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  • September 27, 2010
  • 08:42 AM

News about the Integrated Microbial Genomes (IMG) resource

by Jennifer in OpenHelix

I’ve got a few news items regarding IMG, or Integrated Microbial Genomes, from the DOE Joint Genome Institute. The first item is that their Sept 2010 release occurred this week. IMG is now on version 3.2, has updated features and a bunch of new/revised genomes. I’ve begun updating our tutorial & will let you know when that is released. It’s not the craziest level of tool changes that I’ve seen from this group, but dang, they SURE don’t rest on their laurels! They are constantly changing and improving their interface and database.
If you are involved in microbial research and haven’t already checked out this powerful resource, I strongly suggest that you do. We’ve been training on this resource since 2006 and really believe in its value, which seems to increase with each of their releases. Mary & Trey presented an IMG workshop at NIH recently and it was surprising how many of their researchers were not aware of IMG. We hear that pretty often and it is too bad, it has so much to offer the microbial community and others as well.
The second item is that IMG has an annotation tool specifically designed for undergraduate education. Iddo Friedberg  describes this as ‘Way cool’ in a recent tweet. The program/interface is named the “Integrated Microbial Genomes Annotation Collaboration Toolkit (IMG-ACT)“, and is somewhat associated with the “Interpret a GEBA Genome for Education” project from JGI. “GEBA” stands for Genomic Encyclopedia of Bacteria and Archaea.  Both efforts are aimed at encouraging undergraduate research in microbial genome annotation, which might lead to the ‘alternative science career’ as a biocurator!
You can read all about the tool in their PLoS Biology article “Incorporating Genomics and Bioinformatics across the Life Sciences Curriculum“, or see a tour of the program/interface here. The tour makes the interface seem a bit clunky to me, but well thought out with lots of solutions to problems/issues often associated with undergraduate classes. The paper really provides a nice overview of the concept, collaborations, and initial outcomes of the 2008-2009 program.
Sign-ups are occurring for the 2011-2012 version of the program. The time frame is as follows:
Timeline to Participate:
1. Apply to be part of the 2011-2012 team by Monday, November 5, 2010 (download the application)
2. After acceptance, attend the workshop at the JGI (January 2011)
3. Implement in 2011-2012 academic year
as can be seen at the bottom of this page.
IMG-ACT Reference:
Ditty, J., Kvaal, C., Goodner, B., Freyermuth, S., Bailey, C., Britton, R., Gordon, S., Heinhorst, S., Reed, K., Xu, Z., Sanders-Lorenz, E., Axen, S., Kim, E., Johns, M., Scott, K., & Kerfeld, C. (2010). Incorporating Genomics and Bioinformatics across the Life Sciences Curriculum PLoS Biology, 8 (8) DOI: 10.1371/journal.pbio.1000448

... Read more »

Ditty, J., Kvaal, C., Goodner, B., Freyermuth, S., Bailey, C., Britton, R., Gordon, S., Heinhorst, S., Reed, K., Xu, Z.... (2010) Incorporating Genomics and Bioinformatics across the Life Sciences Curriculum. PLoS Biology, 8(8). DOI: 10.1371/journal.pbio.1000448  

  • September 27, 2010
  • 07:11 AM

How do miRNAs affect protein production?

by Becky in It Takes 30

A recent paper from the Bartel and Weissman groups (Guo et al. Mammalian microRNAs predominantly act to decrease target mRNA levels, Nature 466 835-40, PMID: 20703300) provides an interesting snapshot of the journey of a field from consensus to controversy to (one day?) consensus again. At issue is the question of how microRNAs — small [...]... Read more »

  • September 27, 2010
  • 05:08 AM

You've discovered a whacky wood-eating catfish? So what's new? | GrrlScientist

by GrrlScientist in GrrlScientist

The press has recently been abuzz with news of a newly discovered species of catfish that eats wood, of all things... Read more »

  • September 27, 2010
  • 03:35 AM

Story of X

by Razib Khan in Gene Expression

A month ago I pointed to a short communication in Nature Genetics which highlighted differences in the patterns of variation between the X chromosome and the autosome. I thought it would be of interest to revisit this, because it’s a relatively short piece with precise and crisp results which we can ruminate upon.
Sometimes there is [...]... Read more »

  • September 26, 2010
  • 10:59 PM

Humans 1, Environment 0

by CJA Bradshaw in ConservationBytes

While travelling to our Supercharge Your Science workshop in Cairns and Townsville last week (which, by the way, went off really well and the punters gave us the thumbs up – stay tuned for more Supercharge activities at a university near you…), I stumbled across an article in the Sydney Morning Herald about the state [...]... Read more »

Australian Bureau of Statistics. (2010) Measures of Australia's Progress. Report. info:other/

Raudsepp-Hearne, C., Peterson, G., Tengö, M., Bennett, E., Holland, T., Benessaiah, K., MacDonald, G., & Pfeifer, L. (2010) Untangling the Environmentalist's Paradox: Why Is Human Well-being Increasing as Ecosystem Services Degrade?. BioScience, 60(8), 576-589. DOI: 10.1525/bio.2010.60.8.4  

  • September 26, 2010
  • 08:14 PM

Cold start of Life: Ice as a protocellular medium for RNA replication

by Olexandr Isayev in

The hot spot for life on early Earth may have been a very cold place. Tiny pockets and channels that form inside ice can contain and protect replicating molecules, researchers report September 21 in Nature Communications. The paper suggests that life could have sprung from icy slush covering a freshwater lake, rather than a broiling [...]... Read more »

Attwater, J., Wochner, A., Pinheiro, V., Coulson, A., & Holliger, P. (2010) Ice as a protocellular medium for RNA replication. Nature Communications, 1(6), 1-8. DOI: 10.1038/ncomms1076  

  • September 26, 2010
  • 02:55 PM

Guest Post - Survival of the fittest?

by Lab Rat in Lab Rat

I'm very excited about this post, which is a guest post from my sister! She's an undergrad doing biochemistry at Bristol University, and she's currently taking a year working in a research laboratory as part of her degree. She's working with Plasmodium at the moment (which is the little protist that causes malaria) but has sent me a bacteria-related post because she knows me, and she knows my blog and who doesn't love bacteria?Post - survival of the fittest?Bacteria have always been very adaptable when it comes to surviving evolutionary stressful situations, such as exposure to antibiotics. Usually some form of mutation will arise leading to the creation of resistant strains of bacteria. These will be selected for via ‘natural selection’ processes and go on to replicate to produce a whole population of resistant bacteria that are able to survive.However new research looked at a colony of wild type E.coli bacteria in a bioreactor under exposure to increasing levels of the antibiotic norfloxacin and found that no more than 60% of growth was inhibited to maintain a sizable population. The resistance levels of the population as a whole, and of 12 random individuals, was checked every day and it was found that they did not correspond to one another.The majority of the individual isolates were less resistant than the population as a whole but there was one mutant found that was highly resistant. By isolating the supernatant from the high resistance individual, and conducting gel electrophoresis to separate out the intracellular components, a protein was found that was produced in very high numbers.This was the enzyme tryptophanase which has the main job of breaking down tryptophan to ammonia, pyruvate and indole. Experiments were done to show that the third molecule, Indole, provided an obvious survival benefit under antibiotic conditions. It upregulated multi-drug efflux pumps which helped in the physical export of the drug and it also had a role in activating various oxidative stress protective mechanisms. The mass production of Indole by the highly resistant mutant allows more vunerable cells in the surrounding area to survive. a) no antibiotic stress, bacteria naturally produce indole.b) dead and dying bacteria fail to produce indolec) mutant appears and supplies indole at a fitness cost to itself.The resistant bacteria is therefore not selfishly replicating to outgrow the rest of the population but, in helping others to survive, is enduring a fitness cost of its own by mass producing Indole.This experiment was also carried out using various different antibiotics and the same bacterial altruism was found to exist. The survival of the weaker bacteria does have some advantages as it allows further exploration of mutations that could be even more beneficial to the population. Also, it keeps the opportunity for the bacteria to return to their original state if the stress is temporary, rather than keeping up the energetically wasteful production of antibiotic resistance genes.So, bacteria working as a team to ensure not just temporary survival but long term advantages for the whole population. Not just survival of the fittest.---Lee HH, Molla MN, Cantor CR, & Collins JJ (2010). Bacterial charity work leads to population-wide resistance. Nature, 467 (7311), 82-5 PMID: 20811456... Read more »

Lee HH, Molla MN, Cantor CR, & Collins JJ. (2010) Bacterial charity work leads to population-wide resistance. Nature, 467(7311), 82-5. PMID: 20811456  

  • September 26, 2010
  • 01:07 PM

FDA: there to protect us

by Science Exploiter in Science Exploits

Yesterday while walking home from the store, I bumped into a neighbor who seemed out of sorts.  Pulling me aside, he told me of numerous health problems which have developed recently, most of which he blames on a new medicine.  I don't doubt his sincerity, but it did raise some questions. For instance: has he imagined the symptoms?  It sounds terrible to suggest such a thing, but when starting a new treatment how many of us have suddenly noticed something which perhaps we never took notice of before?  It doesn't necessarily apply to health, but to all aspects of life.  I recall having trouble with a cell phone, and noticing what looked like a malfunction on the screen.  I took it to the store and they told me that all phones of that brand have that, not a blemish, but part of the background which appears as soon as you turn on the phone on day 1.  The customer service rep then showed me his phone, which had what I had perceived as a part of the problem.  I accepted my mistake.  So too must we consider that such mistakes happen with regard to health.Another thing to consider: could something else explain the symptoms?  Could it be that the treatment prescribed fixed one problem, allowing another to take hold?  Or perhaps the treatment did not address the problem appropriately, allowing symptoms to exacerbate; either because the treatment is incorrect, or because the condition is refractory to that treatment. My neighbor only wanted a shoulder to lean on, but nonetheless his suspicions about the medication got me thinking: how much do we trust the FDA?  All things considered, nobody wants to think about such things as I have highlighted above.  If we can blame it on a pill, then a simple fix is to either remove or replace the pill.  Easy enough.  Something I think we would all hope for, rather than receiving other tough news. In general, to get a drug approved, a company needs to meet strict requirements: laboratory work which suggests effectiveness of the drug, animal testing which shows a benefit, and finally human testing.  Prior to human testing the FDA reviews the drug's merit in both laboratory data and animal models.  Assuming the drug acquires approval, it then moves on to safety testing: will it negatively affect people simply by merit of taking of it?  If it passes this step, then it moves on to those with the targeted condition, to see if it works as expected.  After reviewing the collective picture, the FDA will then make a decision as to whether or not to allow the drug to hit the market.  If it does approve the drug, it is then monitored: does it work as expected?  Does it have unexpected side effects or reactions?  Etc.  The process moves slowly, but as such it helps protect people from potentially harmful drugs.  In the lab a formula may appear like a cure, but in practice it may be everything but. Given these rigorous guidelines, I would not expect any approval without a hard look at the data, a review of the benefits to risks ratio, and a discussion on how best to prescribe the drug (ie: will it require weekly blood tests, etc.).  However, not all pills fall under the FDA's jurisdiction.  And this is where it gets iffy.  Vitamins and supplements needn't go through the FDA approval process.  I have heard many people proclaim the benefits of vitamins and supplements.  Often these accolades include such statements as: they are natural, they don't have the side effects of drugs. Let's look at this: they don't have side absurd.  Most will recall the terrible outcome of the supplement, ephedra. But other supplements have discouraging associations as well: primrose oil lowers seizure threshold, echinacea suppresses the immune system with prolonged use, St. John's wort can affect the efficacy of certain prescription drugs, and so on.  Unfortunately, such side effects often do not see the light of day when browsing for a supplement.  If someone hears that Vitamin A promotes good eye health, might they not assume that taking large amounts may offer more benefit?  As a teratogen at high doses, a pregnant woman would want to avoid large amounts of Vitamin A.  Yet how many people know of this association?  The list of risks of supplements is long, and with valid research might reveal worse and more compromising information. I for one feel that supplements have a time and a place.  But I want to see the FDA taking a more active role in their claims of effectiveness.  Just like companies promoting brand name and generic drugs, companies in the supplement business should have to provide testable data to the FDA which suggests veracity of their claims.  They should also have to go through an approval process.  Perhaps not the same as that for prescription drugs, but nonetheless something stringent on data, a hard look at the proposed indications for the supplement, and whether its benefits outweigh the risks.  Who knows, some supplements may provide data such that they actually require prescription status!  There is a strong push against further FDA involvement with the supplement business, but just look at the possibility: if the FDA approves a supplement's claims based on data, shouldn't defenders of the supplement industry rejoice in knowing that the government has essentially backed their claims of the effectiveness of supplements?  P.J. Landrigan (2000). Bad Policy, Worse Medicine Pediatrics, 106 (6), 1482-1483Eugene Pergament, MD, PhD; Amy Schechtman, MS, CGC; Carrie Curell, BA (1996). Vitamin A and Pregnancy ITIS Newsletter, 4 (6)... Read more »

P.J. Landrigan. (2000) Bad Policy, Worse Medicine. Pediatrics, 106(6), 1482-1483. info:/

  • September 26, 2010
  • 11:00 AM

Evo-devo of digital reduction in amphibians

by Kele in Kele's Science Blog

Synopsis: Alberch and Gale: “A Developmental Analysis of an Evolutionary Trend: Digital Reduction in Amphibians” (1985). In this paper, the authors looked at different foot morphologies in extant amphibians and performed some experimental embryology with a few of the species. The induced developmental change followed the natural variation found by the authors! Details below! This [...]... Read more »

  • September 26, 2010
  • 10:06 AM

Shadows on the wall: « Truth never triumphs, but its opponents eventually die »

by Rogue in Into Oblivion

Gregory Petsko wrote a small comment in the very last Genome Biology titled Shadows on the wall. A very angry but still contained one, nicely written and important to think about. Here is some of my thoughts about. Gregory Petsko discusses a question related to what people call « paradigms » and innovation. Paradigm is a word [...]... Read more »

Petsko GA. (2010) Shadows on the wall. Genome biology, 11(9), 136. PMID: 20863416  

  • September 26, 2010
  • 07:28 AM

Big Pharma Explain How To Pick Cherries

by Neuroskeptic in Neuroskeptic

Here at Neuroskeptic, we see a lot of bad science. Maybe, over the years (all 2 of them) that I've been writing this blog, I've become a bit jaded. Maybe I'm less distressed by it than I used to be. Cynical, even.But this one really takes the biscuit. And then it takes the tin. And relieves itself in it: A New Population-Enrichment Strategy to Improve Efficiency of Placebo-Controlled Clinical Trials of Antidepressant Drugs.Don't worry - it's from a big pharmaceutical company (GlaxoSmithKline), so I don't have to worry about hurting feelings.It's is full to bursting with colourful graphs and pictures, but the basic idea is very simple. As in "simpleton".Suppose you're testing a new drug against placebo. You decide to do a multicentre trial, i.e. you enlist lots of doctors to give the drug, or placebo, to their patients. Each clinic or hospital which takes part is a "centre". Multicentre trials are popular because they're an easy way of quickly testing a drug on a large number of patients.Anyway, suppose that the results come in, and it turns out that the drug didn't work any better than placebo, which unfortunately is what happens rather often in modern trials of antidepressants. Oh dear. The drug's crap. That's the end of that chapter....or is it?!? say GSK. Maybe not. They have a clever trick. Look at the results from each centre individually. Placebo response rates will probably vary between centres: in some of them, the placebo people don't get better, in others, they get lots better.Now, suppose that you just chucked out all of the data from centres where the people on placebo got much better, on the grounds that there must be something weird going on in those ones. They reanalyzed the data from 1,837 patients given paroxetine or placebo, across 124 centres. In the dataset as a whole, paroxetine barely outperformed placebo. However, in the centres where people on placebo only improved a little, the drug was much better than placebo!Well, of course it was. Imagine that the drug has no effect. Some people just get better and others don't. Let's assume that each person randomly gets between 0 and 25 better, with an equal chance of any outcome. Half are on drug and half are on placebo, but it makes no difference.Let's further assume that there are 50 centres, with 20 people per centre (1000 people total). I knocked up a "simulation" of this in Excel (it took 10 minutes). Here's what you get:The blue dots show, for each imaginary centre, drug improvement vs. placebo improvement. There's no correlation (it's random), and, on average, there is no difference: both average out at 12 points. The drug doesn't work.The red dots show the "Treatment Effect" i.e. [drug improvement - placebo improvement]. The average is 0 - because the drug doesn't work. But there's a strong negative correlation between Treatment Effect and the placebo improvement - in centres where people improved lots on placebo, the drug worked worse.This is exactly what Glaxo show in Figure 1a (see above). They write:The analysis of the surface response indicated the predominant role of center specific placebo response as compared with the dose strength in determining the Treatment Effect of paroxetine.But of course they correlate. You're correlating placebo improvement with itself: the "Treatment Effect" is a function of the placebo improvement. It's classic regression to the mean.Of course if you chuck out the centres where people on placebo do well (the grey box in my picture), the drug seems to work pretty nicely. But this is cheating. It is cherry-picking. It is completely unscientific.The authors note that this could be a source of bias, but say that it wouldn't be one if it was planned out in advance: "in order to overcome the bias risk, the enrichment strategy should be accounted for and pre-planned in the study protocol." This is like saying that if you announce, before playing chess, that you are going to cheat, it's not cheating.To be fair to the authors, assuming the drug does work, this method would improve your chances of correctly detecting the effect. Centres with very high placebo responses quite possibly are junk. Assuming the drug works.But if we're assuming the drug works, why are we bothering to do a trial? The whole point of a trial is to discover something we don't know. The authors justify their approach by suggesting that it would be useful for drug companies who want to do a "proof-of-concept" trial to find out whether an experimental drug might work under the most favourable conditions, i.e. whether they should bother continuing to research it.They say that such trials "are inherently exploratory in their conception, aimed at signal detection, open to innovation..." - in other words, that they're not meant to be as rigorous as late-stage trials.Fair enough. But this method is not even suitable for proof-of-concept, because it would (as I have shown above in my 10 minute simulation) increase your chance of finding an "effect" from a drug that doesn't work.Whatever the truth is, this method will give the same result, so it's not useful evidence. It's like saying "Heads I win, tails you lose". You've set it up so that I lose - the coin toss doesn't us anything.All of the author's results are based on trials in which the drug "should have worked": they do not appear to have simulated what would happen if they used this method on trials where it didn't work, as I just did. So I'm doing Pharma a big favour by writing this post, because if they adopt this approach, they're more likely to waste money on drugs that don't work.They should be paying me for this stuff.Merlo-Pich E, Alexander RC, Fava M, & Gomeni R (2010). A New Population-Enrichment Strategy to Improve Efficiency of Placebo-Controlled Clinical Trials o... Read more »

  • September 25, 2010
  • 01:25 PM

Kinetic Traps of Single Biomolecule Refolding

by Michael Long in Phased

David Rueda (Wayne State University, United States) and coworkers have quantitated kinetic barriers to refolding in DNA and RNA, uncovering rare and transient events only addressable on the single molecule level. This news feature was written on September 25, 2010.... Read more »

Zhao, R., Marshall, M., Alemán, E. A., Lamichhane, R., Feig, A., & Rueda, D. (2010) Laser-Assisted Single-Molecule Refolding (LASR). Biophysical Journal, 99(6), 1925-1931. DOI: 10.1016/j.bpj.2010.07.019  

  • September 25, 2010
  • 09:13 AM

The Structural Basis of Peptide-Protein Binding Strategies

by Nir London in Macromolecular Modeling Blog

How can peptides overcome the entropic cost involved in switching from an unstructured, flexible peptide to a rigid, well-defined bound structure? What are the strategies used by peptides in order to bind their protein receptor? How is this different than protein-protein interactions? In this work we performed A structure-based analysis of peptide-protein interactions to try and answer these questions.

... Read more »

London N, Movshovitz-Attias D, & Schueler-Furman O. (2010) The structural basis of peptide-protein binding strategies. Structure (London, England : 1993), 18(2), 188-99. PMID: 20159464  

  • September 24, 2010
  • 06:50 PM

How vaccines work Pt.2

by James Byrne in Disease Prone

In my last post I spoke about how vaccines work from the point of view of the person receiving the jab or pill. In that case we were talking about immunological memory but vaccines also work in another very important way from the point of view of the community and it is referred to as ‘herd immunity’.... Read more »

Fung KS, Yeung WL, Wong TW, So KW, & Cheng AF. (2004) Pertussis--a re-emerging infection?. The Journal of infection, 48(2), 145-8. PMID: 14720490  

  • September 24, 2010
  • 06:41 PM

How Vaccines Work Pt.2

by James Byrne in Disease Prone

In my last post I spoke about how vaccines work from the point of view of the person receiving the jab or pill. In that case we were talking about immunological memory but vaccines also work in another very important way from the point of view of the community and it is referred to as [...]... Read more »

Fung KS, Yeung WL, Wong TW, So KW, & Cheng AF. (2004) Pertussis--a re-emerging infection?. The Journal of infection, 48(2), 145-8. PMID: 14720490  

  • September 24, 2010
  • 11:23 AM

Risk, Insurance, LUST, and Fish

by Noam Ross in Noam Ross

Two papers crossed my desk yesterday highlighting the role insurance can play in mitigating environmental risk.  The first, by Yin et. al. in Risk Analysis, discusses three appoaches to mitigating the risk of leaking underground storage tanks (a problem with the fantastic acronym LUST).  
Large fines for spills, as it turns out, are not a particularly efficient enforcement tool, as most LUSTs are owned by small businesses like gas stations that would likely go bankrupt before paying all the fines and cleanup costs.  Many large firms outsource or spin off their tank operations to smaller companies so that they can declare bankruptcy in such an event.
Another option is to have a set of safety regulations that are strictly enforced.  However, the EPA and state regulators have lacked the resources to send inspectors into the field to make sure USTs are up to code.
Mandating insurance for tank owners, on the other hand, lowers the burden on regulators and also spreads the cost to operators out into a string of premium payments.  Some states have created public quasi-insurance funds by forcing industry to pay for cleanups through a gasoline tax.  However, it turns out that private insurers are better and forcing their customers to manage their tanks for safety.  The authors are able to show that in states that have robust private insurance markets for LUSTs, there are about 35% fewer spills.
In Ecological Econmics, D.S. Holland writes about possible insurance options for fishery markets.  Some fisheries have total bycatch quotas, meaning that the fishery is shut down when a total amount of bycatch is caught.  For example, if, collectively, all the Pacific flounder fisherman catch 20 loggerhead turtles, then regulators declare no more Paciifc flounder fishing for the year.
This can lead a "race to fish", where fisherman try to catch all they can before the fishery is shut down.  Holland explores the possibility of bycatch insurance where fisherman are compensated for a loss of revenue if the fishery is shut down earlier than expected.  This is only tangentially related to the LUST insurance above, but it again creates an interesting situation where the insurance company is incentivized to reduce its clients' environmental damages.  In this case, would insurers force fisherman to find ways to reduce bycatch?
I'm interested to see how insurance models scale up to addressing large scale, systemic ecological risks.  There's an intruiging example of the potential of private insurance in the underwriting of reforestation in the Panama Canal.  Where else is it applicable?
(For more on lust, see Christine O'Donnell.)
Yin, H., Pfaff, A., & Kunreuther, H. (2010). Can Environmental Insurance Succeed Where Other Strategies Fail? The Case of Underground Storage Tanks Risk Analysis DOI: 10.1111/j.1539-6924.2010.01479.x
Holland, D.S. (2010). Markets, pooling and insurance for managing bycatch in fisheries Ecological Economics : 10.1016/j.ecolecon.2010.08.015... Read more »

Holland, D.S. (2010) Markets, pooling and insurance for managing bycatch in fisherie. Ecological Economics. info:/10.1016/j.ecolecon.2010.08.015

  • September 24, 2010
  • 11:15 AM

What species of skate is for dinner? New research challenges elasmobranch fisheries policy

by WhySharksMatter in Southern Fried Science

I write a lot about shark conservation issues, but I rarely focus on their fellow elasmobranchs. Rays and skates have similar life history strategies as sharks, and many species are similarly overfished.  A friend just sent me a cool paper about the conservation of skates, which provides an excellent opportunity to remedy this oversight.
A major issue [...]... Read more »

  • September 24, 2010
  • 10:32 AM

What Killed Europe’s Hyenas?

by Laelaps in Laelaps

Mass extinctions are often typified by the catastrophic loss of charismatic animals. Even though ammonites, pterosaurs, many forms of marine reptiles, and even some lineages of mammals all succumbed during the great dying at the end of the Cretaceous, that event will always be cast as the unexpected curtain-fall on the Age of the Dinosaurs. [...]... Read more »

  • September 24, 2010
  • 08:46 AM

Symbiotic Foreclosure: coral bleaching predictions and a potential acclimation mechanism

by Uncharted Atolls in Uncharted Atolls

NOAA—the National Oceanic and Atmospheric Administration—issued a press release on September 22nd declaring coral bleaching likely in the Caribbean.  NOAA reports that: With temperatures above-average all year, NOAA’s models show a strong potential for bleaching in the southern and southeastern … Continue reading →... Read more »

  • September 24, 2010
  • 08:38 AM

Introducing Peptide-Protein Interactions

by Nir London in Macromolecular Modeling Blog

Peptide-protein interactions are gaining much interest of late. The Furman group have recently published a series of papers on the subject of peptide-protein interactions (disclaimer - these were partly authored by yours truly). In this post I will introduce the subject and the motivation to investigate these interactions and in later posts of this 'mini-series' I will get into more details on this on-going research.

... Read more »

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