, FS, E-2, and P-4 and raised cell number. In the absence of FSH or IGF, coculture with oocytes had no effect on any of the measured hormones, although cell number was increased up to 1.8-fold (P < 0.0001). Addition of oocytes to FSH-stimulated cells dose-dependently suppressed (P < 0.0001) inh A (6-fold maximum suppression), act A (5.5-fold), FS (3.6-fold), E-2 (4.6-fold), and P-4 (2.4-fold), with suppression increasing with FSH dose. Likewise, oocytes suppressed (P < 0.001) IGF-induced secretion of inh A, act A, FS, and E-2 (P < 0.05) but enhanced IGF-induced P-4 secretion (1.7-fold; P < 0.05). Given the similarity of these oocyte-mediated actions to those we observed previously following epidermal growth factor (EGF) treatment, we used immunocytochemistry to determine whether bovine oocytes express EGF or transforming growth factor (TGF) alpha. Intense staining with TGFalpha antibody (but not with EGF antibody) was detected in oocytes both before and after coculture. Experiments involving addition of TGFalpha to granulosa cells confirmed that the peptide mimicked the effects of oocytes on cell proliferation and on FSH- and IGF-induced hormone secretion. These experiments indicate that bovine oocytes secrete a factor(s) capable of modulating granulosa cell proliferation and responsiveness to FSH and IGF in terms of steroidogenesis and production of inhibin-related peptides, bovine oocytes express TGFalpha but not EGF, and TGFalpha is a prime candidate for mediating the actions of oocytes on bovine granulosa cells.

Physiological mechanisms mediating aspartame-induced satiety

Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid + 224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to cat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r = -.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite. (C) 2003 Elsevier Science Inc. All rights reserved.

The AcrAB-TolC efflux system of Salmonella enterica serovar Typhimurium plays a role in pathogenesis

The ability of an isogenic set of mutants of Salmonella enterica serovar Typhimurium L354 (SL1344) with defined deletions in genes encoding components of tripartite efflux pumps, including acrB, acrD, acrF and tolC, to colonize chickens was determined in competition with L354. In addition, the ability of L354 and each mutant to adhere to, and invade, human embryonic intestine cells and mouse monocyte macrophages was determined in vitro. The tolC and acrB knockout mutants were hyper-susceptible to a range of antibiotics, dyes and detergents; the tolC mutant was also more susceptible to acid pH and bile and grew more slowly than L354. Complementation of either gene ablated the phenotype. The tolC mutant poorly adhered to both cell types in vitro and was unable to invade macrophages. The acrB mutant adhered, but did not invade macrophages. In vivo, both the acrB mutant and the tolC mutant colonized poorly and did not persist in the avian gut, whereas the acrD and acrF mutant colonized and persisted as well as L354. These data indicate that the AcrAB-TolC system is important for the colonization of chickens by S. Typhimurium and that this system has a role in mediating adherence and uptake into target host cells.

The role of dust in climate changes today, at the last glacial maximum and in the future.

Natural mineral aerosol (dust) is an active component of the climate system and plays multiple roles in mediating physical and biogeochemical exchanges between the atmosphere, land surface and ocean. Changes in the amount of dust in the atmosphere are caused both by changes in climate (precipitation, wind strength, regional moisture balance) and changes in the extent of dust sources caused by either anthropogenic or climatically induced changes in vegetation cover. Models of the global dust cycle take into account the physical controls on dust deflation from prescribed source areas (based largely on soil wetness and vegetation cover thresholds), dust transport within the atmospheric column, and dust deposition through sedimentation and scavenging by precipitation. These models successfully reproduce the first-order spatial and temporal patterns in atmospheric dust loading under modern conditions. Atmospheric dust loading was as much as an order-of-magnitude larger than today during the last glacial maximum (LGM). While the observed increase in emissions from northern Africa can be explained solely in terms of climate changes (colder, drier and windier glacial climates), increased emissions from other regions appear to have been largely a response to climatically induced changes in vegetation cover and hence in the extent of dust source areas. Model experiments suggest that the increased dust loading in tropical regions had an effect on radiative forcing comparable to that of low glacial CO2 levels. Changes in land-use are already increasing the dust loading of the atmosphere. However, simulations show that anthropogenically forced climate changes substantially reduce the extent and productivity of natural dust sources. Positive feedbacks initiated by a reduction of dust emissions from natural source areas on both radiative forcing and atmospheric CO2 could substantially mitigate the impacts of land-use changes, and need to be considered in climate change assessments.

The power of perceptions: exploring the role of urban design in cycling behaviours and healthy ageing

Good urban design has the power to aid in the provision of inclusive journey environments, yet traditionally neglects the perspective of the cyclist. This paper starts from the premise that more can be done to understand and articulate cyclists’ experiences and perceptions of the urban environment in which they cycle, as part of a closer linking of urban design qualities with transport planning and infrastructure interventions. This approach is particularly applicable in relation to older cyclists, a group whose needs are often poorly understood and for whom perceptions can significantly influence mobile behaviours. Currently, knowledge regarding the relationship between the built environment and physical activity, including cycling, in older adults is limited. As European countries face up to the challenges associated with ageing populations, some metropolitan regions, such as Munich, Germany, are making inroads into widening cycling’s appeal across generations through a combination of urban design, policy and infrastructure initiatives. The paper provides a systematic understanding of the urban design qualities and built environment features that affect cycling participation and have the potential to contribute towards healthy ageing. Urban design features such as legibility, aesthetics, scale and open space have been shown to influence and affect other mobile behaviours (e.g. walking), but their role as a mediator in cycle behaviour remains under-explored. Many of these design ‘qualities’ are related to individual perceptions; capturing these can help build a picture of quality in the built environment that includes an individual’s relationship with their local neighbourhood and its influences on their mobility choices. Issues of accessibility, facilities, and safety in cycling remain crucial, and, when allied to these design ‘qualities‘, provides a more rounded reflection of everyday journeys and trips taken or desired. The paper sets out the role that urban design might play in mediating these critical mobility issues, and in particular, in better understanding the ‘quality of the journey’. It concludes by highlighting the need for designers, policy makers, planners and academics to consider the role that design can play in encouraging cycle participation, especially as part of a healthy ageing agenda.

A role for adhesion and degranulation-promoting adapter protein in collagen-induced platelet activation mediated via integrin α(2) β(1)

Platelet aggregation and phosphorylation of phospholipase Cγ2 induced by collagen were attenuated in ADAP(-/-) platelets. However, aggregation and signaling induced by collagen-related peptide (CRP), a GPVI-selective agonist, were largely unaffected. Platelet adhesion to CRP was also unaffected by ADAP deficiency. Adhesion to the α(2) β(1) -selective ligand GFOGER and to a peptide (III-04), which supports adhesion that is dependent on both GPVI and α(2) β(1), was reduced in ADAP(-/-) platelets. An impedance-based label-free detection technique, which measures adhesion and spreading of platelets, indicated that, in the absence of ADAP, spreading on GFOGER was also reduced. This was confirmed with non-fluorescent differential-interference contrast microscopy, which revealed reduced filpodia formation in ADAP(-/-) platelets adherent to GFOGER. This indicates that ADAP plays a role in mediating platelet activation via the collagen-binding integrin α(2) β(1). In addition, we found that ADAP(-/-) mice, which are mildly thrombocytopenic, have enlarged spleens as compared with wild-type animals. This may reflect increased removal of platelets from the circulation.