The DNA Network |
| Can Virgin Trick You Into Better Health? [Epidemix] Posted: 19 Jun 2008 06:34 PM CDT
That’s well established in public health research. Despite millions of dollars and thousands of studies trying to get people to change their habits and improve their health, and despite plenty of evidence that shows that when people in fact *do* change their behavior their health improves, well, most people keep acting pretty much the same way. I’ve written about this before, but it’s one of the big cunundrum’s behind personalized medicine or, more specifically, personal genomics. It’s one thing to know that we have an elevated risk, and it’s a second thing to know that by changing our diet or exercise habits we can ameliorate that risk. But it’s quite a different thing to actually go out and do that. And this fact puts tremendous strain on our healthcare system, and means that, despite the promise of predictive medicine, we will always be dealing with late-stage conditions that could’ve been avoided. Here I’ll quote from an email sent by a secret physician source:
It’s especially frustrating, because so much of what we mean by “behavior change” boils down to two things: Eat better. Get more exercise. (there’s a third: Quit smoking. But that has all sorts of separate implications, which I hope to deal with later.) All this is prelude to mentioning one novel approach to behavior change: Virgin HealthMiles. Part of the Richard Branson Virgin empire, Virgin HealthMiles is a web-based tool to help people exercise more and more regularly. It is a fancied up exercise diary: you join, enter some exercise goals, and track your progress. There are a growing number of tools like this out there (Nike+ is a cool one for runners, that allows open sharing of routes and stats). But Virgin HealthMiles is different because it adopts the “miles” concept from frequent flier programs as a reward system. The more exercise you do, and the closer you track to your goals, the more miles you get; miles can be redeemed for hot fudge sunda… oops, redeemed for HealthCash, which can be converted into gift certificates at various stores. Right now, HealthMiles is open only through employer health benefits programs; it’s not open to individuals. And the million dollar question: Does it work? Well, there’s no evidence on the site, besides some anecdotal information. But my guess is it is likely more effective for people than just trying to remember that they should be exercising. The traditional way of advocating behavior change - the way the NIH does it - advocates similar principals (goals, targets, etc) Especially for the data-inclined, the life-hacker crowd, this sort of stuff is like catnip - you keep coming back to check you stats. And the thing is, as Kevin Kelly has noted, more and more of us are finding utility in tracking our lives. This isn’t a fringe thing, it’s an early adopter thing, and the masses are catching on (see the popularity of Nike+ and all the spin off mapping sites). |
| DNA Traits among the 13 [The Gene Sherpa: Personalized Medicine and You] Posted: 19 Jun 2008 06:24 PM CDT I just finished emailing David Ewing Duncan (Who has a great new blog) about the frustration I have. You see, everyone is saying....these SNP tests are information/data, not really medicine. But I... [[ This is a content summary only. Visit my website for full links, other content, and more! ]] |
| Scientists get pwned, conference ends in total carnage. [T Ryan Gregory's column] Posted: 19 Jun 2008 05:49 PM CDT Video games and I get along well. Always have. When I was a kid, my father and I went regularly to the local arcade to play our favourites. (Guess the decade: I usually played centipede and Tron). I haven't owned a console system since the original Nintendo, but games have occupied a significant portion of my PC hard drive since high school. |
| How Accurate are Your Pipettes? [Bitesize Bio] Posted: 19 Jun 2008 05:35 PM CDT Your pipettes are probably most used tools in your lab and (I’ve said it before, but it’s worth repeating) without accurate pipetting you are asking for problems with your experiments. Pipette manufacturers quote accuracy of pipettes but the truth is that pipetting accuracy is a very personal thing. It depends not only on the condition of your pipettes but also on your own pipetting technique. It’s a very useful exercise to periodically measure your pipetting accuracy because this error is incorporated into every pipetting action you perform in the lab. For most experiments the error might be too small to be significant but in some cases it might be very significant - e.g. if you are using a pipette to measure out a dilution for a very sensitive technique like HPLC. The point is this: to know whether you pipette is accurate enough for the job you want it to do, you need to know the systematic error in your own pipetting. It’s easy to measure your pipetting accuracy - just pipette the same volume of water ten times onto a tared balance, note the weight each time. Then measure the relative standard deviation in the dispensed masses by calculating the standard deviation and expressing it as a percentage of the average. This is your pipetting error. Repeat this for several different volumes using each of your pipettes and you’ll get a pretty good idea of your overall pipetting accuracy that you can keep in mind when deciding whether your pipetting is accurate enough for the experiment you are doing. Photo: scouse dan |
| A receptor for dopamine and a mismapped mutation [Discovering Biology in a Digital World] Posted: 19 Jun 2008 03:52 PM CDT Right or wrong, the word "dopamine" always conjures up images in my head of rats pushing levers over and over again, working desperately hard to send shots of dopamine into their tiny little rodent brains. |
| Kristin-gate at the OHRI [Bayblab] Posted: 19 Jun 2008 02:13 PM CDT   Notice anything strange with these blots? Apparently the data on it was faked and photoshoped along with "19 panels of Western blot data, appearing in 11 figures in 3 publications" by a post-doc fellow who shared working space with some bayblab readers and contributors. The story is all over the news today as we learned that her employment with the OHRI was terminated. You can find coverage of the whole story in the Ottawa Citizen and the National Post. The OHRI is trying to do some damage control, and thankfully the fraud wasn't commited here in the Ottawa lab but during Kristin's PhD at the university of Pennsylvania. The Office of Research Intergrity has taken the following disciplinary actions:"for a period of five (5) years, beginning on June 7, 2007: (1) Dr. Roovers is debarred from eligibility for any contracting or subcontracting with any agency of the United States Government and from eligibility or involvement in nonprocurement programs of the United States Government referred to as ``covered transactions'' as defined in HHS' implementation of OMB Guidelines to Agencies on Governmentwide Debarment and Suspension at 2 CFR part 376, et seq.; and (2) Dr. Roovers is prohibited from serving in any advisory capacity to PHS, including but not limited to service on any PHS advisory committee, board, and/or peer review committee, or as a consultant." This is bad news for everybody involved, the university, the institute and the scientific community. How could such blatant fraud make it past peer review? I would hate to be one of the innocent co-authors. Science is stressful and sometimes frustrating, and there can be tremendous pressure to have experiments work, but I am still baffled by the extent of fogery in this case. Any thoughts on the subject? |
| Evolution 2.0 [Sciencebase Science Blog] Posted: 19 Jun 2008 01:00 PM CDT
Now, researchers from the European Molecular Biology Laboratory’s European Bioinformatics Institute have revealed the source of these systematic errors in comparative genetic sequencing and have devised a new computational tool that avoids these errors and provides accurate insights into the evolution of DNA and protein sequences. Their work suggests that sequence turnover is much more common than assumed. “Evolution is happening so slowly that we cannot study it by simply watching it,” explains Nick Goldman, group leader at EMBL-EBI, “we learn about the relationships between species and the course and mechanism of evolution by comparing genetic sequences.” At the core of the evolutionary process are random changes in the DNA of all living things, incorrect copying of a single DNA base, or substitution, the loss of a base by deletion, and the inadvertent insertion of a new base. Such changes can lead to functional and structural changes in genes and proteins. If those mutations confer a reproductive advantage on the individual concerned then they will be carried on to the next generation. The accumulation of enough mutations over the course of many generations leads to the formation of new species. Reconstructing the history of these mutation events reveals the course of evolution.
“Our new The team’s work (published in the June 20 issue of Science) suggests that insertions are much more common than previously assumed, while deletion numbers have been overestimated. Now, that tools are being developed to reveal such issues our understanding of evolution can only become clearer. A post from David Bradley Science Writer |
| It is not all bad news [Mailund on the Internet] Posted: 19 Jun 2008 12:17 PM CDT
Since it is on neighbour-joining, we weren’t that optimistic. We’ve had problems publishing on this before, but this time it was very well received.
It’s really Martin SImonsen’s work. He is a Mater’s student at BiRC and in one of our algorithmics courses the students were asked to implement neighbour-joining and try to speed it up. Usually, they come up with some clever ideas, but they never before managed to beat my own version, QuickJoin. Martin did come up with a faster approach. Well, pretty close to, anyway. With mine and Christian Storm’s help, we managed to fix a few things here and there, and speed his approach up to one that not only beats QuickJoin but also all other methods we could get our hands on. QuickJoin uses a lot of tricks to speed up the search for nodes to join in the algorithm, but the data structures makes it slow on small data sets and also rather memory hungry. Martin’s approach is much simpler and this helps it a lot in the small data sets and doesn’t seem to hurt it on the larger data sets. As for QuickJoin, the trick is to only look at pairs of nodes that can potentially be joined and avoid looking at nodes that we can rule out as the next pair to be joined. Instead of using quad-trees and various functions to rule out pairs, Simon simply sorts nodes in a way where most likely pairs are considered first, and such that we can recognize when new pairs will not be better than those we have already seen. Read the actual paper — it is quite easy to understand the algorithm from there — if you want the details. Simonsen, M., Mailund, T., Pedersen, C.N. Accelerated neighbour-joining. Proceedings of WABI 2008 |
| Steven Pinker and Evolutionary Psychology in The Guardian [adaptivecomplexity's column] Posted: 19 Jun 2008 11:30 AM CDT The Guardian has an interesting interview with Harvard Evolutionary Psychologist Steven Pinker:
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| Posted: 19 Jun 2008 10:09 AM CDT Maybe there’s a chance I could end up back in this wonderful city and have a career, too.
The HPS consulting firm’s assessment is less sanguine, but overall deems the success of the center “likely”. Just to help paint the picture of things, the projected patient mix is: 13-21% Medicare .gif) This post is about development, louisiana, New OrleansRelated posts |
| Database and clinical implications of African genetic diversity [Yann Klimentidis' Weblog] Posted: 19 Jun 2008 10:03 AM CDT Establishment of a biobank and pharmacogenetics database of African populations Alice Matimba, Margaret N Oluka, Benjamin U Ebeshi, Jane Sayi, Oluseye O Bolaji, Anastasia N Guantai and Collen M Masimirembwa European Journal of Human Genetics (2008) 16, 780–783 There's no abstract, so here are the more more interesting parts: We here report the results of the first phase of this initiative that has seen research groups from five different African countries with collaborative support from leading experts in Europe and America establish a biobank of blood and DNA from nine ethnic groups from across the African continent. The biobank of anonymous samples has been used to establish baseline frequency distribution of SNPs of genes important in drug metabolism, hence the initiation of a pharmacogenetics database (http://www.aibst.com/biobank.html). The biobank consists of 1488 DNA samples from nine ethnic groups (Yoruba, Hausa, Ibo, Luo, Kikuyu, Maasai, Shona, San and Venda)regarding within-Africa diversity: We further analyzed the data for possible stratification of the African ethnic groups alone. No distinct differentiation was observed. Studies using other genetic markers have demonstrated that there is great genetic diversity among African populations compared to Caucasian or Oriental populations.12 These preliminary findings from our studies could indicate that the number and/or type of genes and/or SNPs analyzed do not carry enough resolution power to capture the genetic diversity of African populations reported in other studies.some clinical implications: The high frequency of individuals who are homozygous for the CYP2B6*6 allele (18–25% ) in African populations is predictive of reduced capacity to metabolize and dispose efavirenz compared to Caucasians where lower genotype frequencies of 5–10% have been reported.17, 18 This is in agreement with clinical observations in which Africans have been reported to have significantly higher plasma concentrations of the drug compared to Caucasians when given at the standard 600 mg per day doses.19 Ongoing studies in our laboratory in HIV/AIDS patients taking the anti-HIV drug, efavirenz, indicate the need to lower the dose of this drug in people of African origin homozygous for the CYP2B6*6 allele (Nyakutira et al, unpublished). This could go a long way in reducing adverse effects hence increase treatment compliance. This could also reduce the costs for individuals requiring lower doses and thus partly contributes to the diagnostic costs of identifying such individuals. For the African specific CYP2D6*17 variant20 similar clinical effects could be explored in the use of antipsychotic drugs21, 22 in African populations based on the observed high frequency of the variant (14–34% ) across the major African populations reported in this study (Table 1). Though the current pharmacogenetics database carries no direct phenotype information linked to carriers of the variants, clinical extrapolations from well-established in vivo effects of these polymorphisms give an important baseline that can be the basis for population-specific clinical trial design for optimal use of some medicines. |
| Death of a Mac… [Mailund on the Internet] Posted: 19 Jun 2008 09:56 AM CDT My new iMac died on me today. It crashed unexpectedly three times — and it has never crashed on me before — and after the last crash it didn’t come back up. I cannot even turn it on anymore, so I guess it is a hardware problem. I guess the warranty is still good — I bought it this year and there should be one year as I recall — so I’ll send it back to have it fixed. It still annoys the hell out of me, ’cause I was just getting used to using a Mac instead of Linux. Oh well, at least I get to test if my Time Machine backup is working. |
| A lesson in genetic testing: the I148T mutation [Mary Meets Dolly] Posted: 19 Jun 2008 09:01 AM CDT There has been a lot in the news lately about how California Health officials have ordered 13 genetic testing companies to stop testing California residents. I think many people do not understand why public health officials are concerned about the flood of new genetic tests offered directly to the public. I think I have an example that may illustrate the problem. Cystic Fibrosis (CF) is a devastating disease that is caused by mutations in the CFTR gene. To have CF, you must inherent one mutation from your mother and one from your father, which means that both copies of your CFTR gene do not work properly. If you only have one mutation in your CFTR gene you are called a carrier for CF, which means that while one copy of the CFTR gene isn't up to snuff, you at least have one working copy. The one working copy is enough to prevent you from developing CF symptoms. But, being a carrier is no picnic because if you were to have a child with a person who was also a carrier, there is a 25% chance that child will have CF. Most CF carriers have no idea that they carry a mutation in their CFTR gene. About 1 in every 30 North American caucasians is a carrier. So that brings us to the I148T mutation. When researchers were studying the causes of CF, they discovered that there were a significant amount of people that had CF that also had a mutation in the CFTR gene that causes a substitution of a threonine amino acid for an isoleucine at position 148 of the CFTR protein. Hence the name I148T. Researchers made the assumption that the I148T was one of the two mutations that caused the patients' CF. So, anyone who was found to have the I148T mutation, but did not have CF symptoms was labeled a carrier for CF. The I148T mutation was included in the testing panel for many labs, including mine. Unfortunately, that isn't the end of the story. As more people were tested, researchers found that there were people who had the I148T mutation with another known mutation, but did not have CF. If the I148T mutation was actually was a disease causing mutation, then these people should definitely have symptoms of CF, but they did not. What researchers eventually found was that I148T was actually what is called a benign polymorphism, which means that it is a mutation that does not cause disease. What they found was that the disease causing mutation is really a deletion of 6 base pairs at nucleotide number 3199. The mutation is called 3199del6 and just happens to be inherited in high frequency with the I148T mutation. Long story short: Lots of people were told they were carriers of a CF causing mutation, namely the I148T mutation, when actually, they just carried a benign polymorphism. Time and more information revealed a more complex picture of CF mutations. To this day the I148T is on the CF testing panel in commercial CF testing kits. We used it as a flag to conduct further testing for the 3199del6 mutation. So the lesson is, just because a mutation is present does not mean it causes disease. Any genetic test has to have a mound of research proving that it has any clinical relevance. A reputable genetic counselor would be able to sift through the data and give you an interpretation of your results. |
| Fishy phylogenetics figures found. [T Ryan Gregory's column] Posted: 19 Jun 2008 07:04 AM CDT Currently working on a paper about fishes, I came across some interesting figures. (Well, mildly interesting, as they are more of the same actually). |
| Wired on regulation of DTC genetic testing [Genetic Future] Posted: 19 Jun 2008 03:04 AM CDT The Wired website is abuzz with news and opinions regarding the California Public Health Department's recent letter to direct-to-consumer genetic testing companies, which advised them to cease testing customers until they have demonstrated compliance with state regulations - importantly, including the provision that all "clinical laboratory tests" (apparently including a genome scan) be ordered through a doctor. Such regulation goes against the general Wired philosophy of unfettered access to technology, so the response is not positive. Wired began the day with a list of the Top 10 Reasons that Regulators Should not Hinder Genetic Testing, followed with an exclusive release of the letter that started it all, a report on a 3-hour health department conference call on the issue last Friday, and then a summary of the whole debacle. I'm not going to go on about this topic (this will hopefully be my last post on it for a while) but the links above are well worth a scan for anyone concerned about the future of the personal genomics industry.  Subscribe to Genetic Future. |
| Crap [Mailund on the Internet] Posted: 19 Jun 2008 02:40 AM CDT First they tell us that alcohol hurts our publication record, and now it causes cancer? Stop researching alcohol! |
| Neuroscientists show insulin receptor signaling regulates structure of brain circuits [Think Gene] Posted: 19 Jun 2008 02:16 AM CDT A team of neuroscientists at Cold Spring Harbor Laboratory (CSHL) has demonstrated for the first time in living animals that insulin receptors in the brain can initiate signaling that regulates both the structure and function of neural circuits. The finding suggests a significant role for this class of receptors and perhaps for insulin, not only in brain development, but also in cognition and in pathological processes in which cognition is impaired, as in Alzheimer’s disease, for example. Insulin receptors on the surface of cells throughout the body have long been understood to play a central role in controlling metabolism through the regulation of glucose. When a molecule of insulin, a hormone, “docks” with the receptor, a complex signaling cascade is set in motion inside a cell, culminating in the cell’s uptake of insulin.
The Brain Is Not “Insulin-Insensitive” After All
Although insulin receptors are observed in certain parts of the mammalian brain, most scientists, until a few years ago, had assumed the organ was “insulin-insensitive,” knowing that glucose could be taken up by brain cells without the involvement of either insulin or insulin receptors. In recent years, however, it has been shown that the brain is indeed an insulin target, and in cell-culture experiments that insulin receptor signaling in neurons can have an impact on the formation and development of neural circuits. This had never been demonstrated in living organisms until it was shown in experiments performed in the laboratory of CSHL Professor Hollis Cline, Ph.D., and reported this week in the journal Neuron. These experiments, in Xenopus tadpoles, show that insulin receptor signaling in neurons regulates the maintenance of synapses, contributes to the processing of sensory information and is also involved in adjusting the plasticity of brain circuits in response to experience. The latter function is particularly interesting, notes Dr. Cline, since “it is required for the incorporation of neurons into brain circuits.”
Blocking the Receptor
To test the idea that insulin receptor signaling regulates the formation of brain circuits during development, the Cold Spring Harbor team used two different techniques to block the function of the receptor in neurons located in the visual pathway of tadpoles. One method “knocked down” expression of the receptors genetically, while the other left them in place but prevented them from initiating signaling cascades within the cell. “Tadpoles are wonderful creatures for such experiments,” Dr. Cline explained, “in part because they have translucent bodies, which makes it easy for us to visualize and record what happens to individual neurons as we manipulate the insulin receptors on their surface.” When insulin receptor function was blocked, neurons in the visual pathway connecting the tadpole’s retina to a brain region called the tectum responded very poorly to light stimuli. The tectum is the area in which brain cells process incoming visual signals. “We showed that the insulin receptor is critical for the proper operation of this circuit, and also that defects in receptor signaling cause a reduction in the animal’s visual responses,” Dr. Cline said.
Time-Lapse Images of Dendritic Branching
The team went on to perform other experiments that demonstrated two remarkable facts. One is that insulin receptor signaling correlates with the density of the synapses, or neuron-to-neuron connections, in brain circuits. In more technical terms, they found that insulin receptors maintain synaptic density and that synapse density decreases when insulin receptors are removed or dysfunctional. The team also secured time-lapse images of dendritic formations, the ethereal, branch-like structures that receive chemical signals sent from one neuron to the next. Again, they found that when insulin receptors are engaged and sending signals inside the neuron, dendritic growth is enhanced, specifically in response to visual stimulation. In this, as in the findings about synaptic density, the team found that insulin receptor signaling regulates the form and function of brain circuits in response to incoming visual information. Another way to put this is that the receptor regulates brain circuits in response to “experience.”
Possible Links to Disease
This suggests that insulin receptors in the brain may play a key role not only in the brain’s development early in life, but also in disease processes that usually occur late in life. People with advanced diabetes suffer memory loss and cognitive deficits, possibly because insulin receptor signaling in the brain is disrupted, synaptic connections are lost and brain circuits don’t work optimally. In addition, other researchers have found a correlation between diminished insulin receptor signaling and Alzheimer’s disease. Results of the Cold Spring Harbor team’s research raise the question of whether deficits in learning and memory associated with Alzheimer’s might be linked causally to decreased synaptic density as a consequence of lowered insulin receptor signaling. “We are a long way from knowing this for sure, but it’s the direction in which our work now takes us,” Dr. Cline said. Source: Cold Spring Harbor Laboratory Josh says: If this turned out to be true, it could have huge implications for our eating habits and offer an even larger incentive to eat healthier other than the risk of type II diabetes. |
| Lifestyle can alter gene activity, lead to insulin resistance [Think Gene] Posted: 19 Jun 2008 02:15 AM CDT A Finnish study of identical twins has found that physical inactivity and acquired obesity can impair expression of the genes which help the cells produce energy. The findings suggest that lifestyle, more than heredity, contributes to insulin resistance in people who are obese. Insulin resistance increases the chance of developing diabetes and heart disease. The study, “Acquired obesity and poor physical fitness impair expression of genes of mitochondrial oxidative phosphorylation in monozygotic twins discordant for obesity,” appears in the online edition of the American Journal of Physiology-Endocrinology and Metabolism, published by The American Physiological Society (www.the-aps.org). The study was carried out by Linda Mustelin and Kirsi Pietiläinen, of Helsinki University Central Hospital and the University of Helsinki; Aila Rissanen, Anssi Sovijärvi and Päivi Piirilä of Helsinki University Central Hospital; Jussi Naukkarinen, Leena Peltonen and Jaakko Kaprio, University of Helsinki and National Public Health Institute; and Hannele Yki-Järvinen of Helsinki University Central Hospital and Minerva Medical Research Institute.
Environment can influence genes
Recent studies have suggested that defects in expression of genes involved in the body’s conversion of food to energy, known as mitochondrial oxidative phosphorylation, can lead to insulin resistance. The researchers wanted to know if defects in the expression of these genes are primarily a result of heredity or lifestyle. Because the twins in the study were identical, any differences that were found could be attributed to environmental factors, the researchers reasoned. Twenty four pairs of identical twins, born in Finland between 1975 and 1979, took part in the study. Fourteen pairs (eight male and six female) were discordant for obesity, that is, one twin was obese, while the other was not. The control group consisted of five male and five female twin pairs who were concordant for weight. Some of the concordant pairs were normal-weight while some pairs were overweight. The researchers measured whole body insulin sensitivity, body composition and cardiorespiratory fitness. They also obtained a needle biopsy of abdominal subcutaneous fat tissue, although they were unable to obtain this measurement for one of the discordant pairs. Among the discordant pairs, the study found the obese twin had significantly lower:
Heredity may still play role
“These data suggest that physical inactivity may have contributed to the defects in mitochondrial oxidative phosphorylation described in type 2 diabetic patients and prediabetic subjects,” the authors wrote. The authors also noted that, although environment plays a role in how these genes work, there still may be a hereditary component. “Although we found that the reduced transcript levels of genes encoding mitochondrial oxidative phosphorylation in obesity is influenced by environmental and acquired factors, it does not exclude the possibility that genetic factors contribute to regulation of mitochondrial oxidative metabolism,” lead author Linda Mustelin noted. The next step is to do a clinical study to see if exercise and other lifestyle changes can increase the expression of these genes. Source: American Physiological Society Josh says: This is certainly possible, since so many things in our body are regulated by feedback mechanisms. Cells, and the body for that matter, are very adaptive. Take for example tolerance to drugs. Though, I’ve always assumed that insulin resistance was dietary more so than hereditary. Unfortunately, the paper is not yet available. |
| Self Assembly: New Communication Channels for Biology [business|bytes|genes|molecules] Posted: 19 Jun 2008 12:01 AM CDT
Going to San Diego has its own charm. I lived there for almost six years, the longest I have ever stayed in any place for a continuous stretch. I haven’t gone back since I moved to the Seattle area, so hopefully I will get a chance to say hello to old friends and my brother-in-law. I also get a chance to catch up with other members of the online science community (Jean-Claude, Moshe), and with some whom I am acquainted with virtually, but have never met (Hilary Spencer, Jason Kelly, Michael Nielsen). Further reading Technorati Tags: Scientific Communication  |
| Breathlessly Back From BIO2008 [] Posted: 18 Jun 2008 11:26 PM CDT
We spent the day at Bio2008. The turnout seemed pretty good, and the conference was spectacularly well organized. Special Aminopop shout-out to Erin Reese for arranging a press pass.
What comes to mind, while we’re still catching our breath: Biotech industry people are healthier, better dressed and better groomed than people in infotech — we haven’t seen that many ties and perfect creases at a trade show since 1985. The gargantuan exhibition hall was jammed with booths. But, unlike an infotech trade show, a whole lot of them — maybe even a majority — weren’t fronting for individual biotech companies… but instead for various consortia (government sponsored and commercial associations), biotech industry-stimulating efforts of various nations (“Biotechnology in Sweden!” “The Malaysian Miracle!” etc.), and … law firms. A ton of them. All of them wanting to help you protect your valuable intellectual property. Probably a good sign; to paraphrase Stewart Brand, if you want to find out where the action is in a culture, follow the lawyers. Based on the showing of litigants at Bio2008, there’s evidently a ton of cultural action in Biotech.
The one major disappointment was the almost singular focus on pharma. Despite the conference’s slogan of “Heal, Fuel, Feed The Planet”, there was little feeding or fueling in evidence. Amazingly, the Wednesday Ernst&Young supersession (okay, so we left after 90 minutes, so sue us if we missed something) didn’t contain a single reference to agriculture or biofuels. This is a little weird, and very un-Aminopop to boot; we’re pretty certain the first world-changing Biotech killer app isn’t going to be a drug. Yet, to outward appearances at Bio2008, Biotech seems to be all about antibodies and small-molecule drugs. Oh, and litigation.
There were plenty of exceptions, though. We did turn up a whole lot of fun stuff, which we’ll write up over the next few days — hands-on fun stuff like nanotech fluorescence tags, a desktop microfluidics rig, and a korean hand-held PCR unit that looks like a klunky iPod. We also collected a pile of fun booth-bait tchochkes we’ll roll out in separate post.
All in all, though, the show left us yearning for that Juan Enriques-brand vision, enthusiasm and irreverent prognostication we find so charming and, well… fun. Maybe next year. Right now, Biotech people seem to be buttoned up a little tightly because of capitalization cycles and gloomy equity markets. We think they need another good 2001-style bubble to bring them out of their shells a bit.
More later. |
| Collective Intelligence in the hospital [business|bytes|genes|molecules] Posted: 18 Jun 2008 10:13 PM CDT
Doc Searls is sick, but like Jon Udell in the comments, I was drawn to the lines above. In medicine, where information and knowledge is truly built via the collective, and where you might find non-obvious linkages, wouldn’t we really benefit from capturing this collective intelligence, across doctors and patients. A lot of healthcare systems focus on building hospital efficiency and on a per-patient level. I wonder if they do as good a job of capturing this knowledge, and potentially alerting doctors of possible diagnoses or help that add to the knowledge they have built on their own? If not, there is an opportunity there, which someone needs to tap into. And yes, I think ontologies underlying data entry would be a huge plus. Technorati Tags: Collective Intelligence, Doc Searls, Hospitals  |
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1 comment:
If you are needing pipetting for making up reagents, then disposable plastic graduated pipettes that can use a vacuum assisted drawing bulb or plunger would be ideal.
lisa
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