Friday, June 13, 2008

The DNA Network

The DNA Network

Open Metagenomics: Selenium in the Oceans [The Tree of Life]

Posted: 13 Jun 2008 05:37 PM CDT

Well, I have started previous an "Open Evolution" series here and now I am starting an "Open Metagenomics" series. I know, I have gotten grief from some out there (yes, you Rob Edwards - see comments here) about my support for somewhat non open things in metagenomics, so I am going to try and make up for that as much as possible.

In the first installment, I am pointing people to a new paper on PLoS Genetics "Trends in Selenium Utilization in Marine Microbial World Revealed through the Analysis of the Global Ocean Sampling (GOS) Project" by Yan Zhang, Vadim N. Gladyshev (hat tip to Katie Pollard for pointing out this paper).

In this paper the authors study selenium utilization using data from the first part of the Venter Global Ocean Survey (GOS) which was metagneomic sequencing from multiple samples - mostly surface ocean water.  The GOS data they use comes from the Rusch et al. paper in PLoS Biology (note for full disclosure ... I was an c0-author on this paper).  

There have been challenges with getting and using metagenomic data from other people's publications in the past and I note that the authors here obtained the data sets from CAMERA, a metagenomics database supported by the Moore Foundation.  I note - it is my support of this database that Rob Edwards gave me grief about since the database is not currently completely open (e.g., you need to register to use it and the software that runs it is not currently all open source). 

Anyway, they got the data from CAMERA, and then did a pretty comprehensive analysis to search for genes and features in the data that would be indicative of selenium utilization. Selenium is of great interest to many biologists for many reasons, including that it is required for the synthesis and function of Selenocysteine (Sec), which , if you do not know, goes occasionally by the nickname "The 21st amino acid"

Without going into all the details of the paper, the last paragraph sums up the major features
In this study, we report a comprehensive analysis of Sec utilization in marine microbial samples of the GOS expedition by characterizing the GOS selenoproteome. This is the first time that the microbial selenoprotein population is described in a global biogeographical context. Our analysis yielded the largest selenoprotein dataset to date, provided a variety of new insights into Sec utilization and revealed environmental factors that influence Sec utilization in the marine microbial world.
My favorite part of the paper is that they map some of the selenium related features onto the globe.  For example, in one figure they show the inferred selenoprotein "richness" in 
the different samples. (Selenoproteins are proteins that have selenocysteine in them).  Now I am sure there are many assumptions they made in leading to the inferences they have made about selenium utilization and I am also sure some of these will turn out to be a bad idea.  But to me, this paper is a good example of what researchers will be able to do with metagenomic data in the future.  Sitting at their computers anywhere in the world, researchers can now ask questions about the distribution patterns of functions in microbes in the world.  Pretty cool.  And the more open we are with the papers, the tools, and the data, the more likely this type of work is to spread.

The figures are from the paper and I am permitted to use them here because they were published under a Creative Commons license that allows anyone to use them as long as the source is cited. The source is Zhang Y, Gladyshev VN (2008) Trends in Selenium Utilization in Marine Microbial World Revealed through the Analysis of the Global Ocean Sampling (GOS) Project. PLoS Genet 4(6): e1000095. doi:10.1371/journal.pgen.1000095 

No one wants to believe Carl Icahn’s offer of $15 B for Biogen- even when he says he will increase R&d Spending [Microarray and bioinformatics]

Posted: 13 Jun 2008 05:34 PM CDT


CNN once referred him as shrewdest investor on the planet. Carl Icahn who is now in the eye of storm for his involvment to throw the board of Yahoo for rejecting bid offer from Microsoft. The Billionaire corporate raider has made a beeline for the Lifescience Industry.

Carl Icahn, embroiled in a proxy battle with Biogen Idec, offered to pay as much as $15 billion last year for the company, the largest maker of drugs for multiple sclerosis. This week his move to throw out the board of Biogen has been rejected by shareholders as they voted in favor of the biotech's own slate of directors instead of those nominated by activist investor Carl Icahn.

Seems like no one wants to believe him when he says he will pump in more money into R&D. Really?

according to a memo to shareholders filed today with the ( SEC) Securities and Exchange Commission. Icahn wants to boost spending on research and development, improve employee morale, mend relations with partners, and possibly cut expenses outside research,

In the biggest biotechnology deal of 2007, Icahn pushed MedImmune Inc. to sell itself to London-based AstraZeneca Plc for $15.2 billion

Wealth of genomic hotspots discovered in embryonic stem cells [Think Gene]

Posted: 13 Jun 2008 05:09 PM CDT

In a paper published in Cell on June 13, 2008, Singapore scientists at the Genome Institute of Singapore (GIS) and the National University of Singapore (NUS) unveil an atlas that showing the location of “genomic hotspots” of essential protein “switches” (transcription factors) that are critical for maintaining the embryonic stem (ES) cell state.

Using advanced high throughput sequencing technology, the scientists discovered over 3,000 hotspots. These findings could improve understanding of the unique properties of stem cells that enable them to maintain their intriguing ability to grow and differentiate to virtually any cell type.

“This is the first time such a large scale study has been conducted in Singapore and
obtaining such groundbreaking results has caused much excitement,” said Wei Chia Lin, Ph.D., Senior Group Leader at GIS. “This blueprint that we obtained is like a treasure map, pointing us to specific sites where we can further study how these switches interact within the cell. Hopefully, this will eventually allow us unlock the secrets of stem cells.”

Ng Huck Hui, Ph.D., also a Senior Group Leader at GIS, added, “we think that these ’stemness’ hotspots are the most critical points in the genetic blueprint of ES cells. By targeting these hotspots, we may be able to reconnect the wiring in non-stem cells and jump-start the stem cell program in them. This can potentially create an inexhaustible source of clinically useful cells for regenerative medicine or cell based therapies in the future.” The team has already started work to investigate further into this area of research.

“Using cutting edge sequencing technology, scientists from the GIS and NUS have identified hotspots in embryonic stem cells,” said Prof. Lee Eng Hin, Executive Director of A*STAR’s Biomedical Research Council. “These are important hubs of the genome of embryonic stem cells. This piece of work illustrates how scientists from different disciplines and across institutions can come together to define fundamental features of these intriguing cells.”

“In this new paper in Cell, the team at the GIS continues their remarkable progress in
defining the precise DNA sequences to which an important group of 13 transcriptional
factors bind in mouse embryonic stem cells,” said Alan Colman, Ph.D., Executive Director of
Singapore’s Stem Cell Consortium. “This particular group of factors is responsible for maintaining the self renewal and pluripotency of the embryonic stem cells. The team shows that many of the factors which bind to the same gene regions (’hotspots’) and their work provide a working model of the transcriptional networks at play within the cells, and how these intracellular networks are linked to events that can be influenced by external stimuli.”

The researchers performed genome-wide mapping of the in vivo binding sites for 13
sequence-specific transcription factors in ES cells. These transcription factors play
different roles in self-renewal, pluripotency, reprogramming and chromatin insulation.
This study uncovers two major modes of binding that give rise to transcription factor co-
localization hotspots. The Nanog/Oct4/Sox2 centric hotspots are commonly co-bound
by Smad1 and STAT3 and they represent points of integration for the intrinsic and
external signaling pathways. The combinatorial wiring of transcription factors is
important in deciphering the code behind gene expression program in ES cells.

Source: Agency for Science, Technology and Research (A*STAR), Singapore

Integration of External Signaling Pathways with the Core Transcriptional Network in Embryonic Stem Cells. Xi Chen, Han Xu, Ping Yuan, Fang Fang, Mikael Huss, Vinsensius B. Vega, Eleanor Wong, Yuriy L. Orlov, Weiwei Zhang, Jianming Jiang, Yuin-Han Loh, Hock Chuan Yeo, Zhen Xuan Yeo, Vipin Narang, Kunde Ramamoorthy Govindarajan, Bernard Leong, Atif Shahab, Yijun Ruan, Guillaume Bourque, Wing-Kin Sung, Neil D. Clarke, Chia-Lin Wei, and Huck-Hui Ng. Cell. June 13, 2008: 133 (6).

Josh says:

Previous reports showed that these transcription factors are sufficient to induce pluripotent stem cells, but this is unique in that it shows what genes these transcription factors activate.

Synthetic cocoa chemical slows growth of tumors in human cell lines [Think Gene]

Posted: 13 Jun 2008 05:01 PM CDT

A synthetic chemical based on a compound found in cocoa beans slowed growth and accelerated destruction of human tumors in laboratory studies, and should be tested further for cancer chemoprevention or even treatment, say researchers at Georgetown University Medical Center.

“We have all heard that eating chocolate is good for you; this study suggests one reason why that might be true,” says the study’s lead author Min Kim, Ph.D., a research scientist in the Department of Oncology at Lombardi Comprehensive Cancer Center.

Published online today in Cell Cycle, the researchers describe how four different human tumor cells lines out of 16 tested were sensitive to the chemical, known as GECGC. The strongest response was seen in two different colon cancers; growth was cut in half and most of the tumor cells were damaged.

Normal cells were not affected by GECGC, which makes the chemical a candidate for cancer chemoprevention, says Kim.

“This chemical seems to be safe, which makes sense because it has a structure similar to a natural product in cocoa beans - the same beans that are used to make chocolate,” he says.

The researchers have long studied the beneficial effects of flavanols, which are molecules in vegetables and fruits that exhibit potent anti-oxidant and, potentially, anti-tumor properties. As part of these studies, investigators have been testing a new synthetic version of natural procyanidins, a class of flavanols, created and patented by the confectionery company, Mars Incorporated. (The company provided GECGC as a gift, and this project was funded in part by Mars Incorporated.)

In these studies, the scientists tested the effects of three different doses of GECGC on the cancer cell lines - the first time that a synthetic cocoa derivative has been used to screen human cancer cell lines. None of the doses tested were extreme, Kim points out. “The effective concentrations were considered similar to what a person might eat or use,” he says.

They found sensitivity to GECGC in both colon cancer cell lines they tested, in cervical cancer cells and in one line of leukemia, tumor cells. Other cell lines were resistant, including ovarian and prostate cancer cells.

Overall, GECGC showed the most effect in treating cancer cells that are normally fast growing, Kim says. And the fact that it demonstrated the most killing power in colon cancer suggests the chemical “could serve as a promising therapeutic for colon cancer,” he says. “So far, these data are very convincing.”

The researchers do not yet clearly understand the mechanism by which GECGC disrupts tumor growth, but they think it inhibits the physical connections between cancer cells and blocks internal cell signaling pathways.

Kim says that animal studies testing the anticancer power of GECGC are currently underway. “While this work is indeed promising, we have much more study to do before we can say with authority that GECGC has anticancer properties.”

Source: Georgetown University Medical Center

Selective cytotoxicity of synthesized procyanidin 3-O-Galloylepicatechin-4b,8-3-O-galloylcatechin to human cancer cells. Min Kim, Xiaofang Wu, Insun Song, Maofu Fu, Seo-Hee Chang, Michael P. Lisanti and Richard G. Pestell. Cell Cycle. Volume: 7 | Issue: 11 | Pages: 1648 - 1657

Josh says:

I really wonder what its mode of action really is, and why it doesn’t affect normal cells.

Scientists confirm that parts of earliest genetic material may have come from the stars [Think Gene]

Posted: 13 Jun 2008 04:46 PM CDT

Scientists have confirmed for the first time that an important component of early genetic material which has been found in meteorite fragments is extraterrestrial in origin, in a paper published on 15 June 2008.

The finding suggests that parts of the raw materials to make the first molecules of DNA and RNA may have come from the stars.

The scientists, from Europe and the USA, say that their research, published in the journal Earth and Planetary Science Letters, provides evidence that life’s raw materials came from sources beyond the Earth.

The materials they have found include the molecules uracil and xanthine, which are precursors to the molecules that make up DNA and RNA, and are known as nucleobases.

The team discovered the molecules in rock fragments of the Murchison meteorite, which crashed in Australia in 1969.

They tested the meteorite material to determine whether the molecules came from the solar system or were a result of contamination when the meteorite landed on Earth.

The analysis shows that the nucleobases contain a heavy form of carbon which could only have been formed in space. Materials formed on Earth consist of a lighter variety of carbon.

Lead author Dr Zita Martins, of the Department of Earth Science and Engineering at Imperial College London, says that the research may provide another piece of evidence explaining the evolution of early life. She says:

“We believe early life may have adopted nucleobases from meteoritic fragments for use in genetic coding which enabled them to pass on their successful features to subsequent generations.”

Between 3.8 to 4.5 billion years ago large numbers of rocks similar to the Murchison meteorite rained down on Earth at the time when primitive life was forming. The heavy bombardment would have dropped large amounts of meteorite material to the surface on planets like Earth and Mars.

Co-author Professor Mark Sephton, also of Imperial’s Department of Earth Science and Engineering, believes this research is an important step in understanding how early life might have evolved. He added:

“Because meteorites represent left over materials from the formation of the solar system, the key components for life — including nucleobases — could be widespread in the cosmos. As more and more of life’s raw materials are discovered in objects from space, the possibility of life springing forth wherever the right chemistry is present becomes more likely.”

Source: Imperial College London

“Extraterrestrial nucleobases in the Murchison meteorite”, Earth and Planetary Science Letters, Sunday 15 June 2008.

Josh says:

Since we know that nucleobases form well in ice, it seems logical for these molecules to be in meteors. In the early Earth, there were a lot of meteors hitting, so these nucleobases were probably the most common, relatively complex molecules available. It seems natural then that since they can so easily polymerize, that they did, forming the initial enzymes (proteins evolved later. RNA can act as an enzyme, and in fact still does in our bodies now. Take for example the splicing out of introns).

Finch 3, Linking Samples and Data [FinchTalk]

Posted: 13 Jun 2008 04:18 PM CDT

One of the big challenges with Next Gen sequencing is linking sample information with data. People tell us: "It's a real problem." "We use Excel, but it is hard." "We're losing track." Do you find...

Is this what they mean by blood money? [genomeboy.com]

Posted: 13 Jun 2008 04:10 PM CDT

I can only hope that this is still active, because I’m sure every homeless hospital patient in New York would be glad to know that his/her genome is worth five gallons of gas, four Sunday Times, three six packs, and a partridge in a freaking pear tree.

The hospital plans to offer a $20 incentive to any patient who donates an eight-milliliter vial of blood to a new Biobank, a warehouse of DNA and plasma that is a central component of the hospital’s Institute for Personalized Medicine. “Personalized medicine,” an approach that incorporates molecular analysis into managing a patient’s health, has been touted as the future of medicine ever since scientists completed the map of the human genome in 2003.

Woo hoo! Muchos gracias, Mt. Sinai! Can I give 16 mls and get $40? Can I bring my kids in, too? How much for my dog’s lymphocytes?

Rumours about the next 454 update [Next Generation Sequencing]

Posted: 13 Jun 2008 03:06 PM CDT

PolITiGenomics have posted some details about the upcoming update to the 454 system. According to the blog, the next upgrade will be called Titanium and will have twice the number of cycles increasing  the average read length from 250 to around 400 bases. Furthermore, the new version will have smaller, more densely packed wells on the [...]

I just hate page limits [Mailund on the Internet]

Posted: 13 Jun 2008 02:14 PM CDT

This is a typical situation for me: I submit a paper to a journal or conference that is just to  under the page limit.  I get review reports back, and each reviewer has a few reasonable suggestions to additional experiments or possible extensions or papers worth referencing.  I want to do the extra work — it is reasonable and I will learn something from it — but there just isn’t room in the paper to write about it!

Right now, I’m editing a paper for Bioinformatics, where the page limit is seven pages.  I’ve done all the work suggested by the reviewers but I’m practically putting it all in the cover letter instead of the paper.  The cover letter is now as long as the paper itself.

What do you do in a situation like this?

The reviewers’ decision is based on the submitted paper, so there is a limit to how much I can remove.  I cannot completely rewrite the paper, since the journal want me to mark up all changes (and I doubt that they will be happy with markups showing that I’ve changed everything).  So with the submitted manuscript being seven pages, I can only make very minor changes to the paper, and I still need to find a way to address all reviewer comments.

It is an impossible task!

I guess I should always leave a page or so for the second submission, but usually I find it hard to get down to the page limit in the first place…

Ahead of Google Health and HealthVault: PointOne [ScienceRoll]

Posted: 13 Jun 2008 01:38 PM CDT


Google Health and Microsoft HealthVault seem to be the leading forces in the market of electronic health records. Now I would like to show you something that can shape the future of healthcare. Robert S. Pothier, the President and CEO of PointOne Systems, answered some of my questions about the RedBox system.

  • Please tell us what RedBox is about.

RedBox is the core technology of PointOne. It is a software that takes in patient information from a variety of sources, analyzes the information based on established medical best practices, research findings and our own algorithms, and then provides reports that can focus on overall health assessments, risks and next steps.

  • What do I need to do to use it?

Although RedBox has been in development since 1998 and PointOne has been marketing its capability since 2001, the tool has not been available at a consumer level until this year. PointOne is now working on interfaces that will allow consumers direct access. At the end of July PointOne will launch a website called ClearSense that will allow consumers to get reports directly and use their Personal Health Records as a source of information for the reports. The new website will be Beta tested with a select group for a short time and then available to the public for free initially.

  • Why do you think it is beneficial to have online health records?

Consumers need to be in control of their own healthcare and having immediate access to our own health records is key to that. If we expect individuals to manage their own health, they need the data to do so. It is ridiculous that I can't see everything that's been done to me, my wife or my children from a health perspective in one place. How can I monitor my blood pressure or cholesterol if I don't have access to that data over time? The doctor has it in his records, along with my immunizations and other things. Why don't I have it? We talk about it being "private" and "confidential" but right now it's only "private" and "confidential" to the doctor. For me it's just a hassle to get access to it.

  • Where does the health data come from that is used in RedBox?

Initially the data will come directly from the consumer (answers to a questionnaire) or from a PHR (likely not a lot of these at first). Eventually, however, we'd like to see RedBox access data from anywhere health data resides, whether it's a fitness club, blood donation center or even home monitoring devices.

  • In some of the reports you published, there are action items that can improve my health (e.g. get an annual physical exam or schedule a hypertension evaluation). Are these suggestions made by physicians or this is an automatic feature of the software?

This is an automatic feature of the software. The reports we provide are not dispositive, meaning we don't say "you have diabetes" or "you have breast cancer". That's for a doctor to decide. However, our reports are designed to be educational. In addition to learning something about yourself, it also lists what you should be doing to monitor your health or providing information about tests you should consider. For example, many women do not know that the BRCA1/2 tests are even available. If you had a family history of breast or cervical cancer on one of our reports, the action item would mention the test as something to consider. It's pushing the right information to the right people.

  • What do you expect from the next months? How many users do you think will register?

We do not expect that this is a technology that will explode onto the scene. The use of this technology will be a gradual development as PHRs develop, as people become use to the idea that these reports are possible, as health data becomes more consolidated and cleaner. We use the following analogy to describe the process:

(True Story: http://www.niagarakite.com/history.html) – In 1847 in the United States Charles Ellet was trying to build a suspension bridge over the Niagara Falls gorge. The gorge was 800 feet across and 225 feet deep and the river was very swift. In order to get the suspension cables across the gorge they needed a way across that didn't involve hiking down, taking the boat across and going back up the other side. So, Mr. Ellet sponsored a kite flying contest to get one thread across the gorge. In 1948 a 15 year old boy got his kite across and won the contest. Mr. Ellet used that single thread to tie ever-increasing gauges of string, rope, wire and ultimately the steel wire cables that supported the bridge.

PointOne has the same approach. We are trying to build the bridge of health data analytics being accessible to everyone. Initially, however, we realize we will need to cast some small threads across and pull ever increasing applications across before we will be able to accomplish our goal in full.

The future of healthcare IT is the analytics. Right now everyone's focused on the collection, management, movement and protection of health data. That's an IT exercise. The eventual holy grail of healthcare IT will be the analysis of that data to provide information to the ultimate consumer.

Check out more about it at PointOne.

The Distraction of Google is Changing Our Brains [adaptivecomplexity's column]

Posted: 13 Jun 2008 01:04 PM CDT

The Atlantic is asking Is Google Making Us Stupid? They quote a pathologist at the University of Michigan School of Medicine:

"I now have almost totally lost the ability to read and absorb a longish article on the web or in print... I can't read War and Peace anymore. I've lost the ability to do that. Even a blog post of more than three or four paragraphs is too much to absorb. I skim it."

Can we still think in the age of online distraction?

Tomorrow's Table in Boston [Tomorrow's Table]

Posted: 13 Jun 2008 12:08 PM CDT

Next week I fly out to Boston to give a talk about organic farming, genetics and the future of food. The lecture is hosted by the Department of Molecular Biology at Massachusetts General Hospital and the Department of Genetics, Harvard Medical School.

The lecture will be held from 2-3 p at the Richard B. Simches Research Center, Room #3110. There will be time after the lecture to discuss the book. If you are in the boston area, please do drop by and introduce yourself.

Why Pfizer planning a $5B USD counter bid for the largest Indian branded generics [Microarray and bioinformatics]

Posted: 13 Jun 2008 09:53 AM CDT


While Invitrogen is making news merging into Applied Biosystems, with its $ 6.7 B USD deal creating the first of its kind of company, that can boast to own and invade every sphere of biological research from wet lab to information systems.

Pfizer is planning to counter bid the $4.6 billion offer by Japan’s Daiichi Sankyo Co Ltd  for the Indian generic drug maker Ranbaxy Laboratories Ltd. Ranbaxy has been a thorn in the big pharma fight against, generics and branded generics. Reason Ranbaxy just got FDA approval–and 180-day exclusivity–to sell a copycat version of Pfizer’s cholesterol lowering drug lipitor beginning in March 2010. Why should  lose all that cholesterol-drug revenue when, with a buyout, it could recapture it?

Raising fears that Indian companies that supply WHO and other World Organizations with cheap medicine will go under the hammer of Big multinationals, prompting hike in prices of drugs for treating  AIDs to cancer, cholestrol , hyper-tension or even antibiotics to fight infections, whose prices are the lowest in the world . Perhaps the era of cheap drugs may be over.

India is the biggest supplier of cheaper versions of essential drugs to the developing world and has a share of nearly 25% in the overall generic space. Domestic generic biggies particularly Ranbaxy and Cipla have been recognized globally, not only for their low-cost medicines, but also of their ability to produce quality medicines.

For instance, Cipla offers a first line AID Medicine which is a combination of three drugs, at a price of $100 per patient per year as against the MNC tag of $10,349, a huge reduction of over 100 times.

On not seeing the forest for the trees [Bayblab]

Posted: 13 Jun 2008 07:21 AM CDT

N: which is correct, seven and five IS thirteen, or seven and five ARE thirteen?
Joker: Neither.
Joker: Because it's twelve.

[From bash.org]

Midsummer Alchemist [Sciencebase Science Blog]

Posted: 13 Jun 2008 07:00 AM CDT

Midsummer alchemistFirst online in The Alchemist, this week, is an award for pioneering work in mass spectrometry and the study of molecules colliding with surfaces.

A way to create the thinnest polyethylene plastic bag ever has been devised by a team in Germany, while Australian researchers are hoping to defeat HIV by thickening the protective keratin layer of the penis using the female hormone estrogen. The Alchemist also learns that the Brits are turning to waste oil from that wondrous delicacy Fish & Chips to power up their cars.

Also in this week’s issue, Japanese chemists have synthesized what at first site looks to be a hexavalent carbon compound. Finally, with the long summer months stretching ahead of those of us in the Northern Hemisphere, The Alchemist cracks open a tinny and discovers that researchers in Venezuela have uncovered the secret to making beer last longer - add a little poison.

Grab all leads in my Alchemist column on Chemweb.com

Also live this week, the latest Intute Spotlight, covering rule-breaking quantum mechanics, exploiting pathological proteins in polymer science, and size does matter (on a planetary scale). Switch on the Spotlight. You may also like to check out the recent scientific discoveries archive on Sciencebase.

A post from David Bradley Science Writer

Midsummer Alchemist

Around the Blogs [Bitesize Bio]

Posted: 13 Jun 2008 05:55 AM CDT

This week you get two “around the blogs” articles for the price of one!

Seems Dan and Nick got their wires crossed this week as both have written an “around the blogs” post at the same time. Still, best not to let a good round-up go to waste, so here are both of them:

Dan’s Around the Blogs


These are busy days still, so here are a roundup of links from across the blogs.
Careers

Want to be successful? learn to write quickly and efficiently - I could take some tips on writing efficiency - we all could.

Academic Promises - “Here’s the deal. Oral promises in academia don’t mean jack.”

Reflections on my first year as a faculty member - Personal career reflections. Check ‘em out.

Science

Growing new brain cells to treat depression: A clinical trial

Evolution of Phage Capsid and Genome Size

Miscellaneous

Cuddle up to a phage! - Simply amusing.

Science is so much more than its technical details - Comments on Brian Greene’s recent opinion piece in the NY Times. Another good response: Rethinking Science education

…and Nick’s Around The Blogs


Career paths into biotechnology.
Sandra at Discovering Biotechnology in a Digital World discusses the variety of training paths that US students take to reach their first biotech job.

…and career paths out of biotechnology. Dan has been talking about the difficulties in moving out of the biotech/science career path this week, and so has Chris at chrisdellavedova.com.

Egg in our face (terrible pun, sorry). BayBlab carries some amazing photos of human ovulation captured by surgeons performing a partial hysterectomy.

Have you ever been mortified in the name of science? David at The World’s Fair has, and he along with his commenters are sharing. Maybe you should too?

It’s ok if your gel looks crappy. Janet in Adventures in Ethics and Science comments on the surprisingly common practice of tampering with images intended for publication. A lot of people apparently do this to “beautify” their images, but there is a very fine line between this and tampering with data.

DNA Quote: Sir William Bragg on Science [Eye on DNA]

Posted: 13 Jun 2008 03:25 AM CDT

150px-William Henry Bragg

The important thing in science is not so much to obtain new facts as to discover new ways of thinking about them.

~Sir William Bragg, 1862-1942, British physicist and chemist, winner of the 1915 Nobel Prize in Physics

via Quotes of the Day

Heavweight Cryptographer Squares Off With The Code Of Life []

Posted: 13 Jun 2008 02:24 AM CDT

cryptodna.jpg

Here’s a really interesting New York Times piece about heavyweight cryptographer Nick Patterson. The guy should be a character in a Neil Stephenson novel: he worked at the NSA, then Renaissance Capital as a Wall Street quant. All too boring for him. He wanted to sink his teeth into something really tough — like the human genome — which he’s taking on despite zero training in the life sciences. Definitely one to follow.

Survival in Prostate Cancer: It May Be Affected By Your Genes [Cancer and Your Genes]

Posted: 13 Jun 2008 02:00 AM CDT

We frequently hear about connections between our genes and the risk of developing prostate and other cancers.  However, a new study provides further evidence in support of an old idea that our genes may affect something much more important than the development of cancer; indeed, this new research supports the concept that our genes affect survival from prostate cancer

Dr. Kari Hemminki and colleagues, in a fascinating piece of epidemiologic sleuthing published in the Journal of Clinical Oncology, utilized the Swedish Family-Cancer Database to determine whether survival patterns from prostate cancer clustered within families.  By assessing survival data for more than 600 prostate cancer-affected sons and their fathers (who also had prostate cancer), they were able to show that sons of fathers with shorter survival from prostate cancer tended to survive for a shorter period as well.  Likewise, sons of fathers who survived for a longer period of time after the diagnosis tended to survive for a longer period of time as well. 

Although these results shouldn't be utilized at this point to guide treatment decisions, as they may be subject to some biases and need further confirmation, they should pave the way for future studies aimed at identification of genes underlying this familial risk.  This would be a refreshing approach in an area of medicine beset with substantial uncertainty surrounding best treatments - particularly with respect to decisions regarding prostatectomy versus "watchful waiting."  It will be very interesting to see how this turns out, and it is important to remember that genes that may confer risk of metastatic disease and/or poor survival may not be genes that are involved in risk of developing prostate cancer (i.e., they only affect the rate of progression or metastasis of the disease once it is already established). 

Selected References

K Hemminki et al.  Concordance of survival in family members with prostate cancer.  Journal of Clinical Oncology 26: 1705-9, 2008.

Resources

Prostate Cancer Foundation


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High-risk, high-reward and the NIH [business|bytes|genes|molecules]

Posted: 13 Jun 2008 01:43 AM CDT

National Institutes of HealthImage via Wikipedia

(The NIH needs to) continue to maximize the freedom of scientists to pursue high-risk, high-impact research

Those words were spoken by Elias Zerhouni, Director of the National Institutes of Health (via Genomeweb, free sub reqd). I have many questions, but foremost I would like to understand what the NIH considers “high-risk” and “high-impact”

The NIH really needs to start consider how to fund projects which could fail completely, and how to fast track funding. The funding process doesn’t work for teams that want to act fast, especially when you are a new group without too much of a track record.

I am not an academic, haven’t been since I finished grad school, but would love to hear what your expectations are, and perhaps what you really think will happen.

Further reading
NIH funding
HHMI goes farming

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Ancient antibody molecule offers clues to how humans evolved allergies [Think Gene]

Posted: 13 Jun 2008 12:57 AM CDT

Scientists funded by the Biotechnology and Biological Sciences Research Council (BBSRC) have discovered how evolution may have lumbered humans with allergy problems. The team from the Randall Division of Cell & Molecular Biophysics, King’s College London are working on a molecule vital to a chicken’s immune system which represents the evolutionary ancestor of the human antibodies that cause allergic reactions. Crucially, they have discovered that the chicken molecule behaves quite differently from its human counterpart, which throws light on the origin and cause of allergic reactions in humans and gives hope for new strategies for treatment. The work is published today (13 June) in The Journal of Biological Chemistry.

Researcher, Dr Alex Taylor said: “This molecule is like a living fossil – finding out that it has an ancient past is like turning up a coelacanth in your garden pond. By studying this molecule, we can track the evolution of allergic reactions back to at least 160 million years ago and by looking at the differences between the ancient and the modern antibodies we can begin to understand how to design better drugs to stop allergic reactions in their tracks.”

The chicken molecule, an antibody called IgY, looks remarkably similar to the human antibody IgE. IgE is known to be involved in allergic reactions and humans also have a counterpart antibody called IgG that helps to destroy invading viruses and bacteria. Scientists know that both IgE and IgG were present in mammals around 160 million years ago because the corresponding genes are found in the recently published platypus genome. However, in chickens there is no equivalent to IgG and so IgY performs both functions.

Lead researcher, Dr. Rosy Calvert said: “Although these antibodies all started from a common ancestor, for some reason humans have ended up with two rather specialised antibodies, whereas chickens only have one that has a much more general function.

“We know that part of the problem with IgE in humans is that it binds extremely tightly to white blood cells causing an over-reaction of the immune system and so we wanted to find out whether IgY does the same thing.”

By examining how tightly IgY binds to white blood cells the researchers have found that it behaves in a much more similar way to the human IgG, which is not involved in allergic reactions and binds much less tightly.

Professor Brian Sutton, head of the laboratory where the work was done said: “It might be that there was a nasty bug or parasite around at the time that meant that humans needed a really dramatic immune response and so there was pressure to evolve a tight binding antibody like IgE. The problem is that now we’ve ended up with an antibody that can tend to be a little over enthusiastic and causes us problems with apparently innocuous substances like pollen and peanuts, which can cause life-threatening allergic conditions.”

The next stage of the work is to examine in very fine detail the interaction between the antibodies and the surface of the white blood cell. This is with a view to designing drugs that could alter this interaction and therefore ‘loosen’ the binding of IgE, making it more like its chicken counterpart.

Source: Biotechnology and Biological Sciences Research Council

Alexander I. Taylor, Hannah J. Gould, Brian J. Sutton, and Rosaleen A. Calvert. Avian IgY Binds to a Monocyte Receptor with IgG-like Kinetics Despite an IgE-like Structure. J. Biol. Chem. 2008 283: 16384-16390. First Published on April 9, 2008; doi:10.1074/jbc.M801321200

Josh says:

I’ve always found the immune system fascinating. IgG, IgE, IgM, and IgA are all extremely similar, so it makes sense that they started as one gene that was later duplicated, in this case producing IgG and IgE.

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