Genetics  

CRISPR gene drives allow scientists to change sequences of DNA and make that the resulting edited genetic trait is inherited by future generations, opening up the possibility of altering entire species forever. More than anything, the technology has led to questions: How will this new power affect humanity? What are we going to use it to change?

CRISPR genetic engineering now gives scientists the ability to change sequences of DNA and guarantee that the resulting edited genetic trait is inherited by future generations, opening up the possibility of altering entire species forever. More than anything, the technology has led to questions: How will this new power affect humanity? What are we going to use it to change?

At a recent TED talk, Jennifer Kahn questions and shares a potentially powerful application of gene drives: the development of disease-resistant mosquitoes that could knock out malaria and Zika.

Kahn talks about the work of Kevin Esvelt, the scientist behind gene drives. Gene drive systems are capable of altering the traits of wild populations and associated ecosystems.

"It's like a global search and replace, or in science terms, it makes a heterozygous trait homozygous.."

Named for the ability to "drive" themselves and nearby genes through populations of organisms over many generations, these genetic elements can spread even if they reduce the fitness of individual organisms. They do this by ensuring that they will be inherited by most - rather than only half - of offspring. Preferential inheritance can more than offset costs to the organism, permitting rapid spread through the population. CRISPR-based genome editing allows us to build gene drive systems capable of spreading different useful changes, including those that will eventually suppress or eliminate the target population.

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So, what does this mean asks Kahn? For one thing, it means we have a very powerful, but also somewhat alarming new tool. "Up until now, the fact that gene drives didn't work very well was actually kind of a relief. Normally when we mess around with an organism's genes, we make that thing less evolutionarily fit. So biologists can make all the mutant fruit flies they want without worrying about it. If some escape, natural selection just takes care of them."

Gene drives might not stay confined to what we call the target species, says Kahn. That's because of gene flow, or species interbreeding. If that happens, it's possible a gene drive could cross over, like Asian carp could infect some other kind of carp. That's not so bad if your drive just promotes a trait, like eye color. In fact, there's a decent chance that we'll see a wave of very weird fruit flies in the near future. But it could be a disaster if your drive is deigned to eliminate the species entirely.

Science journalist Kahn likes to seek out complex stories, with the goal of illuminating their nuances. She teaches in the magazine program at the UC Berkeley Graduate School of Journalism, and is a contributing writer for the New York Times Magazine; she has written features and cover stories for The New Yorker, National Geographic, Outside, Wired and many more.

Her work has appeared in the Best American Science Writing anthology series four times, most recently for the New Yorker story “A Cloud of Smoke,” a story on the complicated death of a policeman after 9/11.

SOURCE  TED

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Genomics  

Recently Andrew Hessel presented a tremendous keynote address at the Congress On the Future of Engineering Software on the state-of-the-art in genetic engineering and what the future of biotechnology might bring. This is must-watch material.

In his keynote address at the recent Congress On the Future of Engineering Software (COFES) conference, the former co-chair of bioinformatics and biotechnology at Singularity University, Andrew Hessel presented the current state of biotechnology and what lays beyond in the not-too-distant future.

In his talk titled, “Virus Engineering and Beyond” (available below), Hessel, now with Autodesk as a research scientist, talked about the programming of living things. He believes that we are now advancing from reading genetic code to writing it. This means that we can design tools specific for living organisms and prototype the processes to bring these designs into the real world.

"Now that we have this foundation in genomics we can start to think about writing code."

As Hessel explains, the exponential nature of genetic engineering technology. "This is the golden age of sequence, and it is only going to keep going," he states."Computer technology moved pretty fast, but DNA sequencing has broken every record."

More than just a futurist on the subject, Hessel is taking a leading role in bringing about the writing of genetic code as part of the leadership of the recently announced Human Genome Project-write initiative. The project aims to build a human genome from the ground up. "Now that we have this foundation in genomics we can start to think about writing code," says Hessel.

Hessel describes how viruses can be the simplest way to make big changes in healthcare and genomics. He makes fighting cancer sound very simple with the idea of viral engineering, which encompasses using software to design and make viruses — and 3D print them.

Looking ahead, Hessel says that as biotechnology tools continue to get cheaper, it will get weirder as well. He describes how researchers are now modifying yeast to produce beer with nearly any gene including creating medical beer and caffeinated beer as well.

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Genomics breakthroughs also may dramatically extend our life spans. Hessel points to a recent study where scientists were able to modify cells in mice to essentially commit suicide as they became too old, thereby keeping the overall organism healthier. The results were mice that lived over 20% longer than average.

Continuing on Hessel predicts that real life Eldon Tyrell's and J.S. Sebastian's that will push forward engineering that blends silicon and carbon. The corporate and open-source versions portrayed in Blade Runner will be reality claims Hessel.

Hessel also points to Alec Ross's book, The Industries of the Future, which states that, "The last trillion-dollar industry was built on a code of 1s and 0s. The next will be built on our own genetic code."

Hessel’s work extends CAD and 3D printing into biology, a vast design space that is largely unexplored. Hessel says that cells are the ultimate 3D printers; they can be programmed to produce millions of compounds, including medicines, foods, or fuels—or used as ink in 3D printers.

Hessel is a futurist and catalyst in biological technologies, helping industry, academics, and authorities better understand the changes ahead in life science. He is a Distinguished Researcher with Autodesk Inc.’s Bio/Nano Programmable Matter group, based out of San Francisco. He is also the co-founder of the Pink Army Cooperative, the world’s first cooperative biotechnology company, which is aiming to make open source viral therapies for cancer.

We are sure you will agree that the talk is inspiring and Hessler's enthusiasm is contagious.

SOURCE  COFES 2016

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 Genetic Engineering  

Researchers have developed a way to program DNA in such a way that genes can be turned on or off in living cells. The new tool can affect two different genes at the same time, an advance that will allow scientists to treat even the most complex genetic disorders.

Bioengineers at Stanford and other universities have developed a sort of programmable genetic code that allows them to preferentially activate or deactivate genes in living cells.

The research is published in the current issue of Cell, and could help usher in a new generation of gene therapies.

The technique is an adaptation of CRISPR, itself a relatively new genetic tool that makes use of a natural defense mechanism that bacteria evolved over millions of years to slice up infectious virus DNA.

Standard CRISPR consists of two components: a short RNA that matches a particular spot in the genome, and a protein called Cas9 that snips the DNA in that location. For the purposes of gene editing, scientists can control where the protein snips the genome, insert a new gene into the cut and patch it back together.

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Inserting new genetic code, however, is just one way to influence how the genome is expressed. Another involves telling the cell how much or how little to activate a particular gene, thus controlling how much protein a cell produces from that gene and altering its behavior.

"We could eventually synthesize tens of thousands of RNA molecules to control the genome over a whole organism."

It's this action that Lei Stanley Qi, an assistant professor of bioengineering and of chemical and systems biology at Stanford, and his colleagues aim to manipulate.

In the new work, the researchers describe how they have designed the CRISPR molecule to include a second piece of information on the RNA, instructing the molecule to either increase (upregulate) or decrease (downregulate) a target gene's activity, or turn it on/off entirely.

They also designed it so that it could affect two different genes at once. In a cell, the order or degree in which multiple genes are activated can produce different metabolic products.

"It's like driving a car. You control the wheel to control direction, and the engine to control the speed, and how you balance the two determines how the car moves," Qi said. "We can do the same thing in the cell by up- or downregulating genes, and produce different outcomes."

To prove the principle, the scientists used the technique to take control of a yeast metabolic pathway, turning genes on and off in various orders to produce four different end products. They then tested it on two mammalian genes that are important in cell mobility, and were able to control the cell's direction and how fast it moved.

The ability to control genes is an attractive approach in designing genetic therapies for complex diseases that involve multiple genes, Qi said, and the new system may overcome several of the challenges of existing experimental therapies.

"Our technique allows us to directly control multiple specific genes and pathways in the genome without expressing new transgenes or uncontrolled behaviors, such as producing too much of a protein, or doing so in the wrong cells," Qi said.

Next, Qi plans to test the technique in mice and refine the delivery method. Currently the scientists use a virus to insert the molecule into a cell, but he would eventually like to simply inject the molecules into an organism's blood. "I'm optimistic because everything about this system comes naturally from cells, and should be compatible with any organism."


SOURCE  Stanford University

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 Down's Syndrome  

Researchers have identified a compound that dramatically bolsters learning and memory when given to mice with a Down syndrome-like condition on the day of birth.

Researchers at Johns Hopkins and the National Institutes of Health have identified a compound that dramatically bolsters learning and memory when given to mice with a Down syndrome-like condition on the day of birth. As they reported in Science Translational Medicine, the single-dose treatment appears to enable the cerebellum of the rodents’ brains to grow to a normal size.

"We were able to completely normalize growth of the cerebellum through adulthood with that single injection."

The scientists caution that use of the compound, a small molecule known as a sonic hedgehog pathway agonist, has not been proven safe to try in people with Down syndrome, but say their experiments hold promise for developing drugs like it.

“Most people with Down syndrome have a cerebellum that’s about 60 percent of the normal size,” says Roger Reeves, Ph.D., a professor in the McKusick-Nathans Institute of Genetic Medicine at the Johns Hopkins University School of Medicine. “We treated the Down syndrome-like mice with a compound we thought might normalize the cerebellum’s growth, and it worked beautifully. What we didn’t expect were the effects on learning and memory, which are generally controlled by the hippocampus, not the cerebellum.”

Reeves has devoted his career to studying Down syndrome, a condition that occurs when people have three, rather than the usual two, copies of chromosome 21. As a result of this “trisomy,” people with Down syndrome have extra copies of the more than 300 genes housed on that chromosome, which leads to intellectual disabilities, distinctive facial features and sometimes heart problems and other health effects. Since the condition involves so many genes, developing treatments for it is a formidable challenge, Reeves says.

For the current experiments, Reeves and his colleagues used mice that were genetically engineered to have extra copies of about half of the genes found on human chromosome 21.

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The mice have many characteristics similar to those of people with Down syndrome, including relatively small cerebellums and difficulty learning and remembering how to navigate through a familiar space. (In the case of the mice, this was tested by tracking how readily the animals located a platform while swimming in a so-called water maze.)

Based on previous experiments on how Down syndrome affects brain development, the researchers tried supercharging a biochemical chain of events known as the sonic hedgehog pathway that triggers growth and development. They used a compound — a sonic hedgehog pathway agonist — that could do just that.

The compound was injected into the Down syndrome-like mice just once, on the day of birth, while their cerebellums were still developing. “We were able to completely normalize growth of the cerebellum through adulthood with that single injection,” Reeves says.

But the research team went beyond measuring the cerebellums, looking for changes in behavior, too. “Making the animals, synthesizing the compound and guessing the right dose were so difficult and time-consuming that we wanted to get as much data out of the experiment as we could,” Reeves says. The team tested the treated mice against untreated Down syndrome-like mice and normal mice in a variety of ways, and found that the treated mice did just as well as the normal ones on the water maze test.

Reeves says further research is needed to learn why exactly the treatment works, because their examination of certain cells in the hippocampus known to be involved in learning and affected by Down syndrome appeared unchanged by the sonic hedgehog agonist treatment. One idea is that the treatment improved learning by strengthening communication between the cerebellum and the hippocampus, he says.

As for the compound’s potential to become a human drug, the problem, Reeves says, is that altering an important biological chain of events like sonic hedgehog would likely have many unintended effects throughout the body, such as raising the risk of cancer by triggering inappropriate growth. But now that the team has seen the potential of this strategy, they will look for more targeted ways to safely harness the power of sonic hedgehog in the cerebellum. Even if his team succeeds in developing a clinically useful drug, however, Reeves cautions that it wouldn’t constitute a “cure” for the learning and memory-related effects of Down syndrome. “Down syndrome is very complex, and nobody thinks there’s going to be a silver bullet that normalizes cognition,” he says. “Multiple approaches will be needed.”




SOURCE  Johns Hopkins Medicine

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 Gene Therapy  

By using a a new gene-editing system based on bacterial proteins, researchers have effectively cured mice of a rare liver disorder caused by a single genetic mutation.

Using a new gene-editing system based on bacterial proteins, MIT researchers have cured mice of a rare liver disorder caused by a single genetic mutation.

The findings, described in Nature Biotechnology, offer the first evidence that this gene-editing technique, known as CRISPR, can reverse disease symptoms in living animals.

CRISPR, which offers an easy way to snip out mutated DNA and replace it with the correct sequence, holds potential for treating many genetic disorders, according to the research team.

“What’s exciting about this approach is that we can actually correct a defective gene in a living adult animal,” says Daniel Anderson, the Samuel A. Goldblith Associate Professor of Chemical Engineering at MIT, a member of the Koch Institute for Integrative Cancer Research, and the senior author of the paper.

The recently developed CRISPR system relies on cellular machinery that bacteria use to defend themselves from viral infection. Researchers have copied this cellular system to create gene-editing complexes that include a DNA-cutting enzyme called Cas9 bound to a short RNA guide strand that is programmed to bind to a specific genome sequence, telling Cas9 where to make its cut.

At the same time, the researchers also deliver a DNA template strand. When the cell repairs the damage produced by Cas9, it copies from the template, introducing new genetic material into the genome. Scientists envision that this kind of genome editing could one day help treat diseases such as hemophilia, Huntington’s disease, and others that are caused by single mutations.

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Scientists have developed other gene-editing systems based on DNA-slicing enzymes, also known as nucleases, but those complexes can be expensive and difficult to assemble.

“The CRISPR system is very easy to configure and customize,” says Anderson, who is also a member of MIT’s Institute for Medical Engineering and Science. He adds that other systems “can potentially be used in a similar way to the CRISPR system, but with those it is much harder to make a nuclease that’s specific to your target of interest.”

"What’s exciting about this approach is that we can actually correct a defective gene in a living adult animal."

For this study, the researchers designed three guide RNA strands that target different DNA sequences near the mutation that causes type I tyrosinemia, in a gene that codes for an enzyme called FAH. Patients with this disease, which affects about 1 in 100,000 people, cannot break down the amino acid tyrosine, which accumulates and can lead to liver failure. Current treatments include a low-protein diet and a drug called NTCB, which disrupts tyrosine production.

In experiments with adult mice carrying the mutated form of the FAH enzyme, the researchers delivered RNA guide strands along with the gene for Cas9 and a 199-nucleotide DNA template that includes the correct sequence of the mutated FAH gene.

Using this approach, the correct gene was inserted in about one of every 250 hepatocytes — the cells that make up most of the liver. Over the next 30 days, those healthy cells began to proliferate and replace diseased liver cells, eventually accounting for about one-third of all hepatocytes. This was enough to cure the disease, allowing the mice to survive after being taken off the NCTB drug.
“We can do a one-time treatment and totally reverse the condition,” says Hao Yin, a postdoc at the Koch Institute and one of the lead authors of the Nature Biotechnology paper.

Gene therapy is one area of science that has consistently failed to achieve its therapeutic potential. Now, our abilities may finally be able to unlock some of the promise of real-world DNA manipulation, making hereditary and acquired genetic disease much more treatable. This study marks the beginning of a new era of usability in genetic manipulation, and everyone with DNA stands to benefit.


SOURCE  MIT News Top Image - Christine Daniloff/MIT

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 Medicine  

Researchers have discovered the fundamental biology of calcium waves in relation to heart arrhythmias. The findings published this month in the Jan. 19 edition of Nature Medicine outlines the discovery of this fundamental physiological process that researchers hope will one day help design molecularly tailored medications that correct the pathophysiology.

Researchers have discovered the fundamental biology of calcium waves in relation to heart arrhythmias.

The findings published recently in Nature Medicine outlines the discovery of this fundamental physiological process that researchers hope will one day help design molecularly tailored medications that correct the pathophysiology.

Heart arrhythmias cause the heart to beat irregularly, resulting in symptoms such as dizziness and fainting, or in severe cases, sudden arrhythmic death. While many factors contribute to the development of arrhythmias, including genetics, scientists know that a common mechanism of cardiac arrhythmias is calcium overload in the heart, i.e. calcium-triggered arrhythmias that can lead to sudden death. The underlying mechanism of these calcium-triggered arrhythmias has remained a mystery for decades.

Using a combination of molecular biology, electrophysiology, and genetically engineering mice, scientists at the University of Calgary's and Alberta Health Services' Libin Cardiovascular Institute of Alberta (Libin Institute)have discovered that a calcium-sensing-gate in the cardiac calcium release channel (ryanodine receptor) is responsible for initiation of calcium waves and calcium-triggered arrhythmias.

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Utilizing a genetically modified mouse model they were able to manipulate the sensor and completely prevented calcium-triggered arrhythmias.

"The calcium-sensing- gate mechanism discovered here is an entirely novel concept with potential to shift our general understanding of ion channel gating, cardiac arrhythmogenesis, and the treatment of calcium-triggered arrhythmias," says SR Wayne Chen, PhD, the study's senior author and University of Calgary- Libin Institute researcher. "These findings open a new chapter of calcium signaling and the discovery fosters the possibilities of new drug interventions."


SOURCE  EurekAlert

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 Genetic Engineering  

Two parallel projects at Harvard’s Wyss Institute have created new genomes inside the bacterium E. coli in ways that test the limits of genetic reprogramming and open new possibilities for increasing flexibility, productivity. and safety in biotechnology.

In two parallel projects, researchers have created new genomes inside the bacterium E. coli in ways that test the limits of genetic reprogramming, opening new possibilities for increasing flexibility, productivity and safety in biotechnology.

In one project, researchers created a novel genome—the first-ever entirely genomically recoded organism—by replacing all 321 instances of a specific “genetic three-letter word,” called a codon, throughout the organism’s entire genome with a word of supposedly identical meaning. The researchers then reintroduced a reprogrammed version of the original word (with a new meaning, a new amino acid) into the bacteria, expanding the bacterium’s vocabulary and allowing it to produce proteins that do not normally occur in nature.

In the second project, the researchers removed every occurrence of 13 different codons across 42 separate E. coli genes, using a different organism for each gene, and replaced them with other codons of the same function. When they were done, 24 percent of the DNA across the 42 targeted genes had been changed, yet the proteins the genes produced remained identical to those produced by the original genes.

“The first project is saying that we can take one codon, completely remove it from the genome, then successfully reassign its function,” said Marc Lajoie, a Harvard Medical School graduate student in the lab of George Church. “For the second project we asked, ‘OK, we've changed this one codon, how many others can we change?’”

Of the 13 codons chosen for the project, all could be changed.

“That leaves open the possibility that we could potentially replace any or all of those 13 codons throughout the entire genome,” Lajoie said.

The results of these two projects appearred recently in the journal Science. The work was led by Church, Robert Winthrop Professor of Genetics at Harvard Medical School and founding core faculty member at the Wyss Institute for Biologically Inspired Engineering. Farren Isaacs, assistant professor of molecular, cellular, and developmental biology at Yale School of Medicine, is co-senior author on the first study.

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Recoded genomes can confer protection against viruses—which limit productivity in the biotech industry—and help prevent the spread of potentially dangerous genetically engineered traits to wild organisms.

“In science we talk a lot about the ‘what’ and the ‘how’ of things, but in this case, the ‘why’ is very important,” Church, author of Regenesis: How Synthetic Biology Will Reinvent Nature and Ourselves said, explaining how this project is part of an ongoing effort to improve the safety, productivity and flexibility of biotechnology.

“These results might also open a whole new chemical toolbox for biotech production,” said Isaacs. “For example, adding durable polymers to a therapeutic molecule could allow it to function longer in the human bloodstream.”

But to have such an impact, the researchers said, large swaths of the genome need to be changed all at once.

“If we make a few changes that make the microbe a little more resistant to a virus, the virus is going to compensate. It becomes a back and forth battle,” Church said. “But if we take the microbe offline and make a whole bunch of changes, when we bring it back and show it to the virus, the virus is going to say ‘I give up.’ No amount of diversity in any reasonable natural virus population is going to be enough to compensate for this wildly new genome.”

In the first study, with just a single codon removed, the genomically recoded organism showed increased resistance to viral infection. With several additional codons reassigned, a “wildly new genome” would make it impossible for engineered genes to escape into wild populations, Church said, because they would be incompatible with natural genomes. This could be of considerable benefit with strains engineered for drug or pesticide resistance, for example. What’s more, incorporating rare, non-standard amino acids could ensure strains only survive in a laboratory environment.

Since a single genetic flaw can spell death for an organism, the challenge of managing a series of hundreds of specific changes was daunting, the researchers said. In both projects, the researchers paid particular attention to developing a methodical approach to planning and implementing changes and troubleshooting the results.

“We wanted to develop the ability to efficiently build the desired genome and to very quickly identify any problems—from design flaws or from undesired mutations — and develop workarounds,” Lajoie said.

The team relied on number of technologies developed in the Church lab and the Wyss Institute and with partners in academia and industry, including next-generation sequencing tools, DNA synthesis on a chip, and MAGE and CAGE genome editing methods. But one of the most important tools they used was the power of natural selection, the researchers added.

“When an engineering team designs a new cellphone, it’s a huge investment of time and money. They really want that cell phone to work,” Church said. “With E. coli we can make a few billion prototypes with many different genomes, and let the best strain win. That’s the awesome power of evolution.”



SOURCE  Harvard Medical School

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 Genetics  

Researchers working with induced pluripotent stem cells have found a way to block the extra chromosome responsible for Down syndrome—the work may eventually lead to chromosome-level gene therapy to treat Down's and other conditions.

According to a study published in Nature, he insertion of one gene can muzzle the extra copy of chromosome 21 that causes Down’s syndrome,. The method could help researchers to identify the cellular pathways behind the disorder's symptoms, and to design targeted treatments.

“It’s a strategy that can be applied in multiple ways, and I think can be useful right now,” says Jeanne Lawrence, a cell biologist at the University of Massachusetts Medical School in Worcester, and the lead author of the study.

“Genetic correction of hundreds of genes across an entire extra chromosome has remained outside the realm of possibility,” said Lawrence in a release. “Our hope is that for individuals with Down syndrome, this proof-of-principle opens up multiple exciting new avenues for studying the disorder now, and brings into the realm of consideration research on the concept of ‘chromosome therapy’ in the future.”

Image Source: Jeanne Lawrence Lab

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Lawrence and her team came up with an approach to mimic the natural process that silences one of the two X chromosomes carried by all female mammals. Both chromosomes contain a gene called XIST(the X-inactivation gene), which, when activated, produces an RNA molecule that coats the surface of a chromosome like a blanket, blocking other genes from being expressed. In female mammals, one copy of the XIST gene is activated — silencing the X chromosome on which it resides.

Lawrence’s team spliced the XIST gene into one of the three copies of chromosome 21 in cells from a person with Down’s syndrome. The team also inserted a genetic 'switch' that allowed them to turn on XIST by dosing the cells with the antibiotic doxycycline. Doing so dampened expression of individual genes along chromosome 21 that are thought to contribute to the pervasive developmental problems that comprise Down's syndrome.

The experiment used induced pluripotent stem cells (iPS), which can develop into many different types of mature cells, so the researchers hope that one day they will be able to study the effects of Down’s syndrome in different organs and tissue types. That work could lead to treatments that address degenerative symptoms of Down’s syndrome, such as the tendency of people with the disorder to develop early dementia.

The approach could yield fresh treatments for Down's syndrome — and prove useful for studying other chromosome disorders such as Patau syndrome, a developmental disorder caused by a third copy of chromosome 13.

For those of you seeking additional information about the dental issues for caregivers of individuals with Down syndrome please have a look at this informative guide: Dental Care Guidance for Caregivers of Patients with Down Syndrome. It looks at some of the common dental issues seen in patients with Down syndrome as well as practical advice for caregivers.

 
SOURCE  Nature

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