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"The researchers found 14 that did the trick, but one molecule—named RNPA1000—was especially effective against S. aureus. RNPA1000 killed cells from all 12 major strains of methicillin-resistant S. aureus (MRSA)."
Biochemistry and molecular biology informing anti-bacterial targets. Quite cool.
15 February 2011
14 February 2011
13 February 2011
12 February 2011
07 February 2011
05 February 2011
02 February 2011
29 January 2011
28 January 2011
25 January 2011
Are scientists afraid of blogs and tweets?
Nature has a nice wee article (no subscription required to read this one, FTW!) on the state of what one might call "informal" peer review - the challenges and questions to published works that come from blogs and tweets and the like.
For those of us who have been talking about the changes needed in the whole infrastructure and culture of science discourse (particularly the lock publishers have on research papers), this Nature article holds no surprises. Indeed, it comes off making some scientists seem a bit whiny.
The article points to some recent events where scientists have been skewered online for papers or claims made. This reminds me of the early days of blogging when folks were trying hard to control the message and were freaking out when anyone said anything.
The paper does have some great examples and quotes though. For example, David Goldstein, from Duke's Center for Human Genome Variation, is quoted saying, "if the work is solid, it hold up over time". And the efforts by PLoS with comments on papers, how arXiv.org works, and ratings from F1000 are good to show to those who are probably reading the article to figure out how to survive the blogosphere.
My favorite comment by the author, though, is:
One solution may lie in new ways of capturing, organizing and measuring all these scattered inputs, so that they end up making a coherent contribution to science instead of just fading back into the blogosphere.
I've been harping on this for a while and still think there's an opportunity to create a solution like this. I think there is a lot of good thinking, plenty of examples in other industries, and folks are doing parts of this solution, such as trying to think of other ways to change how we calculate the impact of a paper (à la Technorati or through real-time stats), author ID systems, or ways to turn the science paper into the social object. The article also mentions Jason Priem's work on alternate paper metrics (alt-metrics).
It feels like 2004 all over again as another industry discovers the power of devolving the power back to the masses. And the Web was initially designed by scientists, for scientist - what's there to fear?
UPDATE 28jan11: Related to this topic, Zachary Knight has an incisive commentary on how all this was protrayed.
Image from Mike Babcock
24 January 2011
Human microbial ecology - cool study
I mentioned a few weeks back a review in Nature about a trio of scientists studying the contributions of gut microbial ecology in preemies that get necrotizing enterocolitis (NEC). Sneaky, sneaky, it turns out that a paper on this work was posted that the review didn't mention or link to. I subsequently found a great article out of the UC Berkeley media relations team that is an even better review of the work, with some excellent quotes from the investigators themselves.
Link: Scientists sequence gut microbes of premature infant
It's a fascinating story. The microbes in preemie feces were collected daily and either sequenced completely or identified by 16S rRNA sequences. The investigators were then able to visualize a time course of the abundance of different microbes (image to upper-right) and to start to understand the contributions of these microbes to pathology, particularly NEC.
It's cool to see the shifts in population as the gut microbes settle in. Interestingly (and not surprising), there were some microbes that are known to be pathogenic, but didn't really affect the preemie's health.
The thought, though, is that there might be some strain specificity within microbe species, or something related to the balance of all the other bacteria. This seems to correlate well with the findings from folks studying the contribution of gut microbes to immune system development.
If you're into developments in human microbial ecology (which I highly recommend new grad students study), I urge you to read this paper (here's the link from the article linked above) and the back story in the article linked above.
What do you think of this?
Image from the paper showing a time course of the gut microbial species
23 January 2011
22 January 2011
Doing stand-up at IgniteAmherst Feb 8th
Just a note that I'll be doing a 5-minute stand-up act at IngiteAmherst at the Eric Carle Museum of Picture Book Art (125 West Bay Road, Amherst, MA).
Link: IngiteAmherst: Making stuff
Our theme is "Making Stuff". Our valley is steeped in a rich history of making stuff, from the straw hat industry of Amherst to Holyoke and Springfield and Northampton. That tradition continues and we'll hear thought-provoking Ignites from folks Making Stuff in our valley.
There'll be folks talking about Fish, Games, Museums, and Biz. I'll be on hand to give a whirlwind tour of DIYBio (working title "The past, present, and future of making stuff through biology").
My plan (working on talk today) will be about all the ways we use biology to make stuff, starting with practical microbiology (of course), then making the leap to synthetic biology, and then spending some time showing examples of all the cool things happening among DIYbio folks. Of course, the emphasis will be on all the "making". And, I'm sure as I develop the outline, I'll start winnowing away the extra and find that one thing I am excited to focus on.
Let's see what actually turns out. The talks will be pecha kucha - 20 slides automatically flipping in 5 minutes - which I've never done before. Thankfully, I do NOT think 5 minutes is too short to share something that excites me.
Looking forward to a great evening!
21 January 2011
19 January 2011
Functional roles for noise in genetic circuits
I have a thing about noise (see my ramblings here). And as folks try to turn elements of biological circuits into well-behaving engineered parts, I’ve been trying to put my finger on why biological noise means so much to me.
A series of articles in Nature back in September covered the cost of feedback control, the fundamental limits on the suppression of molecular fluctuations, the functional roles for noise in genetic circuits (subscription required for all three).
The main review mentions that noise is a nuisance in the design of deterministic (engineered) circuits. But goes on to show that noise in biological systems provides critical functions that are hard to achieve with deterministic circuits.
Noise in biological systems is unavoidable, there are limits to how much a feedback system can reduce noise. And the review goes on to discuss many areas where noise is integral to the stability or responsiveness of a process, such as gene expression coordination, state-switching, positive feedback, differentiation, and in development.
How might we understand this noise and actually engineer it into our deterministic circuits?
One thing, though, that tempers my bias towards keeping noise in biologically engineered circuits is that digital electronics also had their start in a noisy analog world. Will engineering biological circuits be forever mired in the analog noisy world of biology or will these circuits eventually be complex enough to exhibit the precise nature that biological engineers seem to want? Should biological engineers seek to incorporate noise into their calculations or strive to limit stochastic fluctuations?
Really, that’s a bit beyond my ability to understand circuit design and noise and all, so I leave it to smarter folk than I. :-)
Image from BarelyFitz
18 January 2011
17 January 2011
The subtlety of life - clever codon usage
Here’s a paper from September I haven’t had a chance to comment on.
Zhang et al reported in Science (review, paper - subscription required) how two almost identical protein sequences can have different translational modifications. In this case, β-actin and γ-actin are 98% identical, the differences are marginal and don’t explain why one protein is modified with arginine and the other is not.
The difference is actually quite subtle - there is one amino acid in the protein sequence that is lysine in both proteins, but the codons in the RNA are different. That difference is enough to change the relative translation speed of β-actin so that it rapidly folds and gets arginylated but not degraded as happens in the slower translation of γ-actin. In the end, this affects the relative lifetime of each protein in the cell, leading to differential functions.
That’s so cool.
It seems like every so often, things we view as well understood turn out to have another layer of subtlety built in. For example, differential codon usage is usually considered a synonymous change, nothing momentous. Sure, there’s been studies of codon usage relative to the abundance of corresponding tRNAs and how that might be used to modulate abundance of a protein (a quick Google search revealed some interesting codon-usage papers). But I think this case is novel, differential codon usage actually affecting the post-translational modification of a protein simply by tweaking the speed of translation.
How might we create a codon usage table that takes into account tRNA abundance, contribution to translational speed of different codons, and speed of post-translational processes to be able to model and predict things like the differences between the functions of β-actin and γ-actin.
Also, how prevalent is this subtle effect on post-translational modification and how susceptible is it to breaking and causing trouble in a cell?
image from Science review (found via Google images, mind you)
14 January 2011
Co-operative evolution of the immune system in humans?
Lee and Mazmanian, from Caltech, published this great review in Science on microbes in the gut and how different bacteria might have been involved in the evolution of the human immune system.
Link (subscription required): Has the Microbiota Played a Critical Role in the Evolution of the Adaptive Immune System? by Yun Kyung Lee and Sarkis K. Mazmanian
They discuss research that shows different bacteria modulating the maturation and function of different types of T-cells. And this modulation not only affects what happens immunologically in the gut, but also the rest of the body.
The thought is that this modulation not only keeps the body from rejecting the bacteria outright, but also might provide a protective environment favoring that bacteria, including keeping out other competing bacteria. They also suggest some potential connection with auto-immunity as well.
How cool is that?
Of course, all this requires a proper balance of bacterial populations and T-cell modulation - any imbalance can lead to disease. Indeed, they use the term “pathobionts” for bacteria that normally colonize the gut without adverse affects, but still remain pathogenic under certain circumstances.
There has been lots of research in understanding the molecular mechanisms that underly our relationship as host to a whole ecosystem of bacteria in and on our body. This review provides a great overview of what’s known about the potential modulation of the evolution of our immunity. It’s worth a read if you can get the paper.
Image from striatic
13 January 2011
More on bacteria and asthma
There’s a theory going around to explain the rise in asthma: we’re too clean. Research in the past 5 years has slowly been teasing out how this might be.
Link (subscription required): Bacteria and Asthma: Untangling the Links by Jennifer Couzin-Frankel, Science
Scientists have been studying the difference in the incidence of asthma in babies born by cesarian and babies born through vaginal birth, where they are exposed to birth canal bacteria and fungi; or the incidence in children who receive lots of antibiotics or not. Children who are born by C-section or receive lots of antibiotics have a higher incidence of asthma.
Another study is comparing the bacterial flora of children from farms and from non-farm rural settings - farm kids seem to get less asthma.
So far, the link between bacterial diversity and asthma has been an association not proof that bacteria are causing or inhibiting the development of asthma. Yet, it does point to a future where we are less aseptic, less clean in the post-Pasteurian sort of way.
What do you think?
Image from net_efekt
12 January 2011
11 January 2011
The new germ theory
Lizzie Buchen from Nature (link below) wrote a great article on some cool work folks are doing to change the way we view bacteria.
For example, one group (like a joke, it’s a microbiologist of extremophiles, a neonatologist, and a human microbial geneticist) is studying the effect of bacteria on a devastating intestinal disease in premature babies. They want to know if there’s a role or not for bacteria in this disease.
What’s interesting is that up to now, most understanding of bacteria in humans has been stuff that is pathogenic and can be cultured easily. Bringing in someone who is skilled at finding and characterizing microbes from extremely inhospitable places might help discover new things about our own microbiota.
I don’t know if it’s because I’m all interested now in human microbial ecology or if indeed there has been a resurgence in the study of human microbiology, all I know is that not a week goes by without a new paper or review in this area.
Quite exciting, isn’t it?
Here’s the article: Microbiology: The new germ theory in Nature (no subscription required FTW!).
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