On BioScience and Life and Such

Archive for October, 2008|Monthly archive page

No I do not need a genetic scan to know my kids

In Uncategorized on October 31, 2008 at 10:40 am

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I have three children. I know them very well. Every parent should. I know that they have strengths, – some things they do very well (they know it too). I know that they struggle with other things (they are aware of this too). I tell them to tell me if I can help them learn something new or manage something they find complicated. I encourage them when I see that they are enjoying something they are good at. I tell them that it does not matter if there are things they do not master, – everyone can’t be good at everything I tell them. They accept that. We all do.

I can see if they are sick or are feeling unwell. I tell them to tell me if they feel sick or uncomfortable for some reason. I tell them I will do my best to make them well again. I comfort them and tell them that this will pass, and you’ll be fit as a fiddle again soon. I tell them to eat right, I tell them to stay active. We do this together. I tell them this is because we do not want to be permanently ill in the future.

I know my family, not only my kids. I know which diseases my father and mother have had, and their fathers and mothers too. I tell my kids to do things that will minimize the risk for similar ailments in the future. I try and minimize risk myself too, because that benefits me as well as my children.

When they grow up and can make informed medical decisions, I will tell them that they are free to scan their genetic sequence if they choose to.

I do not however, need a genetic scan to see what is good for them and what is not. I know them.

If you do not know your kids, – please start getting to know them now. To do that you do not need genetic testing, you need attentiveness and presence.

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A tribute to Dr. Sergio Stagnaro, – consider yourself warned…

In Uncategorized on October 30, 2008 at 10:04 am

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Such as problem is really difficult to resolve, when the interest of all individuals, i.e., drug companies and patients, is central. Every drug, if it’s such, must be burden by beside effects, sometimes dangerous. In addition, we must remember that the statement “post hoch ergo propter hoch” not always is right, according to Hume! In spite of the above mentioned remarks, in my opinion, if all physicians around the world would know precisely both Biophysical Semeiotic Constitutions and related inherited real risks, harmful results should be less numeorus.

If you are a regular blog/news reader, you are certain to come across writings from people with views removed, to a varying extent, from the mainstream. This applies not only to those who themselves blog or write news stories, but just as often, to the people that are commenting on these pieces.

Dr. Sergio Stagnaro is such a person. He seems not to have a blog on his own even though he is an obvious blogger-candidate. He is frequently commenting on other peoples web-writings voicing ideas and views (especially on diagnostics) that are well removed from the mainstream (rather on a mountain top somewhere, – not necessarily in the vicinity of any running liquid whatsoever). These are features that usually fits well in the blogging genre.

I’ve consequently, taken on the task of blogging some of his comments since he strikes me as an interesting person and I believe he means no harm. Admittedly, the risk of his ideas causing harm is hard for me to assess since I find myself unable to evaluate most of the medical points he is making (see the first and the last quotes in this post). But, I’ll take that risk – on to the quotes:

On climate change:

Surely, climate change is real, as states wisely Obama. On the contrary, I believe that NHS Programs are unfortunately stable all around the world, generating the present Mean Age of Medicine and – as a consequence – Psychological Terrorism. For instance read http://www.nature.com/news/2008/081006/full/news.2008.1154.html

On why there are so few women speaking at medical conferences” (in two parts):

Now I am an old and diseased man, as a consequence I am working exclusively with computers without attending and speaking at Italian Congresses, as usually in the past decades. I remember that I meet once numerous women, who spoke in so fascinating way, but your information gehnerally were OLD to me. In any case, they were really nice!


Dear Fi,
in my former comment there are two trivial errors.I wrote “your” information, instead of THEIR; “gehnerally” and not generally! In addition, I admitt that not ALL women were “really nice”.I should agree with cancelling both of messages.
Please, excuse me.

From NEJM on Diet and Risk of Type 2 Diabetes:

To the Editor: In their article on diet, lifestyle, and type 2 diabetes mellitus in women (Sept. 13 issue),1 Hu et al. point out that obesity is an important cause of type 2 diabetes mellitus. I wish to point out that since diabetes does not develop in all overweight women (or men, of course), there must be other factors that predispose patients to the condition, as I illustrated in earlier reports.2,3,4,5,6 Therefore diet is certainly important, but particularly for women and men for whom this overlooked risk factor is involved.

And I’ll include this to illustrate his frustration caused by the lack of response to his diagnostic methods (from bmj):


As I wrote recently (as usual without receiving any response, of course) in an open letter to Italian Health Minister Prof Sirchia …….

More on his diagnostic methods, from International Seminars in Surgical Oncology

Sergio Stagnaro (06 December 2007)  Biophysical Semeiotics Research Laboratory email


the authors write:”The typical clinical presentation of idiopathic granulomatous mastitis often mimics infection or malignancy”. Unfortunately, it’s clear that authors ignore Biophysical Semeiotics (1-5) (www.semeioticabiofisica.it). In addition, using breast cancer genetic risk assessment tools and going through the process of assessing breast cancer risk by this expensive way, can answer many women’s questions about what puts them at relatively higher or lower risk. Certainly such as evaluation is to expensive for both NHS and single patient, and not applicable on women (and men!, of course) on very large scale.

In fact, based on 51 year-long clinical experience, for all women (and men!), an original clinical assessement may be desirable that in a easy and reliable manner allows to recognize the possible presence of maternally-inherited CAEMH-dependent, Oncological Terrain and oncological Real Risk, conditio sine qua non of cancer (1, 2), without following with genetic testing, but ascertaining especially breast cancer oncological INHERITED “real risk” in well-defined breast quadrant(s), characterized by newborn-pathological, type I, subtype a) i.e., oncological, Endoarteriolar Blocking Devices (1-5). In addition, testing for mutations of breast cancer susceptibility genes or for their diminished expression adds to our ability to assess breast cancer risk at an individual level. Really, we cannot localise in a (or more) mamma quadrant the possible breast cancer risk in BRCA 1 and BRCA 2, as well as a lot of other gene mutations-positive women (and men!). Biophysical Semeiotics (http://www.semeioticabiofisica.it, Breast Cancer in Practical Application; Oncological Terrain) allows doctor to recognize firstly oncological terrain in a quantitative way, and then, bu “not” in all cases, of course, breast cancer real risk: individuals with oncological terrain do not show generally real risk in all biological systems (3). Interestingly, the absence of both Oncological Terrain and breast oncological “Real Risk”, the later in a subject with Oncological Terrain, excludes beyond every doubt the possibility of occurrence of breast cancer (2, 3). As a consequence, we can perform nowadays an efficacious clinical, primary prevention of breast cancer (4), on very large scale, based on the Single Patient Based Medicine (5-10), as suggests also Planning for the EU public Health Portal at URL:

http://www.google.it/search?q=cache:U5A-DtWmRDsJ:europa.eu.int/comm/health/ph_information/documents/ev_20030710_co01_en.pdf+single+patient+based+medicine+and+stagnaro&hl=it&ie=UTF-8 Pg 36.

Finally, “real” sentinel limphonodes are trigger-points for autoimmune syndrome (3)

And finally you have his own compilation of comments that you can find here.

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Hammering nails in the “junk-DNA” coffin

In Uncategorized on October 28, 2008 at 2:12 pm

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A replica of the coffin used for Abraham Linco...

Image via Wikipedia

Enough talk (see this previous post and links within), on to the peer-reviewed science. Below you will find a list of references that I hope will contribute to the fall of the term “junk-DNA“, – some of it may (currently) lack a known function, but it is not junk !!!

Disclaimer: This is a list of useful references when arguing against the common overestimation of the amount of “junk”-DNA. By listing these I am not claiming anything beyond what I have already posted on this blog or in a comment somewhere. Also and importantly, I have not myself  had the time to review these articles as thoroughly as I would have wanted to, – some have been read carefully, others lightly and yet others just skimmed through. Thus, you are more than welcome to comment on these references if you have opinions on any of them, or find them unsuited for this list.

The list will be continuously expanded, and if you have references you would like to add, please notify me with a comment to the post.

The references are unsorted. Feel free to copy, rearrange and use as desired…

Last updated 5/8-13:

  1. Alu elements as regulators of gene expression. Häsler J, Strub K, Nucleic Acids Res. 2006;34(19):5491-7. Epub 2006 Oct 4.
  2. RNA editing, DNA recoding and the evolution of human cognition
    Trends in Neurosciences, , Volume 31, Issue 5, May 2008, Pages 227-233
    John S. Mattick, Mark F. Mehler
  3. Evolution of the mammalian transcription factor binding repertoire via transposable elements, Bourque, Guillaume, Leong, Bernard, Vega, Vinsensius B., Chen, Xi, Lee, Yen Ling, Srinivasan, Kandhadayar G., Chew, Joon-Lin, Ruan, Yijun, Wei, Chia-Lin, Ng, Huck Hui, Liu, Edison T. Genome Res. 2008 0: gr.080663.108. DOI: 10.1101/gr.080663.108
  4. Lin L, Shen S, Tye A, Cai JJ, Jiang P, et al. 2008 Diverse Splicing Patterns of Exonized Alu Elements in Human Tissues. PLoS Genetics 4(10): e1000225 doi:10.1371/journal.pgen.1000225
  5. Dispensability of mammalian DNA. McLean C, Bejerano G., Genome Res. 2008 Oct 2. [Epub ahead of print]
  6. Functional Demarcation of Active and Silent Chromatin Domains in Human HOX Loci by Noncoding RNAs. John L. Rinn et al., Cell 129, 1311–1323, June 29, 2007
  7. A Strategy for Probing the Function of Noncoding RNAs Finds a Repressor of NFAT. A. T. Willingham, A. P. Orth, S. Batalov, E. C. Peters, B. G. Wen, P. Aza-Blanc, J. B. Hogenesch, and P. G. Schultz (2 September 2005). Science 309 (5740), 1570. [DOI: 10.1126/science.1115901]
  8. Dinger, M. E. et al. Long noncoding RNAs in mouse embryonic stem cell pluripotency and differentiation, Genome Res. doi: 10.1101/gr.078378.108
  9. Non-coding RNAs in the nervous system, Mark F. Mehler and John S. Mattick, J Physiol Volume 575, Number 2, 333-341, September 1, 2006 DOI: 10.1113/jphysiol.2006.113191
  10. Specific expression of long noncoding RNAs in the mouse brain, Tim R. Mercer* et al., PNAS  January 15, 2008   vol. 105  no. 2  716-721
  11. RNA Maps Reveal New RNA Classes and a Possible Function for Pervasive Transcription, Philipp Kapranov et al., Science 8 June 2007: Vol. 316. no. 5830, pp. 1484 – 1488 DOI: 10.1126/science.1138341
  12. Intergenic transcription is required to repress the Saccharomyces cerevisiae SER3 gene, Joseph A. Martens, Lisa Laprade and Fred Winston, Nature 429, 571-574 (3 June 2004) | doi:10.1038/nature02538
  13. Regulation of an intergenic transcript controls adjacent gene transcription in Saccharomyces cerevisiae, Joseph A. Martens, Pei-Yun Jenny Wu and Fred Winston, GENES & DEVELOPMENT 19:2695-2704, 2005
  14. Neuronal Untranslated BC1 RNA: Targeted Gene Elimination in Mice, Boris V. Skryabin et al., Molecular and Cellular Biology, September 2003, p. 6435-6441, Vol. 23, No. 18 0270-7306/03/$08.00+0 DOI: 10.1128/MCB.23.18.6435-6441.2003
  15. Pellionisz, A. (2008) The Principle of Recursive Genome Function. The Cerebellum (Springer), DOI 10.1007/s12311-008-0035-y
  16. Evolution of the mammalian transcription factor binding repertoire via transposable elements, Guillaume Bourque, Bernard Leong, Vinsensius B. Vega, et al.
    Genome Res. published online August 5, 2008; doi:10.1101/gr.080663.108
  17. Natural selection on gene function drives the evolution of LTR retrotransposon families in the rice genome. Regina S. Baucom et al. Genome Res. Published in Advance November 24, 2008, doi: 10.1101/gr.083360.108
  18. Bekpen C, Marques-Bonet T, Alkan C, Antonacci F, Leogrande MB, et al. (2009) Death and Resurrection of the Human IRGM Gene. PLoS Genet 5(3): e1000403. doi:10.1371/journal.pgen.1000403.
  19. Local DNA Topography Correlates with Functional Noncoding Regions of the Human Genome. Stephen C. J. Parker, Loren Hansen, Hatice Ozel Abaan, Thomas D. Tullius, Elliott H. Margulies. Published Online March 12, 2009. Science DOI: 10.1126/science.1169050.
  20. A Functional Role for Transposases in a Large Eukaryotic Genome.
    Mariusz Nowacki, Brian P. Higgins, Genevieve M. Maquilan, Estienne C. Swart, Thomas G. Doak, Laura F. Landweber. Science 15 May 2009: Vol. 324. no. 5929, pp. 935 – 938 DOI: 10.1126/science.1170023.
  21. Unstable Tandem Repeats in Promoters Confer Transcriptional Evolvability. Marcelo D. Vinces, Matthieu Legendre, Marina Caldara, Masaki Hagihara, Kevin J. Verstrepen. Science 29 May 2009: Vol. 324. no. 5931, pp. 1213 – 1216. DOI: 10.1126/science.1170097.
  22. The regulated retrotransposon transcriptome of mammalian cells. Geoffrey J Faulkner1, Yasumasa Kimura2, Carsten O Daub2, Shivangi Wani1, Charles Plessy2, Katharine M Irvine3, Kate Schroder3, Nicole Cloonan1, Anita L Steptoe1, Timo Lassmann2, Kazunori Waki2, Nadine Hornig4,5, Takahiro Arakawa2, Hazuki Takahashi2, Jun Kawai2, Alistair R R Forrest2,6, Harukazu Suzuki2, Yoshihide Hayashizaki2, David A Hume7, Valerio Orlando4,5, Sean M Grimmond1 & Piero Carninci2. Nature Genetics 41, 563 – 571 (2009)
  23. Distributions of selectively constrained sites and deleterious mutation rates in the hominid and murid genomes. Eory L, Halligan DL, Keightley PD. Mol Biol Evol.2009; 0: msp219v1-msp219
  24. Characterization of viral and human RNAs smaller than canonical microRNAs. Zhihua Li, Sang Woo Kim, Yuefeng Lin, Patrick S. Moore, Yuan Chang, and Bino John. J. Virol. doi:10.1128/JVI.01325-09.
  25. SVA retrotransposons: Evolution and genetic instability. Dustin C. Hancksa and Haig H. Kazazian Jr. Seminars in Cancer Biology, doi:10.1016/j.semcancer.2010.04.001
  26. High-throughput sequencing reveals extensive variation in human-specific L1 content in individual human genomes. Adam D Ewing and Haig H Kazazian. Genome Res.  gr.106419.110; Published in Advance May 20, 2010, doi:10.1101/gr.106419.110
  27. A coding-independent function of gene and pseudogene mRNAs regulates tumour biology. Laura Poliseno, Leonardo Salmena, Jiangwen Zhang, Brett Carver, William J. Haveman & Pier Paolo Pandolfi. Nature Volume:465, Pages: 1033–1038. Date published: (24 June 2010). doi:10.1038/nature09144
  28. Orchestrated Intron Retention Regulates Normal Granulocyte Differentiation. Justin J.-L. Wong1, William Ritchie, Olivia A. Ebner, Matthias Selbach, Jason W.H. Wong, Yizhou Huang, Dadi Gao, Natalia Pinello, Maria Gonzalez, Kinsha Baidya, Annora Thoeng, Teh-Liane Khoo, Charles G. Bailey, Jeff Holst, John E.J. Rasko. Cell, Volume 154, Issue 3, 1 August 2013, Pages 583–595
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After whole genome sequencing comes PCR

In Uncategorized on October 23, 2008 at 8:56 am

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I attended an Applied Biosystems SOLiD seminar the other day. Let me tell you this: the SOLiD system packs some serious sequencing power (as does it’s competitors like Illumina, -and possibly others). Only imagination sets limits to the potential uses for such whole genome (and whole transcriptome !) sequencing. Thus, I found myself continuously drifting off, dream-designing new projects we could set up. But, at the same time I couldn’t keep from thinking that in terms of diagnostics, this a massive overkill. Too much information is not always a good thing when it comes to disease and disease predisposition. If one particular genetic variation is relevant to the symptoms presented, then there’s hardly necessary to return the whole genome or transcriptome. You would end up giving the patient information on a whole range of diseases, – the patient may not want/need to know this. Especially since we know that (currently) there is considerable uncertainty surrounding the future disease-risk associated with most genetic markers. Besides, once you know the relevant genetic regions it would probably be sufficient to run a couple of million markers to determine any predisposition.

Early model of a Polymerase Chain Reaction mac...

Good (?, and really) old PCR.

Image via Wikipedia

Thus, all of these projects ended with good old PCR, which is kind of strange since sequencing one would think, is the superior of the two technologies. Here’s how I figured my (would be) whole genome sequencing projects would go:

  1. Pick species/subspecies/individual trait or disease group
  2. Sequence everything you can get your hands on
  3. Characterize genetic differences be it SNPs, indels, repeats, CNV or any other
  4. And then, …..design PCR/real-time PCR assays for diagnostics/further research and such.

Because, obviously, once everything is sequenced, there’s no need to keep sequencing. My prediction is that at that point (real-time) PCR (and quite possibly Sanger sequencing capillary electrophoresis) will regain it’s lost status as preferred tools for molecular biologists.

So, as a comfort to all those who are unable to jump on the whole genome sequencing train: Not to worry ! We’re just going through a phase. This too shall pass.

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Here’s why I get fat when I exercise

In Uncategorized on October 20, 2008 at 9:03 pm

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In an attempt to probe deeper into my ongoing exercise/obesity confusion, I have read three papers (1,2,3)  that illuminated the issue to some extent. And the answer is, not surprisingly: I’m not exercising enough.

It turns out that you need something like 225 to 275 minutes of weekly exercise to loose 5-10 % of your body weight over 16-24 months. Which means exercising a minimum of 45 minutes a day 5 days a week over a long period of time to achieve……in my case, – not that much. Which again translates into: not bloody likely to happen. Or as stated more elegantly in Donnelly JE et al.:

Application of the results from the present study to the general population will require considerable help from behavioral scientists to encourage adoption and adherence to a long-term exercise program that becomes part of an individual’s lifestyle and can be maintained indefinitely.

The intensity of the training does not seem to matter too much. Any hint of comfort in that however, is swept away by the fact that the rather unimpressive 5 % weight loss from 45 minute exercise pr. day was achieved by young people, ….- I’m not that young anymore and that’s a big chunk of the problem at hand…..

Relentlessly, I will keep exercising of course. There are after all so many other benefits to it. Plus, the exercise I do is fun and inspiring. The conclusion therefore still is: exercise helps, – even if it does so mostly as in “exercise restraint” (when it comes to food intake).

That’s it, it took me 4 blog posts to reach the conclusions I started out with in the first place:

1) Less food = desired weight loss

2) Exercise not essential to loose weight.

And then one would think I am all done on this subject.

But alas no, there’s more to it, – plenty more. Have a look at this “Obesity System Influence Diagram” (Thank you Laura for pointing me here through friendfeed):

Sometimes knowledge it seems, is just confusing. The only reasonable conclusion from this diagram is that the interplay between factors contributing to obesity is extremely complex.

It’s tempting to leave it at that, – it’s all just very complex, let’s move on. But, instead I’ll try and take this as a challenge: Plenty more posts to come…..perhaps on aging and obesity, – seems like a natural next step.

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It’s not all about the genes, well it’s not all about the environment either

In Uncategorized on October 16, 2008 at 8:23 pm

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When having a good debate on a given topic, there will usually be arguments ranging from one extreme to the other (and anywhere in between). The true answer you will find, is never those extremes.

The middle ground is sometimes hard to maintain in discussions and debates because the extremes keep hitting each other in the head, making impenetrable noise as they do so. Examples I have been involved in lately are debates on race, IVF, abortion, junk-DNA and open access publishing. Arguably, this mechanism is present for almost any discussion.  So also for the the debate on how much of human nature is shaped by genes and how much by the surrounding environment, -the nature vs. nurture discussion.

Reassuringly though, as most debates mature, they do tend to move towards the golden mean. Most people are confident now that human biology (behavior) is a result of a combination of our genes and the environment in which we live and grow. I am confident about this too, but I see research giving support to this notion far to seldom. First example I remember, was this article on domestic violence and genetics:

A functional polymorphism in the gene encoding the neurotransmitter-metabolizing enzyme monoamine oxidase A (MAOA) was found to moderate the effect of maltreatment. Maltreated children with a genotype conferring high levels of MAOA expression were less likely to develop antisocial problems. These findings may partly explain why not all victims of maltreatment grow up to victimize others, and they provide epidemiological evidence that genotypes can moderate children’s sensitivity to environmental insults. – Caspi A et al. Role of genotype in the cycle of violence in maltreated children.Science. 2002 Aug 2;297(5582):851-4.

I remember reading it and thinking, – yes !! Finally some evidence proving what we all thought we already knew . And I’ve kept waiting for other reports to similarly illustrate this gene/environment interplay so clearly (for the record, I know that the MAOA-results have not been unequivocally reproduced). Now, I have seen sporadic reports on other gene/environment interactions, but the mountain of evidence I had been expecting since 2002 just has not appeared.

That’s why when I read this review on ADHD the other day, which was exemplary in referencing and discussing gene/environment interactions, I was pleased and reassured that this field is far from forgotten about. Here are some descriptive quotes:

The neurobiology of psychiatric disorders is not about inevitability but is instead about vulnerability and propensity; it is only in certain environments that the disease is likely to emerge.


One of the explanations why results of genetic studies of ADHD have been contradictory is that not all individuals carrying a vulnerable genotype develop the disorder as the genetic effect may only become apparent among the subgroup of individuals exposed to a certain environmental risk. Thus, the importance of studying gene–environment interactions in behavioral disorders lies in the hypothesis that some genes show effects only in groups of individuals subjected to specific environmental stressors. – Kieling C at al. Neurobiology of attention deficit hyperactivity disorder.Child Adolesc Psychiatr Clin N Am. 2008 Apr;17(2):285-307, viii.

There is the definite possibility that I may not have paid enough attention and contrary to what I believe, one can find a mountain of publications on gene/environment interactions. If not (and I’m right), the reason there aren’t that many publications on this topic may be that research into this field is really hard to do. And that of course, is a good excuse.

But, regardless of the presence of this mountain or not: in order to use genetic research with any confidence in medical practice (and future research), the exact contributions from genes and environment needs to be worked out for as many traits as possible. And that (I hope) is our inevitable future – knowing our genes and what they will do to/for you given your surroundings. Subsequently, being able to manipulate these two factors will transform both nature and nurture. Potentially, we’ll reach the golden mean.

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The Likes of Blog Publishing (Open Access Day 08 entry)

In Uncategorized on October 14, 2008 at 5:03 am

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This post is my entry for Open Access Day 2008. It is about blogging, peer-review publishing, open access, elitism, prejudice and exclusion.

I had this dream: publishing directly on the web mixed with interactive comments to individual publications was to replace traditional peer-reviewed publishing in scientific journals. I set up SciPhu.com to achieve this. The core idea was (and still is) that any publication would remain fluid in its format and content since communication with referees was continuous and interactive. By letting the publication evolve in this way it should asymptote towards perfect.

Inspiration of how a series of comments can serve to paint the whole picture, I took from posts (and their comment-threads) like Anna Koushnir’s post on female scientists (where the comments are sometimes borderline harassment, but the comments taken together as a whole, nails the relevant issues, I think) and Olivia Judson’s post “The monster is back” (I could have taken any post with more than say -10- comments)……

I realize now that I was a bit naive in believing this could completely replace a system that has worked so well for so long. The system has after all allowed the scientific community to retain an unsurpassed credibility, worldwide.

But……..I am not accepting defeat just yet, because traditional peer-review publishing has it’s problems.

Firstly, most articles published are not open access. That means that if you need a scientific article and you do not work in an institution that has paid a large amount of money for subscription to the given journal (or you have a private subscription) you will not be able to access it (you can pay for individual articles, but that will become very expensive over time). In contrast, blog publishing would be free and accessible to all. The cost of publishing on a blog is very low indeed. It does not need printing and it will not need conventional employees. Editors and peer-reviewers (those who comment) would all be doing work on a volunteer basis. Consequently, no need to charge the readers,…….- at least not for scientific use (commercial use could potentially have a different set of rules).

Secondly, traditional paper-publishing is painstakingly slow and, compared to web-publishing, extremely inefficient. Blogs and scientific news-sites can publish in a matter of minutes and provide continuous updates (and corrections) on almost any topic. Also, web-publishing allows you to track your readers in an unprecedented way, – and most importantly, it provides a feedback channel for them. This feedback I think is essential in the next era of publishing. It does however, need some structure. The commenting anarchy of today will not suffice.

Thirdly, – the complete lack of such anarchy, has been one the strengths of the traditional peer-review model. But, to such an extent has peer-review been controlled that it has become the opposite of anarchy, namely dictatorship. Reviewers are handpicked by the publishers, creating potential old boy networks, with the journal editors as presidents. To add to this, reviewers are usually anonymous, potentially masking any conflicts of interest, be it financial, work-related or personal. In addition editors and peer reviewers tend to have agenda’s different to those who submit their papers. Thus, the traditional system does not serve to get as much quality scientific information out as possible, – this is contrary to the intentions. Below, I’ll quote from a discussion I had with (editor) T Ryan Gregory, to illustrate elitism, prejudice and exclusion, as examples of editor-agendas (comments from this genomicron post):

1. Elitism

My concern is that publish first, comment second represents an easy way around the rigors of review by experts in which publication is dependent on positive reviews and revision. I am all for open discussion, but initiatives started by people who don’t publish much in the peer-reviewed literature or do not themselves review many manuscripts do not really appeal to me because it adds to my sense of concern that this is a backdoor. I am not trying to seem elitist, I am just saying that peer review, for all its problems, is there for a reason. Submitted by T Ryan Gregory on 22 May 2008 – 8:10am.

2. Prejudice

May I ask what your record is in terms of reviewing manuscripts and publishing peer reviewed articles?  Submitted by T Ryan Gregory on 22 May 2008 – 9:00am.

One might also be forgiven for thinking that someone with only a few publications might be looking to skip the hard (but necessary) stage of getting through reviewers. Isn’t it a bit odd to complain about the anonymous nature of peer review while moderating a “review” blog anonymously? Submitted by T Ryan Gregory on 22 May 2008 – 9:00am.

3. Exclusion

Peer review isn’t supposed to be democratic. It is supposed to be done by peers — a set of individuals with highly specific knowledge in a particular field. The democratic part comes only once the paper gets through that filter, when it is made accessible to the entire community. Peer review is a vetting process, not a rating process. Submitted by T Ryan Gregory on 22 May 2008 – 9:42am.

By now I have concluded that SciPhu or similar blog-publishing alternatives is not going to replace traditional publishing, and that other alternatives will have to. Blogs can/will however, still be a valuable addition to traditional publishing, perhaps serving to correct some of the flaws:

“….fact is, at least now, if you come up for review and your citations are all on SciPhu or PLoS, you are going to get clobbered.”

This is very true. What I am saying is that I hope that it will be different in the future. Sciphu is probably not the final solution, but it is a starting point. And hopefully one of many similar initiatives to come. A site like this can be developed into a wiki or it can have staffed (unpaid) experts in given fields as reviewers or it can develop in any other direction. But, and this is important, it should never require fees of any sort from either referees, authors or readers. There are no fees attached to the sciphu site (it doesn’t even have google adds), it’s all non-profit scientific idealism. Submitted by Sciphu (not verified) on 22 May 2008 – 10:21am.

Money and open access, – this is the imperative issue that needs to be sorted out. Development of new publishing methods will most certainly follow. Peer-review publishing is dead, long live peer-review publishing.

Hence I pledge my complete and unrestricted support to any open-access initiative.

Some other views on peer review: nature debate on peer review, Certifying Online Research

Hitting three peeves with one stone

In Uncategorized on October 11, 2008 at 10:36 am

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Everyone’s talking about their pet peeves, I thought maybe I should too. Here are three of them

1. Labeling DNA with unknown function as “junk”

2. Scientists in ivory towers and on top of their high horses.

3. Holding back on scientific arguments in fear that someone will use them in an unscientific way.

The two last ones are really about how scientists communicate with the rest of the world, and I’ll get back to that

The post that lets me comment on these issues all at the same time is: Scientists Cynical use of “Junk DNA” at Michael Eisens blog (I know the post is rather old, but it is new to me). Coincidentally his post allows me to sum up my recent “junk” posts and the “creationist terror” post.

Quotes for each peeve

Unfortunately, for initially practical reasons, a disproportionate amount (surely in excess of 90%) of research has focused on protein-coding genes, fostering the faulty impression – amongst scientists as well as science writers – that the ~3% of the human genome that is protein-coding contains > 90% of the function.

This is good…..if it means what I mean: that labeling DNA of unknown function as “junk” by default is wrong. Which it most certainly is. For more on this topic, see my 6 post discussion with Larry Moran (1,2,3,4,5,6).

But, then Eisen starts criticizing the press release for the fact that they used this “junk” term:

They work on non-coding DNA precisely because they know it is NOT junk. So why, when it’s time to make a pitch to the local press officer, do they fall back on this old bromide? It obviously appeals to writers – who love it when they can pitch a story as overturning orthodoxy. It seems minor, but pegging it this way leads to some really attrocious misrepresentations of current biological knowledge.

This is bad, because of two reasons. Firstly, the term is not wrong, it’s used on a piece of DNA with an previously unknown function. A lot of this DNA is currently labeled “junk” by the “junk-people“. The only wrongdoing here is that they didn’t specify that regulatory elements have been known for some time, – that’s hardly a grave error. On the contrary, phrasing it like this in the press release underscores and highlights that much of what we previously labeled as “junk” in fact isn’t. That is really, really good, in fact it’s an excellent way of enlightening the public that non-coding DNA isn’t necessarily “junk”. Secondly, when scientists communicate with the rest of the world it is important to use terms that will not serve to alienate. Only to a certain extent of course, because oversimplification can easily distort the true message. But, this press release is not an example of oversimplification. The critique of these news-pieces constitutes nitpicking, and strengthens the view of scientist as locked inside ivory towers or sitting on top of their high horses. There are plenty of examples of press releases that is misrepresenting science, are inaccurate or just plain wrong. The over-hyping of imminent cures for cancer, diabetes and Alzheimer are good examples of bad science news reporting, and this happens almost daily all over the world. Another example is getting statistics all wrong in reporting on genetic tests (there are however, initiatives to try and fix this situation. You are hereby encouraged to go see HelixGene, I also strongly recommend you to join if you can help, or report bad news coverage of science if you find any).

Towards the end of the post I find my third pet peeve:

A second, and less obvious, problem is that this view has played into the hands of the intelligent design crowd.


And every time a new study comes out reporting that “junk DNA” is not junk, the ID’ers jump on it as validation of the predictions of ID. It’s hooey of course, but we needn’t give them the opportunity.

Which shows us Eisen is a victim of creationist-terror (see my previous post on this topic), and it makes me sad that we as scientists do not have the guts to stand up against this terror. We must feel free to express whichever valid scientific argument we find relevant in a given topic or field. That some of us don’t makes me really, really unhappy….

Are you Suffering under the Creationist Terror Regime

In Uncategorized on October 8, 2008 at 9:23 pm

post to news.thinkgene.com

Then free yourself……now !!

While reading “Postmodern evolution?” (a Nature News feature by John Whitfield) I found myself ripped out of the general feeling of bliss (caused by the fact that evo-devo is finally gaining some momentum). Because, first I read this:

Günter Wagner, an evolutionary theorist at Yale University in New Haven, Connecticut, puts up a slide bearing the words ‘Postmodern Synthesis’. Pigliucci is moved to make an editorial suggestion from the floor: “I’d really rather we didn’t use that term.” Wagner says the slide was intended to be tongue-in-cheek, but Pigliucci is worried about the impression the word creates: “If there’s one thing we don’t want, it’s for people to get the idea that there’s a bunch of evolutionary theories out there, and that they’re all equal.”

So, …. are we all forced into silence by the creationists ? The advice is not to use a term because it illuminates that there are new ways of thinking about an existing (and accepted) theory. We cannot speak in fear of being misinterpreted ? Such a coward attitude !

And then to make things worse, towards the end I read this:

…the dominant political concern was a fear of attack from fundamentalists. As Gould discovered, creationists seize on any hint of splits in evolutionary theory or dissatisfaction with Darwinism. In the past couple of decades, everyone has become keenly aware of this, regardless of their satisfaction or otherwise with the modern synthesis. “You always feel like you’re trying to cover your rear,” says Love. “If you criticize, it’s like handing ammunition to these folks.

Well, discussing in this cover-up manner will in my opinion, provide even stronger ammunition. Science is not about keeping your silence, quite the contrary.

Sometimes accusations of damaging the Darwinistic cause are used by scientists towards other scientist, – an indication of a societal reign of terror. To illustrate, here’s a comment to Oliwia Judsons blog post on Hopeful Monsters:

A “jumpy sort of evolutionary process” explains the complex organism’s sudden appearance, because there isn’t fossil evidence? Be careful or you’ll soon be agreeing with the Intelligent Design folk that there is such a thing as irreducible complexity. And “so far the data are suggestive rather than definitive”? Well, that opens a whole another box of problems, doesn’t it, Ms. Scientist Judson? Speculative articles such as these masquerade as science and do great harm to the whole field.— Posted by Charles M

Many are, of course aware of the situation, but nevertheless ends up bowing in fear of creationist attack (again from the Nature News feature):

” So don’t criticize in a grandstanding way, says Coyne: “People shouldn’t suppress their differences to placate creationists, but to suggest that neo-Darwinism has reached some kind of crisis point plays into creationists’ hands,” he says.

The glue holding a regime of terror together, are terrorized people. But, why be afraid, – facts are on our side. We are free to safely discuss the implications of these facts. There is no danger in this.

So please, please, stop holding your arguments back. It does not serve the cause of solidifying evolution as a fundamental force in biology. Speaking clearly on all scientific views of evolution theory on the other hand will, and holding back only makes things worse.

Quote of the month October 08

In Uncategorized on October 7, 2008 at 1:35 pm

I mostly disagree with Rebecca Taylor at Mary Meets Dolly, but this quote has a point, – several points actually, – and different ones I guess, depending on where you stand on religion….

Because science has no internal way to decide on ethical issues, it needs philosophy, history, theology and the law to be it’s moral compass. Nothing is quite as scary to me than the idea of science with no ethical constraints. Science without guidance from such scientifically distasteful things as “religion, politics, and personal ideolgies” is a horror I never want to witness.