Does Open Access benefit small universities?

There has been quite a lot of chatter recently about different scientific publishing models. Prompted by Elsevier’s support for the Research Works Act, and the resulting proposed  academic boycott.

Let there be no mistake: I value the Open Access (OA )model of publication, for both moral and practical reasons that have been elaborated upon in many other places. Briefly: 1) OA is the right thing to do, as the results of publicly funded research should be available to the public and 2) it is the practical thing to, as the broadest sharing of knowledge possible is fundamental to educational and scientific advances.

This post deals with the difficulty  that still exists on the ground. I see the current author-pays model of OA publishing as still somewhat problematic, with the result of driving many of my colleagues away from OA. One supporting argument for OA is that small universities and four-year colleges, and institutes in developing countries can ill-afford to subscribe to a large number of close-access publications. this places researchers and students at a disadvantage. Therefore, the OA model of publishing does them a favor by reducing subscription fees, granting broader access to publications.

On the the flip side , it is in those very same institutes that researchers have less “disposable income” to pay for publications.  $2500, a typical OA fee, for a lab funded by an R15  (small NIH grants given to less research-intensive institutes) or a small NSF grant is a larger chunk of change than $2500 for a lab holding a couple of R01s (the larger NIH “workhorse” grant). Knowing the limit on these grants, a researcher squeezed for funding would rather budget for an extra month for a graduate student than for OA publication fees.  In way, OA fees are something of a regressive tax: it hurts those with less disposable income more. The OA advocates would say that the money saved by the institute from the reduction of library fees can be rolled into subsidizing publications. Some institutions do that by subscribing to OA journals, thus reducing the publication fees their authors are required to pay. However, many do not, and 10% of $2500 still leaves $2250 to pay.

Yes, PLoS grants “hardship” fee waivers, but many other publishers do not. However, requesting waivers in many cases is something of a dilemma: Prof. SmallU may have the $2500, but using those towards publication would mean running out of lab materials earlier than needed, or letting a graduate student off for the summer. In many cases it is not that the money is not there (after all, Prof. SmallU did manage to fund the research!) but facing this tough choice is problematic, and many people would be reluctant to ask for a subsidy or a waiver. Also, there is hardly any reward in small universities  for publishing in OA. Publishing OA, by itself, figures very little, if at all in promotion & tenure  decisions.

Therefore, when publishing those journals which have both options, OA and closed access, there is very little incentive to shell out the $2500 (usually more in the “two option” journals)  once the paper is accepted. OA-only journals are often shunned altogether.

So what would be the solution? I agree with FakeElsevier that it has to come from the funding agencies. But maybe, instead of OA being a flat-fee, and hence regressive, it can be turned, with the help of the granting agencies, into a progressive fee. After all, those same agencies know how much funding a lab has anyhow, as this must be provided with every grant request, award, and progress report. If a lab is able to demonstrate a “publication hardship”, perhaps an extra subsidy can be given once a paper is accepted, provided it is used towards an OA publication. Knowing that this extra money is there may help nudge Prof. SmallU in the direction of publishing in OA. Also, the subsidy can be contingent upon the university subscribing to the OA journal, thus sharing the burden and creating and incentive for departmental library committees to pressure administrators to allocate funds towards OA access.

As it stands now, the motivation for low-budget labs, the supposed best beneficiaries of OA publishing, is not to publish OA. Unless stronger incentives are given, those labs will continue to get their reading material via those journals their library subscribes to, and through emailed electronic copies. Incidentally, a practice that the scientific publishing industry is starting to notice and is even attempting to stop.

 

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Music Monday: Androgynetics

My man Joel Griggs (guitar, right) playing with Us, Today at MOTR Pub in Cincinnati. Enjoy the groove.

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Science Funding: Aging Researchers and Funding Recipients

Here is a video produced by Sally Rockey and her team showing changes in age distribution of NIH Principal Investigators and medical school faculty. Rockey is NIH’s Deputy Director for Extramural Research, serving as the principal scientific leader and advisor to the NIH Director on the NIH extramural research program. The video compares the average age of NIH PIs to the age of faculty in medical schools over the years 1980-2009. Since about 55% of R01* recipients are in medical schools, this provides an interesting comparison of the faculty age, and the age of the funded faculty, and how this distribution has changed over the years. In 1980 the distribution both of funding and of faculty age was skewed toward the younger faculty, with a lower median age. Over time, the distribution becomes less skewed, with a higher median age which is also closer to the mean age.

Two other things that jump out:

In 1980, less than 1% of PIs were over age 65, and now PIs over age 65 constitute nearly 7% of the total. In parallel, in 1980, close to 18% of all PIs were age 36 and under. That number has fallen to about 3% in recent years.

Also:

Another factor that jumps out is the increasing gap between entry into faculty and receipt of the first R01. Although not all AAMC faculty members apply for NIH research grants, the gap is interesting and suggests that institutions and other non-NIH funding sources are increasingly responsible for research start-up costs.

 

You can read more in the full Rock Talk.  Also, Drugmonkey outlines a five-point plan to fix the aging funded faculty problem.

——————-
* An R01 is the main vehicle for funding single labs by the NIH. It is typically a 5 year renewable grant.

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Life is short

ResearchBlogging.org

Continuing with rather philosophical musings about life, Ed Trifonov has recently suggested a new approach to defining life:  let’s just vote on the definition.
So how does that work? And why should it work in the first place?
Note that I am diving straight into the subject, and not prefacing this post with a review of the various definitions of life. I assume that this blog’s readers have been exposed to some aspects of the debate on how to define life. Wikipedia and the references therein are a decent starting point, in case you want to refresh your memory. But just so we have something, here is the definition from the American Heritage dictionary:
LIFE:  the condition that distinguishes organisms from inorganic objects and dead organisms, being manifested by growth through metabolism, reproduction, and the power of adaptation to environment through changes originating internally.
Trifonov’s rationale for doing what he does is as follows:
The definitions [of life, IF] are more than often in conflict with one another. Undeniably, however, most of them do have a point, one or another or several, and common sense suggests that, probably, one could arrive to a consensus, if only the authors, some two centuries apart from one another, could be brought together. One thing, however, can be done – sort of voting in absentia – asking which terms in the definitions are the most frequent and, thus, perhaps, reflecting the most important points shared by many. Such analysis is offered below, revealing those most frequent terms that may be used for tentative formulation of the consensus.
Where to start?  Trifonov decided to take two book chapters which together list 123 non-redundant definitions of life. He then counted the words in those chapters, omitting connecting words and grouped them by meaning , then ordered them by the definientia (the words serving to define another word or expression) frequency (click to enlarge):

By word count, seems like life has mainly to do with living. Well, no surprises there, but somewhat tautological and less-than-informative.  However, rejoice O system biologists, for SYSTEM is the second most frequent keyword grouping. Then we have organic stuff, CHEMICAL, COMPLEXITY, REPRODUCTION with ENERGY and ABILITY trailing. Trifonov continues:

Thus, the consensus of the life definition patched from these nine definientia would be: Life is [System, Matter, Chemical (Metabolism), Complexity (Information), (Self-)Reproduction, Evolution (Change), Environment, Energy, Ability,…] where the square brackets correspond to some compact expression containing the words listed within. For example, one possibility is:

Life is metabolizing material informational system with
ability of self-reproduction with changes (evolution),
which requires energy and suitable environment.    

(I added the underlines.) Hm.  Actually, not bad for a definition culled from a simple exercise in word counting. Of course, to put these definientia together one would need some knowledge of life, this the exercise is not completely automatic and unbiased, nor does it profess to be so.

But Trifonov wants to condense this definition even more. To quote Hemingway: “boil it down; know what to leave out; tell a story in six words”. Is there still some redundancy in the definientia themselves that would let us boil it down and tell the story in only six words? Trifonov argues that metabolism implies the existence of energy and materials.  Whereas the existence of materials already implies a suitable environment. But self-reproduction subsumes all the above, as it requires metabolism, energy, materials and environment. However, variations and self-reproduction  are actually mutually exclusive. Both must be noted. The boiled down, Hemingwayan definition would therefore be:

 Life is self-reproduction with variations.

And, to top it off, six words! Hemingway achievement unlocked.

Of course, this succinct definitions renders all sorts of problems. trifonov admits to that:

One unforeseen property of the minimalistic definition is its generality. It can be considered as applicable not just to “earthly” life but to any forms of life imagination may offer, like extraterrestrial life, alternative chemistry forms, computer models, and abstract forms. It suggests a unique common basis for the variety of lives: all is life that copies itself and changes.

Here is where I think things go a bit too far: is self-reproducing (and mutating) software alive? Is the Weasel program alive? Are viruses alive? All of those examples fulfill, at least technically, the above definition. In a previous post, I talked about going from life to non-life on a scale roughly correlating to size and thus the amount of information and sustaining materials life can carry with it. The difference between life and non-life seems to be not only in self-reproduction with variations, but the ability to do so at some level of autonomy. When adding the caveat of autonomy, viruses are not alive, since they require the transcriptional and translational machinery of their host cells. Neither are organelles such as mitochondria, since most of their proteins are encoded by the nucleus. But requiring autonomy raises another problem, which I find hard to solve: how far does this requirement of autonomy go? After all, all heteretrophs are, to some degree non-autonomous, as they require basic materials produced only by autotrophs. So the definition becomes fuzzy again: humans are alive, although they cannot self-sustain without plants. Plants are alive, but they cannot fix nitrogen and require bacteria to do so. So are we to say that  autotrophic nitrogen-fixing bacteria the only living species on earth?  So maybe the autonomy criterion be limited to self-reproduction rather than metabolism? But those are hard to separate: without sugar, there is no DNA. Without essential amino acids, which most heretrophs acquire by consuming other organisms, there are no proteins to effect reproduction.

despite the difficulties,  my definition would be (seven words, unfortunately):

 Life is autonomous self-reproduction with variations.

 Fuzzy? You betcha. That’s life.

PS: as you can see from the article’s Pubmed page, it generated a flurry of comments. Those make for a great read too. Enjoy.

 


 

Trifonov EN (2011). Vocabulary of definitions of life suggests a definition. Journal of biomolecular structure & dynamics, 29 (2), 259-66 PMID: 21875147

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Music Monday: OK Go

OK Go’s video for their song Needing/Getting. Pretty crazy.

From the details section in the YouTube page

The new music video from OK Go, made in partnership with Chevrolet. OK Go set up over 1000 instruments over two miles of desert outside Los Angeles. A Chevy Sonic was outfitted with retractable pneumatic arms designed to play the instruments, and the band recorded this version of Needing/Getting, singing as they played the instrument array with the car. The video took 4 months of preparation and 4 days of shooting and recording. There are no ringers or stand-ins; Damian took stunt driving lessons. Each piano had the lowest octaves tuned to the same note so that they’d play the right note no matter where they were struck. For more information and behind-the-scenes footage, see http://www.LetsDoThis.com and http://www.okgo.net. Many thanks to Chevy for believing in and supporting such an insane and ambitious project, and to Gretsch for providing the guitars.

Director: Brian L. Perkins & Damian Kulash, Jr.
Director of Photography: Yon Thomas
Editor: Doug Walker
Producer: Luke Ricci

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Wikipedia pages on protein function prediction

I just received an email from Julian Gough , one of last year’s CAFA participants. He started a Wikipedia initiative on protein function prediction, which are barely stubs at the moment. EDIT: He alerted me to the fact that protein function prediction has virtually no presence on Wikipedia. So all you protein function predictors out there, please contribute. Yes, you too!

I guess that as a CAFA organizer, I should really contribute to the second page. And I will. But I really don’t mind if someone else jump-starts it. 😉

http://en.wikipedia.org/wiki/Protein_function_prediction

http://en.wikipedia.org/wiki/Critical_Assessment_of_Function_Annotation

 

 

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Operating systems and sandwiches

Ubuntu Linux: “You can have your sandwich any way you like, but recently we started wrapping it in this really ugly wrapper. Still yummy though, and you can ask for a different wrapper. But you have to ask”.

Mac OSX: “We only serve ham & cheese on white bread. If you don’t like it, go somewhere else.”

Windows: “Lettuce and lots of Mayo. $400. That will be extra for the ham, extra for the turkey, no, you can’t have cheese with it if you have turkey. Well, you can, but you’ll have to add mustard. You don’t like mustard? Tough. So the sandwich is dripping all over you and falling apart? You can buy a sandwich-handler anti-drip across the street. $40/ year. Sandwich too big for your hands? Get someone else to hold it for you. No you can’t make your own. If you do, I’ll have you arrested.”

Gentoo Linux: “Here’s a sickle. Go to the field outside town, and harvest some wheat. Then you will see a cabin. Go inside, there are five types of grindstones there. Grid the flour you like. Then add water, we can give you mineral water, stream water, or tapwater. We also have different types of yeast. Make your dough. Bake bread (we have fire brick ovens, electric ovens, gas, traditional Bedouin oven, and a new plasma-jet oven). What would you like? Chicken? Go kill one in the back yard, pluck it, gut it, and cook it. You can roast it, fry it, grill it, or boil it. All in all, you can have your sandwich in just under a week if you’re good at what you do.”

Puppy Linux: here is a cracker and a bit of cheese. Enjoy your sandwich.

FreeBSD: Like Gentoo, but we also have a 30-.06 if you want a venison sandwich.

Credit: Joe Shlabotnik, Flickr

 

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The Search for Small finds Life on a Gradient

In Chapter 3 of The House at  Pooh Corner, Rabbit organizes a search for Small, “One of my friends and relations.”  Like a good manager (or scientist) Pooh lays out a program:


As soon as Rabbit was out of sight, Pooh remembered that he had forgotten to ask who Small was, and whether he was the sort of friend-and-relation who settled on one’s nose, or the sort who got trodden on by mistake, and as it was Too Late Now, he thought he would begin the Hunt by looking for Piglet, and asking him what they were looking for before he looked for it.
“And it’s no good looking at the Six Pine Trees for Piglet,” said Pooh to himself, “because he’s been organdized in a special place of his own. So I shall have to look for the Special Place first. I wonder where it is.”
And he wrote it down in his head like this:

ORDER OF LOOKING FOR THINGS

  1. Special Place
  2. Piglet
  3. Small
  4. Rabbit
  5. Small again
(To find Piglet)
(To find who Small is)
(To find Small)
(To tell him I’ve found Small)
(To tell him I’ve found Rabbit)

“Which makes it look like a bothering sort of day,” thought Pooh as he stumped along.

Of course, it does turn out to be a bothering sort of day, and nothing goes according to plan. Pooh does find Small but that is almost an afterthought considering the other things he discovered that day.


Just like science. You set out looking for something, you find a bunch of other things. You may or may not find what you  to originally set out to look for, but by the time you get to finding Small, finding him may not be the accomplishment you originally thought it may be. Something else has superseded it.

I started writing this post about the search for the smallest organism. Why? Because life in small packages fascinates me. How small can a biological package be, and still be considered living? Or: “The Search for Small(est)”.

But like Pooh, I bumbled along into other things.

So what is the smallest living thing? Starting at the smallest scale, viruses  are considered by most scientists to be replicators, rather than organisms. They do not metabolize, and do not carry a full complement of reproduction machinery. They affect life profoundly, but they are missing a few essential components to actually be living.  This view has been shaken up recently with the discovery of giant viruses that have genomes larger than some bacteria. These genomes are also quite complex, including coding for a large part of the reproductive machinery, having a selective membrane, and other of life’s goodies. Still, even if we consider giant viruses (or mimiviruses, as they are called)  have crossed the border between non-life and life and are considered to be living, they are already not the smallest around. Not in genome size, and not in the particle size. Indeed, mimivirus were, for a long time, mistaken for bacteria due to their size, which is where they go their name: “mimi”  is short for microbial mimic.

So: small bacteria? The bacterium Candidatus carsonella rudii is really small: its genome is just shy of 160,000 base pairs and it codes for about 182 predicted genes. But carsonella is an obligatory endosymbiont: it lives inside the cells of a special organ in the jumping plant louse or psyllid, an insect that feeds on plant phloem. Carsonella cannot survive outside its host and, in fact, its genome has lost so many genes that it is practically an organelle, not much larger than a mitochondrion. (A mitochondrion  has 16,000 base-pairs and 32 genes.) Mitochondria are not living, although they originated from bacteria. Is carsonella there yet? Has it crossed into from life into non-life just as mimiviruses may have crossed from life into life? Buchnera, another insect endosymbiont is not much larger, with about 400 genes.

Mycoplasma genitalium is parasitic,  but at least it codes for (almost) all of its proteins. It is usually heralded as “the smallest organism that can be grown in cell-free culture”. Its genome is  521 genes strong: just 3 times more than that of carsonella. It is not an obligatory endosymbiont, but it is a parasite: we can trick it to live and grow in a nutrient-rich soup, but in nature you will not find it outside a host.

Pelagibacter ubique, a marine bacterium, is, as far as we know, the smallest free-living organism, with approximately 1390 predicted genes.

So in searching for Small, I was asking a question that seemed to become more awkward each time I thought I found him: is this Small I found  living or not?  Each of the Smalls has certain characteristics of life, but where on the scale outlined by pelagibacter, mycoplasma, carsonella and a mitochondrion does life turn into non-life?

When a question you ask makes you feel weird, you may want to consider whether you are asking the right question. So maybe I was asking the wrong question. Maybe the definition of life is not a binary one and we should not think in terms of “living” and “not living”. Life may very well be a quantitative thing.  Life sheds itself into non-life gradually, from free-living to parasitic to endiosymbiont to organelle.  Indeed, self-replicating proteins (prions) and self-replicating RNA (viroids) are the byproduct of much more complex life, which has arisen before those replicators were derived. As they are, they are non-living, but they owe their existence to life.

So there is no single boundary where “life”  crosses over to “non-life”. That’s not the right way to look at it. When journeying  from virus through mimivirus,  through organelle, various endosymbionts, parasites to free-living we are are simply hitting milestones on a continuum. Perhaps not that different from the continuum from which life emerged in the first place.

Understanding this probably beats actually finding Small.

 

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Music Monday: War Again

Balkan Beat Box, from “Blue Eyed Black Boy”. I like the animated rendering of Tomer Yosef.

 

 

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Microbial Pancakes

 

Prepared by daughter. Not to scale. Species not yet identified. Delicious.

 

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Gut microbes and diabetes

It seems that every day we are discovering more about the role of microbes to our health. We really have to revise our definition of what a human (or any other animal or plant) is: we are not just a creatures of 10,000,000,000,000 cells containing the DNA we got from mother and father. We have 10 times that many cells which are microbial, and we are only now beginning to understand how profoundly they affect us.

Together with obesity, insulin resistance is the harbringer of metabolic syndrome. Insulin resistance is when the body cannot use insulin effectively. Insulin is needed to help control the amount of sugar in the body. As a result, blood sugar and fat levels rise.  Therein lies the path to morbid obesity, diabetes, stroke, and heart problems.

ResearchBlogging.org

This post was chosen as an Editor's Selection for ResearchBlogging.org

So what’s the connection of metabolic disease to bacteria? Well, for one thing, we know that in obese people the bacterial population in the gut is different, and the different population of bacteria may lead to a vicious cycle contributing to obesity.

Another possible connection has to do with an  important group of molecules in our body called Toll-like receptors, or  TLRs. TLRs are a family of  membrane proteins that sense a wide variety of bacterial populations and activate our innate immune system. TLRs are like a first-defense warning station: they sense the bacterial enemy first, and, if needed, activate the proper defense mechanisms. Researchers studying TLR-2 have created knockout mice lacking TLR-2, and they discovered is that many of TLR-2 knockout mice do not develop insulin resistance when fed with a high-fat diet. Think about it: all the McCrap you can eat, yet your blood sugar level remains normal (although you still grow fat).  So why does that happen? How come these mice lacking a bacterial sensor also seem immune to insulin resistance?

 

To answer this, we must understand that TLR receptors (quite a few are known so far) are known to serve as a bridge (or “mediate crosstalk”) between the immune system and the body’s metabolism.  Mice without TLR-5 develop eating disorder known as hyperphagia which is characterized by an increased appetite; they also show other pre-diabetic  symptoms: hypertension, high lipids, and insulin resistance. I have posted before about how TLR-5 may control the type of gut bacteria mice have and, in turn, control their propensity for obesity.

TLR-4 deficient mice, on the other hand, seem to be protected from insulin resistance, just like TLR-2 deficient mice. So a connection between these front-line sensors of the immune system and whole body metabolism is well-known.

A group of researchers from Brazil have decided to look further into these “diabetes resistant” mice. The thing about mutant TLR deficient mice, is that they are normally grown in sterile conditions because possible infections and because the uncontrollable gut microbes add uncontrolled variables to any experiment. When scientists cannot precisely control for experimental conditions, they face two choices: One, they can deviate from the model to emulate “real world” better, but sacrifice control of one or more of the variables in an experiment. Or, maintain full control of the experiment and sacrifice a simulation whatever they are trying to model. Most scientists go with the second option: they would prefer to have a well-controlled model, even if it supposedly detracts from its supposed practicality and application to “real life”. That is because a model (in our case, mutant TLR mice), is somewhat removed from the real thing anyway: mutant TLR-deficient are basically a  an artificial construct used to investigate the effect of knocking out a TLR from the mouse, so hopefully we can draw conclusions about humans. So the second type of possible error is the one scientists generally prefer to make.

 

Toll-like receptors: it's complicated.

But Andrea Caricilli and colleagues have decided to look at TLR-2 knockout mice in non-sterile conditions. Rememebr: TLR-2 knockouts seem to have protection from insulin resistance. What Caricilli and her colleagues discovered was quite the opposite of what was known so far: TLR-2 knockout mice were not protected from insulin resistance. Quite the opposite: the mutant mice developed metabolic syndrome. But did  the gut bacteria do it? To check that, the researchers treated the mice with broad-spectrum antibiotics for 20 days. After that, the bacterial species that re-colonized the mice’s guts were quite different in their composition from the bacterial species that originally inhabited them. And they did not have meteabolic disease, or the symptoms were much less severe.

So here it is: changing the mice’s gut microbiota changed them from mice with insulin resistance to mice without insulin resistance. Yes, there are mutant mice, but still: insulin resistance was turned off  by changing the types of microbes in the gut.

They then transplanted the microbiota from TLR-2 mutants which had insulin resistance to regular mice. And what do you know: the regular mice then showed symptoms of insulin resistance and metabolic disease.

There is a lot more to this paper than these two experiments: they have also investigated many other parameters, trying to come up with the chain of events that bacteria trigger when causing metabolic disease. I won’t get into that, the paper is quite long with some 20(!)  figures. A lot of work went into this. But the bottom line again supports what has been shown in other studies: the bacteria that live in our gut are responsible for our metabolism, and it is the interaction between the bacteria and our immune system that not only protects us from pathogens, but also protects us (or not) from metabolic disease.

 

 Update: this post has been slashdotted. Exercise extreme caution.


Caricilli, A., Picardi, P., de Abreu, L., Ueno, M., Prada, P., Ropelle, E., Hirabara, S., Castoldi, A., Vieira, P., Camara, N., Curi, R., Carvalheira, J., & Saad, M. (2011). Gut Microbiota Is a Key Modulator of Insulin Resistance in TLR 2 Knockout Mice PLoS Biology, 9 (12) DOI: 10.1371/journal.pbio.1001212

 

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Nobody knows you

With deepest apologies to the memory of Jimmy Cox.

EDIT: I got a couple of concerned emails. No, this did not happen to me. Yet.

Once I lived the life of a PI so rich,
Research was going along without a hitch.
Lab manager, four postdocs and grad students eight,
My lab took up the whole floor, and that felt great.

Five years later it all went to hell,
My renewal was declined, because no papers in Cell.
But I just read an RFA that is out,
I’m going to apply, and get it, without a doubt.

Nobody knows you,
when you lose your grant.
In your funding, not one penny,
and as for postdocs, I haven’t any.

If I ever get back on my feet again,
My department chair will not treat me with disdain.
It’s mighty strange, which is why I’m doing this rant,
Nobody knows you when you lose your grant.

Best version of the original, IMHO:

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Seriously?

I get the weirdest emails sometimes….

 

Dear  professor  Iddo Friedberg,

    

    First of all, I would like to introduce myself, my name is _____, 30 years old I  occupy a staff position of instructor at the department of pharmaceutical microbiology, faculty of pharmacy, ____ University, _____.

I was graduated in 2003 with an overall grade “excellence with honors” & I was the second among 1000 students.  I have a PhD scholarship totally funded by the ______ Ministry of High Education. The scholarship includes tuition fees, residence, health insurance and everything. Here is the link of the scholarships offered _________. I am interested in doing my PhD study in the field of molecular biology under your supervision. To fulfill the requirements of the scholarship, I should have a research proposal including the following items. I will apply to The University as soon as I receive the proposal.

 

The research proposal includes:

·                   Title Page (including Title, Keywords).

·                   Abstract

·                   General Overview of Research Area and Literature

·                   Key Research Questions and Objectives

·                   Methodology

·                   Tentative Timetable

·                   Selective Research Bibliography

 

I will be so grateful to you if you generously send me  a research proposal few days before the deadline(January 10, 2012)

 

 

N.B. other information is available in the attached C.V.

If you need any additional information or documents, please let me know

I am waiting for your reply as soon as possible in case of either acceptance or refusal.

Kind regards

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Open Cancer Research

 

“We seek to download from the amazing successes of the computer industry two principles: that of open source, and that of crowdsourcing; to quickly, responsibly accelerate the delivery of targeted therapeutics to cancer patients. Our business model involves all of you. This research is funded by the public.”

 

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Music: The Black Keys, El Camino

The Black Keys‘ new album El Camino is coming out today. I am not entirely sure why they called the album El Camino, and placed a picture of a 1994 Chrysler Town & Country van:

 

What a Chevrolet El Camino might look like:

1968 El Camino

 

Anyhow, the music is great. Here is the first track, Lonely Boy. Enjoy:

 

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