Postdoc position in Computational Biology / Infectious Disease w/ Ashlee Earl at the Broad

My friend, the brilliant Ashlee Earl is recruiting a post doc ... posting this for her.


POSTDOC – COMPUTATIONAL BIOLOGIST (INFECTIOUS DISEASE)
Requisition Number: 1571 http://www.broadinstitute.org/careers/job-openings/job-openings-0

The goal of the Bacterial Genomics Group at Broad is to develop and implement genomic and metagenomic methods to answer pressing questions related to bacteria and their role in human health. Specifically, we seek to understand the evolution and spread of bacterial pathogens (and antibiotic resistance) including the interactions that these pathogens have with their host and host-associated microbiota. We devise and carry out large-scale studies that employ genomic, metagenomic and transcriptomic data sets to understand human pathologies caused by e.g., Mycobacterium tuberculosis, carbapenem resistant Enterobacteriaceae, enterococci and uropathogenic Escherichia coli. We do this in close collaboration with clinical and academic researchers from across the Broad community and around the globe.

We are seeking a creative and highly motivated postdoctoral researcher in Computational Biology.  The ideal candidate should be broadly conversant with bioinformatics techniques for genomic data analysis including metagenomic analysis. They should also be familiar with microbial ecology principles, statistics and have made significant contributions to their area of study.

Responsibilities include:

  • Developing data analysis strategies, writing algorithms and deploying computational tools for the exploration of large genomic, metagenomic and metatranscriptomic data sets
  • Collaborating closely with experimental and computational researchers to interpret analytical results for publication
  • Communicating scientific findings in writing and orally

A Ph.D. in Computer Science, Bioinformatics, Biostatistics, Physics, Biological Sciences or a related field

  • Must be proficient in working in the Unix environment.  Solid coding proficiency in some combination of Python, Perl, Scala, Java, C/C++ and R. Experience with cluster computing and parallelization preferred.
  • Comfort and experience with programming for biological data analysis
  • Demonstrated ability to analyze and interpret metagenomic data
  • Excellent ability to communicate scientific material
  • Excellent collaborative skills and unrelenting enthusiasm for genomic science


EOE/Minorities/Females/Protected Veterans/Disabilities

Haloferax volcanii, model archaea, and me

When I was a graduate student I was looking around for an extremophile - especially an evolutionarily novel one.  And I settled on this species Haloferax volcanii - a model halophilic archaeon largely because Ford Doolittle and colleagues had started to turn it into a genetic model organism (and because Patrick Keeling, from Ford's lab convinced me it was a good thing to do).  So I started work on this species - doing DNA repair studies in the lab.  See my PhD thesis for some of the work I did which I never published outside of the thesis for multiple reasons.  But I continued to be interested in this species.  And when I was working at TIGR, an NSF Program Officer approached me asking me to help get the genome sequencing done for this species.  So, well, I did: The Complete Genome Sequence of Haloferax volcanii DS2, a Model Archaeon.  And I became interested in other haloarchaea and eventually started working with Marc Facciotti, in the lab next to mine, in sequencing from across the diversity of the haloarchaea: Sequencing of Seven Haloarchaeal Genomes Reveals Patterns of Genomic Flux and Phylogenetically Driven Sequencing of Extremely Halophilic Archaea Reveals Strategies for Static and Dynamic Osmo-response.

Anyway - enough about me.  The whole point here is to point people to a new paper:  BMC Biology | Abstract | Generation of comprehensive transposon insertion mutant library for the model archaeon, Haloferax volcanii , and its use for gene discovery.  Further evidence for the use of Haloferax volcanii as a model species.  Tools continue to become available for genetic and experimental studies in this species.  So - if you are looking for an unusual and interesting organisms to work on - consider working on this species ...

Really shameful overselling the microbiome from the American Society for Microbiology regarding lupus

Well, this press release is from October:Study Suggests Altering Gut Bacteria Might Mitigate Lupus But I just discovered it and it definitely deserves an award.  An Overselling the Microbiome Award.  The PR, sadly and amazingly from the American Society for Microbiology which should know better, discusses a paper from the ASM Published journal Applied and Environmental Microbiology.  The PR does an OK job discussing what was in the paper - a study of the microbiome in mice including those that are a model for lupus.  The researchers characterized the microbiome is mice with and without the lupus model disease and also compared over time and between sexes.  And they found some interesting correlates of microbial patterns that are found during flare ups of lupus for example and also in drug induced worsening of symptoms.  But they never showed ANY causal connection between any of the mcirobes and the lupus like disease.  And the never showed ANY benefit of treating the lupus-like symptoms in the mice.  Yet amazingly they go over board in making such claims including
Title: STUDY SUGGESTS ALTERING GUT BACTERIA MIGHT MITIGATE LUPUS.
No - the study did not suggest that at all.  The authors suggested that, yes.  And the study is consistent with that.  But it is also consistent with altering gut bacteria having NO EFFECT on lupus.  So this title is simply deceptive.

In the text other statements are like this:
These results suggest that the gut bacteria may contribute to lupus.
Stunningly, the PR includes some really inappropriate comments including:
Nonetheless, Luo suggests that people with lupus should eat Lactobacillus-containing probiotics, such as live culture yogurts, to reduce lupus flares.
Seriously?  Shame on ASM for allowing this garbage to be in the PR. No evidence at all is presented that this is helpful.

Also in the PR:
More generally, "The use of probiotics, prebiotics, and antibiotics has the potential to alter microbiota dysbiosis, which in turn could improve lupus symptoms," says co-principal investigator Husen Zhang. Ultimately, says Luo, fecal transplant might prove valuable as a treatment for lupus.
Again, shame on ASM.  No evidence is presented for this either.

And then the PR ends with
"We were inspired in part to perform this research by a study on type 1 diabetes, which found that that disease is dependent on gut microbiota," says Zhang. "Like type 1 diabetes, lupus is an autoimmune disease that is even more prevalent [than type 1 diabetes] in women."
What?  I know of no research that shows that type 1 diabetes is dependent on gut microbiota.  I really don't even know what to say here.

This is one of the worst Press Releases I have ever seen in terms of misleading statements about microbiomes.  And ASM should be embarassed about it.  And ASM should retract it.  And ASM should never ever put out something like this again.  And for this, I am awarding a coveted "Overselling the Microbiome Award" to ASM for putting out this inappropriate press release.  If any with lupus goes out and gets even remotely worse from taking such probiotics, prebiotics, or antibiotics, ASM will bear some of the responsibility for their problems.  Shameful.



UPDATE 1: Jan 2, 2015

I did some searching for "probiotics" and "lupus" and found some much more tempered claims from other places. For example in "Lupus Studies Point to Gut Microbes, Epigenetics"
 "The long-standing anecdotal patient reports of certain diets worsening or improving flares might be more real than we thought. They should be studied more systematically, now that we know that almost any dietary component acts on the gut microbiota, [which] in turn has profound effects on the immune system," Dr. Kriegel said. He also warned that patients should not assume that the various "probiotic" products now available to consumers would have a beneficial effect in lupus. "Probiotics could theoretically even worsen a disease state, since it is possible that physiologic immune responses against benign commensals could fuel autoimmune responses via cross-reactivity (as we hypothesize) or other mechanisms," he said.
Dr. Kriegel concluded, "I think the best will be to wait until we have a better understanding of which commensals or commensal-derived products might be driving which autoimmune disease and then target those with a diet that is known to modulate these strains or products. Ideally, the field will also develop eventually novel types of antibiotics or vaccinations against certain commensals. Such approaches would allow us, in the future, to more specifically modulate the gut microbiota in autoimmunity." 
Now that is responsible commenting on lupus and the microbiome.  Too bad ASM allowed complete BS to get into this PR instead of more reasonaed statements.

See also

Quick post: Viruses - don't forget about the viruses

OK OK.  Everyone, everywhere keeps telling me "Viruses - don't forget about the viruses" whenever I talk about microbial communities or discuss work we are doing in my lab.  Yes, I say "I know, I know" but then I panic and think "We can't even deal with the diversity of bacteria and archaea out there.  We generally ignore the microbial eukaryotes.  How the hell are we going to include viruses too?"  But, in the end, if we are going to study microBIOMEs (as in, ecosystems that include viruses), then, well, we need to include all the players.

(I note - as I am writing this, my son asked me what I am doing and I said I am writing about viruses.  He got excited and sad "Write about Ebola").

What got me on my viral kick today?  Well, I have been thinking about viruses a lot recently.  And then I saw this paper: The ISME Journal - Diversity of viral photosystem-I psaA genes.  And it reminded me of the largely unknown diversity of viruses out there in the world.

Anyway - I was going to write a longer post about viruses, but I have to go and do something with my son.

Paper of possible interest: Exploring interactions of plant microbiomes



Just got alerted to this new (open access) paper that seems like it should be of interest to those working on plant microbiomes Scientia Agricola - Exploring interactions of plant microbiomes. It has some useful summaries of work that has been done on plant microbiomes.

Do preprints count for anything? Not according to Elife & G3 & some authors ..



Well, just got pointed to this paper: Metagenomic chromosome conformation capture (meta3C) unveils the diversity of chromosome organization in microorganisms | eLife by Martial Marbouty, Axel Cournac, Jean-François Flot, Hervé Marie-Nelly, Julien Mozziconacci, Romain Koszul.  Seems potentially really interesting.

It is similar in concept and in many aspects to a paper we published in PeerJ earlier in the year (see Beitel et al., 2014 Beitel CW, Froenicke L, Lang JM, Korf IF, Michelmore RW, Eisen JA, Darling AE. (2014) Strain- and plasmid-level deconvolution of a synthetic metagenome by sequencing proximity ligation products. PeerJ 2:e415 http://dx.doi.org/10.7717/peerj.415.

Yet despite the similarities to our paper and to another paper that was formally published around the time of ours, this new paper does not mention these other pieces of work any where in the introduction as having any type of "prior work" relevance.  Instead, they wait until late in their discussion:
Taking advantage of chromatin conformation capture data to address genomic questions is a dynamic field: while this paper was under review, two studies were released that also aimed at exploiting the physical contacts between DNA molecules to deconvolve genomes from controlled mixes of microorganisms (Beitel et al., 2014; Burton et al., 2014).
Clearly, what they are trying to do here is to claim that since they paper was submitted before these other two (including ours) was published, that they should get some sort of "priority" for their work.  Let's look at that in more detail.  Their paper was received May 9, 2014.  Our paper was published online May 27 and the other related paper by Burton et al. was published online May 22.  In general, if a paper on what your paper is about comes out just after you submit your paper, while your paper is still in review, the common, normal thing to be asked to do is to rewrite your paper to deal with the fact that you were, in essence, scooped.  But that does not really appear to be the case here.  They are treating this in a way as "oh look, some new papers came out at the last minute and we have commented on them."  The last minute would be in this case, 6 months before this new paper was accepted.  Seems like a long time to treat this as "ooh - a new paper came up that we will add a few comments about".

But - one could quibble about the ethics and policies of dealing with papers that were published after one submitted one's own paper.  From my experience, I have always had to do major rewrites to deal with such papers.  But maybe E-Life has different policies.  Who knows.  But that is where things get really annoying here.  This is because it was May 27 when our FINAL paper came out online at PeerJ. However, the preprint of the paper was published on February 27, more than two months before their paper was even submitted.  So does this mean that the authors of this new paper do not believe that preprints exist?  It is pretty clear on the web site for our paper that there is a preprint that was published earlier.  Given what they were working on - something directly related to what our preprint/paper was about, one would assume they would have seen it with a few simple Google searches.  Or a reviewer might have pointed them to it.  Maybe not.  I do not know.  But either way, our preprint was published long before their paper was submitted and therefore I believe they should have discussed it in more detail.

Is this a sign that some people believe preprints are nothing more than rumors?  I hope not.  Preprints are a great way to share research prior to the delays that can happen in peer review.  And in my opinion, preprints should count as prior research and be cited as such.  I note - the Burton group in their paper in G3 also did not reference our preprint in what I consider to be a reasonable manner.  They add some comments in their acknowledgements
While this manuscript was in preparation, a preprint describing a related method appeared in PeerJ PrePrints (Beitel et al. 2014a). Note added in proof: this preprint was subsequently published (Beitel et al. 2014b). 
Given that our preprint was published before their paper was submitted too, I believe that they also should have made more reference to it in their paper.   But again, I can only guess that both the Burton and the Marbouty group just do not see preprints as being respectable scientific objects.  That is a bad precedent to set and I think the wrong one too.  And it is a shame.  A preprint is a publication.  No - it is not peer reviewed.  But that does not mean it should not be considered part of the scientific literature in some way.  I note - this new paper from the Marbouty group seems really interesting.  Not sure I want to dig into it any deeper if they are going to play games with the timing of submission vs. published "papers" as part of how they are positioning themselves to be viewed as doing something novel.

Buzzfeed includes microbiomes in "77 facts" but alas, gets the facts (and the math) wrong

Well, I admit it - I clicked on this Buzzfeed link someone posted on Facebook - 77 Facts That Sound Like Huge Lies But Are Actually Completely True.  There are some pretty funny and interesting things on the list.  However, I note - I did not click on the link per se for entertainment.   I clicked on it to see if there was anything about microbes on the list.  And happily, there was.  Alas, what there was, was, well, a bit wrong:


Let's start with #67.  "There is 10 times more bacteria in your body than actual body cells".  Well, alas, this is a nice bit of information.  But it is not based on facts.  See Peter Andrey Smiths wonderful article in the Boston Globe about this issue. The Buzzfeed article links to a 2010 Discover Magazine bit about this topic.  So they were trying to use facts.  But alas, that was not based on facts itself.

Then, let's go to #68.  "And 90% of the cells that make us up of aren’t human but mostly fungi and bacteria.".  So - I am at a bit of a loss on this.  First, isn't this really just rehashing #67 with the addition of fungi to the story?  Also - I note the math here is weird.  #67 would lead one to conclude that 90.9% of the cells in your body are bacterial (10:1 = 10/11 = 90.9%).  So then if one adds fungi to the picture the percent of cells in our bodies that are not human goes DOWN to 90%.  How does that work exactly?

So not only do they get the 10x as many cells fact wrong, they do something really weird by basically repeating #67 and then doing some weird math.

Oh well, glad they have something on microbiomes.  Too bad it came out a bit wrong.

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الجمعة، 9 يناير 2015

Postdoc position in Computational Biology / Infectious Disease w/ Ashlee Earl at the Broad

My friend, the brilliant Ashlee Earl is recruiting a post doc ... posting this for her.


POSTDOC – COMPUTATIONAL BIOLOGIST (INFECTIOUS DISEASE)
Requisition Number: 1571 http://www.broadinstitute.org/careers/job-openings/job-openings-0

The goal of the Bacterial Genomics Group at Broad is to develop and implement genomic and metagenomic methods to answer pressing questions related to bacteria and their role in human health. Specifically, we seek to understand the evolution and spread of bacterial pathogens (and antibiotic resistance) including the interactions that these pathogens have with their host and host-associated microbiota. We devise and carry out large-scale studies that employ genomic, metagenomic and transcriptomic data sets to understand human pathologies caused by e.g., Mycobacterium tuberculosis, carbapenem resistant Enterobacteriaceae, enterococci and uropathogenic Escherichia coli. We do this in close collaboration with clinical and academic researchers from across the Broad community and around the globe.

We are seeking a creative and highly motivated postdoctoral researcher in Computational Biology.  The ideal candidate should be broadly conversant with bioinformatics techniques for genomic data analysis including metagenomic analysis. They should also be familiar with microbial ecology principles, statistics and have made significant contributions to their area of study.

Responsibilities include:

  • Developing data analysis strategies, writing algorithms and deploying computational tools for the exploration of large genomic, metagenomic and metatranscriptomic data sets
  • Collaborating closely with experimental and computational researchers to interpret analytical results for publication
  • Communicating scientific findings in writing and orally

A Ph.D. in Computer Science, Bioinformatics, Biostatistics, Physics, Biological Sciences or a related field

  • Must be proficient in working in the Unix environment.  Solid coding proficiency in some combination of Python, Perl, Scala, Java, C/C++ and R. Experience with cluster computing and parallelization preferred.
  • Comfort and experience with programming for biological data analysis
  • Demonstrated ability to analyze and interpret metagenomic data
  • Excellent ability to communicate scientific material
  • Excellent collaborative skills and unrelenting enthusiasm for genomic science


EOE/Minorities/Females/Protected Veterans/Disabilities

الجمعة، 2 يناير 2015

Haloferax volcanii, model archaea, and me

When I was a graduate student I was looking around for an extremophile - especially an evolutionarily novel one.  And I settled on this species Haloferax volcanii - a model halophilic archaeon largely because Ford Doolittle and colleagues had started to turn it into a genetic model organism (and because Patrick Keeling, from Ford's lab convinced me it was a good thing to do).  So I started work on this species - doing DNA repair studies in the lab.  See my PhD thesis for some of the work I did which I never published outside of the thesis for multiple reasons.  But I continued to be interested in this species.  And when I was working at TIGR, an NSF Program Officer approached me asking me to help get the genome sequencing done for this species.  So, well, I did: The Complete Genome Sequence of Haloferax volcanii DS2, a Model Archaeon.  And I became interested in other haloarchaea and eventually started working with Marc Facciotti, in the lab next to mine, in sequencing from across the diversity of the haloarchaea: Sequencing of Seven Haloarchaeal Genomes Reveals Patterns of Genomic Flux and Phylogenetically Driven Sequencing of Extremely Halophilic Archaea Reveals Strategies for Static and Dynamic Osmo-response.

Anyway - enough about me.  The whole point here is to point people to a new paper:  BMC Biology | Abstract | Generation of comprehensive transposon insertion mutant library for the model archaeon, Haloferax volcanii , and its use for gene discovery.  Further evidence for the use of Haloferax volcanii as a model species.  Tools continue to become available for genetic and experimental studies in this species.  So - if you are looking for an unusual and interesting organisms to work on - consider working on this species ...

الخميس، 1 يناير 2015

Really shameful overselling the microbiome from the American Society for Microbiology regarding lupus

Well, this press release is from October:Study Suggests Altering Gut Bacteria Might Mitigate Lupus But I just discovered it and it definitely deserves an award.  An Overselling the Microbiome Award.  The PR, sadly and amazingly from the American Society for Microbiology which should know better, discusses a paper from the ASM Published journal Applied and Environmental Microbiology.  The PR does an OK job discussing what was in the paper - a study of the microbiome in mice including those that are a model for lupus.  The researchers characterized the microbiome is mice with and without the lupus model disease and also compared over time and between sexes.  And they found some interesting correlates of microbial patterns that are found during flare ups of lupus for example and also in drug induced worsening of symptoms.  But they never showed ANY causal connection between any of the mcirobes and the lupus like disease.  And the never showed ANY benefit of treating the lupus-like symptoms in the mice.  Yet amazingly they go over board in making such claims including
Title: STUDY SUGGESTS ALTERING GUT BACTERIA MIGHT MITIGATE LUPUS.
No - the study did not suggest that at all.  The authors suggested that, yes.  And the study is consistent with that.  But it is also consistent with altering gut bacteria having NO EFFECT on lupus.  So this title is simply deceptive.

In the text other statements are like this:
These results suggest that the gut bacteria may contribute to lupus.
Stunningly, the PR includes some really inappropriate comments including:
Nonetheless, Luo suggests that people with lupus should eat Lactobacillus-containing probiotics, such as live culture yogurts, to reduce lupus flares.
Seriously?  Shame on ASM for allowing this garbage to be in the PR. No evidence at all is presented that this is helpful.

Also in the PR:
More generally, "The use of probiotics, prebiotics, and antibiotics has the potential to alter microbiota dysbiosis, which in turn could improve lupus symptoms," says co-principal investigator Husen Zhang. Ultimately, says Luo, fecal transplant might prove valuable as a treatment for lupus.
Again, shame on ASM.  No evidence is presented for this either.

And then the PR ends with
"We were inspired in part to perform this research by a study on type 1 diabetes, which found that that disease is dependent on gut microbiota," says Zhang. "Like type 1 diabetes, lupus is an autoimmune disease that is even more prevalent [than type 1 diabetes] in women."
What?  I know of no research that shows that type 1 diabetes is dependent on gut microbiota.  I really don't even know what to say here.

This is one of the worst Press Releases I have ever seen in terms of misleading statements about microbiomes.  And ASM should be embarassed about it.  And ASM should retract it.  And ASM should never ever put out something like this again.  And for this, I am awarding a coveted "Overselling the Microbiome Award" to ASM for putting out this inappropriate press release.  If any with lupus goes out and gets even remotely worse from taking such probiotics, prebiotics, or antibiotics, ASM will bear some of the responsibility for their problems.  Shameful.



UPDATE 1: Jan 2, 2015

I did some searching for "probiotics" and "lupus" and found some much more tempered claims from other places. For example in "Lupus Studies Point to Gut Microbes, Epigenetics"
 "The long-standing anecdotal patient reports of certain diets worsening or improving flares might be more real than we thought. They should be studied more systematically, now that we know that almost any dietary component acts on the gut microbiota, [which] in turn has profound effects on the immune system," Dr. Kriegel said. He also warned that patients should not assume that the various "probiotic" products now available to consumers would have a beneficial effect in lupus. "Probiotics could theoretically even worsen a disease state, since it is possible that physiologic immune responses against benign commensals could fuel autoimmune responses via cross-reactivity (as we hypothesize) or other mechanisms," he said.
Dr. Kriegel concluded, "I think the best will be to wait until we have a better understanding of which commensals or commensal-derived products might be driving which autoimmune disease and then target those with a diet that is known to modulate these strains or products. Ideally, the field will also develop eventually novel types of antibiotics or vaccinations against certain commensals. Such approaches would allow us, in the future, to more specifically modulate the gut microbiota in autoimmunity." 
Now that is responsible commenting on lupus and the microbiome.  Too bad ASM allowed complete BS to get into this PR instead of more reasonaed statements.

See also

السبت، 27 ديسمبر 2014

Quick post: Viruses - don't forget about the viruses

OK OK.  Everyone, everywhere keeps telling me "Viruses - don't forget about the viruses" whenever I talk about microbial communities or discuss work we are doing in my lab.  Yes, I say "I know, I know" but then I panic and think "We can't even deal with the diversity of bacteria and archaea out there.  We generally ignore the microbial eukaryotes.  How the hell are we going to include viruses too?"  But, in the end, if we are going to study microBIOMEs (as in, ecosystems that include viruses), then, well, we need to include all the players.

(I note - as I am writing this, my son asked me what I am doing and I said I am writing about viruses.  He got excited and sad "Write about Ebola").

What got me on my viral kick today?  Well, I have been thinking about viruses a lot recently.  And then I saw this paper: The ISME Journal - Diversity of viral photosystem-I psaA genes.  And it reminded me of the largely unknown diversity of viruses out there in the world.

Anyway - I was going to write a longer post about viruses, but I have to go and do something with my son.

الجمعة، 26 ديسمبر 2014

Paper of possible interest: Exploring interactions of plant microbiomes



Just got alerted to this new (open access) paper that seems like it should be of interest to those working on plant microbiomes Scientia Agricola - Exploring interactions of plant microbiomes. It has some useful summaries of work that has been done on plant microbiomes.

الأربعاء، 24 ديسمبر 2014

Do preprints count for anything? Not according to Elife & G3 & some authors ..



Well, just got pointed to this paper: Metagenomic chromosome conformation capture (meta3C) unveils the diversity of chromosome organization in microorganisms | eLife by Martial Marbouty, Axel Cournac, Jean-François Flot, Hervé Marie-Nelly, Julien Mozziconacci, Romain Koszul.  Seems potentially really interesting.

It is similar in concept and in many aspects to a paper we published in PeerJ earlier in the year (see Beitel et al., 2014 Beitel CW, Froenicke L, Lang JM, Korf IF, Michelmore RW, Eisen JA, Darling AE. (2014) Strain- and plasmid-level deconvolution of a synthetic metagenome by sequencing proximity ligation products. PeerJ 2:e415 http://dx.doi.org/10.7717/peerj.415.

Yet despite the similarities to our paper and to another paper that was formally published around the time of ours, this new paper does not mention these other pieces of work any where in the introduction as having any type of "prior work" relevance.  Instead, they wait until late in their discussion:
Taking advantage of chromatin conformation capture data to address genomic questions is a dynamic field: while this paper was under review, two studies were released that also aimed at exploiting the physical contacts between DNA molecules to deconvolve genomes from controlled mixes of microorganisms (Beitel et al., 2014; Burton et al., 2014).
Clearly, what they are trying to do here is to claim that since they paper was submitted before these other two (including ours) was published, that they should get some sort of "priority" for their work.  Let's look at that in more detail.  Their paper was received May 9, 2014.  Our paper was published online May 27 and the other related paper by Burton et al. was published online May 22.  In general, if a paper on what your paper is about comes out just after you submit your paper, while your paper is still in review, the common, normal thing to be asked to do is to rewrite your paper to deal with the fact that you were, in essence, scooped.  But that does not really appear to be the case here.  They are treating this in a way as "oh look, some new papers came out at the last minute and we have commented on them."  The last minute would be in this case, 6 months before this new paper was accepted.  Seems like a long time to treat this as "ooh - a new paper came up that we will add a few comments about".

But - one could quibble about the ethics and policies of dealing with papers that were published after one submitted one's own paper.  From my experience, I have always had to do major rewrites to deal with such papers.  But maybe E-Life has different policies.  Who knows.  But that is where things get really annoying here.  This is because it was May 27 when our FINAL paper came out online at PeerJ. However, the preprint of the paper was published on February 27, more than two months before their paper was even submitted.  So does this mean that the authors of this new paper do not believe that preprints exist?  It is pretty clear on the web site for our paper that there is a preprint that was published earlier.  Given what they were working on - something directly related to what our preprint/paper was about, one would assume they would have seen it with a few simple Google searches.  Or a reviewer might have pointed them to it.  Maybe not.  I do not know.  But either way, our preprint was published long before their paper was submitted and therefore I believe they should have discussed it in more detail.

Is this a sign that some people believe preprints are nothing more than rumors?  I hope not.  Preprints are a great way to share research prior to the delays that can happen in peer review.  And in my opinion, preprints should count as prior research and be cited as such.  I note - the Burton group in their paper in G3 also did not reference our preprint in what I consider to be a reasonable manner.  They add some comments in their acknowledgements
While this manuscript was in preparation, a preprint describing a related method appeared in PeerJ PrePrints (Beitel et al. 2014a). Note added in proof: this preprint was subsequently published (Beitel et al. 2014b). 
Given that our preprint was published before their paper was submitted too, I believe that they also should have made more reference to it in their paper.   But again, I can only guess that both the Burton and the Marbouty group just do not see preprints as being respectable scientific objects.  That is a bad precedent to set and I think the wrong one too.  And it is a shame.  A preprint is a publication.  No - it is not peer reviewed.  But that does not mean it should not be considered part of the scientific literature in some way.  I note - this new paper from the Marbouty group seems really interesting.  Not sure I want to dig into it any deeper if they are going to play games with the timing of submission vs. published "papers" as part of how they are positioning themselves to be viewed as doing something novel.

الثلاثاء، 23 ديسمبر 2014

Buzzfeed includes microbiomes in "77 facts" but alas, gets the facts (and the math) wrong

Well, I admit it - I clicked on this Buzzfeed link someone posted on Facebook - 77 Facts That Sound Like Huge Lies But Are Actually Completely True.  There are some pretty funny and interesting things on the list.  However, I note - I did not click on the link per se for entertainment.   I clicked on it to see if there was anything about microbes on the list.  And happily, there was.  Alas, what there was, was, well, a bit wrong:


Let's start with #67.  "There is 10 times more bacteria in your body than actual body cells".  Well, alas, this is a nice bit of information.  But it is not based on facts.  See Peter Andrey Smiths wonderful article in the Boston Globe about this issue. The Buzzfeed article links to a 2010 Discover Magazine bit about this topic.  So they were trying to use facts.  But alas, that was not based on facts itself.

Then, let's go to #68.  "And 90% of the cells that make us up of aren’t human but mostly fungi and bacteria.".  So - I am at a bit of a loss on this.  First, isn't this really just rehashing #67 with the addition of fungi to the story?  Also - I note the math here is weird.  #67 would lead one to conclude that 90.9% of the cells in your body are bacterial (10:1 = 10/11 = 90.9%).  So then if one adds fungi to the picture the percent of cells in our bodies that are not human goes DOWN to 90%.  How does that work exactly?

So not only do they get the 10x as many cells fact wrong, they do something really weird by basically repeating #67 and then doing some weird math.

Oh well, glad they have something on microbiomes.  Too bad it came out a bit wrong.