Photo 51

Rosalind Franklin doodle

Today’s Google Doodle honors Rosalind Franklin, whose work on X-ray diffraction was instrumental in determining the double helix structure of DNA. In the Doodle she’s staring at an X-ray diffraction image, known as Photo 51, that got the ball rolling. If you’d like to learn more about how the structure of DNA was determined, Nova has a great interactive dissection of Photo 51 that helps unravel the double helix structure from what looks like just an “X.”

After her work on DNA, she “conducted pioneering work into the structure of viruses.” Sadly, she died due to complications of ovarian cancer in 1958–four years before the Nobel Prize was awarded to Watson and Crick for their research on nucleic acids, and at the time much of her contribution was overlooked.

I can’t help but wonder what else she would have accomplished had she not passed away.

Should I start patenting the cDNAs I’ve made in the lab?

In a unanimous decision today, the SCOTUS struck down patents for genes by ruling against Myriad Genetics in Association for Molecular Pathology vs. Myriad Genetics. The Court, however, did leave some wiggle room for companies to patent cDNAs, or complementary DNA.

“In Myriad, the high court held cDNA is patentable, because it involves actual work in the laboratory and inverts the normal process found in nature. The synthetic DNA is an edited version of a gene, stripped of non-coding regions that the court said makes it “not naturally occurring.”

Critics say even the edited sequences are directly analogous to naturally occurring DNA.”

In many labs, cDNAs are routinely made, manipulated, and used for research. cDNA is DNA that is engineered in reverse using messenger RNA (mRNA) as the template. As the above quote alludes, a cDNA is not a carbon copy of its corresponding gene. Interspersed along the length of a gene are regions of non-coding DNA sequence. These are segments of DNA that aren’t represented in the sequence of the encoded protein. When a gene is initially transcribed into mRNA some of these non-coding regions, called introns, are included. Introns, however, are ultimately removed by the cell before the mRNA is translated into protein. Since mRNA is used to make cDNA, the introns are excluded from the cDNA sequence.

gene expression
During gene expression, a gene is first transcribed into a primary RNA transcript, which includes non-coding introns (blue). Through a process called splicing the introns are removed from the transcript resulting in a mature mRNA molecule. The sequences found in mRNA are called exons (red and yellow). The mRNA is  then translated into protein. Since cDNA is made from mature mRNA, it will consist only of exon sequences.

Although gene and cDNA are different, they both carry essentially the same DNA sequence for a protein. (It should be noted, however, that many genes encode multiple forms of a protein, for which each form has its own corresponding cDNA.) So, I’m not sure why the “patentable” emphasis is on cDNAs as opposed to making mutations* to the underlying sequence that result in say, new or altered function of a protein. At least there I could see an inventive process happening–or am I missing something here?

*I’m talking about generating novel mutations. Of course, I’m not sure what should happen if said mutations are discovered to be “naturally occurring” after the fact.

Related Reading:

Patents on Nature

 

 

Crossposted at Scientopia

Blight-Resistant Potato: an “Acceptable” GMO?

1280px-Phytophtora_infestans-effects
“Potato Blight Effects”

Last week, I wrote about a disease-causing nematode that infects the roots of soybean plants and  a mutation in one strain of soybeans that makes them resistant to these nematodes. In the post I mused,

what if an already existing gene variant with a desired trait from one organism is genetically engineered into another organism of the same species? Would this make GMOs a little bit more palatable to their detractors?

While intended to be more of a thought experiment, a commenter alerted me to a very similar scenario playing out in Ireland, where potato crops are still affected by blight–yes, as in the blight responsible for the Great Famine of the mid-1840s. Blight makes potatoes rot and is caused by infestation of a fungus-like organism (oomycetes) called Phytophthora infestans.

In recent years, scientists have developed blight-resistant GMO strains of potato plants by introducing a blight-resistance gene called RB into the potato’s genome. This gene was identified in Solanum bulbocastanum, a wild potato plant native to Mexico that is closely-related to potatoes. Resistance to blight most likely developed as a result of coevolving with P. infestans, which is considered to be native to Mexico as well.

The scenario facing GMO potatoes, however, is a little bit different from the question I posed earlier since the RB gene isn’t found in cultivated potato plants. Furthermore, traditional breeding methods have been unsuccessful in making hybrids between cultivated potatoes and S. bulbocastanum, therefore necessitating genetic engineering. There are, however, other blight-resistant wild Solanum plants, such as Solanum venturii, that can be hybridized with cultivated potatoes. But using the RB gene from S. bulbocastanum remains the most attractive option because S. bulbocastanum is resistant to the most number of blight-causing P. infestans strains

The response from one anti-GM campaigner to using genetic engineering in this case?

It is just there to make GM more palatable to the general public. The fact that it comes from a related plant doesn’t make it any different. The real danger is the process.

I guess that answers my question.

Immigration Reform: A Second Chance for Undocumented Immigrant Health?

When the Affordable Care Act was signed into law in March of 2010, many immigration advocates were disappointed that the bill left undocumented immigrants out in the cold. While the law kickstarts the process of bridging the gap for millions of uninsured Americans, specific language was written into the legislation to bar undocumented immigrants from being “eligible for public insurance or any type of private coverage obtained through exchanges.” At the time of the bill’s signing, approximately 7 million out of an estimated 11 million undocumented immigrants in the US were without insurance, and many of whom were living in poverty. These numbers are only expected to increase [1]. With immigration reform highly visible in Obama’s second term, immigration advocates are now viewing this as a second chance to address a growing public health concern.

Read more at PLOS Blogs…

Dengue Fever, GMOsquitos, and a “Wolbachian” Invasion

In my recent Public Health Perspectives post for PLOS Blogs, I discussed two ways to control the transmission of dengue fever. The first was through the release of genetically-modified (GM) male mosquitoes that mate with wild females and pass on a gene that is lethal to its offspring–a strategy called Release of Insects carrying a Dominant Lethal (RIDL) (1). If released in sufficient numbers, the GM male mosquitoes will cause a collapse of the mosquito population.

Diagram of the RIDL transgene (image from Oxitec website)
Diagram of the RIDL transgene (image from Oxitec website)

The RIDL transgene (a) that has been engineered into the OX513A strain of mosquitoes carries instructions for the production of a protein called tetracycline transactivator (tTA). tTA , itself, is a product of genetic engineering, created by the fusion of parts of two proteins. One “half” of tTA acts as transcriptional activator–it can turn on and amplify the expression of certain genes. The other “half” can bind to specific DNA sequences called tetO binding sites. By engineering tetO binding sites into the RIDL transgene this allows the tTA protein, itself, to amplify expression of the tTA gene thereby producing even more tTA protein (b). This results in what is known as a positive feedback loop. At high enough levels, the tTA protein interferes with cellular process causing mosquito larvae to die. The expression of the tTA gene can be turned off by tetracycline, however (c). Tetracycline binds to the tTA protein and prevents it from binding to DNA, which short circuits the feedback loop.

“This allows scientists to raise the mosquitoes in the lab by adding tetracycline to the diet of the larvae. Without a source of tetracycline in the wild, however, any mosquito offspring that inherits the gene will live not beyond the larval stage.”

The other strategy I discussed was using Wolbachia infection of mosquitos to prevent dengue transmission. Wolbachia is an symbiotic bacteria that has been shown to protect mosquitos against dengue infection by interfering with the ability of the dengue virus to replicate. Wolbachia can invade and establish itself in insect populations quite rapidly and stably–an ideal characteristic if Wolbachia is to be used in limiting the transmission of dengue. It accomplishes this by employing a cunning strategy called “cytoplasmic incompatibility (2).” In short, when Wolbachia-infected males mate with uninfected females all their offspring die. However, the offspring of Wolbachia-infected females are viable regardless of the infection status of the male. This means that Wolbachia infection confers a reproductive advantage to infected females over uninfected females–infected females are more likely to have offspring because they can mate with both infected and uninfected males. Furthermore, Wolbachia infection is passed on from mother to offspring. It is through this process that Wolbachia “invades” and secures its place in an insect population.

Field studies conducted in Australia showed that when  mosquitoes infected with the wMel Wolbachia strain are released into the wild, within several months stable wMel infection became established in two wild A. aegypti populations (3). The speed at which wMel invaded the natural mosquito populations demonstrated the potential of using Wolbachia infection to control the spread of dengue.

You can read more about this topic here:

Could Wolbachia be an alternative to dengue-fighting GMOsquitos?

References:

1) Phuc HK, Andreasen MH, Burton RS, Vass C, Epton MJ, Pape G, Fu G, Condon KC, Scaife S, Donnelly CA, Coleman PG, White-Cooper H, Alphey L. Late-acting dominant lethal genetic systems and mosquito control. BMC Biol. 2007 Mar 20;5:11. PubMed PMID: 17374148; PubMed Central PMCID: PMC1865532.

2) Walker T, Johnson PH, Moreira LA, Iturbe-Ormaetxe I, Frentiu FD, McMeniman CJ, Leong YS, Dong Y, Axford J, Kriesner P, Lloyd AL, Ritchie SA, O’Neill SL, Hoffmann AA. The wMel Wolbachia strain blocks dengue and invades caged Aedes aegypti populations. Nature. 2011 Aug 24;476(7361):450-3. doi: 10.1038/nature10355. PubMed PMID: 21866159.

3) Hoffmann AA, Montgomery BL, Popovici J, Iturbe-Ormaetxe I, Johnson PH, Muzzi F, Greenfield M, Durkan M, Leong YS, Dong Y, Cook H, Axford J, Callahan AG, Kenny N, Omodei C, McGraw EA, Ryan PA, Ritchie SA, Turelli M, O’Neill SL. Successful establishment of Wolbachia in Aedes populations to suppress dengue transmission. Nature. 2011 Aug 24;476(7361):454-7. doi: 10.1038/nature10356. PubMed PMID: 21866160.

Featured image:
Detail from the original by Emil August Goeldi (1859 – 1917) [Public domain or Public domain], via Wikimedia Commons

by Viet Le

Rhino horns: From traditional medicine to recreational drug

Rhino horns are a precious commodity. On the black market, they can fetch an absurd price upwards of $60,000/kg. That’s more than the price of gold. Put in a different perspective, drop me a kilo of rhino horn and that pays two years of my graduate stipend…plus a Christmas bonus.* But that price also cost 618 rhinos their lives in 2012. This all-time high continues a rapidly increasing trend dating back to 2008 when poachers killed 83 rhinos–a noticeable uptick from the yearly average of 15 rhinos killed from 2000-2007. The practice is in no way humane, as poachers often cut horns off of tranquilized rhinos and then leave them to die from their wounds. I’ll spare you the grisly photos, but gruesome Internet images abound.

Adapted from Infographic- Understanding the rhino wars
Adapted from Infographic- Understanding the rhino wars

Fueling this demand for rhino horns are East Asian countries like China and Vietnam (I’m shaking my head in disapproval at you, my peoples in Vietnam). There, rhino horns are coveted by practitioners of traditional Chinese medicine who believe its extract can be used for treating fevers as well as other “conditions.” While most news coverage is quick to point out that rhino horns are little more than keratin (the protein found in our hair and nails) and that they lack any curative properties, little discussion is devoted to any actual research on their medicinal value. While published data is scarce–this probably reflects the obstacles in obtaining rhino horns for research–what little that has been published certainly doesn’t support using rhino horn as medicine.

In the early 1990s, Chinese researchers published in the Journal of Ethnopharmacology two studies that tested the ability of rhino horn extract to reduce fever (1,2). In the first study, researchers induced fever in rats by injecting them with turpentine oil, a known fever-causing agent. This was followed by injections of rhino horn extract prepared in either saline or in the herbal concoction traditionally prescribed for fevers. Both preparations of rhino horn extract were able to slightly decrease fevers in rats, but the effect required using rhino horn extract at 20 times the concentration normally prescribed by traditional medicine. Furthermore, the researchers observed that similarly high concentrations of horn extracts from saiga antelope, water buffalo, and cattle, also reduced fever in rats. This result meant that there was nothing special or magical about rhino horns in particular. The researchers concluded that, at least for the purpose of traditional medicine, rhino horns could be swapped out for horns from non-endangered animals.

Image credit: Jim Epler
Rhino horn. Image credit: Jim Epler

Still, the Chinese studies had two other problems. First, they injected the rhino horn extract into the rats, whereas in traditional medicine rhino horn extract is ingested. Second, their study didn’t compare how effective rhino horn extract reduced fever against known anti-fever drugs. These issues were addressed by Laburn and Mitchell, who published their results in the Journal of Basic and Clinical Physiology and Pharmacology (3). In their study, rabbits were injected with bacterial lipopolysaccharide (LPS), a component of bacterial cell walls. Since LPS is foreign to the rabbit’s body, it triggers the rabbit’s immune system and induces fever. To test their fever-reducing abilities, either rhino horn extract, reedbuck (a non-endangered African antelope) horn extract, indomethacin (an anti-fever drug), or water was fed “gavage-style” to the LPS-injected rabbits. This meant that the samples were pumped directly into the rabbit’s stomach through a tube passed through its mouth. To monitor the effect of each agent on fever, rectal temperature was monitored over the course of 250 minutes. The researchers found that neither the rhino nor the reedbuck horn extract did anything to reduce fever in rabbits. More importantly, indomethacin was very effective at reducing the fever. These findings are similar to another report which found that acetaminophen was more effective than rhino horn extract at reducing fever in children.

Rabbits were injected with bacterial lipopolysaccharide (LPS) to induce fever and simultaneously administered rhino horn extract (black circle), reedbuck extract (white square), water (white circle), or the anti-fever drug, indomethacin (black triangle). Rectal temperature was measured to monitor fever over the course of 250 minutes. Only indomethacin (black triangle) was able to reduce LPS-induced fever after about 75 minutes.
Rabbits were injected with bacterial lipopolysaccharide (LPS) to induce fever and simultaneously administered rhino horn extract (black circles), reedbuck extract (white squares), water (white circles), or the anti-fever drug, indomethacin (black triangles). Rectal temperature was measured to monitor fever over the course of 250 minutes. Only indomethacin (black triangles) was able to reduce LPS-induced fever after about 75 minutes (3).

Despite little scientific support for using rhino horns as medicine, the demand for rhino horns in China and Vietnam continues to soar. This week, in response to the growing poaching problem, Vietnam signed a no-poaching agreement with South Africa, where the majority of rhinos have been killed. Whether this will have any appreciable effect on poaching, however, is debatable considering that the demand for rhino horns in Vietnam has overshadowed its own conservation efforts. In 2010, the last of the Javan rhino subspecies native to Vietnam was killed by poachers.

Dehorned rhino
A dehorned rhino just looks so sad. Brent Stirton/National Geographic

Other ways to curb poaching have also been explored, such as routinely shaving off rhino horns. While rhino horns eventually grow back, this practice is unpopular among conservationists since rhinos depend on their horns for defense. It’s also worth noting that many dehorning advocates are also rhino owners whose true financial motives may lie in their support for legalizing the rhino horn trade. Another suggestion that’s been floated around to reduce poaching is to implant GPS devices into rhino horns. This would serve as a sort of RhinoJack that can be used to track down poachers. Others, on the other hand, suggest taking even more drastic actions.

These measures, of course, serve only to make poaching less desirable without dealing directly with demand. What’s troubling is that the demand for rhino horns is now being propped up by new and kookier, unscientific ideas, which extend far beyond its traditional use. Reports from China and Vietnam indicate that con men are peddling rhino horn extract as a miracle cure for whatever malady suits their fancy. As John Platt, of SciAm blogs, reports, “In Vietnam con men recently started marketing rhino horn as a cure for cancer or as a party drug to lessen the effects of alcohol.” (Do I smell a pseudo-cure for Asian Glow as well?) In other cases, rhino horns are being crushed and snorted like cocaine, sprinkled on food, or mixed with alcoholic cocktails as over-the-top displays of wealth popular among Vietnam’s “nouveaux riches.” By linking rhino horns with status symbols, the affluent are only driving up prices. Unfortunately for rhinos, as the price for their horns go up, so does the incentive for poachers. 

*We don’t receive Christmas bonuses.

Featured image: 

untitled (Walter Corno) / CC BY-NC-SA 3.0

References:

1. But PP, Lung LC, Tam YK. Ethnopharmacology of rhinoceros horn. I: Antipyretic
effects of rhinoceros horn and other animal horns. J Ethnopharmacol. 1990
Sep;30(2):157-68. PubMed PMID: 2255207.

2. But PP, Tam YK, Lung LC. Ethnopharmacology of rhinoceros horn. II: Antipyretic
effects of prescriptions containing rhinoceros horn or water buffalo horn. J
Ethnopharmacol. 1991 May-Jun;33(1-2):45-50. PubMed PMID: 1943172.

3. Laburn HP, Mitchell D. Extracts of rhinoceros horn are not antipyretic in
rabbits. J Basic Clin Physiol Pharmacol. 1997;8(1-2):1-11. PubMed PMID: 9363565.

 

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David Byrne explains the neuroscience of music and mirror neurons but skips the skepticism.

David Byrne, one of my favorite musicians, is out with a new book that is part-memoir and part-collection-of-essays titled, “How Music Works.” In an excerpt featured in Smithsonian magazine, Byrne explains why sometimes he prefers silence over listening to music–and who can blame him? I’d be pretty tired of hearing artists copping my style for the past 10 years too. But at about a third of the way through, interestingly enough, Byrne switches gears and tries his hand at a little science writing.

Expounding on the neurological basis of how our brains process music, Byrne cites a UCLA study that proposed “our appreciation and feeling for music are deeply dependent on mirror neurons. When you watch, or even just hear, someone play an instrument, the neurons associated with the muscles required to play that instrument fire. Listening to a piano, we ‘feel’ those hand and arm movements, and as any air guitarist will tell you, when you hear or see a scorching solo, you are ‘playing’ it, too.” The mirror neurons to which he’s referring “fire” when an individual performs an action or observes another performing that same action. This has been interpreted to mean that

“when you observe someone performing a movement, particular mirror neurons embedded in your motor system are activated, enabling you to simulate yourself performing that movement using your own motor system. This simulation then allows you to access your own associated intentions, goals, emotions and social values (perhaps through activity of other brain areas including the limbic system) and assign them to the person you are observing.”[1]

Mirror neurons have been implicated as the basis for our capacity to learn through mimicking, our ability to understand and anticipate both the actions and intentions of others. In addition, they are believed to be the foundation of human empathy–much of which is repeated by Byrne throughout the excerpt. Not surprisingly, it has also been proposed that impaired mirror neuron function underlies autism spectrum disorders[2]. More hyperbolically, mirror neurons have also been proclaimed to be “the driving force behind the great leap forward in human evolution.” You’ll have to excuse me, but this is all starting to sound a bit, well, oxytocin-y.

Mirror neurons are the basis for “Monkey see Monkey Do”

Although it allows him to craft a neat and tidy story, Byrne’s narrow focus on mirror neurons is problematic because it disregards the skepticism surrounding both the existence and importance of mirror neurons. Originally identified in monkeys, mirror neurons have yet to be directly observed in humans, mainly because in order to do so you have to be able to stick a probe into the brain to detect single neurons. The existence of mirror neurons in humans is generally based on measurements of the activity from populations of neurons in functional magnetic resonance (fMRI) studies, which detect changes in blood flow that are correlated with neuronal activity. Regions of the human brain that “light up” in mirror neuron experiments correspond to where scientists have identified mirror neurons in monkeys. But as Dinstein et al. point out, interpreting these fMRI studies is complicated by the fact that other neurons also “light up” in regions of the brain not expected to contain mirroring activity[1]. The best we can conclude from these studies is that there are areas of the brain that look and act like a mirror neuron system.

These fMRI images reveal areas of the brain that “light up” upon seeing faces (left) or houses (right). Adapted from source.

Even employing different methods that circumvent the limitations of fMRI can prove to be complicated. Adaptation is a counterintuitive process by which the activity of neurons specific for a particular action decreases as that action is repeated. For instance, let’s say there are specific neurons that fire when you drink from a cup. As you drink more and more from a cup the activity from those “drinking-from-a-cup” neurons diminishes. Therefore, the neurons for a specific action can be revealed by looking for the neurons that exclusively lose activity in response to the action being repeated. A 2009 study from Alfonso Caramazza’s lab tried to identify mirror neurons by exploiting this phenomenon[3]. The assumption in this study was that the activity of mirror neurons would “adapt” in response to either the execution or the observation of an action as though they were equivalent. In this experiment, the action being performed or watched was a hand gesture. Adaptation was observed in scenarios where subjects only performed the gesture repeatedly or only watched the gesture repeatedly. Adaptation also occurred when subjects observed the gesture first and then performed it. However, adaptation did not happen when the subject first executed the gesture and then watched it. To Camarazza, these results called into question the existence of mirror neurons. Nevertheless, later in 2009, a study led by James Kilner that used similar techniques yielded conflicting data [4]. This time adaptation was observed when a person performed an action first and then observed it.

Assuming a mirror neuron system does exist, determining its role in the human brain presents a whole different problem. One way scientists test the importance of a component within a system is to remove it and observe the consequences. For instance, you can remove a bike chain and see that without it you wouldn’t be able to pedal the bike. Unfortunately, scientists don’t have the luxury to remove parts of the brain to see what happens. This is where studying individuals with brain injuries or disorders might be informative. As stated before, it has been suggested that mirror neurons play a vital role in our capacity to understand and anticipate the actions and intentions of others. Because one of the features of autism spectrum disorders (ASD) is misunderstanding social cues, it has been hypothesized that this could be due to dysfunctional mirror neurons. In fact, a 2006 study revealed that when test subjects were asked to imitate facial expressions of others, fMRI scans revealed less brain activity in regions associated with mirror neurons in individuals with autism spectrum disorder than in the control group [2]. However, even the links between mirror neuron dysfunction and autism are contentious. A study from 2010, revealed that regions of the brain thought to contain mirror neurons behaved similarly between people with autism and control groups[5].

In this study, test subjects were asked to imitate facial expressions of others. fMRI scans revealed less brain activity in regions associated with mirror neurons in individuals with autism spectrum disorder(b) than in the control group (a) [2].

Due to both inadequacies in imaging techniques and lack of evidence, the cognitive and empathic roles associated with mirror neurons remain speculative at best[1]. The same can be said about the role of mirror neurons in how our brains process music. Unfortunately, Byrne skimps out on any discussion of this skepticism surrounding mirror neurons. Now, I recognize that as a writer and musician, David Byrne isn’t obligated to express any scientific skepticism. To his credit he at least uses some cautious language (“proposed,” “might explain,” etc.), but absent a healthy dose of skepticism, Byrne gives mirror neurons the appearance of settled science and the sheen of a TED talk. David Byrne remains one of my favorite musicians, but not science writer. Maybe next time Byrne writes about science he’ll hear the alarms of skepticism ringing over his much sought-after silence.

(Thanks to Jerry Nguyen, Justin Kiggins, and Pascal Wallisch for their input and discussion.)

References:

1. Dinstein I, Thomas C, Behrmann M, Heeger DJ. A mirror up to nature. Curr Biol. 2008 Jan 8;18(1):R13-8. Review. Erratum in: Curr Biol. 2008 Feb 12;18(3):233. PubMed PMID: 18177704; PubMed Central PMCID: PMC2517574.

2. Dapretto M, Davies MS, Pfeifer JH, Scott AA, Sigman M, Bookheimer SY, Iacoboni M. Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders. Nat Neurosci. 2006 Jan;9(1):28-30. Epub 2005 Dec 4. PubMed PMID: 16327784.

3. Lingnau A, Gesierich B, Caramazza A. Asymmetric fMRI adaptation reveals no evidence for mirror neurons in humans. Proc Natl Acad Sci U S A. 2009 Jun 16;106(24):9925-30. Epub 2009 Jun 2. PubMed PMID: 19497880; PubMed Central PMCID: PMC2701024.

4. Kilner JM, Neal A, Weiskopf N, Friston KJ, Frith CD. Evidence of mirror neurons in human inferior frontal gyrus. J Neurosci. 2009 Aug 12;29(32):10153-9. PubMed PMID: 19675249; PubMed Central PMCID: PMC278815

5. Dinstein I, Thomas C, Humphreys K, Minshew N, Behrmann M, Heeger DJ. Normal movement selectivity in autism. Neuron. 2010 May 13;66(3):461-9. PubMed PMID: 20471358; PubMed Central PMCID: PMC2872627.

Related Reading:

While, some scientists have challenged the existence of mirror neurons, others have questioned their importance in understanding action. Greg Hickok over at TalkingBrains.org (I know, what a coincidence) has also raised the red flag that mirror neurons represent an unfalsifiable theory:

“…there is apparently no empirical result that can falsify the theory. If a mirror neuron shows up in an unexpected place, it is a new part of the mirror system. If a mirror neuron’s activity dissociates from action understanding, it was not coding understanding at that moment. If damage to the motor system doesn’t disrupt understanding, it is because that part of the motor system isn’t mirroring.”

The Sonification of Science

“If music is inherent in all things and places, then why not let music play itself? The composer, in the traditional sense, might no longer be necessary. Let the planets and spheres spin.” – David Byrne

As science becomes further entrenched in the era of Big Data, scientists are facing the increasing challenges of how to organize large data sets generated by computation and automation in useful ways. Visualization is the standard method of representing scientific information and often yields visually striking images that can help reveal patterns in the data.

“This visualization depicts the carbon dioxide from various sources that are advected individually as tracers in the atmosphere model. Carbon dioxide from the ocean is shown as plumes during Feb. 1900.
Image courtesy of Forrest Hoffman and Jamison Daniel of Oak Ridge National Laboratory.”

Recently, however, scientists have been tinkering with different ways to experience scientific data–namely, through hearing it. Scientists, often in collaboration with artists, have used these large data sets to generate music. Here’s a recent sampling of science, musically-sonified:

The Music of Microbes

 “The English Channel project involves sequencing DNA found in the seawater and trying to piece together a sense of how some of these microbial systems work. How do thevarious organisms interact with one another? How do they respond to changing conditions like temperature, nutrients, acidity? The research generates terabytes upon terabytes of data.

To turn some of it into music, Larsen mapped environmental conditions–daylight, temperature, phosphorous level–to specific chords. When the conditions change, the chords change. Then he took the microbial concentrations at each of those environmental conditions—how much of a certain type of microbe exists at a certain temperature, say—and mapped each one to a scale. The chords play in a particular scale, depending on how the environmental conditions affect the size of the microbe communities.” (read more)

Listen to the Higgs Boson

‘Vicinanza led the Higgs sonification project collaborating with Mariapaola Sorrentino of ASTRA Project (Cambridge), who contributed to the sonification process, and Giuseppe La Rocca (INFN Catania), who was in charge of  the computing framework.

“Sonification worked by attaching a musical note to each data. So, when you hear the resulting melody you really are hearing the data,” Vicinanza said.

The researchers mapped intervals between values in the original data set to interval between notes in the melody. The same numerical value was associated to the same note. As the values increased or decreased, the pitch of the notes grew or diminished accordingly.’ (read more)

Scientists translate gamma rays to music

Published Thursday on the Fermi blog, this cosmic concert came from GRB-080916C, an especially strong gamma-ray burst that NASA recorded in September 2008. To make it audible, Fermi researchers converted the GRB’s energy signature into musical notes played on a harp, a cello and a piano. They also made an animation of its photon frequency, and then paired these sights and sounds” (read more)

Related Reading:

Music from tiny particles’ movements set to debut

Scientists listen to the sun in new sonification project

Joy Division’s Iconic Album Cover Is Actually a Data Visualization

Voters also have a right to know the science behind GMOs

On November 6th, California voters will decide if foods containing genetically modified organisms (GMO) will require labeling. Prop37 argues that consumers have a right to know so that they can make informed choices regarding the foods they buy. One of the issues that scientists have with this initiative is that Prop37, as well as media coverage of GMOs, contain misleading language that distorts the science behind how GMOs are made and how safe they are for consumption. This raises, then, the question of how useful would labeling of GMO foods be if there is general public misconception of the topic.

Katie PhD explains “what exactly IS a genetically modified plant” on her blog.

Many scientists and science communicators are seizing this opportunity to educate the public about GMOs. Some are taking the opportunity to explain to the public what a GMO actually is while others are providing insight concerning the safety of GMO foods. Others are exposing flaws in a recent study that claims GMO maize causes cancer (More related links can be found in Keith Kloors’ article in Slate).


Unsurprisingly, those entering the fray can also expect to have their credibility questioned. The food industry corporations, having spent a considerable amount of money in an effort to defeat Prop37, have provided the anti-GMO/pro-labeling crowd with a convenient way to dismiss or discredit scientists defending GMOs: they are all corporate shills (or worse). This, of course, is absurd. Could industry money be swaying scientist’s stance on GMOs? Maybe. But if scientists are that easily corruptible by money, why aren’t more scientists anti-climate change? Absent polling data, it’s unclear to me where scientists fall on the issue of GMO labeling (although, you can help by filling out this survey being conducted by @Katie_PhD). Anecdotally, in my interactions with other scientists, the stances on GMO labeling are not monolithic. Some are pro, some are anti, while others are ambivalent.

The issue for most scientists, I think, is not so much the labeling requirement itself, but the distortion of information being used to justify it and how that ultimately undermines science. The difficulty of course is that scientists are trying to engage the public dispassionately about a topic the public takes very personally. In my view, I don’t think GMO foods require labeling, but I certainly respect the public’s right to vote on this issue. However, by Prop37’s logic, if the consumer has a right to know if their foods contain to GMOs so that they can make informed decisions, then the public has the right to information so they can make an informed vote. Scientists are just making sure that they are getting accurate information.

Related Reading:

How California’s GMO Labeling Law Could Limit Your Food Choices and Hurt the Poor

The transfer of genes between unrelated organisms happens. All. The. Time.

Autism in the News

Autism is coming off a big week in the news. The New York Times covered a recent study, which suggested that the risk of autism in children is linked to paternal age since older fathers pass on more mutations to their children. In another New York Times piece, this time an Op-Ed, Moises Velasquez-Manoff offers up the possibility that autism might be an autoimmune disorder. This is an idea with roots in the hygiene hypothesiswhich proposes that conditions like asthma and allergies are the result of a “bored” immune system, no longer burdened with fending off parasites (hence the hygiene), mounting an inappropriate response against the body or otherwise, unharmful, environmental substances (e.g. pollen). Lastly, there was the announcement of an FDA-approved trial using stem cells as a therapy for autism. In a week when headlines were dominated by autism, here were my favorite reads that offered some balance and insight:

On the Paternal Age and Autism linkVirginia Hughes gives us the “Top 3 Reasons to Stop Fretting About Being an Old Dad,” while Seth Mnookin writes about an overlooked implication of this study–“that the genetic health of the species is now facing a serious threat.” With regard to the stem cell trial for autism, Youssef Rizk explores how the design of the trial sidesteps ethical complications by using the patient’s own cord blood stem cell, and Kathleen Raven, rather than simply calling the trial a “cure,” explains the hypothesis being tested in the trial and the, “study’s primary goal…assessing changes in patients’ speaking and understanding of vocabulary.” As for Velaquez Manoff’s Op-Ed piece on autism as an autoimmune disease, Jonathan Eisen laments the “lack of a discussion of the distinction between correlation and causation.” And finally, Emily Willingham, in her critique, isn’t quite buying what Velaquez-Manoff is selling:

“From the headline to the final paragraphs focused on using parasitic worms to treat or even prevent autism, the science as Velasquez-Manoff presents it is limited at best, and frequently unsourced and unreferenced. Where a source is given or traceable, the conclusions are overstated or cherry-picked.”