StemCell Therapy

Seanan McGuire, Laughter at the Academy (Subterranean Press 978-1-59606-928-2, $40.00, 374pp, hc) October 2019. Cover by Carla Speed McNeil.

McGuires introduction calls this her first single-author short story collection, which isnt exactly true, but it is her first collection of non-series stories, 22 of them, all originally published from 2009-2017. The bulk of them are dark tales; she has a tendency to pick one creepy idea and then push it to extremes. Many of the story introductions include trigger warnings, ranging from unapologetic to outright boasting. Most symptomatic, perhaps, is The Tolling of Pavlovs Bells which Contains a remarkably high death toll, even for me, and detailed discussion of disease progression. The story, about a mad doctor determined to teach the world a lesson about not taking the risk of plagues seriously, is truly scary yet amusingly over-the-top germophobes and hypochondriacs beware. The title story also plays with mad science, though with a twist. McGuire likes twisting things like tropes, urban legends, and familiar stories; two look at the legend of Peter Pan, while one of my favorite stories, Emeralds to Emeralds, mixes elements of film noir and Oz, with Dorothy a bitter witch investigating a murder in an Oz where the arrival of too many visitors from Earth has caused the natives of Oz to turn against them. We Are All Misfit Toys is a near-future horror story of what happens when AI toys become too attached to their children. Plague and mad science, AI, genetic engineering, ghosts, Lovecraftian beingstheres a lot of variety here, and not a little humor, but the dark thread is what sticks with you. There are so many ways to envision the end; even a fish story, Threnody for Little Girl, With Tuna, At the End of the World, that had me tearing up. Just a little.

Margaret Rogerson, Sorcery of Thorns (McElderry 978-1-4814-9761-9, $17.99, 453pp, hc) June 2019. Cover by Charlie Bowater.

Libraries and books come alive in this young-adult fantasy about an orphan raised to protect books of spells from the demon-wielding sorcerers who would misuse them. Elisabeth Scrivener, an apprentice librarian in the Great Library of Summershall, dreams of becoming one of the magic-fighting wardens, but things start going wrong. The librarys Director is killed, and a grimoire gets loose and turns into an evil Malefict and has to be destroyed. Elisabeth, who managed to stop the Malefict, is accused of the crime, and carted off to the capital by the powerful sorcerer Nathaniel Thorn who, it turns out, is only 18, and not pure evil as Elisabeth had been raised to expect. Even his demon, Silas, turns out to be less terrifying than punctilious, at least most of the time. Someone is out to stop Elisabeth from telling the truth, and she ends up fighting for her life, facing a high society she doesnt understand, escaping an appalling hospital for disturbed females, and ultimately works to save the world from a sorcerer backed by an ancient conspiracy. With Nathaniels help, she ultimately succeeds, but at a cost. The fantastic battles and magical encounters are nearly non-stop, leavened by Elisabeth and Nathaniels rocky relationship, which is beset by all sorts of absurd misconceptions that both have to get past if they are to work together. The humor and touches of romance make a charming counterpoint to the grim magics they face. Add books that want to join in the fighting and libraries that can choose whom to help, statues that come alive, and otherworldly encounters, and its a wonderfully dramatic and colorfully weird fantasy with a special appeal for book lovers.

Carolyn F. Cushman, Senior Editor, has worked for Locus since 1985, the longest of any of the current staff, and handles our in-house books database, writes our New and Notable section, and does the monthly Books Received column. She is a graduate of Western Washington University with a degree in English. She published a fantasy novel, Witch and Wombat, in 1994.

This review and more like it in the November 2019 issue of Locus.

While you are here, please take a moment to support Locus with a one-time or recurring donation. We rely on reader donations to keep the magazine and site going, and would like to keep the site paywall free, but WE NEED YOUR FINANCIAL SUPPORT to continue quality coverage of the science fiction and fantasy field.

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Carolyn Cushman Reviews Laughter at the Academy by Seanan McGuire and Sorcery of Thorns by Margaret Rogerson - Locus Online

One of the more dramatic retcons that Star Wars: The Rise of Skywalker established was making Snoke a puppet of Palpatine all along. I have been every voice you have ever heard inside your head, Palpatine says early in the film, transitioning from his own voice to Snokes and then to Darth Vaders to really drive that point home. I made Snoke! Then we see a few Snoke clones growing in a vat, implying that the Supreme Leader was always just some kind of artificial humanoid alien created and used by Palpatine.

A new canon comic, however, complicates matters by trying to make Snoke even more of his own person. Has Star Wars become the war of the retcons? And which version of Snoke are we supposed to believe?

Star Wars: The Rise of Kylo Ren #2 was released Wednesday, and in it, we see more of Ben Solos visit to Snoke that began in the first issue. After he flees from the destruction of Luke Skywalkers Jedi academy, he heads straight to some small space station thats a floating greenhouse of sorts. There, Snoke admits that he was not born Snoke.

If he was not born Snoke, then who was he before? Were meant to see an obvious parallel between Darth Vader and Anakin Skywalker, between Ben Solo and Kylo Ren, the idea that to fully embrace the Dark side, a person has to cast aside their original identity and become something new.

This makes it seem like hes not just an empty vessel controlled by Palpatine, assuming hes telling the truth about being somebody other than Snoke at some point. Was he a sentient person that became Snoke when he embraced the Dark side, and then Palpatine took control over that body and cloned it? Or are we supposed to believe this is Palpatine saying these words through Snokes mouth and lying? Something doesnt quite add up here.

All this talk of names comes up when Ben Solo complains about the legacy of his own name. Theres Ben after Obi-Wan Kenobi, the fake name assumed by a famous Jedi he never even met, yet another reflection of the lofty expectations of his legacy. Then theres Solo, the fake surname assigned to his father by an Imperial soldier. To Ben Solo, both of his names feel like a lie.

Who will you become? Snoke asks Ben Solo. The way of the Dark side is to embrace this new identity, and The Rise of Kylo Ren is setting up an inevitable confrontation between Ben Solo and Ren, who at this point in time leads the Knights of Ren. Hes not around for the new trilogy, so Ben Solo will probably have to kill him by the end of this series and assume his name.

This isnt even the first time that The Rise of Kylo Ren writer Charles Soule has adjusted Snokes story in surprising ways. In The Rise of Kylo Ren #1, Ben Solo says, Snoke look what Master Luke did to you. Ben Solo has known Snoke for a long time, and Snokes scarring is due to some kind of attack from Luke. However, in The Rise of Skywalker, the Snoke clones on Exogol also have the scarring. Thats not how genetic engineering works.

Theres always the possibility that everything Snoke says in these comics is just Palpatine lying so he can manipulate Ben Solo, but these comic books seem like theyre overcomplicating Snokes identity in ways that are hard to grasp.

Star Wars: The Rise of Kylo Ren #3 will be released February 12, 2020.

Read the original here:
'Rise of Skywalker' theory: Kylo comic joyfully retcons Snoke's big twist - Inverse

Welcome back and happy new year.

The turn of a decade is always a great time for taking stock, for predictions and forecasts about the new era to come. In case you missed it, the Upside published its review of the super-trends of 2010s over the Christmas period and asked readers what they thought the dominating tendencies of the 2020s would be.

There were some thought-provoking responses.

John Simke predicted that the 2020s would mark the end of seven decades of overenthusiastic consumerism:

By 2030, buying consumer goods will not only be looked down on, increasingly it will not be done, particularly in the rich world. This will go far beyond conscious consumption to complete cessation of consumption. This will be led by the younger generation but will be picked up by everyone. Our economy will shift from being consumption led to being savings and investment led, as we spend trillions of dollars on a new energy system and climate change adaptation. Obviously this will be driven by the need to mitigate climate change.

Kevin Fisher in Los Angeles forecast a series of ends. The end of work as we know it, the end of human contact, the end of disease:

I think even in the next decade we will see more and more diseases eradicated completely and as we start to treat illness with in-body genetic engineering we will see hereditary conditions also disappear.

Robbie Morrison in Berlin is buoyant about prospects for a more open society:

I predict open will become a supertrend: more specifically, open civil society organizations and open analysis in pursuit of solutions to our existential crisis of sustainability.

It was the opensource world that bequeathed the ethos, the community norms, the decision processes, the copyleft and permissive open licensing models, the versioning and issues tracking tools, the concept of predominantly online collaboration, and the web platforms in support.

So I see this fledgling supertrend in the raft of new selforganizing civil society communities confronting climate change, including Extinction Rebellion, GermanZero, Fridays for Future, and Scientists for Future.

To this end, Ive embarked on trying to build a community to analyze future zerocarbon energy systems thus, with some background here.

And finally, Tom Forster ran through an exotic list of predictions including skyrocketing pet ownership, drug liberalisation, the return of the city state, anti-fashion, nationalist art and my own favourite, ocean travel:

I think ocean/rail liners will start targeting #generationeasyjet, diversifying their onboard services to subcontract for millennial appetites such as rage rooms, food/beer markets, vegan cuisine, axe throwing, escape games, gin tastings, etc.

As for me, I predict a giddy torrent of optimistic journalism. Already in the last week or so, we have published:

US greenhouse gas emissions fell 2% in 2019, according to preliminary estimates, as cheaper natural gas supplanted coal at a prodigious rate.

Also falling in the US is the cancer death rate, by 2.2% in the latest year on record the biggest ever reported decline.

And it was a good week for auto workers in the US and bakers in the UK. Automakers GM and Ford made more than 1,500 temporary workers permanent members of staff under a new union deal. British baker Greggs gave its 25,000 staff a bonus of up to 300 each, as the company continued to thrive.

Vogue Italias startling decision to publish its January edition without any photos.

Also, various media reports detailing Australian generosity to raise money to battle the bushfires.

But most of all, we loved this NPR piece about the scary moms and crowdfunded activists pressuring the Pakistani government to do something about apocalyptic air pollution.

We had plenty of further suggestions for Upside Legends, following our article just before new year highlighting the unsung heroes who really deserve public acclamation.

Inka Wienbarg wrote:

Salma Zulfiqar started the Migration Project in 2016, she has been producing artwork and delivering her ARTconnects workshops to change perceptions in communities and promote cultural understanding and empower women, in particular vulnerable young women. Her passion and drive to create peaceful communities and have a positive impact has meant that hundreds of people have engaged in her ARTconnects workshops in the Midlands, Manchester, London, Norwich, Greece, the UAE, France and Italy that have all have benefited from her work at a critical time when racism and hate crimes are increasing.

Nicholas Hale nominated his sister, Rachel Bramwell:

Rachel is a reception and special needs teacher at Thatto Heath Community Primary School in St. Helens, Merseyside. Its quite a deprived area and my sister has taught at the Thatto Heath since she qualified as a teacher, 26 years ago. Come rain, shine or freezing snow, my sister is there for her class - day after day, week after week, year after year. I cant even begin to imagine how many childrens lives shes changed for the better.

My sister and I have always shared a love of literature. In her masterpiece, Middlemarch, the great novelist George Eliot writes: The growing good of the world is partly dependent on unhistoric acts; and that things are not so ill with you and me as they might have been, is half owing to the number who lived faithfully a hidden life.

In the British royal household, where the Duke and Duchess of Sussex showed the way towards a more streamlined monarchy.

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'The good of the world partly depends on unhistoric acts' - The Guardian

CEDAR RAPIDS Losing your vision can be an isolating experience, but a new Cedar Rapids-based support groups aims to create a community among blind and visually impaired area residents.

The Blindness Support Group is made up of more than a dozen blind and visually impaired individuals who meet once a month to learn from one another how to overcome barriers specific to their disability.

The group was formed by Jonathan Ice, a Cedar Rapids resident and longtime advocate. The group held its first meeting in March.

When people go blind and by that I mean the whole range of vision loss they feel very isolated, Ice said. They feel like theyre the only one going through this.

To find out youre not alone in this is really a very helpful thing. Not only are you not alone in this, but there are other people who are finding ways of dealing with it, he said.

But Ice emphasized the group is focused on positive experiences.

If its just people having a pity party about how awful it is being blind, its not going to do any good, Ice said. But if you can have people who can share ideas and patterns to cope with the challenges you have as a person, you can do a lot.

For Sarah McDonough, a 42-year-old Coralville resident, the Blindness Support Group has helped her navigate the world safely after her vision was damaged by a stroke two years ago. She has learned how to use a knife and how to cook safely with a hot stove, among other skills, she said.

That has been a huge help to me that I know I have support and help that I can ask for, McDonough said.

In addition to sharing ideas among themselves, the Blindness Support Group invites guests to speak at its meetings. For example, Ice said they have invited an official with the city of Cedar Rapids to learn about public transportation options.

The support group also plans to invite an ophthalmologist, or a vision care specialist, to next months gathering.

Ice found a passion for teaching blindness skills during his time at the Iowa Department for the Blind, where he worked for more than 17 years.

Although Ice was born legally blind, he said he didnt know it until he was diagnosed at age 20.

I just thought my vision was bad, Ice said. Suddenly, I get this label when I was 20, but it was a bit amusing because it didnt really change my life. I was still doing things like playing softball and riding a bike and all the things I was doing before.

But then, Ice said he began to notice things he didnt have in common with people who werent visually impaired. They didnt face job discrimination or lowered expectations from others like he did.

Ice saw the impact support groups statewide had on his clients at the Iowa Department for the Blind, and said he felt it was important to bring a group back to Cedar Rapids.

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Support groups for blind and visually impaired individuals have existed in the past, but they have tapered off over the years.

The second-largest city in the state should have (a support group), too, Ice said.

Meetings are held from 1 to 3 p.m. the fourth Thursday of the month at Cottage Grove Place, Sedlacek Hall, 2115 First Ave. SE, Cedar Rapids. For more information, call Ice at (319) 298-2919 or email jkice89@q.com.

Comments: (319) 368-8536; michaela.ramm@thegazette.com

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Cedar Rapids group formed to support blind, visually impaired residents - The Gazette

January 11, 2020

By Jana ReissReligion News Service

Drawn from his fiction and nonfiction writings, The Reading Life: The Joy of Seeing New Worlds Through Others Eyes takes snippets of C.S. Lewis various writings, all themed around the capacious love he had for books and reading, and gathers them into a gift book perfect for the new year.

Nostalgia for childhood

The pieces are short and well-chosen, and often draw upon nostalgia. Several times in different essays, Lewis reflects on childrens literature as a nourishing source of adult reflection. He says those stories meant something different to him as a mature man than they did in childhood, but that very timelessness is what makes them important to revisit.

When I became a man I put away childish things, including the fear of childishness and the desire to be very grown up, he writes.

This attraction to myth and childrens fantasy leads him to review his friend J.R.R. Tolkiens work. Lewis early reviews of The Hobbit and The Fellowship of the Ring are included in the collection and make for fascinating reading for anyone who loves the series.

He urges people to take The Lord of the Rings books seriously as literature, asserting readers who revisit The Hobbit again and again will realize what deft scholarship and profound reflection have gone to make everything in it so ripe, so friendly, and in its own way so true.

Prediction is dangerous, Lewis writes, but The Hobbit may well prove a classic.

In a similar vein, he notes that true readers just dont have an age-based timetable for what they find interesting:

The neat sorting-out of books into age-groups has only a very sketchy relation with the habits of any real readers. Those of us who are blamed when old for reading childish books were blamed when children for reading books too old for us. No reader worth his salt trots along in obedience to a time-table.

Lewis covers some familiar and controversial questions is it permissible to dog-ear a book? No, he insists; such behavior ought to fill us with shame. (I stubbornly dog-eared that page.) Yet he gives the thumbs-up to marginalia: He underlines, indexes and comments in his books, particularly ones he didnt think were very good, thereby making them his own.

Many an otherwise dull book which I had to read I have enjoyed in this way, with a fine-nibbed pen in my hand: one is making something all the time and [a] book so read acquires the charm of a toy without losing that of a book.

Not all of the essays are lighthearted love letters to the act of reading. In The Case for Reading Old Books, he takes on a question that plagues me constantly: What will turn out to have been the blindnesses of our own age?

When we read writers across the centuries, we are alive to their false assumptions in a way they were not able to be:

Nothing strikes me more when I read the controversies of past ages than the fact that both sides were usually assuming without question a good deal which we should now absolutely deny. We can be sure that the characteristic blindness of the 20th century the blindness about which our posterity will ask, But how could they have thought that? lies where we never would have suspected it, and concerns something about which there is untroubled agreement.

Magic about the past

When we read this collection more than half a century after Lewis death, his own blind spots will seem obvious to us his utter lack of attention to questions of gender, race and colonialism; and his assumption that the Western canon of literature is canonical because it is superior and not simply because it helps to reify those assumptions about gender, race and colonialism.

But thats not the point. Or at least, thats not the only point. That essay, like all great literature, should make us pause and turn the tables on ourselves, and try to spot our own Achilles heels. Its not that there is any magic about the past, as Lewis makes clear. People were not cleverer or more moral then than they are now.

But a regular habit of keeping the clean breeze of the centuries blowing through our minds, as Lewis wrote, broadens our perspective and makes us challenge the unquestioned assumptions of our age in a way that reading only contemporary writers cannot.

Read more from the original source:
Review: Readers will love 'The Reading Life' compiled from CS Lewis' writings - Alabama Baptist

Inclusive education for the specially-abled is one of the most effective ways through which we can move towards a just society that is more sensitive to the needs of the less fortunate among us.

Our society is developing at a rapid pace, the message that needs to be delivered among the people is of social acceptance and inclusion along with creating an environment that is supportive for the learning of people with any form of disability. A socially inclusive society is one in which all people enjoy the same rights and where no one experiences any stigma and discrimination. In India and around the world, many times, people with disabilities are denied the right to go to school, find a job, access health care and take part in political processes. Addressing this very issue and to propagate the idea of inclusivity, Sightsavers supports comprehensive education and social inclusion to ensure that children who are blind or visually impaired are included in mainstream education and people with disabilities such as blindness or visual impairments have an equal right to achieve their full potential, just like everyone else. This is crucial to boosting the confidence of the people with any form of disabilities and making them an equal part of society.

Importance of inclusive education

India is home to nearly 8 million blind people, which is approximately one-fourth of the total blind population in the world. Inclusive education enables children with disabilities to realise their rights, facilitating their participation in, and contribution to society; supports poverty reduction and can tackle discrimination through social integration.

The vision we want to inculcate in the society is for them to practice a system of inclusive education that will ensure people with disabilities to have access to equal educational opportunities. People may be born without a completely functional organ or senses but that shouldnt deter anyone from leading a life of independence and dignity.

Holistic education of children with visual impairment is necessary, as when children with disabilities participate in mainstream education on an equal basis with other children, they learn from an early age that they are valued members of society. A plethora of initiatives are taken by the government and NGOs to ensure people with any form of disability are registered in mainstream schools. Moreover, the practice of inclusive education in schools helps them to participate more actively in general community activities throughout their lives and will promote social acceptance.

Now, the challenge is to ensure learning outcomes, to find the right teacher that is skilled to teach children with disabilities and to create an environment that is supportive of the learning of children with visual impairment. For inclusive education in India to succeed, training of specialist teachers is required. Assistive devices and accessible educational material should be made available, provision of compensatory skills training, suitable infrastructure, better accessibility and building education management and leadership among others for people with visual impairment are of primary importance. Our government should demonstrate scalable, cost-effective approaches to education for children with disabilities.

Need for socially inclusive society

Change is the only constant, hence change in the attitudes of communities, schools and governments by ensuring they adopt socially inclusive policies towards people with disabilities is an important step for making a disabled-friendly India. For a socially inclusive society, it is required to equip disabled people with skills; tools and assistance they need to earn a living and lead an independent life. Access to digital platforms and technology has made it easier for people to learn, adapt and upskill technologically in the recent years. It has created more opportunities and new possibilities for disabled in helping them overcome discrimination, for example, a visually impaired person can now listen to audiobooks and learn. As citizens of this society, we should encourage people with disabilities converse with other children to be active participants in society. For the development of the society, a standardised approach is required for mainstreaming inclusive education and disability inclusion.

We all have to create an environment to make our society more aware and discrimination-free for people with disability. And the situation is improving now. The disabled people are also contributing greatly towards society. Sightsavers India has been working to achieve governments goal on Accessible Elections. The campaignTowards an inclusive election: Leaving no one behind aims at creating awareness regarding accessible election and in ensuring increased participation of the PwDs in voting. Inclusion in the election process with complete participation of people with disabilities (PWDs) is a step in the right direction to ensure that no voter is left behind. Through this initiative, Sightsavers India is encouraging more voters and empowering DPO members (Disabled Peoples Organisation) all the more.

It is important to create an environment where disabled can equally participate in the society and share classrooms with other children in a mainstream education environment from an early age. This can be achieved when we take a step forward to create an inclusive society, where everyone including people with disability (PwDs) are treated alike with equal opportunities and pay. It is crucial to uplift the disableds confidence and send a message to the society that how there are no limitations for people with visual disability.

The author is director-funding and marketing, Sightsavers India

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Education is the first step towards an inclusive India - The Sunday Guardian

PITTSBURGH (KDKA) With the new year upon us, its a good time to take a health check for your family. Have you had your childrens vision checked lately?

Dr. Todd Wolynn, CEO of Kids Plus Pediatrics, explains why its important, when you should have it done and how its improved with the help of technology. Heres his edited conversation with KDKAs Kristine Sorensen.

Kristine Sorensen: Vision care is important because it can have long term impacts, right?

Dr. Todd Wolynn: Absolutely. If not picked up, a vision disorder in childhood can cause permanent disability. Actually, vision problems are the number one cause of disability in children.

Kristine Sorensen: What should parents do?

Dr. Todd Wolynn: Do your regular checks with your pediatrician. We used to not be able to do vision checks until close to age 4, but now have a phone-based application where we can screen kids down to age 1. The American Academy of Pediatrics recommends annual photo screening between the ages of one and three.

Kristine Sorensen: Why is it important to do it as young as possible?

Dr. Todd Wolynn: You want to pick up an eye disorder as early as possible to get treatment early. Sometimes parents may have concern about eye strain, sometimes they call it lazy eye. If that can get detected and diagnosed early, if it is a true vision impairment, the ophthalmologist can take care of that early and help avoid things like surgery down the road.

Kristine Sorensen: And even possibly blindness?

Dr. Todd Wolynn: Yes, amblyopia is one of the leading causes for childhood blindness.

Kristine Sorensen: If your pediatrician doesnt have that app, because its so new, what should you do?

Dr. Todd Wolynn: If your pediatrician or family practice doctor doesnt have it but you have concerns, bring it up to them. If theyre unsure of whats going on, theyll then refer you over to the pediatric ophthalmologist.

Kristine Sorensen: Ive worn glasses since I was about 10 years old, so Im very aware of how important it is. Thank you so much for the advice.

Read the original post:
Kidsburgh Kidcast: Importance of Vision Screening - CBS Pittsburgh

Jesse Bloom, left, and Lea Starita are genetic scientists pursuing advances with the technique known as Deep Mutational Scanning, which will be the subject of a symposium and workshop at the University of Washington in Seattle on Jan. 13 and 14. (GeekWire Photo / Todd Bishop)

It has been nearly two decades since scientists accomplished the first complete sequencing of the human genome. This historic moment gave us an unprecedented view of human DNA, the genetic code that determines everything from our eye color to our chance of disease, unlocking some of the biggest mysteries of human life.

Twenty years later, despite the prevalence of genetic sequencing, considerable work remains to fulfill the promise of these advances to alleviate and cure human illness and disease.

Scientists and researchers are actually extremely good at reading genomes, but were very, very bad at understanding what were reading, said Lea Starita, co-director of Brotman Baty Institute for Precision Medicines Advanced Technology Lab, and research assistant professor in the Department of Genome Sciences at the University of Washington.

But that is changing thanks to new tools and approaches, including one called Deep Mutational Scanning. This powerful technique for determining genetic variants is generating widespread interest in the field of genetics and personalized medicine, and its the subject of a symposium and workshop on Jan. 13 and 14 at the University of Washington.

I think approaches like Deep Mutational Scanning will eventually allow us to make better countermeasures, both vaccines and drugs that will help us combat even these viruses that are changing very rapidly said Jesse Bloom, an evolutionary and computational biologist at the Fred Hutchinson Cancer Research Center, the Howard Hughes Medical Institute and the University of Washington Department of Genome Sciences.

Bloom, who researches the evolution of viruses, will deliver the keynote at the symposium, held by the Brotman Baty Institute and the Center for the Multiplex Assessment of Phenotype.

On this episode of the GeekWire Health Tech Podcast, we get a preview and a deeper understanding of Deep Mutational Scanning from Bloom and Starita.

Listen to the episode above, or subscribe in your favorite podcast app, and continue reading for an edited transcript.

Todd Bishop: Lets start with the landscape for precision medicine and personalized medicine. Can you give us a laypersons understanding of how personalized medicine differs from the medicine that most of us have encountered in our lives?

Lea Starita: One of the goals of precision medicine is to use the genomic sequence, the DNA sequence of the human in front of the doctor, to inform the best course of action that would be tailored to that person given their set of genes and the mutations within them.

TB: Some people in general might respond to certain treatments in certain ways and others might not. Today we dont know necessarily why thats the case, but personalized medicine is a quest to tailor the treatment or

Starita: To the individual. Exactly. Thats kind of personalized medicine, but you could also extend that to infectious disease to make sure that youre actually treating the pathogen that the person has, not the general pathogen, if you would. How would you say that, Jesse?

Jesse Bloom: I would elaborate on what Lea said when it comes to infectious diseases and other diseases. Not everybody gets equally sick when they are afflicted with the same underlying thing, and people tend to respond very differently to treatments. That obviously goes for genetic diseases caused by changes in our own genes like cancer, and it also happens with infectious diseases. For instance, the flu virus. Different people will get flu in the same year and some of them will get sicker than others, and thats personalized variation. Obviously wed like to be able to understand what the basis of that variation is and why some people get more sick in some years than others.

TB: Where are we today as a society, as a world, in the evolution of personalized medicine?

Starita: Pretty close to the starting line still. Theres been revolutions in DNA sequencing, for example. Weve got a thousand dollar genome, right? So were actually extremely good at reading genomes, but were very, very bad at understanding what were reading. So you could imagine youve got a human genome, its three billion base pairs times two, because youve got two copies of your genome, one from your mother, one from your father, and within that theres going to be millions of changes, little spelling mistakes all over the genome. We are right now very, very, very I cant even use enough verys bad at predicting which ones of those spelling mistakes are going to either be associated with disease or predictive of disease, even for genes where we know a lot about it. Even if that spelling mistake is in a spot in the genome we know a lot about, say breast cancer genes or something like that, we are still extraordinarily bad at understanding or predicting what effects those changes might have on health.

Bloom: In our research, were obviously also interested in how the genetics of a person influences how sick they get with an infectious disease, but we especially focus on the fact that the viruses themselves are changing a lot, as well. So theres changes in the virus as well as the fact that were all genetically different and those will interact with each other. In both cases, it really comes back to what Lea is saying is that I think weve reached the point in a lot of these fields where we can now determine the sequences of a humans genome or we can determine the sequence of a virus genome relatively easily. But its still very hard to understand what those changes mean. And so, thats really the goal of what were trying to do.

TB: What is deep mutational scanning in this context?

Lea Starita: A mutation is a change in the DNA sequence. DNA is just As, Cs, Ts and Gs. Some mutations which are called variants are harmless. You can think of a spelling mistake or a difference in spelling that wouldnt change the word, right? So the American gray, which is G-R-A-Y versus the British grey, G-R-E-Y. If you saw that in a sentence, its gray. Its the color.

But then it could be a spelling mistake that completely blows up the function of a protein, and then in that case, somebody could have a terrible genetic disease or could have an extremely high risk of cancer, or a flu virus could now be resistant to a drug or something like that, or resistant to your immune response. Or, mutations could also be beneficial, right? This is what allows evolution. This is how flu viruses of all the bacteria evolve to become drug resistant or gain some new enzymatic function that it needs to survive.

Bloom: For instance, in the case of mutations in the human genome, we know that everybody has mutations relative to the average human. Some of those mutations will have really major effects, some of them wont. The very traditional way or the way that people have first tried to understand what those mutations do is to sequence the genomes of a group of people and then compare them. Maybe here are people who got cancer and here are people who didnt get cancer and now you look to see which mutations are in the group that got cancer versus the group that didnt, and youll try to hypothesize that the mutations that are enriched in the group that did get cancer are associated with causing cancer.

This is a really powerful approach, but it comes with a shortcoming which is that theres a lot of mutations, and it gets very expensive to look across very, very large groups of people. And so the idea of a technique like deep mutational scanning is that we could simply do an experiment where we test all of the mutations on their own and we wouldnt have to do these sort of complicated population level comparisons to get at the answer. Because when youre comparing two people in the population, they tend to be different in a lot of ways, and its not a very well-controlled comparison. Whereas you can set up something in the lab where you have a gene that does have this mutation and does not have this mutation, and you can really directly see what the effect of that mutation is. Really, people have been doing that sort of experiment for many decades now. Whats new about deep mutational scanning is the idea that you can do that experiment on a lot of mutations all at once.

Starita: And its called deep because we try to make every possible spelling mistake. So every possible change in the amino acid sequence or the nucleotide sequence, which is the A, C, Ts and Gs, across the entire gene or the sequence were looking at.

Bloom: Lets say we were to compare me and Lea to figure out why one of us had some disease and other ones didnt. We could compare our genomes and theres going to be a lot of differences between them, and were not really going to know what difference is responsible. We dont even really know if it would be a change in their genomes thats responsible. It could be a change in something about our environment. So the idea behind deep mutational scanning is we would just take one gene. So in the case of Lea, she studies a particular gene thats related to breast cancer, and we would just make all of the individual changes in that gene and test what they do one by one. And then subsequently if we were to see that a mutation has some effect, if we were to then observe that mutation when we sequenced someones genome, we would have some idea of what it does.

Starita: The deep mutational scanning, the deep part is making all possible changes. We have all of that information at hand in an Excel file somewhere in the lab that says that this mutation is likely to cause damage to the function of the protein or the activity of the protein that it encodes. Making all of the possible mutations. Thats where the deep comes from.

TB: How exactly are you doing this? Is it because of advances in computer processing or is it because of a change in approach that has enabled this increase in volume of the different mutations you can look at?

Bloom: I would say that theres a number of technologies that have improved, but the really key one is the idea that the whole experiment can be done all at once. The traditional, if you were to go back a few decades way of doing an experiment like this, would be take one tube and put, lets say the normal or un-mutated gene variant in that, and then have another tube which has the mutant that you care about, and have somehow do an experiment on each of those two tubes and that works well.

But you can imagine if you had 10,000 tubes, it might start to become a little bit more difficult. And so the idea is that really the same way that people have gotten very good at sequencing all of these genomes, you can also use to make all of these measurements at once. The idea is you would now put all of different mutants together in the same tube and you would somehow set up the experiment, and this is really the crucial part of the whole thing, set up the experiment such that the cell or the virus or whatever youre looking at, how well it can grow in that tube depends on the effect of that mutation. And then you can just use the sequencing to read out how the frequencies of all of these mutations have changed. You would see that a good mutation that lets say helped the cell grow better would be more representative in the tube at the end, and a bad mutation would be less representative in the tube. And by doing this you could in principle group together tens of thousands or even hundreds of thousands or millions of mutations all at once and read it all out in one experiment.

Starita: This has been enabled by that same revolution that has given us the thousand dollar genome. These DNA sequencers that were now using, not really to sequence human genomes, but were using them as very expensive counting machines. So, were identifying the mutation and were counting it. Thats basically what were using the sequencers for. Instead of sequencing human genomes, were using them as a tool to count all of these different pieces of DNA that are in these cells.

TB: At what stage of development is deep mutational scanning?

Starita: It started about 10 years ago. The first couple of papers came out in 2009 and 2010 actually from the Genome Sciences department at University of Washington. Those started with short sequences and very simplified experiments, and we have been working over the years to build mutational scanning into better and more accurate model systems, but that are increasing the complexity of these experiments. And so weve gone from almost, Hey, thats a cute experiment you guys did, to doing impactful work that people are using in clinical genetics and things like that.

TB: When youre at a holiday party and somebody asks you what you do and then they get really into it and they ask you, Wait, what are the implications of not only personalized medicine but this deep mutational scanning? Whats this going to mean for my life?

Starita: Right now it hasnt been systematically used in the clinic, but well get phone calls from UW pathology that says, Hey, I have a patient that has this variant. We found the sequence variant and this patient has this phenotype. What does this mutation look like in your assay? And were like, Well, it looks like its damaging. And then they put all of that information together and they can actually go back to that patient and say, You are at high risk of cancer. Were going to take medical action. That has happened multiple times. Were working right now to try to figure out how to use the information that we are creating. So these maps of the effect of mutations on these very important proteins and how to systematically use them as evidence for or against their pathogenicity. Right now for a decent percentage of these people who are telling them, Well, youve got changes but we dont know what they do. We want those tests to be more informative. So you go, you get the test, they say, That is a bad one. That ones fine. That mutation is good. That ones OK. That one, though. That ones going to cause you problems. We want more people to have more informative genetic testing because right now in a decent proportion of tests come back with an I have no idea, answer.

Bloom: You can also think about mutations that affect resistance to some sort of drug. For many, many types of drugs, these include drugs against viruses, drugs against cancers and so on, the viruses and the cancers can become resistant by giving mutations that allow them to escape from that drug. In many cases there are even multiple drugs out there and you might have options of which drug to administer, but you might not really know which one. Clinicians have sort of built up lore that this drug tends to work more often or you try this one and then you try this other one, but because how well the drug works is probably in general determined by either the genetic mutations in lets say the cancer or the person or the genetic mutations in the virus or pathogen, if you knew what the effects of those mutations were ahead of time, you could make much more intelligent decisions about which drugs to administer. And there really shouldnt be a drug that works only 50 percent of the time; youre probably just not giving it in the right condition 50 perfect of the time. Wed like to be able to pick the right drug for the right condition all the time.

TB: And thats what precision medicine is about.

Starita: Yes.

TB: Deep mutational scanning as a tool.

Starita: To inform precision medicine.

Bloom: These deep mutational scanning techniques were really developed by people like Jay Shendure and Stan Fields, and Lea and Doug Fowler to look at these questions of precision medicine from the perspective of changes in our human genomes affecting our susceptibility to diseases. I actually work on mutations in a different context, which has mutations in the viruses that infect us and make us sick. These viruses evolve quite rapidly. In the case of flu virus, youre supposed to get the flu vaccine every year. The reason why you have to get it every year is the virus is always changing and we have to make the vaccine keep up with the virus. The same thing is true with drugs against viruses like flu or HIV. Sometimes the viruses will be resistant, sometimes the drugs will work. These again have to do with the very rapid genetic changes that are happening in the virus. So, were trying to use deep mutational scanning to understand how these mutations to these viruses will affect their ability to, lets say, escape someones immunity or escape a drug that might be used to treat that person.

TB: How far along are you on that path?

Bloom: Were making progress. One of the key things weve found is that the same mutation of the virus might have a different impact for different people. So we found using these approaches that the ways that you mutate a virus will allow the virus sometimes to escape from one persons immunity much better than from another persons immunity. And so were really right now trying to map out the heterogeneity across different people. And hopefully that could be used to understand what makes some people susceptible to a very specific viral strain versus other people.

TB: And so then would your research extend into the mutations in human genes in addition to the changes in the virus?

Bloom: You could imagine eventually wanting to look at all of those combinations together, and we are very interested in this, but the immediate research were focusing on right now actually probably is not so much driven by the genetics of the humans. In the case of influenza virus, like I was saying, we found that if theres a virus that has some particular mutation, it might, lets say, allow it to escape from your immunity but not allow it to escape from the immunity of me or Lea. That doesnt seem to be driven as much we think by our genetics, but rather our exposure histories. So in the case of influenza, were not born with any immunity to influenza virus. We build up that immunity over the course of our lifetime because we either get infected with flu or we get vaccinated with flu and then our body makes an immune response, which includes antibodies which block the virus. Each of us have our own personal history, not genetic history, but life history of which vaccinations and which infections weve gotten. And so, that will shape how our immune response sees the virus. As a result, we think that that doesnt really have so much of a genetic component as a historical component.

TB: Just going with the flu example, could this result in a future big picture where I go in to get my flu vaccine and its different than the one the next person might go in to get?

Bloom: What we would most like to do is use this knowledge to just design a vaccine that works for everybody. So that would just be the same vaccine that everyone could get. But its a very interesting I think at this point I would say its almost in the thought experiment stage to think about this. When you think of something like cancer, like Lea was saying, you can use these tools to understand when people have mutations that might make them at risk for a cancer, but thats actually often a very hard thing to intervene for, right? Its not so easy to prevent someone from getting cancer even if you know theyre at risk. But obviously if people are able to do that, theyre interested in spending a lot of money to do it, because cancer is a very severe thing and you often have a very long window to treat it.

Something like a flu virus is very much at the other end. If I had the omniscient capability to tell you that three days from now youre going to get infected with flu and youre going to get really sick, we could prevent that. We have the technology basically right now to prevent that, if its nothing else than just telling you to put on a bunch of Purell and dont leave your bedroom. But theres also actually some pretty good interventions including prophylactics to flu that work quite well. But the key thing is, right now we think of everyone in the world as being at risk all the time and you cant be treating everybody in the world all the time against flu. Theres just too many people and the risk that any person

Starita: Not that much Tamiflu on the market.

Bloom: Not that much, and the risk of it So I think to the extent that we could really identify whos at the most risk in any given year, that might allow us to use these interventions in a more targeted way. Thats the idea.

TB: And how does deep mutational scanning lead to that potentially?

Bloom: Yeah. So the idea, and at this point, this is really in the research phase, but the idea is if we could identify that say certain people or certain segments of the population, that because of the way their immunity, lets say, is working makes them very susceptible to the viral mutant that happens to have arisen in this particular year, we could then somehow either suggest that theyre more at risk or, as you suggested, design a vaccine thats specifically tailored to work for them. So thats the idea. I should make clear that that is not anywhere close to anybody even thinking of putting it into economic practice at this point because even the concepts behind it are really quite new. But I do think that theres a lot of potential if we think of these infectious diseases not so much as an act of God, where you just happened to someone sneezed on you as youre walking down the street, but actually a complex interaction between the mutations in the virus and your own either genetics or immune system, we can start to identify who might be more at risk for certain things in certain years, and that would at least open the door to using a lot of interventions we already have.

Starita: The first year was three years ago, and some very enthusiastic graduate students started it. Basically, it was almost like a giant lab meeting where everybody who is interested in this field came. Somebody tweeted it out and then all of a sudden people from UCSF were there and were like, What the heck? It was great and we all talked about the technology and how we were using it. The next year, the Brotman Baty Institute came in and were like, OK, well, maybe if we use some of this gift to support this, we can have a bigger meeting. And then it was 200 people in a big auditorium and that was great. And now this year, its a two-day symposium and workshop, and its also co-sponsored by a grant from the National Human Genome Research Institute. But now weve got hundreds of people, so about 200 people again, but now flying in from all over the world. Weve got invited speakers, and the workshop, which is Tuesday, is a more practical, If youre interested in this, how do you actually do these experiments?

TB: Whats driving the interest in deep mutational scanning?

Bloom: We are starting to have so much genetic information about really everything. It used to be, going back a couple of decades, a big deal to determine even the sequence of a single flu virus. It was totally unthinkable to determine the sequence of a human genome, right? If you dont know what mutations are there, you dont really care that much what they do. Now we can determine the sequence of tens of thousands of flu viruses. I mean, this is happening all the time, and we can determine the sequence of thousands, even tens of thousands of human genomes. So now it becomes, as Lea said, really important to go from just getting these sequences to understanding what the mutations that you observe in these sequences actually will mean for human health.

See this site for more on the Brotman Baty Institute for Precision Medicine and the Deep Mutational Scanning Symposium and Workshop, Jan. 13 and 14 in Seattle. The symposium is free to attend if youre in the Seattle area, and it will also be livestreamed, with archived video available afterward.

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Scientists pursue new genetic insights for health: Inside the world of deep mutational scanning - GeekWire

Doctors say digital technology and data are driving change that will create a different world of medicine in the next couple of decades, a new report from Stanford Medicine finds.

In a survey, physicians, residents and medical students say they expect almost a third of their current duties could be automated in 20 years. And doctors are preparing for that very different healthcare future now, according to the report (PDF).

Nearly half of physicians (73%) and most medical students (73%) are seeking additional training in areas such as advanced statistics, genetic counseling, population health and coding. One-third are studying artificial intelligence, according to the national survey of more than 700 physicians, residents and medical students commissioned by Stanford Medicine to understand how changing trends will reach the doctors office and shape patient care.

"We found that current and future physicians are not only open to new technologies but are actively seeking training in subjects such as data science to enhance care for their patients," saidLloyd Minor, M.D., dean of theStanford UniversitySchool of Medicine, in a statement.

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"We are encouraged by these findings and the opportunity they present to improve patient outcomes. At the same time, we must be clear-eyed about the challenges that may stymie progress, he said.

Key trends that are reshaping healthcare include a maturing digital health market, new health laws opening patient access to data and AI gaining regulatory traction for medical use.

And the jurys still out when it comes to whether the private industrys foray into healthcarein the form of companies such as Amazon, Google and Apple will solve problems.

Physicians, residents and students had mixed views about the impact these companies will have on healthcare, with 30% of students and residents and 21% of physicians still undecided. While patient outcomes are likely to improve, respondents are divided on whether physician effectiveness will improve and say physician job satisfaction will likely decrease, while healthcare costs likely increase.

Other findings include:

The value of data. The survey also showed that providers are heavy digital users and they believe patient data from wearables can be clinically valuable. Nearly half the survey respondents wear a health monitoring device, and most of them use the data to inform their personal healthcare decisions (71% of physicians, 60% of students and residents). A majority of students and residents (78%) and physicians (80%) say self-reported data from a patients health app would be clinically valuable in supporting their care. They also see value in data from consumer genetic testing reports.

Doctors arent prepared to implement innovations. However, most providers dont believe the current generation of practitioners is ready for the data-driven future, even current medical students and residents. When asked to rate the effectiveness of their education to prepare them for these developments, only 18% of current medical students and residents surveyed said that their education was very helpful. And 44% of physicians surveyed said their education was either not very helpful or not helpful at all.

The report pointed to the need to modernize curriculum and training programs so current and future physicians can make the most of new technologies.

The ongoing struggle with medical practice burdens. And, no surprise, physicians and residents say they are struggling under medical practice burdens. Nearly 1 in 5 would change their career path if given the opportunity, citing poor work-life balance and administrative burdens as the top reasons to reconsider their decision.

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Physicians expect almost one-third of their jobs to be automated by 2040, Stanford Medicine report finds - FierceHealthcare

The NHS states that it will be the world-leading healthcare system in its use of cutting-edge genomic technologies to predict and diagnose inherited and acquired disease, and to personalise treatments and interventions. As all diseases are either inherited or acquired, this is no modest claim.

This approach to medical care is known as precision medicine, and given the hype that surrounds the model, you might be forgiven for thinking that the usual practice of imprecise medicine is greatly inferior. And yet it has been the routine and, in many respects, indiscriminate use of effective treatments for a range of common diseases that has improved the health of large numbers of patients over the past few decades.

Precision medicine assumes that genes play a big role in causing diseases and that new treatments targeting genes and their processes can have significant benefits. The government is so enthusiastic about this new approach that in 2019 it offered gene sequencing to the entire UK population, albeit for a fee. In announcing this initiative, Health Secretary Matt Hancock said there are huge benefits to sequencing as many genomes as we can every genome sequenced moves us a step closer to unlocking life-saving treatments.

But just how big are the benefits likely to be? How relevant is precision medicine to preventing and treating the diseases responsible for most premature deaths and hospital admissions in the UK, such as heart disease, stroke, hip fracture and dementia diseases where genetic links are not clear.

In a study of half a million participants in the UK Biobank project, 1.7 million separate gene variants were shown to be associated with heart disease. Yet in combination, these variants accounted for less than 3% of heart disease after considering known causes such as smoking and high cholesterol.

Precision medicine seems likely to offer most promise for preventing and treating less common diseases, as they are more likely to have a major genetic cause. The poster child for precision medicine is the drug trastuzumab (also known as Herceptin), which was developed following the discovery of HER2, a genetic factor implicated in about 20% of breast cancer cases.

Trastuzumab targets a specific biological mechanism that is involved in HER2 positive cancer, and treatment with this drug improves survival and reduces cancer recurrence. But the effects are not quite as remarkable as has been sometimes suggested. A meta-analysis of clinical trials reported that after ten years, 74% of patients treated with trastuzumab remained alive and recurrence-free compared with 62% of those who did not receive trastuzumab. A worthwhile effect for sure, but only for about 10-15% of patients.

Comparing these important but small gains with the impact of an imprecise approach taken to other diseases offers a stark contrast. For example, HIV used to be a death sentence. Today, 94% of people with the disease are still alive after 30 years, thanks to antiretroviral drugs. Similarly, deaths in the five-year period following a heart attack declined by 70% between 1979 and 2013, largely due to the routine use of drugs such as aspirin, ACE inhibitors and statins.

Interestingly, for both heart attacks and HIV, when efforts have been made to personalise treatment, it has generally led to worse outcomes; in large part as a consequence of doctors withholding treatments they believe may not be beneficial or could be dangerous for a particular person. Unfortunately, such clinical insights are more often wrong than right.

Its hard not to conclude that the nations health would be better served by the NHS if it aspired to be a global leader in the standardisation of care for common serious diseases. Lets not let the current enthusiasm for precision medicine blind us to the benefits of the imprecise medicine we know saves millions of lives every year.

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In defence of imprecise medicine: the benefits of routine treatments for common diseases - The Conversation UK

SOUTH SAN FRANCISCO, Calif., Jan. 10, 2020 /PRNewswire/ -- IDEAYA Biosciences, Inc. (NASDAQ:IDYA), an oncology-focused precision medicine company committed to the discovery and development of targeted therapeutics, announced that the company has entered into a Sponsored Research Agreement with Boston Children's Hospital for preclinical evaluation of the role of protein kinase C (PKC) in Sturge Weber syndrome (SWS), a rare neurocutaneous disorder characterized by capillary malformations and associated with mutations in GNAQ.

Under the agreement, IDEAYA will collaborate with and support research at Boston Children's Hospital in the laboratory of Dr. Joyce Bischoff, Ph.D., Research Associate, Department of Surgery and Professor, Harvard Medical School, who is Principal Investigator of the research studies. The preclinical research will evaluate IDE196, a potent, selective PKC inhibitor, in vitro to assess whether pharmacological inhibition of PKC in endothelial cells having GNAQ mutations will restore normal cell function, as well as in vivo to assess whether pharmacological inhibition of PKC can regulate blood vessel size in murine models that recapitulate enlarged vessels seen in SWS capillary malformations.

SWS is a rare disease characterized by a facial birthmark, neurological abnormalities (e.g. seizures) and glaucoma, which occurs in 1 to 20,000 to 50,000 live births. The disease is believed to be mediated by a somatic GNAQ mutation in skin or brain tissue which enhances signaling in the PKC pathway in a reported 88% (n=26) of SWS patients. (NEJM Shirley et al., May 2019). "SWS is a rare disease that can present debilitating symptoms for patients, such as choroidal hemangiomas which may lead to glaucoma. There are no current FDA approved treatments specifically developed for SWS highlighting the high unmet medical need for these patients," noted Dr. Bischoff, Ph.D.

IDE196 is a potent, selective, small molecule inhibitor of protein kinase C (PKC), which IDEAYA is evaluating in a Phase 1/2 basket trial in patients with Metastatic Uveal Melanoma or other solid tumors, such as cutaneous melanoma, having GNAQ or GNA11 hotspot mutations which enhance signaling in the PKC pathway. "We are excited to work with Boston Children's Hospital to evaluate IDE196 activity in preclinical models relevant to Sturge Weber, a rare disease believed to be driven by genetic mutation of GNAQ. This important work is part of our broader strategy to deliver precision medicine therapies for patients with GNAQ or GNA11 mutations, by targeting the underlying biology of the disease," said Yujiro S. Hata,Chief Executive Officer and President at IDEAYA Biosciences.

About IDEAYA Biosciences

IDEAYA is an oncology-focused precision medicine company committed to the discovery and development of targeted therapeutics for patient populations selected using molecular diagnostics. IDEAYA's approach integrates capabilities in identifying and validating translational biomarkers with small molecule drug discovery to select patient populations most likely to benefit from the targeted therapies IDEAYA is developing. IDEAYA is applying these capabilities across multiple classes of precision medicine, including direct targeting of oncogenic pathways and synthetic lethality which represents an emerging class of precision medicine targets.

Forward-Looking Statements

This press release contains forward-looking statements, including, but not limited to, statements related to IDE196 activity in preclinical models relevant to Sturge Weberand IDEAYA's ability to deliver precision medicine therapies. Such forward-looking statements involve substantial risks and uncertainties that could cause IDEAYA's preclinical and clinical development programs, future results, performance or achievements to differ significantly from those expressed or implied by the forward-looking statements. Such risks and uncertainties include, among others, the uncertainties inherent in the drug development process, including IDEAYA's programs' early stage of development, the process of designing and conducting preclinical and clinical trials, the regulatory approval processes, the timing of regulatory filings, the challenges associated with manufacturing drug products, IDEAYA's ability to successfully establish, protect and defend its intellectual property and other matters that could affect the sufficiency of existing cash to fund operations. IDEAYA undertakes no obligation to update or revise any forward-looking statements. For a further description of the risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to the business of IDEAYA in general, see IDEAYA's recent Quarterly Report on Form 10-Q filed on November 13, 2019 and any current and periodic reports filed with the U.S. Securities and Exchange Commission.

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IDEAYA Biosciences and Boston Children's Hospital Collaborate on Preclinical Evaluation of IDE196 for Sturge Weber Syndrome - a Rare Disease...

Biofidelity assay has potential to make high precision, cost-effective and non-invasive diagnosis more widely available, improving treatment and patient outcomes

Cambridge, UK, 9th January 2020 Biofidelity Ltd, a company developing high performing novel molecular assays for the detection of targeted, low-frequency genetic mutations, today announced the successful completion of a study to detect key lung cancer mutations in collaboration with Agilent Technologies, a global leader in life sciences, diagnostics, and applied chemical markets.

The collaboration, using an assay developed by Biofidelity, demonstrated an improvement in sensitivity of 50 times that achieved with current FDA-approved PCR-based diagnostics, matching that of specialized NGS assays, which require error-correction technology, while providing a dramatic simplification of workflows from more than 100 steps, to just 4 (four). Assays were performed using standard laboratory instrumentation, demonstrating the potential for straightforward adoption of Biofidelitys panels in decentralised testing laboratories around the world.

As well as extremely high sensitivity, 100% specificity was achieved in the detection of multiplexed panels of mutations from both tissue and plasma, with no false positives observed across more than 750 assays. Analysis of results is also dramatically simpler than sequencing-based assays, providing physicians a clear, simple, actionable result, with a turnaround time of less than 3 hours, making the Biofidelity assay suitable for recurrent patient monitoring.

Genetic testing for lung cancer mutations is usually carried out through invasive tissue biopsy, an expensive procedure carrying significant risk for patients with advanced disease. Up to 10% of such tests fail due to the lack of sensitivity of current testing solutions and poor sample quality.

Liquid biopsy, or testing directly from the patients blood, offers a non-invasive alternative with significant potential benefits to patients. However, its use has been limited by the lack of cost-effective, robust and rapid tests which are sufficiently sensitive to enable detection of the very small fractions of tumor DNA present in such samples.

Of the nearly 2 million new cases of non-small-cell lung cancer (NSCLC) diagnosed each year worldwide, fewer than 5% of patients receive high-sensitivity, non-invasive genetic testing. The assay developed by Biofidelity could provide a simple solution, enabling access to high-precision genetic testing for more than 1.7m new NSCLC patients every year with a test that outperforms DNA sequencing in a fraction of the time.

Work was supported by InnovateUK grant number 105202 as part of the Investment Accelerator: Innovation in Precision Medicine program.

Dr Barnaby Balmforth, Chief Executive Officer of Biofidelity, commented: Our goal is to improve patient outcomes in oncology by enabling much greater access to the highest precision diagnostic tests. This collaboration with Agilent in lung cancer has again demonstrated that Biofidelitys molecular assays dramatically increase the effectiveness and speed of diagnosis, supporting early detection of disease, better targeting of therapies and improved patient monitoring. By combining diagnostic outperformance and rapid results in a simple, cost-efficient format using existing instrumentation, we believe we have the potential to bring high precision testing to many more NSCLC patients, substantially reducing the need for invasive biopsies.

Tad Weems, Managing Director, Agilent Early Stage Partnerships, commented: As both a scientific collaborator and an investor in the company, Agilent has been impressed by the data from Biofidelitys assays, which detected a selection of NSCLC DNA mutations at extremely low frequencies in both tissue and plasma samples without the need for DNA sequencing. Biofidelitys assays are specific and sensitive, with the potential to provide improved and rapid routine cancer diagnostics.

Notes To Editors

About Biofidelity

Biofidelity has developed a molecular assay with a simple workflow and fast time-to-result which can transform the detection of genetic abnormalities within a sample by reliably detecting large panels of DNA mutations at extremely low frequencies.

This assay has a simple workflow and is suitable for routine use in diagnostics labs around the world, without the need for investment in new instrumentation or infrastructure.

Biofidelity is developing genetic panels for use in precision medicine and patient monitoring across a range of diseases including NSCLC and colorectal cancer

Located in Cambridge, UK, Biofidelity is a private company founded in 2019.

For more information, visit http://www.biofidelity.com, or follow us on LinkedIn: Biofidelity.

Issued for and on behalf of Biofidelity by Instinctif Partners.For more information please contact:

BiofidelityDr Barnaby Balmforth, CEOT: +44 1223 358652E: info@biofidelity.com

Instinctif PartnersTim Watson / Genevieve WilsonT: +44 20 7457 2020E: Biofidelity@instinctif.com

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Biofidelity and Agilent complete successful molecular assay study for rapid and accurate detection of key lung cancer mutations - BioSpace

The advent of large data sets from many sources (big data), machine learning, and artificial intelligence (AI) are poised to revolutionize asthma care on both the investigative and clinical levels, according to an article published in the Journal of Allergy and Clinical Immunology.

According to the researchers, a patient with asthma endures approximately 2190 hours of experiencing and treating or not treating their asthma symptoms. During 15-minute clinic visits, only a short amount of time is spent understanding and treating what is a complex disease, and only a fraction of the necessary data is captured in the electronic health record.

Our patients and the pace of data growth are compelling us to incorporate insights from Big Data to inform care, the researchers posit. Predictive analytics, using machine learning and artificial intelligence has revolutionized many industries, including the healthcare industry.

When used effectively, big data, in conjunction with electronic health record data, can transform the patients healthcare experience. This is especially important as healthcare continues to embrace both e-health and telehealth practices. The data resulting from these thoughtful digital health innovations can result in personalized asthma management, improve timeliness of care, and capture objective measures of treatment response.

According to the researchers, the use of machine learning algorithms and AI to predict asthma exacerbations and patterns of healthcare utilization are within both technical and clinical reach. The ability to predict who is likely to experience an asthma attack, as well as when that attack may occur, will ultimately optimize healthcare resources and personalize patient management.

The use of longitudinal birth cohort studies and multicenter collaborations like the Severe Asthma Research Program have given clinical investigators a broader understanding of the pathophysiology, natural history, phenotypes, seasonality, genetics, epigenetics, and biomarkers of the disease. Machine learning and data-driven methods have utilized this data, often in the form of large datasets, to cluster patients into genetic, molecular, and immune phenotypes. These clusters have led to work in the genomics and pharmacogenomics fields that should ultimately lead to high-fidelity exacerbation predictions and the advent of true precision medicine.

This work, the researchers noted, if translated into clinical practice can potentially link genetic traits to phenotypes that can for example predict rapid response, or non-response to medications like albuterol and steroids, or identify an individuals risk for cortisol suppression.

As with any innovation, though, challenges abound. One in particular is the siloed nature of the clinical and scientific insights about asthma that have come to light in recent years. Although data are now being generated and interpreted across various domains, researchers must still contend with a lack of data standards and disease definitions, data interoperability and sharing difficulties, and concerns about data quality and fidelity.

Machine learning and AI present their own challenges; namely, those who utilize these technologies must consider the issues of fairness, bias, privacy, and medical bioethics. Legal accountability and medical responsibility issues must also be considered as algorithms are adopted into routine practice.

We must, as clinicians and researchers, constructively transform the concern and lack of understanding many clinicians have about digital health, [machine learning], and [artificial intelligence] into educated and critical engagement, the researchers concluded. Our job is to use [machine learning and artificial intelligence] tools to understand and predict how asthma affects patients and help us make decisions at the patient and population levels to treat it better.

Reference

Messinger AI, Luo G, Deterding RR. The doctor will see you now: How machine learning and artificial intelligence can extend our understanding and treatment of asthma [published online December 25, 2019]. J Allergy Clin Immunol. doi: 10.1016/j.jaci.2019.12.898

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Machine Learning and Artificial Intelligence Are Poised to Revolutionize Asthma Care - Pulmonology Advisor

More than 250,000 participants in Pennsylvania and New Jersey have enrolled in Geisingers groundbreaking precision medicine project, MyCode. With DNA sequence and health data currently available on 145,000 of these participants, MyCode is the largest study of its kind in the world.

The program has the potential to help nearly 1,500 people who are at increased risk for potentially life-threatening conditions. Results will allow patients to work with their care providers to prevent or detect disease in its early stages, leading to better health outcomes.

Geisinger has reached a major milestone in precision health, said David H. Ledbetter, Ph.D., executive vice president and chief scientific officer for Geisinger and one of the principal investigators of the MyCode study. This number of enrolled participants speaks to the trust that our community has in Geisingers expertise and the ability we have through this project to make precision health accessible to all of our patients.

MyCode analyzes DNA samples to look for genes known to increase the risk of developing 35 specific health conditions. These include the BRCA1 and BRCA2 genes known to increase risk for breast and ovarian cancer; as well as genes for familial hypercholesterolemia, which can cause early heart attacks and strokes; Lynch syndrome, which can cause early colon, uterine and other cancers; and several heart conditions, including cardiomyopathy and arrythmia.

The project has also identified several genes that can contribute to the development of cognitive disorders. While not always medically actionable, these results can provide valuable information to patients about probable genetic causes for neuropsychiatric conditions like epilepsy, bipolar disorder and depression, as well as learning disabilities and other similar conditions.

There are a lot of genes that have medical actionability, like finding a change in a gene that causes breast cancer and doing more frequent mammograms as a result, said Christa Martin, Ph.D., associate chief scientific officer and one of the principal investigators of the MyCode study. But there are other ones that might not be medically actionable but could have important implications to patients. So, one of our research projects is exploring reporting information back to individuals who have certain brain conditions.

When given the option to receive test results that included genetic changes that could explain their brain condition, more than 90 percent of patients responded in favor of receiving the results. The majority found the information personally useful to explain medical diagnoses they had been dealing with most of their lives.

Giving these patients a unifying medical explanation for their multiple, apparently unrelated learning, behavioral and psychiatric conditions had a powerful impact on these patients and their family members, Dr. Ledbetter said.

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DNA project will aid in early disease detection - Reading Eagle

The U.S. Food and Drug Administration (FDA) has approved avapritinib (Ayvakit; Blueprint Medicines, previously known as BLU-285) for the treatment adults patients with unresectable or metastatic gastrointestinal stromal tumor (GIST), a type of tumor that occurs in the gastrointestinal tract, most commonly in the stomach or small intestine, harboring a platelet-derived growth factor receptor alpha (PDGFRA) exon 18 mutation.

The approval includes GIST that harbors a PDGFRA D842V mutation, which is the most common exon 18 mutation. Avapritinib is a kinase inhibitor, meaning it blocks a type of enzyme called a kinase and helps keeps the cancer cells from growing.

Each year, approximately 5,000 new cases of GIST are diagnosed in the United States. However, GISTs may be more common because small tumors, without clear signs or symptoms, often remain undiagnosed.

CauseGastrointestinal stromal tumors are caused by genetic changes in one of several genes

About 80% of cases are associated with a mutation in the KIT gene, and about 10 percent of cases are associated with a mutation in the PDGFRA gene. Mutations in the KIT and PDGFRA genes are associated with both familial and sporadic GISTs. A small number of affected individuals have mutations in other genes.

GISTs arise from specialized nerve cells found in the walls of the gastrointestinal tract. One or more mutations in the DNA of one of these cells may lead to the development of GIST. These cells aid in the movement of food through the intestines and control various digestive processes.

More than half of GISTs start in the stomach. Most of the others start in the small intestine, but GISTs can start anywhere along the gastrointestinal tract. The activating mutations in PDGFRA have been linked to the development of GISTs, and up to approximately 10% of GIST cases involve mutations of this gene.

Response to PDGFRAGIST harboring a PDGFRA exon 18 mutation do not respond to standard therapies for GIST. However, todays approval provides patients with the first drug specifically approved for GIST harboring this mutation, noted Richard Pazdur, M.D., director of the FDAs Oncology Center of Excellence and acting director of the Office of Oncologic Diseases in the FDAs Center for Drug Evaluation and Research.

Clinical trials showed a high response rate with almost 85% of patients experiencing tumor shrinkage with this targeted drug, Pazdur added.

ApprovalThe FDA approved avapritinib based on the results of a clinical trial involving 43 patients with GIST harboring a PDGFRA exon 18 mutation, including 38 patients with PDGFRA D842V mutation.

In this trial, patients received avapritinib 300 mg or 400 mg orally once daily until disease progression or they experienced unacceptable toxicity. The recommended dose was determined to be 300 mg once daily.

The trial measured how many patients experienced complete or partial shrinkage of their tumors during treatment, referred to as overall response rate or ORR. For patients harboring a PDGFRA exon 18 mutation, the overall response rate was 84%, with 7% having a complete response (CR) and 77% having a partial response (PR).

For the subgroup of patients with PDGFRA D842V mutations, the overall response rate was 89%, with 8% having a complete response and 82% having a partial response. While the median duration of response was not reached, 61% of the responding patients with exon 18 mutations had a response lasting six months or longer (31% of patients with an ongoing response were followed for less than six months).

The full approval of [avapritinib] is based on robust data from our Phase I NAVIGATOR study. This is an incredibly exciting milestone for our company and, more importantly, for GIST patients with a PDGFRA exon 18 mutation, who have been waiting for a new treatment option, explained Jeff Albers, Chief Executive Officer at Blueprint Medicines.

[Avapritinib] is the first of what we hope will be many approved medicines enabled by our research platform. Now, as we begin to deliver [avapritinib] to patients and their healthcare providers, we aim to fortify our leadership in the field of precision medicine and build a foundation for our broader portfolio by pairing our strong research and development capabilities with an equally talented commercial organization focused on addressing patient needs, accelerating diagnostic testing and enabling access, Albers added.

Adverse eventsCommon side effects for patients taking avapritinib were edema (swelling), nausea, fatigue/asthenia (abnormal physical weakness or lack of energy), cognitive impairment, vomiting, decreased appetite, diarrhea, hair color changes, increased lacrimation (secretion of tears), abdominal pain, constipation, rash and dizziness.

Avapritinib can cause intracranial hemorrhage (bleeding that occurs inside the skull) in which case the dose should be reduced, or the drug should be discontinued. The newly approved agent can also cause central nervous system effects including cognitive impairment, dizziness, sleep disorders, mood disorders, speech disorders and hallucinations.

If this happens, the highlights of prescription information specifies that, depending on the severity, the drug should be withheld and then resumed at the same or reduced dose upon improvement or permanently discontinued.

Breakthrough TherapyThe FDA granted this application Breakthrough Therapy designation, which expedites the development and review of drugs that are intended to treat a serious condition, when preliminary clinical evidence indicates that the drug may demonstrate substantial improvement over available therapies.

Avapritinib was also granted Fast Track designation, which expedites the review of drugs to treat serious conditions and fill an unmet medical need. Avapritinib received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs for rare diseases.

New Drug ApplicationAs part of the approval process, the FDA administratively split the proposed indications for avapritinib under the initial New Drug Application (NDA) into two separate NDAs. These NDAs include one for the indication for PDGFRA exon 18 mutant GIST, and one for fourth-line GIST.

The Prescription Drug User Fee Act (PDUFA) action date for the fourth-line GIST indication is currently February 14, 2020. For the NDA for fourth-line GIST an extension of up to three months for the PDUFA action date will likely be required to enable Blueprint Medicines to provide top-line data to the FDA from VOYAGER, a Phase III clinical trial evaluating avapritinib versus regorafenib (Stivarga; Bayer) in third- or fourth-line GIST.

Ongoing studiesIn addition to the approved indication in GIST, Blueprint Medicines is investigating avapritinib in the treatment of acute myeloid leukemia and systemic mastocytosis and systemic mastocytosis with an associated hematologic neoplasm and mast cell leukemia.[1]

These studies are based on the understanding that mutations in two type-3 receptor tyrosine kinases, KIT and FLT3, are common in acute myeloid leukemia and systemic mastocytosis, leading to hyperactivation of key signalling pathways. [1]

Based on the structural similarity between FLT3 and KIT, researchers have found that tyrosine kinase inhibitors targeting either FLT3 or KIT offer significant clinical benefit. [1]

These benefits have been shown in the ongoing PIONEER study, a multicenter, randomized, double-blind, placebo-controlled, phase II study in patients with indolent or smoldering systemic mastocytosis whose symptoms are not adequately controlled by best supportive care. These patients typically have a single driver gain-of-function KIT mutation making them promising candidates for KIT D816V inhibitor therapy, including avapritinib.

Avapritinib is now being studies to help identify the recommended phase II dose (RP2D) in indolent systemic mastocytosis and to investigate efficacy of avapritinib vs. placebo in patients with indolent and smoldering systemic mastocytosis.

Clinical trialsStudy of BLU-285 in Patients With Gastrointestinal Stromal Tumors (GIST) and Other Relapsed and Refractory Solid Tumors (NAVIGATOR) NCT02508532Study of Avapritinib vs Regorafenib in Patients With Locally Advanced Unresectable or Metastatic GIST (VOYAGER) NCT03465722Early Access Program (EAP) for Avapritinib in Patients With Locally Advanced Unresectable or Metastatic GIST NCT03862885Study to Evaluate Efficacy and Safety of Avapritinib (BLU-285), A Selective KIT Mutation-targeted Tyrosine Kinase Inhibitor, in Patients With Advanced Systemic Mastocytosis (PATHFINDER) NCT03580655Study to Evaluate Efficacy and Safety of Avapritinib (BLU-285), A Selective KIT Mutation-targeted Tyrosine Kinase Inhibitor, Versus Placebo in Patients With Indolent and Smoldering Systemic Mastocytosis (PIONEER) NCT03731260

Reference[1] Weisberg E, Meng C, Case AE, et al. Comparison of effects of midostaurin, crenolanib, quizartinib, gilteritinib, sorafenib and BLU-285 on oncogenic mutants of KIT, CBL and FLT3 in haematological malignancies. Br J Haematol. 2019;187(4):488501. doi:10.1111/bjh.16092

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First Targeted Therapy Approved for Rare Mutation of Gastrointestinal Stromal Tumors - OncoZine

As a doctor of Chinese medicine, I'm always looking for ways to get toxins out of my life. Whether it be skin care products, clean eating, or plastics, health is affected by lifestyle behaviors. And, in our current society, we are exposed to an unhealthy amount of chemicals throughout our lifetime, and I believe that they eventually take a toll on our body.

Nutrigenomics is a facet of epigenetics that integrates genomic science with nutrition and other environmental factors such as cigarette smoking, alcohol consumption, and exercise. Each of us carries a blueprint, if you will, within our genetic code, that signals our body to express genetic variations. This means that by studying your individual genetic code, you can help your body minimize unfavorable genetic expressions, like chronic disease.

Even though our genes are fundamental for determining expression and function, what we put in our mouth directly affects the extent to which certain genes are expressed.

This gives an individual a certain power over their genetic expression. But first, you must understand your genes and epigenetics.

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Are You Doing The Wrong Detox For Your Genes? Plus, Foods & Habits To Use - mindbodygreen.com

According to Barringer, rigid hereditary determinism predetermined the absolute limit of African Americans biological and social advancement. He argued that with emancipation came reversion of African Americans to savage status, creating a new, degenerate black generation that could not possibly survive in contact with civilized white society.

Barringer believed that under the conditions of slavery, blacks had advanced beyond their natural selection through selective breeding by slave owners. With emancipation came reversion of African Americans to their original savage nature, which put them on a path toward extinction, accelerated by an irrational procreation which further exacerbated their genetic inferiority and susceptibility to disease and criminality.4

The drastically high incidence of tuberculosis, syphilis and typhoid fever among African Americans (locally and in cities around the country) indicated nothing to Barringer about overcrowded housing or lack of clean water, sanitation or safe meats and pasteurized milk. Instead the high morbidity and mortality rates of African Americans proved the genetic unfitness of a markedly criminal race. Without white intervention, Barringer condemned blacks to a life of barbarism and death. To Barringer, the Negro Problem was more than a political problem; it was a huge public health threat to whites.

Barringers tripartite solution to the Negro Problem was political disfranchisement, transferring responsibility for African American education from black to white teachers, and training blacks to be law-abiding laborers and artisans. As he wrote, Every Negro doctor, lawyer, teacher or other leader in excess of the immediate needs of his own people is an antisocial produce, a social menace.5

Eugenics flourished under the leadership of President Edwin Alderman (1903-27) as he set out to build the research base of the University with recruitment of leading men of eugenic science into schools across Grounds: These included Harvey Jordan, Robert Bean and Lawrence Royster in the medical school; George Ferguson in education; Orlando White as director of UVAs biological station; and Ivey Lewis as chair of biology.

Together these faculty created eugenics research and education programs at UVA and throughout the state, and in doing so, trained UVA students as well as high school and college teachers in eugenic racism. They also collaborated with nationally renowned eugenics investigators, and presented their work at international eugenics meetings. Fully immersed in race science, these men contributed directly and indirectly to ethically contemptuous laws and policies designed to maintain a culture of white supremacy, and exclusionary white privilege.

Jordan, a professor of embryology, genetics and histology, was one of Aldermans early recruits. Joining the faculty in 1907, he served as dean of the medical school from 1939 to 1949. Believing that blacks inherited a susceptibility to contracting diseases such as syphilis and tuberculosis, Jordan called for compulsory registration of all who were ill. He argued that proposed eugenic marriage, segregation and sterilization laws, were public and racial health measures that should form part of the health code, to be administered under the State Police powers.6 The promise of eugenics as a solution to societys ills, and the power of physicians in solving such problems was best summed up when Jordan declared at the 1st International Congress of Eugenics in 1912 that the future physician must also take a more active part in helping to shape legislation in the interest of race welfare.7

Chair of Anatomy Dr. Robert Bean argued that the physical features of African Americans confirmed their inferiority when compared to whites. Furthermore, he advanced human types that represent different degrees of susceptibility of disease may be segregated and given differential treatment.8 Through medical school core courses, Jordan and Bean, combined, taught about 20% of the medical school curriculum.

Along similar lines, George Oscar Ferguson, a professor in the education school, in his use of intelligence testing among blacks, mixed-race and white children concluded, It does not seem possible to raise the scholastic attainment of the Negro to an equality with that of the white. [N]o expenditure of time or money would accomplish this end, since education cannot create mental power, but can only develop that which is innate.9

Eugenics began to shape public policy nationally as early as 1907, when Indiana passed a sterilization law. Two Virginia eugenics laws, both passed in 1924, had a profound impact in the commonwealth and throughout the country. The Virginia Sterilization Act and the Racial Integrity Act not only legalized sterilization of the mentally ill and persons of low literacy, but also cemented discrimination against marginalized and vulnerable populations, including African Americans. These laws codified Jim Crow into every aspect of community life, and in doing so, denied African Americans access to medical care, jobs and fair wages, as well as higher education and professional training. Simply put, eugenic laws created the one drop rule, where one drop of African American blood restricted a person of color to life behind the veil.10

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UVA and the History of Race: Eugenics, the Racial Integrity Act, Health Disparities - UVA Today

(Mainichi)

Some iPS cells for regenerative medicine, distributed by a stock project at Kyoto University's Center for iPS Cell Research and Application (CiRA), showed cancer-related genetic and chromosomal abnormalities when differentiated to the target cells, several sources close to the project revealed.

Some of the iPS cells, even those produced at the same time, showed various abnormalities while others did not, depending on the research institution they were distributed to, prompting experts to voice concerns over their safety. The CiRA has acknowledged the facts, and the cells that developed abnormalities were not used in patients.

The project stockpiles iPS cells provided by the same suppliers at the same time in a cell line. In clinical research and a trial, iPS cells and differentiated cells go through genome analysis, and are transplanted into mice to check whether they turn cancerous. It is then decided which cell line should be distributed to implementing agencies.

Of the 27 cell lines distributed since August 2015, test results were revealed for four. Of these, abnormalities were found in two cell lines. The two cell lines were distributed in several containers to two research institutions, respectively, and were differentiated to the same target cells at each institution.

For one of the cell lines, one institution found a genetic abnormality in relation to cancer, while the other found a numerical disorder in the chromosome. For the other cell line, one institution found a different genetic abnormality, while the other institution did not find any irregularities. Furthermore, the institution that found the abnormality did not find any problems in the cells kept in a different container.s

Genetic abnormalities included a high-risk abnormality, similar to those found in humans with cancer. When implanted in mice, abnormal tissue growth that cannot be seen with normal cells was confirmed.

"No matter what kind of cell, an error could occur during the process of cultivation and differentiation," said specially appointed professor and manufacturing supervisor Masayoshi Tsukahara of the iPS cell stock project. He explained, "There's no other choice but to conduct careful tests before putting them to use."

Several experts in Japan, however, expressed concerns that safety cannot be ensured if test results vary depending on containers.

Michael Snyder, professor at Stanford University's School of Medicine and the director of the Center for Genomics and Personalized Medicine, pointed to the need to evaluate the matter in an open discussion.

(Japanese original by Momoko Suda, Science & Environment News Department)

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Kyoto Univ.-distributed iPS cells found with abnormalities after differentiation - The Mainichi

That's the equivalent of more than 130 every week.

Every year more than 7,000 British drivers lose their licence as a result of poor eyesight, new research has revealed.

Figures uncovered by insurance company Direct Line through a Freedom of Information request show that 19,644 drivers had their licences revoked between January 2017 and September 2019 because their eyesight did not meet the required standard. Thats the equivalent of 134 drivers per week, or more than 7,100 a year.

The figures also show that an average of 12 people a week fail their driving test before it has begun because their eyesight isnt good enough. According to the government, all drivers must be able to read a clean number plate in daylight from a distance of 20 metres - something that is checked by an examiner before the driving test begins.

Night driving eyeglasses on car arm rest

However, it seems that most drivers arent having their eyes tested regularly to find out whether theyre up to scratch. Direct Line quizzed 2,000 UK adults and found that a fifth (21 percent) have not had their eyes tested in the past two years, while three percent confess to never having had an eye test.

Perhaps more worryingly, a quarter of respondents (24 percent) said they would rather wait until their licence was revoked, rather than voluntarily giving up driving because their eyesight had deteriorated. And Direct Line says people are unwilling to report friends and family with worsening eyesight to the DVLA, with only four percent of respondents having taken that course of action.

Elderly man in glasses driving a car

Steve Barrett, head of motor insurance at Direct Line, said drivers should take regular eye tests to make sure they arent putting themselves and others at risk.

If people do not have regular eye tests, they may not even realise their vision is impaired when they get behind the wheel, which leaves them a danger to themselves and other road users, he said. A simple eye test, that takes a moment in time, can ensure drivers have the appropriate corrective glasses or contact lenses so that their vision is adequate to drive.

Senior patient checking vision with special eye equipment

And Dr Nigel Best, clinical spokesperson for Specsavers opticians, said eye tests could uncover changes to our vision that we might struggle to notice.

Our vision can deteriorate slowly, meaning it is sometimes difficult to detect a change ourselves but subtle variations can increasingly affect both perception and reaction time when driving, he said. We welcome this research and hope it will make more road users aware of the risks they run by not having regular eye tests, whether it is potentially losing your driving license or worse, causing a collision on the road.

It takes around 25 minutes for an optician to conduct a thorough vision and eye health check. To take this simple step every two years or more, if recommended by your optician, isnt an arduous task, particularly when you weigh up the potentially negative consequences of driving with impaired vision.

Optician in surgery giving man eye test

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7,000 drivers a year lose their licence over eyesight concerns - Yahoo News UK

These days, when Nancy Cowan greets her famous falcon named Banner, she offers a bow and utters a little chup as a hello.

Banner, who went through a landmark cataract surgery in 2014, does the same in return. This bird of prey and her falconer have a unique relationship the human saved the falcon from an early demise by insisting that Banners eyesight be corrected, and thanks to animal imprinting, the falcon now sees Cowan as her mate.

She sees me as her boyfriend, husband, whatever, Cowan explained.

The imprinting process started after the surgery that gave Banner new lenses in her eyes so she could see again. Everything to Banner was new again and she needed to relearn the world, Cowan said.

Banners eyes were very blurry because she had stitches in the eyes. She had lots of medications and stuff poured into her eyes, Cowan said. We got her home. We thought she could see but we werent sure.

The same perch she sat on every day, the same one she could easily master without sight, became a foreign object. Even her favorite meal, a freshly plucked quail, was strange to her.

Cowan reintroduced Banner to her surroundings through her sense of touch. Once her talons touched the perch, she was able to identify it. The same went for the quail.

Months after the initial procedure, Cowan and her husband, Jim, who run the New Hampshire School of Falconry on their Deering property, discovered one of the implanted lenses in Banners eye had curled up, leaving her with enduring poor sight.

Cowan got back to work.

After a human goes through cataract surgery, a follow-up procedure using lasers to clear up any scar tissue is routine. Cowan found a doctor at Concord Eye Center willing to do the procedure and then pleaded to the New Hampshire Board of Medicine to allow a human procedure to be performed on an animal. Once again, Cowan prevailed.

After the laser cleared up her vision, Banner was seeing the world anew. Thats when she began to view Cowan as Mr. Right.

When falcons get ready to mate they will make a food transfer, Cowan explained.

Thats the males job to bring food to the female, Cowan said. In exchange, the female will offer a piece of food back to the male.

Twice a year, during the mating season for falcons, Banner will excitedly greet Cowan when she delivers a quail and offer a piece back. That was the telltale sign that Banner was in the mood for love, Cowan said.

Cowan is considering whether she could breed Banner, a lanner falcon, with a male gyrfalcon she has at the school. But thats just an idea.

Besides the occasional desire for avian hanky panky, Banners life has mostly returned to normal for a captive bird of prey, except for one thing she isnt used for hunting anymore.

If I can just handle her and have her have a happy life, interact with her as an imprint, thats all I want to do, Cowan said. Im not going to ask her to go into an environment where if she doesnt come back to me shes gonna get killed within a day or two via great horned owl or red tailed hawk. Im not going to ask that.

Visitors still come to the school looking for Banner, who was quite the local celebrity after her story went international, including an article in the London Daily Mail.

It was fantastic, Cowan said. In London, they were very excited. It went all over the world. Shes world-famous.

As a result of Banners celebrity-status and all she has learned from the bird, Cowan is working on a second book, which has the working title Eyesight and Insights, she said.

Boy, they teach you a lot of things that you never would have suspected when you have 11 birds youre dealing with. You really get a different viewpoint of the world than you do normally, Cowan said. So the insights will be there and the eyesight part is going to be about restoring Banners vision. And thats a long story.

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With restored sight, Banner the falcon has relearned the world - Concord Monitor