Biomedicine on Display

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“Why Proteins Have to Die So That We May Live”. This was the title of the talk given by Nobel Laureate Dr. Aaron Ciechanover at the international symposium entitled Protein Chemistry: Applications to Combat Diseases held at the University of Copenhagen earlier this week. Three days packed with talks from the world’s leading protein chemists and researchers. The focus of the conference was the life of proteins from their synthesis to their degradation. This was highlighted by talks from three Nobel Prize laureates: Ada Yonath, Avram Hersko and Aaron Chiechanover – each of whom have contributed immensely to our understanding of these processes.

The symposium featured talks from invited speakers only, and as such the quality of the talks reflected this in being very high. The papers presented were mostly already published, but some did include unpublished data (although I’m sure these were already on their way to being submitted). Each speaker was given twenty-five minutes to present their papers, and unfortunately due to a complete lack of control by the chairs, this was exceeded over and over again. Annoying. Not only are breaks important when you sit through three hours of talks, they are also where a lot of the magic happens! They must be respected and cherished! Thumbs down, organizers!

The conference format for communicating science is interesting. It takes the researchers out of their daily routines (well, more or less), and to some extent forces them to listen in on subjects that they otherwise wouldn’t have paid the slightest attention. This is good. Even the most experienced researchers cannot keep up with all the data being published. Meeting colleagues in an informal setting and discussing work over food and wine also works great. It’s brilliant for networking! However, this must happen organically and cannot be forced. The organizers attempted to schedule informal meetings betweens speakers and audience during breaks (“science dating”), but I think that defies the point of informality. In this case, a lot of empty slots emphasized this. Or maybe it was just the lack of breaks?

What about social media? I’ve been going to a number of medical conferences over the past few years, and to be honest I haven’t really noticed anyone actively using it. My first conference in the museum world was very different. Granted, it was a conference about the web, but everyone was tweeting throughout the entire event. Online forums were being used actively for discussions. And (of course) all information about the conference was available online. Including all abstracts. This is very far from the case at medical meetings I’ve attended. Where the rest of the world is moving towards Web 3.0, they remain an early beta. And this is sad. It seems there is too much focus on controlling information rather than letting it flow free. Sharing. Engaging. Not only for the benefit of the meeting attendees, but perhaps also the rest of the world? Am I being naïve?

A lot of scientific and non-scientific discoveries are known to have been done by chance or even accident. We all know the story of how Alexander Fleming accidentally discovered penicillin when one of his staph bacteria cultures got infected by a fungus. Another example that might not be as well-known is sildenafil, also known as Viagra. Originally developed to treat high blood pressure and angina (chest pains), this drug was quickly discovered to have other more “exciting” uses. Teflon, microwave ovens and LSD are other examples of common-day (well, for some anyway) appliances that were discovered by accident.

Science by chance happens all the time. Researchers looking for answers to one question find themselves answering another. Last week, I went to a seminar entitled “The role of actin cytoskeleton in glucose metabolism and the accumulation of fat” by Professor Peter Gunning from the University of New South Wales in Australia. He is the head of the Oncology Research Unit at the School of Medical Sciences and an expert on the protein tropomyosin (list of publications). Alongside the proteins actin and myosin, these are responsible for the contractile activity of muscle cells. But they also have functions in virtually all other cells in regulating cell structure, motility, division, adhesion and even signaling.

In searching for proteins that could be targeted in cancer treatment, they happened to discover that when mice were genetically engineered to overexpress a specific protein they had visibly increased fat mass in certain areas of the body. Similarly, when the same gene was knocked out (eliminated), the same areas of fat were smaller. Interestingly, and also rather counter-intuitively, the same overexpressing mice showed an increased glucose tolerance and insulin sensitivity – parameters that are usually impaired in association with type 2 diabetes. Thus while the mice had more fat and therefore supposed to be more likely to develop type 2 diabetes, these mice showed quite the opposite. So, while looking for cancer target genes, they accidentally came across some very interesting findings that might prove important in a completely different area of research!

I wonder how often such discoveries are made – and do researchers always take the time to share findings that aren’t necessary relevant to their own work? I certainly hope so!