Weekend Suitcase

“JJ had long known that something else was wrong with her — that no one should touch her blood. She had seen doctors every few months since birth and taken medicine since a plastic syringe delivered it to her mouth. “A rare blood disease,” Lee had told her, and JJ never pressed for more details.” John Cox at the Washington Post on telling a child she has HIV.

Stephen Curry reviews Photograph 51 at The Guardian, starring Nicole Kidman as Rosalind Franklin“Here is a hard problem: how to write a play about science that captures the real complexities of research while remaining accessible – and dramatic?” 

“Well, this is just plain awful: Are Antibiotics Ruining Your Libido? – The Daily Beast.  In this article, Robynne Chutkan argues that people’s sex drives may be being ruined by antibiotics.  And she presents zero evidence for this other than handwaving.” Jonathan Eisen continues to fight the good fight against microbial hype at Tree of Life.

David Dobbs at The Atlantic on the cost of misconduct in clinical trials. “A year before, in 2001, a much-publicized paper described a clinical trial that showed Paxil to be safe and effective in teenagers as well as adults. Study 329, as it became known, helped spur a huge increase in Paxil prescriptions. In 2002 alone, over 2 million prescriptions were written for children and teens, and many more for adults. (…) The study is now again in the news, as a new reanalysis of the its original dataincluding about 77,000 pages of formerly inaccessible patient records—shows that Paxil was neither effective nor safe.”

“Some readers may have never heard of The American Chestnut, but it might have been considered the counterpart to the vast conifer forests of the West, like the Douglas fir (Pseudotsgua douglasii). The American chestnut dominated eastern forests from Georgia to Maine (1 in 4 trees was a Chestnut). Until a blight, a fungus, from Asia was introduced with imported Chinese Chestnut trees. With no resistance, the blight wiped out almost all The American Chestnut trees.” Ian Street at The Quiet Branches on a new approach to an old epidemic.

Chris Stringer at Elife on our newest relative, Homo naledi, and all the questions it raises:(…) despite the wealth of information about the physical characteristics of H. naledi that this collection provides, many mysteries remain. How old are the fossils? Where does H. naledi fit in the scheme of human evolution? And how did the remains arrive deep within the cave system?”

“Light travels at around 300,000 km per second. Why not faster? Why not slower?” Sidney Perkowitz asks at Aeon.

Finding Stories: A Conversation With Daniel Davis

Something that has always interested me in science are the people that do it. Every single scientist, in every continent, has a story of how they got there, you know? Not just the really famous scientists, but all of the every-day scientists struggling, and winning, and going through the same process of groping around, trying to find a story from their data”, says University of Manchester immunologist Daniel Davis.

In The Compatibility Gene, he tells the story of how a sprawling cast of characters solved the mystery of the MHC, and explores the current research frontiers in the field, from modern immunology to neuroscience. Dr Davis spoke to us about his own journey from doing a PhD in Physics to his lab’s work at the cutting edge of imaging the immune system, and going down to a shed at the bottom of his garden to write a book.

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Illustration by Madalena Parreira.

You did a PhD in Physics?

DD I did Physics initially because I thought “what could be more fundamental than laws that are constant across the whole universe?” That’s what I should study. Then, during my PhD I did feel like it was a bit esoteric, the specific Physics that I was doing. I thought that I could have more impact if I studied Biology, and then I thought that maybe how life works is in some ways more fundamental than how Physics works. So I decided to switch, and then it was a little bit random as to which part of Biology I would go into. I actually just wrote letters to very different types of biological scientists, the kind of people that caught my attention for one reason or another. Some of the people I wrote to were in the kinds of fields that people that come from Physics often go into, like protein folding or structural biology. One of the people I wrote to was Jack Strominger in Harvard and he took me*. I thought, “it sounds great, to study how the immune system works”. It was a little bit random how I ended up in Immunology, but that’s kind of how it went.

Why did you decide to write a book for the general public?

DD In your day job in your lab, you have to be immersed in all the detail, because obviously to get a paper in your journal, you’ve got to get all the details right. Everything has got to be very well controlled, and you’re discussing with the students and postdocs. I had my own lab since I was twenty-nine, and then twelve, thirteen years later, I wanted to take stock of the big picture. Coming from Physics, you’re sort of trained as a physicist to try to think about the broader picture- the universal laws again. So I wanted to write a popular level book as a way of taking time out, to take stock of the big picture of how the immune system works.

DD There’s another reason that’s important to me. A lot of the greatest tragedies that have happened through history- I’m Jewish, so the Holocaust is one thing that comes to mind- come from a misunderstanding of the differences between people. One of the greatest themes that we get from studying the immune system is quite a deep understanding of what the differences between people really mean, and that was a really important story for me to tell. For example, if you asked people in the general public “what genes would you think might be different from one person to the next?” they’ll probably think of things like “the genes that control our hair color, our eye color, or our skin color” for example. In fact, the genes that vary the most from one person to the next are in our immune system. Not only are the genes that vary the most in our immune system, it’s actually crucial that they do vary, that they have that exceptional diversity. Because the way that we have evolved to survive disease requires this exceptional diversity in our immune system genes, or specifically, our MHC genes. So, in a way, it’s a really powerful celebration of human diversity, and I wanted to tell that story.

How did you keep a lab running during the writing of the book?

DD I took a year’s sabbatical leave. That basically meant I didn’t have to do my usual teaching and administrative duties. I still ran the lab. I still came in, did lab meetings. But I didn’t come in to the lab and do a lot of the stuff I would normally do, and I turned down a lot of invitations to conferences during that period of a year. We built a shed at the bottom of my garden and basically I sat in that shed for a year and wrote this book. I did also interview of course many of the scientists that were involved. I wanted to tell this sixty year long journey of the discovery of the MHC genes, and then how we learned all the things that they do in the human body. I interviewed a lot of the people that did the primary work, and if they were no longer with us, I also interviewed some members of their families just to get a sense of their state of mind, of how they did the work, and what they went through to win us that knowledge.

How did you find a publisher?

DD I didn’t have a good idea about that at the outset- I actually just thought, you know, I’ll write the book and it will be published somehow, just like I might do a paper and send it to J Exp Med. It took me a while to figure out how that worked. It turned out that it’s not so different from what we’re used to, in the sense that you essentially have to write a proposal, like I would normally have to write a grant proposal to do the research. That basically means an outline, a description of what would be in each chapter, and then some stuff about why the book is going to be important, who’s going to read the book, why I’m the right person to write the book- or at least I’m a person who could write that book. You have to certainly sell it a bit, to send that proposal to literary agents. There’s just a lot of guidance out there on the web about how to find an appropriate literary agent. Or you could just look in any other popular science book and see who their literary agent is, and send it to them. By chance, my proposal ended up with a literary agent in London whose other client was J.K. Rowling, of the Harry Potter books, so that seemed like it would be a great literary agent to be associated with**.

What is your lab currently working on?

DD What we’re working on now is using super-resolution microscopes to look at what happens at the immune cell surface when immune cells are switched on or off. The thing I love about microscopy is, as well as using it to answer specific questions, you know, to work out the details of some mechanisms by which some process works- the wonderful thing about microscopy is you might discover unexpected new phenomena. It’s a great tool for explorative science. That’s what led me to initially co-discover the immune synapse and membrane nanotubes. Now we’re using these newer microscopes that work at even higher resolution and we’re seeing that the same kind of cell can have subtle changes to the organization of its proteins at the cell surface which correlate with different states of health and disease. I’m now also much more connected to pharmaceutical companies. I’ve recently moved from Imperial College in London to Manchester and one of the things about that move is that I’m Director of Research for a center that’s connected to pharmaceutical companies. I’m trying to find out really what might be druggable in the way cell surfaces are organized, and how that may be used to impact the outcome of immune cell recognition.

* Some of their work on HLA and NK cells was published in JEM.

** Dan’s agent is Caroline Hardman.

The Viral Shake

A kerfuffle over whether or not the University of California at Berkeley was a place for serious scientists led directly to the creation of our sibiling publication, The Journal of General Physiology. Dr Flexner’s old Professor, Jacques Loeb, was banned from the pages of The American Journal of Physiology when he moved from the University of Chicago to the West Coast in 1902 (and thus “no longer represented a ‘major’ institution”). Eight years later, Flexner recruited Loeb to the Rockefeller Institute, and eight years after that, in 1918, Loeb launched The Journal of General Physiology.

So it’s numerologically appropriate that eight years after Avery and colleagues demonstrated in JEM that DNA was the “transforming principle”, Alfred Hershey and Martha Chase should publish their own work on the chemical nature of the hereditary material of viruses in JGP. These are the beloved Waring Blendor (sic) experiments*- Hershey had found the setting where phage** (and phage “ghosts”, i.e. protein shells) clinging to the bacteria would be spun-off without bursting the bacteria themselves.

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T2 phage (illustration by Madalena Parreira).

The key to understanding Hershey and Chase’s experimental setup is quite simple: proteins contain sulfur & DNA doesn’t; the reverse is true of phosphorous. Growing phage in the presence of radioactive sulfur-35 or phosphorus-32 isotopes allows tracking of the different compounds’ fate simply by measuring radiation in bacterial cultures. By shaking the bacteria in the blender (or blendor), and then spinning the whole mix in a centrifuge, Hershey and Chase could use a Geiger counter to find which viral molecules were passed on the next generations (via synthesis in the bacteria). They conclude that:

“The experiments reported in this paper show that one of the first steps in the growth of T2 is the release from its protein coat of the nucleic acid of the virus particle, after which the bulk of the sulfur-containing protein has no further function.”

or, in other words

“We have concluded above that the bulk of the sulfur-containing protein of the resting phage particle takes no part in the multiplication of phage, and in fact does not enter the cell. It follows that little or no sulfur should be transferred from parental phage to progeny.”

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Hershey and Chase, JGP 1952, figure 1.

Though Hershey & Chase’s work is often referred to as “definitive” confirmation of the Avery group’s work, it is worth noting that the levels of contamination in their work vastly exceed those published in 1944- a fact the authors do not attempt to conceal:

“The radiochemical purity of the preparations is somewhat uncertain, owing to the possible presence of inactive phage particles and empty phage membranes.”

“The following experiments show that this is readily accomplished by strong shearing forces applied to suspensions of infected cells, and further that infected cells from which 80 per cent of the sulfur of the parent virus has been removed remain capable of yielding phage progeny.”

Even the best-case scenario

“The experiments described below show that this expectation is correct, and that the maximal transfer is of the order 1 per cent”

was unimaginable in Avery’s meticulous, painstaking biochemical work, and contamination had led Hershey to the wrong conclusion only a year before:

“The properties described explain a mistaken preliminary report (Hershey et al., 1951) of the transfer of S 35 from parental to progeny phage.”

Perhaps the most salient aspect of Hershey and Chase’s landmark study, what immediately stands out when reading the original manuscript and the rationale behind the experimental design, is that these experiments were not set up to test if DNA was the genetic material at all. They were optimized to examine if protein could be. But the idea of DNA as the genetic material was much more acceptable in 1952, and the use of radioactive isotopes labeling was very appealing in the heyday of the Atomic Age. So for many scientists at the time, Hershey and Chase’s 1952 JGP classic marked the definitive acceptance of deoxyribonucleic acid as the chemical agent of heredity.

* Matthew Cobb kills this romantic image: “This apparatus is often called a kitchen blender, which conjures up some kind of retro 1950s domestic device, all chrome and glass. Sadly this was not the case (…) the apparatus used by Hershey and Chase was a highly specialized, unstylish bronze-coloured piece of laboratory equipment’”. Dr Cobb may or may not be available to come to your kid’s party and tell him there is no Santa.

** A group of viruses that infect bacteria (short for bacteriophage).

Andersen, O.S. A Brief History of The Journal of General Physiology. 2005. 125:3.

Hershey, A.D., and Chase, M. Independent functions of viral protein and nucleic acid in growth of bacteriophage. Journal of General Physiology. 1952. 36:39-56.

Painting the Invisible.

Artist Emilie Clark painted the beautiful watercolor on our August 24th issue cover. Originally from San Francisco, Emilie lives and works in New York City. She took a short break from her summer vacation to talk about her work with JEM, the role of science and natural history in her art, and being chosen to represent a deadly sin.

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Emilie Clark, JEM August 2015 cover.

How did you start working with JEM?

EC Well, let’s see… It’s been some years now. I was trying to remember the other day the first time I did one for them, and I’m not entirely sure what year was that.

I think it was 2004.

EC 2004? Ok, so that’s quite a while ago. I got an email out of the blue from them, and there had been somebody working there who had seen an exhibit of mine. She said that they were trying to expand the kind of illustration that they had.

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Emilie Clark, lymph nodes. JEM cover September 2004.

I’m not an illustrator. I’m more in the kind of fine arts context of doing more conceptually motivated work. But all of my work deals with the history of science in some way. At the time, I was working on a project that dealt with carnivorous plants, and that’s what this person from JEM had seen. She said that they wanted to work with artists that weren’t necessarily doing straight medical illustration, but could get more of the dynamic of what the authors were talking about in their papers. That was really exciting to me. I had actually thought about doing medical illustration way back, when I was a teenager. So I said I would love to do it, and then I did one, and we just kind of went from there. They’ve kept coming back, which has been great. I really love doing the covers for JEM. I’m really happy when I get the email in my inbox from Marlowe (Tessmer, JEM executive editor, ed. note).

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Emilie Clark, JEM cover September 2010.

What kind of input do you get from JEM?

EC I really wanted to see an abstract or a description summary of what the paper was about, because a lot of my work has been response to historical text- sometimes medical, sometimes natural history or other kinds of scientists, botanical scientists, animal scientists. Reading a description is often more provocative to me than looking at a photograph, or a cartoon, or a medical illustration. I always get a description or the abstract for the paper. Then JEM often will send an electronic microscopic image that’s more diagrammatic, or they’ll send a diagram that is part of what they’re describing. But it’s very rare that there is an existing diagram of whatever it is that is being spoken about. I have to be able to make sense of the science enough to be able to make a drawing that is going to communicate what they are talking about, but I also try to keep within the way that I work. I would describe the way that I work to be more abstract, and more kind of getting at the dynamic than being like a straight up kind of illustration. Does that make sense?

Yes.

EC So if you looked at the diagram it might be clearer, or the relationships of scale in my work sometimes might be more loose than they would be realistically. But that’s to try to emphasize whatever the argument is.

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Emilie Clark, JEM cover July 2011.

You’ve worked also as artist in residence in the Brooklyn Botanical Garden.

EC When they invited me to come, I spent a lot of time talking to the botanists there, and the different horticulturalists that worked there. I discovered that the Garden was suffering from a devastating virus in their rose garden, and also a bacterial gall. Because of those things, they were going to have to remove something like a third of the rose population, the soil, and keep them fallow for two years, I think. That’s what ended up capturing my fascination. So I worked closely with the botanist who was studying the virus, and we had access to these amazing microscopes. But a lot of it involved a kind of fantasy on my part, because much of when I wasn’t looking at the microscope I was working in the garden and what I was looking at mostly not visible to the human eye. So that’s interesting to me, that sort of space that you can’t see, that you can only imagine and project on to. I think a lot of science is like that- you have to hypothesize and take what you do know and then apply to what you don’t know. That’s sort of what I did at the garden, and it was really fun and I learned a lot from it. And it was nice to work directly with some scientists as well.

What are you currently working on?

EC Right now I have a solo exhibit up at the Katonah Museum of Art, which is just north of the city in Katonah, New York. There’s a consortium of seven museums in the New York area that decided to team up and put together exhibits that dealt with the seven deadly sins. The Katonah Museum had chosen to work with gluttony and they chose me to represent that sin. I have a large exhibit that responds to that theme, and in a way the work that I did is about the opposite of gluttony. It’s more about seeking a sustainable relationship to the environment. It’s an exhibit of large watercolors and there’s an installation of food detritus. I spent a year saving all of my family’s food waste, and preserved every part of it, and so there’s a large table with all of that food waste on it. There’s also a sculpture that functions as a research station. Those are the three components of my work. I always do watercolor drawings or paintings depending on how you want to talk about them, it doesn’t matter; and then I make sculptures, part of which are functional and have something like a research interactive station to them. So that research station has a microscope and certain specimens that visitors to the Museum can examine. That’s up til October. It opened in the beginning of July. Then I’ll be having a big exhibit at the gallery that represents me in New York, which is called Morgan Lehman Gallery. That will be in February.

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Emilie Clark, JEM cover November 2012.

Weekend Suitcase

“So, yogurt. In 2007 scientists working for Danisco, a Danish food ingredient company now owned by Dupont, invented a method for encouraging virus resistance in Streptococcus thermophilus, a bacterium critical to yogurt and cheese production. “ Anne Fausto-Sterling at Boston Review takes a critical look at CRISPR.

Consider the octopus “an intelligent animal with entwining arms so filled with neurons that each of them possesses a separate personality”, says Philip Hoare at the New Statesman.

“And then there’s the truly wild card!  All of these risks are based on the combinations of past exposures to measured lifestyle factors, but the mix of those and the rise of other new lifestyle factors, or the demise of past ones, means that the most fundamental of all predictors can itself not be predicted, not even in principle!” Anne Buchanan at The Mermaid’s Tale goes down the rabbit-hole of prediction in complex diseases.

Steve Silberman at Buzzfeed, on Oliver Sacks and autism: ‘“The autistic mind, it was supposed at that time, was incapable of self-understanding and understanding others and therefore of authentic introspection and retrospection,” Sacks told me. “How could an autistic person write an autobiography? It seemed a contradiction in terms.”’

“No one is entirely clear on how Brian Nosek pulled it off, including Nosek himself. Over the last three years, the psychologist from the University of Virginia persuaded some 270 of his peers to channel their free time into repeating 100 published psychological experiments to see if they could get the same results a second time around.” Ed Yong at The Atlantic wants to know How Reliable Are Psychology Studies.

The increasingly Dickensian experience of grant application. “it was the epoch of belief, We are totally going to get this grant! Science! How could anyone not think fetal surgery is the awesomest. This grant is great. The science so solid. The ideas so unique. Hashtag fundableIt was the epoch of incredulity, Why granting gods, oh why? Peer review will be a disaster. This is never going to fly. It’s due in 2 weeks and we still have so much to dooooooooo.” By Sally Winker at Beta Pleated Chic.

“Two years away from retirement, Dr Madhusudana is still haunted by the death of a 21-year-old student who was once in his care. Like Bhuvan and Veena she lived in a rural village, hours from Bangalore, in the southern state of Karnataka. She had been washing dishes behind her home in May 2013 when she was bitten twice by a street dog. The girl was injected with the rabies vaccine, but her treatment ended there. ” Mary-Rose Abraham at Mosaic on the fight against rabies.

Arjun Raj thinks of the trainees, and proposes his Top 10 Signs That a Paper/Field Is Bogus.

To finish on a lighter note, the latest viral scientific hashtag made the LA Times: “One minute later, Helena Ledmyr, a development officer at the International Neuroinformatics Coordinating Facility in Stockholm, copied the tweet and added the hashtag #scienceamoviequote”, by Karen Kaplan.

Dr Zon & The Zebrafish: The Origin Story

As promised, here is part two of our talk with Harvard and HHMI investigator Leonard Zon, in which he shares with us why he left frogs, how he came to work on zebrafish, and the importance of getting by with a little help from your friends. (Click here for Part I).

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Illustration by Madalena Parreira.

You spent some time working on Xenopus?

LZ When I started my lab, I thought I wanted to do mouse genetics. I went over to MIT on a Friday afternoon and dissected out day 7.5 mouse embryos, looking for the very first blood island. It took us 6 hours and at the end of that time I had a dish that had 6 embryos in it. I realized that everything that I wanted to do wasn’t going to be possible. So I was pretty depressed. I came back to the lab and I saw a friend of mine, Celeste Simon, and she said that I looked terrible. I said I’d had this bad experience with what I wanted to start my lab in. I didn’t think it was practical anymore. She said, “Well I can’t help you with that. But I’m having a party at my house and I’d like you to come”.

So I was there at the party and I had a beer in my hand and this guy walks up, and his name is Jerry Thomsen, who’s at Stony Brook. Jerry worked on frog embryos in Doug Melton’s lab. So we started talking and I told him about my mouse experience. He said, “You know, you really have to think about an externally fertilized animal, because you could have thousands of embryos, like a frog. Then everything will be one-cell, two-cell, four-cell… and eventually you would make blood and you could study that process, in a facile system”. The next week I made an appointment with Doug and started doing frogs. A couple of years in, I realized that the frog didn’t have very good genetics. There were no morpholinos or anything at that time, so everybody was not really doing anything except injecting a dominant negative construct in the frog. I felt like I needed to switch systems, so I decided to switch to the zebrafish.

I could tell you more about how I did that, or we could go on. I had kind of an amazing week that transformed my group into a zebrafish lab.

That sounds like an interesting story.

LZ I went to a hemoglobin switching meeting and presented my frog work. After the presentation this transgenic mouse person, Frank Grosveld, came up to me and said, “You know, I really felt like your talk was fantastic. The frog is a good system but, you’re never going to do genetics. Have you heard about the zebrafish as a model system?

I actually had been thinking about switching to zebrafish already because Janni (Christiane) Nusslein-Volhard was going to start doing zebrafish. So I’d been thinking about it. We spent actually about an hour together. He helped crystalize the reasons for going into a new model system, how it could be a good thing. So I came back really charged up about zebrafish. Literally the next day, I had a call from Bill Dietrich, who’s an investigator at Northeastern University. He worked on the Antarctic icefish. The icefish has lost its red blood cells, because it is a competitive disadvantage in cold water to have red blood cells, you end up stroking out. So he convinced me that I should study cold adaptation of transcription in this icefish. I said, “I don’t care about icefish, what about zebrafish?” He said, “That sounds really interesting, sign me up for a sabbatical.” So I had my first person on day 2. Then, on day 3, an investigator in Wally Gilbert’s lab at Harvard called. He had been doing a few zebrafish experiments and found a mutant fish that had no blood. They were going to throw it out, but they said, “We heard you like these things, so you can have it.” So that was it.

Now you have over three thousand tanks?

LZ Yeah, it’s actually three thousand. It’s amazing. Three hundred thousand fish. It’s actually split in two facilities right now.

You identified the first human disease-causing gene in zebrafish. Can you tell us a bit about that?

LZ It was very interesting in the early days. We had very few reagents to do research. We had a mutant where we did a chromosomal walk of a megabase. Literally took us about three years. We found the gene. This mutant was Sauternes. Sauternes ended up being an ALAS2 mutant- this is one of the major steps in heme biosynthesis. It was a human disease gene. So we really found the first human disease-relevant gene in fish. That was really exciting. We published a Nature Genetics paper. About half of the community was very excited about it, that it was possible to clone this type of gene, and the other half was “Well, we already knew about that gene, because it was already a human disease gene. Will you ever find anything novel?”

Luckily our second gene was Weissherbst. We did a comparative approach to actually clone this gene. The human locus and the fish locus had the genes in the same order. So it was nice because we had candidates to walk through this locus. We found this gene which we named ferroportin, which is an iron exporter. This mutant had iron in the yolk, but it couldn’t get it to the baby, because it missed the transporter to do that. That was a very exciting gene because it was completely novel.

When we looked at it, we realized that it was evolutionarily conserved, because the human gene was there. We made antibodies to the human gene product, and we found that it had binding in the placenta. This yolk sac iron transporter and the placental iron transporter were the same. Mothers get their babies iron through this ferroportin. Then we started staining adult tissues and we found that in the duodenum there was specific staining for ferroportin. What we realized was that there was this basolateral iron transporter in the gut that many people had hypothesized to exist, and shown it should be there. It turned out to be ferroportin. That was also exciting, and later we found mutations in people that had hemochromatosis. So it became not only a novel gene, but the first time that a zebrafish mutant predicted a new human disease.

Weekend Suitcase

“I’ve spent months investigating the problems hounding science, and I’ve learned that the headline-grabbing cases of misconduct and fraud are mere distractions. The state of our science is strong, but it’s plagued by a universal problem: Science is hard — really fucking hard.” Christie Aschwanden at FiveThirtyEight on why “Science Isn’t Broken”.

“Certain genes (…) have no known relatives, and they bear no resemblance to any other gene. They’re the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.” Emily Singer at Quanta on genes from junk.

Personalized tragedy: Tom Junod at Esquire on Stephanie Lee, precision medicine’s patient zero. “Without prelude, a deus ex machina had arrived upon the scene, and the race against time had begun.” 

Pseudo-science and the justice system, by Jeremy Stahl at Slate. “‘The howls of protest from fire investigation ‘professionals’ were deafening,” fire scientist John Lentini wrote of the initial response to NFPA 921. ‘If what was printed in that document were actually true, it meant that hundreds or thousands of accidental fires had been wrongly determined to be incendiary fires. No investigator wanted to admit to the unspeakable possibility that they had caused an innocent person to be wrongly convicted.'”

Architects, doctors, janitors, police, and gardeners. Ferris Jabr at Nautilus on the cells in your brain (not those, the other ones).

“The intro, discussion, and conclusion have value because I don’t view them as opinion, but as argument.” PaleoGould on the virtues of reading the whole paper.

The vast majority of scientific papers today are published in English. What gets lost when other languages get left out?” Adam Huttner-Koros at The Atlantic wants to know.

In Memoriam: obituaries for genetic algorithm pioneer John Henry Holland and cell biologist Chris Marshall.