VIRGINIA MILLEN, SWINBURNE UNIVERSITY VENTURE MAGAZINE |
How do you decide which running shoes to buy? Why do you prefer the iPhone over all other smart phones? Why did smokers crave a cigarette after watching an ad designed to turn people off smoking, while non-smokers were disgusted by it? These are the questions advertisers, marketers and market researchers are constantly faced with and Swinburne Neuroscience Professor Richard Silberstein has some of the answers.
Neuromarketing or consumer neuroscience is a relatively new area of research that combines neuroscience with market research. It uses brain-measuring technology to find out what consumers really think of advertising. Until recently, market research companies had access to limited methods to assess the effectiveness of an ad. According to Professor Silberstein, these methods rely on assessment using the right hemisphere of the brain, which focuses on details and specifics, to explain why we did or didn’t like an ad. “Basically, the current research tools that people are using for market research are good for fact-based ads, but they are no good for advertising that is more creative and emotional, which we are getting more and more of,” he says. “More and more advertising is directed at emotion. People are very poorly aware of their emotional processes and it’s even harder to vocalise or express them.” Brain-measuring technology Research is proving that emotions are the most powerful drivers of our decision-making. But there’s another reason why advertising is working to appeal to our emotions. And that is due to heavy competition between brands that have little to set them apart, except for our emotional connection to them. Take a tube of toothpaste, for example. Why do some people buy Colgate Total White Stripe over Macleans Ultimate White Ice Sensation? Professor Silberstein explains we make these decisions based on emotion, not fact. It is important to note, however, that there are some cases when rational processes come in to play. People will often choose a home loan, for example, based on the lowest interest rate a bank can offer. Professor Silberstein’s company Neuro-Insight uses a technology invented at Swinburne called Steady State Topography (SST) to measure the effectiveness of a piece of commercial communication by tracking rapid changes in the speed of neural processing in different parts of the brain. “When a part of the brain becomes more active it tends to process neural information faster. SST is probably the only technology that can measure that particular feature of brain response,” he says. “The right hemisphere of our brain is concerned with imagery, but also with the emotional connection and that’s the one that’s hard to get at by using traditional market research methodologies.” SST can measure if an ad is being stored in our long-term memories – probably the most important aspect of judging whether an ad is effective or not. “One of our measures for advertising effectiveness is if there is a high level of memory encoding during either the key message of the ad or during the branding of the ad,” says Professor Silberstein. The company can also measure whether the subject likes or dislikes something, their engagement with the ad, and emotional intensity experienced while watching an ad. “When you put all of that together we can give a profile of psychological processes and we can see how they change on a second-by-second basis. “We can give an insight into the mind and emotions of the people a company is trying to communicate with. We can tell not what are people thinking, but how people are thinking,” says Professor Silberstein. Your decision-making personality Swinburne’s Dr Joseph Ciorciari has been working in the same area, but specialises in how the biology of personality and thinking style impact decision-making. Through their joint research, Dr Ciorciari and Dr John Gountas, from Murdoch University, recently found that there is a neurobiological validation for the four broad personality types Dr Gountas believes each of us lean towards when making decisions. These four personality types are logical, pragmatic, emotional and imaginative. “When we make a decision we have a dominant personality [thinking style] and we may shift to another depending on the impact our environment is having on us,” says Dr Ciorciari, a senior lecturer who has taught in the biomedical sciences, biomedical engineering and psychophysiology undergraduate, honours and postgraduate programs, and is the program coordinator for the undergraduate psychology/psychophysiology course at Swinburne. Targeted advertising Examining consumer behaviour through the prism of these personality types allows marketers to better target advertising. Dr Ciorciari and Dr Gountas have done studies on advertisements designed to curb the road toll. “We did a couple of studies on young men watching these ads, using an EEG technique called LORETA, which looks at the source of where the electrical activity is emanating from the brain. It gives you a better estimation of which region is involved in decision-making,” says Dr Ciorciari. The research showed that certain ads caused young men to completely switch off. “The ads had absolutely no impact. We didn’t find memory systems activating. We saw systems working because they were watching, but the information wasn’t getting in.” However, one ad shown to the men took a completely different approach. “It pulled on the heart strings, it gave the young men who were watching it an opportunity to see the suffering of those who were left behind. It was extremely effective,” says Dr Ciorciari. The ability of consumer neuroscience to determine whether an ad is effective is the reason more corporations, including Google, Coca-Cola and General Motors are using it to influence consumer attitudes. “If you want to put together a better ad, you can work out where the negative bits are, based on neuroscience. You can then better construct the ad to help maintain attention, to make it more effective,” says Dr Ciorciari. This technology and research is illuminating the human mind and our decision-making processes. It offers insight into the most effective ways companies can communicate with us and helps scientists and advertisers to understand what resonates, and therefore what is most powerful. It is shaping advertising.
Editor's Note: Original story from Swinburne's Venture magazine can be found here.
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ScienceDaily — Behaving something like ravenous monsters, tumors need plentiful supplies of cellular building blocks such as amino acids and nucleotides in order to keep growing at a rapid pace and survive under harsh conditions. How such tumors meet these burgeoning demands has not been fully understood. Now chemists at the California Institute of Technology (Caltech) have shown for the first time that a specific sugar, known as GlcNAc ("glick-nack"), plays a key role in keeping the cancerous monsters "fed." The finding suggests new potential targets for therapeutic intervention.
The new results appear in this week's issue of the journal Science.
The research team -- led by Linda Hsieh-Wilson, professor of chemistry at Caltech -- found that tumor cells alter glycosylation, the addition of carbohydrates (in this case GlcNAc) to their proteins, in response to their surroundings. This ultimately helps the cancerous cells survive. When the scientists blocked the addition of GlcNAc to a particular protein in mice, tumor-cell growth was impaired.
The researchers used chemical tools and molecular modeling techniques developed in their laboratory to determine that GlcNAc inhibits a step in glycolysis (not to be confused with glycosylation), a metabolic pathway that involves 10 enzyme-driven steps. In normal cells, glycolysis is a central process that produces high-energy compounds that the cell needs to do work. But Hsieh-Wilson's team found that when GlcNAc attaches to the enzyme phosphofructokinase 1 (PFK1), it suppresses glycolysis at an early phase and reroutes the products of previous steps into a different pathway -- one that yields the nucleotides a tumor needs to grow, as well as molecules that protect tumor cells. So GlcNAc causes tumor cells to make a trade -- they produce fewer high-energy compounds in order to get the products they need to grow and survive.
"We have identified a novel molecular mechanism that cancer cells have co-opted in order to produce intermediates that allow them to grow more rapidly and to help them combat oxidative stress," says Hsieh-Wilson, who is also an investigator with the Howard Hughes Medical Institute.
This is not the first time scientists have identified a mechanism by which tumor cells might produce the intermediates they need to survive. But most other mechanisms have involved genetic alterations, or mutations -- permanent changes that lead to less active forms of enzymes, for example. "What's unique here is that the addition of GlcNAc is dynamic and reversible," says Hsieh-Wilson. "This allows a cancer cell to more rapidly alter its metabolism depending on the environment that it encounters."
In their studies, Hsieh-Wilson's team found that this glycosylation -- the addition of GlcNAc to PFK1 -- is enhanced under conditions associated with tumors, such as low oxygen levels. They also found that glycosylation of PFK1 was sensitive to the availability of nutrients. If certain nutrients were absent, glycosylation was increased, and the tumor was able to compensate for the dearth of nutrients by changing the cell's metabolism.
When the researchers analyzed human breast and lung tumor tissues, they found GlcNAc-related glycosylation was elevated two- to fourfold in the majority of tumors relative to normal tissue from the same patients. Then, working with mice injected with human lung-cancer cells, the researchers replaced the existing PFK1 enzymes with either the normal PFK1 enzyme or a mutant form that could no longer be glycosylated. The mice with the mutant form of PFK1 showed decreased tumor growth, demonstrating that blocking glycosylation impairs cancerous growth.
The work suggests at least two possible avenues for future investigations into fighting cancer. One would be to develop compounds that prevent PFK1 from becoming glycosylated, similar to the mutant PFK1 enzymes in the present study. The other would be to activate PFK1 enzymes in order to keep glycolysis operating normally and help prevent cancer cells from altering their cellular metabolism in favor of cancerous growth.
Hsieh-Wilson's group has previously studied GlcNAc-related glycosylation in the brain. They have demonstrated, for example, that the addition of GlcNAc to a protein called CREB inhibits the protein's ability to turn on genes needed for long-term memory storage. On the other hand, they have also shown that having significantly lower levels of GlcNAc in the forebrain leads to neurodegeneration. "The current thinking is that there's a balance between too little and too much glycosylation," says Hsieh-Wilson. "Being at either extreme make things go awry, whether it's in the brain or in the case of cancer cells."
Additional Caltech coauthors on the paper, "Phosphofructokinase 1 Glycosylation Regulates Cell Growth and Metabolism," were lead author Wen Yi, a postdoctoral scholar in Hsieh-Wilson's group; Peter Clark, a former graduate student in Hsieh-Wilson's group; and William Goddard III, the Charles and Mary Ferkel Professor of Chemistry, Materials Science, and Applied Physics. Daniel Mason and Eric Peters of the Genomics Institute of the Novartis Research Foundation and Marie Keenan, Collin Hill, and Edward Driggers of Agios Pharmaceuticals were also coauthors.
The work was supported by the National Institutes of Health, the Department of Defense Breast Cancer Research Program, and a Tobacco-Related Disease Research Program postdoctoral fellowship.