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The Backstreet Boys sing genetics (not really) but their latest album is called "DNA"
Other that the promotional artwork, cover art and the title, the Backstreet Boys pop band does not seem to have taken science or DNA (deoxyribonucleic acid)/genetics to heart in their latest oeuvre. As for what chickens have to do with it, I I gather this is some sort of humorous nod to a past hit song. Still, I am weirdly fascinated by this January 25, 2019 video news item on Billboard,
Having looked at the list of songs on the DNA album (they're listed in the Billboard news item where they've embedded audio samples), I can't find anything that suggests an interest in genetics but perhaps you can: Don't Go Breaking My Heart? Nobody Else? Breathe? New Love? Passionate? Is It Just Me? Chances? No Place? Chateau? The Way It Was? Just Like You Like it? OK? Anyone who can figure out how the songs relate to DNA, please let me know in the Comments.
Frankly, that's as much analysis as I can offer on the topic. Thankfully, Karen James (an independent educator, researcher, and consultant in molecular biology) has written a February 5, 2019 article (I Want DNA That Way; The Backstreet Boys' new album and tour features a very old-school depiction of DNA) for slate.com where she unpacks the imagery in the promotional material and on the cover (Note: Links have been removed),
The Backstreet Boys are back. Credit: Dennis Leupold [downloaded from https://slate.com/technology/2019/02/backstreet-boys-dna-album-cover-gene-sequencing.html]
The Backstreet Boys released a new album. I never thought I'd start a science article—or any article—with that sentence, but here we are.
We are here because the promotional artwork for the album (above) is a photograph of the boy band (man band?) lit by a projection of DNA bands. The image, and the album's title, DNA, jumped out of my Twitter timeline because I'm a geneticist, I work with DNA, and I've seen countless images just like it in textbooks and research articles. I've even made them myself in the lab.
What struck me as funny (both funny-ha-ha and funny-odd) is that the lab methods that could have produced this image are old—older even than the Backstreet Boys' first album. One of the methods—called Sanger sequencing—was published in 1977, making it even older than two of the Backstreet Boys themselves, scientist Kristy Lamb pointed out. Genetics is a particularly fast-moving science. New technologies are constantly emerging and eclipsing prior ones. Yet this 40-year-old imagery persists, and not just in the promotional artwork for DNA. Just do a Google image search for "DNA sequencing" and you'll see plenty of images like this mixed in with the double helices and long GATTACA readouts.
After her description of Sanger sequencing James offers another 'sequencing' possibility, almost as old as the Sanger technique,
Careful readers might have noticed that I suggested there was more than one method that produces images like this. At first glance, I thought the projection in the Backstreet Boys' publicity photo was modified from an image made with Sanger sequencing. But when I looked again in preparation for writing this article, I had second thoughts. Why aren't the lanes clustered in groups of four? Why are some of the bands in adjacent lanes the same size? (They shouldn't be if you're doing Sanger sequencing.) It could be that the photo was heavily modified with individual lanes copied and pasted. Indeed, some of the lanes are even identical to each other (*suppresses fake ivory tower scoff*).
Or it could be that this image was made with another old method: DNA fingerprinting. Made famous in so many crime TV shows, DNA fingerprinting was invented in 1984 by Alec Jeffreys, who, though he did not win a Nobel Prize, was made a knight of the British Empire for his contribution to science, among many other prestigious awards, which is nice.
I suspect the Backstreet Boys weren't going for a tongue-in-cheek reference to their own advancing age. While today's DNA sequencing methods produce images that scarcely resemble those produced by Sanger sequencing and DNA fingerprinting, the old-school imagery is still everywhere. The Backstreet Boys' promotional team probably just went with a stock image that looked compelling and worked well as a projection.
James returns to her theme, why use imagery associated with outdated techniques? (Note: Links have been removed),
But that doesn't answer the real question: Why is 40-year-old imagery still so ubiquitous? As science writer and editor Stephanie Keep tweeted, one reason may be that, despite its age, the Sanger method is still taught in high school classrooms: "It's so visual and intuitive." It's true. When I teach students about DNA sequencing, I always start with Sanger sequencing and use that as the basis for explaining newer technologies, adding more complexity as I go, following the historical timeline.
Another reason the old imagery is still in use may be that the images produced by newer, so-called next-generation sequencing methods aren't visually scored by a scientist sitting at a lab bench, but by computers. As such, the images themselves often go unseen by human eyes [emphasis mine], despite their colorful beauty.
Interesting, eh? The latest imagery is not seen by human eyes. So the newest imagery is intended for machines. James presents an example of the 'new' imagery,
An image generated using a next-generation DNA sequencing method.. Credit: Illumina [downloaded from https://slate.com/technology/2019/02/backstreet-boys-dna-album-cover-gene-sequencing.html]
According to James, this image was not easily obtained according to one of her tweets. [https://twitter.com/kejames/status/1092888034322845696] So, big thanks to Illumina (there's also a Wikipedia entry about the company). Getting back to James' and her article, she asks why the band titled their latest album, DNA,
But why did the Backstreet Boys call their album DNA in the first place? The official RCA Records press release announcing the album says, "BSB analyzed their individual DNA profiles to see what crucial element each member represents in the groups DNA." It links to a YouTube video that supposedly explains "how their individual strains, when brought together, create the unstoppable and legendary Backstreet Boys."
The video is a futuristic, spy movie–esque montage, complete with a computerized female voice describing the various characteristics of each Backstreet Boy. Reader, I confess: I cringed. There were so many tropes and misconceptions about DNA packed into the 83-second video, I would have to write a follow-up to this just to explore them. The cringeworthiness doesn't end there, though. The cover of DNA has each Backstreet Boy on his own spiral staircase.
The staircases are surely meant to evoke the structure of DNA: the famous double helix. But there's a problem, as the social media account for the journal Genome Biology tweeted: The staircases are spiraling in the wrong direction. DNA is usually right-handed. If you stick out your right thumb, your fingers will naturally curl in a right-handed spiral as you move your hand in the direction your thumb is pointing. The Backstreet Boys' staircases are left-handed.
Here's the promotional trailer for DNA,
It's everything James says it is. As for those wrongly spiraling DNA staircases,
RCA Records [downloaded from https://slate.com/technology/2019/02/backstreet-boys-dna-album-cover-gene-sequencing.html]
Thank you to Karen James for this illuminating article. If you have time, I encourage you to read her piece in its entirety:
I Want DNA That Way; The Backstreet Boys' new album and tour features a very old-school depiction of DNA.
As for why the Backstreet Boys called their album DNA and you likely guessed. it would seem to be a promotional gimmick meant to leverage the perceived interest in commercial DNA testing by companies such as 23andMe and Ancestry, amongst others.
This entry was posted in Music, pop culture, science and tagged Alec Jeffreys, Backstreet Boys (BSB), Dennis Leupold, deoxyribonucleic acid, DNA, DNA (album), DNA fingerprinting, DNA sequencing, double-helix, Genetics, I Want DNA That Way; The Backstreet Boys' new album and tour features a very old-school depiction of DNA, Illumina, Karen James, Kristy Lamb, Sanger sequencing, Stephanie Keep on February 5, 2019 by Maryse de la Giroday.
Diatoms show off their nanofabrication skills
Base-pairing properties of DNA were used to construct tiny structures that accumulated a silica outer skeleton similar to shell-building organisms known as diatoms. Credit: Yan Lab. [downloaded from https://phys.org/news/2018-07-single-celled-architects-nanotechnology.html]
The gif below isn't quite so pretty as the image above but it's both an example of the kind of imagery (lots of grey), that scientists routinely work with and it shows the work in more detail,
3D cube made using DNA Origami Silicification (DOS), which deposits a fine layer of silica onto the DNA origami framework. Credit: Yan Lab [downloaded from https://phys.org/news/2018-07-single-celled-architects-nanotechnology.html]
A July 16, 2018 news item on phys.org describes the 'diatom' work,
Diatoms are tiny, unicellular creatures, inhabiting oceans, lakes, rivers, and soils. Through their respiration, they produce close to a quarter of the oxygen on earth, nearly as much as the world's tropical forests. In addition to their ecological success across the planet, they have a number of remarkable properties. Diatoms live in glasslike homes of their own design, visible under magnification in an astonishing and aesthetically beautiful range of forms.
Researchers have found inspiration in these microscopic, jewel-like products of nature since their discovery in the late 18th century. In a new study, Arizona State University (ASU) scientists led by Professor Hao Yan, in collaboration with researchers from the Shanghai Institute of Applied Physics of the Chinese Academy of Sciences and Shanghai Jiaotong University led by Prof. Chunhai Fan, have designed a range of diatom-like nanostructures.
To achieve this, they borrow techniques used by naturally-occurring diatoms to deposit layers of silica—the primary constituent in glass—in order to grow their intricate shells. Using a technique known as DNA origami, the group designed nanoscale platforms of various shapes to which particles of silica, drawn by electrical charge, could stick.
A July 16, 2018 ASU news release (also on EurekAlert) by Richard Harth, which originated the news item, provides more detail,
The new research demonstrates that silica deposition can be effectively applied to synthetic, DNA-based architectures, improving their elasticity and durability. The work could ultimately have far-reaching applications in new optical systems, semiconductor nanolithography, nano-electronics, nano-robotics and medical applications, including drug delivery.
Researchers like Yan and Fan create sophisticated nanoarchitectures in 2- and 3-dimensions, using DNA as a building material. The method, known as DNA origami, relies on the base-pairing properties of DNA's four nucleotides, whose names are abbreviated A,T,C and G.
The ladder-like structure of the DNA double-helix is formed when complementary strands of nucleotides bond with each other—the C nucleotides always pairing with Gs and the As always pairing with Ts. This predictable behavior can be exploited in order to produce a virtually limitless variety of engineered shapes, which can be designed in advance. The nanostructures then self-assemble in a test tube.
In the new study, researchers wanted to see if architectures designed with DNA, each measuring just billionths of a meter in diameter, could be used as structural frameworks on which diatom-like exoskeletons composed of silica could grow in a precise and controllable manner. Their successful results show the power of this hybrid marriage of nature and nanoengineering, which the authors call DNA Origami Silicification (DOS).
"Here, we demonstrated that the right chemistry can be developed to produce DNA-silica hybrid materials that faithfully replicate the complex geometric information of a wide range of different DNA origami scaffolds. Our findings established a general method for creating biomimetic silica nanostructures," said Yan.
Among the geometric DNA frameworks designed and constructed in the experiments were 2D crosses, squares, triangles and DOS-diatom honeycomb shapes as well as 3D cubes, tetrahedrons, hemispheres, toroid and ellipsoid forms, occurring as single units or lattices.
Once the DNA frameworks were complete, clusters of silica particles carrying a positive charge were drawn electrostatically to the surfaces of the electrically negative DNA shapes, accreting over a period of several days, like fine paint applied to an eggshell. A series of transmission- and scanning electron micrographs were made of the resulting DOS forms, revealing accurate and efficient diatom-like silicification.
The method proved effective for silicification of framelike, curved and porous nanostructures ranging in size from 10-1000 nanometers, (the largest structures are roughly the size of bacteria). Precise control over silica shell thickness is achieved simply by regulating the duration of growth.
The hybrid DOS-diatom nanostructures were initially characterized using a pair of powerful tools capable of unveiling their tiny forms, Transmission Electron Microscopy (TEM) and Atomic Force Microscopy (AFM). The resulting images reveal much clearer outlines for the nanostructures after the deposition of silica.
The method of nanofabrication is so precise, researchers were able to produce triangles, squares and hexagons with uniform pores measuring less than 10 nm in diameter—by far the smallest achieved to date, using DNA origami lithography. Further, the technique outlined in the new study equips researchers with more accurate control over the construction of 3D nanostructures in arbitrary forms that are often challenging to produce through existing methods.
One property of natural diatoms of great interests to nanoengineers like Yan and Fan is the specific strength of their silica shells. Specific strength refers to a material's resistance to breakage relative to its density. Scientists have found that the silica architectures of diatoms are not only inspiringly elegant but exceptionally tough. Indeed, the silica exoskeletons enveloping diatoms have the highest specific strength of any biologically produced material, including bone, antlers, and teeth.
In the current study, researchers used AFM to measure the resistance to breakage of their silica-augmented DNA nanostructures. Like their natural counterparts, these forms showed far greater strength and resilience, displaying a 10-fold increase in the forces they could withstand, compared with the unsilicated designs, while nevertheless retaining considerable flexibility.
The study also shows that the enhanced rigidity of DOS nanostructures increases with their growth time. As the authors note, these results are in agreement with the characteristic mechanical properties of biominerals produced by nature, coupling impressive durability with flexibility.
A final experiment involved the design of a new 3D tetrahedral nanostructure using gold nanorods as supportive struts for a DOS fabricated device. This novel structure was able to faithfully retain its shape compared with a similar structure lacking silication that deformed and collapsed.
The research opens a pathway for nature-inspired innovations in nanotechnology in which DNA architectures act as templates that may be coated with silica or perhaps other inorganic materials, including calcium phosphate, calcium carbonate, ferric oxide or other metal oxides, yielding unique properties.
"We are interested in developing methods to create higher order hybrid nanostructures. For example, multi-layered/multi-component hybrid materials may be achieved by a stepwise deposition of different materials to further expand the biomimetic diversity," said Fan.
Such capabilities will open up new opportunities to engineer highly programmable solid-state nanopores with hierarchical features, new porous materials with designed structural periodicity, cavity and functionality, plasmonic and meta-materials. The bio-inspired and biomimetic approach demonstrated in this paper represents a general framework for use with inorganic device nanofabrication that has arbitrary 3D shapes and functions and offers diverse potential applications in fields such as nano-electronics, nano-photonics, and nano-robotics.
Complex silica composite nanomaterials templated with DNA origami by Xiaoguo Liu, Fei Zhang, Xinxin Jing, Muchen Pan, Pi Liu, Wei Li, Bowen Zhu, Jiang Li, Hong Chen, Lihua Wang, Jianping Lin, Yan Liu, Dongyuan Zhao, Hao Yan, & Chunhai Fan. Nature (2018) DOI: https://doi.org/10.1038/s41586-018-0332-7 Published 16 July 2018
This entry was posted in biomimcry, electronics, medicine, nanophotonics, nanotechnology, robots and tagged 3D cube made with DNA Origami Silicification (DOS), atomic force microscopy (AFM), bio-inspired, biomimetic, biomimetic silica nanostructures, Bowen Zhu, China, Chinese Academy of Sciences, Chunhai Fan, Complex silica composite nanomaterials templated with DNA origami, deoxyribonucleic acid, diatom-like exoskeletons, diatom-like nanostructures, diatoms, DNA, DNA origami, DNA origami framework. Arizona State University (ASU), DNA origami lithography, DNA Origami Silicification (DOS), Dongyuan Zhao, Fei Zhang, glass, gold nanorods, Hao Yan, Hong Chen, hybrid DOS-diatom nanostructure, Jiang Li, Jianping Lin, Lihua Wang, Muchen Pan, nanofabrication, nanorobotics, Pi Liu, Richard Harth, Shanghai Institute of Applied Physics, Shanghai Jiaotong University, silica, silica deposition, silica shells, synthetic DNA-based architectures, transmission electron microscopy (TEM), US, Wei Li, Xiaoguo Liu, Xinxin Jing, Yan Liu on January 30, 2019 by Maryse de la Giroday.
Why not monetize your DNA for 2019?
I'm not a big fan of DNA (deoxyribonucleic acid) companies that promise to tell you about your ancestors and, depending on the kit, predisposition to certain health issues as per their reports about your genetic code. (I regularly pray no one in my family has decided to pay one of these companies to analyze their spit.)
During Christmas season 2018, the DNA companies (23andMe and Ancestry) advertised special prices so you could gift someone in your family with a kit. All this corporate largesse may not be wholly in service of the Christmas spirit. After all, there's money to be made once they've gotten your sample.
Monetizing your DNA in 2016
I don't know when 23andMe started selling DNA information or if any similar company predated their efforts but this June 21, 2016 article by Antonio Regalado for MIT (Massachusetts Institute of Technology) Review offers the earliest information I found,
"Welcome to You." So says the genetic test kit that 23andMe will send to your home. Pay $199, spit in a tube, and several weeks later you'll get a peek into your DNA. Have you got the gene for blond hair? Which of 36 disease risks could you pass to a child?
Run by entrepreneur Anne Wojcicki, the ex-wife of Google founder Sergey Brin, and until last year housed alongside the Googleplex, the company created a test that has been attacked by regulators and embraced by a curious public. It remains, nine years after its introduction, the only one of its kind sold directly to consumers. 23andMe has managed to amass a collection of DNA information about 1.2 million people, which last year began to prove its value when the company revealed it had sold access to the data to more than 13 drug companies. One, Genentech, anted up $10 million for a look at the genes of people with Parkinson's disease.
That means 23andMe is monetizing DNA rather the way Facebook makes money from our "likes." What's more, it gets its customers to pay for the privilege. That idea so appeals to investors that they have valued the still-unprofitable company at over $1 billion. "Money follows data," says Barbara Evans, a legal scholar at the University of Houston, who studies personal genetics. "It takes a lot of labor and capital to get that information in a form that is useful."
Monetizing your DNA in 2018 and privacy concerns
Starting with Adele Peters' December 13, 2018 article for Fast Company (Note: A link has been removed),
When 23andMe made a $300 million deal with GlaxoSmithKline [GSK] in July[2018]–so the pharmaceutical giant could access a vast store of genetic data as it works on new drugs–the consumers who actually provided that data didn't get a cut of the proceeds. A new health platform is taking a different approach: If you choose to share your own DNA data or other health records, you'll get company shares that will later pay you dividends if that data is sold.
Before getting to the start-up that would allow you rather than a company to profit or at least somewhat monetize your DNA, I'm including a general overview of the July 2018 GSK/23andMe deal in Jamie Ducharme's July 26, 2018 article for TIME (Note: Links have been removed),
Consumer genetic testing company 23andMe announced on Wednesday [July 25, 2018] that GlaxoSmithKline purchased a $300 million stake in the company, allowing the pharmaceutical giant to use 23andMe's trove of genetic data to develop new drugs — and raising new privacy concerns for consumers
The "collaboration" is a way to make "novel treatments and cures a reality," 23andMe CEO Anne Wojcicki said in a company blog post. But, though it isn't 23andMe's first foray into drug discovery, the deal doesn't seem quite so simple to some medical experts — or some of the roughly 5 million 23andMe customers who have sent off tubes of their spit in exchange for ancestry and health insights
Perhaps the most obvious issue is privacy, says Peter Pitts, president of the Center for Medicine in the Public Interest, a non-partisan non-profit that aims to promote patient-centered health care.
"If people are concerned about their social security numbers being stolen, they should be concerned about their genetic information being misused," Pitts says. "This information is never 100% safe. The risk is magnified when one organization shares it with a second organization. When information moves from one place to another, there's always a chance for it to be intercepted by unintended third parties.
That risk is real, agrees Dr. Arthur Caplan, head of the division of medical ethics at the New York University School of Medicine. Caplan says that any genetic privacy concerns also extend to your blood relatives, who likely did not consent to having their DNA tested — echoing some of the questions that arose after law enforcement officials used a genealogy website to find and arrest the suspected Golden State Killer in April [2018].
"A lot of people paid money to 23andMe to get their ancestry determined — fun, recreational stuff," Caplan says. "Even though they may have signed a thing saying, 'I'm okay if you use this information for medical research,' I'm not sure they understood what that really meant. I'm not sure they understood that it meant, 'Yes, we'll go to Glaxo, and that's where we're really going to make a lot of money off of you.'"
A 23andMe spokesperson told TIME that data privacy is a "top priority" for the company, emphasizing that customer data isn't used in research without consent, and that GlaxoSmithKline will only receive "summary statistics from analyses 23andMe conducts so that no single individual can be identified."
Yes the data is supposed to be stripped of identifying information but given how many times similar claims about geolocation data have been disproved, I am skeptical. DJ Pangburn's September 26, 2017 article (Even This Data Guru Is Creeped Out By What Anonymous Location Data Reveals About Us) for Fast Company illustrate the fragility of 'anonymized data',
… as a number of studies have shown, even when it's "anonymous," stripped of so-called personally identifiable information, geographic data can help create a detailed portrait of a person and, with enough ancillary data, identify them by name
Curious to see this kind of data mining in action, I emailed Gilad Lotan, now vice president of BuzzFeed's data science team. He agreed to look at a month's worth of two different users' anonymized location data, and to come up with individual profiles that were as accurate as possible
The results, produced in just a few days' time, range from the expected to the surprisingly revealing, and demonstrate just how "anonymous" data can identify individuals.
Last fall Lotan taught a class at New York University on surveillance that kicked off with an assignment like the one I'd given him: link anonymous location data with other data sets–from LinkedIn, Facebook, home registration and mortgage records, and other online data.
"It's not hard to figure out who this [unnamed] person is," says Lotan. In class, students found that tracking location data around holidays proved to be the easiest way to determine who, exactly, the data belonged to. "Basically," he says, "visits to private homes that are owned and publicly registered."
In 2013, researchers at MIT and the Université Catholique de Louvain in Belgium published a paper reporting on 15 months of study of human mobility data for over 1.5 million individuals. What they found is that only four spatio-temporal points are required to "uniquely identify 95% of the individuals." The researchers concluded that there was very little privacy even in raw location data. Four years later, their calls for policies rectifying concerns about location tracking have fallen largely on deaf ears.
Getting back to DNA, there was also some concern at Fox News,
Other than warnings, I haven't seen much about any possible legislation regarding DNA and privacy in either Canada or the US.
Now, let's get to how you can monetize your self.
Me making money off me
I've found two possibilities for an individual who wants to consider monetizing their own DNA.
Health shares
Adele Peters' December 13, 2018 article describes a start-up company and the model they're proposing to allow you profit from your own DNA (Note: Links have been removed),
"You can't say data is valuable and then take that data away from everybody," says Dawn Barry, president and cofounder of LunaPBC, the public benefit corporation that manages the community-owned platform, called LunaDNA, which recently got SEC approval to recognize health data as currency. "What we're finding is that [our early adopters are] very excited about the transparency of this model–that when we all come together and create value, that value flows down to the individuals who shared their data.
The platform shares some anonymized data with nonprofits, such as foundations that study rare diseases. In that case, money wouldn't initially change hands, but "there could be intellectual property that at some point in time is monetized, and the community would share in that," says Bob Kain, CEO and cofounder of LunaPBC. "When we have enough data in the near future, then we'll work with pharmaceutical companies, for instance, to drive discovery for those companies. And they will pay market rates.
The company doesn't offer DNA analysis itself, but chose to focus on data management. If you've sent a tube of spit to 23andMe, AncestryDNA, MyHeritage, or FamilyTree DNA, you can contribute that data to LunaDNA and get shares. (If you'd rather not let the original testing company keep your data, you can also separately take the steps to delete it.
"We looked at a number of different models to enable people to have ownership, including cryptocurrency, which is a proxy for ownership, too," says Kain. "Cryptocurrency is hard to understand for most people, and right now, the regulatory landscape is blurry. So we thought, to move forward, we'd go with something much more traditional and easy to understand, and that is stock shares, basically.
For sharing targeted genes, you get 10 shares. For sharing your whole genome, you get 300 shares. At the moment, that's not worth very much–the valuation takes into account the risk that the data might not be monetized, and the fact that the startup isn't the exclusive owner of your data. The SEC filing says that the estimated fair market value of a whole genome is only $21. Some other health information is worth far less; 20 days of data from a fitness tracker garners two shares, valued at 14¢. But as more people contribute data, the research value of the whole database (and dividends) will increase. If the shareholders ever decided to sell the company itself, they would also make money that way.
Luna's is a very interesting approach and I encourage you to read the December 13, 2018 article in its entirety.
Blockchain and crypto me
At least one effort to introduce blockchain/cryptocurrency technology to the process for monetizing your DNA garnered a lot of attention in February 2018.
A February 8, 2018 article by Eric Rosenbaum for CNBC (a US cable tv channel) explores an effort by George Church (Note: Links have been removed),
It's probably wise to be skeptical of anyone who says they have a new idea for a blockchain-based company, or worse still, a company changing its business model to focus on the crypto world. That ice tea company that shifted its model to the blockchain, or Kodak saying its road back to riches was managing photo rights using a blockchain system. Raise eyebrow, or move directly onto outright shake of head
However, when a world renown Harvard geneticist announces he's launching a blockchain-based start-up, it merits some attention. And it's not the crypto-angle itself that might make you do a double-take, but the assets that will be managed, and exchanged, using digital currency: your DNA
Harvard University genetics guru George Church — one of the scientists at the forefront of the CRISPR genetic engineering revolution — announced on Wednesday a start-up, Nebula Genomics, that will use the blockchain to not only allow individuals to share their personal genome for research purposes, but retain ownership and monetize their DNA through trading of a custom digital currency.
The genomics revolution has been exponentially advanced by drastic reductions in cost. As Nebula noted in a white paper explaining its business model, the first human genome was sequenced in 2001 at a cost of $3 billion. Today, human genome sequencing costs less than $1,000, and in a few years the price will drop below $100
In fact, some big Silicon Valley start-ups, led by 23andMe, have capitalized on this rapid advance and already offer personal DNA testing kits for around $100 (sometimes with discounts even less)
Nebula took direct aim at 23andMe in its white paper, and one reason why it can offer genetic testing for less
"Today, 23andMe (23andme.com) and Ancestry (ancestry.com) are the two leading personal genomics companies. Both use DNA microarray-based genotyping for their genetic tests. It is an outdated and significantly less powerful alternative to DNA sequencing. Instead of sequencing continuous stretches of DNA, genotyping identifies single letters spaced at approximately regular intervals across the genome. …
Outdated genetic tests? Interesting, eh? Zoë Corbyn provides more information about Church's plans in her February 18, 2018 article for the Guardian,
"Under the current system, personal genomics companies effectively own your personal genomics data, and you don't see any benefit at all," says Grishin [Dennis Grishin, Nebula co-founder]. "We want to eliminate the middleman.
Although the aim isn't to provide a get-rich-quick scheme, the company believes there is potential for substantial returns. Though speculative, its modelling suggests that someone in the US could earn up to 50 times the cost of sequencing their genome – about $50,000 at current rates – taking into account both what could be made from a lifetime of renting out their genetic data, and reductions in medical bills if the results throw up a potentially preventable disease
The startup also thinks it can solve the problem of the dearth of genetic data researchers have to draw on, due to individuals – put off by cost or privacy concerns – not getting sequenced.
Payouts when you grant access to your genome would come in the form of Nebula tokens, the company's cryptocurrency, and companies would need to buy tokens from the startup to pay people whose data they wanted to access. Though the value of a token is yet to be set and the number of tokens defined, it might, for example, take one Nebula token to get your genome sequenced. An individual new to the system could begin to earn fractions of a token by taking part in surveys about their heath posted by prospective data buyers. When someone had earned enough, they could get sequenced and begin renting out their data and amassing tokens. Alternatively, if an individual wasn't yet sequenced they may find data buyers willing to pay for or subsidise their genome sequencing in exchange for access to it. "Potentially you wouldn't have to pay out of pocket for the sequencing of your genome," says Grishin.
In all cases, stress Grishin and Obbad [Kamal Obbad, Nebula co-founder], the sequence would belong to the individual, so they could rent it out over and over, including to multiple companies simultaneously. And the data buyer would never take ownership or possession of it – rather, it would be stored by the individual (for example in their computer or on their Dropbox account) with Nebula then providing a secure computation platform on which the data buyer could compute on the data. "You stay in control of your data and you can share it securely with who you want to," explains Obbad. Nebula makes money not by taking any transaction fee but by being a participant providing computing and storage services. The cryptocurrency would be able to be cashed out for real money via existing cryptocurrency exchanges.
Hopefully, Luna and Nebula, as well as, any competitors in this race to allow individuals to monetize their own DNA will have excellent security.
For the curious, you can find Luna here and Nebula here.Note: I am not endorsing either company or any others mentioned here. This posting is strictly informational.
This entry was posted in business, science and tagged 23andMe, Adele Peters, Ancestry, Anne Wojcicki, Antonio Regalado, Arthur Caplan, blockchain, Bob Kain, cryptocurrency, Dawn Barry, Dennis Grishin, deoxyribonucleic acid, DJ Pangburn, DNA, DNA microarray-based genotyping, DNA sequencing, Eric Rosenbaum, Even This Data Guru Is Creeped Out By What Anonymous Location Data Reveals About Us, FamilyTree DNA, George Church, Gilad Lotan, GlaxoSmithKline (GSK), Google, Jamie Ducharme, Kamal Obbad, LunaDNA, LunaPBC, MyHeritage, Sergey Brin, Zoë Corbyn on January 14, 2019 by Maryse de la Giroday.
Café Scientifique Vancouver (Canada) talk on August 28th 2018: Getting the message: What is gene expression and why does it matter?
Here's more about the latest Café Scientifique talk from an August 22, 2018 announcement received via email,
Our next café will happen on TUESDAY, AUGUST 28TH at 7:30PM in the back
room at YAGGER'S DOWNTOWN (433 W Pender [St., Vancouver]). Our speaker for the
evening will be DR. KATIE MARSHALL from the Department of Zoology at
UBC [University of British Columbia]. Her topic will be:
GETTING THE MESSAGE: WHAT IS GENE EXPRESSION AND WHY DOES IT MATTER?
Many of us think that DNA is like a light switch; you have a particular
sequence of base pairs or a particular chromosome, and these directly
cause a large change in biological functioning. But the truth is that
any given gene can be up or downregulated through a dizzying array of
biochemical "dimmer switches" that finely control how much that
particular gene is expressed. Understanding how this works is key to
answering questions like "How does a sequence of base pairs in DNA
become a whole organism?" and "Why is it that every cell has the
same DNA sequence but different function?". We'll chat about the
advances in computing needed to answer these questions, the importance
of gene expression in disease, and how this science can help us
understand social issues better too.
I wasn't able to find out too much more about Dr. Katie but there is this profile page on the UBC Zoology Department website,
The long-term goal of my research is to understand how abiotic stress filters through physiology to shape species abundance and distribution. While abiotic stressors such as temperature have been used very successfully to predict population growth, distribution, and diversity of insect species, integration of the mechanisms of how these stressors are experienced by individuals from alteration of physiology through to fitness impacts has lagged. Inclusion of these mechanisms is crucial for accurate modelling predictions of individual (and therefore population-level) responses. My research to date has focused on how the impact of frequency of stress (rather than the duration or intensity of stress) is a superior predictor of both survival and reproductive success , and used insect cold tolerance as a model system.
At UBC I'll be focusing on the cold tolerance and cryobiology of invertebrates in the intertidal. These organisms face freezing stress through the winter, yet remarkably little is known about how they do so. I'll also be investigating plasticity in cold tolerance by looking for interactive effects of ocean acidification and community composition on thermal tolerance.
This entry was posted in environment, science communication, Vancouver and tagged abiotic stress, abiotic stressors, Cafe Scientifique, chromosomes, cold tolerance, cryobiology, deoxyribonucleic acid, disease, DNA, gene expression, Getting the message: What is gene expression and why does it matter?, human biology, insect cold tolerance, intertidal, invertebrates, Katie Marshall, marine environment, ocean acidification, Physiology, plasticity in cold tolerance, temperature, thermal tolerance, UBC, University of British Columbia on August 23, 2018 by Maryse de la Giroday.
Being smart about using artificial intelligence in the field of medicine
Since my August 20, 2018 post featured an opinion piece about the possibly imminent replacement of radiologists with artificial intelligence systems and the latest research about employing them for diagnosing eye diseases, it seems like a good time to examine some of the mythology embedded in the discussion about AI and medicine.
Imperfections in medical AI systems
An August 15, 2018 article for Slate.com by W. Nicholson Price II (who teaches at the University of Michigan School of Law; in addition to his law degree he has a PhD in Biological Sciences from Columbia University) begins with the peppy, optimistic view before veering into more critical territory (Note: Links have been removed),
For millions of people suffering from diabetes, new technology enabled by artificial intelligence promises to make management much easier. Medtronic's Guardian Connect system promises to alert users 10 to 60 minutes before they hit high or low blood sugar level thresholds, thanks to IBM Watson, "the same supercomputer technology that can predict global weather patterns." Startup Beta Bionics goes even further: In May, it received Food and Drug Administration approval to start clinical trials on what it calls a "bionic pancreas system" powered by artificial intelligence, capable of "automatically and autonomously managing blood sugar levels 24/7."
An artificial pancreas powered by artificial intelligence represents a huge step forward for the treatment of diabetes—but getting it right will be hard. Artificial intelligence (also known in various iterations as deep learning and machine learning) promises to automatically learn from patterns in medical data to help us do everything from managing diabetes to finding tumors in an MRI to predicting how long patients will live. But the artificial intelligence techniques involved are typically opaque. We often don't know how the algorithm makes the eventual decision. And they may change and learn from new data—indeed, that's a big part of the promise. But when the technology is complicated, opaque, changing, and absolutely vital to the health of a patient, how do we make sure it works as promised?
Price describes how a 'closed loop' artificial pancreas with AI would automate insulin levels for diabetic patients, flaws in the automated system, and how companies like to maintain a competitive advantage (Note: Links have been removed),
[…] a "closed loop" artificial pancreas, where software handles the whole issue, receiving and interpreting signals from the monitor, deciding when and how much insulin is needed, and directing the insulin pump to provide the right amount. The first closed-loop system was approved in late 2016. The system should take as much of the issue off the mind of the patient as possible (though, of course, that has limits). Running a close-loop artificial pancreas is challenging. The way people respond to changing levels of carbohydrates is complicated, as is their response to insulin; it's hard to model accurately. Making it even more complicated, each individual's body reacts a little differently.
Here's where artificial intelligence comes into play. Rather than trying explicitly to figure out the exact model for how bodies react to insulin and to carbohydrates, machine learning methods, given a lot of data, can find patterns and make predictions. And existing continuous glucose monitors (and insulin pumps) are excellent at generating a lot of data. The idea is to train artificial intelligence algorithms on vast amounts of data from diabetic patients, and to use the resulting trained algorithms to run a closed-loop artificial pancreas. Even more exciting, because the system will keep measuring blood glucose, it can learn from the new data and each patient's artificial pancreas can customize itself over time as it acquires new data from that patient's particular reactions.
Here's the tough question: How will we know how well the system works? Diabetes software doesn't exactly have the best track record when it comes to accuracy. A 2015 study found that among smartphone apps for calculating insulin doses, two-thirds of the apps risked giving incorrect results, often substantially so. … And companies like to keep their algorithms proprietary for a competitive advantage, which makes it hard to know how they work and what flaws might have gone unnoticed in the development process.
There's more,
These issues aren't unique to diabetes care—other A.I. algorithms will also be complicated, opaque, and maybe kept secret by their developers. The potential for problems multiplies when an algorithm is learning from data from an entire hospital, or hospital system, or the collected data from an entire state or nation, not just a single patient. …
The [US Food and Drug Administraiont] FDA is working on this problem. The head of the agency has expressed his enthusiasm for bringing A.I. safely into medical practice, and the agency has a new Digital Health Innovation Action Plan to try to tackle some of these issues. But they're not easy, and one thing making it harder is a general desire to keep the algorithmic sauce secret. The example of IBM Watson for Oncology has given the field a bit of a recent black eye—it turns out that the company knew the algorithm gave poor recommendations for cancer treatment but kept that secret for more than a year. …
While Price focuses on problems with algorithms and with developers and their business interests, he also hints at some of the body's complexities.
Can AI systems be like people?
Susan Baxter, a medical writer with over 20 years experience, a PhD in health economics, and author of countless magazine articles and several books, offers a more person-centered approach to the discussion in her July 6, 2018 posting on susanbaxter.com,
The fascination with AI continues to irk, given that every second thing I read seems to be extolling the magic of AI and medicine and how It Will Change Everything. Which it will not, trust me. The essential issue of illness remains perennial and revolves around an individual for whom no amount of technology will solve anything without human contact. …
But in this world, or so we are told by AI proponents, radiologists will soon be obsolete. [my August 20, 2018 post] The adaptational learning capacities of AI mean that reading a scan or x-ray will soon be more ably done by machines than humans. The presupposition here is that we, the original programmers of this artificial intelligence, understand the vagaries of real life (and real disease) so wonderfully that we can deconstruct these much as we do the game of chess (where, let's face it, Big Blue ate our lunch) and that analyzing a two-dimensional image of a three-dimensional body, already problematic, can be reduced to a series of algorithms.
Attempting to extrapolate what some "shadow" on a scan might mean in a flesh and blood human isn't really quite the same as bishop to knight seven. Never mind the false positive/negatives that are considered an acceptable risk or the very real human misery they create.
Moravec called it
It's called Moravec's paradox, the inability of humans to realize just how complex basic physical tasks are – and the corresponding inability of AI to mimic it. As you walk across the room, carrying a glass of water, talking to your spouse/friend/cat/child; place the glass on the counter and open the dishwasher door with your foot as you open a jar of pickles at the same time, take a moment to consider just how many concurrent tasks you are doing and just how enormous the computational power these ostensibly simple moves would require.
Researchers in Singapore taught industrial robots to assemble an Ikea chair. Essentially, screw in the legs. A person could probably do this in a minute. Maybe two. The preprogrammed robots took nearly half an hour. And I suspect programming those robots took considerably longer than that.
Ironically, even Elon Musk, who has had major production problems with the Tesla cars rolling out of his high tech factory, has conceded (in a tweet) that "Humans are underrated."
I wouldn't necessarily go that far given the political shenanigans of Trump & Co. but in the grand scheme of things I tend to agree. …
Is AI going the way of gene therapy?
Susan draws a parallel between the AI and medicine discussion with the discussion about genetics and medicine (Note: Links have been removed),
On a somewhat similar note – given the extent to which genetics discourse has that same linear, mechanistic tone [as AI and medicine] – it turns out all this fine talk of using genetics to determine health risk and whatnot is based on nothing more than clever marketing, since a lot of companies are making a lot of money off our belief in DNA. Truth is half the time we don't even know what a gene is never mind what it actually does; geneticists still can't agree on how many genes there are in a human genome, as this article in Nature points out.
Along the same lines, I was most amused to read about something called the Super Seniors Study, research following a group of individuals in their 80's, 90's and 100's who seem to be doing really well. Launched in 2002 and headed by Angela Brooks Wilson, a geneticist at the BC [British Columbia] Cancer Agency and SFU [Simon Fraser University] Chair of biomedical physiology and kinesiology, this longitudinal work is examining possible factors involved in healthy ageing.
Turns out genes had nothing to do with it, the title of the Globe and Mail article notwithstanding. ("Could the DNA of these super seniors hold the secret to healthy aging?" The answer, a resounding "no", well hidden at the very [end], the part most people wouldn't even get to.) All of these individuals who were racing about exercising and working part time and living the kind of life that makes one tired just reading about it all had the same "multiple (genetic) factors linked to a high probability of disease". You know, the gene markers they tell us are "linked" to cancer, heart disease, etc., etc. But these super seniors had all those markers but none of the diseases, demonstrating (pretty strongly) that the so-called genetic links to disease are a load of bunkum. Which (she said modestly) I have been saying for more years than I care to remember. You're welcome.
The fundamental error in this type of linear thinking is in allowing our metaphors (genes are the "blueprint" of life) and propensity towards social ideas of determinism to overtake common sense. Biological and physiological systems are not static; they respond to and change to life in its entirety, whether it's diet and nutrition to toxic or traumatic insults. Immunity alters, endocrinology changes, – even how we think and feel affects the efficiency and effectiveness of physiology. Which explains why as we age we become increasingly dissimilar.
If you have the time, I encourage to read Susan's comments in their entirety.
Scientific certainties
Following on with genetics, gene therapy dreams, and the complexity of biology, the June 19, 2018 Nature article by Cassandra Willyard (mentioned in Susan's posting) highlights an aspect of scientific research not often mentioned in public,
One of the earliest attempts to estimate the number of genes in the human genome involved tipsy geneticists, a bar in Cold Spring Harbor, New York, and pure guesswork.
That was in 2000, when a draft human genome sequence was still in the works; geneticists were running a sweepstake on how many genes humans have, and wagers ranged from tens of thousands to hundreds of thousands. Almost two decades later, scientists armed with real data still can't agree on the number — a knowledge gap that they say hampers efforts to spot disease-related mutations.
In 2000, with the genomics community abuzz over the question of how many human genes would be found, Ewan Birney launched the GeneSweep contest. Birney, now co-director of the European Bioinformatics Institute (EBI) in Hinxton, UK, took the first bets at a bar during an annual genetics meeting, and the contest eventually attracted more than 1,000 entries and a US$3,000 jackpot. Bets on the number of genes ranged from more than 312,000 to just under 26,000, with an average of around 40,000. These days, the span of estimates has shrunk — with most now between 19,000 and 22,000 — but there is still disagreement (See 'Gene Tally').
… the inconsistencies in the number of genes from database to database are problematic for researchers, Pruitt says. "People want one answer," she [Kim Pruitt, a genome researcher at the US National Center for Biotechnology Information {NCB}] in Bethesda, Maryland] adds, "but biology is complex."
I wanted to note that scientists do make guesses and not just with genetics. For example, Gina Mallet's 2005 book 'Last Chance to Eat: The Fate of Taste in a Fast Food World' recounts the story of how good and bad levels of cholesterol were established—the experts made some guesses based on their experience. That said, Willyard's article details the continuing effort to nail down the number of genes almost 20 years after the human genome project was completed and delves into the problems the scientists have uncovered.
In addition to opaque processes with developers/entrepreneurs wanting to maintain their secrets for competitive advantages and in addition to our own poor understanding of the human body (how many genes are there anyway?), there are same major gaps (reflected in AI) in our understanding of various diseases. Angela Lashbrook's August 16, 2018 article for The Atlantic highlights some issues with skin cancer and shade of your skin (Note: Links have been removed),
… While fair-skinned people are at the highest risk for contracting skin cancer, the mortality rate for African Americans is considerably higher: Their five-year survival rate is 73 percent, compared with 90 percent for white Americans, according to the American Academy of Dermatology.
As the rates of melanoma for all Americans continue a 30-year climb, dermatologists have begun exploring new technologies to try to reverse this deadly trend—including artificial intelligence. There's been a growing hope in the field that using machine-learning algorithms to diagnose skin cancers and other skin issues could make for more efficient doctor visits and increased, reliable diagnoses. The earliest results are promising—but also potentially dangerous for darker-skinned patients.
… Avery Smith, … a software engineer in Baltimore, Maryland, co-authored a paper in JAMA [Journal of the American Medical Association] Dermatology that warns of the potential racial disparities that could come from relying on machine learning for skin-cancer screenings. Smith's co-author, Adewole Adamson of the University of Texas at Austin, has conducted multiple studies on demographic imbalances in dermatology. "African Americans have the highest mortality rate [for skin cancer], and doctors aren't trained on that particular skin type," Smith told me over the phone. "When I came across the machine-learning software, one of the first things I thought was how it will perform on black people."
Recently, a study that tested machine-learning software in dermatology, conducted by a group of researchers primarily out of Germany, found that "deep-learning convolutional neural networks," or CNN, detected potentially cancerous skin lesions better than the 58 dermatologists included in the study group. The data used for the study come from the International Skin Imaging Collaboration, or ISIC, an open-source repository of skin images to be used by machine-learning algorithms. Given the rise in melanoma cases in the United States, a machine-learning algorithm that assists dermatologists in diagnosing skin cancer earlier could conceivably save thousands of lives each year.
… Chief among the prohibitive issues, according to Smith and Adamson, is that the data the CNN relies on come from primarily fair-skinned populations in the United States, Australia, and Europe. If the algorithm is basing most of its knowledge on how skin lesions appear on fair skin, then theoretically, lesions on patients of color are less likely to be diagnosed. "If you don't teach the algorithm with a diverse set of images, then that algorithm won't work out in the public that is diverse," says Adamson. "So there's risk, then, for people with skin of color to fall through the cracks."
As Adamson and Smith's paper points out, racial disparities in artificial intelligence and machine learning are not a new issue. Algorithms have mistaken images of black people for gorillas, misunderstood Asians to be blinking when they weren't, and "judged" only white people to be attractive. An even more dangerous issue, according to the paper, is that decades of clinical research have focused primarily on people with light skin, leaving out marginalized communities whose symptoms may present differently.
The reasons for this exclusion are complex. According to Andrew Alexis, a dermatologist at Mount Sinai, in New York City, and the director of the Skin of Color Center, compounding factors include a lack of medical professionals from marginalized communities, inadequate information about those communities, and socioeconomic barriers to participating in research. "In the absence of a diverse study population that reflects that of the U.S. population, potential safety or efficacy considerations could be missed," he says.
Adamson agrees, elaborating that with inadequate data, machine learning could misdiagnose people of color with nonexistent skin cancers—or miss them entirely. But he understands why the field of dermatology would surge ahead without demographically complete data. "Part of the problem is that people are in such a rush. This happens with any new tech, whether it's a new drug or test. Folks see how it can be useful and they go full steam ahead without thinking of potential clinical consequences. …
Improving machine-learning algorithms is far from the only method to ensure that people with darker skin tones are protected against the sun and receive diagnoses earlier, when many cancers are more survivable. According to the Skin Cancer Foundation, 63 percent of African Americans don't wear sunscreen; both they and many dermatologists are more likely to delay diagnosis and treatment because of the belief that dark skin is adequate protection from the sun's harmful rays. And due to racial disparities in access to health care in America, African Americans are less likely to get treatment in time.
I'll add one thing to Price's article, Susan's posting, and Lashbrook's article about the issues with AI , certainty, gene therapy, and medicine—the desire for a happy ending prefaced with an easy solution. If the easy solution isn't possible accommodations will be made but that happy ending is a must. All disease will disappear and there will be peace on earth. (Nod to Susan Baxter and her many discussions with me about disease processes and happy endings.)
The solutions, for the most part, are seen as technological despite the mountain of evidence suggesting that technology reflects our own imperfect understanding of health and disease therefore providing what is at best an imperfect solution.
Also, we tend to underestimate just how complex humans are not only in terms of disease and health but also with regard to our skills, understanding, and, perhaps not often enough, our ability to respond appropriately in the moment.
There is much to celebrate in what has been accomplished: no more black death, no more smallpox, hip replacements, pacemakers, organ transplants, and much more. Yes, we should try to improve our medicine. But, maybe alongside the celebration we can welcome AI and other technologies with a lot less hype and a lot more skepticism.
This entry was posted in medicine, robots and tagged Adewole Adamson, African-Americans, AI, Andrew Alexis, Angela Brooks Wilson, Angela Lashbrook, artificial intelligence (AI), artificial intelligence algorithms, artificial intelligence systems, artificial pancreas, Avery Smith, bionic pancreas system, cancerous skin lesions, Cassandra Willyard, cholesterol, close-loop artificial pancreas, darker-skinned patients, data, deep learning, deep-learning convolutional neural networks (CNN), demographic imbalances in dermatology, deoxyribonucleic acid, dermatology, diabetes, diagnosing eye diseases, DNA, European Bioinformatics Institute (EBI), Ewan Birney, fair-skinned people, FDA, finding tumors, GeneSweep contest, Germany, Gina Mallet, glucose monitors, Guardian Connect system, health risk, human genome sequence, IBM Watson, IBM Watson for Oncology, illness, insulin pump, insulin pumps, International Skin Imaging Collaboration (ISIC), Kim Pruitt, Last Chance to Eat: The Fate of Taste in a Fast Food World, machine learning, machine learning algorithms, machine learning software, magnetic resonance imaging, medical AI systems, Medtronic, melanoma, Moravec's paradox, MRI, race, radiologists, skin cancer, Super Seniors Study, Susan Baxter, University of Texas at Austin, US, US Food and Drug Administration, US National Center for Biotechnology Information (NCB), W. Nicholson Price II on August 21, 2018 by Maryse de la Giroday.
The CRISPR ((clustered regularly interspaced short palindromic repeats)-CAS9 gene-editing technique may cause new genetic damage kerfuffle
Not unexpectedly, CRISPR-Cas9 or clustered regularly interspaced short palindromic repeats-CRISPR-associated protein 9 can be dangerous as these scientists note in a July 16, 2018 news item on phys.org,
Scientists at the Wellcome Sanger Institute have discovered that CRISPR/Cas9 gene editing can cause greater genetic damage in cells than was previously thought. These results create safety implications for gene therapies using CRISPR/Cas9 in the future as the unexpected damage could lead to dangerous changes in some cells.
Reported today (16 July 2018) in the journal Nature Biotechnology, the study also revealed that standard tests for detecting DNA changes miss finding this genetic damage, and that caution and specific testing will be required for any potential gene therapies.
This CRISPR-Cas9 image reminds me of popcorn,
CRISPR-associated protein Cas9 (white) from Staphylococcus aureus based on Protein Database ID 5AXW. Credit: Thomas Splettstoesser (Wikipedia, CC BY-SA 4.0)[ downloaded from https://phys.org/news/2018-07-genome-crisprcas9-gene-higher-thought.html#jCp]
A July 16, 2018 Wellcome Sanger Institute press release (also on EurekAlert), which originated the news item, offers a little more explanation,
CRISPR/Cas9 is one of the newest genome editing tools. It can alter sections of DNA in cells by cutting at specific points and introducing changes at that location. Already extensively used in scientific research, CRISPR/Cas9 has also been seen as a promising way to create potential genome editing treatments for diseases such as HIV, cancer or sickle cell disease. Such therapeutics could inactivate a disease-causing gene, or correct a genetic mutation. However, any potential treatments would have to prove that they were safe.
Previous research had not shown many unforeseen mutations from CRISPR/Cas9 in the DNA at the genome editing target site. To investigate this further the researchers carried out a full systematic study in both mouse and human cells and discovered that CRISPR/Cas9 frequently caused extensive mutations, but at a greater distance from the target site.
The researchers found many of the cells had large genetic rearrangements such as DNA deletions and insertions. These could lead to important genes being switched on or off, which could have major implications for CRISPR/Cas9 use in therapies. In addition, some of these changes were too far away from the target site to be seen with standard genotyping methods.
Prof Allan Bradley, corresponding author on the study from the Wellcome Sanger Institute, said: "This is the first systematic assessment of unexpected events resulting from CRISPR/Cas9 editing in therapeutically relevant cells, and we found that changes in the DNA have been seriously underestimated before now. It is important that anyone thinking of using this technology for gene therapy proceeds with caution, and looks very carefully to check for possible harmful effects."
Michael Kosicki, the first author from the Wellcome Sanger Institute, said: "My initial experiment used CRISPR/Cas9 as a tool to study gene activity, however it became clear that something unexpected was happening. Once we realised the extent of the genetic rearrangements we studied it systematically, looking at different genes and different therapeutically relevant cell lines, and showed that the CRISPR/Cas9 effects held true."
The work has implications for how CRISPR/Cas9 is used therapeutically and is likely to re-spark researchers' interest in finding alternatives to the standard CRISPR/Cas9 method for gene editing.
Prof Maria Jasin, an independent researcher from Memorial Slone Kettering Cancer Centre, New York, who was not involved in the study said: "This study is the first to assess the repertoire of genomic damage arising at a CRISPR/Cas9 cleavage site. While it is not known if genomic sites in other cell lines will be affected in the same way, this study shows that further research and specific testing is needed before CRISPR/Cas9 is used clinically."
For anyone who'd like to better understand the terms gene editing and CRISPR-Cas9, the Wellcome Sanger Institute provides these explanatory webpages, What is genome editing? and What is CRISPR-Cas9?
For the more advanced, here's a link and a citation for the paper,
Repair of double-strand breaks induced by CRISPR–Cas9 leads to large deletions and complex rearrangements by Michael Kosicki, Kärt Tomberg, & Allan Bradley. Nature Biotechnology DOI: https://doi.org/10.1038/nbt.4192 Published 16 July 2018
The kerfuffle
It seems this news has affected the CRISPR market. From a July 16, 2018 article by Cale Guthrie Weissman for Fast Company,
… CRISPR could unknowingly delete or alter non-targeted genes, which could lead to myriad unintended consequences. This is especially frightening, since the technology is going to be used in human clinical trials.
Meanwhile, other scientists working with CRISPR are trying to downplay the findings, telling STAT [a life sciences and business journalism website] that there have been no reported adverse effects similar to what the study describes. The news, however, has brought about a market reaction–at least three publicly traded companies that focus on CRISPR-based therapies are in stock nosedive. Crispr Therapeutics is down by over 6%; Editas fell by over 3%; and Intellia Therapeutics dropped by over 5%. [emphasis mine]
Gaetan Burgio (geneticist, Australian National University) in a July 16, 2018 essay on phys.org (originating from The Conversation) suggests some calm (Note: Links have been removed),
But a new study has called into question the precision of the technique [CRISPR gene editing technology].
The hope for gene editing is that it will be able to cure and correct diseases. To date, many successes have been reported, including curing deafness in mice, and in altering cells to cure cancer.
Some 17 clinical trials in human patients are registered [emphasis mine] testing gene editing on leukaemias, brain cancers and sickle cell anaemia (where red blood cells are misshaped, causing them to die). Before implementing CRISPR technology in clinics to treat cancer or congenital disorders, we must address whether the technique is safe and accurate.
There are a few options for getting around this problem. One option is to isolate the cells we wish to edit from the body and reinject only the ones we know have been correctly edited.
For example, lymphocytes (white blood cells) that are crucial to killing cancer cells could be taken out of the body, then modified using CRISPR to heighten their cancer-killing properties. The DNA of these cells could be sequenced in detail, and only the cells accurately and specifically gene-modified would be selected and delivered back into the body to kill the cancer cells.
While this strategy is valid for cells we can isolate from the body, some cells, such as neurons and muscles, cannot be removed from the body. These types of cells might not be suitable for gene editing using Cas9 scissors.
Fortunately, researchers have discovered other forms of CRISPR systems that don't require the DNA to be cut. Some CRISPR systems only cut the RNA, not the DNA (DNA contains genetic instructions, RNA convey the instructions on how to synthesise proteins).
As RNA [ribonucleic acid] remains in our cells only for a specific period of time before being degraded, this would allow us to control the timing and duration of the CRISPR system delivery and reverse it (so the scissors are only functional for a short period of time).
This was found to be successful for dementia in mice. Similarly, some CRISPR systems simply change the letters of the DNA, rather than cutting them. This was successful for specific mutations causing diseases such as hereditary deafness in mice.
I agree with Burgio's conclusion (not included here) that we have a lot more to learn and I can't help wondering why there are 17 registered human clinical trials at this point.
This entry was posted in medicine, risk, science, synthetic biology and tagged Allan Bradley, Australian National University, Cale Guthrie Weissman, cancer, cells, clustered regularly interspaced short palindromic repeats-CRISPR-associated protein 9, CRISPR (clustered regularly interspaced short palindromic repeats), CRISPR Therapeutics, CRISPR-Cas9, CRISPR/Cas9 gene editing, deoxyribonucleic acid, DNA, Editas, Gaetan Burgio, gene editing, genetic damage, genome editing tools, genome editing treatments, HIV, Intellia, Kärt Tomberg, Maria Jasin, Memorial Slone Kettering Cancer Centre, Michael Kosicki, Repair of double-strand breaks induced by CRISPR–Cas9 leads to large deletions and complex rearrangements, ribonucleic acid, RNA, sickle cell disease, UK, unforeseen mutations, Wellcome Sanger Institute, What is CRISPR-Cas9?, What is genome editing? on July 17, 2018 by Maryse de la Giroday.
CRISPR-Cas12a as a new diagnostic tool
Similar to Cas9, Cas12a is has an added feature as noted in this February 15, 2018 news item on ScienceDaily,
Utilizing an unsuspected activity of the CRISPR-Cas12a protein, researchers created a simple diagnostic system called DETECTR to analyze cells, blood, saliva, urine and stool to detect genetic mutations, cancer and antibiotic resistance and also diagnose bacterial and viral infections. The scientists discovered that when Cas12a binds its double-stranded DNA target, it indiscriminately chews up all single-stranded DNA. They then created reporter molecules attached to single-stranded DNA to signal when Cas12a finds its target.
A February 15, 2018 University of California at Berkeley (UC Berkeley) news release by Robert Sanders and which originated the news item, provides more detail and history,
CRISPR-Cas12a, one of the DNA-cutting proteins revolutionizing biology today, has an unexpected side effect that makes it an ideal enzyme for simple, rapid and accurate disease diagnostics.
(iStock)
Cas12a, discovered in 2015 and originally called Cpf1, is like the well-known Cas9 protein that UC Berkeley's Jennifer Doudna and colleague Emmanuelle Charpentier turned into a powerful gene-editing tool in 2012.
CRISPR-Cas9 has supercharged biological research in a mere six years, speeding up exploration of the causes of disease and sparking many potential new therapies. Cas12a was a major addition to the gene-cutting toolbox, able to cut double-stranded DNA at places that Cas9 can't, and, because it leaves ragged edges, perhaps easier to use when inserting a new gene at the DNA cut.
But co-first authors Janice Chen, Enbo Ma and Lucas Harrington in Doudna's lab discovered that when Cas12a binds and cuts a targeted double-stranded DNA sequence, it unexpectedly unleashes indiscriminate cutting of all single-stranded DNA in a test tube.
Most of the DNA in a cell is in the form of a double-stranded helix, so this is not necessarily a problem for gene-editing applications. But it does allow researchers to use a single-stranded "reporter" molecule with the CRISPR-Cas12a protein, which produces an unambiguous fluorescent signal when Cas12a has found its target.
"We continue to be fascinated by the functions of bacterial CRISPR systems and how mechanistic understanding leads to opportunities for new technologies," said Doudna, a professor of molecular and cell biology and of chemistry and a Howard Hughes Medical Institute investigator.
The new DETECTR system based on CRISPR-Cas12a can analyze cells, blood, saliva, urine and stool to detect genetic mutations, cancer and antibiotic resistance as well as diagnose bacterial and viral infections. Target DNA is amplified by RPA to make it easier for Cas12a to find it and bind, unleashing indiscriminate cutting of single-stranded DNA, including DNA attached to a fluorescent marker (gold star) that tells researchers that Cas12a has found its target.
The UC Berkeley researchers, along with their colleagues at UC San Francisco, will publish their findings Feb. 15 [2018] via the journal Science's fast-track service, First Release.
The researchers developed a diagnostic system they dubbed the DNA Endonuclease Targeted CRISPR Trans Reporter, or DETECTR, for quick and easy point-of-care detection of even small amounts of DNA in clinical samples. It involves adding all reagents in a single reaction: CRISPR-Cas12a and its RNA targeting sequence (guide RNA), fluorescent reporter molecule and an isothermal amplification system called recombinase polymerase amplification (RPA), which is similar to polymerase chain reaction (PCR). When warmed to body temperature, RPA rapidly multiplies the number of copies of the target DNA, boosting the chances Cas12a will find one of them, bind and unleash single-strand DNA cutting, resulting in a fluorescent readout.
The UC Berkeley researchers tested this strategy using patient samples containing human papilloma virus (HPV), in collaboration with Joel Palefsky's lab at UC San Francisco. Using DETECTR, they were able to demonstrate accurate detection of the "high-risk" HPV types 16 and 18 in samples infected with many different HPV types.
"This protein works as a robust tool to detect DNA from a variety of sources," Chen said. "We want to push the limits of the technology, which is potentially applicable in any point-of-care diagnostic situation where there is a DNA component, including cancer and infectious disease."
The indiscriminate cutting of all single-stranded DNA, which the researchers discovered holds true for all related Cas12 molecules, but not Cas9, may have unwanted effects in genome editing applications, but more research is needed on this topic, Chen said. During the transcription of genes, for example, the cell briefly creates single strands of DNA that could accidentally be cut by Cas12a.
The activity of the Cas12 proteins is similar to that of another family of CRISPR enzymes, Cas13a, which chew up RNA after binding to a target RNA sequence. Various teams, including Doudna's, are developing diagnostic tests using Cas13a that could, for example, detect the RNA genome of HIV.
(Infographic by the Howard Hughes Medical Institute)
These new tools have been repurposed from their original role in microbes where they serve as adaptive immune systems to fend off viral infections. In these bacteria, Cas proteins store records of past infections and use these "memories" to identify harmful DNA during infections. Cas12a, the protein used in this study, then cuts the invading DNA, saving the bacteria from being taken over by the virus.
The chance discovery of Cas12a's unusual behavior highlights the importance of basic research, Chen said, since it came from a basic curiosity about the mechanism Cas12a uses to cleave double-stranded DNA.
"It's cool that, by going after the question of the cleavage mechanism of this protein, we uncovered what we think is a very powerful technology useful in an array of applications," Chen said.
CRISPR-Cas12a target binding unleashes indiscriminate single-stranded DNase activity by Janice S. Chen, Enbo Ma, Lucas B. Harrington, Maria Da Costa, Xinran Tian, Joel M. Palefsky, Jennifer A. Doudna. Science 15 Feb 2018: eaar6245 DOI: 10.1126/science.aar6245
This entry was posted in medicine and tagged antibiotic resistance, blood, cancer, Cas12a, Cas13a, Cas9 protein, cells, Cpf1, CRISPR enzymes, CRISPR-Cas12a protein, CRISPR-Cas12a target binding unleashes indiscriminate single-stranded DNase activity, CRISPR-Cas9, deoxyribonucleic acid, DETECTR, diagnostic system, DNA, DNA Endonuclease Targeted CRISPR Trans Reporter (DETECTR), Emmanuelle Charpentier, Enbo Ma, gene editing, genetic mutations, human papilloma virus (HPV), isothermal amplification system, Janice Chen, Janice S. Chen, Jennifer A. Doudna, Jennifer Doudna, Joel M. Palefsky, Joel Palefsky, Lucas B. Harrington, Lucas Harrington, Maria Da Costa, polymerase chain reaction (PCR), recombinase polymerase amplification (RPA), ribonucleic acid, RNA, Robert Sanders, saliva, single-stranded DNA, stool, targeted double-stranded DNA sequence, UC Berkeley, UC San Francisco, University of California at Berkeley, University of California at San Francisco, urine, US, Xinran Tian on May 17, 2018 by Maryse de la Giroday.
Cloaking devices made from DNA and gold nanoparticles using top-down lithography
This new technique seems promising but there've been a lot of 'cloaking' devices announced in the years I've been blogging and, in all likelihood, I was late to the party so I'm exercising a little caution before getting too excited. For the latest development in cloaking devices, there's a January 18, 2018 news item on Nanowerk,
Northwestern University researchers have developed a first-of-its-kind technique for creating entirely new classes of optical materials and devices that could lead to light bending and cloaking devices — news to make the ears of Star Trek's Spock perk up.
Using DNA [deoxyribonucleic acid] as a key tool, the interdisciplinary team took gold nanoparticles of different sizes and shapes and arranged them in two and three dimensions to form optically active superlattices. Structures with specific configurations could be programmed through choice of particle type and both DNA-pattern and sequence to exhibit almost any color across the visible spectrum, the scientists report.
A January 18, 2018 Northwestern University news release (also on EurekAlert) by Megan Fellman, which originated the news item, delves into more detail (Note: Links have been removed),
"Architecture is everything when designing new materials, and we now have a new way to precisely control particle architectures over large areas," said Chad A. Mirkin, the George B. Rathmann Professor of Chemistry in the Weinberg College of Arts and Sciences at Northwestern. "Chemists and physicists will be able to build an almost infinite number of new structures with all sorts of interesting properties. These structures cannot be made by any known technique."
The technique combines an old fabrication method — top-down lithography, the same method used to make computer chips — with a new one — programmable self-assembly driven by DNA. The Northwestern team is the first to combine the two to achieve individual particle control in three dimensions.
The study was published online by the journal Science today (Jan. 18). Mirkin and Vinayak P. Dravid and Koray Aydin, both professors in Northwestern's McCormick School of Engineering, are co-corresponding authors.
Scientists will be able to use the powerful and flexible technique to build metamaterials — materials not found in nature — for a range of applications including sensors for medical and environmental uses.
The researchers used a combination of numerical simulations and optical spectroscopy techniques to identify particular nanoparticle superlattices that absorb specific wavelengths of visible light. The DNA-modified nanoparticles — gold in this case — are positioned on a pre-patterned template made of complementary DNA. Stacks of structures can be made by introducing a second and then a third DNA-modified particle with DNA that is complementary to the subsequent layers.
In addition to being unusual architectures, these materials are stimuli-responsive: the DNA strands that hold them together change in length when exposed to new environments, such as solutions of ethanol that vary in concentration. The change in DNA length, the researchers found, resulted in a change of color from black to red to green, providing extreme tunability of optical properties.
"Tuning the optical properties of metamaterials is a significant challenge, and our study achieves one of the highest tunability ranges achieved to date in optical metamaterials," said Aydin, assistant professor of electrical engineering and computer science at McCormick.
"Our novel metamaterial platform — enabled by precise and extreme control of gold nanoparticle shape, size and spacing — holds significant promise for next-generation optical metamaterials and metasurfaces," Aydin said.
The study describes a new way to organize nanoparticles in two and three dimensions. The researchers used lithography methods to drill tiny holes — only one nanoparticle wide — in a polymer resist, creating "landing pads" for nanoparticle components modified with strands of DNA. The landing pads are essential, Mirkin said, since they keep the structures that are grown vertical.
The nanoscopic landing pads are modified with one sequence of DNA, and the gold nanoparticles are modified with complementary DNA. By alternating nanoparticles with complementary DNA, the researchers built nanoparticle stacks with tremendous positional control and over a large area. The particles can be different sizes and shapes (spheres, cubes and disks, for example).
"This approach can be used to build periodic lattices from optically active particles, such as gold, silver and any other material that can be modified with DNA, with extraordinary nanoscale precision," said Mirkin, director of Northwestern's International Institute for Nanotechnology.
Mirkin also is a professor of medicine at Northwestern University Feinberg School of Medicine and professor of chemical and biological engineering, biomedical engineering and materials science and engineering in the McCormick School.
The success of the reported DNA programmable assembly required expertise with hybrid (soft-hard) materials and exquisite nanopatterning and lithographic capabilities to achieve the requisite spatial resolution, definition and fidelity across large substrate areas. The project team turned to Dravid, a longtime collaborator of Mirkin's who specializes in nanopatterning, advanced microscopy and characterization of soft, hard and hybrid nanostructures.
Dravid contributed his expertise and assisted in designing the nanopatterning and lithography strategy and the associated characterization of the new exotic structures. He is the Abraham Harris Professor of Materials Science and Engineering in McCormick and the founding director of the NUANCE center, which houses the advanced patterning, lithography and characterization used in the DNA-programmed structures.
Building superlattices from individual nanoparticles via template-confined DNA-mediated assembly by Qing-Yuan Lin, Jarad A. Mason, Zhongyang, Wenjie Zhou, Matthew N. O'Brien, Keith A. Brown, Matthew R. Jones, Serkan Butun, Byeongdu Lee, Vinayak P. Dravid, Koray Aydin, Chad A. Mirkin. Science 18 Jan 2018: eaaq0591 DOI: 10.1126/science.aaq0591
As noted earlier, it could be a while before cloaking devices are made available. In the meantime, you may find this image inspiring,
Caption: Northwestern University researchers have developed a new method to precisely arrange nanoparticles of different sizes and shapes in two and three dimensions, resulting in optically active superlattices. Credit: Northwestern University
This entry was posted in environment, medicine, nanotechnology and tagged Building superlattices from individual nanoparticles via template-confined DNA-mediated assembly, Byeongdu Lee, Chad A. Mirkin, cloaking devices, deoxyribonucleic acid, DNA, gold nanoparticles, Jarad A. Mason, Keith A. Brown, Koray Aydin, light bending devices, Matthew N. O'Brien, Matthew R. Jones, Megan Fellman, metamaterials, nanoparticle superlattices, Northwestern University, optical materials, optically active superlattices, programmable self-assembly driven by DNA, Qing-Yuan Lin, Serkan Butun, Spock, Star Trek, top-down lithography, Vinayak P. Dravid, Wenjie Zhou, Zhongyang on April 11, 2018 by Maryse de la Giroday.


EAST HARTFORD >> A 51-year-old man has died after he was hit by a car in Connecticut.
Police say the man was crossing a street Monday night in East Hartford when he was struck.
He was taken to a hospital with serious injuries, but was later pronounced dead.
Police tell WFSB-TV that the driver of the car involved in the crash remained on the scene and is cooperating with the investigation. At this point, no charges have been filed.


We have been building quality audio turntables for over 35 years now, which makes us one of the oldest manufacturers still in business. The GyroDec turntable has been around for over 25 years, and even its first incarnation can still be upgraded to the latest status. Michell turntables are precision instruments, built to last, and to reproduce sound as close as possible to the mastertape.
Making a turntable...The task of a turntable seems to be simple. At audio frequencies, the arm should be kept locked above the groove, without any extraneous motion relative to the cartridge. And the groove should be dragged at a constant angular speed underneath the stylus. This means that over the whole frequency band of 10Hz up to 20kHz and beyond, the whole loop made by record, platter, bearing, (sub)chassis, arm board, tone arm, and cartridge body should behave in an utterly rigid and non-resonant fashion. Any flexure of the same dimensions as the microscopic undulations in the groove detracts from sonic fidelity. At lower-than-audio frequencies, the arm should be made able to freely follow the groove's warps and excentricities, so as not to damage LP or cartridge, and this without inducing any spurious signals into the cartridge's generator. Only when these demands are fulfilled can the stylus trace the actual information embedded in the record's groove walls. A simple task, you said?
The platter should be supported so that it can revolve smoothly, without any extraneous vibrations and motion. This is the job for the main bearing, the very heart of a turntable.
The LP/cartridge/arm trio is to reside on its own 'island'. The suspension decouples them from the outside world with its motor noise, footfall, acoustic vibrations, and other potential disturbances. All of our turntables, except the TecnoDec, suspend the heavy subchassis and platter from three extension springs. This is an elegant and self-stabilising solution as the center of gravity of the floating mass is conveniently put below the suspension points. Rocking and nodding modes of the subchassis are hence discouraged, while overall turntable setup is straightforward, and drift is virtually inexistent. In addition, the total suspended mass of about eleven kilograms ensures that any incoupled energy can not result in large displacements. The spring towers double as the actual turntable supports, terminated in heavy aluminium cones. The towers are sectioned in two vertical parts, making a high-pressure point-contact with a bearing ball. This makes for a true three point support, which gives the springs and the suspended subchassis a firm reference to ground. The floating chassis' task is to keep the bearing and arm board rigidly in relation to each other. It is a heavy and rigid cast aluminium component, internally strengthened with beams and ribs. The Orbe and Orbe SE benefit from an additional layer of DensoDamp mastic which results in an acoustically inert subchassis with excellent self-damping properties. Offering a wide range of custom-made arm boards, we can keep the mass, and the mass-distribution, of the subchassis, platter, and arm a known constant. This translates into a suspended chassis turntable that works optimally with almost any existing tone arm. Off-the-shelf boards can be delivered for the following tone arms: Michell, Rega, SME (both types), Graham, Wilson-benesch, Morch, Origin-Live, and Linn. Others can be made to order.
The most obvious task of a turntable is to keep the record at a constant and precise angular speed, without low-rate drift, without audible wow, and without high-frequency noise components which detract from the music's delicacy. The 3.5 kg heavy platter, precision balanced, acts as a large flywheel. The Orbe's platter is made of three GyroDec platters bonded together to form one massive slab of acrylic. The GyroDec and Gyro SE employ a single-thickness acrylic platter, loaded with the gold-plated brass weights which over time have become Michell's signature. Once up to speed, and aided by the low-friction bearing, the platter only wants to maintain its motion, and not much extra input from the motor is needed. This motor is a very precise, reliable, and low-noise DC motor that has been selected only after extensive listening sessions and reliability tests. The Orbe models use a version of the same motor with a tacho speed control loop back to the supply. With all turntables the motor is a stand-alone unit, housed in a heavy base of metal (almost 3kg for the Orbe), to elimate vibrational breakthrough to the turntable. The HR and Orbe Controller NC supplies effectively isolate the motor from the potentially poluted mains network. Drive is relayed to the platter via a precision-ground soft round-section neoprene belt, which runs around the platter's circumference. This results in a very high reduction of noise transfer from the motor.


Episode 782 of One Piece has been released and the fans gave it a good response. The excitement of the fans has shot up for the upcoming episode. They are eagerly waiting for the next segment to arrive.
Though the filler arc was used in the previous series of the episodes in which the chase and hurdles for stealing food from the marine base by Luffy and his teammate were shown. But in new the episode of One Piece, a new interesting turn will begin.
From episode 783, the Whole Cake Island arc will be shown. This arc will twenty-ninth arc of the series One Piece and the second arc in Yonko Saga.
In the upcoming events, Luffy will be seen saving Sanji from the trap of Big Mom. Big Mom is after Sanji and Luffy know that. As from the previous episode, we encountered that Sanji is all set to marry Big Mom's daughter, Lady Pudding. But Luffy wants to stop him from doing that. It will be very interesting to see Sanji and his team facing the challenges while saving the cook of the Straw Hat Pirates.
The twisted point in the story will be Sanji falling madly in love with Lady Pudding and this will become a problem for Luffy as he is trying to stop Sanji to change is mind and going back to his weakness for love. He wants to save him from doing the same mistake again. Also, many visuals are also released by studios behind the series which give us some vague idea about the latest arc in the story.
The videos show Sanji getting angry on Luffy and about to kick which shows he is going against him at some point in this arc. The fans will also finally get to see Luffy going against a Yonko in next episodes.
One Piece episode 783 will be aired on April 9, 2017. Finally, the viewers will get to some new interesting turn of events in the former series.
One Piece Chapter 929 Release Date and Manga Spoilers: Is the new character a thief?


Named by chefs "the Kobe beef of pork": find out where to source the prized Mangalitsa pork, whether direct from the farms or at Michelin restaurants.
James Sharman and his One Star House Party travelling restaurant pop up will pitch up at Everest base camp in December. Find out how you can be there.
Aska in New York has been awarded two Michelin stars barely a month after opening – see the dishes.
The Michelin Guide to New York 2017 has been leaked early – see the full list.
Wondering how to use caviar? Try these elegant recipes perfect for entertaining. Plus, don't miss a video tutorial for making chocolate caviar!
A new gadget turns home composting into a mere 24-hour process – find out how it works.