874 resultados para Impact on R
Resumo:
"GAO-04-758."
Resumo:
At head of title: 93d Congress, 1st session. Committee print.
Resumo:
Distributed to some depository libraries in microfiche.
Resumo:
Includes bibliographical references (p. 24).
Resumo:
"September 1990."
Resumo:
"December 1979."
Resumo:
Event Marketing represents a common promotional strategy that involves direct contact between brands and consumers at special events, namely concerts, festivals, sporting events and fairs. Brands have been investing in sponsorship as a means of associating themselves with particular events, essentially with the goal to enhance brand image and brand awareness. Interestingly, the response of consumers to event marketing has not yet been fully understood. This dissertation fills this gap. More specifically, it intends to determine the extent to which sponsoring brands at events favors brand awareness (recall and recognition) and how it relates to brand attitude. Based on three Portuguese music festivals, two studies were conducted to ascertain event sponsorship’s impact on consumer memory, notably Brand Recall and Brand Recognition, and correlation with attitudes towards the brands such as familiarity and liking. The key findings of these studies show that recognition is much higher for those respondents who attended the festivals, presenting a score of 73,9%, in comparison with recall, presenting a much lower score of 37,5%. Further, and surprisingly, it suggests that the ability to recall and recognize sponsoring brands is not associated to consumer attitudes towards the brands. Instead, it relates to the time consumers dedicated to these particular events, that is, the number of music festivals attended.
Resumo:
The GH receptor (GHR) mediates metabolic and somatogenic actions of GH. Its extracellular domain (ECD; residues 1-246) has two subdomains, each with seven beta strands organized into two antiparallel beta sheets, connected by a short hinge region. Most of the ECD residues involved in GH binding reside in subdomain 1, whereas subdomain 2 harbors a dimerization interface between GHR dimers that alters conformation in response to GH. A regulated GHR metalloprotease cleavage site is in the membrane-proximal stem region of subdomain 2. We have identified a monoclonal anti-ECD antibody, anti-GHR(ext-mAb), which recognizes the rabbit and human GHRs by immunoprecipitation, but less so after GH treatment. By immunoblotting and immunoprecipitation, anti-GHR(ext-mAb) recognized a glutathione-S-transferase (GST) fusion incorporating subdomain 2, but not one including subdomain 1. In transient transfection experiments, anti-GHR(ext-mAb) failed to recognize by immunoprecipitation a previously characterized dimerization interface mutant GHR that is incompetent for signaling. In signaling experiments, brief pretreatment of GH-responsive human fibrosarcoma cells with anti-GHR(ext-mAb) dramatically inhibited GH-induced Janus kinase 2 and signal transducer and activator of transcription 5 tyrosine phosphorylation and prevented GH-induced GHR disulfide linkage (a reflection of GH-induced conformational changes). In contrast, anti-GHR(ext-mAb) only partially inhibited radiolabeled GH binding, suggesting its effects on signaling were not simply via inhibition of binding. Furthermore, anti-GHR(ext-mAb) prevented phorbol ester-stimulated GHR proteolysis, but GHR cleavage site mutants were normally recognized by the antibody, indicating that the stem region cleavage site is not a direct epitope. A Fab fragment of anti-GHR(ext-mAb) inhibited GH-induced GHR disulfide linkage and signaling, as well as phorbol ester-induced GHR proteolysis, in a fashion similar to the intact antibody. Thus, our findings suggest that anti-GHR(ext-mAb) has promise as a GH antagonist and as a tool in studies of conformational changes required for GHR activation.
Resumo:
Inorganic arsenic compounds are known carcinogens. The human epidemiologic evidence of arsenic-induced skin, lung, and bladder cancers is strong. However, the evidence of arsenic carcinogenicity in animals is very limited. Lack of a suitable animal model until recent years has inhibited studies of the mechanism of arsenic carcinogenesis. The toxicity and bioavailability of arsenic depend on its solubility and chemical forms. Therefore, it is critical to be able to measure arsenic speciation accurately and reliably. However, speciation of arsenic in more complex matrices remains a real challenge. There are tens of millions of people who are being exposed to excessive levels of arsenic in the drinking water alone. The source of contamination is mainly of natural origin and the mass poisoning is occurring worldwide, particularly in developing countries. Chronic arsenicosis resulting in cancer and non-cancer diseases will impact significantly on the public health systems in their respective countries. Effective watershed management and remediation technologies in addition to medical treatment are urgently needed in order to avoid what has been regarded as the largest calamity of chemical poisoning in the world.