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| New: CliniChats by Gene Sherpas! [Think Gene] Posted: 15 Aug 2008 07:42 PM CDT CliniChats are regular, informal videos about genomics in health and the latest news in personalized medicine. Subscribe to the NEW CliniChats YouTube channel! (I may or may not be affiliated with the production of CliniChats…) CliniChats #1: Genomic Medicine
CliniChats #2: Abacavir Testing
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| Do not drink liquid nitrogen [Bayblab] Posted: 15 Aug 2008 12:56 PM CDT Because of safety reasons all my bottles of reagents on my shelf are labeled "do not drink" (except my ddH2O, that one is labeled "only drink if very thirsty"). I always thought it was a ridiculous precaution because who in their right mind would drink from a bottle in a lab. I mean if you're going write that, might as well add "do not use for enema". Well I guess I'm just not gifted: August 15, 2008 -- A gifted 15-year-old student from India had to be rushed to the hospital after drinking liquid nitrogen during a science class at Princeton University. The class was part of a program run by the Connecticut-based Summer Institute for the Gifted. |
| Scientists discover major genetic cause of colorectal cancer [Think Gene] Posted: 15 Aug 2008 11:00 AM CDT Josh: This is an extremely high penetrance mutation. More doctors and physicians need to be trained to order genetic tests for mutations such as this for their patients, especially those with a family history of colorectal cancer. If someone has this mutation, chances are they are going to get colorectal cancer, so routine screenings may be enough to save their life…preventative medicine at its best. About one-third of colorectal cancers are inherited, but the genetic cause of most of these cancers is unknown. The genes linked to colorectal cancer account for less than 5 percent of all cases. Scientists at Northwestern University’s Feinberg School of Medicine and colleagues have discovered a genetic trait that is present in 10 to 20 percent of patients with colorectal cancer. The findings strongly suggest that the trait is a major contributor to colorectal cancer risk and likely the most common cause of colorectal cancer to date. If a person inherits this trait — which is dominant and clusters in families — the study found the lifetime risk of developing colorectal cancer is 50 percent, compared to 6 percent for the general population. The study will be published August 14 in an advanced on-line report in the journal Science. “This probably accounts for more colorectal cancers than all other gene mutations discovered thus far,” said Boris Pasche, M.D., a lead author of the paper and director of the Cancer Genetics Program at the Feinberg School and the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. Pasche also is a physician at Northwestern Memorial Hospital. “The reasonable expectation is this finding will save some lives,” Pasche said. “We will be able to identify a larger number of individuals that are at risk of colorectal cancer and, in the long term, maybe decrease the cases of colorectal cancer and of people dying from it by being able to screen them more frequently.” Colorectal cancer is the second leading cause of cancer death in the U.S. The trait, which has been named TGFBR1 ASE, results in decreased production of a key receptor for TGF-beta, the most potent inhibitor of cell growth. With less of this vital protective substance to inhibit cell growth, colon cancer can more easily develop. In 1998, Pasche and colleagues discovered the first mutation of this gene and in 1999 they showed that it was linked to a higher risk of colorectal cancer. The results presented in this new study are the first to show that decreased production of this receptor for TGF-beta was present in 10 to 20 percent of patients with colorectal cancer. Decreased production of the same receptor was present in only 1 to 3 percent in healthy control groups. The findings, which are based on a Caucasian population, need to be confirmed in other studies and may show strong variation between ethnic groups, Pasche said. Pasche expects that a clinical test will soon be developed that could be offered to families with a history of colorectal cancer and other individuals to determine whether they carry this mutation. Source: Northwestern University Germline Allele-specific Expression of TGFBR1 Confers an Increased Risk of Colorectal Cancer. Laura Valle, Tarsicio Serena-Acedo, Sandya Liyanarachchi, Heather Hampel, Ilene Comeras, Zhongyuan Li, Qinghua Zeng, Hong-Tao Zhang, Michael J. Pennison, Maureen Sadim, Boris Pasche, Stephan M. Tanner, and Albert de la Chapelle. Science. Published online August 14 2008; 10.1126/science.1159397 (Science Express Reports) |
| And the junk DNA train rolls on... [Genomicron] Posted: 15 Aug 2008 07:40 AM CDT This appeared in my weekly automated journal search. I have ordered the paper as I can't find an online copy, but the abstract pretty much covers what the argument will be. Same old pre-1980s adaptationist idea presented as radically novel. Mallik, M. and Lakhotia, S.C. 2008. Noncoding DNA is not "junk" but a necessity for origin and evolution of biological complexity. Proceedings of the Indian National Science Academy Section B - Biological Sciences 77 (Sp. Iss.): 43-50.See also: Junk DNA and the Onion Test. |
| wiki for reporter assay? [Reportergene] Posted: 15 Aug 2008 04:58 AM CDT According to my referrals, these are the keywords most searched in the last period (wordle elaboration). Lot of people is looking for a wiki of reporter genes (top left), does this resource eventually be useful for you? I'll think about it at the seaside. Holidays!  |
| Around the Blogs [Bitesize Bio] Posted: 15 Aug 2008 01:49 AM CDT In this week’s round-up of bio-related blogs: The smell of the sea breeze, corporal punishment in the lab and a surprising side-dish that comes with your sushi.
Oh I do like to be beside the seaside. Alan at Microbiology Bytes picks up on a Microbiology Today articles on the microbial genetic origins of that seaside tang. A hard Knight. The Black Knight thinks that lab newbies just aren’t scared enough these days. For your information. Alex at The Daily Transcript gives his viewpoint on Dan’s recent article about Sir Paul Nurse’s use of information processing as an analogy for biological processes. Blood-line. Nobel Intent’s John Timmer describes how Japanese scientists have managed to produce human red blood cells from embryonic stem cells. United Colors of Biotech. Aminopop has a nice succinct description of green, red and white biotech, and a nice image to go with it. Mad on Virophages. Mike the Mad Biologist highlights a Nature article on Virophages; viruses that prey on viruses. Less is more. Jonathan at Working the Bench gives a good tip for anyone having PCR problems. and finally… Do you love Sushi? Not anymore. |
| Posted: 14 Aug 2008 09:21 PM CDT Josh: This is certainly an interesting study. I suppose the primary question I have is why do cells decrease the expression of the lysosomal receptors with age? Knowing that would be helpful, I think not only for aging and neurodegenerative research, but also for cancer research. Too bad this won’t really be a realistic treatment in its current state…however, perhaps a drug could be used to increase expression. As people age, their cells become less efficient at getting rid of damaged protein — resulting in a buildup of toxic material that is especially pronounced in Alzheimer’s, Parkinson’s disease, and other neurodegenerative disorders. Now, for the first time, scientists at the Albert Einstein College of Medicine of Yeshiva University have prevented this age-related decline in an entire organ — the liver — and shown that, as a result, the livers of older animals functioned as well as they did when the animals were much younger. Published in the online edition of Nature Medicine, these findings suggest that therapies for boosting protein clearance might help stave off some of the declines in function that accompany old age. The study’s senior author was Dr. Ana Maria Cuervo, associate professor in the departments of developmental & molecular biology, medicine and anatomy & structural biology at Einstein. The cells of all organisms have several surveillance systems designed to find, digest and recycle damaged proteins. Many studies have documented that these processes become less efficient with age, allowing protein to gradually accumulate inside cells. But aging researchers continue debating whether this protein buildup actually contributes to the functional losses of aging or instead is merely associated with those losses. The Einstein study was aimed at resolving the controversy. One of these surveillance systems — responsible for handling 30 percent or more of damaged cellular protein — uses molecules known as chaperones to seek out damaged proteins. After finding such a protein, the chaperone ferries it towards one of the cell’s many lysosomes — membrane-bound sacs filled with enzymes. When the chaperone and its cargo “dock” on a receptor molecule on the lysosome’s surface, the damaged protein is drawn into the lysosome and rapidly digested by its enzymes. In previous work, Dr. Cuervo found that the chaperone surveillance system, in particular, becomes less efficient as cells become older, resulting in a buildup of undigested proteins within the cells. She also detected the primary cause for this age-related decline: a fall-off in the number of lysosomal receptors capable of binding chaperones and their damaged proteins. Could replenishing lost receptors in older animals maintain the efficiency of this protein-removal system throughout an animal’s lifespan and, perhaps, maintain the function of the animal’s cells and organs as well? To find out, Dr. Cuervo created a transgenic mouse model equipped with an extra gene — one that codes for the receptor that normally declines in number with increasing age. Another genetic manipulation allowed Dr. Cuervo to turn on this extra gene only in the liver and at a time of her choosing, merely by changing the animals’ diet. To keep the level of the receptor constant throughout life, Dr. Cuervo waited until mice were six months old (the age that the chaperone system’s efficiency begins to decline) before turning on the added receptor gene. When the mice were examined at 22 to 26 months of age (equivalent to approximately 80 years old in humans), the liver cells of transgenic mice digested and recycled protein far more efficiently than in their normal counterparts of the same age — and, in fact, just as efficiently as in normal six-month old mice. Does maintaining efficient protein clearance in liver cells of an older animal translate into better functioning for the liver as a whole? Since a key function of the liver is metabolizing chemicals, Dr. Cuervo answered this question by injecting a muscle relaxant into very old transgenic mice and very old normal mice. The very old transgenic mice metabolized the muscle relaxant much more quickly than very old normal mice and at a rate comparable to young normal mice. “Our study showed that functions can be maintained in older animals so long as damaged proteins continue to be efficiently removed — strongly supporting the idea that protein buildup in cells plays an important role in aging itself,” says Dr. Cuervo. “Even more important, these results show that it’s possible to correct this protein ‘logjam’ that occurs in our cells as we get older, thereby perhaps helping us to enjoy healthier lives well into old age.” Dr. Cuervo next plans to study animal models of Alzheimer’s, Parkinson’s and other neurodegenerative brain diseases to see whether maintaining efficient protein clearance in the brain might help in treating them. “Most people with these conditions are born with a mutation that gives rise to defective proteins, but they don’t experience symptoms until later in life,” says Dr. Cuervo. “We think that’s because their protein-clearance systems can handle abnormal proteins when the person is younger but get overwhelmed as their efficiency falls with age. By preventing this decline in protein clearance, we may be able to keep these people free of symptoms for a longer time.” Dr. Cuervo will also investigate whether maintaining efficient protein clearance in all the body’s tissues will influence longevity and prevent the functional losses associated with growing old. “There’s reason to hope that drugs exerting a similar effect throughout the body may help us enjoy healthier lives well into old age,” says Dr. Cuervo. Meanwhile, she notes, evidence is mounting that two dietary interventions —low-fat and calorie-restricted diets — help cells to maintain efficient protein clearance. Source : Albert Einstein College of Medicine |
| Larry Ellison, please join the 21st century! [Omics! Omics!] Posted: 13 Aug 2008 11:14 PM CDT I've sniped at Microsoft at least once, so in the interest of balance I'll take a crack at the other software giant I rely on but also frequently complain about: Oracle. Oracle is truly amazing. Now, I don't have much experience with other relational database systems, so this isn't comparative. But relational databases are amazing. I give it a query of what I want and if I cross all my t's and dot all my i's, then huge databases are searched rapidly (often a matter of seconds). My first complaint is with inconsistency in syntax. Oracle has several flavors of text types depending on how big you might let your text get. I mostly query databases, not create them, and so I generally want to treat them all the same. Now there might be some good reason I need to use a different function to get the substring from each type, but I really don't want that hassle. But if I'm stuck with it, why couldn't you keep the argument orders the same? Standard substring, like every substring method I've ever met, has the order: string, start, length. But for the really big text columns ("CLOB"s), it's string, length, start. WHY??? But worse, is when I'm having trouble dotting those i's and crossing the t's, Oracle really doesn't give much help. The error messages are somewhere out of the 60's. For example, one handy feature of Perl (and other environments) is some attempt to identify common pitfalls and give hints about them in the error messages. A common mistake for me is to include an extra , in my query
In this example, of course, it's small -- but many of my queries are 30-40 lines long. Surely it could detect that the unrecognized field name is a reserved word and therefore hint that I've included an extra comma. Another example. For one query I have I've been parsing out a numeric string and then trying to convert it to a number. Alas, somehow my parse is failing and I'm getting some unconvertable strings back. Oracle gives me an error that it can't convert something to a number -- but keeps that something a secret from me! I could go on-and-on. Line numbers for the error are frequently non-helpful, the error messages don't give the context of the offending bit, etc, etc. The one thing I haven't tried is to edit my queries in Visual Studio, which has an SQL mode. I really should try that -- not that VS's error messages are always golden, but it is good about highlighting the likely neighborhood of mistakes in a way SQL Developer (the Oracle interface I use) just doesn't even attempt Ah well, I'll live. Larry probably has bigger fish to fry. Personally, though, if it was my software I'd be cringing. |
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