The DNA Network |
| Posted: 10 Jun 2008 05:34 PM CDT The NY Times today has a profile on Congress's 3 PhD physicists. Congressman Vernon Ehlers (R, Michigan), PhD, tells the NY Times that he has had to stop his Congressional colleagues from trying to cut funding for research on game theory and ATM - apparently some politicians thought that game theory is about sports, and that ATM in a science proposal really does stand for automatic teller machines. (In the particular case, ATM means Asynchronous Transfer Mode, a fiber-optic data transfer protocol). |
| Getting John Henry and his hammer into a scientific paper [The Tree of Life] Posted: 10 Jun 2008 01:05 PM CDT Gotta love a scientific paper that quotes John Henry stories. In Andy Ellington's primer on ribozyme evolution (PLoS Biology - Man versus Machine versus Ribozyme) he leads off with His point here is to talk about man versus machine and to then discuss the recent article in PLoS Biology on a "Darwinian Machine" which I wrote about previously. (I think he is also making a bit of a play on words with the hammerhead ribozyme, but I am not sure). Anyway, Ellignton's article is worth checking out. I especially like the ending Machine-based continuous evolution should be the best of all worlds, combining man's mental ability to chart the future with automated control of selection stringency with the still unpredictable mode and tempo of evolution's relentless drive. Figure from Ellington's PLoS Biology paper. I can put it here because it is a fully Open Access paper using a broad Creative Commons license. All I have to do is cite the source. And so I am. Andy Ellington. PLoS Biol 6(5): e132 doi:10.1371/journal.pbio.0060132 |
| The Big Switch [business|bytes|genes|molecules] Posted: 10 Jun 2008 12:30 PM CDT
As some of you are aware this is my last week in my current job. Later this month I will be starting a new position in the business development group at Amazon Web Services, where I will jump headfirst into the world of web services and utility computing. Many eons ago, I promised myself, never to take up a job where I didn’t believe in the underlying fundamentals and that has been the case throughout my career. Any reader of this blog is more than aware of my belief in the impact of cloud computing in general and Amazon’s web services stack and business model in particular. It’s an opportunity that I just could not resist, even though it takes me out of being directly involved with science in one way or another for the first time since 1989 when I decided to choose science as my specialty in high school. Hopefully along the way, I’ll get to play some role in the adoption of the cloud for scientific computing. What does this mean for bbgm? To be quite honest, I am not 100% sure, but do have some ideas. Obviously the disclaimers will change. In some ways it also makes it easier to blog about science. There have been many occasions where an in depth analysis was not feasible due to potential conflicts of interest, or where I had access to privileged information. That’s no longer an issue now, so I hope to be able to blog more freely about science, perhaps even starting that industry watch column I have always wanted to. I won’t have access to all the newsletters and journals as before (will really miss BioInform), so I will be following blogs a little more closely :). One hope is that being around developers and the freedom to do some garage science without conflict with my day job will get be coding actively and participating in BioGang projects. Otherwise, it’s still the good ole bbgm. Computing, in silico science, the Semantic Web, Open Data, Personalized Medicine, and Bursty Work are all going to remain staples. I suspect time is going to be a big issue, so will have to become more efficient or so I suspect. We’ll see. And here is the cool footnote. While not quite Second Life, this whole chain of events started unfolding on Twitter, including sending a resume in 140 characters or less. Technorati Tags: Amazon Web Services  |
| Posted: 10 Jun 2008 12:30 PM CDT I have written quiet often about this subject and companies that promises solution for personalized medicine. especially the use of genomics information in organ transplant patients and cancer treatment. XDx and Genomic Health are two such companies . XDX has applied microarray, to monitor the immune system, with the help of Gene expression to address the challenge of balancing the risk of acute cellular rejection against the known adverse effects of immunosuppressants; especially inexpression testing for patients with heart transplants. Genomic Health provides individualized genomic profiling of tumor tissue may help improve cancer management. personalized medicine is still dismissed of by many as the cost are still high, and there are very few trained physicians who can use this extra information for better clinical outcome. US institutes Biodesign Institute at Arizona State University, Fred Hutchinson Cancer Center Translational Genomics Research Institute (TGen), the Institute for Systems Biology, and the Partnership for Personalized Medicine will help the government of Luxembourg start a three-pronged, $200 million-plus biomedical initiative focused on harnessing genomics technologies to study human health problems. For those who wants to cry foul that genomic information can lead to discrimination against individuals by insurance companies or others can take solace on GINA . In may 21.2008 President George Bush has signed into law the Genetic Information Nondiscrimination Act (GINA) that will protect Americans against discrimination based on their genetic information when it comes to health insurance and employment. The most immediate benefit of GINA is to remove barriers to identifying individuals at high risk for diseases due to genetic mutations before the onset of the disease         |
| DRD4 and BMI in nomadic vs. settled Kenyans [Yann Klimentidis' Weblog] Posted: 10 Jun 2008 10:23 AM CDT This paper (abstract below) looks at the association between BMI and the 7R variant of DRD4 often associated with ADHD and novelty seeking behavior (in humans and birds) and inter-racial mating - by same two first authors as this paper. It's also been invoked as a variant that could be selected for in a multilevel (i.e. group selection) density dependent way. I've been very interested in this gene ever since Harpending and Cochran's paper a few years back in PNAS called "In our genes" about what groups in the world have the 7R allele at a high frequency and the link to potential selection benefits - migratory behavior, cad vs. dad male behavior, warfare etc... it's been a while since I've read it. In this paper they find an association between the 7R variant and BMI among the nomadic, but not among the settled group in Kenya. I have yet to read the paper, and would like to see how they attempt to explain this. They don't find a difference in 7R allele frequency between the two groups. Razib also blogged on this paper and put up a map of the worldwide distribution of the 7R DRD4 allele, a table from this paper, and a link to "In our genes". Dopamine receptor genetic polymorphisms and body composition in undernourished pastoralists: An exploration of nutrition indices among nomadic and recently settled Ariaal men of northern Kenya Dan T.A. Eisenberg , Benjamin Campbell , Peter B. Gray and Michael D. Sorenson BMC Evolutionary Biology 2008, 8:173 Abstract (provisional) Background Minor alleles of the human dopamine receptor polymorphisms, DRD2/TaqI A and DRD4/48bp, are related to decreased functioning and/or numbers of their respective receptors and have been shown to be correlated with body mass, height and food craving. In addition, the 7R minor allele of the DRD4 gene is at a higher frequency in nomadic compared to sedentary populations. Here we examine polymorphisms in the DRD2 and DRD4 genes with respect to body mass index (BMI) and height among men in two populations of Ariaal pastoralists, one recently settled (n = 87) and the other still nomadic (n = 65). The Ariaal live in northern Kenya, are chronically undernourished and are divided socially among age-sets. Results Frequencies of the DRD4/7R and DRD2/A1 alleles were 19.4% and 28.2%, respectively and did not differ between the nomadic and settled populations. BMI was higher in those with one or two DRD4/7R alleles in the nomadic population, but lower among the settled. Post-hoc analysis suggests that the DRD4 differences in BMI were due primarily to differences in fat free body mass. Height was unrelated to either DRD2/TaqI A or DRD4/48bp genotypes. Conclusions Our results indicate that the DRD4/7R allele may be more advantageous among nomadic than settled Ariaal men. This result suggests that a selective advantage mediated through behaviour may be responsible for the higher frequency of the 7R alleles in nomadic relative to sedentary populations around the world. In contrast to previous work, we did not find an association between DRD2 genotypes and height. Our results support the idea that human phenotypic expression of genotypes should be rigorously evaluated in diverse environments and genetic backgrounds. |
| Acceptance of evolution in Canada. [T Ryan Gregory's column] Posted: 10 Jun 2008 07:40 AM CDT About a year ago an Angus Reid poll provided some information regarding the acceptance of evolution in Canada, which was taken by some as the basis for claiming that the level of acceptance of this unifying principle of biology is roughly the same in Canada as in the United States. |
| The adaptive origins of attention deficit disorder [Genetic Future] Posted: 10 Jun 2008 07:28 AM CDT  Razib from Gene Expression describes a potentially fascinating study on a variant of the DRD4 gene, which was first shown to be associated with attention deficit hyperactivity disorder (ADHD) more than ten years ago. (It's worth emphasising, by the way, that DRD4 is just one of the many genes likely to be involved in this complex trait). Interestingly, the same variant has also been reported to show a signature of recent positive selection in some human populations, suggesting that the behavioural "problems" displayed by modern individuals with ADHD may actually result from a mis-match between the environment our hunter-gatherer ancestors were adapted to and the bizarre, restrictive environment of Homo suburbanensis.
In other words, behaviour that would result in a rapid trip to the headmaster (followed by the psychiatrist) in stable, industrialised society may actually have been extremely useful in the relatively uncertain world of the hunter-gatherer tribesman.  Subscribe to Genetic Future. |
| deCODEme Genome Browser Review [Think Gene] Posted: 10 Jun 2008 05:13 AM CDT deCODEme Genome Browser (demo account) What if you could see your genome DNA like sound tracks in mixing software? What if you wanted to listen to music, but could only play it in mixing software? With deCODEme’s new genome browser, now officially launched, you can.
I previewed the Genome Browser in Reykjavík a few months ago, and my response was then as it is now: “No.” Now, I like deCODE, I love this industry, and I want people to be excited. So, I get a bit overheated when I see something with so much potential grow in the wrong direction, like some geeky math genius with basketball dreams. Put that bling where it belongs, son: in the bank, not in your teeth. and… that’s deCODEme’s Genome Browser: right bling, wrong places. The Bling: Genome Browser is the best, most accessible, most personally relevant genome browsing software today. I can seamlessly zoom from chromosome, to gene, to individual nucleotide sequence. I can see where deCODEme SNPs are geographically aligned in the genome. I can search for a term, like “CCR5,” and Genome Browser zooms to results in real-time. And, I can cross-reference against the top three genomic public databases. Very cool. Similar Products. Note that these are scary, ugly science tools: The Teeth: So who are the users of Genome Browser? Scientists? I can’t reference it. I can’t link to it (because of Java). It doesn’t have the technical depth to be a better scientific tool. And, I can’t import or export tracks —my own data. Amusing, but not useful. A tool for casual enthusiasts? I have to wait several minutes to install Java and wait fifteen seconds to load the application? (waiting is bad) I have to read instructions because the interface isn’t self-descriptive and intuitive? (reading is bad) Where are the hyperlinks? Where are the scrollbars? Why can I do something annoying, like drag rows to arbitrary positions, but I can’t do something useful, like click-drag zoom directly in tracks? Why is there a mostly empty row for every deCODEme phenotype instead of a compact, single row? Confusing, and not useful. Ultimately, deCODEme’s genome browser is like an average modern linux application: written for its programmers’ gratification, not for its users’. That’s something not even the shiniest transparency effects can fix. The Bank Genome Browser has value, but it’s misplaced in a bad interface. This can be fixed:
Conclusion Eventually, hopefully, someone at deCODEme, 23andMe, or Navigenics is going to realize that their product is a crude, disposable prototype for cheap full genome sequencing, and that their actual job is market finding, not product building. Thus, personal genome products TODAY aren’t the REAL business, they’re just early loss-leaders for building company brand and expertise. So, if I were the CEO of deCODEme (or 23andMe), I wouldn’t budget a penny for any deCODEme project, including new releases for the deCODEme Genome Browser, unless my team could tell me in three sentences how that project would:
I am having a difficult time composing those three sentences for this release of deCODEme Genome Browser as it is now. |
| The Illuminati Trades On Nasdaq, Apparently… [] Posted: 10 Jun 2008 02:05 AM CDT
Wow. All we can say is wow. Apparently twenty-year-old technology is hot news to Wallstrip. Listen to their YouTube Video rant about gene chip manufacturer Illumina… it’s the kind of tin-foil-hat, they’re-beaming-thoughts-into-my-head rambling usually reserved for ambulatory psychotics:
“They look through your DNA and discover your genetic code. that’s right… they discover. your. genetic. code. This stuff is for real. They’re going to look inside of you and discover your code. And they’re tricking us into paying for it.”
Totally incoherent. Just the kind of BioLuddite insanity Aminopop encounters so often out there. We can’t believe anybody would… [pause] Um, wait a minute: Illumina. Illuminati. Oh, wait… now we get it. It’s a satire. They actually had us going for a minute… In that case, we’re a little hasty. And this video is kind of brilliant. |
| TGG Interview Series V - Whit Athey [The Genetic Genealogist] Posted: 10 Jun 2008 02:00 AM CDT The name Whit Athey is undoubtedly very familiar to many genetic genealogists. Whit’s Haplogroup Predictor, used to predict an individual’s paternal haplogroup based on DNA test results, is one of the most valuable online (and FREE) tools for genetic genealogists. Among Whit’s many contributions to the field, he is also the Editor (and frequent contributor) of the Journal of Genetic Genealogy. From his biosketch:
In the following interview, we talk about Whit’s introduction to genetic genealogy, the creation of the JoGG, and Whit’s thoughts about the future of the field. TGG: How long have you been actively involved in genetic genealogy, and how did you become interested in the field? Whit Athey: I have always been interested in molecular biology, and my graduate work, though primarily in physics, was partly in molecular biology. When the article by Cann, Stoneking, and Wilson came out about 20 years ago, I was really struck by the potential for a better understanding of human origins. However, at that time I was heavily involved in other things, so I was just an interested bystander for many years. I bought Bryan Sykes's book, The Seven Daughters of Eve, when it was published in 2001, and this rekindled my interest. I almost ordered the mtDNA sequencing that his company was offering, but it was rather pricey in those days, so I again held off getting personally involved. I did develop a course that I called "The Human Family," and presented it several times in 2001 and 2002 to local groups. In 2003 I finally took the plunge and ordered both Y-STR tests and mtDNA sequencing for myself, and I started a surname project for my own surname. I started five other projects during 2004 and 2005. TGG: You are one of the founders of the Journal of Genetic Genealogy. How did this journal come about, and what are the journal's goals? WA: JoGG was really the brainchild of Ann Turner and Dennis Garvey. They had really brought a lot of good work to bear on our fledgling field, and the journal was really their idea. Ann and Dennis can better address the question of why they thought that we needed a journal. The idea immediately appealed to me because of the quality of some of the "amateur" genetics studies that I was aware of. I thought that a number of these studies were worthy of publication in some form. Anyway, Ann and Dennis organized a meeting of several interested people, including myself, just after the first Family Tree DNA (FTDNA) conference in Houston in November 2004, with the purpose of discussing the possibilities of a new journal. I volunteered to help with getting the journal off the ground. Probably because I seemed to have the most time available, I ended up as its editor. TGG: Have you undergone genetic genealogy testing? Were you surprised with the results? Did the results help you break through any of your brick walls or solve a family mystery?
WA: Yes, I have tested myself on over 115 Y-STR markers and I have had a full mtDNA sequence done. I am a hopeless test junkie. My Y haplogroup was quite a surprise to me, considering that my paternal line came to the U.S. from Galway, which is in a part of Ireland that is over 95% R1b. I am in Haplogroup G2-U8, which occurs in northwest Europeans at only about a 1.5% frequency. Furthermore, my cluster of 20 G2 Atheys is a considerable genetic distance from any other G2's, except for one small family cluster that has the surname, Whitfield. This is quite a coincidence since my given name is Whitfield. So far, we cannot see how it is possible that our two lines are so similar when it appears that the common ancestor must have lived prior to the year 1400. Most people seem to think that mtDNA has little role to play in genealogy. If you are simply looking for matches in the large databases, then I would agree that most matches that are found are likely to be meaningless for genealogy. However, in the area of hypothesis testing, I think that it can be quite useful. If you are comparing the mtDNA of two people who are suggested (by traditional genealogical methods) to be related along a matrilineal line, then the mtDNA results can either disprove or support your hypothesis. TGG: What do you think the future holds for genetic genealogy? WA: I can't help but believe that we will see a continuing decrease in price and an increase in the number of tests that are available. For the Y-chromosome phylogenetic tree it appears to me that the addition of new SNPs will probably double every 2-3 years. We are also likely to see many new complete mtDNA sequences added to the world's databases. This increase in resolution for both Y-chromosome and mtDNA trees, together with more people participating in testing, will bring new understanding of human migrations. I believe that "amateurs" will continue to play a key role in new developments in the future, probably even more than at present. We have the ability to move quickly on a new question and a vast population available of people who have been tested. I think that the time has past when our community just waits on the professional population geneticists to bring new data to us through publications in traditional journals. I think that we will be playing a leading role in the future. TGG: Thank you, Whit, for a terrific interview! Other posts in the TGG Interview Series:
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| Livermore researchers use carbon nanotubes for molecular transport [Think Gene] Posted: 10 Jun 2008 12:41 AM CDT Molecular transport across cellular membranes is essential to many of life’s processes, for example electrical signaling in nerves, muscles and synapses. In biological systems, the membranes often contain a slippery inner surface with selective filter regions made up of specialized protein channels of sub-nanometer size. These pores regulate cellular traffic, allowing some of the smallest molecules in the world to traverse the membrane extremely quickly, while at the same time rejecting other small molecules and ions. Researchers at Lawrence Livermore National Laboratory are mimicking that process with manmade carbon nanotube membranes, which have pores that are 100,000 times smaller than a human hair, and were able to determine the rejection mechanism within the pores. “Hydrophobic, narrow diameter carbon nanotubes can provide a simplified model of membrane channels by reproducing these critical features in a simpler and more robust platform,” said Olgica Bakajin, who led the LLNL team whose study appeared in the June 6 online edition of the journal Proceedings of the National Academy of Sciences. In the initial discovery, reported in the May 19, 2006 issue of the journal Science, the LLNL team found that water molecules in a carbon nanotube move fast and do not stick to the nanotube’s super smooth surface, much like water moves through biological channels. The water molecules travel in chains - because they interact with each other strongly via hydrogen bonds. “You can visualize it as mini-freight trains of chain-bonded water molecules flying at high speed through a narrow nanotube tunnel,” said Hyung Gyu Park, an LLNL postdoctoral researcher and a team member. One of the most promising applications for carbon nanotube membranes is sea water desalination. These membranes will some day be able to replace conventional membranes and greatly reduce energy use for desalination. In the recent study, the researchers wanted to find out if the membranes with 1.6 nanometer (nm) pores reject ions that make up common salts. In fact, the pores did reject the ions and the team was able to understand the rejection mechanism. “Our study showed that pores with a diameter of 1.6nm on the average, the salts get rejected due to the charge at the ends of the carbon nanotubes,” said Francesco Fornasiero, an LLNL postdoctoral researcher, team member and the study’s first author Fast flow through carbon nanotube pores makes nanotube membranes more permeable than other membranes with the same pore sizes. Yet, just like conventional membranes, nanotube membranes exclude ions and other particles due to a combination of small pore size and pore charge effects. “While carbon nanotube membranes can achieve similar rejection as membranes with similarly sized pores, they will provide considerably higher permeability, which makes them potentially much more efficient than the current generation of membranes,” said Aleksandr Noy, a senior member of the LLNL team. Researchers will be able to build better membranes when they can independently change pore diameter, charge and material that fills gaps between carbon nanotubes. Source: DOE/Lawrence Livermore National Laboratory Josh says: This does have a lot of implications. They must work very similar to ion channels in membranes, where only certain ions can travel through. I wonder if it would be possible to design custom transmembrane membrane channels to help with drug delivery? |
| Stem cell discovery sheds light on placenta development [Think Gene] Posted: 10 Jun 2008 12:34 AM CDT Researchers studying embryonic stem cells have explored the first fork in the developmental road, getting a new look at what happens when fertilized eggs differentiate to build either an embryo or a placenta. By manipulating a specific gene in a mouse blastocyst — the structure that develops from a fertilized egg but is not yet an actual embryo — scientists with the University of Florida’s McKnight Brain Institute and the Harvard Stem Cell Institute caused cells destined to build an embryo to instead change direction and build the cell mass that leads to the placenta. Writing in today’s (Monday, June 9) online edition of Nature Genetics, the scientists reveal a cellular signaling mechanism in place at the earliest developmental stage. Understanding the conditions that cause these cells to go off to different fates may have a bearing on health problems such as ectopic pregnancy, which occurs when the embryo develops outside of the womb in about 1 of 60 pregnancies, or molar pregnancy, which is abnormal tissue growth within the uterus that affects about 1 in every 1,000 pregnancies. “We originally were exploring factors that might cause embryonic stem cells to become malignant — there is a concern that these cells may cause tumors,” said Chi-Wei Lu, Ph.D., an associate neuroscientist at the UF College of Medicine and lead author of the study. “Our experiments led us to discover the signal that initiates the process of embryonic tissue differentiation.” By activating a gene called Ras in cells bathed in a very specific culture medium, scientists were able to cause embryonic stem cells — which originate from the inner cell mass of the blastocyst — to become more like the trophoblastic stem cells that give rise to the placenta from the outer portion of the blastocyst. Researchers marked these newly minted cells, which they called ES-TS cells, and injected them into mouse embryos. Instead of joining the stem cells that build the embryo, ES-TS cells joined the stem cells that build the placenta. Furthermore, when scientists transferred the engineered mouse embryos to foster mothers, the ES-TS cells went to work exclusively laying the foundation for the placenta. “This paper highlights the value of embryonic stem cells for understanding early development,” said senior author George Q. Daley, M.D., Ph.D., an associate professor of biological chemistry and molecular pharmacology at Harvard Medical School and an associate professor of pediatrics at Children’s Hospital Boston. “Embryonic stem cells are more plastic than we had thought. By simply activating the Ras gene, we changed the fate of embryonic stem cells to an entirely unexpected tissue — the placenta. This surprising result has given us an unanticipated insight into early embryo development.” The technique of genetically modifying the cells and growing them in a special medium could be valuable for additional research. “This is exciting because events that only occur in the early stages of embryonic development are very difficult to study,” Lu said. “Just a few models exist, and even in mice, only a limited amount of embryos can be harvested. Now we can culture these cells and have unlimited material to study.” Researchers are only beginning to understand the natural chemical environments that allow for production of different tissues. “What is nice is that what she has observed in cultures appears to be quite similar to what goes on in early development in animals,” said R. Michael Roberts, D.Phil., a professor of molecular biology at the C.S. Bond Life Sciences Center at the University of Missouri-Columbia who did not participate in the research. “Normally, mouse embryonic stem cells aren’t easily converted along the pathway to form placental cells, while human embryonic stem cells undergo this transition quite easily. This has always been a puzzle. What she has shown is you can make mouse embryonic stem cells convert unidirectionally to trophoblasts by activating a single gene. This is very helpful for understanding how the placenta develops.” Source: University of Florida Josh says: As the one author said, this certainly does show the importance of working with stem cells. It’s interesting though that a cancer gene, Ras, lead to the stem cells becoming placenta. |
| A Simple Lab Notebook Admin System [Bitesize Bio] Posted: 10 Jun 2008 12:31 AM CDT All of the hard work you do in the lab goes into your lab book. So if you’re not careful it can get quite difficult to find stuff in there after a while, especially if, like me, you use a number of different lab books at the same time. This simple numbering system can help you keep track of your lab book data more easily. Give each lab book a unique ID. The key to this numbering system is to give your lab book a unique and systematic identification code. A good format is your initials, followed by a numbering code. So Bitesize Bio’s first 3 lab books might be numbered BSB-001, BSB-002, BSB-003. But I prefer letters so I’ll use the alternative: BSB-AA, BSB-AB, BSB-AC. Now the pages have a unique ID too Now each lab book has a unique ID so if we number the pages of our lab book, each page we work on will have a unique ID too. So the first page in our first lab book would be numbered BSB-AA-01, and no other page we ever use will have this number. Why is this useful? Giving each page a unique and totally systematic name is very useful because now if we routinely label samples, experiments and protocols with the ID number of the page they were created/performed on we can easily track back to the original data. It is also very easy to identify samples. For example if we are doing an time course experiment with 5 different samples, the sample labeling can normally get a bit ambiguous and/or cumbersome, especially if we are looking at the samples a few weeks after performing the experiment. But, if in our lab book page (with it’s unique ID number) we make a table showing the 5 samples and label them 1-5, then it’s easy to make a unique identifier for each sample and time point. e.g. sample 2 at the 24 hour time point would be BSB-AA-01-1-24h. And no other sample can have that identifier, ever. The diagram below shows some examples where this labeling system can be used.
Would/do you do it like this? …or do you have a better way? Tell us in the comments. |
| Posted: 10 Jun 2008 12:12 AM CDT In PNAS: Intraspecific phylogenetic analysis of Siberian woolly mammoths using complete mitochondrial genomes (doi):
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| Friendfeed Comments [business|bytes|genes|molecules] Posted: 09 Jun 2008 11:34 PM CDT Those of you who have not done so better install FriendFeed Comments. The plugin pulls in comments and likes from a blog post on FriendFeed. Here is an example of the plugin in action  Further reading Technorati Tags: FriendFeed, Wordpress |
| Medicine and the iPhone [business|bytes|genes|molecules] Posted: 09 Jun 2008 10:31 PM CDT
Netter’s Anatomy is an app from Modality Learning. Here is a description of the product
While apps from Modality have been available on classic iPods in the past, the multitouch controls of the iPhone and other features are likely to take this to another level. One can easily extend this concept to other life science/biomedical applications, e.g. pathways, drug libraries, protein structures, etc. Think that is far fetched? Not so fast. The second app demoed was a product from MIMvista, which allows you to examine MRI’s and other images. Given the wi-fi capabilities, new sync capabilities, etc this is a powerful tool for anyone looking for rich, mobile applications. These announcements remind me of the BioIT World keynote by Josh Boger of Vertex, where he talked about how the iPhone can be used to track RFID tagged pill bottles, patient exercise regimens, carry patient records, monitor weight, etc. The future is NOW!!! Further reading Image by Getty Images via Daylife iphone, biomedical, mobile computing  |
| Pavlov's Bacteria [adaptivecomplexity's column] Posted: 09 Jun 2008 10:15 PM CDT One of the most useful things about having our brains is the ability to anticipate predictable events: we can see that it's going to rain, or that it's getting dark, and prepare accordingly. Some things in life are completely random, some are almost perfectly predictable (like the sun rising tomorrow at 5:35 AM in the Midwest US), and most other things are not quite so regular as the sunrise, but predictable nonetheless. We use neural networks in our brain to anticipate these events, but anticipation is obviously not limited to organisms that have brains. How do other organisms, like the single-celled E. coli anticipate change? |
| Worldwide differentiation at disease related SNPs [Yann Klimentidis' Weblog] Posted: 09 Jun 2008 09:59 PM CDT the objective: To address the strength of the CDCV model on a worldwide scale and to evaluate the effects of local positive selection on worldwide risk allele frequencies, we present allele frequencies and levels of population differentiation across 53 populations for 25 SNPs which show replicated association with the following common complex human diseases: Crohn's disease, type 1 diabetes, type 2 diabetes, rheumatoid arthritis, coronary artery disease and obesity [17, 26-42]the conclusion: disease-associated SNPs do not show more population differentiation than random SNPsI'm not so sure why one would expect a different result if you're looking at a set of polymorphisms related to risk to a bunch of different "diseases" (am I the only one getting tired of this term?). Also, I wonder, how exactly did they pick the 25 SNPs? Do the diseases in question differ in prevalence between worldwide populations? They may answer these in the paper, but my cursory reading of the paper did not find answers. Also, I remember someone blogging about this paper a while back, because one of the figures looked very familiar. I thought it was someone at GNXP, but I can't find it... anyone know?? Worldwide population differentiation at disease-associated SNPs. Myles S, Davison D, Barrett J, Stoneking M, Timpson N. BMC Med Genomics. 2008 Jun 4;1(1):22. [Epub ahead of print] Abstract: BACKGROUND: Recent genome-wide association (GWA) studies have provided compelling evidence of association between genetic variants and common complex diseases. These studies have made use of cases and controls almost exclusively from populations of European ancestry and little is known about the frequency of risk alleles in other populations. The present study addresses the transferability of disease associations across human populations by examining levels of population differentiation at disease-associated single nucleotide polymorphisms (SNPs). METHODS: We genotyped ~1000 individuals from 53 populations worldwide at 25 SNPs which show robust association with 6 complex human diseases (Crohns disease, type 1 diabetes, type 2 diabetes, rheumatoid arthritis, coronary artery disease and obesity). Allele frequency differences between populations for these SNPs were measured using Fst. The Fst values for the disease-associated SNPs were compared to Fst values from 2750 random SNPs typed in the same set of individuals. RESULTS: On average, disease SNPs are not significantly more differentiated between populations than random SNPs in the genome. Risk allele frequencies, however, do show substantial variation across human populations and may contribute to differences in disease prevalence between populations. We demonstrate that, in some cases, risk allele frequency differences are unusually high compared to random SNPs and may be due to the action of local (i.e. geographically-restricted) positive natural selection. Moreover, some risk alleles were absent or fixed in a population, which implies that risk alleles identified in one population do not necessarily account for disease prevalence in all human populations. CONCLUSIONS: Although differences in risk allele frequencies between human populations are not unusually large and are thus likely not due to positive local selection, there is substantial variation in risk allele frequencies between populations which may account for differences in disease prevalence between human populations. |
| Radioactive beer belly determined early in life [Bayblab] Posted: 09 Jun 2008 09:24 PM CDT  Apparently you can tell how old cells are based upon pulse chase-like experiments. A group of researchers has done this on human subjects and found that the turnover rate for fat cells is about 10% per year. This result was independent of body mass index and suggests that in early childhood the number of fat cells is determined. Not only is that interesting itself but also interesting is the fact that the 'pulse' used in these experiments were provided by nuclear bomb tests. Genius. At my current computer I can't access the paper, but I wonder if they looked at any other tissues? |
| Plant kin recognition? (Caution - Anthropocentrism ahead) [The Tree of Life] Posted: 09 Jun 2008 09:17 PM CDT A fascinating story in the New York Times today on kin recognition in plants (see Plants Found to Show Preferences for Their Relatives ). They report The sea rocket, researchers report, can distinguish between plants that are related to it and those that are not. And not only does this plant recognize its kin, but it also gives them preferential treatment.And
The notion that plants sense and respond to their surroundings is apparently controversial. Or, maybe a better way to put it is, the attempts to compare plant to animal neural functions is controversial. So much so that many plant scientists got together to say enough is enough Thirty-six authors from universities that included Yale and Oxford were exasperated enough to publish an article last year, "Plant Neurobiology: No Brain, No Gain?" in the journal Trends in Plant Science. The scientists chide the new society for discussing possibilities like plant neurons and synapses, urging that the researchers abandon such "superficial analogies and questionable extrapolations." I personally think there is an enormous amount of anthropocentrism here. Sure, plants may not have true brains. But even though many people like to think of animals in general and humans in particular as the be all end all of evolution, last time I checked, plants have been evolving for a long time. And there is no reason to think that they do not have all sorts of cool and wacky ways to sense and respond to the world around them. The same anthropocentric point of view has led scientists to grossly underestimate the complexity of phenomena in microbes too. Microbes in fact can sense and respond to kin, they can count, they can tell time, they have immune systems. In other words, whether small or large, furry or not, simple or complex (in appearance) lots of cool things have evolved in lineages that do not lead up to humans. Well, everyone. As we continue to delve into the biology of non animals more deeply, we are going to find all sorts of cool things out there. And yes, some of it will be even more complex and interesting and wacky than what we see in animals. For other stuff on this story see |
One of the cooler moments in my life was when 
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