Recently I wrote a meeting report on the SENS3 conference for a very prestigious science journal, but finally it did not go through the filters. I knew that the chance for publication is small as the journal rarely publish such meeting reports and as it was in many respects an unconventional science conference. The standards were really high and the genre itself is strictly restricted: no more than 900 words and only 1-2 conference topic could be covered focusing on new data. On the whole it was a really good science writing experience for me. I finally realized how challenging it is to introduce the concept of robust scientific life extension for the mainstream science audience although it is not impossible at all.
But if a man has an interactive blog with a quality readership even an officially unpublished text could be useful, so please read my draft in its final form and think about it. Links of the video versions of the referred presentations and references are included, a perpetual advantage of the web comparing to offline publication. I’d like to say thanks for the folks who helped me with the draft: Aubrey de Grey, Michael Rae, Mark Hamalainen from within the SENS camp, Matthew Oki O’ Connor and Chris Patil, fellow scientists-bloggers and first of all, Anna.
Subject scrapline: Biotechnology
Title: Translating ageing
Summary: A recent unconventional strategic conference on translational science in ageing related damages helps to put some puzzle pieces together.
Changes in the adult tissue stem cells or in the mitochondria are two main processes under constant investigation amongst researchers curious about the ins and outs of the ageing process. At the SENS3 conference in Cambridge scientists and laymen shared their results and ideas, respectively.＊
Despite its mixed population with a scientist majority, the conference resembled a mainstream life science conference due to its topic sessions focusing on the different types of lifelong, ageing accumulated damages. SENS decodes as Strategies for Engineered Negligible Senescence, which aims to suggest a panel of interventions on how to robustly extend the mean and maximum human life span and claims to identify the adequately exhaustive list of main age-related pathologies ranging from cell depletion to mitochondrial mutations. SENS is by definition a flexible enough umbrella term to include other coming life extension technologies and concepts under its brand. Also, it is an engineering project compiled by main organizer Aubrey de Grey, a computer scientist turned theoretical biologist with a grand mission and hypotheses yet to be experimentally tested. The presentations were mainly reviewing the progress in the related branches, with enough new data to keep the experts interested.
The Nobel Assembly at Karolinska Institute has today decided to award The Nobel Prize in Physiology or Medicine for 2007 jointly to Mario R. Capecchi, Martin J. Evans and Oliver Smithies for their discoveries of “principles for introducing specific gene modifications in mice by the use of embryonic stem cells” Link
It’s rather a 2/3 gene technology, 1/3 stem cell methodology Prize, but shows how those technologies are interrelated.
Evans is still an active scientist but here are 2 famous papers he authored or coauthored:
Linda Powers is the managing director and co-founder of Toucan Capital Corp, a $120 million venture capital fund (SBIC) focused on seed and early-stage life science and advanced technology investments (the fund markets itself as the The Leading US Investor in Stem Cells and Regenerative Medicine). Out of here insights and facts presented on the SENS3 conference (I caught some of her slides with my iPhone, see below) I’d like to highlight the following ones:
- the anti-aging market today is approx. 42 billion dollars,
- the number of issued and published U.S. stem cell patents has been decreased for the first time since 2000 compared to the earlier year,
- viable business models in regenerative medicine are still missing,
- first-to-trial and -market is not always advantageous in regmed.
Rutledge Ellis-Behnke from M.I.T. talked on “a nano hemostatic agent that immediately stops bleeding. Hemostasis is a major problem after trauma and during surgery; as much as 50% of surgical time can be spent packing wounds to reduce or control bleeding and there are few effective methods to stop it without causing secondary damage. We show that hemostasis can be achieved in less than 15 seconds, in multiple tissues as well as a variety of different wounds, using a self-assembling peptide, demonstrating the first time that nanotechnology has been used to stop bleeding in a surgical setting for animal models that does not rely on heat, pressure, platelet activation, adhesion, or desiccation to stop bleeding.” The video he showed us was pretty convincing.
Embedded on the slideshow below 9 slides of Michael Rose’s presentation called Slowing and then stopping aging on the SENS3 conference on the 9th of September. (Photos made by me with the iPhone.) Rose’s argument was: Aubrey de Grey’s original SENS proposal is based on the non-evolutionary assumption that aging is a process of accumulating damage, while according to the evolutionary SENS version of Rose aging should be interpreted as a loss of adaption. The script is: breed mice with delayed reproduction over multiple generations (let evolution by natural selection give us the answer of how to build a long-lived animal), and then reverse engineer this answer to develop anti-aging therapies for genetically unaltered humans. The experimental basis of this proposal: Rose’s own ancient experiments with fruit flies (sorry, no reference yet, that’s what I’ve heard) showed that there is a plateau in mortality rates after many generations of breeded Drosophilas with delayed reproduction time which leads to the cessation of the aging process.
Does this method sound as one that gives us a complete engineering toolkit to achieve robust healthy life extension for early generations of humans under the reverse engineered treatment?
Well, I’ve lost the first part of this MacBook made iSight video as I used the iMovie file’s backup version on my Windows partition but out of this segment of the talk you can form some idea on what was going on during Kurzweil’s talk. The distance talk was orchestrated from a little Sony laptop by Richard Schueler. As Kurzweil’s friend Terry Grossman (they together wrote the book the Fantastic Voyage) informed me, Ray does not really like to leave the United States. Anyway, his talk was not typical, the conference was basically a biology-biotechnology conference with an amazingly broad range of the topics, covered.
I am off to Cambridge to the SENS3 conference. The New Orleans - Washington - Heathrow London - Cambridge trip is about 16 hours from house to house. I’ll be based at Pembroke College. The picture was made by Anna last year in Cambridge at the steps of the old Cavendish Laboratory Building on Free School Lane, near to the Eagle Pub.
Network biology is a way to integrate fragmented benchwork data in order to understand complex biological phenomena. In a recent Nature paper, entitled Integrating molecular and network biology to decode endocytosis Cambridge (UK) researchers authors Eva Schmid and Harvey McMahon of MRC, Cambridge give a good example of a predictive and experimentally useful systems biology approach. As in many cases in the current literature, the formal, printed article is just the tip of the iceberg, and the “supplementary information” section is as crucial.
Clathrin-mediated endocytosis (CME) is an important vesicle biogenesis pathway. Cargo is packaged into vesicles that are surrounded by a coat predominantly made of the protein clathrin and adaptor protein complexes. For instance at the synapse, clathrin-coated vesicles (CCVs) participate in retrieval of synaptic vesicles following exocytosis.
Authors identify 2 hubs in this pathway: AP2 and clathrin triskelion and instead of putting them into the existing hub subtypes (‘date’ and ‘party’ hubs) they argue that neither are hubs at the beginning of CME, but mature into hubs by clustering either on the membrane or through polymerization. It is likely that many pathway/party hub proteins will oligomerize or cluster to function as pathway hubs. ‘Clustered hubs’ are a new subtype of hubs not previously described
I found Figure 3 particulary refreshing which depicts functional and connectivity views of vesicle formation in nerve terminals. (2 pieces included)
I am visiting the third Strategies for Engineered Negligible Senescence (SENS3) conference, which will be held from 6-10 September 2007 at Queens’ College, Cambridge.
Aubrey de Grey (with whom I made a blogterview in 2006), the main organizer and soul behind the conference is clear about the purpose: “The purpose of the SENS conference series, like all the SENS initiatives (such as the journal Rejuvenation Research and the Methuselah Mouse Prize), is to expedite the development of truly effective therapies to postpone and treat human aging by tackling it as an engineering problem: not seeking elusive and probably illusory magic bullets, but instead enumerating the accumulating molecular and cellular changes that eventually kill us and identifying ways to repair — reverse — those changes, rather than merely to slow down their further accumulation.“
So after SciFoo I have the chance to visit another unconventional science gathering. SciFoo was unconventional by definition as it was an unconference with no strict schedule defined earlier (remember Henry Gee: Someday, all conferences will be like this), while SENS3 is unconventional due to its mission statement. SciFoo, SENS: ideal meeting points for young scientists with strong drive for change and looking for the new.
SENS3 is not an average conference in any respect and I am really happy to participate for 5 reasons, firstly, as this was the only conference I found where there are both good mitochondrial and stem cell biology sessions and those are my 2 major biological topics, b., there will be a lot of biogerontology presentations on aging and thirdly, because this is the only scientific conference that includes the heavyweight life extension supporter scholar fellows, including the organizer Aubrey de Grey or the practical life extensionist Ray Kurzweil. Fourthly, the conference clearly has some broader science politics implications as there is the more and more important question whether how it is possible to do research directly aiming human life extension or is it contradictory somehow as what scientists can do is just answering strictly restricted and well defined experimental questions. Last but not least I can meet my Cambridge friends and colleagues I’ve met last year during my 3 months Cambridge visiting period.
I am in Budapest again from December 23. The Cambridge months were extremely useful from a scientific point of view. (You can hunt down my 2 AA batteries on the photo)
Is is easy to realize on a conference when you are hearing a good talk. The audience starts to take notes and gets focused. That happened today during Austin Smith’s talk (look at Day 1 picture). Straightforward, not overcomplicated line of thought presented by easily conceivable, step by step slides, and hardcore science (facts). These are the elements of a compelling scientific argument. Starting with a dogma, which is that the default in vitro state of embryonic stem cells without any additional factor is neural differentiation, attacking this dogma through carefully executed independent experiments, and proposing a replacement claim: in the case of culture grown hESCs self-renewal is the default state. The “neural commitment by default” is a constructive dogma anyway, it can give rise to nice hypotheses because it captures the imagination with its counterintuitive offer: undifferentiated, pluripotent, self-renewing cells become neural type of cells in normal simple medium by themselves, although neurons are one of the most specialized cell type of the human body, and the nerve system is a young organ system measured on the scale of philogenesis.
Another fruit of the talk for me was meeting with the term “stiff upper lip“. Thanks, Hannah.
Recently I wrote a meeting report on the SENS3 conference for a very prestigious science journal, but finally it did not go through the filters. I knew that the chance for publication is small as the journal rarely publish such meeting reports and as it was in many respects an unconventional science conference. The standards were really high and the genre itself is strictly restricted: no more than 900 words and only 1-2 conference topic could be covered focusing on new data. On the whole it was a really good science writing experience for me. I finally realized how challenging it is to introduce the concept of robust scientific life extension for the mainstream science audience although it is not impossible at all.
Network biology is a way to integrate fragmented benchwork data in order to understand complex biological phenomena. In a recent Nature paper, entitled 
Authors identify 2 hubs in this pathway: AP2 and clathrin triskelion and instead of putting them into the existing hub subtypes (
So after SciFoo I have the chance to visit another unconventional science gathering. SciFoo was 
