April 2, 2012
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Last year, my research into the mechanisms of breast cancer development hit a roadblock. As a postdoctoral candidate at the University of Miami, I needed to conduct immunology experiments outside my expertise, but had difficulty finding potential collaborators or providers to work with. There was simply no efficient way to access specialist services, compare pricing across laboratories, or exchange payment across institutions.
Such inefficiencies were by no means unique to me, but represented an emerging impediment to the progress of scientific research. I realized that we now live in an increasingly specialized world, where no scientist can be an expert in all fields. There was no medium to fill gaps in expertise, few mechanisms to transfer expert information, and even fewer platforms sufficient for exchanging services. Whether its basic research or translational work, it was now clear to me that research institutions have become closed ecosystems, with siloed laboratories and opaque mediums of exchange. The current system of scientific collaboration, as it stood, needed to be changed.
Thankfully, I’ve had the honor of interacting with several ventures and initiatives to lead a movement in changing this dynamic.
Startups in Silicon Valley are providing the infrastructural change needed to improve scientific collaboration. Ventures like Academia.edu have established social platforms for researchers to connect and exchange academic papers online. Organizations like Breakout Labs are providing early-stage non-dilutive funding for radical scientific ideas. And Science Exchange, a startup I co-founded last year, is helping researchers collaborate across institutions, and exchange services over a transparent marketplace.
Such organizations lay the groundwork to accelerate scientific research. They create a dynamic that helps fill gaps in expertise, and efficiently exchange services as needed. Sustainable change and adoption of such platforms however, must now emerge from the bottom-up: from the students, postdocs, and professors themselves.
Recognizing this, Science Exchange has recently received backing from nonprofits like the Kauffman Foundation, and venture capital groups including Y Combinator and Andreessen Horowitz, to launch the Science Advocates initiative.
Science Advocates will be ambassadors for open innovation and efficiency in science. Science needs leaders in the academic community to work within their institutions, helping to push for infrastructural change in scientific processes. Whether its through peer communications, seminars, or conferences, Science Advocates will be at the forefront of the changing pace of scientific research, working within their institutions to improve access to shared resources, and open science platforms.
Together, I believe we can initiate a movement to fundamentally transform the way science is conducted, and the pace at which research is produced.
Interested in becoming a Science Advocate? Check out www.scienceexchange.com/advocates for more info.
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Good idea.
I could point some mechanisms in academia which produce narrow specialists and make people unwilling to cooperate. But they are quite well known.
Link to thisCancer research should be more focused to cancer metabolism, as underlined also by James D. Watson (Nobel Prize) on NYT (“we may have to turn our main research focus away from decoding the genetic instructions behind cancer and toward understanding the chemical reactions within cancer cells.” (http://www.nytimes.com/2009/08/06/opinion/06watson.html?pagewanted=all)) and “Science” (http://sciencecareers.sciencemag.org/career_magazine/previous_issues/articles/2011_03_25/science.opms.r1100102). For example, DCA (dichloroacetate) was discovered on 2007 to cause apoptosis in some cancer cells (http://www.sciencedirect.com/science/article/pii/S1535610806003722#sec1) but who is studying the four PDK isoenzymes and where?: “Thus, although DCA inhibits growth of a variety of cancer cells, the effect and the underlying mechanisms seem to be cell-type dependent. A likely explanation for these differential effects could be the difference in expression of the PDK isoenzymes in the cancer cells examined. Dichloroacetate is a non-specific inhibitor of PDK (Whitehouse and Randle, 1973), and has a different Ki for each of the four PDK isoenzymes (Bowker-Kinley et al, 1998). In addition, the four PDK isoenzymes are known to be differentially expressed in various tissues. Thus, there is a need to develop inhibitors to the individual PDK isoenzymes that should allow cancer cell-type-specific metabolic manipulation.”
(Dichloroacetate induces apoptosis and cell-cycle arrest in colorectal cancer cells. , http://www.nature.com/bjc/journal/v102/n12/full/6605701a.html)
Thanks
Link to thisDanilo