Let the Libertarian candidate have a say – Bluefield Daily Telegraph

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The Commonwealth of Virginia is set to elect a new governor in November. There are three candidates qualified to be on the ballot but the Republican and Democratic parties are blocking the Libertarian candidate Cliff Hyra from participating.

The voters are entitled to hear from all eligible candidates not just those of the two majority parties. I would like the Bluefield Daily Telegraph and its readers to ask that Mr. Hyra be included in all future debates as the citizens of Virginia need to know all of the options that are available in November.

As three newspapers in Virginia have endorsed this idea as well as this issue being addressed by WVTF-TV in Roanoke as well as Virginia public radio. I think that the Bluefield Daily Telegraph should have the courage to take such a stand.

Greg Gruchacz

Bluefield, Va.

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Let the Libertarian candidate have a say - Bluefield Daily Telegraph

Mosquitoes with West Nile virus found on Toronto Islands – Toronto Star

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Flooding has kept the Toronto Islands closed since the spring. ( Anne-Marie Jackson / Toronto Star file photo )

Mosquitoes carrying the West Nile virus have been found on the Toronto Islands, which are set to reopen Monday following extensive flooding throughout the spring and summer.

An email from a Toronto Public Health official sent Tuesday informed an Island residents group of the latest development in a summer that has left attractions rained out, parks underwater and businesses without customers.

For your information, mosquitoes collected from our traps on the Toronto Islands tested positive for West Nile virus this week, the email stated.

We are continuing to work with Parks, Forestry and Recreation in identifying and remediating mosquito breeding sites on the Islands on a regular basis. It is not only a local problem, as West Nile virus and vector mosquitoes are spread across Toronto and Ontario, but we did want to share this finding with you.

The email included a fact sheet about measures islanders can take to steer clear of the virus.

The city recommends wearing light-coloured, long-sleeved shirts and pants when outdoors and applying bug spray. Residents should also make sure their homes have tight-fitting screens on windows and doors to prevent mosquitoes from getting inside.

The warning comes less than a week before the islands are supposed to reopen to the public, as the city has been working towards a July 31 target.

Toronto Island Park has been closed to the general public since May and ferry service to the Wards Island Dock has been restricted to residents.

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Australia’s Best Islands for Families with Kids – HuffPost

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Australia, the worlds sixth largest country, is not just a single massive landmass. It also boasts beautiful little islands, which serve as one-stop mini vacation destinations that will leave you mesmerized.

Australias smallest islands pack a big punch! Frolick in the Great Barrier Reefs white sand beaches and then watch kangaroos hop around deep-blue ocean waters. Shop for locally made products then enjoy the views on record breaking sea cliffs. Or see where the reef meets the rainforest. For one of a kind vacation combinations, take the kids for a quick trip in one of the best islands in Australia.

Making the top of our list of the best islands in Australia is Hamilton Island. The island known for its white sandy beaches and picturesque turquoise blue waters. Its perfectly situated as a luxurious Great Barrier Reef launch point and the beginning of an unforgetable getaway. Getting to the the island is an easy with a quick ferry ride from the mainland. Stay at one of the top three hotels there: The Beach Club, The Reef View, and Qualia. But try to avoid booking during Australian scoolies week.

Daydream Island is a kids paradise and one of the best island in Australia. Also located in the Whitsundays, it literally brings the reef to you with its famous living reef lagoon. This living reef makes for a uniquely intimate way to experience life on the reef. It is home to more than 140 species of marine fish and 82 species of coral. For vacationing families wanting to get in the water, theres access paddleboards, kayaks, and snorkeling equipment. As it is a popular vacation spot for Australians, avoid going during their school break periods including the first three weeks in April.

Located off the coast of South Australia, Kangaroo Island is home to some of Australias most famous land and sea life. Kangaroos, koalas, Penguins, sea lions and birds galore all call this island home. Its truly one of the best islands in Australia to visit with kids. Take a hike to the top of the jagged sea cliffs or meander along the sandy beaches. As one third of the island being a protected nature reserve, theres not a bad view to be had. Easily accessible from the mainland via the Adelaide airport, this little island is an ocean and animal lovers paradise. The best time to visit for warmer temps: December through February.

Where the rainforest meets the reef is Fitzroy Island, one of the best islands in Australia. A quick ferry or fast cat boat ride from Cairns, Fitzroy Island is an all in one reef-slash-rainforest retreat. It puts you within the waters of the Great Barrier Reef while being surrounded by lush tropical rainforest. You can enjoy the island by hitting the water with some rented snorkeling gear or a glass bottom kayak. Or take in the tropical rainforest and amazing views on one of the islands many hiking trails. Round out your time by scheduling a guided dive in the Great Barrier Reef. Stay on the island for just the day, or choose to stay at one of the resorts. They typically offer three-night or longer package deals for an even more inspired nature experience.

Its a small but mighty island located off the southeastern coast of Tasmania where locally produced everything rule the scene. Bruny Island is known for its locally-produced cheeses, wines, berries, seafood and whiskies. And everything is set among an intensely beautiful and ever-changing landscape of bushwalks and sea cliffs. North and South Bruny Island are connected by a narrow isthmus called the neck. A quick walk here leads you to one of the most striking 360-degree views in all of Australia. While there take a wildlife cruise on the yellow boats, with the Southern Hemispheres tallest sea cliffs against the bright blue sky. If youre looking to spend an artisanal day or two on the one of the best islands in Australia, this ones an excellent pick.

Julie McNamara contributed this to MiniTime.

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Love Island’s Marcel and Gabby reveal they have finally had sex and it was ‘absolutely banging’ – The Sun

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Patience certainly paid off for the pair

LOVE Islands Gabby Allen and Marcel Somerville finally had sex after the Love Island final.

The loved up pair managed to share a bed in the villa for almost two months and not do the deed, but confirmed they had sex as soon as they were away from the cameras.

SWNS:South West News Service

Marcel cheered: We done it yesterday! We done it yesterday!

Gabby added: We had sex last night after the wrap party. We were in a villa with no cameras so we flip reversed it.

And Gabby says her her Blazin Squad boyfriend didnt disappoint.

It was amazing. It definitely lived up to expectations. I was glad I waited.

I would rather have got out and it be absolutely banging than us be underneath the covers trying not to get caught.

He may have had weeks of pent up sexual tension, but Marcel insisted Gabby wasnt left short-changed.

ITV Plc

It wasnt difficult to make the session long lasting. I pre-warned Gabby about my stamina. I lived up to it.

Gabby added: It was impressive. I was like come on! It was after the party too so I was exhausted.

Last week Gabby failed a lie detector test after it said she wasnt telling the truth when she claimed she was looking forward to having sex with Marcel something which she refuses to accept.

The lie detector test this is a bloody machine, its a robot thats telling me how I feel.

They are designed to day yes and no, and there are massive grey areas that you cant go into, but I know what I think and how I feel.

Rex Features

And the he may have came fourth in the show last night, but Marcel admitted when he first joined the island and failed to couple with anyone he wondered whether hed made the worst choice of his life.

Marcel said: I was like, What have you put yourself into, this is the worst choice of your life. What have you done to yourself? Then she came in and I thought boom there she is.

Explaining why it took so long for him to couple up, he said: I was the first boy in I came boom down the steps and obviously I was oozing confidence, but then they realised I was a nice guy.

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Love Island's Marcel and Gabby reveal they have finally had sex and it was 'absolutely banging' - The Sun

Woman, 67, living on one of the world’s most remote islands by … – The Sun

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The citizen scientist spends her days collecting horse skulls to help with research

A WOMAN who has lived alone on a remote island for 40 years insists she never gets lonely as long as shes got her binoculars to hand to admire its stunning wildlife.

Zoe Lucas, 67, livesin a wooden-clad houseon Sable Island off the coast of Canada,which is covered in fog for around 127 days of the year.

Sadie Whitelocks/ MailOnline

Sadie Whitelocks/ MailOnline

But despite that, Zoe feels perfectly at home in the peace and quiet with 400 horses, 300,000 grey seals and 350 species of bird to keep her company on the 26-mile island.

She first fell in love with Sable Island when visiting as a 21-year-old student in 1971 and soon made it her home.

Speaking to MailOnline Travel, Zoe said: I squawked and squawked, I wanted to come so bad. I originally came out here for the horses.

Now a citizen scientist, the 67-year-old rarely returns to her hometown of Halifax in Nova Scotia and instead depends on supplies being flown in on a weekly basis.

There is no way to reach the island, other than by boat or charter plane.

It earned the nickname graveyard of the Atlantic after more than 300 shipwrecks.

Sadie Whitelocks/ MailOnline

Sadie Whitelocks/ MailOnline

SABLE Island is 26 miles long and 0.93 miles across at its widest point.

It is situated 190 miles away from Halifax on the Nova Scotian mainland.

The island is home to400 horses, 300,000 grey seals and 350 species of bird.

In the winter,temperatures average near freezing on the island, with peaks of 20 degrees in the summer.

Sable Island is covered in fog 127 years of the year which is thought to be the reason there have been more than 300 shipwrecks on its shores.

Its only possible to visit the island by boat or charter plane.

On June 20, 2013, Sablebecame a National Park Reserve.

Sadie Whitelocks/ MailOnline

During her four decades living on the island, a refrigerator, crateful of fresh peppers from a shipping container, popped balloon carcasses and even a fake LEG has washed up on the beach.

Zoe spends her days studying ecology and collecting horses skulls so that scientists can discover how the animals have been able to adapt to the islands stark landscape.

In 2013 Sable Island was made a National Park Reserve on June 20, 2013.

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Woman, 67, living on one of the world's most remote islands by ... - The Sun

Human Ancestor Mated with ‘Ghost Lineage’ And the Proof Is in Your Spit – Live Science

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Scientists have found that a "ghost" lineage of archaic human may have interbred with the ancestors of modern humans in what is now sub-Saharan Africa around 200,000 years ago.

A protein that helps make human spit slimy reveals signs that the ancestors of modern humans interbred with an extinct human lineage that was an even more distant relation than Neanderthals, a new study finds.

The ancestors of modern humans once shared the world with ancient human lineages such as the Neanderthals, the closest extinct relatives of modern humans, as well as the Denisovans, which might have once roamed a vast range stretching from Siberia to Southeast Asia. In previous research, DNA extracted from fossilized bones and teeth of Neanderthalsand Denisovanshas revealed that the ancestors of modern humans interbred with both of these groups.

Previous research also suggested that the ancestors of modern humans may have interbred with other human lineages not known from the fossil record. For example, a 2011 studyanalyzing modern human DNA found that the species may have bred with a now-extinct lineage of humanity before leaving Africa. [Denisovan Gallery: Tracing the Genetics of Human Ancestors]

Now, researchers suggest that a "ghost" lineage of ancient humans may have contributed the DNA for a protein called mucin-7 found in the saliva of modern humansliving in sub-Saharan Africa today.

"About 5 to 7 percent of every population in sub-Saharan Africa has this divergent protein," said Omer Gokcumen, study co-senior author of the new study and an evolutionary genomicist at the University at Buffalo in New York.

The scientists were investigating mucin-7 in order to learn more about its role in human health. This molecule helps give saliva its slimy consistency and binds onto microbes, potentially helping rid the body of dangerous germs.

The researchers examined copies of the gene for mucin-7 the gene is called MUC7 in more than 2,500 modern human genomes. The scientists found that a number of genomes from sub-Saharan Africa possessed a version of the MUC7 gene that was wildly different from versions found in other modern humans. In fact, the Neanderthal and Denisovan versions of this gene more closely resembled those of other modern humans than this outlier did.

The researchers suggested the most plausible explanation for this mysterious version of the MUC7 gene is that it came from what they called a "ghost" lineage that is, one that scientists have not found the fossils of yet.

"We were not looking for this discovery we essentially stumbled onto it," Gokcumen told Live Science.

That this variant is so widespread across Africa suggests that it may have entered the modern human gene pool before the ancestors of modern humans separatedinto different regions across that continent, Gokcumen said. Given the usual rate at which genes mutate during the course of time, the researchers estimated the interbreeding event with this mystery lineage "may have happened about 200,000 years ago, but this lineage separated from the ancestors of modern humans maybe 500,000 years or 1 million years ago," Gokcumen added.

The scientists said they aren't sure how the variants of this protein might differ in function. "We do know that MUC7 has two major functions," said study co-senior author Stefan Ruhl, an oral biologist also at the University at Buffalo. "One is helping to lubricate the oral cavity for eating and swallowing, and the other, and this may be more important, is to let good microbes stay in the body and sort out the undesirable ones."

An analysis of mouth, skin, stool and other biological samples from 130 people revealed that different versions of MUC7 were strongly associated with different oral microbiomes the collections of microbes within the mouth. "This suggests that MUC7 is interacting with the oral microbiome and plays a role in terms of viruses, bacteria, parasites or fungi," Ruhl told Live Science. "On the other hand, we haven't ruled out that it may play a role in lubrication say, when it comes to environmental conditions such as dryness of the air."

Future research can explore when and where this interbreeding happened, "and if it happened just once or multiple times," Gokcumen said.

The scientists detailed their findingsonline July 21 in the journal Molecular Biology and Evolution.

Original article on Live Science.

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Human Ancestor Mated with 'Ghost Lineage' And the Proof Is in Your Spit - Live Science

Scientists raise ethics alarm over use of DNA for research – Wired.co.uk

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Grafner

When we choose to donate to biobanks, we often give up ownership of our own blood, saliva, urine and DNA for the sake of scientific research.

Now, ethics commentators are raising questions about whether asking someone for consent when they donate a sample, which can then be used for research purposes long after they die, is sufficient.

In a report published on 25 July in PLOS Biology, University of Alberta health law researchers Timothy Caulfield and Blake Murdoch argue that the legal and ethical principles surrounding consent for biobanking are worryingly vague.

We can volunteer to give our health information to researchers at biobanks so they can help prevent, diagnose and treat a wide range of serious and life-threatening illnesses for future generations. Yet the report argues that a consensus on who owns the samples of blood, urine and saliva, as well as what participants are agreeing to, doesn't exist. These issues are only going to intensify as more people question their rights.

Andrew Trehearne from UK Biobank, which asks donors to agree to give up ownership of samples, questions why a consensus is even necessary: "It's an interesting set of views, but it doesn't seem to offer any suggestions for improvement, and I can't see any detailed specifics. I am not sure why there has to be a consensus on consent type."

The report states that the 'broad' or 'blanket' consent strategies that biobanks use deviate from traditional legal norms. 'Broad consent' refers to when a donor consents to his/her samples being used once at the beginning of a research experiment it's the consent type used by UK Biobank, among others. Biobanks can then continue to use the samples for research purposes, without asking for further consent.

Is such 'passive' consent an issue? It's certainly something which has been debated before. Back in 2013, an article was published in the European Journal of Human Genetics which concluded that the 'broad consent' model is still preferable to using 'dynamic consent', where participants are asked to re-consent to every new experiment or use of their samples.

But the new report out this week says this view is outdated and that the arguments against using specific consent simply because it is 'inefficient and costly', just don't hold up. It's now very easy and cheap to keep in contact with participants electronically, for instance.

The crux of the issue with non-specific consent strategies is that participants might not fully understand what their DNA is being used for. The report argues that only 55 per cent of people agree with blanket consent if their specimens are being used to make profit for commercial companies.

Essentially, they lose trust in biobanks once they think they are receiving funding from industry. Biobanks, however, are reliant on such funding. They work largely on developing personalised medicine, and to get these studies to the clinical trial stage requires money.

What has given rise to these consent concerns now? The report refers to 'social trends', which have led to a discussion on policy namely a rise in support for biorights, the increasing involvement of industry, growing concern about privacy and high profile research controversies.

Biorights centre on the idea that research participants have an ongoing right to control their research samples, to benefit directly from the research, and/or to be financially compensated for their contribution.

People certainly seem not to like the fact they aren't in control, when consent is only given once. A 2016 study in the US found that nearly 44 per cent of a nationally representative sample believed blanket consent was unacceptable, while 38 per cent felt it was the worst in a range of consent policy options.

This hasn't dampened the success of UK Biobank, whose 500,000 participants joined them under broad consent and have remained with them for the duration.

One criteria participants must agree to is: "I give permission for long-term storage and use of my blood and urine samples for health-related research purposes (even after my incapacity or death), and relinquish all rights to these samples which I am donating to UK Biobank."

"We think it's important that [our participants] know what they are doing and what we are using their samples for, which is why we send out annual news letters and host events. Participants are also allowed to withdraw at any time," says Trehearne.

Part of 'what they are doing', is giving permission for long-term storage and use of blood and urine samples for health-related research purposes (even after incapacity or death), and relinquishing all rights to these samples.

Considering participants receive no payment or results on their own health, the vast number that still sign up are contributing, altruistically, to biomedical research.

Still, the issue of whether this is fair and whether agreeing to something once is enough to last a lifetime, is still up for discussion.

In the meantime, biobanks must strive to ensure they obtain proper, legal consent, or risk having to destroy an abundant amount of health data.

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Scientists raise ethics alarm over use of DNA for research - Wired.co.uk

Senate rejects proposal to repeal and replace Obamacare …

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But hours later, the Senate decisively rejected a Republican proposal to repeal-and-replace Obamacare, a sign of the chaos expected to envelop Capitol Hill as GOP leaders work to find a plan their conference can agree to.

Wednesday morning, floor debate on the legislation to overhaul the Affordable Care Act will continue, even though there aren't any guarantees the votes are there to eventually pass it -- and it's unclear what a final bill will look like.

But little may match the drama of Tuesday's vote on the motion to proceed, when Sen. John McCain returned from Arizona to applause from fellow senators to cast what would be a critical vote for the Republicans. Two GOP senators -- Susan Collins and Lisa Murkowski -- sided with all Democrats in opposition, meaning all remaining Republicans and Pence were necessary for the motion to pass.

The vote came as Senate Majority Leader Mitch McConnell and President Donald Trump dared their fellow Republicans to block their seven-year campaign promise to repeal and replace Obamacare.

Senators late Tuesday cast their first vote on what could be dozens of amendments considered to it.

This first vote dealt with a measure that combined a previous Senate proposal known as the Better Care Reconciliation Act -- that was rejected by several Republican senators -- with $100 billion in extra money for people on Medicaid desired by moderate Republicans and a proposal from conservative Sen. Ted Cruz, R-Texas, to allow bare-bones health insurance plans.

Democrats moved successfully to kill the amendment, which was possible because it had not been officially scored by the Congressional Budget Office and therefore didn't meet the complicated reconciliation rules that the Senate is using to consider the bill.

Republicans needed 60 votes to keep the amendment alive. It died on a 43 to 57 vote.

The vote came after a Senate clerk was forced to read the text of the amendment aloud in the Senate chamber, all part of the delaying tactics Democrats employing to express their overall unhappiness with the bill.

On Wednesday, senators are expected to cast a vote on a "repeal-only" proposal. It too is expected to be defeated because many Republicans as well as all Democrats reject repealing without a replacement ready.

The vote was up in the air until the last moments, when several Republican holdouts announced their support, including Sens. Rand Paul, Dean Heller, Rob Portman and Shelley Moore Capito.

Trump, who has repeatedly said he's ready to sign any repeal legislation, celebrated the vote, which creates a path to give him the major congressional victory that's eluded the White House thus far.

"I'm very happy to announce that with zero of the Democrats' votes, the motion to proceed on health care has moved past and now we move forward toward truly great health care for the American people. We look forward to that. This was a big step," Trump said at a White House news conference.

"I want to thank Sen. John McCain," he added. "A very brave man. He made a tough trip to get here."

But while Trump was happy with the result, he also acknowledged there's a long road ahead for the legislation and criticized the two GOP senators who opposed the motion.

"We had two Republicans that went against us, which is very sad, I think," Trump said. "It's very, very sad -- for them. But I'm very, very happy with the result. I believe now we will, over the next week or two, come up with a plan that's going to be really, really wonderful for the American people."

Democrats are united against the bill, saying it would end health care coverage for millions of Americans.

"Anyone who thinks this is over is sadly mistaken," said Minority Leader Chuck Schumer, D-New York. "There are many, many Republicans who don't like this bill, who don't want to vote for it. They are under enormous pressure to vote for it. ... Anyone who voted to move to proceed and certainly anyone who votes to send this bill to conference is virtually, certainly, voting to kick millions off health care, to make it much harder to get coverage if you have a pre-existing condition, to slash Medicaid and give a huge amount of tax cuts to the rich."

Sen. Bernie Sanders Monday called the bill the "cruelest, most destructive and irresponsible piece of legislation ever brought to the United States Senate in the modern history of this country."

In a speech at the NAACP national convention, highlighted the possible effects of the bill's provisions, which include cutting Medicaid, defunding Planned Parenthood and roadblocks for those with pre-existing conditions.

McConnell won over key holdouts on the procedural vote, but those senators haven't said they will back the final measure.

Paul, a Kentucky Republican, said he would support the procedural motion to open debate on the health care bill, so long as leadership guarantees a vote on a full repeal of Obamacare.

"If this is indeed the plan, I will vote to proceed and I will vote for any all measures that are clean repeal," Paul tweeted. Such an amendment would be expected to fail, however.

Heller, who has complained that Obamacare repeal efforts could hurt Nevada residents dependent on Medicaid, nevertheless said he'd vote to move forward. Heller is facing a tough re-election campaign in Nevada next year.

"Obamacare isn't the answer, but doing nothing to try to solve the problems it has created isn't the answer either," Heller said in a statement. "If the final product isn't improved for the state of Nevada, then I will not vote for it; if it is improved, I will support it."

Republican leaders Tuesday worked thread any needle they can to appease other holdouts.

"The only goal is to get onto the bill. Nothing happens until we do, so that's the only goal," a Republican aide said.

"These are the moments legislatively when you get creative. We're getting creative."

This story has been updated.

CNN's Tami Luhby contributed to this report.

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Senate rejects proposal to repeal and replace Obamacare ...

Senate Health Care Vote: Where the Debate Left Off and What Happens Next – New York Times

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An explainer:

When the Senate voted 51-50 to begin debating the repeal of the Affordable Care Act, technically senators were bringing the repeal bill that was passed in the House to the Senate floor. For now, that is the bill that senators are trying to reshape.

On Tuesday night, Senate Republican leaders brought to the floor their most complete version of a plan to repeal and replace the Affordable Care Act. That measure had been worked out behind closed doors by the majority leader, Senator Mitch McConnell of Kentucky, and it would dismantle major parts of the current health care law, including the requirement that most people have health insurance.

But it also included an overture to Senate conservatives, a measure championed by Senator Ted Cruz, Republican of Texas, that would allow insurance companies to sell stripped down, low-cost insurance plans as long as they also offer insurance policies that comply with federal standards, including the requirement that plans cover essential services like maternity care, mental health treatment and prescription drugs.

Three major proposals are being discussed.

For moderates, the legislation includes $100 billion to help pay out-of-pocket medical costs for low-income people.

Because that broad version of the Senate health care measure had not yet been assessed by the nonpartisan Congressional Budget Office, it needed 60 votes to overcome a Democratic objection that it violated Senate rules.

But it got only 43 votes, demonstrating that even after weeks of refining the legislation, Senate leaders still fell far short of enough support for their replacement plan, from both ends of the partys ideological spectrum.

Mr. McCain had previously made clear that he wanted to secure amendments to that broad repeal-and-replace bill. The vote on Tuesday night could be interpreted as a sign of support for that general approach.

The debate goes on.

Senator John McCain, who was recently diagnosed with brain cancer, spoke to the Senate after casting his vote to begin debating legislation to repeal the Affordable Care Act.

Mr. Trump opened the day by attacking Ms. Murkowski.

But Mr. Trumps public shaming is not an effective strategy for Ms. Murkowski, who has dealt with worse from her party. In 2010, Ms. Murkowski retained her Senate seat in a historic win as a write-in candidate. She had lost Alaskas Republican primary that year to a Tea Party challenger and was largely abandoned by Republican leadership. Since then, she has not felt beholden to her party.

Senators are set to consider a different repeal measure on Wednesday.

This measure would repeal major parts of the health law but would not provide a replacement. The legislation resembles a bill that passed the Senate in 2015 but was vetoed by President Barack Obama in early 2016.

Senator Rand Paul, Republican of Kentucky, supports that approach. But some Republicans worry that repealing the law without providing a replacement would leave many Americans without health care coverage. Such a repeal only measure is not expected to garner enough votes for passage.

The vote for this measure had been expected to take place around midday Wednesday, but it has now been delayed until later in the afternoon.

Republicans are using special budget rules to try to pass a repeal bill, so the debate is limited to 20 hours, and Democrats cannot delay it with a filibuster. Later this week, the Senate will hold what is known as a vote-a-rama, an exhausting marathon of amendment votes.

The nine Republicans who voted against the comprehensive replacement measure on Tuesday night are an indication of the problem that Senate Republican leaders continue to confront: The party caucus still does not agree on what should be in a health care repeal bill that would have enough support to win Senate approval.

One solution might be to pass a pared-down health plan that has support from at least 50 of the 52 Republican senators, and then turn to working out a compromise with the House.

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Senate Health Care Vote: Where the Debate Left Off and What Happens Next - New York Times

Senate delays vote on healthcare repeal – The Hill

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The Senate has delayed a vote on a proposal to repeal much of ObamaCare.

The Senate had been expected to vote on the amendment, which would repeal most of the law in two years, from Sen. Rand PaulRand PaulSenate delays vote on healthcare repeal Senate rejects ObamaCare repeal, replacement amendment Overnight Healthcare: Senate votes to begin ObamaCare repeal debate | McCain returns to vote | GOP floats scaled-down healthcare bill MORE (R-Ky.) late Wednesdaymorning, but made a last-minute announcement that it was being delayed until3:30 p.m.

There was a kerfuffle over the point of order. They need to ... make some other arguments to the parliamentarian, he told reporters.

Asked if it was tied to abortion language included in the bill, he said, I believe so.

Democrats were expected to use the Senates rulebook to try to strip out a provision in the repeal amendment that included restrictions on using tax credits to buy insurance that covers abortions.

The repeal-only amendment would also cut off federal funding for Planned Parenthood.

The ObamaCare repeal amendment is expected to fail, regardless of the abortion fight.

The Senate also voted down an amendment to repeal and replace ObamaCareon Tuesdaynight. They are the first of what are expected to be hundreds of amendments during the days-long healthcare debate.

Three GOP senators have already come out against a repeal-only approach, and Sen. Lamar AlexanderLamar AlexanderSenate delays vote on healthcare repeal Senate Dems launch talkathon ahead of ObamaCare repeal vote This week: ObamaCare repeal vote looms over Senate MORE (R-Tenn.), chairman of the Senates health committee, predicted the Senate would not get 40 votes to repeal ObamaCare without a replacement.

But conservatives ramped up pressure for GOP senators to support the proposal, noting Senate Republicans passed a repeal bill in 2015 when they knew then-President Obama would veto it.

Republicans promised to repeal ObamaCare, and as we move forward in this process, I urge them to join me in supporting a clean repeal of as much of this disastrous law as possible, Paul said ahead of the vote.

FreedomWorks, a conservative outside group, blasted out a key vote notice hours ahead of Wednesdaysvote, arguing President Trump would sign a repeal-only bill.

Repealing portions of ObamaCare without enacting a replacement could leave 18 million people without health insurance the following year, according to a report released by Congressional Budget Office (CBO) in January.

After the elimination of ObamaCare's Medicaid expansion and insurance subsidies, 27 million people would lose insurance, rising to 32 million by 2026, the CBO found.

The proposal comes as senators are searching to find a path forward to fulfill their yearsofcampaign pledges to repeal and replace ObamaCare.

Senate Majority Leader Mitch McConnellMitch McConnellHuffPost writer: McCain 'will die with dishonor' for yes vote on healthcare White House, GOP close to releasing joint tax-reform principles Senate delays vote on healthcare repeal MORE (R-Ky.) scored a victory Tuesdaywhen he wrangled 50 GOP senators to agree to start debate on the matter. Vice President Pence broke the 50-50 tie.

But during the first amendment voteon Tuesdayevening, nine GOP senators joined with Democrats to vote against a key repeal-and-replace proposal, known as the Better Care Reconciliation Act (BCRA). The setback doesnt prevent GOP leadership from offering another version of BCRA during what is expected to be a days-long floor debate.

McConnell acknowledged the healthcare effort certainly wont be easy.

Well consider many different proposals throughout this process from senators on both sides of the aisle. Ultimately, we want to get legislation to finally end the failed ObamaCare status quo through Congress, and to the presidents desk for his signature, he said Wednesdaymorning.

Republicans have a 52-seat majority and will need the support of at least 50 GOP senators to pass a proposal.

GOP leadership could ultimately try to pass a skinny repeal, which would include a repeal of the individual and employer mandate and the medical device tax, if broader proposals arent able to garner enoughsupport.

The move could buy Republicans time to work out a deal as they try to merge their healthcare bill witha proposal passed earlier this year by the House.

I think the endgame is to be able to move somethingat the end of thisprocess across the Senate floor that can get 50 votes and then get into conference with the House, Sen. John ThuneJohn ThuneSenate delays vote on healthcare repeal Senate might not act on must-pass aviation bill until September Senate votes to begin ObamaCare repeal debate MORE (R-S.D.) told reporters.

Cornyn added Wednesdaythat the GOP is looking for a way to get to conference quick but no decisions had been made aboutwhat the Senate could ultimately pass, or what could be included in a "skinny repeal."

Democrats, however, have blasted that path as a setupto try to ultimately pass full repeal of ObamaCare.

Make no mistake about it, skinny repeal is equal to full repeal. Its a Trojan horse designed to get the House and Senate into conference where the hard-right flank of the Republican caucus, the FreedomCaucus, will demandfull repeal orsomething very close to it, SenateMinority Leader CharlesSchumer (D-N.Y.)said ahead of the vote.

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That was Massachusetts Sen. John Kerry trying, unsuccessfully, to explain his vote(s) on federal funding for the American troops in Iraq and Afghanistan during the 2004 presidential campaign. President George W. Bush took that comment and turned it into this devastating TV ad.

Kerry's argument -- and the reason he said the whole voted-for-it-before-I-voted-against-it thing -- was that he had voted for a bill to fund the troops via the repeal of a series of Bush-era tax cuts before he had voted against the Republican-favored plan. The Senate votes a lot, Kerry's case went, and Republicans were cherry-picking what was one in a series of votes.

Sound familiar?

Republican after Republican who got off the fence to support the "motion to proceed" on Tuesday was careful to note that they were not yet supportive of the broader GOP health care bill but rather were expressing their support to allow debate on the measure to begin.

"I voted for the motion to proceed to allow debate to continue and amendments to be offered," John McCain said on the Senate floor. "I will not vote for the bill as it is today."

What that logic presumes is that the average voter distinguishes between a procedural vote to start debate on health care and a vote on some sort of actual health care measure.

Here's some breaking news: They don't!

Just ask John Kerry. Trying to explain the arcane and complicated ways in which the Senate cast votes -- motion to proceed, motion to recommit, final passage etc. -- is a total political loser. Peoples' eyes fog over and it reminds them of all the things they don't like about Washington. It sounds like gobbledy-gook and double speak to them even if, technically speaking, Kerry DID vote for $87 billion for the war and reconstruction efforts before he voted against it.

(Sidebar: The number of votes that senators take -- and the complex ways in which these votes play out -- is the leading reason why senators rarely make good presidential candidates. Too many votes to defend.)

Democrats, stung by Kerry's experience, are already preparing to give Republicans a taste of their own medicine.

The one silver lining, politically speaking, for Republicans is they have very little vulnerability in 2018. Only Sen. Dean Heller of Nevada, who voted for the motion to proceed, is up for re-election in a state Hillary Clinton won in 2016. And, in total, only 10 Republican seats are up for re-election.

Still, health care -- as President Obama and Democrats found out in the 2010 and 2014 elections -- is an issue where voters have a long memory. And the "he voted for the heath care bill before he voted against it" attack is a very, very potent one. Just ask John Kerry.

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"If you're expecting an instant panacea or an instant cure, it's not going to be provided by anybody here in Washington," Scaramucci said on CNN's "New Day" Wednesday.

Scaramucci cast the current deliberations in Congress on repealing Obamacare as incremental steps on health care.

They are expected on Wednesday to continue the health care debate, and it is unclear what a final bill could look like.

Scaramucci seemed to dismiss the nuances of the debate and advised senators to move forward with something on health care.

"Don't focus on the micro nature of this today if you're a senator," Scaramucci said.

He lamented not being able to push through a major overhaul on health care, and said "we have to start with incrementalism" on the issue because of the "webs in Washington."

As for Attorney General Jeff Sessions, whom President Donald Trump has publicly complained about and left open the possibility of firing, Scaramucci said he advised all Cabinet members to "have a tough skin."

Asked if Trump had talked directly with Sessions, Scaramucci said, "I don't know the answer."

Besides facing opposition from his own party, Trump has also demonstrated a willingness to move against one of his earliest prominent supporters. Scaramucci, however, denied that Trump was demanding loyalty in exchange for returning none back.

"He is a symmetrical loyalist for sure," Scaramucci said. "If you take care of him, he's going to take care of you."

Turning to his own role as the new communications chief, Scaramucci spoke at length about his desire to tamp down on leaks coming from the White House. He said he knew he could not eliminate the leaks entirely, but said he could dial them back.

When asked if the higher-ranking person was Trump, Scaramucci deferred and said he was "getting so subtle and surgical" with his answers.

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Trump calls out Murkowski over health care vote – CNN

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"Senator @lisamurkowski of the Great State of Alaska really let the Republicans, and our country, down yesterday. Too bad," he tweeted.

Murkowski and Sen. Susan Collins of Maine were the only two GOP senators to vote against a procedural vote backed by Senate Majority Leader Mitch McConnell Tuesday afternoon. They were also among the nine Republicans who voted Tuesday night against the Better Care Reconciliation Act, a version of the health care overhaul bill.

Murkowski responded to Trump Wednesday afternoon.

"Every day shouldn't be about campaigning," the Alaska senator added. "Quite honestly, I don't think it's wise to be operating on a daily basis thinking about what -- a statement or a response -- that causes you to be fearful of your electoral prospects."

Notably, Trump has not yet publicly criticized Collins on social media in the wake of Tuesday's vote.

But the President subtly warned Republicans that their political futures could be in jeopardy if they don't support his efforts.

"Any senator who votes against repeal and replace is telling America that they are fine with the Obamacare nightmare, and I predict they'll have a lot of problems," he said at a rally in Youngstown, Ohio, Tuesday night.

For her part, Murkowski noted to MSNBC that she is not up for re-election again until 2022, "a long time away."

Trump has publicly pressured other members of his own party who haven't backed him on health care.

At a recent White House meeting, the President predicted that Sen. Dean Heller, who is facing a tough re-election fight in 2018, would reverse himself and vote to advance the GOP's health care bill.

Back in March, Trump called out House members when the chamber was debating the issue.

He added: "Where are @RepMarkMeadows, @Jim_Jordan and @Raul_Labrador? #RepealANDReplace #Obamacare."

CNN's Dylan Stafford contributed to this report.

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Remember: The strategy for passing the bill depends on secrecy. Mitch McConnell, Paul Ryan and their allies understand that their plans are deeply unpopular. So the best way to prevent them from taking health coverage from people is to call attention to their efforts. On Tuesday night, one Obamacare replacement bill had already failed.

Spiro suggested that people with Democratic senators call them to urge them to fight as hard as possible, by filibustering and offering unlimited amendments. Locking in the tentative no votes from the Republican senators Lisa Murkowski (of Alaska) and Susan Collins (of Maine) is also critical.

Meanwhile, people who live in Ohio, Nevada, West Virginia, Arizona, Wisconsin, Kentucky, Kansas, Colorado, Louisiana and Utah are represented by Republican senators who could provide the swing vote.

Senate leadership wants to pass a bill this week, Marianna Sotomayor of NBC reported. One worrisome possibility, as Senator Chris Murphy noted, is the Senate passing a bare-bones bill, under the guise of fixing it during so-called conference negotiations with the House. That would almost certainly lead to massive losses in insurance coverage.

If you were ever tempted to get involved in politics, now would be a good time to make a phone call or urge friends and relatives to do so. And if youre a United States senator who is tempted to put Americans well-being above partisan loyalty, now would be a really good time.

The McCain moment: John McCain, who rushed back to Washington from a diagnosis of aggressive brain cancer, faces an especially stark choice.

He suggested yesterday that he was disgusted by the process so far and blasted it for violating the Senates regular order but he also voted to move ahead. For him, voting against any bill produced by this process would be the most consistent stand in favor of regular order, Adam Jentleson, a former Democratic Senate aide, wrote. If Im wrong & McCain votes for whatever monstrosity comes out of this process, hell lose all authority on the Senate as an institution.

David A. Graham, in The Atlantic, was struck by the same tension: Senate floor speeches can stir the heart strings. But if McCain intends to return the body to regular order, at some point, hes actually going to have to vote to do that.

Intriguingly, FiveThirtyEights Nate Silver argues that younger political writers were more critical of McCains speech than older writers.

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With the Senate having voted Tuesday to open debate on repealing and replacing Obamacare -- exactly how is yet to be determined -- here's still another possible repercussion from that effort: A hit to the U.S. economy.

If the Republican efforts to replace the Affordable Care Act fail and the exchanges are left to twist in the wind, it's likely the U.S. will see a potential decline in health care consumption, said Paul Ashworth, chief U.S. economist at Capital Economics. In a recent report, he said that "could conceivably become a significant drag on GDP growth next year."

It also casts even more doubt on the Trump administration's rosy predictions of 3 percent GDP growth next year. That estimate has already been met with plenty of skepticism even without the prospect of taking health insurance away from as many as 30 million people by 2026.

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The U.S. potential economic growth rate has been declining from an average of over 3 percent in the 1990s to between 1.5 percent and 2 percent in the 2010s, according to Jeremy Lawson, chief economist at asset management firm Standard Life Investments. He believes short-term future growth is unlikely to return to previous highs without an acceleration of structural reforms well beyond health care.

If Obamacare is repealed with no replacement, the result would be an estimated $417 billion decline in the budget deficit over a 10-year period, according to the Congressional Budget Office analysis. That would have a modest impact on GDP growth, said Lawson. But that estimate assumes no Obamacare replacement whatsoever is implemented, which is unlikely to happen over a decade.

Both the Senate and House versions of replacement would restrict Medicaid spending and reduce the number of insured people by about 20 million. "Both plans would have a more modest negative effect on the economy than just repeal," Lawson predicted. But because the plans would likely reduce access to health insurance, you may see more personal bankruptcies and other disruptive economic impacts, Lawson said.

It's also important to look at health care's impact on the U.S. economy in terms of productivity, Lawson explained. Health care spending accounts for 18 percent of total U.S. GDP, a much higher percentage than in most other world economies. A lot of that spending is inefficient because individuals, especially those with employer-sponsored insurance, and the health care industry itself don't have incentives to make health care a more cost-efficient and thus productive system.

As health care spending continues to grow more quickly than the rest of the economy, Lawson explained, it squeezes out potential spending in other, more efficient sectors, which would in turn help boost overall economic growth. He added: "One could argue inefficient health care systems are holding back the U.S. economy over the long term."

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Patient information can be vulnerable when health care facilities are the focus of cyberattacks. Eric Audras/Onoky/Getty Images hide caption

Patient information can be vulnerable when health care facilities are the focus of cyberattacks.

In the neonatal intensive care unit of Cook Children's Hospital in Fort Worth, Texas, a father is rocking a baby attached to a heart monitor. While doctors roam the halls trying to prevent infections, Chief Information Officer Theresa Meadows is worried about another kind of virus.

"The last thing anybody wants to happen in their organization is have all their heart monitors disabled or all of their IV pumps that provide medication to a patient disabled," Meadows says.

Meadows manages IT and cybersecurity for nearly 7,000 employees at more than 50 locations in Texas. After co-chairing an evaluation of hospital cybersecurity across the U.S., she says there's a lot to improve.

Dr. John Halamka, chief information officer of Beth Israel Deaconess Medical Center in Boston, agrees. "Health care has traditionally underinvested in information technology," Halamka says.

Halamka, who has been a CIO since the 1990s, says just a decade ago, pretty much all health records were paper. Then, in a period of a few years, hospitals switched to electronic records. But the security of digital health data has not kept up with its growth. Other industries, like financial services and the federal government, have devoted more than 12 percent of their IT budgets to cybersecurity. Health care averages just half that.

At the same time, the cost of mitigation has soared, with the average breach costing $355 per stolen record for health care organizations. And hackers have gotten creative. Back in 1997, Halamka says, the threats he faced were students trying to hack the network.

"In 2017, what threats do I face? State-sponsored cyberterrorism, organized crime and hacktivism."

It's no wonder demand for cybersecurity talent in health care has exploded. But it's not that easy to recruit.

Digital health care consultant Drexel DeFord jokes that he's a "recovering CIO. CIOs are overly stressed with everything from security to regulation," he says. "When I talk to them about maybe coming into health care, the answer I usually get is 'No way, it's too complicated. It's way simpler to do banking or oil and gas.' "

It's also much more lucrative to work in other industries. According to Burning Glass Technologies, the average advertised pay for health care cybersecurity positions is 25 percent lower than in finance.

Plus you're on the line every minute, not just for keeping someone's social media profile working, but for helping keep them alive.

Meadows says a good CIO is familiar with complex medical devices and comfortable with software and complicated regulations. Also, a CIO needs to keep the hospital staff educated on the latest threats, sometimes by running mock cyberattacks. Meadows conducts regular phishing exercises paired with educational campaigns.

The average cost of a health care breach is estimated to be more than $2.2 million, not to mention the reputation damage. Meadows says the price of hiring a cybersecurity leader might seem high, but leaving the job open is an invitation for trouble.

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Medicine’s Movable Feast: What Jumping Genes Can Teach Us about Treating Disease – Scientific American

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When the groundbreaking geneticist Barbara McClintock was born in Hartford, Connecticut, in 1902, her parents initially named her Eleanor. But they soon felt that the name was too delicate for their daughter and began to call her Barbara instead, which they thought better suited her strong personality. Her parents accurately predicted her determination.

To say that McClintock was a pioneer is an understatement. In 1944, she became the third woman to be elected to the US National Academy of Sciences and the first woman to lead the Genetics Society of America. Shortly afterwards, she discovered that certain genetic regions in maize could jump around the chromosome and, consequently, influence the color of mottled ears of maize with kernels ranging from golden yellow to dark purple. She dubbed these jumping bits of genetic code controlling units, which later became known as transposons or transposable elements. Unfortunately, by the mid-1950s, McClintock began to sense that the scientific mainstream was not ready to accept her idea, and she stopped publishing her research into this area to avoid alienation from the scientific establishment. But scientific ideas can re-emerge and integrate into the mainstream, and 30 years later, McClintock received a Nobel Prize in Physiology or Medicine for her revolutionary insights into these moving chunks of genetic code.

In recent years, medical research has uncovered new evidence showing that moving parts of the genome in humans can contribute to life-threatening diseases ranging from cancer to diabetes. For example, a handful of hemophilia cases have been traced to transposable elements that, at some point before the patient was born, or even, perhaps, conceived, inserted themselves into and disrupted genes that facilitate blood clotting. At the same time, experiments also offer mounting data to suggest that some transposable elementsand the genes that these roving bits of DNA help to resurrecthave beneficial roles.

The study of transposable elements is a hotbed of research, according to Josh Meyer, a postdoctoral fellow who studies these bits of DNA at Oregon Health & Science University in Portland. Way back in the mists of time for the field, the general category of these things was junk DNA, he explains. Now, he says, researchers have begun to understand that transposable elements aren't always neutral genetic components: There's nothing that transposon biologists love more than to have the discussion of whether these things are, on balance, bad for us or good for us.

Since McClintock's breakthrough, researchers have identified different classes of transposable elements in the genomes of every organism in which they have sought them, ranging from fruit flies to polar bears. About 3% of the human genome consists of transposons of DNA origin, which belong to the same class as the ones that McClintock studied in maize. The other type of transposable elements, known as retrotransposons, are more abundant in our genome. These include the transposable elements that originate from viruses and make up as much as 10% of the human genome1. These elements typically trace back many millennia. They arise when viruses integrate into the genome of sperm or egg cells, and thus get passed down from one generation to the next.

The ancient viruses that became 'fossilized' in the genome remain dormant for the most part, and degenerate over time. However, there are hints that they might have the ability to re-emerge and contribute to illnesses that some scientists say could include autoimmune disease and schizophrenia2. In one example, a 2015 study found elevated levels of one embedded virus, known as human endogenous retrovirus K, in the brains of individuals with amyotrophic lateral sclerosis, also known as Lou Gehrig's disease3. However, researchers stress that the data do not yet establish a causal link.

Yet another category of retrotransposons, called long interspersed nuclear elements-1, or LINE-1 for short, make up a whopping 17% or more of the human genome4. When LINE-1 retrotransposons move within the genome of reproductive cells and insert themselves in new places, they can disrupt important genes. Researchers have so far identified more than 120 LINE-1 gene insertions, resulting in diseases ranging from muscular dystrophy to cystic fibrosis5.

Much of the focus on transposable elementsand particularly, on endogenous retroviruses and LINE-1shas centered on the possible negative repercussions of these DNA insertions. But work tracing back to the 1980s has suggested that endogenous retroviruses may also support reproductive function in some way6. In 2000, scientists found that remnants of an ancient virus in the human genome encode a protein called syncytin, which cell experiments indicate is important for placental development7. And although it is not shown definitely, there are also hints that an endogenous retrovirus that became embedded in the DNA of a primate ancestor might help boost the production of the digestive enzyme amylase, which helps to break down starch, in our saliva8, 9.

To peer deeper into the effects of transposable elements in humans, geneticist Nels Elde and his colleagues at the University of Utah in Salt Lake City used CRISPRCas9 gene editing to target an endogenous retrovirus called MER41, thought to come from a virus that integrated into the genome perhaps as far back as 60 million years ago. The scientists removed the MER41 element from human cells cultured in a dish. In humans, MER41 appears near genes involved in responding to interferon, a signaling molecule that helps our immune response against pathogens. Notably, as compared with normal cells, cells engineered to lack MER41 were more susceptible to infection by the vaccinia virus, used to inoculate people against smallpox. The findings, reported last year, suggest that MER41 has a crucial role in triggering cells to launch an immune response against pathogens through the interferon pathway10.

Meyer stresses that these insights elevate the already eminent discoveries by McClintock. I would hope she would be extremely gratified and vindicated, he says. She recognized a type of sort of factor of genomic dynamism that no one else had seen before. And I am firmly convinced that it's going to only become more and more and more central to our understanding of how genomics works.

In 2005, with a freshly minted doctorate in molecular genetics, Nels Elde landed a job as a research fellow in Seattle and was tasked with studying the evolution of the immune system of gibbons, a type of ape. Each morning as he biked to the lab downtown, he would pass the city's zoo and hear its gibbons calling to each other. Occasionally, he would visit the zoo and look at them, but he had no idea at the time that the squirrel monkeys that he also saw there would feature so largely in his future research. At work, Elde's primate investigations focused on the gibbon DNA that he was responsible for extracting and analyzing using sequencing machinery.

Then, six years ago, Elde received his first lab of his own to run, at the University of Utah. He did not expect his team's first discovery there to come so swiftly, or that it would involve transposable elements. Elde had arrived at the university with the intention of learning how cells recognize and defeat invading viruses, such as HIV. But he hadn't yet obtained the equipment that he needed to run experiments, despite already having two employees who were eager to do work, including his lab manager, Diane Downhour. Given the lack of lab tools, the two lab staff members spent their time on their computers, poking around databases for interesting patterns in DNA. After just two weeks of this, Downhour came into Elde's office and told him that they had found a couple of extra copies of a particular gene in New World monkeysspecifically, in squirrel monkeys.

Elde initially brushed off Downhour's insight. I said, 'Why don't you go back to the lab and not worry about it?' he recalls. But a couple of days later, she returned to his office with the idea. I was just in the sort of panicked mode of opening a lab, ordering freezers, trying to set up equipment and hiring people, Elde explains. Diane definitely had to come back and say, 'Come on, wake up here. Pay attention.'

The gene that they detected multiple copies of in squirrel monkeys is called charged multivesicular body protein 3, or CHMP3. Each squirrel monkey seems to have three variants of the gene. By comparison, humans have only the one, original variant of CHMP3. The gene is thought to exist in multiple versions in the squirrel monkey genome thanks to transposable elements. At some point around 35 million years ago, in an ancestor of the squirrel monkey, LINE-1 retrotransposons are thought to have hopped out of the genome inside the cell nucleus and entered the cytoplasm of the cell. After associating with CHMP3 RNA in the cytoplasm, the transposable elements brought the code for CHMP3 back into the nucleus and reintegrated it into the genome. When the extra versions of CHMP3 were copied into the genome, they were not copied perfectly by the cellular machinery, and thus changes were introduced into the sequences. Upon a first look at the data, these imperfections seemed to render them nonfunctional 'pseudogenes'. But as Elde's team delved into the mystery of why squirrel monkeys had so many copies of CHMP3, an intriguing story emerged.

The discovery of pseudogenes is not wholly uncommon. There are more than 500,000 LINE-1 retrotransposons in the human genome11, and these elements have scavenged and reinserted the codes for other proteins inside the cell as well. Unlike with the endogenous retroviral elements in the genome, which can be clearly traced back to ancient viruses, the origin of LINE-1 retrotransposons is murky. However, both types of transposable elements contain the code for an enzyme called reverse transcriptase, which theoretically enables them to reinsert genetic code into the genome in the cell nucleus. This enzyme is precisely what allowed LINE-1 activity to copy CHMP3 back into the genome of the squirrel-monkey ancestor.

Elde couldn't stop thinking about the mystery of why squirrel monkeys had multiple variants of CHMP3. He knew that in humans, the functional variant of the CHMP3 gene makes a protein that HIV uses to bud off of the cell membrane and travel to and infect other cells of the body. A decade ago, a team of scientists used an engineered vector to prompt human cells in a dish to produce a truncated, inoperative version of the CHMP3 protein and showed that the truncated protein prevented HIV from budding off the cells12. There was hope that this insight would yield a new way of treating HIV infection and so prevent AIDS. Unfortunately, the protein also has a role in allowing other important molecular signals to facilitate the formation of packages that bud off of the cell membrane. As such, the broken CHMP3 protein that the scientists had coaxed the cells to produce soon caused the cells to die.

Given that viruses such as HIV use a budding pathway that relies on normal CHMP3 protein, Elde wondered whether the extra, altered CHMP3 copies that squirrel monkeys carry confers some protection against viruses at the cellular level. He coordinated with researchers around the globe, who sent squirrel-monkey blood from primate centers as far-reaching as Bastrop, Texas, to French Guiana. When Elde's team analyzed the blood, they found that the squirrel monkeys actually produced one of the altered versions of CHMP3 they carry. This finding indicated that in this species, one of the CHMP3 copies was a functional pseudogene, making it more appropriately known as a 'retrogene'. In a further experiment, Elde's group used a genetic tool to coax human kidney cells in a dish to produce this retrogene version of CHMP3. They then allowed HIV to enter the cells, and found that the virus was dramatically less able to exit the cells, thereby stopping it in its tracks. By contrast, in cells that were not engineered to produce the retrogene, HIV was able to leave the cells, which means it could theoretically infect many more.

In a separate portion of the experiment Elde's group demonstrated that whereas human cells tweaked to make the toxic, truncated version of CHMP3 (the kind originally engineered a decade ago) die, cells coaxed to make the squirrel-monkey retrogene version of CHMP3 can survive. And by conducting a further comparison with the truncated version, Elde found that the retrogenewhat he calls retroCHMP3in these small primates had somehow acquired mutations that resulted in a CHMP3 protein containing twenty amino acid changes. It's some combination of these twenty points of difference in the protein made by the retrogene that he thinks makes it nontoxic to the cell itself but still able to sabotage HIV's efforts to bud off of cells. Elde presented the findings, which he plans to publish, in February at the Keystone Symposia on Viral Immunity in New Mexico.

The idea that retroCHMP3 from squirrel monkeys can perhaps inhibit viruses such as HIV from spreading is interesting, says Michael Emerman, a virologist at the Fred Hutchinson Cancer Research Center. Having an inhibitor of a process always helps you understand what's important for it, Emerman explains. He adds that it's also noteworthy that retroCHMP3 wasn't toxic to the cells, because this finding could inspire a new antiviral medicine: It could help you to design small molecules or drugs that could specifically inhibit that part of the pathway that's used by viruses rather than the part of the pathway used by host cells.

Akiko Iwasaki, an immunologist at the Yale School of Medicine in New Haven, Connecticut, is also optimistic that the finding will yield progress. What is so cool about this mechanism of HIV restriction is that HIV does not bind directly to retroCHMP3, making it more difficult for the virus to overcome the block imposed by retroCHMP3, Iwasaki says. Even though humans do not have a retroCHMP3 gene, by understanding how retroCHMP3 works in other primates, one can design strategies to mimic the activity of retroCHMP3 in human cells to block HIV replication.

Elde hopes that, if the findings hold, cells from patients with HIV infection might one day be extracted and edited to contain copies of retroCHMP3, and then reintroduced into these patients. Scientists have already used a similar cell-editing approach in clinical trials to equip cells with a variant of another gene, called CCR5, that prevents HIV from entering cells. In these experiments, patients have received infusions of their own cellsmodified to carry the rare CCR5 variant. But although preliminary results indicate that the approach is safe, there is not enough evidence yet about its efficacy. (Another point of concern is that people with the rare, modified version of the CCR5 gene might be as much as 13 times more susceptible to getting sick from West Nile virus than those with the normal version of this gene13.) By editing both retroCHMP3 and the version of CCR5 that prevents HIV entry into cells, Elde suggests, this combination of gene edits could provide a more powerful way of modifying patient cells to treat HIV infection.

You could imagine doing a sort of cocktail genetic therapy in order to block HIV in a way that the virus can't adapt around it, Elde says. His team also plans to test whether retroCHMP3 has antiviral activity against other viruses, including Ebola.

The investigations into how pseudogenes and retrogenes might influence health are ongoing. And there is mounting evidence that the LINE-1 elements that create them are more active than previously thought. In 2015, for example, scientists at the Salk Institute in California reported a previously unidentified region of LINE-1 retrotransposons that are, in a way, supercharged. The region that the researchers identified encodes a protein that ultimately helps the retrotransposons to pick up bits of DNA in the cell cytoplasm to reinsert them into the genome14. The same region also enhances the ability of LINE-1 elements to jump around the genome and thus create variation, adding weight to the idea that these elements might have an underappreciated role in human evolution and in creating diversity among different populations of people.

The active function of transposable elements is more important than many people realize, according to John Coffin, a retrovirus researcher who divides his time between his work at the US National Cancer Institute in Frederick, Maryland, and Tufts University in Boston. They canand havecontributed in important ways to our biology, he says. I think their role in shaping our evolutionary history is underappreciated by many evolutionary biologists.

Squirrel monkeys are not the only animals that might reap protection against viral invaders thanks in part to changes in the genome caused by transposable elements. In 2014, Japanese scientists reported on a chunk of Borna virus embedded in the genome of ground squirrels (Ictidomys tridecemlineatus). The team's results from cellular experiments suggest that this transposed chunk encodes a protein that might interfere with the pathogenicity of external Borna viruses that try to invade these animals15. Humans also have embedded chunks of Borna virus in their genomes. But we don't have the same antiviral version that the ground squirrels haveand we might therefore be less protected against invading Borna viruses.

Other studies of endogenous viruses might have clearer implications for human health, and so scientists are looking at the activity of these transposable elements in a wide range of other animals, including the house cat. This past October, another group of Japanese researchers found that viruses embedded in the genomes of domesticated cats have some capacity to replicate. This replication was dependent on how well the feline cells were able to squelch the endogenous viruses in the genome through a silencing process called methylation16. But perhaps the most striking example of a replicating endogenous retrovirus is in koalas. In the 1990s, veterinarians at Dreamworld, a theme park in Queensland, Australia, noticed that the koalas were getting lymphoma and other cancers at an alarming rate. The culprit turned out to be a retrovirus that was jumping around in the animals' genomes and wreaking havoc. Notably, koalas in the south of the country showed no signs of the retrovirus, which suggests that the virus had only recently begun to integrate into these animals' DNA17.

The risks of transposable elements to human health are a concern when it comes to the tissue transplants we receive from other species, such as from pigs, which have porcine endogenous retroviruses. These embedded viruseswhich have the unfortunate abbreviation PERVscan replicate and infect human cells.

Transplants from pigs, for example, commonly include tissues such as tendons, which are used in ACL-injury repair. But these tissues are stripped of the pig cellsand thus of PERVsso that just the tissue scaffold remains. However, academic institutions and companies are actively designing new ways to use pig tissues in humans. Earlier this year, Smithfield Foods, a maker of bacon, hotdogs and sausages, announced it had launched a new bioscience unit to help supply pig parts to medical companies in the future. Meanwhile, George Church, a Harvard Medical School geneticist and entrepreneur, has formed a company called eGenesis Bio to develop humanized pigs for tissue transplantation. In March, the company announced that it had raised $38 million in venture funding. Church published a paper two years ago showing that his team had edited out key bits of 62 PERVs from pig embryos, disrupting the PERVs' replication process and reducing their ability to infect human cells by 1,000-fold18.

Whereas Church and other scientists have tried disrupting endogenous retroviruses in animal genomes, researchers have also experimented with resurrecting them: a decade ago, a group of geneticists in France stirred up some controversy when the researchers recreated a human endogenous retrovirus by correcting the mutations that had rendered it silent in the genome for millennia. The scientists called it the 'Phoenix' virus, but it showed only a weak ability to infect human cells in the lab19. There was, perhaps unsurprisingly, pushback against the idea of resurrecting viruses embedded in our genomeno matter how wimpy the resulting viral creation.

But emerging data suggest that the retroviruses buried in the human genome might not be quite as dormant as we thought. The ability for these endogenous retroviruses to awaken from the genome is more widespread than has been previously appreciated, says virologist Rene Douville at the University of Winnipeg in Canada. She views this phenomenon as being the rule, rather than the exception within the cell: These retroelements are produced from the genome as part of the cell's normal function to varying degrees.

Interestingly, the cellular machinery involved in keeping cancer at bay might also have a connection to transposable elements. One in three binding sites in the human genome for the important tumor-suppressor protein p53 are found within endogenous retroviruses in our DNA20. And last year, a team led by John Abrams at University of Texas Southwestern Medical Center in Dallas offered preliminary evidence that p53 might do its work by perhaps keeping embedded retroelements in check21.

When I first started openly publicly talking about this story, some of my colleagues here who are in the cancer community said, 'Hey, that's cute, but it can't be true. And the reason it can't be true is that we would know this already,' Abrams recalls. The reason it wasn't seen before, he explains, is that many genetic analyses throw out repeated sequenceswhich often consist of retroelements. So his team had to go dumpster diving in the genetic databases for these sequences of interest to demonstrate the link to p53. Abrams suspects that when p53 fails to keep retrotransposons at bay, tumors might somehow arise: The next question becomes, 'How do you get to cancer?' Abrams says that this is an example of what he calls transposopathies.

Not all scientists are convinced of a causal link between p53 and retroelements in cancer. My question is, if p53 is so vital in suppressing retrotransposon activity in cancer, why do we not find evidence of dysregulated retrotransposons inserting copies of themselves into the tumor genome more often? asks David Haussler, a genomics expert at the University of California, Santa Cruz. Most tumors have p53 mutations, yet only a very small percentage of tumors show evidence of significantly dysregulated rates of new retrotransposon copy insertion.

Still, there are others interested in exploring whether ancient viruses might reawaken in cancer or have some other role in this disease. Five years ago, scientists at the University of Texas MD Anderson Cancer Center reported that a type of viral protein produced by the human endogenous retrovirus type K (HERV-K) is often found on the surface of breast cancer cells. In a mouse experiment, they showed that cancers treated with antibodies against this protein grew to only one-third of the size of tumors that did not receive this therapy22.

But some cancer scientists are thinking about co-opting endogenous retroviruses to use against cancer. Paul Bieniasz of the Rockefeller University in New York City gained insight into this approach by studying human endogenous retrovirus type T (HERV-T)an ancient virus that spread for 25 million years among our primate ancestors until its extinction roughly 11 million years ago and at some point became fossilized in our DNA lineage. In April, his group found that a particular HERV-T encodes a protein that blocks a protein called monocarboxylate transporter 1, which is abundant on the surface of certain types of cancer cells23. It's thought that monocarboxylate transporter 1 has a role in enabling tumors to grow. Blocking it could help to stymie the expansion of malignancies, Bieniasz speculates. He and his colleagues are now trying to build an 'oncolytic virus' that uses elements of HERV-T to treat cancer.

The idea that new viruses might still be trying to creep into our genomes is a scary one, even if they don't appear very effective at achieving this. One of the most recent to integrate into our genome in a way that it is passed down from generation to generation is human endogenous retrovirus type K113 (HERV-K133), which sits on chromosome 19. It's found in only about one-third of people worldwide, most of whom are of African, Asian or Polynesian background. And researchers say that it could have integrated into the genome as recently as 200,000 years ago6.

Although experts remain skeptical that a virus will integrate into the human genome again anytime soon, other transposable elements, such as LINE-1s, continue to move around in our DNA. Meanwhile, the field that Barbara McClintock seeded more than half a century ago is growing quickly. John Abrams, who is studying retroelements, says that we're only just beginning to understand how dynamic the genome is. He notes that only recently have people begun to appreciate how the 'microbiome' of bacteria living in our guts can influence our health. We're really an ecosystem, Abrams says of the gut, and the genome is the same way. There is the host DNAbelonging to usand the retro-elements it contains, he explains, and there's this sort of productive tension that exists between the two.

This article is reproduced with permission and wasfirst publishedon July 11, 2017.

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Medicine's Movable Feast: What Jumping Genes Can Teach Us about Treating Disease - Scientific American

3 Genetics Tests To Improve Prenatal Screening – HuffPost

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This article is authored by the Mayo Clinic Center for Individualized Medicine. The mission of the Center is to discover and integrate the latest in genomic, molecular and clinical sciences into personalized care for patients.

New technology is reshaping prenatal screening to assess the health of a developing baby. Now pregnant women can have their baby initially screened for genetic disorders, such as Down syndrome, through the use of a newer blood test that evaluates DNA present in the mothers blood stream. Another test for couples planning a family uses a single blood sample to assess whether future children might be at risk for developing a genetic disease.

Its an exciting time in perinatal testing, explains Myra Wick, M.D., Ph.D. DNA sequencing and molecular technology have improved and become more cost effective. These tests are important for family planning before pregnancy as well as planning for the care of a baby who is found to have a genetic disorder during pregnancy.

Researchers from Mayo Clinic and the Center for Individualized Medicine have helped implement several of these tests, which use a personalized medicine approach to perinatal screening. Three state-of-the-art perinatal genetic tests are becoming more widely available to expectant parents.

Mayo Medical Laboratories recently launched a blood test to screen for the most common chromosome disorders diagnosed in pregnancy, such as Down syndrome. Its known as a cell-free DNA test. It screens the mothers blood that contains DNA from the baby, looking for genetic disorders in the fetus. The new test generally has a higher detection rate and fewer false positives than traditional screening tests.

Prior to this new test, mothers had the option of traditional first trimester screening, which is a blood test and ultrasound, or second trimester screening, which is a blood test. In general, the cell free DNA blood test can be used in place of the traditional first and second trimester screening, explains Dr. Wick. It is important to remember that the cell free DNA testing is a screening test, and abnormal results should be followed up with additional testing.

The out-of-pocket cost for the new blood test varies depending on insurance coverage, and the specific laboratory performing the testing; a general estimate is approximately $350. Results are usually ready within one week.

2. Expanded carrier screening

In the past, couples had genetic screening based on family history of a genetic disorder, or if they were part of an ethnic group at risk for certain inherited diseases. Previous tests only screened for a small defined group of genetic disorders. Those tests didnt help couples who were uncertain of their ethnic heritage, plus the tests were very limited in scope.

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Its an exciting time in perinatal testing. DNA sequencing and molecular technology has improved and become more cost effective. These tests are important for family planning prior to pregnancy as well as planning for the care of a child who is found to have a genetic disorder during pregnancy. - Dr. Myra Wick

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Now couples may choose a more comprehensive test that looks for 100 or more genetic disorders. Its called expanded carrier screening. This test is done with a blood sample from each prospective parent.

Expanded carrier screening looks at multiple genes associated with genetic diseases. Most of the disorders included on an expanded carrier screen are inherited in an autosomal recessive manner. This means that the parents are carriers of the disorder, with one normal copy of the gene and one abnormal copy of the gene. Carriers of an autosomal recessive disorder do not typically have signs or symptoms of the disease. A child is affected with an autosomal recessive disorder when he or she inherits one abnormal copy of the gene from mom, and one abnormal copy of the gene from dad. Approximately 5% of couples who undergo expanded carrier screening are found to be carriers for the same disorder, and at risk for having an affected says Dr. Wick.

Depending upon insurance coverage, the test costs approximately $350. Test results are returned within one to two weeks.

3. Whole exome sequencing (WES)

In rare cases, an ultrasound during pregnancy reveals that the baby has several medical problems. Traditional genetic testing may not identify a diagnosis. Now whole exome sequencing (WES), which looks at most of the genes linked to growth and health, can be used to evaluate the fetuss condition. It can provide a diagnosis in 30 percent of cases.

For this testing, an amniocentesis is performed first to obtain DNA for genetic analysis.

We are beginning to use WES even before the baby is born. Results can be used to plan for care of an infant who may be born with several complex medical concerns. In addition, parents can use this information for future family planning, says Dr. Wick.

Whole exome sequencing is expensive, with typical costs of approximately $8,000, depending upon the specific test and insurance coverage. Results from this more complex screening usually take several weeks, depending upon the specific test being used.

Dr. Wicks suggests that you ask your health care provider about genetic testing and recommends that all prospective and expectant parents consult with a medical geneticist or genetic counselor before genetic screening.

If your provider is at a large medical center, genetic counseling should be available. At smaller facilities, your primary provider may order initial blood tests, but you may be referred to a larger facility if test results indicate you need genetic counseling.

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3 Genetics Tests To Improve Prenatal Screening - HuffPost

Phase 2/3 Trial of Elamipretide to Treat Barth Syndrome Now Enrolling Patients – Mitochondrial Disease News

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A Phase 2/3 clinical trial of elamipretide,a potential treatment for a rare mitochondrial disease known asBarth syndrome, is now enrolling patients, the therapys developer,Stealth BioTherapeutics, announced.

The TAZPOWER study (NCT03098797) will be conducted in McKusick-Nathans Institute of Genetic Medicine, at the Johns Hopkins University School of Medicine, and is expected to include 12 patients, ages 12 or older, with genetically confirmed Barth syndrome and stable symptoms, butimpaired walking ability.

Our understanding of Barth syndrome and how it manifests has evolved significantly, but current treatment efforts are still limited to the management of symptoms, Hilary Vernon, anassistant professor of pediatrics at the McKusick-Nathans Institute and the studys primary investigator, said in a press release. The initiation of TAZPOWER represents an important milestone in the potential development of a disease-specific treatment option.

Barth syndrome is a rare inherited mitochondrial disease that is almost exclusive to males. This disease is characterized by cardiac abnormalities, skeletal muscle weakness, recurrent infections due to low white blood cell (immune cell) counts, and delayed growth. It is caused by caused by genetic mutations in the TAZ gene, which encodes the protein tafazzin that is essential for the normal functioning of mitochondria.

The severe problems experienced by patients with Barth syndrome are caused by misshapen and dysfunctional mitochondria, which reduce the energy production in the affected tissues. The resulting muscle weakness can lead to severe fatigue, heart failure and death, said Doug Weaver, chief medical officer at Stealth. In this study, we hope to show that elamipretide may have clinical benefit by improving function in these affected mitochondria.

Elamipretidewas designed to restore mitochondrias ability to work as the cells power source. Due to its capacity to penetrate the inner membrane of mitochondria, the therapy as the potential to reduce the levels of damaging oxidative stress produced by mitochondrias dysfunctional activity.

TAZPOWER trial is a placebo-controlled crossover study, designed to evaluate the effects of daily administration of elamipretide in patients with Barth syndrome. All participants will receive single daily subcutaneous injections of elamipretide or placebo for 12 weeks, followed by a four-week wash-out period. This will then be followed by additional 12 weeks of therapy, but this time the patients will switch the treatment received, with those previously givenelamipretide now receivinga placebo and vice-versa.

The drugs efficacy will be measured by changes in the distance that patients are able to walk during the 6-minute walk test (6MWT). Secondary endpoints will include other functional assessments (of muscle strength, balance, etc.), patient-reported outcomes, and overall treatment safety.

This study underscores our commitment to develop elamipretide for the treatment of rare genetic mitochondrial diseases, said Reenie McCarthy, Stealths chief executive officer.

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Phase 2/3 Trial of Elamipretide to Treat Barth Syndrome Now Enrolling Patients - Mitochondrial Disease News

Stanford announces new Center for Definitive and Curative Medicine – Stanford Medical Center Report

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It is a privilege to lead the center and to leverage my previous experience to build Stanfords preeminence in stem cell and gene therapies, said Roncarolo, who is also chief of pediatric stem cell transplantation and regenerative medicine, co-director of the Bass Center for Childhood Cancer and Blood Diseases and co-director of the Stanford Institute for Stem Cell Biology and Regenerative Medicine. Stanford Medicines unique environment brings together scientific discovery, translational medicine and clinical treatment. We will accelerate Stanfords fundamental discoveries toward novel stem cell and gene therapies to transform the field and to bring cures to hundreds of diseases affecting millions of children worldwide.

The center consists of several innovative pieces designed to allow the rapid development of early scientific discoveries into the clinic that in the past have languished. This includes an interdisciplinary team of basic and clinical scientists to shepherd nascent therapies developed at Stanford. The team will be headed by associate directors Matthew Porteus, PhD, associate professor of pediatrics, and Anthony Oro, MD, the Eugene and Gloria Bauer Professor and professor of dermatology.

To help with clinical development, the center boasts a dedicated stem cell clinical trial office with Sandeep Soni, MD, clinical associate professor of pediatrics, as medical director. In addition, the center has dedicated clinical trial hospital beds in the Bass Center for Childhood Cancer and Blood Diseases located on the top floor of the soon-to-open LucilePackardChildrensHospital. From work performed by scientists over the past decade, the center already has a backlog of nearly two dozen early stage therapies whose development the center will accelerate.

The center will provide novel therapies that can prevent irreversible damage in children, and allow them to live normal, healthy lives, said Mary Leonard, MD, professor and chair of pediatrics and physician-in-chief at Stanford Childrens Health. The stem cell and gene therapy efforts within the center are aligned with the strategic vision of the Department of Pediatrics and Stanfords precision health vision, where we go beyond simply providing treatment for children to instead cure them definitively for their entire lives.

One of the unique features of the center is its close association with the recently opened $35 million Stanford Laboratory for Cell and Gene Medicine, a 23,000-square-foot manufacturing facility located on California Avenue in Palo Alto. One of the first of its kind in the world, the laboratory has the ability to produce newly developed cell and gene therapy therapies according to the Good Manufacturing Practice standards as required for patient treatment.

Headed by executive director David DiGiusto, PhD, the lab can produce diverse cellular products for patient use, such as genetically corrected bone marrow cells for sickle cell anemia, genetically-engineered skin grafts for children with the genetic disease epidermolysis bullosa or genetically-engineered lymphocytes to fight rejection and leukemia.

We are fortunate that Stanford researchers have created such a strong portfolio of innovative candidate therapeutics to develop, said DiGusto. The capabilities of the laboratory will bridge the gap between research and clinical investigation so that the curative potential of these exciting cell and gene therapies can be realized.

For more information about the center, or for information about trials associated with the center, please see https://med.stanford.edu/ptrm/faculty.html, or contact Jennifer Howard at jmhoward@stanford.edu.

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Stanford announces new Center for Definitive and Curative Medicine - Stanford Medical Center Report