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When I was in grad school I was doing graph theoretic analysis of human metabolic networks. I had some really interesting and promising preliminary results about the structure of various metabolic pathways and had been invited to present my unpublished work in a multi-departmental lecture. I was making some new visualizations for my talk and spotted something odd, which led me to a bug in my source code that had reversed the direction of several steps in many of the pathways. I was mortified . . . I ran some preliminary tests on the corrected code and saw that many of my results were completely in error. I wouldn't know for sure until I could get several days of cluster time, but I had proof that my last year of work was completely bogus.

I stayed up all night confirming the new code and the extent of my invalidated results and brought this to my advisor the morning before the lecture. He told me to shut up and present it anyways. Being a young idealist I argued with him about the nature of science and the search for truth . . . I refused to go along with it and present something I knew was false. He made one of the research scientists present on their topic at the last second so our lab wouldn't "lose face" and I was pretty much in the dog house forever after.



From someone with no connection to analysis of human metabolic networks (besides having one, I guess): Thank you!


You might not know it sir. But you are a hero. Definitely my hero! Not all heroes wear capes.

This is how Science should be done.


Thank you.


Graph theoretical analysis of human metabolic networks sounds very interesting, can you elaborate on that and/or point to a few papers?


Papers, not really since I was out on the edge at the time and I haven't caught up with the field since then. Nothing I did ever made it into publication but it was pretty interesting. Mostly was focusing on the redundant connectivity of various metabolic pathways in healthy human cell lines and comparing them to the reduced pathways in cancer cells where mutations and large scale chromosomal loss restricted the ability to process and regulate several key compounds. The general idea was to look for pathways that were nearly always preserved even when cancer cells were extremely evolved/mutated from their original lines and map those to drugs that would target the enzymes mediating those reactions. Basically you'd try and knock out a weak link in the cancer metabolic network for which a healthy cell had significant redundancies.

A major conceptual difficulty was the somewhat nebulous definition of a metabolic pathway, beyond what reactions were drawn together in a textbook diagram. Also somewhat thorny was the concept of building a network with any sort of transitive property with a notion of mass conservation built in. I wrote about 30k lines of terrible Perl code exploring this stuff, if I had independent backing I would definitely dust it off and finish the project but it's pretty far in the rearview mirror at this point.




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