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OVER 30000000099999991829127839193847 VISITORS

Hi welcome to my page. Imagine some early 2000's era MIDI files playing while you browse my discussion questions below:

  • Maureen 19:26, 11 October 2017 (PDT) Can I also play Curtis Mayfield while browsing :)?
  • PosertInLab (talk) 15:32, 17 October 2017 (PDT): Of course!
This is my perfect angel cat, Nooch.
Here is another picture

Questions for Oct-5-2017:

  • How much should we focus on early detection, based on both this article and other research showing that early detection doesn't improve ultimate outcomes?
  • What further studies would you recommend?
  • How important is the exact number for replicative error attribution? At what point does this source of mutation justify funding and research?
  • In the 2017 paper, the authors present data that is devoid of reliance on knowledge of stem cell division rates (e.g., pancreatic ductal adenocarcinomas). How convincing do you find these thought experiments? Relative to the meta-analysis presented in the 2015 paper?
  • The models presented in both papers assume a large degree of homogeneity in cancer. Is there a way to incorporate the diversity of different cancers into the model?
  • Stem cell self-renewal is genetically controlled, and trauma can require expansion of cell populations. Can we truly separate out R from G and E?
  • If early detection doesn't improve prognosis, how should we change the way we think about cancer in light of this stochastic model? Should we?

Questions for Oct-12-2017:

  • Structural biochemistry has been pretty good about setting up identifiers for structures (PDB and EMDB IDs). But if PDB went down, we would be stuck relying on other archiving systems for genes, RNAs, or ORFs. How many layers of meta-archiving strike a good balance between reliability and efficient use of resources?
  • Ultimately, even "persistent" identifiers rely on funding for resolvers and database maintenance. Especially if journals rely more and more on these online, how can we future-proof for when funding inevitable runs out?
  • Even companies with archival plans can disappear ("no plan survives contact with the enemy"). Now that storage is cheap, should funding sources require longer local storage?

Questions for Oct-20-2017:

  • Confused about how these 2-D plots work? Figure 1 in this paper is useful, but basically they separate by mass on one axis and by topology on the other axis. You probe topology wth EtBr.
  • Why should we study telomeres? Do you believe the telomere aging hypothesis? And, if so, what can we do to lengthen our telomeres?
  • The proposed mechanism and regulation of TZAP is very cool. What further experiments would you do to test this hypothesis?

Questions for Oct-24-2017:

  • Don't forget that Drosophila don't have telomeres: TRF2 here is a TBP paralogue, not a shelterin protein!
  • I think it's really interesting that moonshiner is only active in the ovaries. Do you think this is an adaptation to protect the germline from deleterious changes, but keep the mutation rate high in the soma?
  • What evolutionary reason could there be for having several different forms of piRNA regulation in Drosophila?

Questions for Nov-9-2017:

  • At what resolution and quality does a simulation of TADs become clinically useful? The broad strokes are replicated here, but the fine details are missing. Yet, they seem pretty happy with the results.
  • What on earth do these multi-dimensional tensors tell us?
  • How could you further interrogate the rates of loop extrusion? This is an interesting gap in their model.

Questions for Nov-16-2017:

  • HSP90 buffers only specific proteins. Is there any way to confer this buffering property on proteins that are not canonically part of this?
  • Have there been any studies about what inhibition of HSP90 does to cells or organisms? I would expect that removing a misfolded protein buffer could be fine or horrible, depending on the proteins and cell.
  • This study presents an interesting global effect of mutations even in seemingly unrelated genes. If general HSP90 load is important in phenotype, then you could imagine two wildly different mutations which both rely on HSP90 for proper folding could have a multiplicative effect.

Questions for Nov-28-2017:

  • How do they measure CDK2 activity? I can only find methods for live-cell imaging and coupling of cyclins and other genes to fluorescence through IRES fluorophores in the same ORF, but no mention of an actual activity assay. Single-cell activity data seem non-trivial to come by.
  • Figure 3e has an N of only two. Can we trust their data?
  • Figure 4i presents a Hill coefficient fitting, but panel one doesn't fit well at all.

Questions for Dec-7-2017:

  • What are the higher weight bands in Figure 1A? Does part of the complex assemble ahead of time, independent of other factors? What does "RT Stops at As" mean, especially since these bands don't seem to line up with adenine bands?
  • I am curious about the evolution of the heat-shock/A-methylation relationship. And how is this accomplished biologically?
  • Are there other RNA modifications of as-yet unknown function? I'm always surprised when we continue to learn something about such a heavily studied molecule!