The DNA Network |
| You say tomato… [genomeboy.com] Posted: 20 May 2008 07:53 PM CDT …I say Onion. |
| around the blogs [the skeptical alchemist] Posted: 20 May 2008 07:28 PM CDT This is a mesh of interesting science-related news gathered from blog and traditional media. But I would not know most of these things if it weren't for my blogging addiction. Alex Palazzo informs us that there is a new networking tool out there for the scientist 2.0 (something tells us that generations X and Y will be all over this). The tool is called SciLink, and it can be described as a version of LinkedIn for scientists and people in academic careers. Apparently it is not completely bug-proof, but it might be worth checking it out. An old piece of DNA has been resuscitated. This does not qualify as a revival or remake of Jurassic Park, but it shows that ancient DNA can sometimes be rescued and even studied in vivo, granted that you had some samples preserved in decent conditions. Some century-old Tasmanian tiger pouch young and a team of Australian scientists need to be credited for this achievement. But fear not, the Tasmanian tiger (just like mammoths and T Rex before it) will not be resuscitated any time soon. And you should not fear dead bodies either - at least, when it comes to natural disasters. Did you know that dead bodies do not cause disease epidemics? If you are unconvinced, pay a visit to Effect Measure. Talking about old, but not dead, the old prejudices and ideologies linked to creationism are so hard to defeat that, it turns out, about 16% of American science teachers might actually subscribe to creationist views. As the authors of the study, reviewed over at The Lay Scientist point out,
And to conclude, have you checked your tissue culture? It might be infected with Mycoplasma hominis. So make sure you always wash your hands after you go to the washroom or after you do...whatever it is you have done! View blog reactions |
| Incense is psychoactive: Scientists identify the biology behind the ceremony [Think Gene] Posted: 20 May 2008 06:52 PM CDT Religious leaders have contended for millennia that burning incense is good for the soul. Now, biologists have learned that it is good for our brains too. In a new study appearing online in The FASEB Journal (http://www.fasebj.org), an international team of scientists, including researchers from Johns Hopkins University and the Hebrew University in Jerusalem, describe how burning frankincense (resin from the Boswellia plant) activates poorly understood ion channels in the brain to alleviate anxiety or depression. This suggests that an entirely new class of depression and anxiety drugs might be right under our noses. "In spite of information stemming from ancient texts, constituents of Bosweilla had not been investigated for psychoactivity," said Raphael Mechoulam, one of the research study's co-authors. "We found that incensole acetate, a Boswellia resin constituent, when tested in mice lowers anxiety and causes antidepressive-like behavior. Apparently, most present day worshipers assume that incense burning has only a symbolic meaning." To determine incense's psychoactive effects, the researchers administered incensole acetate to mice. They found that the compound significantly affected areas in brain areas known to be involved in emotions as well as in nerve circuits that are affected by current anxiety and depression drugs. Specifically, incensole acetate activated a protein called TRPV3, which is present in mammalian brains and also known to play a role in the perception of warmth of the skin. When mice bred without this protein were exposed to incensole acetate, the compound had no effect on their brains. "Perhaps Marx wasn't too wrong when he called religion the opium of the people: morphine comes from poppies, cannabinoids from marijuana, and LSD from mushrooms; each of these has been used in one or another religious ceremony." said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Studies of how those psychoactive drugs work have helped us understand modern neurobiology. The discovery of how incensole acetate, purified from frankincense, works on specific targets in the brain should also help us understand diseases of the nervous system. This study also provides a biological explanation for millennia-old spiritual practices that have persisted across time, distance, culture, language, and religion—burning incense really does make you feel warm and tingly all over!" According to the National Institutes of Health, major depressive disorder is the leading cause of disability in the United States for people ages 15–44, affecting approximately 14.8 million American adults. A less severe form of depression, dysthymic disorder, affects approximately 3.3 million American adults. Anxiety disorders affect 40 million American adults, and frequently co-occur with depressive disorders. Source: Federation of American Societies for Experimental Biology Josh says: After all this time, we’re still finding novel ways in which ion channels are activated in the brain. I’ve always liked burning incense, now I know one reason why. This does seem promising though as a new mode of action for anti-depressants, which have some nasty withdrawal effects when people go off them. |
| “Tweaking” experimental data [Think Gene] Posted: 20 May 2008 05:56 PM CDT Earlier today, I read a blog post by Mark Chu-Carroll titled, Selective Data and Global Warming. The post is primarily concerned a global warming “denialist” Tim Lambert who dishonestly presented global climate data to force it to fit his anti-global warming agenda. While reading it, I couldn’t help but be reminded that this type of dishonesty happens all the time in science. Most often, scientific experiments do not give simple conclusive results. The data must be “interpreted,” and statistical methods must be “applied.” I’ve seen cases where researchers sat and “tweaked” the statistics to favor their hypothesis with the same aggressive dishonesty as this global warming denialist. A perfect example of this is the software for many real time PCR machines. They allow you to adjust parameters in the data interpretation. While the initial results may not support your hypothesis, it’s almost trivial to play around in the program and make the data fit. The data itself is not changed, but merely the interpretation of it is. To avoid this problem, experiments should be repeated in different ways to ensure the interpreted results are the actual results. If several different runs with different controls and different samples are performed, the real results cannot be hidden with these manipulations, however in my experience I’ve only seen this done if the results are not as expected. This leads into my next point: experiments don’t always work. Experiments are supposed to be repeated several times with multiple levels of controls to ensure the reliability and accuracy of the results. However, I know far too many scientists who will take the results of an experiment that matches what they want the outcome to be, and then never repeat the experiment. Or an experiment was not giving the expected results, but one time out of 10 it will. They will simply take these results and ignore the other experiments, claiming there must have been an error the first 9 times. They are not faking the data, but merely selecting the data they want rather than being unbiased as a scientist should be. The greatest enemy of data integrity is Photoshop. Every scientist knows how to use Photoshop. It’s used for many legitimate purposes, such as preparing images and data for publication. It’s also used to clean up images. Unfortunately, it can also be used to manipulate data. An example is to make a band on an agarose gel darker or lighter, or to combine the results of different experiments together into one image. The latter case in many instances is perfectly acceptable, but results can also be mixed and matched to fit the hypothesis. There is simply no way to know. So why do scientists “tweak” their data? One explanation could be vanity and arrogance, but I think the real problem stems to funding and the ever present pressure to publish, publish, publish. The livelihood of many scientists, especially those in the biological sciences, is dependent upon NIH grants or other sources of funding. To get these grants, they must show progress and results. This usually is in the form of papers they publish, which is also tied to them getting tenure at a university. Papers don’t get published about someone’s hypothesis being wrong; they only get published if someone’s hypothesis is correct. If a scientist spends a year investigating a hypothesis he has, and it turns out that the data doesn’t support it, he’s in quite a bind; oftentimes he feels forced to make the data fit to get a paper out. If these practices continue, it will seriously hurt scientific progress. While many scientists do follow correct practices and don’t manipulate their data or its interpretations, there unfortunately are also many who do. |
| SciLink - the LinkedIn for Scientists [The Daily Transcript] Posted: 20 May 2008 03:48 PM CDT I've been receiving requests from the newest networking program. I've given up fighting and just joined in. So what's special about this new networking site? Well, in contrast to LinkedIn there are special features that are more applicable to academics in general. For example you can add papers and awards to your profile. And unlike Facebook's SciBook, SciLink is a true science networking tool. It also comes with a cool scientific genealogy application. (Evil Gomez - someone has finally implemented your idea!) There are some patches that the developers need to iron out, but overall it looks like the best science networking site that I know of. Go sign up now (and feel free to invite me to your network, but let me know if you really know me or just know my blog.) Read the comments on this post... |
| Whad'ya Know About Protists? [evolgen] Posted: 20 May 2008 03:30 PM CDT My advisor has recently got me listening to Whad'ya Know. My first reaction: It's like Wait Wait...Don't Tell Me! Only not as funny, not as interesting, and not as good. I've been downloading the podcasts for the past couple of weeks, and I'm not sure whether I'll keep subscribing in iTunes. I'm only bringing this up because last week's episode contained a very egregious example of someone knowing just enough biology to get themselves in trouble. The sad part was that the person should have known better. Why? She teaches biology at the university level. What happened? At the midpoint of the first hour of the show, Michael Feldman conducted the quiz. The in-house participant was Deb, a grasslands ecologist. Deb was asked about the diet of early Americans, which turned out to be seaweed. Deb then pointed out that seaweed is not a plant. Huh? Then she said it's algae, which is a protist. Really? Deb doth protist too much, methinks. Read the rest of this post... | Read the comments on this post... |
| Posted: 20 May 2008 12:29 PM CDT Every now and then, mycoplasma contamination rears its ugly head and threatens tissue culture experiments. According to a paper in the Journal of Cell Science (albeit published in 1966), the most common variety of mycoplasma found in contaminated cultures is M. hominis type 1. Mycoplasma hominis is most commonly found in the genital area. What are these people doing with thier cultures to get them infected? |
| Evolution: Winning in Court But Losing In Class? [adaptivecomplexity's column] Posted: 20 May 2008 12:27 PM CDT In the perpetual fight over evolution in public schools, there is good news and bad news. The good news is that supporters of science education have largely been successful in shutting down creationist attempts to undermine evolution through state legislatures and state school boards. While there is still mischief going on in many state legislatures, these efforts rarely go anywhere, thanks to vigilance by supporters of good science education. An essay in PLoS Biology today argues that, at the state level, things are going well:
But here comes the bad news:
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| Lord of the Rings is Based on Grad School - Who Knew? [Bayblab] Posted: 20 May 2008 11:43 AM CDT Pretty apt description of the PhD experience. LOLZ. Lord of the Rings: an allegory of the PhD?The story starts with Frodo: a young hobbit, quite bright, a bit dissatisfied with what he's learnt so far and with his mates back home who just seem to want to get jobs and settle down and drink beer. He's also very much in awe of his tutor and mentor, the very senior professor Gandalf, so when Gandalf suggests he take on a short project for him (carrying the Ring to Rivendell), he agrees. Frodo very quickly encounters the shadowy forces of fear and despair which will haunt the rest of his journey and leave permanent scars on his psyche, but he also makes some useful friends. In particular, he spends an evening down the pub with Aragorn, who has been wandering the world for many years as Gandalf's postdoc and becomes his adviser when Gandalf isn't around. After Frodo has completed his first project, Gandalf (along with head of department Elrond) proposes that the work should be extended. He assembles a large research group, including visiting students Gimli and Legolas, the foreign postdoc Boromir, and several of Frodo's own friends from his undergraduate days. Frodo agrees to tackle this larger project, though he has mixed feelings about it. ("'I will take the Ring', he said, 'although I do not know the way.'") Very rapidly, things go wrong. First, Gandalf disappears and has no more interaction with Frodo until everything is over. (Frodo assumes his supervisor is dead: in fact, he's simply found a more interesting topic and is working on that instead.) At his first international conference in Lorien, Frodo is cross-questioned terrifyingly by Galadriel, and betrayed by Boromir, who is anxious to get the credit for the work himself. Frodo cuts himself off from the rest of his team: from now on, he will only discuss his work with Sam, an old friend who doesn't really understand what it's all about, but in any case is prepared to give Frodo credit for being rather cleverer than he is. Then he sets out towards Mordor. The last and darkest period of Frodo's journey clearly represents the writing-up stage, as he struggles towards Mount Doom (submission), finding his burden growing heavier and heavier yet more and more a part of himself; more and more terrified of failure; plagued by the figure of Gollum, the student who carried the Ring before him but never wrote up and still hangs around as a burnt-out, jealous shadow; talking less and less even to Sam. When he submits the Ring to the fire, it is in desperate confusion rather than with confidence, and for a while the world seems empty. Eventually it is over: the Ring is gone, everyone congratulates him, and for a few days he can convince himself that his troubles are over. But there is one more obstacle to overcome: months later, back in the Shire, he must confront the external examiner Saruman, an old enemy of Gandalf, who seeks to humiliate and destroy his rival's protege. With the help of his friends and colleagues, Frodo passes through this ordeal, but discovers at the end that victory has no value left for him. While his friends return to settling down and finding jobs and starting families, Frodo remains in limbo; finally, along with Gandalf, Elrond and many others, he joins the brain drain across the Western ocean to the new land beyond. |
| Helix Health Genomic Medicine Webcast [Eye on DNA] Posted: 20 May 2008 11:38 AM CDT
Fellow DNA Network member, Dr. Steven Murphy, and his company, Helix Health, will be hosting a webcast tomorrow, May 21, 2008 at 1:00 pm EDT. How Genomic Medicine Is Changing the Management of Breast & Ovarian Cancer Registration is free and will feature Jessica Queller, author of Pretty is What Changes: Impossible Choices, The Breast Cancer Gene and How I Defied My Destiny. |
| Helix Health Genomic Medicine Webcast [Eye on DNA] Posted: 20 May 2008 11:38 AM CDT
Fellow DNA Network member, Dr. Steven Murphy, and his company, Helix Health, will be hosting a webcast tomorrow, May 21, 2008 at 1:00 pm EDT. How Genomic Medicine Is Changing the Management of Breast & Ovarian Cancer Registration is free and will feature Jessica Queller, author of Pretty is What Changes: Impossible Choices, The Breast Cancer Gene and How I Defied My Destiny. |
| New pigmentation loci found [Yann Klimentidis' Weblog] Posted: 20 May 2008 11:33 AM CDT IRF4 and SLC24A4, according to this GWAS among people of European ancestry. A Genome-Wide Association Study Identifies Novel Alleles Associated with Hair Color and Skin Pigmentation Jiali Han et al. PLoS Genet 4(5): e1000074 Abstract: We conducted a multi-stage genome-wide association study of natural hair color in more than 10,000 men and women of European ancestry from the United States and Australia. An initial analysis of 528,173 single nucleotide polymorphisms (SNPs) genotyped on 2,287 women identified IRF4 and SLC24A4 as loci highly associated with hair color, along with three other regions encompassing known pigmentation genes. We confirmed these associations in 7,028 individuals from three additional studies. Across these four studies, SLC24A4 rs12896399 and IRF4 rs12203592 showed strong associations with hair color, with p = 6.0×10−62 and p = 7.46×10−127, respectively. The IRF4 SNP was also associated with skin color (p = 6.2×10−14), eye color (p = 6.1×10−13), and skin tanning response to sunlight (p = 3.9×10−89). A multivariable analysis pooling data from the initial GWAS and an additional 1,440 individuals suggested that the association between rs12203592 and hair color was independent of rs1540771, a SNP between the IRF4 and EXOC2 genes previously found to be associated with hair color. After adjustment for rs12203592, the association between rs1540771 and hair color was not significant (p = 0.52). One variant in the MATP gene was associated with hair color. A variant in the HERC2 gene upstream of the OCA2 gene showed the strongest and independent association with hair color compared with other SNPs in this region, including three previously reported SNPs. The signals detected in a region around the MC1R gene were explained by MC1R red hair color alleles. Our results suggest that the IRF4 and SLC24A4 loci are associated with human hair color and skin pigmentation. |
| Lederberg Workshop LiveNotes [The Tree of Life] Posted: 20 May 2008 09:17 AM CDT I am going to keep posting here notes from the various talks ...
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| Lederberg Workshop Intro [The Tree of Life] Posted: 20 May 2008 08:32 AM CDT Well, I am sitting in the Lederberg workshop right now with David Relman talking about Lederberg and the workshop. He is emphasizing how "microbes as threats" (which is similar to the name of the panel that convened this workshop) is a bit of a biased view point and that beneficial microbes are important too and that Lederberg recognized this. Relman is also mentioning the importance of Esther Lederberg (Josh Lederberg's first wife). Now - some update on last night. I got to the hotel around 3 went walking around DC and then came back to the hotel. All the speakers were supposed to be staying there so I lingered in the lobby hoping to bump into people I knew and find someone to go to dinner with. And I sat down and started reading a book I just got - Microcosm by Carl Zimmer. Zimmer's book is about E. coli and the history of studies of this magnificent organisms. And I started by lookng up in the index the stuff on Lederberg and read that. The book really seems to be quite excellent --- it covers a wide range of topics in biology at the same time as highlighting the importance of this organism. And then the gurus of microbiology started coming by. And I snookered my way into dinner with Julian Davies, Bruce Levin and Stanley Cohen. And it ewas a great time --- talking about Lederberg, microbes, plasmids, selection, etc. A good start to the meeting for me. More later. |
| Is this really useful? [Mailund on the Internet] Posted: 20 May 2008 02:16 AM CDT Google Health is up and running. See a review here. My first thought was: “who would use such a service?” I don’t have much of a “medical history” to keep track of. I’m not eating any regular medicine and never had, and in any case it is not something I want to try to keep track of myself. I trust my physician and would want him to figure out what medicine I need, if any. I want him to keep track of my medical history. He is the expert, that is why I go to him. I don’t want to second guess experts in a field where I have very little knowledge. So really, what’s the point in using Google Health? |
| New long read sequencing technology [Mailund on the Internet] Posted: 20 May 2008 01:47 AM CDT At Next Generation Sequencing I saw a review of a new sequencing technology that allows for long reads, unlike all the other new sequencing methods. While the other technologies read sequences of up to a hundred base-pairs, this can potentially read thousands. This is exciting since this longer reads are needed to deal with repetitive regions and since longer reads will enable us to sequence phased chromosomes and not the mix of two chromosomes we usually get. The review is silent on when we can expect this technology in use or how fast it will be and such, but I hope it is not just vapour-ware. |
| TED talks: physics [Mailund on the Internet] Posted: 20 May 2008 01:09 AM CDT I’ve always loved physics, I’ve just never been smart enough to study it… Table of contents for TED Talks
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| Some like it hot! Structure of receptor for hot chili pepper and pain revealed [Think Gene] Posted: 19 May 2008 11:27 PM CDT You can now not only feel the spicy kick of a jalapeno pepper, you can also see it in full 3D, thanks to researchers at Baylor College of Medicine in Houston. Using sophisticated equipment, the research team led by Dr Theodore G. Wensel, professor of biochemistry and molecular biology at BCM, generated the first three dimensional view of the protein that allows you to sense the heat of a hot pepper. The report appears in the current issue of the Proceedings of the National Academy of Sciences. "This protein, known as TRPV1, not only senses spicy foods, but also makes it possible to feel real heat and the pain and inflammation related to other medical conditions," said Wensel, senior author on the study. "This method of viewing the protein now gives us the chance to clearly see the functional relationship between outside stimuli and the nerve cell." The outside stimulus used in this study was the heat of a chili pepper. It has been known for years that the burning sensation results from the action of a chemical known as capsaicin on TRPV1 found on the nerve cell membrane. TRPV1 is an ion channel, a tiny pore on the cell membrane that allows chemicals such as calcium to flux in and out.
Wensel said the three-dimensional image of TRPV1 revealed surprising information about its structure. It is made up of a pore domain embedded in the cell membrane, and a "hanging basket" of regulatory domains that extend into the interior of the cell. "It's an unusual thing. There is a whole hollow 'basket' area but we don't know what's that's for," Wensel said. "Now the search is on to understand how the 'basket' area regulates the channel." Isolating TRPV1 gives researchers an idea of how other channels are structured as well. "Visualization of TRPV1 gives us insight on other TRP channels since they are structurally similar," said Moiseenkova-Bell. "Pharmaceutical companies target these TRP channels to make sure the drug binds properly. With this first structure we can start to build models of binding sites and hopefully in the future design more effective pharmaceuticals for a wide range of medical conditions." Studying these channels is nothing new. In the past, scientists could measure the activity in the cells but it was unclear what each channel was responding to. Determining which proteins interacted with TRPV1, however, required Wensel's lab to create a purified model. The protein had to be removed from cells, purified, and reconstituted in a synthetic membrane so researchers could control channel activity. "Since calcium is involved in cell signaling, following the calcium movement confirmed the protein is active," said Wensel. "We are the first group to purify a TRPV1 channel and control what goes in and out when the channel opens." Source: Baylor College of Medicine |
| Researchers bring new meaning to the term ‘computer bug’ [Think Gene] Posted: 19 May 2008 11:17 PM CDT US researchers have created 'living computers' by genetically altering bacteria. The findings of the research, published in BioMed Central's open access Journal of Biological Engineering, demonstrate that computing in living cells is feasible, opening the door to a number of applications including data storage and as a tool for manipulating genes for genetic engineering. A research team from the biology and the mathematics departments of Davidson College, North Carolina and Missouri Western State University, Missouri, USA added genes to Escherichia coli bacteria, creating bacterial computers able to solve a classic mathematical puzzle, known as the burnt pancake problem. The burnt pancake problem involves a stack of pancakes of different sizes, each of which has a golden and a burnt side. The aim is to sort the stack so the largest pancake is on the bottom and all pancakes are golden side up. Each flip reverses the order and the orientation (i.e. which side of the pancake is facing up) of one or several consecutive pancakes. The aim is to stack them properly in the fewest number of flips. In this experiment, the researchers used fragments of DNA as the pancakes. They added genes from a different type of bacterium to enable the E. coli to flip the DNA 'pancakes'. They also included a gene that made the bacteria resistant to an antibiotic, but only when the DNA fragments had been flipped into the correct order. The time required to reach the mathematical solution in the bugs reflects the minimum number of flips needed to solve the burnt pancake problem. "The system offers several potential advantages over conventional computers" says lead researcher, Karmella Haynes. "A single flask can hold billions of bacteria, each of which could potentially contain several copies of the DNA used for computing. These 'bacterial computers' could act in parallel with each other, meaning that solutions could potentially be reached quicker than with conventional computers, using less space and at a lower cost." In addition to parallelism, bacterial computing also has the potential to utilize repair mechanisms and, of course, can evolve after repeated use. Source: BioMed Central Andrew says: And what kind of problems is this immediately useful? Comparative genomics. From the paper:
Note: “syntenic” is not a typo for “synthetic,” it means when two genes are on the same chromosome. All genetically linked loci are syntenic, but not all syntenic loci are genetically linked. |
| Sherlock Holmes, Omicist [Omics! Omics!] Posted: 19 May 2008 11:02 PM CDT A nice item in GenomeWeb about a new NIH initiative that's just brilliant -- using omics to try to solve rare disease mysteries. I've blogged on this topic before, and it's an obvious way to go -- particularly since the price of these genome studies is dropping so precipitiously. As noted by the patient named in the report, finding a cause is not (alas!) the same as finding a treatment. But if many patients with mystery diseases are screened, there will almost certainly be some clues that do lead to useful remedies. It is also important to remember that very rare syndromes often shed important light on very common disorders. For example, a large number of rare tumor syndromes have illuminated key cellular mechanisms broadly relevant to tumorigenesis -- von Hippel-Lindau, neurofibromatosis, and many others. Having some molecular clue to the disease is infinitely better than a baffling list of symptoms. |
| Vaccine triggers immune response, prevents Alzheimer’s [Think Gene] Posted: 19 May 2008 10:25 PM CDT A vaccine created by University of Rochester Medical Center scientists prevents the development of Alzheimer's disease-like pathology in mice without causing inflammation or significant side effects. Vaccinated mice generated an immune response to the protein known as amyloid-beta peptide, which accumulates in what are called "amyloid plaques" in brains of people with Alzheimer's. The vaccinated mice demonstrated normal learning skills and functioning memory in spite of being genetically designed to develop an aggressive form of the disease. The Rochester scientists reported the findings in an article in the May issue of Molecular Therapy, the journal of The American Society of Gene Therapy. "Our study demonstrates that we can create a potent but safe version of a vaccine that utilizes the strategy of immune response shaping to prevent Alzheimer's-related pathologies and memory deficits," said William Bowers, associate professor of neurology and of microbiology and immunology at the Medical Center and lead author of the article. "The vaccinated mice not only performed better, we found no evidence of signature amyloid plaque in their brains." Alzheimer's is a progressive neurodegenerative disease associated with dementia and a decline in performance of normal activities. Hallmarks of the disease include the accumulation of amyloid plaques in the brains of patients and the loss of normal functioning tau, a protein that stabilizes the transport networks in neurons. Abnormal tau function eventually leads to another classic hallmark of Alzheimer's, neurofibrillary tangle in nerve cells. After several decades of exposure to these insults, neurons ultimately succumb and die, leading to progressively damaged learning and memory centers in the brain. The mice that received the vaccines were genetically engineered to express large amounts of amyloid beta protein. They also harbored a mutation that causes the tau-related tangle pathology. Prior to the start of the vaccine study, the mice were trained to navigate a maze using spatial clues. They were then tested periodically during the 10-month study on the amount of time and distance traveled to an escape pod and the number of errors made along the way. "What we found exciting was that by targeting one pathology of Alzheimer's — amyloid beta — we were able to also prevent the transition of tau from its normal form to a form found in the disease state," Bowers said. The goal of the vaccine is to prompt the immune system to recognize amyloid beta protein and remove it. To create the vaccine, Bowers and the research group use a herpes virus that is stripped of the viral genes that can cause disease or harm. They then load the virus container with the genetic code for amyloid beta and interleukin-4, a protein that stimulates immune responses involving type 2 T helper cells, which are lymphocytes that play an important role in the immune system. The research group tested several versions of a vaccine. Mice were given three injections of empty virus alone, a vaccine carrying only the amyloid beta genetic code, or a vaccine encoding both amyloid beta and interlueikin-4, which was found to be the most effective. "We have learned a great deal from this ongoing project," Bowers said. "Importantly, it has demonstrated the combined strengths of the gene delivery platform and the immune shaping concept for the creation of customized vaccines for Alzheimer's disease, as well as a number of other diseases. We are currently working on strategies we believe can make the vaccine even safer." Bowers expects the vaccine eventually to be tested in people, but due to the number of studies required to satisfy regulatory requirements, it could be three or more years before human trials testing this type of Alzheimer's vaccine occur. Source: University of Rochester Medical Center Josh says: This is fantastic. I see no reason why this can’t also be applied to other similar diseases. I wonder if the same technique could be used for prion diseases like mad cow disease. |
| Turning back the clock for Schwann cells [Think Gene] Posted: 19 May 2008 09:45 PM CDT Myelin-making Schwann cells have an ability every aging Hollywood star would envy: they can become young again. According to a study appearing in the May 19 issue of the Journal of Cell Biology, David B. Parkinson (University College London, London, UK) and collogues have pinned down a protein that returns the cells to their youth, a finding that might help researchers understand why myelin production falters in some diseases. Wrapped around neurons in the peripheral nervous system, Schwann cells can "dedifferentiate" into a state in which they can't manufacture myelin. Reverting to an immature type of cell speeds healing of injured nerves. Researchers knew that the protein Krox-20 pushes immature Schwann cells to specialize and form myelin, but they didn't know what prompts the reversal. One suspect was a protein called c-Jun, which youthful Schwann cells make but Krox-20 blocks. Parkinson et al. cultured neurons with Schwann cells whose c-Jun gene they could activate. Turning on the gene curbed myelination, suggesting that c-Jun prevents young Schwann cells from growing up. c-Jun also prodded mature Schwann cells to become youthful again, the researchers discovered. Schwann cells that are separated from neurons normally dedifferentiate, but the team found that the cells remained specialized if c-Jun was missing. They suspect that c-Jun works in part by activating Sox-2, as this protein also inhibits myelination. The researchers now want to investigate whether c-Jun is involved in illnesses where myelin dwindles, such as Charcot-Marie Tooth disease and Guillain-Barre syndrome. The results might also provide clues about multiple sclerosis, in which immune attacks destroy myelin in the central nervous system. Unlike Schwann cells, oligodendrocytes, the myelin makers in the central nervous system, can't revert to an immature state. Whether c-Jun affects oligodendrocyte differentiation isn't known. Source: Rockefeller University Parkinson, D.B., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200803013 Josh says: Sox-2 is a very common developmental transcription factor. I think it’s really interesting that the same set of proteins and transcription factors is seen over and over again for different uses. During embryogenesis, Sox2 is sometimes used as an epithelial marker and is commonly found in neural precursor cells. |
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