Friday Foolery [3] Showing the invisible

4 09 2009

I always found it difficult to think abstract. It was not until physics class at college, that I started to understand physics formulas,  because our professor gave practical examples from real life, i.e. he made me understand why the sky was blue. Mathematics was all right as long as we stayed in two dimensions, but stereometry was already one dimension too much. Molecules, chemical bonds and atomic structure were also vague especially when wave-particle duality came into play. It was even hard to imagine what DNA really looks like. At one stage I even tried to make a DNA structure at home from matches and colored clay. But the model was so fragile, that it crashed before the first minor groove was finished.

Nowadays, students are so lucky: a computer, the internet, beautiful graphs, videos, 3D-animations.

Below a mixture of recent  and some old animations and 3D representations, that highlight our understanding of numbers and dimensions, the infinite small and the infinite large.

First 3D image of an individual molecule and its bonds!

A real breakthrough was the visualization of the atomic backbone of an individual molecule (pentacene) and its atomic bonds. As reported in the August 28 issue of Science magazine, IBM Research Zurich scientists (in collaboration with Peter Liljeroth of Utrecht University), accomplished this by using an atomic force microsope (ATM) operated in an ultrahigh vacuum and at very low temperatures ( 268oC or 451oF). According to the researchers this is reminiscent of X-rays that pass through soft tissue to enable clear images of bones.

Below you see:

  • the chemical structure of pentacene with 22 carbon atoms (Wikipedia).
  • the force map image of pentacene (IBM).
  • a video-interview with the researchers explaining their research (IBM-Labs).

3-9-2009 23-52-44 pentacene ibm

Hattip: @jensmccabe (twitter) and Greg Laden (twitter and blog)
More info: www.physorg.com and gizmodo.com

The Galaxy mapped

Now quite the opposite infinity: the universe: “what 100,000 nearby large (i.e., Milky Way sized and larger) galaxies, look like reduced each reduced to a point” (translation by @dreamingspires) or “will give you an idea how totally insignificant we are” (@scanman). These tweople referred to Etann Siegel’s blog “It starts with a bang”.

One of the original researchers (Dominique Proust) has also posted a short description of the study and an image on the internet which shows the clustering pattern of about 100,000 nearby galaxies, revealed by the 6dF Galaxy Survey (see here) : “Each galaxy is shown as a dot. The galaxy we live in is at the centre of the pattern” (an enlargement of the image is here).

The astronomers came from all over the world (Australia, the UK, USA, South Africa, France and Japan). Their survey “will reveal not only where the galaxies are but also where they’re heading, how fast, and why. “It’s like taking a snapshot of wildebeest on the African plain. We can tell which waterholes they’re heading to, and how fast they’re travelling,” said D. Heath Jones of the Anglo-Australian Observatory (AAO), lead scientist for the Six-Degree Field Galaxy Survey (6dFGS)”

Dimensions

1, 2, 3 ….no here are 10 dimensions explained

but the 4th dimensions will do for me

Powers of 10

A classical video: the powers of ten. It dates from 1977. I have seen it during college and it made a lasting impression.
Powers of Ten explores the relative size of things from the microscopic to the cosmic. The 1977 film travels from an aerial view of a man in a Chicago park to the outer limits of the universe directly above him and back down into the microscopic world contained in the man’s hand.

There is even a website “powers of ten”. At the right you can click on a power of ten. Like 10 ¹³ and 10 -¹³

13

Measuring in meters, this power of ten is equal to 10 billion kilometers. We see the outer planets as they circulate counterclockwise, all in nearly the same plane.

Measuring in seconds, this power of ten equals

  • Space 10 billion kilometers
  • 317, 097 years.
  • Unmanned Space Probes
  • Johannes Keppler
  • Space First Images Of Jupiter through Time

-13

Measuring in meters, this power of ten is equal to .1 picometer or 100 fermis. We see the kernel of a carbon atom, bound by six neutrons and six protons. This nucleus is dubbed carbon-12.

Measuring in seconds, this power of ten equals 100 femtoseconds.

  • 100 fermis
  • 100 femtoseconds
  • Lasers
  • Niels Bohr

Also the Wikipedia explains large numbers and astronomically large numbers. The Dutch Wikipedia gives more examples from daily life:

Do you still need some help in mathematics? Here is a tip from a Dutch educator @trendmatcher: your free online 24/7 math help, meant to help high school students with their homework. (There is also non-free material)

More frivolous:

Modern steps through time (via @scanman and @drves) : kalman.blogs.nytimes.com

And a  Twitter visualization tool that shows about 11,000 “good morning” tweets over a 24 hour period, between August 20th and 21st. All tweets are color-coded: green blocks are early tweets, orange ones are around 9am, and red tweets are later in the morning. Black blocks are ‘out of time’ tweets which said “good morning” (or a non-english equivalent) at a strange time in the day. Seen at the blog of @zbdigitaal (Edwin)
The original post and the video can be found here

Vodpod videos no longer available.

REFERENCES:
Leo Gross, Fabian Mohn, Nikolaj Moll, Peter Liljeroth, and Gerhard Meyer. “The Chemical Structure of a Molecule Resolved by Atomic Force Microscopy.” Science, 28 August 2009: Vol. 325. no. 5944, pp. 1110 – 1114. DOI: 10.1126/science.1176210.

The 6dF Galaxy Survey: Final Data Release (DR3) and Southern Large Scale Structures
Jones D Heath., Read Mike A., Saunders Will., Colless Matthew., Jarrett Tom., Parker Quentin., Fairall Anthony., Mauch Thomas., Sadler Elaine., Watson Fred., Burton Donna., Campbell Lachlan., Cass Paul., Croom Scott., Dawe John., Fiegert Kristin., Frankcombe Leela., Hartley Malcolm., Huchra John., James Dionne., Kirby Emma., Lahav Ofer., Lucey John., Mamon Gary., Moore Lesa., Peterson Bruce., Prior Sayuri., Proust Dominique., Russell Ken., Safouris Vicky., Wakamatsu Ken-ichi., Westra Eduard., Williams Mary: 2009,
submitted to Monthly Notices of the Royal Astronomical Society

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LoL: Stop Following Me!

28 06 2009

This picture is so cool.
First seen at ScienceRoll of Bertalan Mesko (@berci); this print is from a T-shirt of Zazzle.
More t-shirts and other prictures can be seen here





CMV-infection, plaques and high blood pressure

26 05 2009

A recent experimental study shows that a common virus that hides (becomes latent) after infection can trigger high blood pressure, a leading cause of cardiovascular disease.

The virus is cytomegalovirus (CMV). It belongs to the herpesviruses, hence its alternative name Human Herpesvirus 5 (HHV-5). The herpesviruses have in common that they can become latent (dormant) for a long while. Herpes simplex virus-1 (HSV-1) and varizella zoster virus usually hide in nerves (neurons) and can cause cold sores and shingles respectively after reactivation.

Cytomegalovirus (CMV) can be transmitted by sputum and other bodily fluids. After infection, it stays within the host, hiding primarily in certain white blood cells serving as a reservoir for reactivation.

The study by Cheng et al, consisted of an experimental mouse study and in vitro experiments, using mouse CMV (MCMV) and human CMV (HCMV)

  1. In the in vivo experiment, 4 groups of mice -of 12 animals each- were treated as follows:
    • V: Mice in group 1 were infected by MCMV and fed a regular diet.
    • M: Mice in group 2 were mock-infected and fed a regular diet (control group).
    • V-HD: Mice in group 3 were infected by MCMV and fed a high cholesterol diet.
    • HD: mock-infected and fed a high cholesterol diet (control group).
      systolic diastolic
  2. After 6 weeks the blood pressure, measured in the carotid artery, was significantly enhanced in mice that were infected by the MCMV compared to mock-infected controls. Thus the blood pressure was significantly higher in V versus M and in V-HD versus HD mice. This was both true for the systolic and the diastolic blood pressure (see Fig).
  3. Atherosclerotic plaque formation in mouse aortas was only observed in V-HD mice (MCMV infection and high cholesterol diet together). 3 out of 12 mice showed plaques against 0 out of 12 mice in the other groups.
  4. The serum levels of all 3 pro-inflammatory cytokines tested, IL-6, TNF-α and MCP-1, were higher in the mice infected with MCMV (V-HD and V) than in the mock-infected groups fed with either diet.
  5. CMV infection induced renin and Ang II expression (in vitro cq in vivo). Renin is a rate limiting protein of Renin-Ang-II system and Ang II is the peptide that causes the blood vessels to constrict, thereby enhancing blood pressure.
  6. The renin production was only enhanced in kidney-cells containing CMV-particles.
  7. In mice infected with CMV, Ang II was also increased in serum and in artery tissues.
  8. MCMV RNA and DNA were present in blood vessels post infection. Mice produced the latency-related CMV transcriptional product I-E1.
  9. Next, in vitro experiments were carried out with human cells. Infection of human blood vessel endothelial cells with HCMV induced renin expression in a-dose dependent manner, without lysis of the cells (non-lytic infection). This means that viral gene expression takes place in the absence of a viral cytopathic effect. Only replicating forms of HCMV could induce renin.

Conclusion of the Authors:

“In summary, CMV infection alone caused a significant increase of arterial blood pressure. Enhanced expression of pro-inflammatory cytokines, renin and Ang II underlies the pathogenic mechanism of an active CMV infection to increase blood pressure and aggravate atherosclerosis. Thus, control of CMV infection to restrict development of hypertension and atherosclerosis may provide a new strategy to prevent cardiovascular diseases associated with HCMV infection.”

Review
The present article provides interesting new insights into various mechanisms whereby CMV could ultimately cause cardiovascular disease. Many different assays were performed, both with mouse CMV in vivo and in vitro and with human CMV in vitro.

It should be noted however, that several of the reported findings are not new. CVM DNA and RNA have long been identified in atherosclerotic plaques. CMV and other herpesviruses were known to induce IL-6 and other pro-inflammatory interleukines. And a relation between CMV-infection and cardiovascular disease has been established in the past.

The main new findings are (1) that CVM-infection can raise blood pressure and (2) the demonstration of possible mechanisms involved in the increase of blood pressure: induction of renin and angiotensin by infection of endothelial and renal cells (rather than induction of plaques?) and induction of cytokines. Importantly, the cytokine-enhancing effects were restricted to CMV-infected cells only.

Although the findings are very suggestive of a causal relationship, it remains to be proven whether hypertension via enhanced extrarenal production of renin and angiotensin is the causal factor of CMV-associated cardiovascular disease in the normal human situation. Some statements are not underpinned by the current data. See for instance the blue marked text in the author’s conclusion.

ahc_67444

Arterial wall depicting major inflammatory features common to CMV infection and atherosclerosis. – K. Froberg

The current prevailing hypothesis is that atherogenesis is an inflammatory response to acute or chronic endothelial injury. Possible causes for this endothelial injury include free radicals, modified LDL, hypertension, diabetes mellitus and smoking [4,5]. More recently CMV and other infections have been added to the list of risk factors. It is generally thought that the formation of plaques concurrent with the enhanced induction of cytokines can contribute to atherosclerosis and vascular disease, after many years of chronic, active inflammation of the arterial wall.

In the present model, atherosclerosis was only observed in 3 out of 12 HD-V mice. This indicates that atherosclerosis is not involved in the increase of blood pressure. Instead, the present study shows, that CMV might contribute to cardiovascular disease via an effect on blood pressure, presumably mediated through an enhanced expression of renin and Ang II.

With regard to the statistical analysis, I wonder why each virus-treated group was only compared to its mock-infected control (using the Student’s t-test)? Why weren’t all groups compared to each other, using another statistical test? Is this because another approach would have rendered most differences insignificant? The differences between groups are consistent but not very large and the standard deviations are quite overlapping. (Thus significance might be lost when more rigid test are used)

It would for instance be interesting to know the relative contribution of the fatty diet to the rise in blood pressure, or the risk in the 4 groups relative to each other.
We all have CMV (well about 70-90%), but just few of us get high blood pressure (at young age). So likely other factors come into play, that may enhance the detrimental effects of CMV or vice versa. Therefore, it would for instance be interesting to know, to which extent high fat consumption would contribute to high blood pressure as well. Is the suggested order as we see it real: V alone giving slight elevation of blood pressure, HD alone giving more elevation and VHD giving the highest rise? (2×2 table).

The study has some fascinating results, but it is too soon to think about antiviral treatment as the authors and media [3] suggest. Nor is it necessary to worry the public by stating that: You can find out if you have been infected with CMV by requesting a blood test from your GP”, as the daily mail does. This is useless, because CMV is omnipresent.

It hardly seems to be justified to suggest that everybody should be treated with antivirals. And what about the other viruses or bacteria that may play a role? Furthermore, lifestyle and other (immunological) parameters may be more important ànd lifestyle changes may be easier to implement.

Update: Tuesday 2009-05-26: 17.30 pm.

HATTIP: @microbytes (Twitter)

Figure: Kent Froberg from the University of Minesota (med.umn.edu)

References

ResearchBlogging.org

  1. Cheng, J., Ke, Q., Jin, Z., Wang, H., Kocher, O., Morgan, J., Zhang, J., & Crumpacker, C. (2009). Cytomegalovirus Infection Causes an Increase of Arterial Blood Pressure PLoS Pathogens, 5 (5) DOI: 10.1371/journal.ppat.1000427
  2. http://www.sciencedaily.com/releases/2009/05/090514221915.htm
  3. http://www.dailymail.co.uk/health/article-1186876/Heart-disease-isnt-catching-Oh-yes-scientists-warn.html
  4. Many reviews from Cathrien A. Bruggeman and colleagues, like this review in a Book.
  5. Kent Froberg from the University of Minesota (med.umn.edu)
Human Herpesvirus 5 (HHV-5)




One Third of the Clinical Cancer Studies Report Conflict of Interest

16 05 2009

While many of us just recovered from the news that Elsevier was paid to produce fake Journals to promote pharmaceutical products, another news item has appeared about “conflicts of interests in scientific publications”

This news is based on a new journal article from researchers from the University of Michigan’s Comprehensive Cancer Center in Ann Arbor, published in an early online edition of Cancer [1]

As mentioned in my previous post about the Elsevier “Fake Journals”, pharma-sponsored trials rarely produce results that are unfavorable to the companies’ products [e.g. see 3 for an overview, and many papers of Lisa Bero]. Concerned by these findings, the main medical journals now require researchers to disclose their potential conflicts of interest (COI).

The present study [1] analyzes the frequency of self-reported conflicts of interest (COI), source of study funding, and (their relationship with) other characteristics in original clinical cancer research (thus no reviews or basic research) published in 8 medical Journals in 2006. The 8 journals are high-impact clinical journals, 5 are oncology journals (Journal of Clinical Oncology, the Journal of the National Cancer Institute, Lancet Oncology,Clinical Cancer Research, Cancer) and 3 are core general medical journals (New England Journal of Medicine,JAMA, the Journal of the American Medical Association, Lancet).

In these medical journals 1534 original oncology studies were found. Twenty-nine percent of the oncology articles reported COI: 17% declared industrial funding and the remaining 12% of the studies had authors who were an employee of industry at the time of publication, or were funded by industry.

The study was thoroughly done: 2 students independently coded the articles and 2 other coders, blinded for the initial coding, assessed all randomized trials (within those 1543 papers) for the outcomes. They graded the authors’ subjective interpretations as positive (in favor of the intervention), neutral, or negative (in favor of the control arm). Overall survival was assessed quantitatively.

The main results:

  • Conflicts of interest varied by discipline (P<.001). Studies that had a corresponding author from a medical oncology department or division were most likely to have conflicts (45%), and studies from diagnostic radiology were least likely to have conflicts (4%)
  • Likewise the cancer type mattered, especially with regard to likelihood of industrial funding (P = .001). Studies on the male reproductive system and lung cancers scored highest and studies on neurological cancers scored lowest as to the likelihood of funding. (however there is some contradiction because gynecologic departments have a high score and gynecologic cancers have a relatively low score, conf. figures 1 and 2)
  • Continental origin was also an important variable (P<.001). COI were observed in 33% of the North American studies, 27% of the European studies, 5% of the Asian studies, and 40% of the studies from other locations.
  • COI was most likely in articles with male first and senior authors (P<.001).
  • Industry funded studies were more likely to focus on treatment (P<.001), and less on epidemiology, prevention, risk factors for incidence, screening, or diagnostic methods.
  • The randomized trials (n=124) that assessed survival were more likely to report positive survival outcomes when a COI was present (P=.04). (see below)

The paper has received a lot of media attention, initiated by the press release of the University of Michigan Health System itself. The data however are less shocking then they may seem. The main finding is that “conflicts of interest characterize a substantial minority of the clinically oriented cancer research published in high-impact medical journals”. This and the characteristics of the papers with COI (see above) add to earlier papers that report on the occurrence of COI in published articles, including papers in the field of clinical oncology.”

Some outcomes are not very surprising, such as that pharmaceutical industries and funding will be most involved in intervention studies in medical oncology studies (not so much in radiology or diagnostics).

In itself, COI does not mean that the results cannot be trusted or that they are plain wrong. Credibility could be questioned if only positive results are published or if the results are represented more positive then they really are.

Indeed, Jagsi et al show that “randomized trials with a COI were more likely to report positive survival outcomes (P=.04)”. However, the likelihood that the author interpretation was positive or more positive than the objective effect on overall survival wasn’t influenced by COI. And differences in industrial funding didn’t influence any of the blinded outcomes assessed. Also in this study, the non-neutral findings are emphasized. 😉

On the other hand, authors had to rely on the information given, i.e. not all conflicts of interests may have been reported. Another issue is that not all known COIs are disclosed to the public (i.e. medicalnewstoday)

The following conclusion of the lead author Reshma Jagsi seems most relevant:[2]

“Given the frequency we observed for conflicts of interest and the fact that conflicts were associated with study outcomes, I would suggest that merely disclosing conflicts is probably not enough. It’s becoming increasingly clear that we need to look more at how we can disentangle cancer research from industries”

References
ResearchBlogging.org

  1. Jagsi, R., Sheets, N., Jankovic, A., Motomura, A., Amarnath, S., & Ubel, P. (2009). Frequency, nature, effects, and correlates of conflicts of interest in published clinical cancer research Cancer DOI: 10.1002/cncr.24315
  2. University of Michigan Health System (2009, May 13). 29 Percent Of Cancer Studies Report Conflict Of Interest. ScienceDaily. Retrieved May 14, 2009, from http://www.sciencedaily.com­ /releases/2009/05/090511090846.htm
  3. Smith R. Medical Journals Are an Extension of the Marketing Arm of Pharmaceutical Companies. PLoS Med. 2005 May; 2(5): e138. Published online 2005 May 17. doi: 10.1371/journal.pmed.0020138.

You may also want to read:

Hattip: @sciencebase, Reinout Rietveld (via NRC-next)





Twitter goes Viral: Swine Flu Outbreak – Twitter a Dangerous Hype?

30 04 2009

twitter-network-and-virusTwitter has been praised for its actuality and news breaking character. Remember the earthquakes and the two recent airplane crashes (Hudson River, Schiphol). Twitter often was the first to bring the news.

Twitter’s power lies in its simplicity, -the 140 character limit-, its speed and it’s domino-effect. Tweets (twitter messages) can be read by your followers (I have appr. 650). If they find something important, funny or whatever they could “RT” or Retweet (i.e. resend) the message, and their friends could retweet it as well. Via these secondary networks Twitter can go viral (in its replication and spread).

Below a friends of a friend network of a well known twitter personality Robert Scobleizer, as obtained by Twitterfriends. Only the “relevant network” is shown, directed to someone in particular: tweets beginning with @ (followed by the twitter name of your friend). The actual reach of tweets not starting with @ is greater, because they can be read by all followers.

3136982396_58537a66fb-foaf

Apart from following specific tweople one can also search for certain words or (hash)tags via Twitter Search or #hashtags.

Pushed by celebrities, such as Ashton Kutcher and Oprah Winfrey, who recently joined Twitter. Twitter’s traffic was poised to double and the number of tweeting people has steeply increased.

Twitter has been glorified by the stars. They created a real (meaningless) twitter mania.

But what raises high, can drop low.

Several sources dethroned Twitter because of it’s viral role in the recent swine flu outbreak. One of the first and most serious critiques came from a blog (Foreign Policy: Net Effect). It’s title: Twine flu: Twitter’s power to misinform.swine-flu-totThis is a serious allegation. Evgeny Morozov‘s main critiques:

  1. The “swine flu” meme has led to misinformation, fear and panic. Wrong info includes: fear that it “could be germ warfare” or “that one should not eat pork and certainly not from Mexico”.

  2. Unlike a simple Google search Twitter gives too much noise (irrelevant or wrong information).

  3. Messages from trustworthy sources have as much weight as those from uninformed people.

  4. There is very little context you can fit into 140 characters, even less so if all you are doing is watching a stream.

  5. Evgeny also worries about a future misuse of Twitter by cyber-terrorists shaping conversations on serious topics. A number of corporations are already monitoring and partially shaping twitter conversations about particular brands or products.

In addition some posts highlight that most of the Tweets belong to the category “witty or not so witty”. (also see this post)
And after these comments many similar comments were to follow: In fact these comments and critiques were going viral as well: take a look at this Google Search for Twitter Swine Flu and note the negative sound of most of the headlines.
The CNN website quotes Brennon Slattery, a writer for PC World,

“This is a good example of why [Twitter is] headed in that wrong direction, because it’s just propagating fear amongst people as opposed to seeking actual solutions or key information (..). The swine flu thing came really at the crux of a media revolution.”

Is Twitter just a hype and useless as an information source? Is it dangerous when a wide number of people would turn to Twitter in search of information during an emergency? Or have people just found a stick to beat the dog?

I will go to several aspects of the twitter flu coverage as I have encountered it.

Number of tweets

Indeed, as brought forward by Mashable, Tweets about “Swine Flu” are *now* at 10,000 per hour!!

Yesterday, 5 out of 10 twitter buzzwords were connected to Swine Flu:

  • # · Swine Flu
  • # · swineflu
  • # · Mexico
  • # · H1N1
  • # · Pandemic

Searching for information on Twitter
You can imagine that it is hardly useful to keep track of tweets mentioning *swine flu*, nor is searching for these buzzwords or hastags useful, if not combined with other terms or names, like CDC or laikas (just to find what you tweeted yourself).
I keep track of certain words via Tweetdeck in separate columns, accepting a certain “noise”, knowing this will only yield 20-50 tweets per day. It would not come to my mind to just blindly search for swineflu on Twitter.

The official media
It is said that Twitter doesn’t give useful or correct information, and indeed it hasn’t been designed for that (being merely a social Network). In its primitive form it is just online gossip or as The Register (UK) puts it- “it is not a media outlet. But odd enough, the official media did not behave differently. Cable television programmers went into crisis mode and a look at newspaper front pages and website home pages around the world showed a range of responses, from the almost hysterical to the concerned and more measured (Reuter’s Blog).

Look at this message from AJ Cann, that I retweeted :

laikas: RT @AJCann Totally irresponsible #swineflu journalism in the Dail Mail http://tinyurl.com/cms3km (expand) >>and they say twitter evokes global panic!
Is there really no reason to be worried?
Let’s face it. We don’t know an awful lot about this new virus strain. While it is true that the common flue has killed 13,000 people in the US since in a rather unnoticed way, and while there are relatively few swine flu casualties yet, one never knows how this new H1N1 epidemic will evolve. It might just fade away or it could kill millions of people. We just don’t know. It is a new, deadly virus. Not for nothing (as I learn from Twitter), the WHO has just raised the current level of influenza pandemic alert from phase 4 to phase 5. But this is only meant to be prepared and to inform, not to cause panic.
who-message
AJCann (on twitter)Ben, a doctor writing for the Guardian, excelling in critically informing the public about science (and quack) and a real valibrity, was invited all over by the media to be a naysayer on the “aporkalypse”.
How to deal with Twitter Noise?
Suppose you would listen to all radio channels at once: that would be an unbearable noise. Usually you choose a channel, your favorite one, and just listen what comes next. But you may switch to another channel anytime. And for news you might just go to a specific channel that you know is the most informative.
It is exactly the same with Twitter. I don’t follow everyone. Since I use Twitter mostly for my work (medicine, library, science, web 2.0) and not primarily for a chat or wit, I choose the tweople I follow carefully. If they produce too much noise I might unfollow them. They are my human filter to the news.

6a00d8341bfa9853ef0105368fcb5e970c-400wi-darmano

Furthermore among the ones I follow are News or Health Sources, like @CNN Health, sanjayguptaCNN, @BBC Health, @BreakingNews, @health and recently (because of retweets of friends): @WHOnews , @CDCemergency, Reuters_FluNews, Fluheadlines.

@BreakingNews and @health mentioning real casualties and the WHO calling an emergency meeting, I realized the seriousness of the problem. I was also pointed to @WHOnews and @CDCemergency, the most trustworthy sources to follow.
I also understood that the swine flu might be difficult to contain.

laikas: RT @BreakingNews: BULLETIN — WORLD HEALTH ORGANISATION CALLS EMERGENCY MEETING TO DISCUSS DEADLY SWINE FLU OUTBREAKS IN MEXICO AND THE U.S.

laikas: RT @health WHO, CDC concerned about possible epidemic following reports of 60+ people killed by new flu strain in Mexico http://bit.ly/d3JsO
laikas: RT @TEDchris: Swine flu outbreak. This is how it was SUPPOSED to have been contained. http://is.gd/us6r Worrying. >> WHO protocol
laikas: RT @BreakingNews: Reports of flu outbreak in New Zealand. 22 students may have been infected after a trip to Mexico. BNO trying to confirm. 3:25 AM Apr 26th from TweetDeck

laikas: RT @dreamingspires: RT @AllergyNotes Map of H1N1 Swine Flu of 2009 http://bit.ly/P2mcc (expand) 4:41 AM Apr 26th from TweetDeck

laikas: Map of H1N1 Swine Flu of 2009 http://bit.ly/P2mcc _ New Zealand added to the map. 4:42 AM Apr 26th from TweetDeck


Direct Link to H1N1 Swine Flu Google Map:

Somewhat later came the informative phase. Long before the official media were giving any useful information, some of my twitterfriends alerted me to their own or other (official) news.

@ajcann already wrote a post on his blog Microbiology Bytes (a blog with the latest news on microbiology) :10 things you should know about swine flu. (April 25th)

laikas: Reading @sciencebase Swine Flu http://bit.ly/y5Xqz 7:47 AM Apr 26th from web

laikas: RT @sanjayguptaCNN: I’ll answer your swine flu Q’s LIVE on CNN at 7:30a ET. call 1-800-807-2620. thanks 4he gr8 tweet Q so far.

laikas: RT @consultdoc: Great swine flu summary via @ubiquity http://bit.ly/DK0xV (expand) Thanks Greg.1:18 PM Apr 26th from TweetDeck

laikas: RT @BreakingNews: The WHO is holding a news conference on swine flu. Michael van Poppel is covering it live @mpoppel.
laikas: RT @stejules: RT @mashable HOW TO: Track Swine Flu Online http://tinyurl.com/dh68n8 (expand) (via @tweetmeme) (

At that point I became saturated with all information. I just follow the main news and read some good overviews

end-tweet-flu
Conclusion
For me, Twitter was the first and most accurate news source to get informed and updated on the swine flu pandemics. It was reliable, because “my friends” filtered the news for me and because I follow some trustworthy sources and news sites. Indirectly other tweople also pointed me at good and actual information.
And in my turn I kept my followers informed. The news has alarmed me, but I’m not in panic or frightened. I just feel informed and at the moment I can do nothing more than “wait and see”.

It has often been said: Twitter is what you make of it.
But keep in mind the golden rule:

Information on Swine Flu

News and Blogs

Photo Credits:

* wonderful those different names.





Stories 3. Science or Library Work: what is more rewarding?

20 04 2009

2267526122_f4376fc6bfAmy Tenderich of Diabetesmine, will celebrate her birthday at the very same day as she hosts the next Grand Round. She has therefore chosen a very appropriate theme (see announcement):

I’m favoring any and all posts having to do with birthdays and special occasions – or anything that smacks of serendipity, perks, or gifts related to the work you all do.

First of all I would like to congratulate Amy on her birthday.

I have been hesitating whether I should contribute to this round. It is not an easy subject and a bit out of scope. However, thinking about it, many ideas came up and it even became difficult to choose one. But here it is. It is even the first post in a series: STORIES, a selection of personal stories.

Most of you will know that I’m a medical librarian by profession, but a medical biologist by education. Many years I worked as a scientist, with mice, patients, cells, DNA and proteins.3419163183_91968b96d6

I was an avid scientist. My motivation was to unravel mechanisms and understand life. I liked to ask questions: “why is this? why do I find that? how does it work?” The greatest reward you can get is: looking for explanations and finding the answer to a question. Thinking about it and discussing it with others is exciting.The more difficult a question is, the more rewarding it is to find the answer. The gift that science gives you is science itself.

In those twenty years I did have my little successes. I had a press conference at a congress (1) (because it was the only subject that was understandable for the public) and I had two papers that were frequently cited (2).

The finding that gave rise to those two publications was very serendipitous. We found a very tiny band in B cells that were used as a negative (!) control for follicular lymphoma in a PCR for the t(14;18) chromosomal translocation. This translocation is considered the hallmark of this type of B-cell cancer. If this was true, it would mean that the lymphoma-associated t(14;18) involving the BCL2 oncogene could also occur outside the context of malignancy. My task was to prove that this was true. This was not an easy task, because we had to exclude that the tiny bands in the tonsils were due to contamination with exponentially amplified tumor DNA. A lot of tricks were needed to enable direct sequencing of the tonsil DNA to show that each chromosomal breakpoint was unique. To be honest, there were quite some moments of despair and most of the time I believed I was hunting ghosts. Certainly when the first band I sequenced was from a contaminating tumor. But finally we succeeded.

And although science can be very rewarding:

  • Most ideas aren’t that new.
  • There are many dead leads and negative results (see cartoon).
  • Experiments can fail.
  • There is a lot of competition
  • It takes very long before you get results (depending on the type of experiment)
  • It takes even longer before you get enough results to publish
  • It takes still longer before you have written down the first version of the paper
  • … and to wait for the first comments of the co-authors (see cartoon)
  • … and to rewrite the paper and to wait …
  • … and to submit to the journal and wait..
  • … to get the first rejection, because your paper didn’t get a high enough priority
  • and to rewrite, wait for the comments of the co-authors, adapt and submit
  • to be rejected for the second time by referees that don’t understand a bit of your subject or are competitors
  • to rewrite etcetera, till it is accepted…and published
  • to wait till somebody other than you or your co-authors find the paper relevant enough to cite.
  • but most importantly even with very good results that make you feel very happy and content:
    • each answer raises more questions
    • most research, whatever brilliant, is just a drop in the ocean or worse:
    • it gets invalidated

I loved to do research and I loved to be a researcher. However, it is difficult for post-doc to keep finding a job and wait for the contract renewals each year. So almost 4 years ago, just before another renewal of the contract, I was happy to get the opportunity to become a medical librarian at a place not far from where I lived. In fact, after all these years it is my first permanent job.

And it is a far more rewarding job than I ever had before, although perhaps not as challenging as research.

  • Results are more immediate.
  • Answers are clearcut (well mostly)
  • People (doctors, nurses, students) are very happy when you learn them how to search (well generally)
  • they are also happy when you do the search for them
  • or when you help them doing it
  • It is very rewarding to develop courses, to teach, to educate
  • the job has many facets

The rewards can vary from a happy smile, a hand shake and “a thank you” to acknowledgments and even co-authorships in papers. Sometimes I even get tangible presents, like chocolates, cookies, wine or gift tokens.

Last week a patron suddenly said when seeing the presents gathered: “Is it your birthday?”
Presumably it is about time to drink the wine I got.Cheers!

2717145005_0546fa0755

Photo credits (Flickr-CC):





MnSOD, Carotenoids & Prostate Cancer – “You are what you eat” depends on who you are.

22 02 2009

ResearchBlogging.orgWhen you type Cancer Food Prevention in Google you get about 9 million hits, many of them dotcom sites telling you which nutrients, pills or extracts you should take to prevent cancer. Much of this information is unreliable at least.

Although it is true that numerous observational studies (cohort and case-control) do indicate a relationship between diet and cancer incidence, it is difficult to pinpoint the exact nutrients that may be responsible for a beneficial effect. Furthermore, as explained in “The Best Study Design for Dummies” observational studies provide weaker empirical evidence than RCT’s (randomized controlled trials).

For prostate cancer observational (and preclinical) data indicate that diets high in cruciferous vegetables, soy lecithins and other phytoestrogens, vitamins E and C, lycopene, Selenium, green tea (to name a few) are associated with a lower risk of prostate cancer [1].

However, recent randomized trials did not confirm positive effects of vitamin E and C and Selenium (see previous post on the negative SELECT and the PHS II-trial) and data from the PLCO (Prostate, Lung, Colorectal, Ovarian) Trial [2] suggest that the benefit of lycopene (a powerful anti-oxidant that gives tomatoes their red color) is small and that beta-carotene, an antioxidant related to lycopene, even increases the risk for aggressive prostate cancer.

lycopene-tomato

There may be many reasons why these results discords with the many observational studies performed (3)

  • Earlier positive observational studies have less methodological rigor than (large) RCT’s. In controlled trials, the random assignment of subjects to the intervention eliminates the problems of dietary recall and controls the effects of confounding factors.
  • RCT’s test one or two nutrients in isolation and sometimes in high doses assuming that a single compound may reproduce the beneficial effects of the whole foods.
  • RCT’s are often not stratisfied, differences between individuals are often not taken into account.

That this may be important is shown in a recent study on the manganese superoxide dismutase (MnSOD) polymorfism, prostate cancer and lycopene (4)

The manganese superoxide dismutase (MnSOD) gene encodes an antioxidant enzyme (SOD2) that may protect cells from oxidative damage (which may play an important role in prostatic carcinogenesis). A polymorphism [valine (V) -> alanine (A)] of MnSOD has been recently associated with a higher risk of prostate cancer.

The present study performed by Mikhak et al was a nested case-control study in the Health Professionals Follow-up Study (HPFS) with 612 incident prostate cancer cases and 612 matched controls.

The study not only investigates the role of the MnSOD gene Ala16Val polymorphism in prostate cancer risk, but also measures its interactions with baseline plasma carotenoid concentrations.

In line with several other studies (5), no overall association between MnSOD polymorphism and prostate cancer risk was found. However, a 3-fold [95% confidence interval: 1.37-7.02] increased risk of aggressive prostate cancer was observed among men with the Ala/Ala genotype in the presence of low long-term lycopene status (P-value, test for interaction = 0.02) as compared with men with the Ala/Val+Val/Val genotypes with low long-term lycopene status. In other words when the lycopene blood level is low, the Ala/Ala genotype confers a higher risk of aggressive prostate cancer compared with individuals with the other genotypes.

These results are consistent with findings from an earlier study (6) that reported when total antioxidant status is low, the MnSOD Ala/Ala genotype may be associated with an increased risk of aggressive prostate cancer. In contrast, men with the Val allele were much less sensitive for prediagnostic plasma levels of the anti-oxidants selenium, lycopene and {alpha}-tocopherol.

Thus reasoned the other way around: the anticancer effects of supplemented lycopene and other anti-oxidants may depend on the the MnSOD genotype and the levels of both endogenous and exogenous antioxidants. Similarly, a positive effect of {alpha}-tocopherol (vitamin E) observed in earlier trials appeared to be limited to smokers and/or people with low basal levels of vitamin E (see previous post).

SOURCES

  1. E-medicine/Medscape: prostate cancer and nutrition (2008) (free e-txt)
  2. Peters U, Leitzmann MF, Chatterjee N, Wang Y, Albanes D, Gelmann EP, Friesen MD, Riboli E, Hayes RB. Serum lycopene, other carotenoids, and prostate cancer risk: a nested case-control study in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Epidemiol Biomarkers Prev. 2007 May;16(5):962-8. (free PDF)
  3. Byers T. What can randomized controlled trials tell us about nutrition and cancer prevention? CA Cancer J Clin. 1999 Nov-Dec;49(6):353-61. Review (free PDF)
  4. B. Mikhak, D. J. Hunter, D. Spiegelman, E. A. Platz, K. Wu, J. W. Erdman, E. Giovannucci (2008). Manganese superoxide dismutase (MnSOD) gene polymorphism, interactions with carotenoid levels and prostate cancer risk Carcinogenesis, 29 (12), 2335-2340 DOI: 10.1093/carcin/bgn212
  5. Bag A, Bag N. Target sequence polymorphism of human manganese superoxide dismutase gene and its association with cancer risk: a review.
    Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3298-305. Review. (Abstract)
  6. Li H, Kantoff PW, Giovannucci E, Leitzmann MF, Gaziano JM, Stampfer MJ, Ma J. Manganese superoxide dismutase polymorphism, prediagnostic antioxidant status, and risk of clinical significant prostate cancer.Cancer Res. 2005 Mar 15;65(6):2498-504.

You may also want to read:

Photo Credits





Evolution and Medicine. Cancer and adaptive immune responses as evolutions ‘within’.

29 12 2008

I had almost finished my submission for the Grand Round when I took a look at the site of the host, Moneduloides*, to find that this edition had “the interface of evolution and medicine” as a theme.

What should I write about, considering I only had a few hours to write about this difficult theme?

Quite coincidentally (or not, considering the forthcoming bicentenary of Darwin’s birth (1809) and the 150th anniversary of the publication of ‘On the Origin of Species’) the December 2008 Lancet is a Special Issue: Darwin’s Gifts. But it would be to easy to just summarize one or two articles from this Lancet issue…

Evolution and Medicine can be interpreted differently. One can just see it as the evolution of medicine. Enough to write about this theme….

One can also see the theme in the light of consequences of evolution on medicine or illnesses. Indeed there are ample examples of the consequences of men’s evolution on the susceptibility to certain illnesses, e.g. see moneduloides’ blog about the consequence of human bipedalism.

Yesterday @carlosrizo (twitter) pointed out a link to Darwinian Medicine 2.0″. Since this would be of special interest to this web 2.0 audience, I took a look to see if I could ‘use’ this blogpost. However the post appeared to be based on a rather distorted interpretation of natural selection. Darwinian Medicine 1.0. is considered synonymous with eugenics (!), whereas Darwinian Medicine 2.0 is “gentler, interested in finding “evolutionary causes and remedies for diseases.” while leaving out the genocide”. The counterpart blog being intelligentdesign.org. it is easy to position their view.

Although this blog merits no further discussion, it highlights the often wrong interpretations of the natural selection theories. Eugenics is “just” a political interpretation by some of Darwin’s theorie (see Wikipedia). Darwin himself thought it “absurd to talk of one animal being higher than another” and saw evolution as having no goal.

As a biologist I grew up with the following definition of natural selection.

Natural selection is the process by which favorable heritable traits become more common in successive generations of a population of reproducing organisms, and unfavorable heritable traits become less common, due to differential reproduction of genotypes.

In other words natural selection genetic alterations are mostly random and chance (environment, conditions) will determine whether the genotype exhibiting a new phenotype will continue to exist or even will be more likely to survive (natural selection).

Antibiotic resistance
During my biology study we did all kind of mini-evolution experiments. For instance, we treated bacteria that were deficient for a specific amino-acid (AA) with mutagens and plated them on solid agar plates with or without that particular AA. Only bacteria with a mutation making them independent of that AA would survive on AA-less plates.

Although this is not an experiment of nature, a very similar example of natural selection in action is the development of antibiotic resistance in microorganisms (see wikipedia).

natural-selection-90

Enhancement of antibiotic resistance by natural selection - modified from wikipedia

Natural populations of bacteria contain considerable variation in their genetic material, primarily as the result of mutations. When exposed to antibiotics, most bacteria die quickly, but some (red in Figure) may have mutations that make them less susceptible. If the exposure to antibiotics is short, these individuals will survive the treatment. This selective elimination of maladapted individuals (lighter colors) from a population is natural selection.

Evolutions within
It is not difficult to see how infectious diseases were driven by natural selection (of the organisms causing these diseases). Because all rules that apply to eukaryotic organisms apply to prokaryotic organisms as well. But I would make a point that evolution and natural selection also takes place at a lower level: that of viruses (non-living organisms, see post about sputnik-virus here) and of “individual cells” within an organism. That is to say: the same mechanisms apply.

Clonal selection and B-cell adaptive immune response.
One example of a cellular evolution is the development of the B cell (and T cell) immune repertoire. B and T cells are cells of
the adaptive immune response. In contrast to the innate immune response, which is always ready to respond to whatever intruder, the adaptive immune response matures throughout life, is antigen-specific and long-living. The specificity of B cells lies in the variable region of their immunoglobulins or antibodies, Y-like molecules, anchored in the B cells’ plasma membrane. There are endless antibody variants and each B cell (and its progeny) produces antibodies with one particular specificity.
How is this diversity established?
In the Pre-B cell phase, when B cells do not produce any immunoglobulins individual gene segments coding for the V, (D) and J regions of the heavy and light chain of the immunoglobulin molecule are randomly assembled to one molecule. The random assembly of 51 V, 27 D and 6 J gene segments provides a minimum of 8.300 different possible combinations for the heavy chain alone, but since the recombination process is not precise and extra nucleotides are inserted the number of possibilities of antibody V region diversity turn out to be greater than that.[2]
(The following excellent animation is recommended: www.blink.biz/immunoanimations/ (be sure to choose Open > Antigen Recognition > Recombination)

vdj-recombination-2

When an organism encounters a foreign microorganism or other antigen, only those B cells that recognize the antigen are stimulated to divide and to become plasma cells which produce many antibodies specific for the particular antigen. This process is called clonal selection. It results in a B cell repertoire skewed towards the antigens encountered in life. The advantage is that those B cells are selected that have been proved useful. The next time the same antigen is encountered the response is quicker, stronger and more specific, a process called memory.This is also the principle behind vaccination and boostering.

The principle of clonal B cell selection is very similar to the development of antibiotic resistance, discussed above.

clonal-selection-users-path

Carcinogenesis: Follicular Lymphoma
However, sometimes clones are selected that erroneously react with ‘self’ which results in ‘autoimmunity‘.

Cancer can also be considered as another faulty ‘evolution’, be it within the organism. Cancer cells are better at surviving and reproducing than other cells, because they have escaped the body’s controls. This allows them to increase their population much faster than other cells.

In an interesting editorial, J Breivik comments on the work of Vineis and Berwick[4,5]:

Vineis and Berwick argue that ‘Carcinogenesis, at least for some types of cancer, can be interpreted as the consequence of selection of mutated cells similar to what, in the theory of evolution, occurs at the population level’. Taking a more conclusive stand, I will ague that carcinogenesis is an evolutionary process within the multicellular organism. Evolution by means of natural selection is a scientific principle that reaches far beyond the origin of the species and is applicable to all systems of inheritance, including somatic development.

One example is follicular lymphoma (FL). Follicular lymphoma is characterized by a chromosomal translocation between chromosome 14 and 18, t(14;18), caused by a faulty coupling of the immunoglobulin heavy J chain to the BCL-2 proto-oncogene on chromosome 14 during the normal VDJ-rearrangement process, described above. This mistake leads to a constitutive overexpression of BCL-2, which makes the cell less vulnerable to apoptosis (programmed cell death). Mice bearing a transgene mimicking the BCL-2 translocation have an increased incidence of spontaneous B lymphoid tumors. The lymphomas take many months to develop, however, and the penetrance of disease is low, arguing that BCL-2 overexpression on its own is not highly oncogenic (reviewed in[6]). Indeed our group has shown many years ago that t(14;18) translocations, that were considered specific for follicular lymphoma generally occur in follicular hyperplasias [7] and even in B-cells of healthy individuals [8]. Apparently B cells with the t(14;18) translocation are regularly generated in normal individuals, but only very few cells with the translocation will acquire the additional oncogenic hits necessary to establish the malignant phenotype. Overexpression of BCL-2 only gives the cells a survival advantage. Indeed, according to recent insights [9]:

“Accumulation of genomic alterations and clonal selection account for subsequent progression and transformation. Recently, the role of the immunologic microenvironment of FL in determining clinical behavior and prognosis has been substantiated. Combined genetic and immunologic data may now support a model for the development of FL as a disease of functional B cells in which specific molecular alterations infer intrinsic growth properties of the tumor cells as well as dictate a specific functional cross talk with the immunologic regulatory network resulting in extrinsic growth support.”

The theme of this week inspired me to philosophize about immunity and cancer being examples of evolutionary process. While reading I found that this idea is by no means new; a lot has been written about this concept. For instance in “Understanding Evolution” the writer(s) quite nicely explain the process of evolution within a cell lineage. They first explain that the key elements of the evolutionary process – variation, inheritance, and selective advantage – characterize not just populations of organisms in a particular environment, but also populations of cells within our own bodies.
Furthermore they make the interesting statement that

cancer – even within one person – isn’t a single entity. It’s a diverse and evolving population of cell lineages. A single tumor, for example, is made up of a variety of cell types, produced as the cells proliferated and incurred different mutations. All of this diversity means that the population of cells could easily include a mutant variety that happens to be resistant to any individual chemotherapy drug we might administer. To make matters even more difficult, treating the patient with that drug creates an environment in which the few resistant cancer cells have a strong selective advantage in comparison to other cells. Over time, those resistant cells will increase in frequency and continue to evolve. It’s not surprising then that a simple cure for cancer has yet to be developed: treating even a single type of cancer is a bit like trying to take aim at a whole set of moving targets all at once”

Thus, this challenge helps explain why research has not yet provided us with a cure, but also points the way toward new solutions that take that evolution into account ….

Sources:

  1. Wikipedia (several pages, as indicated)
  2. Kimball Biology Pages: [A] AgReceptorDiversity (very good background information in dictionary-format)
  3. Evolving Immunity – A Response to Chapter 6 of Darwin’s Black Box. Matt Inlay. [blog] Talkdesign: interesting discussion on whether or not clonal selection system could have evolved in the context of irreducible complexity.
  4. Cancer the evolution-within, by Dan [blogpost] on Migrations (2007/04/18) referring to:
  5. Cancer – evolution within. Breivik, J. Int. J. Epidemiol. (2006) 35, 1161-1162.
  6. The Bcl-2 family: roles in cell survival and oncogenesis. Suzanne Cory1, David C S Huang1 and Jerry M Adam. Oncogene (2003) 22, 8590-8607.
  7. Bcl-2/JH rearrangements in benign lymphoid tissues with follicular hyperplasia. Limpens J, de Jong D, van Krieken JH, Price CG, Young BD, van Ommen GJ, Kluin PM. Oncogene. 1991 Dec;6(12):2271-6.(PubMed-link)(
  8. Lymphoma-associated translocation t(14;18) in blood B cells of normal individuals. Limpens J, Stad R, Vos C, de Vlaam C, de Jong D, van Ommen GJ, Schuuring E, Kluin PM. Blood. 1995 May 1;85(9):2528-36.(PubMed-link)(Google Scholar)
  9. Molecular pathogenesis of follicular lymphoma: a cross talk of genetic and immunologic factors. de Jong D. J Clin Oncol. 2005 Sep 10;23(26):6358-63.(PubMed-link)
  10. Another perspective on cancer: Evolution within. [blog] Understanding Evolution with a detailed description on natural selection within, and the evolution of cancer cells plus possible solutions.

Figures:

  1. Antibiotic Resistance: wikipedia
  2. Clonal Selection: http://users.path.ox.ac.uk/~scobbold/tig/clons.gif
  3. Recombination: Evolving Immunity – A Response to Chapter 6 of Darwin’s Black Box, adapted from janeway






Anatomy Lesson 2008: Living in Fear

30 11 2008

You may want to play this music while reading this post: Bach: Gottes Zeit ist die allerbeste Zeit (BWV 106)

amc-homepage

The “Anatomy Lesson” has several meanings:

  1. A lesson in Anatomy
  2. A famous painting of Rembrandt van Rijn (of Nicolaes Tulp) (1632).
  3. The homepage of the AMC, the Academic Medical Center in Amsterdam, inspired on the painting of Rembrandt.
  4. A yearly symposium at the intersecting plane of medicine, art and society, organized by the AMC and the Volkskrant, a Dutch newspaper.

This year I was invited to the yearly “Anatomische Les” in the concertgebouw, Amsterdam’s beautiful concert hall (see Wikipedia). It is a very official happening. The audience had to take their seats long before the start. It took more than 2 hours without any break.

zaal-concertgebouw-anatomische-les

Anatomy Lesson 2008 in the Concertgebouw

This year’s theme was FEAR. The program was as follows:

  • Welcome – Rinnooy Kan
  • Presentation of new work of art of Albert van Westing (1960), recently bought by the AMC – Wim Pybes, director of the “RijksMuseum”
  • “Mit Freud und Freud ich fahr dahin”- Johan Sebastian Bach. 1.”O Jesu Christ, mein’s Lebens Licht” 2. Gottes zeit ist die allerbeste Zeit – Baroque Ensemble “Follia d’ Amsterdam” together with the choir “Nuovo Musico” , conducted by Gustav Leonhardt (above is another version). The cantatas express both fear for death and faith in God.
  • Audiovisual presentation of the assay ” de vertrouwenscrisis” (what went wrong with the fundamental trust in the Dutch society?), written by 19 different publicists.
  • Audiovisual impression of pupils of Amsterdam High Schools attending lectures in psychiatry: funny and disarming.
  • And the climax: a 50 min lecture of Prof. Arieh Y. Shalev, M.D. (Head Department of Psychiatry at the Hadassah University Hospital of Jerusalem, Israel) about living with fear.

I will try to summarize the main points of Shalev’s lecture as I remember them (no notes).

There are several factors that may influence how people react to fear:

  1. DNA (fixed), inherited differences – (written composition in musical notation)
  2. Epigenetic Mechanisms (mostly but not exclusively determined postnatally). (tuning of the piano, quenching the middle register)
  3. (Gene) Expression (Accordion register determining ranks and timbres, determined by the accordionist)
  4. Exogenous factors (i.e. empathy and affection) (the people singing, the acoustics)

Fear is an emotional response to threats and danger, meant to protect against a threat (fright-fight-or-flight). It is a basic survival mechanism occurring in response to a specific stimulus, such as pain or the threat of pain. Recognizing a person in agony is easy. The facial expression of fear includes the widening of the eyes (out of anticipation for what will happen next); the pupils dilate (to take in more light); the upper lip rises, the brows draw together, and the lips stretch horizontally. Muscles used for physical movement are tightened and primed with oxygen, in preparation for a physical fight-or-flight response. When the stimulus is shocking or abrupt, a common reaction is to protect vulnerable parts of the anatomy, particularly the face and head. When a fear stimulus occurs unexpectedly, the victim of the fear response could possibly jump or give a small start. The person’s heart-rate and heartbeat may quicken (from Wikipedia).

brain-amygdalaThe amygdala, an almond shaped complex of related nuclei, located in the middle of the brain, is a critical processor area for fear. Connected to the hippocampus, it plays a role in emotionally laden memories. It is part of the limbic system.

Fear, begins with arousal. For instance:

  1. You hear a sound. The amygdala is alerted.
  2. You see a face, the amygdala is alerted to a greater extent. Your pupils enlarge, your breathing and hartbeat quicken.
  3. You recognize the face; it is nobody to be afraid of: the fear response is dampened. The heartbeat drops to normal levels, because you are reassured that there was no danger.

But suppose (1) you’re walking in a dark alley and (2) you see a gun. (3) Next you see a man holding that gun. (4) He shouts something threatening. There are no breaks anymore (by prefrontal cortex/hippocampus on the amygdala) and the fear machine starts running at full speed. Thus, in case of a major threat, in a split second all alarm bells ring: the abovementioned reflexes occur immediately and with no point of return.

One’s memory of what happens consists of separate “pictures”: (1) the alley, (2) the gun, (3) the man, (4) a loud voice (and perhaps smell). Normally, moments of fear will takes it’s place along other memories, although this may take some time.

However, depending on the kind of fear, your personality and external factors, memories to the incident causing fear may stay at the foreground. It may become a memory that comes to the mind frequently and spontaneously or evoked by one of the remembered associations. For instance any alley may cause the full blown fear response again in the abovementioned example.

Shalev telling this, I suddenly understood my reactions to a car accident. While driving on the highway, the driver lost control of the vehicle, causing it to skid and finally ending against a huge concrete wall. I was sitting in the back and while the car was turning I saw “the wall hitting us”. My “last thought” was “that was it”. The car was total loss, but luckily all 5 (members of a dancing group) survived. Apparently because of the “fear of death”, the impression of that very moment staid long with me. For almost a year I felt frightened not only in a car, but also when I saw a car or motor turning fast around the corner or when moving sideways in an airplane during landing. It must have been a similar feeling as when the car turned and hit the wall. The resemblance of that moment brought the memory and the fear back in quite un uncontrollable way. But as time passed by, so did this emotional reaction. The memory itself was still there, but at the background and slowly all intense associations with that frightful moment faded.

hapThis is what normally happens with frigtening experiences. Fear can be retriggered by a memory (smell, picture, situation) linked to what happened, but can extinguish over time. Thus responding to a conditioned stimulus (CS) spontaneously recovers with the passage of time indicated that extinction does not erase the conditioned memory, but is a form of (active) inhibition. The brain (prefrontal cortex/hippocampus) learns how to coop with it and suppress the emotional fear reflex (amygdala).

However, some fears don’t extinguish and have a lifelong impact. For instance in post-traumatic stress disorder (PTSD), which is a severe and ongoing emotional reaction to extreme physical or psychological trauma.

Shalev gave several examples of people with PTSD other than PTSD in war veterans . For instance, a mother who lost her daughter on the complications of a simple (and unnecesary) intervention. The daughter died of sepsis and from that moment on the mother continued to live in the past, persistently reexperiencing the traumatic event.

This was what the mother remembers as the most frightful moment:

I entered the door, my hand still holding the knob. There she lied staring with pupils so dilatated that her irisses were no longer visible. Death was inevitably approaching. I wanted to scream for help, but there were no doctors present and nurses were all running around. I could do nothing about it.

That was a recurrent theme in all examples: feeling desparate and helpless while facing the inevitable.

In PTSD patients the normal extinction mechanisms don’t work. PTSD patients remain in a state of arousal.

In a longitudinal MRI study Shalev showed that a smaller hippocampal volume is not a necessary risk factor for developing PTSD and does not occur within 6 months of expressing the disorder, thereby dismissing the widely held belief that the volume of the hippocampus is reduced in PTSD patients . (Bonne O et al. Am J Psychiatry. 2001 Aug;158(8):1248-51. Longitudinal MRI study of hippocampal volume in trauma survivors with PTSD.)

Shalev also emphasized that the mere reiteratation of the traumatic event doesn’t help the patient. If the patient is in fear it doesn’t help to bring him to an alley all over again, and to leave the alley again as soon as the patient gets frightened. This only reinforces fear. What should be done is to learn the patient to associate the alley with positive events through psychotherapy. Trust, empathy, friendship can all help as well.

Because extinction is a form of learning some medical treatments given soon after the trauma will not help to reduce the PTSD. In a Randomized Controlled Trial presented at the American College of Neuropsychopharmacology 46th Annual Meeting (December 8-12, 2007), Shalev and coworkers showed that cognitive therapy or prolonged exposure therapy (a type of cognitive behavioral therapy) within 1 month had a reduced prevalence and severity of PTSD at 5 months to 20%, whereas early treatment with a selective serotonin reuptake inhibitor (SSRI) fared no better than individuals randomized to placebo or spontaneous recovery (wait-list) groups (60%). According to Shalev this is a phantastic effect. (Source: Medscape ).

Still, although cognitive therapy is effective, many PTSD patients remain symptomatic despite initial treatment.
————-

This post was (also) written for next Grand Round hosted by Mexican Medical Student. Enrico had a tentative theme in mind (with some flexibility to change it ;) ) but these words should be applicable: renewal, metamorphosis, change, transformation. Well, this story was about how extreme fear can transform you in another person. Furthermore death, referred to in the Bach cantate, is our ultimate transformation.
Finally I hope that Enrico, being both a medical student and a
classical pianist likes Bach.





23andMe: 23notMe, not yet

29 09 2008

23andme cheeper

The company 23andMe was in the news thrice this month:

  1. cutting the price of its service by more than a half
  2. organizing a celebrity spit party
  3. the husband of the 23andMe co-founder Anne Wojcicki, better known as Google co-Founder Sergey Brin, revealed he is at risk for Parkinson’s Disease, as determined by….23andMe.

Coincidence or part of a strategic plan?

23andMe is a ‘direct to consumer genetic testing’ company that as 23andMe puts it: “democratizes personal genetics”. The lowering of the service price from $999 to $399 brings personalized genomics within the range of many.

What do you get for those $399? A spit kit, you do your thing, send the tube to a certified lab, which analyzes your saliva for more than a half-million points (called SNPs) scattered across the 23 pairs of chromosomes you have (hence 23andMe), as well as your mitochondrial DNA. 23andMe shows the digital data and gives you information on certain traits and diseases. 23andMe also gives information on your ancestry and compares your DNA to your relative’s and friend’s-genes, if you want to share that knowledge with them. With your genes in their database you help 23andMe to perform more research for new discoveries, a program called 23andWe. In fact once you sign up you cannot refuse the use your (anonymous) DNA for this purpose.

The main question is: what purpose does this serve (besides as a potential for yielding income)?

According to 23andMe the main purpose is ‘for research’, ‘for education’ and ‘for fun’: “It’s fun to learn about your own genome”.

In this light, we should probably see the recent event 23andMe organized: a spit party where a few hundred people were lured away from the catwalks during the Fashion Week in New York City. On the sound track of “a whole lot of love” celebrities were spitting their DNA-containing saliva in a tube (see here and here). According Guy Kawasaki, who report on it on his blog (see here),

“even Goldie Hawn and Kurt Russell were there providing their spit, but their handlers wouldn’t let me take a picture. I found this ironical: Giving DNA was okay but not a picture.”

The aim for which Sergey Brin let 23andMe test his DNA was less funny. As Sergey (whos mother has Parkinson) explains in his brand new blog:

(…..) Nonetheless it is clear that I have a markedly higher chance of developing Parkinson’s in my lifetime than the average person. In fact, it is somewhere between 20% to 80% depending on the study and how you measure. At the same time, research into LRRK2 looks intriguing (both for LRRK2 carriers and potentially for others).

Thus this shows a 3rd aim: diagnostic?!
Formally 23andMe denies there is a diagnostic purpose (in part, surely, because the company doesn’t want to antagonize the FDA, which strictly regulates diagnostic testing for disease). However, 23andme does give information on your risk profile for certain diseases, including Parkinson.

In addition, 23andMe encourages the formation of networks of people sharing the same traits.

“If you want to have a community around psoriasis,” Ms Wojcicki said, “we’d like to be able to allow you to form a psoriasis-specific community.” (see New York Times article)

Psoriasis-specific community when you only have the genes that may enhance the risk of getting psoriasis??

That sounds like condemning you to a psoriasis patient already?!

Then lets discuss the following burning question: how well does 23andMe predict that you will get the disease?

Even the LRRK2-gene data of Mr. Brin aren’t that conclusive. A marked higher chance of 20% to 80% is often misconceived as meaning that Sergey’s chance of getting Parkison is 20-80%, or “he will almost get the disease for sure”. As explained by the Gene Sherpa in his excellent post on this subject (see here) it only means that the LRRK2-mutation increases the normal chance of Americans/Europeans getting Parkinson from 2-5% to 4-10% at the most (the chance is less than doubled). Furthermore LRRK2 isn’t the most crucial gene for getting Parkinson.

23andMe has chosen to relate personal health info only to common diseases and common genes. Thus whether you have an enhanced or lowered risk for breast cancer (normal 1 out of 8 women) is determined by 2 (not very predictive) SNPs associated with Breast Cancer, but not by determining BRCA1/2 mutations that are highly predictive for breast cancer, but rare in the entire (western) population .

Although 24andMe explicitly mentions that the tests are for non-diagnostic purposes, it is hard to imagine that people will see it otherwise. But:

  • Most genes are only weakly predisposing
  • Often multiple genes are working in concert in a difficult to predict way (seldom one gene-one disease)
  • The environment and chance also play an important role.

Thus the value of these fun predictions is low, but how does it affect people that think they are prone to having a disease? For some it might be reason to adjust their lifestyle (but then, what is the chance you really change “your destiny”), others may get fixed on their presumptive future disease, confused, or depressed. It is not without reason that genetic screening is usually restricted to people with high risks, when a disease can be predicted accurately (without too many false positives and negatives), something can be done about it (prevention or treatment), and only as part of a genetic consultation by professionals.

Sources; further reading




#Sciblog – a bird-eye’s view from the camera

2 09 2008

Last Saturday I learned from @AJCann and @Jobadge (Twitter) that there was a Science Blogging Conference going on in London, that you could virtually attend.

Although I planned to do something else (banking for my mom, pick up my daughter from her overnight stay; Saturday is my-shopping-&-bodyshape-sauna- & blogging-if-I-have-some-spare-time-day), I decided to follow it. In the meantime I tried to blog about something else, which didn’t work.

I largely followed Cameron Neylon’s streamed video on Mogulus. It’s main value was the audio-stream, as well as the candid-camera function peeping at the audience from behind.

I came in late (back from banking) and unfortunately missed the Keynote lecture of Ben Goldacre from Badscience.

The next session didn’t do it for me, partly because the 3 blogging ladies ( Jenny Rohn, Grrl Scientist, Anna Kushnir) were almost inaudible and what they had to say about the bridging function of blogs between scientists and the general public (also figuratively) didn’t catch my ears. In the meantime the virtual attendents including, Fang (Mike Seyfang) from Australia, AJCann, some other guys and me, chatted in Cameron Neylon’s room.

In between I followed Twitter-messages having the hashtag #sciblog (see here). I was not familiar with hashtags, but it is a predefined tag you can add to you microblogging post to easily tract what is being said about a subject (even when you don’t actually follow the persons themselves, so as a spin off you can get acquainted with some real interesting people).

Example of a twitter message on #sciblog:

#sciblog matt woods: friendfeed encourages discussion and closes feedback loop 9 minutes ago from TwitKit

However, Hashtags is an opt-in service. You must follow @hashtags -and it has to follow you- for the service to index your tweets, so it took me some time to get it done (For more information, see this twitter wiki.) Althoug the procedure in itself was very effective, the twitter messages didn’t add much value for people already attending.

Another online backchannel, the Friendfeed room appeared more lively, but I soon stopped following the threads. Furthermore I ‘m so old-fashioned that I think speakers do deserve my attention while they’re talking (but perhaps that is because I’m not yet used to chatting at the back-scene). Checking my notes afterwards with the Friendfeed comments was useful however.

Next I followed Matt Wood’s introduction to microblogging and aggregation services and Breakout 6 “Communicating Primary Research Publicly” by Heather Etchevers (Human in Science), Jean-Claude Bradley (Useful Chemistry) and Bob O’Hara (Deep Thoughts and Silliness).

I found these presentations interesting, but tracking my notes back I couldn’t see where Matt ended and the others began.

During his lively presentation with a lot of gesturing, the heavy “sequencer” Matt Wood from “Green is Good” told us he had decided not to worry to be open and just send the message out to the public. You could use blogs to communicate your scientific findings, but blogposts do not handle versioning, although you can sometimes manipulate the post’s date (WordPress blog). Another tool is microblogging services. Twitter is more of a social platform, whereas Friendfeed is more apt for more information-exchange (no 140 character-limit). A new microblogging service is identi.ca. (see for instance this readwriteweb post)

Labnote books (and wiki’s) were a recurrent subject through the 4 presentations. They are very useful to blog primary research. People should write their motives, use it as a diary (writing down all details and circumstances), recording the results (videorecording, freehand sketches, figures, prints, text), followed by periodic summing up.

Why this is useful?

  • You don’t have to remember it (people tend to forget) (although some lab-scientists don’t like to take the notebook along to the bench)
  • Archive of ideas, (to share with people in the lab, collaborators or even ‘the world’
  • (If open) some results may be available direct outside the lab, which may be very useful for cooperation and exchange of thoughts or help (why did my blot fail?-how to proceed?)
  • It may help as a bridge to the public, i.e. by showing if public money is being spent well or for direct communication of your data to the public.
  • The info is verifiable if you link to the real data
  • Science is far more efficient this way and results are revealed instantly. Why wait till everything is distilled out? The scientist’s approach is as Hans Ricke quoted Richard Feyman from his Nobel Lecture 1966 (at Bob o’Hara ‘s blog) :

“We have a habit in writing articles published in scientific journals to make the work as finished as possible, to cover up all the tracks, to not worry about the blind alleys or describe how you had the wrong idea first, and so on. So there isn’t any place to publish, in a dignified manner,what you actually did in order to get to do the work.”

As Hans said blogs may fill that hole, because they are the place to publish this!

Major Pitfall may be that journals may not accept data reported on a wiki. And another that some people may run away with your ideas. By writing it all down you make it very easy on them. Still if everybody would become open…. For Science that would be a great good.

What I liked most of these presentations is the openness and the creativity of the presenters.
As a (medical) librarian and a scientist these thoughts came to my mind:

  • I’m a bit jealous that I worked as a scientist in the web 1.0 era. This way of approaching science looks very stimulating to me, but maybe that’s only a romantic look from the outside?
  • How do we as librarians step in? Can we play a facilitating role? Should these primary findings be aggregated and made available in a searchable way?
    We should at least keep more in pace with the new scientific developments and the way researchers exchange and find their information. It’s entirely different to what we are used to. (we= most librarians I know, including myself)
  • I wonder if such an approach could also be used in medicine and/or in EBM. Are wiki’s like this useful for CATs for instance? Question, PICO + domain, best study type, search, critical appraisal, summary, power point presentation, pdf-files, video of CAT etc??? link to video of casus perhaps?

To get an impression of the great features of such a wiki/open notebook, take a look at http://usefulchem.wikispaces.com/ (Jean Claude Bradley). You can also go to the Useful Chemistry blog and click at “UsefulChem wiki”. Note for instance the links to the notebooks of the individual scientists. Really impressive.

Below you also find the (short) presentation of Heather. Hope the others will follow soon and share their presentations

Vodpod videos no longer available.

more about “Sciblog2008 Etchevers“, posted with vodpod
Other Info





The Real Sputnik Virus

15 08 2008

I just rewrote the “about” section, saying that this blog was started as part of the web 2.0 SPOETNIK (EN: Sputnik) course, that I saw this blog as an experiment, but that I am now irreversibly infected by the blog/Sputnikvirus.

Coincidentally a real Sputnik virus has been discovered.¹ The virus is called Sputnik (Russian for “travelling companion”), because it “accompanies” the mamavirus, the big ‘mama’ among the recently discovered giant mimiviruses. Both the mamavirus and its satellite were present in an amoeba-species, found in a water cooling tower. Strikingly Sputnik cannot infect the amoeba on its own, but needs the companion of a mimivirus. In fact Sputnik hijackes the ‘viral factory’ of the mimivirus in order to replicate, making the mimivirus less infective. Therefore the Sputnik virus is said to actually “infect” another virus

Wait a minute…!! A virus that ‘lives’ from an other virus and takes over his replicating machinery? This means that the virus that is being ‘infected’ (the mamavirus) is a living organism??? But viruses are ‘dead’, at least that is what I learned.

Definition of a virus in one of my studybooks (Genes IV, Benjamin Lewin, 1990, p41).

“Viruses take the physical form of exceedingly small particles. They share with organisms the property that one generation gives rise to the next; they differ in lacking a cellular structure of their own, instead needing to infect a host cell. Both prokaryotic and eukaryotic cells are subject to viral infections; viruses that infect bacteria are usually called bacteriophages”

Thus ‘per definition’ viruses are not alive ànd they do not infect other viruses?!

But what is in a definition/name?
According to Aristotle a definition of an object must include its essential attributes or its “essential nature”. However humans may only observe part of the essential attributes, especially when it concerns the infinitely small or infinitely large (which limitates the accuracy of our observations). Nature made his own definitions/categorizations and we just trying to find the rules, if any, to bring some order into chaos. But in science rules and concepts can be falsified and this rule may be one of them.

That viruses may be at the boundaries of life is no new discussion. According to wikipedia:

Biologists debate whether or not viruses are living organisms. Some consider them non-living as they do not meet all the criteria used in the common definitions of life. For example, unlike most organisms, viruses do not have cells. However, viruses have genes and evolve by natural selection. Others have described them as organisms at the edge of life.

As you can see from the scheme above (from wikipedia) the classification of living organisms has never been rigid and as time goes more ‘kingdoms’ have been discovered.

The Mimivirus seems to be at “the edge of life”, because it

Besides the what-is-a-living-organism-issue the discovery of the Mimi-Sputnik virus couple raises some other interesting points.

  • The paradigm that viruses are evolutionary latecomers, evolving as parasites after the archaea, bacteria and eukaria had formed is challenged by comparative genome-analysis which suggests that the virus world is the most ancient.
  • There is an abundance of Mimi-like genetic sequences in the (virus-rich) ocean leading to a suspicion that giant viruses are a common parasite of plankton.
  • Sputnik-like DNA is also found in the ocean, raising the possibility that satellite viruses could play a role in regulating the growth and death of (Mimi-infected) plankton. Therefore these marine viruses could be mayor player in the global ecosystem
  • Although Mimiviruses primarily infect amoeba, antibodies have been found to the virus in some human pneumonia cases. If these mimiviruses have their own satellites…. then this might perhaps be therapeutically exploited against large DNA viruses in human.

Finally I would like to close this post with an apt poem of Jonathan Swift (often cited in this context):

So, naturalists observe, a flea
Has smaller fleas that on him prey;
And these have smaller still to bite ’em;
And so proceed ad infinitum.

And another coincidence: There is a popgroup sigue-sigue-sputnik that has an number called virus (on the album ray-of-light.)

NOTES
¹The Sputnikvirus has been detected by the team led by Jean-Michel Claverie and Didier Raoult (CNRS UPR laboratories in Marseilles), the same team that identified the mimivirus as a virus.
²Some of the finding are not completely new, e.g. Sputnik was not the first virus-satellite: Satellite Tobacco Mosaic Virus had been discovered before. Some researches don’t regard a satelite virus as a virus, however, but as subviral

SOURCES
La Scola, B et al The virophage as a unique parasite of the giant mimivirus, Nature DOI:10.1038/nature07218; announced in ‘Virophage’ suggests viruses are alive – Nature News, 2008 august 6th
Other news-coverages:
NRC-handelsblad, 2008-08-09 en wetenschapsbijlage 2008-08-10
telegraph.co.uk 2008-08-06
sciencenow daily news 2008-08-06

BACKGROUND INFO and HYPOTHESES
about the sputnikvirus
:
findingdulcinea.com: good starting point for further information about Sputnik and mimiviruses with links to other sources
scienceblogs.com/grrlscientist/
the-scientist.com/blog/
about the mimivirus :
a general overview in
http://www.microbiologybytes.com (last update 2007)
and “unintelligent-design at discovermagazine.com/2006

about the origin of viruses and their presence in the sea: again….
Nice overview
Viruses in the sea’ in Nature by Curtis A. Suttle et al(2005)
Hypothesis: The ancient Virus World and evolution of cells by Eugene V Koonin in Biomedcentral (2006) (pdf-open access)
General: Wikipedia, ie about Viruses and Bacteriophages

—————

Ik heb net de “about” pagina herschreven: ik schrijf dat ik dit blog ben gestart in het kader van de web 2.0 SPOETNIK cursus, dat ik dit blog als een experiment zag, maar dat ik inmiddels voor altijd geinfecteerd ben met het blog/Spoetnikvirus.

Toevallig las ik afgelopen zaterdag in het NRC dat er een echt Spoetnik virus is ontdekt.¹ Van de Spoetnikcursus weet ik nog dat Spoetnik in het Russisch metgezel betekent. Het virus kreeg deze naam omdat het zich samen met het mamavirus, het grootste virus onder de reusachtige minivirussen, in een amoebe ophoudt. Opmerkelijk genoeg is het Spoetnik virus helemaal niet in zijn eentje in staat om de amoebe te infecteren, maar heeft jij daarbij de hulp van het mimivirus nodig, in die zin dat Spoetnik de virusfabriekjes van het mimivirus inpikt om zichzelf te vermenigvuldigen. Met andere woorden, het Sputnik virus is in staat een ander virus te infecteren.

Wacht even?!……… Een virus dat een ander virus infecteert en ‘ziek maakt’? Dat betekent dat het virus dat geinfecteerd wordt ‘leeft’. Maar virussen zijn dood, dat heb ik tenminste zo geleerd.

Definitie van een virus in een oud studieboek (Genes IV, Benjamin Lewin, 1990, p41).

“Viruses take the physical form of exceedingly small particles. They share with organisms the property that one generation gives rise to the next; they differ in lacking a cellular structure of their own, instead needing to infect a host cell. Both prokaryotic and eukaryotic cells are subject to viral infections; viruses that infect bacteria are usually called bacteriophages”

Dus viruses leven per definitie niet en kunnen andere virussen niet infecteren?!

Maar “what is in a definition/name”?
Volgens Aristoteles moet een een definitie van een voorwerp/begrip essentiële elementen of de ware aard omvatten. Maar mensen zien misschien maar een deel van deze kenmerken, vooral als het om oneinig grote of oneindig kleine dingen gaat. De natuur maakt zijn eigen indelingen en wij proberen om wetten te achterhalen, voor zover deze er zijn, om orde in de chaos aan te brengen.
Volgens de regels der wetenschap zijn wetten en concepten echter toetsbaar en falsifieerbaar. Dat virussen levenloos zijn zou dus ook ontkracht kunnen worden.

Het al dan niet ‘levend zijn’ van virussen is geen nieuwe discussie. Sommige biologen zien virussen als niet-levend, omdat ze niet àlle belangrijke kenmerken van leven hebben, ze hebben bijvoorbeeld geen cellen. Virussen hebben echter wel genen en evolueren door natuurlijke selectie waardoor ze volgens anderen wel op het randje van het leven balanceren.

Het Mimivirus lijkt nog het meest op het randje te balanceren. Het

Behalve bovenstaande implicaties voor wat we ‘leven’ noemen, maakt het Mimi-Spoetnik-koppel nog meer discussie los.

  • Op basis van vergelijkend genoomonderzoek lijkt het onwaarschijnlijk dat virusen evolutionaire nakomertjes zijn, maar meer dat ze aan de voet van de archaea, de bacteriën en de eukaryoten hebben gestaan.
  • Er is heel veel Mimi-achtige genmateriaal in de oceanen gevonden, hetgeen zou kunnen betekenen dat reuzevirussen wel eens een algemene parasiet van plankton zouden kunnen zijn.
  • Spoetnik-achtig DNA wordt óók in de oceaan gevonden. Misschien dat satelliet-virussen wel een slutelrol spelen in de regulatie van de hoeveelheid plankton.
  • Hoewel Mimivirusen vooral amoeben infecteren, zijn antistoffen tegen dit virus ook bij enkele patienten met longontsteking gevonden. Als deze mimivirusen hun eigen satellieten hebben, kunnen deze wellicht ingezet worden tegen de ziekteveroorzakende virussen.

Tenslotte een zeer toepasselijk gedicht van Jonathan Swift (veelvuldig in deze kwestie aangehaald):

So, naturalists observe, a flea
Has smaller fleas that on him prey;
And these have smaller still to bite ’em;
And so proceed ad infinitum.

Nog een toevalligheid Er is een band sigue-sigue-sputnik met een (vrij heftig) nummer virus (album ray-of-light).

NOTES
¹het Spoetnik- en het mimivirus zijn ontdekt door Jean-Michel Claverie en Didier Raoult (CNRS UPR laboratories in Marseilles) en zijn team.
²Niet alle bevindingen zijn echt even nieuw. Vòòr Spoetnik waren er al andere virussatellieten ontdekt, zoals de satelliet(virus)van tabaksmozaïekvirus. Door velen wordt zo’n virus niet als ect virus gezien, maar als subviraal beschouwd.





DAREnet wordt NARCIS

11 04 2008

Net gehoord van een collega: DAREnet gaat samen met Keur der Wetenschappen en de nationale Proefschriftensite onder NARCIS vallen.

Het DARE programma is een gezamenlijk initiatief van alle Nederlandse universiteiten met KB, KNAW en NWO met het doel alle onderzoeksresultaten digitaal op te slaan en toegankelijk te maken met behulp van een netwerk van ‘repositories’.

In januari 2007 heeft de KNAW DAREnet van SURF overgenomen, met de bedoeling deze portal te integreren in de wetenschapsportal NARCIS. Inmiddels is integratie dus een feit, hetgeen echter niet wil zeggen, dat alle functionaliteiten van DAREnet hetzelfde blijven in NARCIS.

Een voordeel heeft het wel voor mij. Ik raadpleeg veel vaker het CRD-bestand DARE (goede synopsissen van systematic reviews) dan DAREnet. ‘Dat zoeken we op in DARE’  gaf daarmee vaak spraakverwarring. Hopelijk is dat met de komst van Narcis verleden tijd. 

En omdat het nu toch de laatste paar dagen echt lente wordt een extra toepasselijk narcissenplaatje.

Zie verder:
http://www.onderzoekinformatie.nl/nl/oi/nieuwsbrief/darenet/

 





Met losse handen publicaties scoren

29 03 2008

losse handen

(naar Bericht in “Status”, maart 2008, Ernst Koelman)

De UvA is doorgedrongen tot de top 50 van ‘s werelds meest productieve universiteiten. Dat komt mede doordat de ‘output’ van het AMC voor het eerst is meegeteld.

Dit heeft alles te maken met de nieuwe electronische registratie van onze Medische Bibliotheek.

Voorheen moesten afdelingen elk jaar zelf een lijst met publicaties aanleveren. Dat gebeurde ‘handmatig’ door Pubmed af te struinen. Overzichten waren zelden compleet of werden soms niet eens ingeleverd. Een volledige registratie is belangrijk, omdat aan de hand van die gegevens in- en extern de wetenschappelijke output bepaald wordt.

Sinds 2007 verzamelt de bibliotheek de gegevens zelf. Met een programma worden automatisch publicaties met het AMC-adres uit PubMed en Web of Science gevist. 85% van de 3000 publicaties wordt daarmee gevangen. De publicaties die gemist zijn, kunnen door de afdeling handmatig worden toegevoegd. Op de bibliotheek-homepage (intern) zijn de recente publicaties te vinden, te rangschikken per auteur of afdeling.

Hulde aan mijn collega’s Cees, Geert en Lieuwe!