What types of conditions does regenerative medicine treat?
Dr. Trevor Bullock of Regen Orthopedics describes the types of injuries and conditions that can be helped by regenerative medicine. These include a number of chronic conditions: arthritis,...

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With a little help from my friends fundraising concert | Frankston TV
We would like to thank all the artists who performed at the fundraising concert for Wayne Higgins on Sunday the 15th of March. EVERYONE, including Glenn Shorrock, Mike Rudd, Andrew Wishart,...

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Measuring the concentration of leukemia cells in patient bone marrow during the first 46 days of chemotherapy should help boost survival of young leukemia patients by better matching patients with the right intensity of chemotherapy. St. Jude Children's Research Hospital investigators led the research, which appears in the March 20 edition of the journal Lancet Oncology.

The findings stem from a study of 498 children and adolescents with acute lymphoblastic leukemia (ALL) enrolled in a St. Jude-led protocol between 2000 and 2007. The clinical trial was the first to use measurement of residual leukemia cells -- or minimal residual disease (MRD) -- in bone marrow to help guide therapy. St. Jude pioneered MRD measurement as a tool to guide leukemia treatment.

"This analysis shows that MRD-directed therapy clearly contributed to the unprecedented high rates of long-term survival that patients in this study achieved," said first and corresponding author Ching-Hon Pui, M.D., chair of the St.Jude Department of Oncology. Overall, 93.5 percent of patients were alive five years after their cancer was diagnosed. "MRD proved to be a powerful way to identify high-risk patients who needed more intensive therapy and helped us avoid over-treatment of low-risk patients by reducing their exposure to chemotherapy," Pui said.

Researchers hope the findings will expand use of MRD measurements to guide leukemia treatment in children and adults.

The technique might also help identify patients who could be cured with less intensive chemotherapy, Pui said. Overall long-term survival was 97.9 percent or better for 244 patients in this study classified as low risk based on a variety of factors including their age at diagnosis and MRD of less than 1 percent on day 19 of treatment. "Given the excellent outcome, it will be important to determine if treatment can be further reduced in this subgroup of patients," Pui said.

In countries with limited resources, Pui said the findings suggest that results of MRD on day 19 can be used to reduce treatment-related deaths by identifying patients who will likely be cured with low-intensity chemotherapy. "This study demonstrates these patients have an extremely low risk of relapse," he said.

The study showed that measuring MRD just twice during remission induction therapy -- at day 19 and day 46 -- rather than multiple times during the more than two years of treatment was sufficient to guide treatment of most pediatric ALL patients. That will help save money and protect patients from the discomfort and risks associated with bone marrow aspiration for MRD testing. MRD measurements should continue, however, to guide treatment of patients with detectable MRD on day 46 of treatment. That is a level of 0.01 percent or more, which translates into one leukemia cell in 10,000 normal cells.

MRD was not a perfect predictor of relapse risk. Cancer returned in 26 of the 430 patients with undetectable MRD when treatment ended after 120 weeks. Researchers are working to develop even more sensitive methods for tracking treatment response in order to identify those at risk for having their cancer return.

Overall, researchers showed that regardless of other risk factors, including age at diagnosis or the initial white blood cell count, patients with an MRD level of 1 percent or more on day 19 of therapy were far less likely than other young leukemia patients to be alive and cancer-free 10 years later. Having detectable leukemia cells on day 46 of treatment was also associated with lower survival.

MRD levels on days 19 and 46 led to the reclassification of 50 patients from low risk to a higher risk leukemia that warranted more intensive therapy. Researchers credited the change with boosting survival.

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Measuring treatment response proves to be a powerful tool for guiding leukemia treatment

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New York, March 20 (IANS): High stress levels can have a critical impact not only on the surface, making our skin age, but also on a molecular level, when stressed cells cannot cope with the pressure and perish much faster than the ones which can.

In a new research report released on Thursday, scientists at the University of California, Berkeley, analysed blood stem cells and found that the cell's ability to repair damage in the mitochondria, their power source, was critical to their survival.

Researchers tried to "relax" these stressed-out cells by slowing down the activity of their mitochondria.

"We found that by slowing down the activity of mitochondria in the blood stem cells of mice, we were able to enhance their capacity to handle stress and rejuvenate old blood. This confirms the significance of this pathway in the aging process," Xinhua news agency quoted Danica Chen, an assistant professor with the Department of Nutritional Sciences and Toxicology.

This pathway lies mainly in the multitude of proteins that need to be folded properly for the mitochondria to function correctly. When the folding goes awry, the mitochondrial unfolded-protein response, or UPRmt, kicks in to boost the production of specific proteins to fix or remove the misfolded protein.

Researchers found that certain proteins known as SIRT7 help cells cope with the stress of unfolding the proteins in the mitochondria, helping those with higher levels of SIRT7 survive longer by making them "unwind". But the levels of SIRT7 decrease as people age.

"The protein level decreases as years go by," Chen said. "But if we increase this protein in blood stem cells, we can make them live longer. Cells in general don't just die suddenly; they are submitted to high stress levels and lose their functions with age."

Chen does not want to encourage the thought that she and other researchers have found the "fountain of youth", but more of a new path for study.

"We still don't know if this would work on other kinds of stem cells, such as pancreatic stem cells or heart cells, and we don't have any expertise with those tissues, so we would be very happy to collaborate with other laboratories to tackle the matter," she said.

The study, published on Thursday in the Science journal, is expected to help researchers gain more insight into the aging process, and even slow it down.

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Cambridge stem cell scientists searching for new cystic fibrosis treatments have grown "mini-lungs" in a laboratory.

The millimetre-wide cell clusters were created using stem cells derived from the skin of patients with the devastating lung disease.

They are the latest in a line of 3D "organoids" produced to mimic the behaviour of specific body tissues, following "mini-brains" for studying Alzheimer's disease and "mini-livers" to model diseases of the liver.

Dr Nick Hannan, led the team from Cambridge University.

He said: "In a sense, what we've created are 'mini-lungs'.

"While they only represent the distal (outer) part of lung tissue, they are grown from human cells and so can be more reliable than using traditional animal models, such as mice.

"We can use them to learn more about key aspects of serious diseases - in our case, cystic fibrosis."

Cystic fibrosis occurs when the movement of water to the inside of the lungs is reduced, causing a build up of thick mucus that leads to a high risk of infection.

The scientists reprogrammed ordinary skin cells to create stem cells that could be transformed into lung tissue.

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Stem cell therapy and me1
Walk without support.

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In this image provided by the National Human Genome Research Institute, a NHGRI researcher monitors a DNA sequencing machine at the NIH in Bethesda, Md.(AP Photo/National Human Genome Research Institute, Maggie Bartlett)

A breakthrough gene-editing process developed in 2012 could potentially be used to eradicate genetic diseases in humansor make a person more intelligent or attractive. The Crispr-Cas9 or "DNA scissors" technique involves making DNA-altering changes to sperm, eggs, or embryos that could then be inherited by future generations.

For example, negative mutations could be replaced with "corrected" DNA strings, Bloomberg reports. The technique is relatively easy for anyone who knows about molecular biology, and it's already been tested in mice, rats, and monkeys, the New York Times reports.

But a group of 18 biologists, including a Crispr-Cas9 inventor, cautions the dangers of genome-editing in a new study and warns "scientists should avoid even attempting, in lax jurisdictions, germline genome modification for clinical application in humans" until the consequences "are discussed among scientific and governmental organizations." In a similar essay last week, several scientists called for a moratorium on gene-editing research that "could be exploited," as "an ethical breach could hinder a promising area of therapeutic development." Scientists around the world won't be forced to abide by the request, but the biologists hope to use their "moral authority" to bar experiments in parts of the world where lab research isn't well regulated.

Similar requests have been agreed to in the past; however, scientists tell Nature that research papers about created human embryos with edited genomes have already been submitted for publication.

Ethicists say editing human DNA to boost intelligence or beauty should never be attempted, but there are also potential dangers as the process can change genes apart from the ones intended.

"You could exert control over human heredity with this technique, and that is why we are raising the issue," an expert says. (Britain is the first nation that will allow three-parent babies.)

This article originally appeared on Newser: Scientists: Let's Halt Gene-Editing in Humans

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Planet Bizzaro Ep Seventeen Genetic Gas
Zoomer and his pals find out Zargon has plagued their food supply with genetically engineered bugs, so Zoomer uses his own genetic engineering to create a super fruit that ends up creating...

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International Centre for Genetic Engineering and Biotechnology
ICGEB: A brief overview and introduction by Mauro Giacca, Director-General, and Researchers in Trieste, Italy.

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A new technology called CRISPR could allow scientists to alter the human genetic code for generations. That's causing some leading biologists and bioethicists to sound an alarm. They're calling for a worldwide moratorium on any attempts to alter the code, at least until there's been time for far more research and discussion.

It's not new that scientists can manipulate human DNA genetic engineering, or gene editing, has been around for decades. But it's been hard, slow and very expensive. And only highly skilled geneticists could do it.

Recently that's changed. Scientists have developed new techniques that have sped up the process and, at the same time, made it a lot cheaper to make very precise changes in DNA.

There are a couple of different techniques, but the one most often talked about is CRISPR, which stands for clustered regularly interspaced short palindromic repeats. My colleague Joe Palca described the technique for Shots readers last June.

Why scientists are nervous

On the one hand, scientists are excited about these techniques because they may let them do good things, such as discovering important principles about biology. It might even lead to cures for diseases.

The big worry is that CRISPR and other techniques will be used to perform germline genetic modification.

Basically, that means making genetic changes in a human egg, sperm or embryo.

Those kinds of changes would be passed down for generations. And that's something that's always been considered taboo in science.

One major reason that it's considered off limits, ethically, is that the technology is still so new that scientists really don't know how well it works.

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Here's the classic, if overly simplistic, example: Children inherit sets of chromosomes from each of their parents, with each chromosome containing the genes for various traits. A blue-eyed child has to inherit the blue-eyed gene from both the mother and the father. Otherwise, the dominant brown-eyed gene trumps the recessive blue-eyed gene.

In reality, eye color is determined by more than one gene. But the same principle applies to genetic defects such as muscular dystrophy: Even if you inherit the mutated gene for muscular dystrophy from one parent, the normal gene from the other parent can compensate and keep you from getting the disease.

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The downside for genetic engineers is that the mechanism makes it harder to introduce desired mutations. Mutagenic chain reaction, or MCR, makes the job easier. The researchers behind the Science study tweaked the CRISPR genome-editing procedure in fruit flies to make a mutation that's generated on one copy of a chromosome spread automatically to the other copy. Thus, both copies of the gene carry the mutation.

"MCR is remarkably active in all cells of the body, with one result being that such mutations are transmitted to offspring via the germline with 95 percent efficiency," study lead author Valentino Gantz, a graduate student at the University of California at San Diego, said in a news release.

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How to get the right treatment to the right patient at the right time

University of Glasgow leads the way in new global drug treatments

The University of Glasgow is launching the first ever Masters programme designed to specifically address the new paradigm in drug discovery stratified medicine which tailors drug therapies to individual patients genetic makeup.

The University of Glasgow is at the forefront of stratified medicine, which involves examining the genetic makeup of patients and their differing responses to drugs designed to treat specific diseases the right treatment to the right patient at the right time.

The course director of the new MSc in Clinical Trials and Stratified Medicine, Professor Matthew Walters, said: Stratified Medicine holds huge potential in the timely development of new treatments for human disease. It is among the most important concepts to emerge in 21stcentury clinical science and will be a crucial component of the global drive to increase the efficacy, safety and cost-effectiveness of new treatments.

He added: There has been global recognition of the need for training in this area so that we have young drug researchers in academia and the commercial environment imbued with the skills required to apply the science for the benefit of patients.

Glasgow is also home to the Stratified Medicine Scotland Innovation Centre, which combines cutting-edge genetic research with state-of-the-art health informatics and imaging technologies. It is a unique collaboration in healthcare between partners from academia, the NHS and the pharmaceutical industry.

There is already huge interest in stratified medicine and pharmaceutical science in Saudi Arabia, said Professor Walters.

China also has a nascent clinical trials industry and Professor Walters is keen to involve Chinese students and academics in this area.

One of the elements we need to be clear about is whether medicines have the same impact across different populations. People handle drugs differently in different parts of the globe. There will be a significant need for people in China with these skills to be running clinical trials over the next few decades, he said.

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Photo: Andrew Brookes/Corbis

In 2005, next-generation sequencing began to change the field of genetics research. Obtaining a persons entire genome became fast and relatively cheap. Databases of genetic information were growing by the terabyte, and doctors and researchers were in desperate need of a way to efficiently sift through the information for the cause of a particular disorder or for clues to how patients might respond to treatment.

Companies have sprung up over the past five years that are vying to produce the first DNA search engine. All of them have different tacticssome even have their own proprietary databases of genetic informationbut most are working to link enough genetic databases so that users can quickly identify a huge variety of mutations. Most companies also craft search algorithms to supplement the genetic information with relevant biomedical literature. But as in the days of the early Web, before Google reigned supreme, a single company has yet to emerge as the clear winner.

Making a functional search engine is a classic big-data problem, says Michael Gonzalez, the vice president of bioinformatics at one such company, ViaGenetics, which was expected to relaunch its platform in March. Before doctors or researchers can use the data, genomic data must be organized so that humans can read and search it. The first step toward that is to put it in a standard form called the variant call format, or VCF. As raw data, a persons complete sequenced genome would take up about 100 gigabytes, so a database that adds the genomes of even 10 patients per day would quickly get out of hand. But VCF files are more compact, requiring only a few hundred megabytes per genome, which helps researchers find the specific variants they want to search in a fraction of the time. Unlike a fully sequenced genome, VCF files point only to where a persons genetic data deviates from the standardthe genome originally compiled by the Human Genome Project in 2001.

With VCF, sifting the genomes themselves for pinpoint mutations isnt the challenge for search engine companies. Most of these companies are allocating their resources toward efforts to seamlessly compile supplementary information about a specific mutation from other databases across the Web, such as the biomedical research archive PubMed or various troves of electronic medical records. Many of these tools have finely tuned algorithms that prioritize the results by credibility or relevance. You want to be able to pull together the information known about a mutation in that position [of the genome] and quickly make an assessment, says David Mittelman, the chief scientific officer for Tute Genomics, based in Provo, Utah, another company designing a genetic-search engine.

In an effort to expand the information that can be attached to a genome under examination, ViaGenetics, based in Miami Beach, Fla., is making its newly updated platform useful for researchers who want to collaborate across institutions. With ViaGenetics tools, researchers can make their data available to other users, so other people can come across these projects, request access, and form a collaboration, Gonzalez says. It helps people connect the dots between different researchers and institutions. This is especially helpful for smaller labs that may not have very extensive genome databases or for researchers from different universities working to decode the same mutation.

Although the genomic-search industry is now focused on serving scientists, that might not always be the case. Mittelman envisions that Tute Genomics could eventually serve consumers directly. People are already demanding information about their genomes just to understand themselves better, Mittelman says, but most companies dont yet consider the average person to be their primary customer. In order to make that shift, the tool will have to be even more intuitive and user-friendly. Fire-hosing someone with data thats not easy to interpret, or using terminology thats not standardized, has the potential to confuse people, he says. Privacy is also a major concern for the average user; the information that Tute users upload isnt stored permanently, Mittelman says, but users will need extra reassurance if the platform becomes available to the lay public.

And a further evolution of the industry is in the offing. Both ViaGenetics and Tute are hoping to be able to run the entire process in-housefrom the initial DNA sequencing to the presentation of final searchable results to users. The market for analyzing and interpreting genomic data is very fragmented, like the computer industry in the 1990s, where you had to go to separate providers to buy a video card or a motherboard and then try to put it together, Mittelman says. Soon this field will consolidate, as the computer industry did.

This article originally appeared in print as A Google for DNA.

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The Race to Build a Search Engine for Your DNA

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A new study from Princeton University sheds light on the handing over of genetic control from mother to offspring early in development. Learning how organisms manage this transition could help researchers understand larger questions about how embryos regulate cell division and differentiation into new types of cells.

The study, published in the March 12 issue of the journal Cell, provides new insight into the mechanism for this genetic hand-off, which happens within hours of fertilization, when the newly fertilized egg is called a zygote.

"At the beginning, everything the embryo needs to survive is provided by mom, but eventually that stuff runs out, and the embryo needs to start making its own proteins and cellular machinery," said Princeton postdoctoral researcher in the Department of Molecular Biology and first author Shelby Blythe. "We wanted to find out what controls that transition."

Blythe conducted the study with senior author Eric Wieschaus, Princeton's Squibb Professor in Molecular Biology, Professor of Molecular Biology and the Lewis-Sigler Institute for Integrative Genomics, a Howard Hughes Medical Institute investigator, and a Nobel laureate in physiology or medicine.

Researchers have known that in most animals, a newly fertilized egg cell divides rapidly, producing exact copies of itself using gene products supplied by the mother. After a short while, this rapid cell division pauses, and when it restarts, the embryonic DNA takes control and the cells divide much more slowly, differentiating into new cell types that are needed for the body's organs and systems.

To find out what controls this maternal to zygotic transition, also called the midblastula transition (MBT), Blythe conducted experiments in the fruit fly Drosophila melanogaster, which has long served as a model for development in higher organisms including humans.

These experiments revealed that the slower cell division is a consequence of an upswing in DNA errors after the embryo's genes take over. Cell division slows down because the cell's DNA-copying machinery has to stop and wait until the damage is repaired.

Blythe found that it wasn't the overall amount of embryonic DNA that caused this increase in errors. Instead, his experiments indicated that the high error rate was due to molecules that bind to DNA to activate the reading, or "transcription," of the genes. These molecules stick to the DNA strands at thousands of sites and prevent the DNA copying machinery from working properly.

To discover this link between DNA errors and slower cell replication, Blythe used genetic techniques to create Drosophila embryos that were unable to repair DNA damage and typically died shortly after beginning to use their own genes. He then blocked the molecules that initiate the process of transcription of the zygotic genes, and found that the embryos survived, indicating that these molecules that bind to the DNA strands, called transcription factors, were triggering the DNA damage. He also discovered that a protein involved in responding to DNA damage, called Replication Protein A (RPA), appeared near the locations where DNA transcription was being initiated. "This provided evidence that the process of awakening the embryo's genome is deleterious for DNA replication," he said.

The study also demonstrates a mechanism by which the developing embryo ensures that cell division happens at a pace that is slow enough to allow the repair of damage to DNA during the switchover from maternal to zygotic gene expression. "For the first time we have a mechanistic foothold on how this process works," Blythe said.

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Letting go of the (genetic) apron strings

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Spring Fling Genetics Seminar AI Panel
The second session of the morning was the AI-Panel. It was made up of 6 past and present AI Sire Analysis #39;s. Roger Turned asked The group questions about how each of them work with breeders....

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*:Sims 4 Perfect Genetics Challenge Dey Getting Married Yo*: Ep8
Hi. I #39;m losingfireflies ( ) Marriage at it #39;s finest. I attempted to make a beautiful wedding anddddd it went okay.. ==================================== Social Media Twitte...

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The Sims 3 - Perfect Genetics Challenge Ep.70 SEASON FINALE!
Come join me on my latest journey into the complex world of sims 3 genetics, as I try to get perfect foals and perfect children. Will I succeed in getting perfect genetics in both? Can I keep...

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The Genetics Of Spirit (Clip) - Sunday Conversations With Roy Masters
The Genetics Of Spirit (Clip) - From Sunday Conversation # 8608 - "Life and the Sin Factor" Recorded March 8th 2015 Watch On This Channel Or At https://www.fhu.com/sunday-conversations/#watch...

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PLoS Genetics : Male-Biased Aganglionic Megacolon in the TashT Mouse Line Due to Perturbation...
Male-Biased Aganglionic Megacolon in the TashT Mouse Line Due to Perturbation of Silencer Elements in a Large Gene Desert of Chromosome 10. Karl-F. Bergeron et al (2015), PLoS Genetics ...

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Minute Genetics Project - Mutations are NOT all harmful
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How to Personalize Your Nutrition Based On Genetics (Revised 3/19/15)
Sign-up for the weekly email newsletter and get a FREE PDF REPORT! http://www.foundmyfitness.com/?sendme=nutrigenomics (Report covers ALL of the information in this video, citations, and more....

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The Sims 4 | Perfect Genetics Legacy | Part 26 - First Teenager
The first season of the Legacy Challenge is coming to an end with Get To Work coming in 11 DAYS!! This means it is time to start winding down getting the family prepared for the future. It...

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Explaining gene therapy for wet AMD
Shows how wet macular degeneration destructs vision, how secretion gene therapy works and how people can benefit.

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Nobel Prize winners raise alarm over genetic engineering of humans.

A group of senior American scientists and ethics experts is calling for debate on the gene-engineering of humans, warning that technology able to change the DNA of future generations is now imminent.

In policy recommendations published today in the journal Science, eighteen researchers, including two Nobel Prize winners, say scientists should accept a self-imposed moratorium on any attempt to create genetically altered children until the safety and medical reasons for such a step can be better understood.

The concern is over a rapidly advancing gene-editing technology, called CRISPR-Cas9, which is giving scientists the ability to easily alter the genome of living cells and animals (see Genome Surgery). The same technology could let scientists correct DNA letters in a human embryo or egg cell, for instance to create children free of certain disease-causing genes, or perhaps with improved genetics.

What we are trying to do is to alert people to the fact that this is now easy, says David Baltimore, a Nobel Prize winner and former president of Caltech, and an author of the letter. We cant use the cover we did previously, which is that it was so difficult that no one was going to do it.

Many countries already ban germ line engineeringor changing genes in a way that would be heritable from one generation to the nextonethical or safety grounds. Others, like the U.S., have strict regulations that would delay the creation of gene-edited children for years, if not decades. But some countries have weak rules, or none at all, and Baltimore said a reason scientists were speaking publicly now was to keep people from doing anything crazy.

The advent of CRISPR is raising social questions of a kind not confronted since the 1970s, when the ability to change DNA in microrganisms was first developed. In a now famous meeting in 1975, in Asilomar, California, researchers agreed to avoid certain kinds of experiments that were then deemed dangerous. Baltimore, who was one of the organizers of the Asilomar meeting, says the scientists behind the letter want to offer similar guidance for gene-engineered babies.

The prospect of genetically modified humans is surprisingly close at hand. A year ago, Chinese researchers created monkeys whose DNA was edited using CRISPR (see 10 Breakthrough Technologies 2014: Genome Editing).

Since then,several teams of researchers in China, the U.S., and the U.K. have begun using CRISPR to change the DNA of human embryos, eggs, and sperm cells, with an eye toward applying the technology at in vitro fertility (IVF) clinics. That laboratory research was described by MIT Technology Review earlier this month (see Engineering the Perfect Baby).

Last week, in Nature, representatives of an industry group, the Alliance for Regenerative Medicine, recommended a wider moratorium that would also include a cessation of such laboratory studies, which it termed dangerous and ethically unacceptable (see Industry Body Calls for Gene-Editing Moratorium).

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Horizon Discovery: The Impact of Horizons Technology Platform (short version)
Horizon #39;s unique gene editing platform powers everything we do. Learn more about how it works, and why the models that are generated are so powerful, changing the way that drugs are being...

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