A new study at Tel Aviv University shows that stem cell therapy, one of the few treatments available to patients with severe and end-stage heart failure, can actually harm them unless it is done differently.

We concluded that stem cells used in cardiac therapy should be drawn from healthy donors or be better genetically engineered for the patient, said lead researcher Jonathan Leor of the universitys Sackler Faculty of Medicine and Sheba Medical Center.

Doctors use tissue or adult stem cells to replace damaged tissue, which encourages regeneration of blood vessel cells and new heart muscle tissue. But cardiac stem cells from a diseased heart can lead to a toxic interaction via a molecular pathway between the heart and the immune system, the study found.

We found that, contrary to popular belief, tissue stem cells derived from sick hearts do not contribute to heart healing after injury, Leor said. Furthermore, we found that these cells are affected by the inflammatory environment and develop inflammatory properties. The affected stem cells may even exacerbate damage to the already diseased heart muscle.

The findings could suggest a way to make stem cell therapy safer for heart disease patients. The treatment is often a last resort, apart from getting a transplant.

Researchers discovered a molecular pathway involved in the toxic interaction while studying stem cells in mice with heart disease. By deleting the gene that makes the pathway, the cells ability to regenerate healthy tissue can be restored, they found.

The researchers are now testing a gene editing technique to delete the problem gene.

We hope our engineered stem cells will be resistant to the negative effects of the immune system, Leor said.

The study was conducted by TAUs Dr. Nili Naftali-Shani and published in the journal Circulation.

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Study says some stem cells dangerous for heart patients | The Times ... - The Times of Israel

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Frances Wang, KXTV 12:07 AM. PDT June 18, 2017

Dawson Deschaine, 8, of Nevada County, passed away after a long battle with leukemia. His family hopes to bring the 'Beads of Courage' program into more hospitals as part of Dawson's legacy.

While most kids try to earn gold stars for their work, Dawson Deschainefelt a little pride every time he earned a bead.

"The Beads of Courage program is these beads that [represent] every poke, every hospital stay, every bone marrow biopsy, every chemotherapy," said Breanna Deschaine, Dawson's mother.

Dawson was diagnosed with leukemia in January 2015 at just 6-years-old. The battle would last two-and-a-half years. It was all Dawson ever knew.

"He mostly knew nurses, doctors, family," said Jason Deschaine, Dawson's father. "He had a lot more adult conversations than kid ones."

Breanna said he was an old soul. He even drank a cup of coffee every morning (decaf, of course).

"They accidentally sent him coffee [instead of hot chocolate] to his room one day," said Breanna.

Dawson's mom said he was an old soul. After getting coffee instead of hot chocolate, that's what he drank every morning (decaf, of course). pic.twitter.com/eYx7Ed57XX

Dawson battled leukemia for 2-and-a half years. Smiled through it all. Chemo, stem cell transplanted, bone marrow biopsies... pic.twitter.com/NN5NoFSFLI

Now you know an infectious smile like Dawson's comes with some pretty funny stories.

Last August, Nevada County made Dawson an honorary firefighter. They called it 'Dawson Day' with a ceremony and all.

Sweet Dawson passed away this Sat. after battling leukemia. He was only 8 years old. Last yr, he became an honorary Nevada Co. firefighter. pic.twitter.com/RkVOY0WGhD

Dawson was given a badge, his own turnouts, and boots. He even got to respond to an injured biker.

"He kept telling the EMTs how to wrap the leg!" said Breanna.

And his firefighter card, he never took for granted.

"He was getting ready to go to clinic one day," said Jason. "He comes back running in the house saying 'I need my ID Card!'...'No no, I need it. Just in case mom gets pulled over, [I can say police officer,] I am with the fire department.

It's reminiscing and laughing about stories like this that keep his family strong and smiling even when it hurts.

"People always ask how we're doing. As you can tell we smile. Dawson would never let us cry in the room," said Breanna.

Dawson's community made sure his last months in this world was full of adventure. Sadly, he got too sick for his Make-A-Wish: to go to Hawaii and swim with dolphins.

Dawson had plenty of adventures his last 6 months. Sadly, he never got to swim with dolphins in Hawaii... it was his dream . pic.twitter.com/UQeAqIwzW3

On June 10th at 6:05 AM, with his parents and his sister by his side, Dawson passed away.

Even up until his very last moment, he gave his family a thumbs up.

"He couldn't talk very much. Just the thumbs up that he was still good. He was Awesome Dawson," said Breanna, through tears. "It was his signature. No matter what...I told him 'It's OK Dawson. You fought the hardest battle and you won.'"

"You're not supposed to cry!" said Melody, Dawson's grandmother. "He's watching you."

And if Dawson was watching, what would they say?

"I would say thank you, for the opportunity...you pulled our community together and made our family so strong," said Melody. "We all love him very, very much. And miss him."

Breanna said she would read to him again from his favorite book 'Love You Forever.'

"His favorite saying from his favorite book: 'I love you forever. I like you for always. As long as I'm living, my baby you'll be," said Breanna.

Dawson's family hopes to continue his legacy by bringing the Beads of Courage program that got him through his darkest days into more hospitals.

Donations can be made on the Beads of Couragewebsite, under Dawson's name.

And until they see Dawson again, the family says they'll live by this motto: 'Don't cry because it's over. Smile because it happened.'

That is what Dawson would've wanted.

2017 KXTV-TV

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Awesome Dawson: The legacy an 8-year-old boy who battled leukemia leaves behind - ABC10

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NICOLE LAWTON

Last updated05:00, June 18 2017

CHRIS MCKEEN/FAIRFAX NZ

Stem cells, skin, red blood cells and platelets are all frozen in liquid nitrogen freezer at the New Zealand Blood Service for later use - but not whole bodies.

Cryonics, the practice of deep-freezing bodies, remains a controversial area of research with many scientists in New Zealand reluctant to wade into the freezer.

Not surprisingly, the art of filling the deceased with antifreeze, suspending them in liquid nitrogen in the vain hopes that scientific break-throughs will one day reanimate them and cure them isnot an accepted academic discipline New Zealand, and therefore isn't pursued in any official capacity.

But that hasn't stopped a few individuals from trying.

CHRIS MCKEEN/FAIRFAX NZ

Dr Richard Charlewood, is the medical director of the national tissue bank, run by the New Zealand Blood Service.

Two New Zealand foundations -The Foundation for Anti-aging Research and the Foundation for Reversal of Solid State Hypothermia - were given the cold shoulder in 2013 when applying to be considered a charity from the Charities Registration Boards (CRB).

READ MORE: Kiwi'sbody hangs upside-down in a -196C vat

The board rejected the foundations on the basis that cryonics was not an accepted academic discipline based on the lack, in mainstream science, of feasibility and benefits of the research.

This decision was then successfully appealed in october 2016 - when Justice Rebecca Ellis found cryonics research to fall squarely under the 'advancement of education' heading and therefore had 'charitable purpose'.

She said there was evidence that the proposed research was likely to lead to advances in areas such as organ transplant medicine, stem cell research, and treating a range of diseases and disorders.

The listed officers and trustees for both foundations have addresses Monaco, Switzerland and Liechtenstein.

Others, Saul Kent and William Faloon bought an old church in downtown Hollywood in 2013 for $880,000 and founded the Church of Perpetual Life.

The pair are big were the cryonics world and both personally signed up for their shot at eternal life.

Nothing has been heard from the foundations since the CRB appeal and all attempts to contact the trustees were unsuccessful.

The closet thing that happens to freezing humans in New Zealand is cryogenically freezing tissue through the tissue banks of the New Zealand Blood Service.

Stem cells, skin, red blood cells and platelets are all submerged in a cryoprotectant and frozen to liquid nitrogen temperatures of around negative 196 degrees Celsius - for later human use.

"The skin cells last for up to 5 years, and stem cells up to ten years," said Richard Charlewood, the national tissue bank's medical director.

"We don't like keeping it for any longer than that because most of the studies only go up as far as ten years.

"At liquid nitrogen temperatures very little is actually happening at molecular level. So it's possible that they would be fine well beyond ten years, we just don't know for sure."

Charlewood said when cryo-preserving, the key thing is to get the cryoprotectant into all the cells that you want to keep alive, otherwise the formation of ice crystals can burst the cells and kill them.

"In terms of whole body freezing, my understanding is that you have to get the cryo-protectant to all the cells in the body, so you'd have to pump it around the body really thoroughly."

Fertility specialists in New Zealand also offer cryogenic preservation of eggs, ovarian tissue, sperm and embryos for reproductively-challenged patients who wish to conceive later.

Otago University's associate professor in botany, David Burritt, also regularly employs cryopreservation in his line of study.

Ina 2016 research paper he said cryopreservation was a great method for long-term storage ofreproductive plant material - such as seeds, pollen, dormant buds, shoot tips, embryos, or isolated plant cells or tissues.

"Plant material is first preconditioned, using chemical and physical treatments, so that it remains viable when it is frozen and during ultra-low temperature storage."

"Following re-warming, seeds and embryos can germinate, buds or shoot tips can be induced to grow, and whole plants can be regenerated from cryopreserved cells or tissues."

He said the samples could, in theory, be conserved indefinitely as "no metabolic activity occurs at these ultra-low temperatures."

'Cryobanking' enables large numbers of important crops, such as wheat, potato and various fruit and forest trees, to be cryopreserved, rewarmed and then allowed to grow into complete plants.

In March, scientists in the UK succeeded in cryogenically freezing and rewarming sections of heart tissue for the first time, in an advance that could pave the way for organs to be stored for months or years.

-Sunday Star Times

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The confounding world of Cryonics, and the Kiwi scientists trying to ... - Stuff.co.nz

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Philly invented the computer then whiffed on becoming home to the tech industry. Will we do better with the next-gen medical breakthroughs were hatching?

Illustration by Muti.

In the conference room of a spacious loft office near 30th Street Station, Usman Oz Azam and Michael Christiano huddle for a meeting. Theyre CEO and chief business officer, respectively, of Tmunity Therapeutics, a start-up launched to commercialize some breakthrough research out of the University of Pennsylvania a method of reengineering a patients own immune system cells so they can destroy cancer tumors.

The two execs are the companys sole employees so far. Their new headquarters still contains chalkboard-style signs and leather couches from the prior tenant, some sort of hipster

telemarketing operation. It looks like an abandoned Cosi restaurant.

Literally the only thing weve done is bring in a coffee machine, Azam says.

Its a microscopically small start to what some people around Philadelphia hope will become very, very big.

Down the hill at the Center for Advanced Cellular Therapeutics, an alliance between Penn Medicine and global drug maker Novartis is working on other pioneering immune system research, which, like Tmunitys technology, comes from the labs of Penns Carl June. It involves extracting T-cells from patients, genetically modifying them so they can attack blood cancer, and putting them back into patients, where the altered cells multiply and become a sort of living medicine. Trials on some leukemia patients have obliterated the disease, and this designed-in-Philly treatment is on track to be the first-ever FDA-approved personalized cellular therapy for cancer.

One floor below, in the same University of Pennsylvania building, scientists at the Parker Institute for Cancer Immunotherapy are working on what could become Americas first use of the genome-editing tool CRISPR in human beings, aimed at cancer. Its funded in part by Sean Parker, the Internet billionaire played by Justin Timberlake in The Social Network (who gave $250 million to six medical schools and cancer centers). Its not the only CRISPR venture in the city. Nearby, on Market Street, the start-up Excision BioTherapeutics is working to commercialize technology from Temple University that uses CRISPR to snip viruses such as HIV out of affected patients.

Just one block up Market Street, in the penthouse-floor laboratory of Spark Therapeutics, researchers cultivate cells in flasks of a liquid that looks like weak cherry Kool-Aid. Spark, founded in 2013 to commercialize research from Childrens Hospital of Philadelphia, is what companies like Tmunity and Excision seek to become. Spark employs around 240 people and has a stock market capitalization of $1.61 billion. In May the company filed with the FDA to create the first gene-therapy treatment for an inherited disease in the United States. The treatment, which involves injecting new genes into patients to replace the imperfect ones they were born with, has reversed a rare form of blindness in clinical trials. It could be approved by the end of the year, with gene treatments for hemophilia to follow. Theyll all be produced right here, at 38th and Market.

And so were having a moment in Philadelphia. Were out to an early lead in the race to become a hub for the next generation of medicine: synthetic biology that augments the human immune system to make it better than nature did. Its a future in which medicine is less about gulping pills to mitigate symptoms than about using targeted gene and cell therapies that begin to approach cures for ailments as serious as blindness, hemophilia, AIDS and cancer. If we dont fumble the opportunity, its also a future that the Philadelphia area can own. People speak hopefully of a regional economy blossoming around these innovations an ecosystem, a magnet, the way Los Angeles is for entertainment, the way Washington is for lobbyists.

I can make the argument that Philadelphia has the greatest concentration of foundational research in gene and cell therapy in the world, says Spark CEO Jeffrey Marrazzo, a Philly native who convinced CHOP to make the company its first commercial spin-off.

Were at a unique moment, says Richard Vague, a managing partner at Philly-based Gabriel Investments who has personally funded some of Carl Junes research. The genome has been mapped. The revolution in technology has occurred. So much that needs to happen has happened. The opportunity for real breakthroughs is palpable.

Some smarties at Penn Medicine have cooked up an optimistic nickname for this region: Cellacon Valley. Its an awkward portmanteau, probably no more likely to catch on than Phillywood. Really, its a brand name for a desire. Maybe this could be our thing (besides cheesesteaks, which we know to be effective in humans). As much as anything, the nickname encapsulates a new attitude, an eagerness to better exploit advances in medicine coming out of local labs. Theres been a history of missed opportunity here, a gap in translating the genius of our academia to the marketplace. Remember, back in 1946, Penn scientists introduced ENIAC, the worlds first electronic computer. But the Delaware Valley didnt become Silicon Valley, or even Vacuum Tube Valley.

Theres a whole negative piece that could be done about what Philadelphia did not do that Boston or San Francisco did, says Steven Nichtberger, a longtime entrepreneur who teaches Wharton undergrads how to commercialize scientific ideas. At MIT and Stanford, pitching moneymaking schemes to venture capitalists is part of the university culture, as routine as joining the Dungeons & Dragons club.

Other places have had reasons they became really good at what they do, Carl June says. Now, this is our chance. I hope we dont blow it.

Looking south fromhis window in the Perelman Center for Advanced Medicine, on Penns rampantly spreading medical campus, Jonathan Epstein can see the smokestacks of Philadelphias industrial legacy.

I think we have a chance to see a new and important industry arise here, he says. Since hes chief scientific officer at Penn Medicine, one of his missions is to help make that happen. On a recent field trip to present Philly to venture capitalists in San Francisco, Epstein floated the phrase Cellacon Valley.

I actually had screens around the auditorium showing the modern parts of Philadelphia, in order to convey the sense that its not the old manufacturing city that many people have in their minds. It is hard to change peoples impressions, he admits.

Epstein thinks of Kendall Square the once-desolate area around MIT in Cambridge, Massachusetts, thats now crawling with shiny biotech buildings as a model. I grew up in Boston, and I like to tell people that Kendall Square is where they used to tow my car, he says. I watched the development of that region.

In West Philly, the makeover has begun. On streets around Penn and Drexel, you can hardly have a conversation that isnt drowned out by the beeps of a construction vehicle erecting another gleaming high-rise. But Penn getting richer or even University City becoming an innovation district isnt the same as success for the region. Around Boston, the prosperity from waves of computer tech and biotech has had a blast radius of 25 miles, to far-flung neighborhoods and suburbs. Its more extreme around San Francisco. Could we have that kind of success here? What would it look like?

If you think of Silicon Valley or Hollywood, theyre places people go with dreams. Its where the jobs they want are. If you leave a company in Mountain View or Kendall Square, theres another across the road or down the highway that needs staff. Small firms grow into big ones and seed new start-ups like acorns. Venture money burns holes in the pockets of investors who live in the area. And behind the headline-making companies are enterprises that support the IPO superstars, providing specialized staffing, equipment and facilities.

Philadelphia has some of these things. It has companies like WuXi AppTech in the Navy Yard, which contracts to do cell production and R&D. Tmunity plans to use a cell-manufacturing facility in East Norriton previously owned by Tengion, whose ambitious plans to grow human tissue ran out of runway, resulting in a 2014 bankruptcy. If you want to make a drug, its easy to hire a contract manufacturer. But if you want to make a cell therapy, it takes particular kinds of facilities and expertise which exist here now, says Nichtberger, the former CEO of Tengion.

The region, of course, has a medical and pharmaceutical legacy that goes back centuries. Ben Franklin founded Pennsylvania Hospital in 1751. In 1830, John K. Smith opened a Philly drugstore that would evolve into Smith, Kline & French and eventually the massive GSK. The Wistar Institute transformed global health with vaccines for rubella, rabies, and other life-threatening diseases. Bob McGrath, who heads Drexels office of technology commercialization, points out that four of the National Cancer Institutes 69 designated cancer centers are here, at Penn, Jefferson, Fox Chase and Wistar. There is infrastructure to build on.

But in this new world, infrastructure isnt enough. Whats also required: money to back academic research, and, no less important, an entrepreneurial culture that lets scientists see a path to making their work available to the world profitably, if possible. Its going to be hard to retain or attract the very best scientists who are entrepreneurial if there isnt an environment here in which they can see their dreams come true, Epstein says.

Thats required a culture change, at Penn in particular.

For Ivy League schools, commercializing technology is a very new event, says June, director oftranslationalresearch at Penns Abramson Cancer Center. Google came out of Stanford. It never could have come out of Penn back then. Ivy League schools kind of turned their nose up at funding from commercial entities. The faculty were encouraged to get peer-reviewed and go for government funding.

These days, the word translational is on business cards and medical buildings all over University City. It means translating science from bench to bedside, from the lab to the patient. That can cost multiple millions of dollars, and government money isnt what it used to be. When I moved to Penn in 1999, I was like most faculty here in that over 80 percent of my research funding was from the NIH, June says. Now, its less than 20 percent. Attracting funding from other sources is more and more important.

Pretty much all the local institutions are trying to get better at it. In a sense, theyve begun throwing open their lab coats to the world and saying, Check us out. Sparks Marrazzo says that in 2011, Steve Altschuler, then CEO at CHOP, invited him to walk the corridors there looking for commercial ideas. Its literally true, Marrazzo says. He said, Why dont you spend three months? Ill give you the authority to walk the halls and meet with scientists, see if theres anything there that you think is worth trying to take a bolder step.

Not-for-profit universities and hospitals cant raise money by selling stock. But they can take equity in the start-up companies built around their intellectual property, which is almost as good. Marrazzo says CHOP invested $35 million in Spark. They have already liquidated between $150 million and $200 million, and they still have 18 or 19 percent of the business, which is worth probably another $300 million to $400 million, he says. CHOP has now spun out three other companies and hired serial entrepreneur Patrick FitzGerald to a new position: Vice President for Entrepreneurship & Innovation.

Penns medical school offers a masters degree in translational research, which MD and PhD candidates can add to their studies. The course helps researchers undergo a Nutty Professor style transformation from meek lab-focused scientists to confident presenters of their assets to potential funders

Theyve got to learn how to articulate their science to different audiences to give the elevator pitch, the TED talk, says Emma Meagher, a cardiologist and clinical pharmacist who runs the program. When they go to the NIH, they have to articulate the science as a scientific discipline. When they go to a not-for-profit foundation, theyve got to articulate the science as it appeals to the unmet medical need for that foundation. To a for-profit funder, its Are you gonna make me money, wheres your business plan?

Drexels McGrath is a matchmaker who connects faculty inventors with commercial partners. A review committee helps them groom pitches. The Lankenau Institute for Medical Research, in Wynnewood, has an incubator to develop companies spawned from its research. CEO George Prendergast calls it a small Bell Labs of bioscience. He invented the word acapreneurial to describe the model marrying academics with entrepreneurship.

At Temples Lewis KatzSchool of Medicine, legal experts from the universitys technology transfer office embed in the med school and look at the facultys papers and grant applications before they go out and see if there are elements we ought to protect with respect to the intellectual property, says Steven Houser, senior associate dean of research there. If you dont protect it, no one in the private sector will ever want to invest in your idea.

Racking up patents isnt an official yardstick for evaluating faculty. Not yet, Houser says. There are discussions at most institutions about whether things like patents should be considered in tenure discussions.

So how do we enter the Valley? It doesnt happen by chance. It happens because people make strategic moves, Penns Epstein says.

The schools outreach to industry is part of it. Public funding and local incentives like tax breaks are also still important, even as the Trump administration pushes for big cuts to NIH and NCI budgets. Pennsylvania has a patchwork of aid. Governor Wolfs new budget proposes selling bonds to raise $45.9 million for CURE, which issues health-research grants. State-supported Ben Franklin Technology Partners offers seed capital to start-ups. Keystone Innovation Zones provide corporate tax credits. But June envies what other states have done. A California voter initiative provided $3 billion for stem-cell therapies. Texas sold bonds to raise $3 billion for cancer research. Its recruiting people and new companies. We need to do that here, June says.

Of course, amid all the possibility, theres a need to proceed carefully. Gene therapy isnt like building a new mobile app. Human health is at stake. Pioneer Jim Wilsons experience tells a cautionary tale and offers another kind of hope.

Wilson created Penns gene-therapy program when he arrived there in 1993. There was a tremendous amount of enthusiasm in the mid-90s, he recalls. Its the natural trajectory of an emerging technology: Theres a lot of expectation and anticipation, a little knowledge, and in this particular area it was fueled by all of us. By the PR machines of the universities. By the investigators, who could garner resources. By patient populations, especially those with rare diseases who just were neglected. Gene therapy sounded different. It wasnt just another drug. It was: I have a bad gene and youre gonna fix it.

Then, in 1999, Jesse Gelsinger died, in a Penn gene-therapy trial directed by Wilson. The 18-year-olds body reacted adversely to the virus used as a vector to deliver a new gene to his system. It turned out Wilson owned stock in a company that was funding the research. There was a lawsuit, and much debate about the conflicts that arise when science gets in bed with business. People walked away from the field, Wilson says.

Humbled and censured, Wilson kept a low profile but continued to work, landing on a safer vector thats part of the current rebirth of gene therapy. Two companies based on his new work, though, located elsewhere. RegenXBio is in Rockville, Maryland. Dimension Therapeutics is in Cambridge, despite the fact that the R&D engine was here at Penn, Wilson says. We tried everything we could to convince management and the investors that it would make more sense to place these companies at Penn.

But ecosystems build one victory at a time. Kevin Mahoney, executive vice dean for integrative services for Penns medical school, had hinted to me about such a victory: a secret new gene start-up coming to the city even though the moneymen tried to insist that it be headquartered in Kendall Square. They said, It can only be in Kendall Square. And we said, No way. It has to be in Philadelphia, Mahoney says.

Wilson wanted to tell me the secret, too. Its a new company called Scout Bio, based on gene therapy technology out of my lab at Penn, he reveals. It uses gene therapies in small animal health pets to deliver therapeutic proteins for anemia, atopic dermatitis, cancer. Were building that in Philadelphia.

Yo, dog. Welcome to Cellacon Valley.

Published as Cellacon Valley? in the July 2017 issue of Philadelphia magazine.

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Welcome to Cellacon Valley? - Philadelphia magazine

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ATLANTA - As an OBGYN with Piedmont Physicians in Newnan, Dr. Tia Guster gets asked a lot about what works for hot flashes.

"It's a little bit of trial and error," Dr. Guster says. "S you have to pack your patience hat on that one."

That's because the triggers are different for each woman, Guster says.

For some, drinking alcohol or caffeine can turn up the heat.

For others, stress, eating spicy food, just being in the heat can trigger that sweaty, flushed feeling.

So, Guster says, start by paying attention to what you're wearing.

"So keep it kind of loose, with flowing maxi-dresses, if you can, at all, wear that as a fashion trend," she says.

And try turning down the temperature at home.

For severe hot flashes, Dr. Guster says, ask your physician whether you're a candidate for hormone replacement therapy, also known asHRT, and what the risks and benefits are.

Your doctor may also prescribe non-hormonal medication to ease your symptoms.

And, Guster says, soy also works for some women.

"Legitimately, soy-based products are helpful, because they act essentially as estrogens in your body," she says. "And we've got those over-the-counter."

Steer clear of soy and soy products if you have a hormone-sensitive condition, like certain breast cancers.Guster says supplements like black cohosh, red clover and evening primrose oil may also help ease your symptoms.

"I think it's worth a try before you go to (prescription) medicine," she says. "But definitely bring all your stuff in and just have a conversation, like, 'Doc, I use this, and I use this. What do you think about this?'"

Finally, Guster says, exercise can be a huge help.

"It boosts your endorphins," she says. "It lowers your weight. It helps with your heart rate and your blood pressure. And all these things are excellent foundations for health."

You don't have to lift weights or run a marathon, Dr. Guster says.

"Just walk up and down your block for 30 minutes," she recommends. "It's also mind-clearing, which goes a long way."

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Tips for easing hot flashes - FOX 5 Atlanta

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In the past half-century, this tiny object has gone from feminist icon to dangerous villain to, incredibly, feminist icon once again. And no, we're not sure why the background is pink.

The IUD is a clever little T-shaped object that does a really good job of babyproofing your uterus. Its relatively safe, last up to 10 years, and is 20 times better at preventing pregnancy than birth control pills, the patch or the ring. Today the IUD, which stands for intrauterine device, has become so trendy that you can find it on necklaces and earrings on Etsy, and read upfront memoirs by women about their experiences. But it wasnt always this way.

In the 1960s and '70s, the device started hittingits stride as an icon of liberated feminism. But in the mid-'70s, disaster hit. For decades, the IUD was roundly shunned in the United States by women and doctors alike. Today it is by far the most-used reversible contraception method in the world, with 106 million women relying on it for long-term contraception. And yet its still relatively rare in the U.S., wherenearly half of all pregnancies are still unintended.

That may be changing. Directly after President Trump took office, news outlets reported on the rush for long-acting birth control, speculating that the new urgency was fueled byfears that the administration would slash Obamacare requirements forinsurers to cover intrauterine devices and other forms of contraception, as well as stop Medicaid reimbursements for Planned Parenthood.(Most forms of the IUD, it turns out, can outlast a presidential term.) Suddenly, it seemedthat the IUD was destined to become a symbol of modern feminism once again.

To which longtime IUD-users say: Duh. What took you so long? Lets go back to the beginning.

Two Strands of Coarse Silkworm Gut

In 1909, a German medical journal published a paper on a funny-sounding device meant to prevent pregnancy. The device, according to the article, consisted of two strands of coarse silkworm gut united by a thin bronze filament, which were inserted into the uterus using a female bladder catheter (ouch!). The idea behind this and other early IUDs was that putting foreign objects in the uterus tended to sparkan inflammatory response that made life tougher for sperm, says David Hubacher, an epidemiologist who studies contraception at FHI 360, a human development nonprofit.

Prior to this point, the main form of internal contraception was known as an interuterine device, a device made of metal or silkworm-and-glass that was originally used for "therapeutic purposes."This device had a major drawback: it crossed both the vagina and the uterus, thus connecting the uterus to the outside environment by way of the vagina. In a time when gonorrhea was more common and had no good cure, these devices resulted in a high rate of pelvic inflammatory disease.

The 1909 papers title, Ein Mittel zur Verhtung der Konzeption (a means of preventing conception), was no doubt shocking to readers at the time, for whom birth control was a taboo topic, according to acontemporary medical journal. That might explain why, although it was the first genuine IUD, it seems not to have been widely used. It wasn't until 1928 thata German physician named Ernest Grafenberg developed a variation on the silkworm gut IUD, made of metal filaments shaped into a ring, which became more well-known.

Still,regulation was poor. As IUDs increased in popularity, so didreports of cases of pelvic inflammatory disease associated with them. By the late 1940s, only a miniscule number of American women were using European IUD technology, says Hubacher,who haswrittenon thehistoryof the device.

The IUD's first heydaydovetailed with the liberated 1960s and '70s. They got another bump when, in the 1970s, Senate hearings featuring safety concerns over the birth control pill pushed many women toward the IUD. Soon the little device had become, in the words of one doctors 1982 history of the IUD, the unofficial status symbol for the liberated woman. IUDs were worn as earrings even as bras were being burned.

It seemed the IUD was finally destined to have its day. At one point in the '70s, nearly 10 percent of American women using contraception were choosing an IUD. But then, just as it had become the anti-pregnancy choice du jour amongliberated women, one popular model turned out to be deadly. Enter: Dalkon Shield.

An American Tragedy

Today just the name "Dalkon Shield" evokes collective wincingamong a certain generation.In the 1970s, this crab-shaped IUD model was beginning to be linked with reports major health problems including pelvic inflammatory disease, septic abortions, infertility and even death. In 1974, amid media reports, congressional hearings and falling sales, the devices manufacturer suspended sales. ByJuly 1975, there were 16 deaths linked to the device, according to the Chicago Tribune.

By 1987, the New York Times was reporting that as many as 200,000 American women have testified that they were injured by the device and have filed claims against the A.H. Robins Company, the one-time maker of Chapstick Lip Balm. (The Washington Post cited more than 300,000 victims.) The manufacturer filed for bankruptcy in 1985, and a $2.4 billion trust was established in the late 80s for women whod been affected. The failure of Dalkon Shield would have consequences for decades to come.

Between 1982 and 1988, the use of IUDs and other long-acting reversible contraceptives in the U.S.declined significantly. That year, updated devices came out that met new FDA safety and manufacturing requirements, but the damage had been done. The shadow of the Dalkon Shield hung over the entire market, dissuading American women from even considering IUDs even as their popularity in Europe grew.

Mary Jane Minkin, a clinical professor of obstetrics, gynecology and reproductive sciences at Yale School of Medicine, says that in the 80s, when she discussed contraceptive options with her patients, IUDs were not even considered as a remote possibility. There was no person who would have let me put one in, she says.

In 1996, The Washington Post ran a story about a family planner from New Jersey working with IUD-using populations in Senegal, Nigeria and Kenya who herself had trouble finding an American physician willing to give her one. (At that time, only 1.4 percent of American women using birth control were using an IUD.) A year later, a Virginia physician trying to test a new IUD for market reported that he couldnt give the device away for free.

The reasons for the Dalkon Shields problems are still a topic of debate. During the fallout of the devices problems, researchers reported that a major problem with the device was the particular design of the Dalkon Shields tail string, which is used bothto help women make sure the device is still in place, and to aid in its eventual removal. Unlike other IUDs at the time, the string on the Dalkon Shield was made not of one filament but of many tightly wound filaments.

According to expert testimony in legal cases and reporting from that time, the multifilament string acted as a wick, pulling bacteria and sexually transmitted viruses into the wombs of Shield wearers, as The New York Times put it in 1987.

But Hubacher and Minkin say it was never clear how much the devices tail string was at fault. Rather, says Minkin, who was an expert witness on behalf of a trust later established to pay out women hurt by the device, the objects pronged, crab-like shape made it difficult to insert. That, possibly combined with poor doctor training, meant that it probably wasnt being placed correctly, she says. As a result, some women got pregnant while wearing the devices, leading to septic abortions and, in some cases, death.

She and Hubacher add that another potential danger for women was the fact that screening for pre-existing STIs like chlamydia and gonorrhea wasnt as good in the 1970s as it is now. Inserting an IUD into a woman with an infection might have spread that infection, potentially leading to pelvic inflammatory disease, which can cause infertility.

What's certain, however, is that the Dalkon Shield's failure rippled out to Americans' perceptions of all IUDs.After the controversy, all but one were pulled from the market by 1986. Even today, says Megan Kavanaugh, a senior research scientist at the Guttmacher Institute, some young women she interviews say their mothers have told them to avoid the devices.

Contraception's Gold Standard

Over the last 15 years, cultural attitudes toward this maligned device have been warming. Ameican IUD use has been on the upward swingsince the early 2000s, and several new brands have hit the market featuring names like Skyla, Kyleena and Liletta(apparently theres a mandate that new IUDs sound like pop stars). In the years 2011 to 2013, around one in 10 American women aged 15 to 44 who relied on contraception usedan IUDa five-fold increase over the previous decade, according to data from the Centers for Disease Control.

A safe IUD is the answer to all birth control prayers, writes a woman on Huffington Post who put her two teenage daughters on the device. I switched over a year ago from the pill to an IUD, and it has made a world of difference, writes another, adding: "I am EXTREMELY forgetful, and it is how we ended up with my now-5-year-old!" A gynecologist who herself wears an IUD recently wrote about the advantages of using a form of birth control that youre supposed to forget.

Kavanaugh attributes the change in great part to a recognition within the scientific community that modern IUDs are extremely safe. It helps, she adds, that a younger generation of women and doctors dont have the strong negative associations as those who grew up during the time of the Dalkon Shield. The American College of Obstetricians and Gynecologists now recommends the IUD as the gold standard of birth control, calling them safe and appropriate... These contraceptives have the highest rates of satisfaction and continuation of all reversible contraceptives.

These days there are two major types of IUDs: hormonal and copper. The copper IUD, physicians believe, is toxic to sperm, slowing and damaging the little wrigglers as they swim toward the egg like heat-seeking missiles. The hormonal IUD releases progestinthe synthetic version of the naturally-produced hormone estrogen, and the same hormone found in the pillwhich makes cervical mucus thicker and more hostile to sperm. While the mechanisms are different, the result is the same: Never the twain shall meet.

Hubacher and Minkin attribute the safety of modern-day IUDs to a number of factors. First of all, screening for STIs is much better nowadays. In addition, because they use copper or hormones rather than merely plastic, modern-day IUDs aremore effective at preventing pregnancy. (That means that IUD users are less likely to get pregnant, which can lead to medical issues like ectopic pregnancy.) Moreover, if the multifilament string was ever at fault, modern-day IUDs use single filament strings, eliminating that potential cause of infection.

Many physicians now back the IUD so much that it's become something of a cause to champion. Kavanaugh points to an organization in Washington, D.C. and a task force in New York City that promote IUD use and offer insertion training to medical professionals. IUD advertising has increased, and magazines like Cosmopolitan and Elle are running stories singing the praises of these tiny objects. Rates of IUD use have been growing across many demographic groups, says Kavanaugh, and the pace is especially rapid among young women. Now, a woman who becomes sexually active at 17 but doesnt want a baby till shes in her late 20s might be a good candidate for an IUD that lasts years.

Anecdotally, gynecologists say theyre seeing a major increase in demand. About six months [ago], I was doing one to two IUD insertions a week and now Im doing one to two a day. It's a huge increase,"says Brandi Ring, an ob-gyn in Denver whos part of a new generation of doctors and patients embracing the IUD. As of 2012, 10.3 percent of women who use contraception were using an IUD slightly more than what it was before the Dalkon Shield fiasco. Of course, because the U.S. population has grown, that means more women in the United States are using an IUD than ever before, Hubacher says.

I break it down for my patients in terms of how often they have to remember or think about their birth control, says Ring. I start with the pill, and I say: In the next year you will have to think about your birth control 365 times. For your IUD, you have to think about it twice: once to tell me you want it, and once when I put it in. Even better, because the IUD gets inserted by the doctor and lasts for years, theres little opportunity for user error. It has a failure rate of about one percentcompared to condoms, which have a 13 percent failure rate over the course of a year, or the pill, at 7 percent.

That said, the IUD isnt perfect. Both formscan cause bleeding and cramping directly after insertion, and ParaGard (the copper version) is known in some cases to initially make periods heavier and cramping more intense. It is possible, while rare,that an IUD could perforate your uterus, particularly if you have never had children or have recently given birth; this serious riskusually happens during insertion. There is also small risk that your body willexpel the device.(Check here for morecommon side effects for each type of IUD.)

The financial downside to IUDs is that women need to pay a chunk of change upfront, depending on insurance coverage. The price ranges: Right now, Obamacare generally covers the bulk of the cost of getting an IUD, sometimes leaving women with a few hundred dollars. Meanwhile, the cost of getting one without any insurance could be upwards of $1000 dollars, according to Kavanaugh.But over the long-term, the IUD ranks among the most cost-effective of contraceptives once you factor in things like the cost of unintended pregnancy.

In the end, it's your body, your choice. But if you do go forth and get an IUD, know that the tiny device in your uterus comes with a long and tangled history.

See more here:
From Medical Pariah to Feminist Icon: The Story of the IUD - Smithsonian

Recommendation and review posted by simmons

wbur Commentary

June 16, 2017

By Dr. Isaac Kohane

Quick: What is the hilly profile in the red figure below?

No, its not my fitness trackers daily step count, but youre close.

Its a set of daily weights, as measured by an electronic scale over a period of several weeks. More specifically, the daily weights of my 90-year-old mother, who continues to live in her own apartment despite all my offers. "I outlived Hitler and Stalin, she says. I can take care of myself."

She can, in fact, take care of herself, but Ive found over recent months that she can take care of herself far better with some digital help. And that experience, though only a single case, persuades me that recent spectacular gains in artificial intelligence could bode far better for our health than studies to date suggest. But also that caring, common-sensical humans will not be replaced by AI any time soon.

My mother has moderate heart dysfunction, and her physician has her on all the right medications, including a daily dose of Lasix, a "water pill" that makes you urinate more and thereby eliminate some of the salt in your blood. Yet last year, over several weeks, her legs became increasingly swollen with fluid, to the point that it oozed out of her skin. Her shins looked as if they were covered withtears. She was also in quite a bit of discomfort.

Her physician sent her to the emergency room, where an ultrasound showed that her heart was enlarged and pumping less effectively than it should. She landed in the hospital for a week, where the most important treatment she received was intravenous Lasix, a far more potent form than her usual pills.

By the time she left the hospital, her legs had not returned to normal but were visibly thinner. As I would have said as a callous medical student, she had been effectively "dried out." She was also considerably weaker from spending a week in a hospital bed, but regained her strength with the help of a physical therapist.

Six months later, a similar scenario played out, but worse. This time, she had to go to a rehabilitation facility after her hospital stay because she was too weak to care for herself or even to walk without help. I suppose if you survive malaria, starvation and typhus as a child, you must be made of tough protoplasm. After two weeks of intensive rehab, she was back at her apartment again.

But two hospital staysin such a short period concerned me. So I decided to try something that in my day job as a researcher in biomedical informatics the use of computing to advance medicine --I knew had been tried before by many health systems with highly variable and often disappointing results.Nonetheless, I was determined to make it work.

The Plan

The plan was to have her watch her weight daily, and every time there was any sign of increased fluid, to recommend an extra dose an extra pill of Lasix, to restore her fluid balance.

This type of thinking has informed doctors for decades. Outside the hospital, it has worked well for some, but multiple trials, several involving computerized alerts every week to change water-pill dosage, have not conclusively shown benefit.

On the other hand, a friends father, a physician, had defied the odds and lived for decades with severe heart failure by weighing himself daily and adjusting his medications accordingly. That was not a trial, true, but it seemed remarkable, and I wanted to emulate it.

Before I go further, let me confess that when I tell this story to my colleagues, especially those trained in internal medicine or cardiology, their responses range from outright alarm to pursed-lip disapproval. It only gets worse when I remind them that I trained in pediatrics. So lets be clear: Don't try this at home, kids. And I would emphasize that I did not remove my mother from her regular internists care. He remained as a safety net, and I communicated with him copiously.

Back to my story: The challenge was to manage my mother within the constraints of my demanding schedule. I decided the first, most crucial task was to get accurate weights sent to me promptly so that I could act on them. I decided to purchase an internet-enabled scale from Fitbit that allowed me to check my mother's weight via Fitbit's web application.

I asked my mother to weigh herself every morning before eating. In the first few weeks, if she forgot to weigh herself I could see that and would call her to nudge her. Within a month, I never had to remind her anymore. Instead, shed call me to see what I thought of her weight.

Now for the easy part, how to control fluid balance. Heart physiology is complex, and many have tried with only partial success to devise computational models that can predict how it will change with perturbations from diet, medications, disease or exercise. But I boiled it down to one question: How to determine whether she should take an extra Lasixon a given day?

I'll call my plan an algorithm, so it will sound authoritative:

1. If her weight increases by more than 1 pound in one day, recommend one extra Lasix pill. 2. If her weight increases by only 1 pound, then wait to see if it increases by another pound in the following two days, in which case, recommend an extra Lasix pill. And if she took the extra pill, then: 3. If the weight does not return to normal by the second day after the extra dose, then give one additional dose the third day. If on the third day the weight has not returned to baseline, go visit her in her apartment and see if her legs are swollen or if her breathing has changed.

This third part of the algorithm I labeled "visiting nurse." If I saw anything that worried me swollen legs, faster breathing, poor skin color I would call her doctor and ask him to evaluate her. At this point, wed be back in the conventional medical management world, but Id have a lot more useful information to share with her doctor than I would otherwise.

The algorithm also included sleuthing out the cause of the weight gain. On the phone Id go over what she had eaten. Often the culprit was a source of additional salt. Only after reviewing a typical salad and pasta dinner would I learn that shed enjoyed a dozen delicious salt-loaded crackers.

Just having these "debugging" phone calls after a weight gain caused these diet-borne risks to be eliminated rapidly. They also provided my mother with a very concrete sense of which foods to avoid.

So What About AI?

Now back to the graph I shared above. It shows a few weeks of what has gone on for over a year. I managed each of those peaks according to the algorithm. Through the miracle of the internet and smartphones, I was able to run the algorithm even when I was in a distant part of the globe to give a talk or on a family vacation.

Best of all, my mother hasn't even come close to needing to go back to the hospital. Her legs remain completely unswollen. Also, I never called her doctor about persistent fluid gain because that part of the algorithm was never triggered.

Moreover, after a few months, my mother startedcallingme to let me know that she had already implemented the algorithm for that day, because shed gotten tired of waiting for me to call her with my recommendation.

So what about AI? If computers can now win Texas hold 'em poker with imperfect information and bluffing human beings, surely they can manage patients like my mother?

Im not so sure.

A frail, elderly patients health may be influenced by single or multiple perturbations that span the full spectrum of human experience: How much salt was in yesterdays food, the appearance of a skin infection on a leg, change in thyroid hormone levels, increased fluid loss due to apartment heat after an air conditioner failure, sad news causing mood changes causing decreased exercise.

That is only a partial list of the challenges that my mother has overcome in the past year.

And though it may seem straightforward, managing an outpatient with heart failure is far more difficult than the apparently more complex tasks that have been featured in the success of "deep learning": finding cancer cells in a pathology slide, or signs of diabetic disease in a photograph of a retina.

Even more challenging: How does a computer program obtain trust and persuasive powers so that skeptics like my mother will comply with recommendations? What discussions, diagrams, pressures or incentives will be sufficient to convince someone who may not be feeling well at all to change a behavior, a medication or diet?

These skills are hard to come by in humans, let alone computers.

So should we give up? On the contrary. Lets not fall into the trap of "the Superhuman Human Fallacy" the demand that computers perform better than even the best of humans. A more useful comparison is to the way humans actually perform.

Even with imperfect hardware and simplistic algorithms, my mother's doing better than before, when weeks would pass between physician visits and treatment adjustments. Im confident she and many other patients can do better still, but only if we shore up the two sides of the clinical compact.

On the one side, organized medicine has to change its practice so that it can ingest the day-to-day or even minute-to-minute measurements made of our fast-growing chronically ill and aging population, and transduce these data into timely treatment. But without thoughtful and broad application of AI techniques into the process of health care, our already struggling and stressed health care workforce will simply be not able to meet this challenge.

And on the other side, AI cannot replace family and friends as guardians of health not now and perhaps not ever.

AI may be good at chess and Go, and at developing expertise once reserved for doctors in arcane areas such as reading X-rays. But AI does not do well at understanding the wide world, at picking up mood or subtle signs of distress, at convincing a resistant human to listen to the doctor. We don't need AI for that; we need a caring village.

Dr. Isaac Kohane is the inaugural chair of the Department of Biomedical Informatics at Harvard Medical School.

Excerpt from:
What My 90-Year-Old Mom Taught Me About The Future Of AI In Health Care - WBUR

Recommendation and review posted by simmons

Posted by Steve Lee, Editor Around the Nation, Online Only, Top Highlights Saturday, June 17th, 2017

NEW YORK By acting out scenarios commonly seen in the clinic, real-life transgender actors can help residents learn to provide more sensitive care to people with a different gender identity than the one they were assigned at birth. This is the main finding of a study published online June 15 in the Journal of Graduate Medical Education.

The opportunity to interact with a transgender patient in a low-stakes setting during medical training increased trainees comfort during future real-world outpatient encounters, says Richard E. Greene, MD, lead author of the study, from NYU Langone Medical Center. Even those who had baseline knowledge of care for transgender patients before the study found that learning in this safe, simulated way added value in helping them provide more sensitive care for transgender patients, adds Greene, an assistant professor in the Department of Medicine at NYU Langone.

As NYU Langones director of gender and health education, Greene designed the current study after many conversations with transgender patients who reported feeling discomfort, discrimination, and insensitivity in health care settings.

To study the problem, the research team employed a common teaching strategy that uses a standardized patient, an average person trained to consistently portray a patient in a certain medical situation. Each trainee in a class interviews the patient, seeking to determine the persons medical needs, communicate options, and offer reassurance. The new NYU research is one of the first published studies to employ transgender persons as standardized patients.

For the study, a transgender actress/standardized patient, who acted out a common outpatient scenario, rated the 23 internal medicine residents on their ability to communicate and to leave the patient satisfied with the interaction. The average scores using a newly designed behavioral measure achieved by the residents were 89 percent for overall communication and 85 percent for satisfaction.

Interestingly, the scores did not differ significantly from those achieved in nine control cases in which the standardized patients were not transgender. This suggests that transgender standardized patients can be just as effective as straight cisgender (or non-transgender) patients in teaching doctors, says Greene.

In the specific clinical scenario used in the study, the transgender actress was taking the anti-androgen hormone spironolactone for reducing masculinization, along with the feminizing hormone estradiol. She also came in for hypertension and had dangerously high blood levels of potassium, a condition known as hyperkalemia. The patient then expressed the desire to undergo an orchiectomy, a procedure for removing the testicles.

The residents were tasked with exploring and respecting the patients treatment goals, given her hormonal transition hormone therapy, and to make a plan for managing her hypertension and hyperkalemia. Additionally, the researchers wanted to see whether the residents asked questions that indicated sensitivity, like a patients preferred pronoun and gender identity, as well as to learn whether the discussion covered sexuality, sexual activity, and associated risks.

The results indicate that good communications skills helped some residents overcome their lack of transgender-specific clinical acumen and that going through this scenario training with a transgender actress helped them to shed preconceptions and be better prepared for the clinic.

On the other hand, most residents in the study did not directly address the patients gender identity and long-term goals of care, says Greene. This underscores the need to include transgender standardized patients in our teaching and curricula. Without them, a substantial gap in care remains.

A 2016 Williams Institute analysis of federal data found that 1.4 million adults identify as transgender across the United States. This figure is double that found a decade earlier.

In addition to Dr. Greene, Kathleen Hanley, MD, Tiffany E. Cook, BGS, Colleen Gillespie, PhD, and Sondra Zabar, MD, all from NYU, were study coauthors. Health Resources Services Administration Grant #T0BHP285770100 provided funding for this research.

Short URL: http://lgbtweekly.com/?p=80468

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New study shows transgender actors effective in teaching new doctors to provide respectful care - LGBT Weekly

Recommendation and review posted by Bethany Smith

Each year, more than 700,000 people suffer myocardial infarction, aka a heart attack. Thanks to medical advances, there are myriad ways for a doctor to get the blood properly pumping and save a persons life. A cardiologist might give a patient medication to clear or loosen blockages. Or a doctor might insert a catheter to remove the clot, or place stents in the artery so it stays open.

These interventions have vastly improved survival rates, but they dont heal the damage caused by a cardiac event. The heart is really just one big muscle, and trauma to any muscle does some damage, which becomes scar tissue. Scar tissue on the heart means it functions far less optimally, which eventually leads to heart failure.

Short of a transplant, there isnt a long-term option to fix a damaged ticker. But a team of researchers say theyve come up with a high-tech solution that could revolutionize cardiology. Using 3-D printing technology, Brenda Ogle, an associate professor of biomedical engineering at the University of Minnesota-Twin Cities, has created a patch a doctor could apply to mend a patients broken heart.

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A false-color scanning electron micrograph (SEM) of a blood clot protruding from an arterial entrance in a heart chamber. This type of clot, known as coronary thrombosis, is the usual cause of myocardial infarction (heart attack). P. Motta/G. Macchiarelli/Sapienza University/Science Photo Libary/Getty

The concept is to imprint proteins that are native to the body, says Ogle. Weve used stem cellderived cardiac musclecardiac myocytesand actually mixed those with other cell types needed for blood vessels. This, she says, prevents what would otherwise happen naturally: The formation of a different type cells known as fibroblasts, which secrete scar tissue.

Ogle and her team of 3-D printing experts, clinical cardiologists and stem cell engineers have successfully tried the patch on mice. First, the team induced cardiac arrest in the rodents. When they then placed the cell patch on a mouse, researchers saw a significant increase in the functional capacity of the organ after just four weeks. We generated the continuous electric signal across the patch, and we can pace it: We can increase the frequency of beating up to three hertz, which is similar to a mouse heart, says Ogle who, this past January, published the findings of their experiment in Circulation Research, a journal from the American Heart Association.

The results of the experiment were so inspiring that in June 2016 the National Institutes of Health awarded her team a grant of more than $3 million, so they can now give pigs heart attacks and fix them with the patch. However, it will take some time to see their innovation in surgical departments, since using biological products such as cells requires a long regulatory process and, of course, quality assurance.

The replacement of muscle has been the holy grail for some time, says Ogle. Now we finally have the ability to take stem cells out of the body and develop the protocols to do that.

Read the original here:
How 3D Printing Can Help Mend a Broken Heart - Newsweek

Recommendation and review posted by Bethany Smith

Asian American Donor Program encourages minorities and mixed heritage to join national registry

Oakland Lisa Marie Evangelista, a 31-year-old Filipina woman who lives in Sacramento, is in a literal fight for her life. Lisa is a speech language pathologist and works at the U.C. Davis Medical Center.

On Dec. 27, 2016, she was diagnosed with Chronic Myelomonocytic Leukemia, a rare and aggressive blood cancer. She needs a bone marrow transplant to survive. Lisas sister is a 5/10 or half match. However, doctors prefer Lisa find a 10/10-donor match. To find a perfect match, Lisa needs a stranger to step forward and help save her life.

Lisa has partnered with the Asian American Donor Program to find a donor similar to her genetic makeup. A bone marrow transplant, which is needed soon, is Lisas only hope for her long-term survival. A committed 10/10 marrow-matching donor must be located to have a successful transplant. Since Lisa is of Filipino, a matching donor will also need to be of Filipino or Asian descent.

More about Lisa

Lisa learned about her diagnosis just nine months after her father died of a blood cancer. Family and friends note how she brings laughter, joy, warmth, and kindness to each day. Lisa is a speech-language pathologist and board certified specialist in swallowing and swallowing disorders. Her clinical interests include the evaluation and treatment of dysphagia resulting from radiation and chemotherapy treatments to the head and neck. She works directly with patients diagnosed with throat cancer. Lisa has lectured at the regional and national levels on pulmonary health and ethical considerations in dysphagia management. Lisa is described by her colleagues as a brilliant clinician and scientific thinker who is devoted to helping her patients. Lisas hobbies include traveling, hiking, and dancing.

Lisa grew up in Laguna Hills in Orange County, California. She attended Laguna Hills High School. From California State University, FresnoLisa received abachelors degree in 2007 and a masters degree in 2009. Lisa received her clinical science doctorate in medical speech-language pathology from the University of Pittsburgh, Pittsburgh, PA in 2014.

Whats the solution?

Minorities are more likely to die of leukemia and other blood cancers because there is a shortage of ethnic and mixed-ethnic donors on the Be The Match national registry. It is vital to expand and build a more diverse registry so everyone has an equal opportunity to survive blood cancers.

Encouraging more people of ethnically diverse backgrounds and those of mixed heritage to be committed and join the Registry, potentially saving a life. Each of us can Be TheOne to Save a Life!

The Asian American Donor Program (AADP,www.aadp.org) is a 27-year-old nonprofit organization, based in Alameda, CA, that works to educate community members about the shortage of ethnic marrow donors and the importance of joining the Be The Match national registry. It is the oldest nonprofit of its kind in the country. AADP staffis dedicated to increasing the availability of potential stem cell donors for patients with life threatening diseases curable by a blood stem cell or marrow transplant.AADP is an official recruitment center for Be The Match.

There is a shortage of committed non-Caucasians on the Be The Match national registry, says Carol Gillespie, the AADP executive director. We need everyone of mixed race ancestry to step forward and join the Registry.When a marrow match is not readily available, patients have to wait longer than is ideal to find a match.Once a match has been found, their disease may have progressed to the point that they are no longer eligible for a transplant.

Shortage of ethnic/multi-ethnic donors

Approximately every three minutes one person in the United States is diagnosed with a blood cancer. An estimated combined total of 172,910 people in the US are expected to be diagnosed with leukemia, lymphoma or myeloma in 2017. New cases of leukemia, lymphoma and myeloma are expected to account for 10.2 percent of the estimated 1,688,780 new cancer cases diagnosed in the U.S. in 2017. (From:http://www.lls.org/http%3A/llsorg.prod.acquia-sites.com/facts-and-statistics/facts-and-statistics-overview/facts-and-statistics)

Of the approximately 816,000 Asians on the Be the Match registry, .5 percent are Filipinos, while Filipino Americans constitute 19.7 percent of Asian Americans (Source: 2010 Census). The Be The Match registry recruits hundreds of thousands of donors each year through an extensive network of more than 155 local and regional Community Engagement Representatives and organizations. You only need to join the Be The Match registry once.

Finding a marrow/stem cell match can be like finding a needle in a haystack, says Gillespie. Multi-racial patients face the worst odds. Those diagnosed with a blood disease need a marrow/stem cell transplant as soon as possible. Building the Registry with committed donors is what patients need. You could potentially match anyone in the world, this is truly a global effort.

Marrow/stem cell matches are very different than blood type matches. Just as we inherit our eyes, hair, and skin color, we inherit our marrow and stem cell tissue type.

For thousands of severely ill blood cancer patients, there is a cure, Gillespie says. You could be the cure. Those whose marrow/stem cells are not a match for a patient in need now may be a match for someone else down the road, anywhere in the world. I encourage multi-ethnic individuals to commit to registering. It is simple to register just a swab of the inside of your cheek.

How you can commit to help

Find a registration drive in your area. Go tohttp://www.aadp.org/drive/.

Register on line here:https://join.bethematch.org/lisa.

You must be 18 to 44 years old and meet general health requirements

Fill out a consent form and do a cheek swab.

Be committed. Be ready to donate to any patient in need.

Contact friends/family and encourage them to go to a registration drive or register online.

Set up a drive in your area or for more information, call AADP at 1-800-593-6667 or visit our websitehttp://www.aadp.org.

Volunteer to help at registration drives.

Please take a few minutes of your time to learn more about how you can help save a life and register as a marrow donor.

Upcoming registration drive

Soy and Tofu Festival, Saturday, June 17 from 11 a.m. to 5 p.m. Open to the public at Saint Marys Cathedral,1111 Gough St., San Francisco, CA 94109.

Malayan SF Outdoor Festival, Philippine Independence Day, Sunday, June 18 from noon to 8 p.m. at Union Square, 333 Post St., San Francisco, 94102.

More about the Asian American Donor Program (AADP)

The Asian American Donor Program (AADP), with its offices in the San Francisco Bay Area,is dedicated to increasing the availability of potential stem cell donors for patients with life threatening diseases curable by a blood stem cell or marrow transplant.

AADP is a community-based nonprofit for social benefit (5013) organization and specializes in conducting outreach and donor registration drives in and with diverse communities. AADP is an official recruitment center of the Be TheMatchregistry.

To learn more about scheduled upcoming marrow drives, visithttp://www.aadp.org/drive/.

Here is the original post:
Filipina urgently needs bone marrow donor - Asianjournal.com

Recommendation and review posted by simmons

Andrew LeClerc knew something was wrong when he heard voices when no one else was around. Some were those of people he knew, others were unfamiliar, but all had the authentic mannerisms of real people, not his imagination. He was in his early twenties, unsure of his direction in life, and had been taking synthetic marijuana to ease stress from past traumas. Disturbed by the voices, he sought help in an emergency room and voluntarily admitted himself to a psychiatric hospital, not realizing he would be kept there for six days. He was diagnosed with psychosis, but had little interaction with a therapist. You mostly sit around with coloring books, he says. It felt like a punishment, when all he wanted was help.

Afterward, he contacted therapists, but many were booked. An online search led him to a research study at Beth Israel Deaconess Medical Center in Boston for people newly diagnosed with psychotic disorders. In January 2014, he entered a two-year study that compared two approaches to psychotherapy to help manage cognitive impairments and other symptoms. He was also prescribed an antipsychotic medication.

Eventually he was diagnosed with schizophrenia. Now, about four years later, at 26, LeClerc is learning to live with the condition. Its hard for a person whos diagnosed with schizophrenia to be told somethings not real when they think its real, he says. He continues to take antipsychotic medications that help control his hallucinations and lives in an apartment below his parents in Middleton, Massachusetts. Hes hoping to start a small business, putting his love of gardening to work as a landscaper.

But more importantly, hes learned to make peace with his mind. He likes to say: I dont hear voices, I hear my own brain. When voices do appear, he recognizes them as a product of an aberrant auditory cortex, and he thinks about engaging his prefrontal cortexthe decision-making part of the brainto help him distinguish fact from fiction. I have tools to pull myself back to the moment, he says.

Not everyone who struggles with schizophrenia is able to find such stability. The illness takes many forms; symptoms may include hallucinations and delusions, lack of motivation, and cognitive problems similar to dementia. It tends to strike in the late teens and early twenties, robbing young people of their mental stability just as theyre entering adulthood, beginning careers, or pursuing a college degree. Some improve, while others experience a long mental decline.

The treatments that we have are useful but not great, says Matcheri Keshavan, Cobb professor of psychiatry at Harvard Medical School (HMS) and the leader of the study that LeClerc participated in. The medications used to treat schizophrenia are decades old, and only ameliorate symptoms. Like other psychiatric illnesses, schizophrenia has suffered from a lack of investment from pharmaceutical companies. Says Keshavan, We need better medications that really address the underlying cause of this illness.

But those causes are still mysterious. What scientists do know is that schizophrenia tends to run in families. About 70 percent to 80 percent of a persons risk of developing the illness, Keshavan says, can be explained by genetic factors. Recently, theres been a surge of effort to capitalize on that fact. Advances in genetics have made it possible to search not only for clues about schizophrenia and other psychiatric illnesses hidden within thousands of human genomesbut also for potential new treatments.

As a result, theres been a renaissance in research on schizophrenia and other psychiatric disorders, and some cautious optimism. Its been possible to make real if still early progress in understanding what genes and molecules influence these illnesses, says Steven McCarroll, Flier associate professor of biomedical science and genetics. At Harvard, the leading force is the Stanley Center for Psychiatric Disease Research at the Broad Institute, which is pouring new funding and resources into amassing data on the genetics of mental illness.

Bringing the power of genomics to psychiatric disease fulfills a long-held goal for the Stanley Centers director, Steven Hyman, professor of stem cell and regenerative biology. An HMS professor of psychiatry before becoming head of the National Institute of Mental Health (NIMH) in 1996, Hyman was frustrated by the sluggish progress on the science of psychiatric disorders, as research on illnesses like cancer, heart disease, and diabetes marched ahead. Schizophrenia in particular is challenging to study because its uniquely human. Scientists can study limited aspects of psychiatric illness in animals if they can measure an observable behavior, such as avoiding social interactions or grooming excessively. But psychosis is a problem of thinking; animals, as far as is known, dont experience it in any way we can measure. Its also challenging because brain tissue is so inaccessible. We were really hampered, Hyman says, and I, frankly, didnt know all that much more when I was at NIMH in the late 1990s than careful observers knew at the turn of the twentieth century.

Steven Hyman, director of the Stanley Center for Psychiatric Disease Research Photograph by Stu Rosner

When he left the position, Hyman was interested in researching psychiatric disease but didnt see a rigorous path to do so; instead, he accepted a position as Harvards provosttaking what he now refers to as a 10-year timeout. During that time, a revolution occurred. Genetic technologies and vastly expanded computer power opened new paths for studying the biological basis of complex diseases.

The Broad Institute launched the Stanley Center in 2007 under inaugural director Edward Scolnick, thanks to an initial $100 million in private funding from philanthropists Ted and Vada Stanley, aiming to bring much-needed innovation to treatments for psychiatric disease by harnessing the power of genomics. (The Stanleys provided another $650 million in 2014, an unprecedented gift for psychiatric research.) Partly as a result, the center has gathered the worlds largest collection of DNA samples for studying not only psychiatric diseasesincluding schizophrenia, autism, ADHD, and bipolar disorderbut also healthy control subjects. The resulting data are freely available to the public.

The human genome has started to give us a really powerful way into the problem, Steven McCarroll explains, because the key source of scientific leverage that we have is we know that schizophrenia and other psychiatric illnesses are heritablethey aggregate in families. Their molecular secrets are almost certainly hidden in the way our genomes vary from person to person.

Much of the research on genetics and disease has focused on what McCarroll calls genetic sledgehammersgenes that when mutated would almost certainly make you sick. But schizophrenia, like most common diseases, is genetically complex. The hereditary component of the disease may be a product of tens to hundreds of genetic nudges, variations that dont cause disease by themselves, but together make people vulnerable to illness.

Studying genetic nudges requires amassing large numbers of DNA samples to achieve the statistical power to find subtle variations that may contribute to disease, a project thats taken enormous collaborative effort by many scientists and institutions around the world. The Psychiatric Genomics Consortiumthe largest scientific collaboration involving psychiatric diseaseformed in 2007 and comprises hundreds of investigators in 38 countries and nearly a million genetic samples. The Stanley Center has served as the hub for data sharing, aggregation, and analysis to further the consortiums discoveries.

One of the key tools for uncovering the genetic basis of disease is the genome-wide association study (GWAS)a way of quickly sorting through the common variations in genomes to find those that are more common in people with a given trait or disease than in those without. Associate professor of medicine Mark Daly, who leads the analytic hub of the consortium, says that scientists originally thought such studies might uncover a handful or two of DNA variants that could be statistically correlated with schizophrenia. But rather than identifying a few standouts, the consortiums Schizophrenia Working Group found a crowd of genetic associations, each contributing just a tiny amount of risk. A landmark paper published in 2014 in the journal Nature, led by Michael ODonovan of Cardiff University, described 108 different locations in the genome that harbored variants associated with schizophrenia.

GWAS studies can identify only stretches of DNA: like flags on a zoomed-out map of a city, they provide a neighborhood, not the exact address. We know where the variants are, one of which is likely to be the causal variant, but cant say for sure which one, says assistant professor of medicine Ben Neale, who is developing methods to analyze genomic data. Another approach is to sift through genomes in finer-grained detail by directly reading each letter of the DNA sequence. Such work is time-consuming, but it can help uncover rare genetic differences that are linked to disease, many of which have a stronger effect than common variants. Work by the consortium has also analyzed areas of DNA that are deleted or duplicated, called copy number variations. People with schizophrenia tend to have more such variations overall, and the genes they affect can provide clues to the diseases origins.

Meanwhile, the Stanley Center and other institutions are working to collect thousands more DNA samples from people with schizophrenia and other psychiatric disorders, hoping to identify even more genetic associations of risk. Hyman doesnt see such data-gathering as an endless project. We should kill this problem, he says, meaning in some reasonable number of yearsseven to 10we should have proceeded so far in the genetics of schizophrenia, bipolar disorders, autism, perhaps some other disorders, that weve reached diminishing returns in terms of biological information.

But so far, the picture is still incomplete. The vast majority of genetic samples, for instance, come from people of European ancestry. From a purely scientific point of view, it means were missing a large proportion of the worlds genetic diversity, says Karesten Koenen, professor of psychiatric epidemiology at the Harvard T.H. Chan School of Public Health. Most of that diversity is in Africa: There is much more diversity in African genomes than in those of people from other parts of the world.

Koenen is leading an effort through the Stanley Center to launch genetic research on psychiatric disease in Ethiopia, Uganda, Kenya, and South Africa. Their researchers are partnering with researchers and academic and clinical institutions in those countries and will be gathering DNA samples and clinical information from people diagnosed with schizophrenia. We really want to build local capacity, she says, and develop sustainable research programs that can be led by local scientists and clinicians. The center also plans to extend the effort to Latin America, beginning in Mexico.

This effort will help fill in the genetic picture of psychiatric illness, and will also help correct a vast imbalance. Geneticists are beginning to use data to classify patients based on their risk of developing complex diseases, including schizophrenia. But these risk profiles, Koenen says, lose accuracy when applied to people of African descent. As this kind of profiling makes its way into medicine, she says, Theres a risk that if we dont extend this research to Africa, the health disparity and treatment gap will widen.

What will all this data amount to? Theres a misconception, McCarroll says, that the goal of this research is to conjure up a crystal ball genetic test that will give people personalized treatments based on their unique portfolio of genes. Thats not the aim. Our goal, he says, is to understand the core biological processes in the illnesses, so that innovative treatments can be developed that can treat anyone. Scientists hope that the dizzying array of schizophrenia-related genes will converge onto a few basic processes in the brain, once the function of those genes is understood.

But even as scientists have made dramatic leaps in discovering genetic risk factors of complex diseases, the task of understanding how those genes work is a different, and slower, task.

Researchers from Harvard and the Broad Institute have grown human brain organoids, three-dimensional organ models cultured from stem cells, to study the genetics of psychiatric illness. This series shows (clockwise from upper left) growth at 1, 3, 6, and 9 months, with development of synapses indicated in green. Quadrato et al./Nature 2017

McCarroll was lead author of a study making one of the strongest links between a specific genetic variant and its role in schizophrenia. Working with Aswin Sekar (then a graduate student, now a research fellow), he focused on the most powerful signal of risk in GWAS studies to date, a stretch of DNA in chromosome 6 that was known to harbor many genes involved in the immune system. They focused on one called C4, which has a high degree of variability in humans: each of its different forms may be present in multiple copies in one individual. By using both genetic data and postmortem brain tissue, they found that people with schizophrenia are more likely to have variants of the C4 gene that lead to higher levels of one gene product, C4A, in brain cells.

C4A is one of several proteins involved in a type of immunity called the complement pathway, which helps clear damaged cells and harmful microbes from the body. As part of their study, McCarroll and Sekar collaborated with associate professor of neurology Beth Stevens, whose previous research with mice clarified an ingenious connection between the complement pathway and the brain. Scientists know that as the brain develops, it churns out new cells, which form billions of connections called synapses. In adolescence and early adulthood, some of these connections are pared back, a process called synaptic pruning. In mice, Stevens has found, this pruning is mediated by the complement pathway, which triggers immune cells called microglia to attack neural connections: literally nibbling at synapses.

Sekar, McCarroll, and Stevens also worked with professor of pediatrics Michael Carroll, who had developed mice with varying copies of the C4 gene, and showed that too much C4 activity in the animals can lead to excess pruning. Its too much of a good thing, Stevens says. Their finding suggests that schizophrenia, in some cases, may be caused by loss of synapses in adolescencean especially promising result because it supports clinical observations: synaptic pruning coincides with the age when schizophrenia typically emerges, and brain imaging shows that many people with schizophrenia experience a thinning of the prefrontal cortex in the early stages of disease.

Steven McCarroll, Flier associate professor of biomedical science and genetics Photograph by Stu Rosner

McCarroll emphasizes that the C4A variation contributes only a small amount of risk of disease, but may collude with other variants to tip the brain past a threshold. There are a lot of genetic findings that map to synapses, says Hyman, so some of those other variants may contribute to a larger disruption in how synapses are formed and maintained. But other processes are likely at work in schizophrenia as well. Some genetic risk variants relate to a chemical signal in the brain called glutamate, and others to ion channels, proteins that determine how electrical signals propagate in brain cells. There are also others, Hyman adds, that, frankly, just have us scratching our heads.

The work on C4 offers an example of how genetics is beginning to help neuroscience move forward. Its opened up a ton of new directions and strategies for our group, says Stevens. Across Harvard and the Stanley Center, a growing community is launching collaborative projects with the goal of taking psychiatric disease research into new territories.

One priority is developing new models for teasing out the role of genes in the brain. Scientists have been able to study some behaviors that relate to mental illness in animals, but there is no animal model for schizophrenia. Michael Carroll is now working to extend the C4 study by creating humanized mice that carry human C4 genes, which may make it possible to study their function in a living brain.

Other researchers are trying to develop new ways to study psychiatric disease in humans. Paola Arlotta, professor of stem cell and regenerative biology, explains that when scientists are able to get samples of human brain tissuefrom patients undergoing surgery, postmortem donations, or even tissue from fetusesthe cells die quickly. They cant be propagated and studied in a laboratory, so there is no renewable source of the actual endogenous tissue.

Stem cells have emerged as a way around that problem. Scientists can now take cells from the skin or hair and transform them into induced pluripotent stem (iPS) cells that are capable of becoming other cell types, including brain cells. (At the Stanley Center, Arlotta and other scientists are exploring how to transform iPS cells into specific types of brain cells.) The iPS cells allow scientists to study how cells derived from a person of one genetic background differ from those of another person. Scientists can also use the genome-editing tool CRISPR-Cas9 to introduce specific genetic changes and study their effects.

But theres very little that can be learned about psychiatric disease from isolated cells: brain activity depends on the constant chatter of many cells that are intricately connected. Arlotta has been investigating whether neural stem cells can be spun into something that behaves more like human brain tissue. So-called organoidsclusters of millions of cells up to a few millimeters in diametercan be formed from growing stem cells in a nutrient-rich solution. Organoids have already been used to study events that happen in early development: last year, a team of researchers used them to study the effects of the Zika virus on developing brains.

But since psychiatric diseases like schizophrenia emerge later in life, Arlotta wants to make organoids grow larger and live longer, and to understand whether they can mimic some of the properties of an older brain. This is a new tissue were making, she says, and so the questions that we want to answer are: can we develop them for a very long time, can we understand the cellular composition, can we see if these organoids make actual networks and communicate with each other?

To better characterize these cell-based models, Arlotta and her colleague Kevin Eggan, a fellow professor of stem cell and regenerative biology, are collaborating with McCarroll to apply a technology his lab developedDropSeqthat makes it possible to analyze gene activity in individual cells. The technology will provide a detailed, cell-by-cell understanding of what these models may reveal. In a Nature paper published in April, Arlottas team demonstrated that its possible to cultivate human brain organoids for nine months or more. Analysis revealed that the organoids are filled with a diverse mix of brain-cell types, and that these cells actually form interconnected networks, suggesting they may begin to function in ways that brains do.

But how much meaningful information about psychiatric disorders can be gleaned by studying individual cells or clusters of artificial tissue remains unclear. And an even bigger question is how to use these models to study the effects of genetic nudges. Disease genetics, typically, has been studied by altering or removing genes, one at a time, in an animal. Studying a whole suite of subtle genetic variations in a model system is a completely new idea.

There is no playbook, says Hyman. He acknowledges that the work is risky; many of these projects are possible only because the Stanley Centers open-ended funding makes it easier for labs to work together to pursue new ideas. We spend many tens of millions of dollars a year, and were accountable only at the end of the year to our scientific advisory board, and we tell them our strategy, he says. It gives us enormous flexibility, but its an enormous responsibility.

Some scientists and clinicians believe that gathering genetic data and studying cells is a misguided strategy for alleviating psychiatric illness. They see it as reductionist, and argue that it emphasizes the inborn biological origins of illnesses rather than other factorslike abuse, trauma, drug use, and emotional stressthat are known to play a role in their development. Hyman answers, Genes are not fate, but genes have an awful lot to say. Genetics and the environment both undoubtedly contribute to disease, but both ultimately must act on the brainand genetics happens to be a more tractable way to study whats happening in the brain.

Genetics is already providing insights that could help alter the way psychiatric disorders are defined. People have studied disorders with a box around them, says Elise Robinson, assistant professor of epidemiology, who has analyzed genetic differences within and between disorders such as schizophrenia, bipolar disorder, depression, and autism, which are usually defined by clinical categories outlined in the Diagnostic and Statistical Manual of Mental Disorders. But Robinson says the idea of distinct boundaries separating these disorders is not necessarily consistent with biology. Genetically, psychiatric disorders look more like Venn diagrams with large overlaps. People with schizophrenia share 60 percent to 70 percent of genome-wide variation with those who suffer bipolar disorder, and about 25 percent with autism.

Similarly, there is no simple dividing line between people who have a psychiatric illness and those who dont. Genetic risk for schizophrenia is not something you either have or dont have, she says. Theres a little bit of risk in all of us. Natural variations in many different genes, she explains, have been shown to relate to the way people perform on tests of cognitive or emotional skills. Schizophrenia may emerge from some combination of factors that are part of normal variation in the development and functioning of the human brain. This is true for other complex diseases and many normal traits, she adds: height, for instance, is largely determined by genetics, but theres no single geneor even handful of genesthat controls it. Its a quality that emerges from many genetic inputs.

Robinson believes that scientists could learn more about these disorders by cutting across diagnostic boxes and studying genetic variants that are linked to multiple traits and disorders. Only by understanding how these variants affect the brain can researchers begin to understand how they contribute both to normal brain function and to the risk of disease.

Such research could help demystify the experiences of people like Andrew LeClerc. He has learned to talk about his schizophrenia as something he struggles with, not something that defines him. He describes his condition as a mental difference.

LeClerc also appreciates that not all the voices in his head are negative: he sometimes hears words of encouragement or helpful warnings. As he speaks, his thoughts dont always follow the linear paths of normal conversation, but they can take him into deeper places; he has a keen understanding of how humans brains create their own realities. He sees an analogy to his condition in the once-expensive glass pieces he has begun collecting from his local dump. Glass that seems like trash, he says, can be reused or recycled, so it isnt really broken. He describes himself the same way: Im fragile, not broken.

It may take decades before genetic research on schizophrenia yields new treatments for people like LeClerc, but clues about the biological underpinnings of schizophrenia could help in other ways. Patients with psychiatric disorders get blamed for those disorders in our culture in a way that people with diseases in other organs dont, says McCarroll. If this research can provide a firmer biological understanding of whats happening in the brain, he says, I would hope that we could generate more empathy.

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Probing Psychoses - Harvard Magazine

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Scientific zeal Jennifer Doudna. Photograph: The Washington Post/Getty Images

It began with the kind of research the Trump administration wants to unfund: fiddling about with tiny obscure creatures. And there had been US Republican hostility to science before Trump, of course, when Sarah Palin objected to federal funding of fruit fly research (Fruit flies I kid you not, she said). The fruit fly has been a vital workhorse of genetics for 100 years. Jennifer Doudnas work began with organisms even further out on the Palin scale: bacteriophages, tiny viruses that prey on bacteria.

Yoghurt manufacturers knew they were important, not least because bacteriophages can destroy yoghurt cultures. Research on the mechanism of this process began in the labs of Danisco (now part of the giant DuPont) in the early 2000s, before spreading through the university biotech labs. In 2012 Doudna and Samuel Sternbergs team at Berkeley (they are co-authors of the book but its written solely in Doudnas voice) came up with probably the greatest biological breakthrough since that of Francis Crick, James Watson and Rosalind Franklin.

Biologists had become intrigued by a curiosity in the genome of some bacteria: they had repeat patterns interspersed always by 20 bases of DNA, which turned out to match sequences found in the phages (as bacteriophages are always known) that prey on them. They had stumbled on a bacterial immune system, now known as Crispr (Clustered regularly interspaced short palindromic repeats) a sequence reading the same forwards and backwards.

An astonishing story of molecular countermeasures against phage invasion was revealed; these enable the bacterium to recognise the phage next time it invades. More than that, Crispr guides a killer enzyme to cut the phages DNA at the point where the 20base sequence is found. Doudna then demonstrated that bacterial Crispr can be reprogrammed to cut any DNA from any organism. This is what has been sought for more than 30 years: an accurate (or almost accurate) way of editing DNA. And there has never been a better example of the unforeseen benefits of pure research because no one guessed that a technique of such power and universality would emerge from what appeared to be a fascinating but arcane corner of biology.

Crispr is not just a triumph for unfettered scientific curiosity, its also a reminder that the secret of life lies in tiny things. The visible world can be beautiful but we are gulled into thinking it must be more important than what we cant see. People have been making that mistake for a long time. In The Citizen of the World (1762), Oliver Goldsmith mocked the supposed pedantry of all who study the tiny creatures revealed by the microscope: Their fields of vision are too contracted to take in the whole Thus they proceed, laborious in trifles, constant in experiment, without one single abstraction, by which alone knowledge may be properly said to increase. But, of course, it is precisely being able to see small things that has unlocked the biological treasure trove.

Very soon after Doudnas paper on the technique appeared in 2012, labs all over the world tried it and found it was surpassingly easy to use; a gold rush began. Its always difficult when something like this happens to sort the hope from the hype, but anticipation is now intense. Doudna does, though, sound many notes of caution. Yes, Crispr is the most accurate form of gene editing so far, but it isnt perfect. There are 3bn bases in the human genome so there is always a chance of a stray 20-base match and a fatal cut in the wrong place. A debate is taking place on whether to allow gene edits only outside the body (with the edited cells reinserted) or to allow editing of eggs and sperm, which changes that germline forever. Doudna comes down cautiously for germline editing, pointing out that mitochondrial replacement therapy, which also leads to permanent genetic alteration, is already a reality in the UK.

Doudna recounts how, soon after her breakthrough, colleagues became rivals, papers were pored over for patent battles

For now the most exciting potential medical application is in single gene diseases, such as cystic fibrosis, sickle-cell anaemia and muscular dystrophy. This is the simplest possible task for Crispr. Just one base has to be corrected out of the 3bn and its not a needle in a haystack: Crispr can find and cut and repair it. Sickle-cell anaemia is caused by a faulty haemoglobin gene, so blood can easily be withdrawn from the body, the gene edited and returned to the body. But this approach demands extreme caution. Genes often have multiple effects and the sickle-cell gene is known to protect against malaria. So if you fixed the sickle-cell gene in the African population (where it is prevalent) there would be many new cases of malaria. But then Crispr can probably fix that, too; other researchers, with Gates Foundation funding, are urgently tackling that problem. There is hardly an area of medicine that could not benefit from Crispr, and on the fringe there is the Jurassic Park fantasy, kept tenuously alive by the work of Crisprs other great name, George Church at Harvard, who is editing the elephant genome to create a creature more like a woolly mammoth.

If medical ethics loom large in debates around Crispr, money and patents loom even larger. Now that this apparently unpromising research has blossomed, the venture capitalists are gathering. Doudna recounts how, so soon after her triumph, colleagues became rivals; papers were pored over for future patent battles. The patent battle in question came to fruition after the book was completed. Doudnas team lost this round, and its not clear what the future holds for Crisprs intellectual property rights. It is unlikely that medical progress will be delayed but there will be some bruised participants and money spent along the way.

It is unusual to have a popular account of a great scientific breakthrough written by the protagonist, so soon after its discovery. Watsons The Double Helix appeared 15 years after the work. We owe Doudna several times over for her discovery, for her zeal to take it from the lab into the clinic, for her involvement in the ethical issues raised, for her public engagement work, and now for this book. Its a fine weapon against the still far too large tribe of those who dont believe in the power of very small things.

Peter Forbess latest book, written with Tom Grimsey, is Nanoscience: Giants of the Infinitesimal. A Crack in Creation is published by Bodley Head. To order a copy for 16.59 (RRP 20) go to bookshop.theguardian.com or call 0330 333 6846. Free UK p&p over 10, online orders only. Phone orders min p&p of 1.99.

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A Crack in Creation review Jennifer Doudna, Crispr and a great ... - The Guardian

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ByMolly Wood and Paulina Velasco

June 16, 2017 | 3:00 PM

In 2012, Jennifer Doudna, along with a small group of scientists, invented a ground-breaking technology to edit DNA known as Crispr. Scientists are still experimenting with it.

Crispr has been in the news recently because a group of scientists released a much-debated study arguing that editing genes can lead to many unintended, unpredictable consequences. In the controversial case, the scientists edited genetic blindness out of a group of mice and said they found two thousand unintended consequences. The scientific community is split on the results, and Doudna said it's hard to conclude anything from the study. But she knows the possible dangers of gene editing, and she warned about them in aWired article in May.

Marketplace's senior tech correspondent Molly Wood spoke withDoudna at the Wired Business Conference in New York earlier this month and asked Doudna whatconcerns her the most about her revolutionary new technology?

The following is an edited transcript of their conversation.

Jennifer Doudna: I guess I worry about a couple of things. I think there's sort of the potential for unintended consequences of gene editing in people for clinical use. How would you ever do the kinds of experiments that you might want to do to ensure safety? And then there's another application of gene editing called gene drive that involves moving a genetic trait very quickly through a population. And there's been discussion about this in the media around the use of gene drives in insects like mosquitoes to control the spread of disease. On one hand, that sounds like a desirable thing, and on the other hand, I think one, again, has to think about potential for unintended consequences of releasing a system like that into an environmental setting where you can't predict what might happen.

Molly Wood: How important is the accessibility? You know, you could buy a Crispr kit online for $150. What does that kind of accessibility lead to, either in terms of opportunity or problems?

Doudna: I think it's mostly a really good thing in the sense that it makes the science more tangible. I honestly feel that things that break down the barriers between scientists and technologists and everybody else, in a way, is a good thing. Although it's easy to use this technology for those that have some training in molecular biology, its actually not going to be very easy to do anything that would be particularly dangerous in my opinion.

Wood: How do you think this technology could change the way we practice medicine? I mean, if we're really talking about potentially curing genetic diseases, it seems like a whole industry will be affected by that.

Doudna: I think it's a fascinating question, and I've been thinking about this a lot and having a number of discussions with folks that work in the pharmaceutical industry to think about really changing the paradigm for how we do human therapeutics, at least for certain types of disease. Imagine that you had a technology or a treatment that allowed, rather than having someone take a pill every day for the rest of their life, that you had a treatment that you could do once and cure them. It also brings along a lot of other issues. Who pays for that? How do you price such a thing? How do you get insurance companies to cover it? Even if there won't be easy answers, I think the first step is really just to realize that that's the moment that we're in right now.

Wood: One of the things I find fascinating is the intellectual property part of the conversation to what extent people might try to patent genetically modified versions of organisms or plants or even human genes?

Doudna: It's very difficult to patent genes. But I think youre touching on an important point. I think the real value of a technology like this that really allows research to move at a much faster pace than it has in the past, is that it opens up opportunities for applications that I think will lead to incredible commercial opportunities and creative things to make products that couldn't have been generated in the past. And along with that, of course, goes all of the issues regarding regulation and pricing and things like that.

Wood: Jennifer, on that question of regulation and pricing, do you have a sense of what body might end up being in charge of that? Because it's really a global issue on some level, right?

Doudna: It is. But I think a lot of it will come down to initial regulatory approval. If we're talking about agricultural products in the U.S. we're talking about the U.S. Department of Agriculture. We might be talking about the Food and Drug Administration, certainly for therapeutics. Of course that affects pricing and valuations, because if there is an onerous regulatory pathway for things, then that adds to the cost of developing them. So this is why I think it's actually very important that scientists be engaging right now with these agencies to set up appropriate regulations, but also not ones that are so onerous that it really prevents development of important products.

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Crispr inventor worries about the unintended consequences of gene ... - Marketplace.org

Recommendation and review posted by Bethany Smith

MUMBAI: Three-year-old Kinaya Shah was diagnosed with thalassemia at the tender age of three months and has been undergoing regular blood transfusions ever since. The only cure for thalassemia is a bone marrow transplant (BMT), a form of stem cell therapy. Typically, the donor of the stem cells would be a sibling of the patient such that the stem cells of the donor are a near perfect match to those of the patient. The only complication was that Kinaya was a lone child.

So, city doctors in a first used stem cells donated by Kinaya's father - who was only a half or haploidentical match - to cure the child of the blood disorder. "We went to Vellore, Bangalore and Pune but no one was willing to do the transplant without a full match donor," said Kinaya's parents, Aneri and Shripal Shah. They approached Dr Santanu Sen at the Kokilaben Dhirubhai Ambani Hospital, Andheri, in October of 2016, after reading about a similar surgery that he had performed.

While haploidentical bone marrow transplants are carried out to cure leukaemia, it has only been done about half a dozen times for thalassemia in a couple of Indian cities. ``Haploidentical transplants are gradually increasing because of better techniques,'' said Dr Sen.

Dr Sen has completed 36 BMTs in the last two years, of which 12 were haploidentical donors. ``But this is the first time that a haploidentical transplant has been done in western India to cure thalassemia,'' he said.

Chennai-based haematologist Dr Revathy Raja said that there is a 85% chance of cure in thalassemia with a fully matched donor. ``The success rate falls to 70% with a half-match or haploidentical donor. We have hence not started it at our Chennai centre. Hopefully, techniques will further improve in the coming years,'' she said.

In order to perform the surgery, Dr Sen conditioned Kinaya's immune system over three months, with slight chemotherapy, to increase the chances of her body accepting the graft. "We found that her father's stem cells were a 70% match through genetic tests and decided to use them for the transplant. In the case that the graft was rejected we froze a couple of Kinaya's stem cells as insurance. The positive is that children have lower rejection rates for foreign cells as they have barely developed any active immunity," said Dr Sen. "BMT is the most viable treatment to cure thalassemia, the only barrier thus far was the necessity of a full match donor," he added.

However, Vinay Shetty of NGO Think Foundation, which works for thalassemia patients, said that it would be prudent to wait for a statistically significant number of successful halploidentical transplants before recommending it to all patients.

Post the three months of conditioning, stem cells were collected from her father's bone marrow and the transplant was performed on May 10, 2017. After several tests to confirm that the graft was accepted, Kinaya was finally discharged from the hospital on June 13.

"The future of thalassemia treatment probably lies in gene therapy, but at the moment, haploidentical transplants have made BMT much more accessible," said Dr Sen, adding that he has two more cases such as Kinaya lined up. Kinaya is expected to be completely independent of medication and any trace of thalassemia in the coming six months.

What is Thalassemia?

Thalassemia is a genetic blood disorder when the body produces abnormal hemoglobin. Patients require regular blood transplant and well as dietary control to ensure that blood irons level stay suppressed.

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In a first, Mumbai doctors use dad's cells to fight blood disorder - Times of India

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Cell harvesting is a technique of collecting stem cells for regenerate, transplant or repair the damaged organ with healthy functioning ones. Cell harvesting is considered as an important step in biopharmaceutical manufacturing industry that can directly affect the product quality and related downstream processes. Stem cells harvesting helps in treating with diseases namely cancers, blood disorders, immune deficiency diseases and various injuries. This therapy is also beneficial for burn victims which help them in grafting new skin cells as a replacement for damaged ones. Many companies are focusing on regeneration of myocardial tissue by injection of cell graft consist of adult stem cells from the patients for manufacturing regenerating medicines. For the treatment of eye diseases new healthy cells are also be grown. For harvesting bone marrow a companies are manufacturing devices with passive flexible drilling unit and suction mechanism which will help in reducing the invasiveness of bone marrow transplantation. Cell harvesting system helps in reducing the invasiveness of bone marrow aspiration from the iliac bone with less punctures. Moreover, helps in reducing procedure time and contamination by T-cells.

Cell Harvesting Systems Market:Drivers and Restraints, Segmentation, Overview, Region-wise Outlook and Key Players

Cell Harvesting Systems Market are witnessing maximum growth owing to increase bone marrow transplantation procedures attributed to high prevalence of blood cancer and anemia. Moreover, improving healthcare expenditure, survival rate after treatment, increasing investment in logistic services, expansion bone marrow transplant registry for heart along with neuronal disorders and growing per capita healthcare expenditure. However, high cost of cumbersome treatment, lack of reimbursement policies, immunological rejection, viable cell density, and identification of stem cells in adult tissues, and complications during cell harvesting and inadequate number of HSCs cells for transplantation is a major barrier to the cell harvesting systems market.

The cell harvesting systems market has been classified on the basis of techniques, application and end user. Based on techniques, the cell harvesting systems market is segmented into the following: Altered Nuclear Transfer, Blastomere Extraction; Based on application, the cell harvesting systems market is segmented into the following: Bone Marrow, Peripheral Blood, Umbilical Cord Blood, Adipose Tissue; Based on end-user, the cell harvesting systems market is segmented into the following: Research Centers, Academics Institutes, Diagnostic Labs, Hospitals

Cell harvesting systems market witnessed substantial growth owing to equipment efficacy and accuracy during stem cells harvest. By application type, bone marrow aspiration is anticipated to hold the major share in the cell harvesting systems market owing to less process error, safe and simple procedure and less side effects. People suffering from Leukemia eligible for bone marrow transplant, is expected to contribute highest share in the global cell harvesting systems market. Cell harvesting systems helps in enhancing proper pigmentation in scar reconstruction which encourage companies for continuous technology advancement in both cell isolation techniques and downstream purification processes.

Depending on geographic region, cell harvesting systems marketis segmented into seven key regions: North America, Latin America, Eastern Europe, Western Europe, Asia Pacific, Japan, and Middle East & Africa. Asia Pacific dominates the cell harvesting systems marketfollowed by Europe, Japan and North America owing to high concentration of bone marrow stem cells harvesting centers and registries along with skilled doctors for the process of harvesting stem cells in these regions. Asia Pacific, Middle East and Africa hold huge potential and shows substantial growth in terms of wide acceptance of new technologyowing to awareness among population, increasing healthcare expenditure along with high number of potential candidate for the procedure.

Key players of cell harvesting systems market are PerkinElmer Inc.Tomtec, Bertin Technologies, TERUMO BCT, INC., hynoDent AG, Avita Medical, Argos Technologies, Inc., SP Scienceware, Teleflex Incorporated., Arthrex, Inc., Thomas Scientific, BRAND GMBH

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Blood Fluid Warming System Market Volume Forecast and Value Chain Analysis 2016-2026

Aptamers Market Dynamics, Forecast, Analysis and Supply Demand 2016-2026

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Cell Harvesting Systems Market Analysis, Segments, Growth and Value Chain 2016-2026 - LANews By Abhishek Budholiya (press release) (blog)

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Thermo Fisher Scientific has launched a program of four-day lecture-based and hands-on CRISPR (clustered regulatory interspaced short palindromic repeats) and TALEN (transcription activator-like effector nuclease) genome-editing workshops at its global training facilities.

The workshops will provide an overview of CRISPR/Cas9 and TALEN technologies through both lecture-based sessions and laboratory practice. The focus will be on topics spanning experimental design strategies, methods for delivering guide RNAs (gRNAs) and Cas9 mRNA/Cas9 proteins into cells for generating gene knockouts, the use of TALs as genome-editing tools for gene knockins, and approaches to analyzing editing efficiency. The workshops will highlight the use of TALEN genome-editing technology for genome-editing applications, including single-nucleotide polymorphism (SNP) repair.

Workshop participants will have the opportunity to design a genome-editing experiment with experts in the field. "Our workshops are designed to equip researchers with the instruction and hands-on training they need to comfortably utilize the leading genome-editing technologies in their own labs," said Helge Bastian, Ph.D., vp and general manager of synthetic biology at Thermo Fisher Scientific. "As the practice of engineering nucleic acids in silico, in vitro, and in living cells evolves at a high-speed pace, it is increasingly important for life science professionals to learn about the basics and the newest formats of these high-precision molecular technologies. This will enable them to unravel the underlying mechanisms of normal cellular processes and disease onset or progression, support the discovery and development of new drugs, and enhance biomanufacturing and therapy solutions."

Thermo Fisher says that as a result of strong demand following workshops in the U.S., Germany, and the U.K., it has now more than doubled the number of workshops offered, and plans to hold courses throughout North America, Europe, the Middle East, and Asia.

Last month, the firm reported a deal to acquire contract development and manufacturing organization (CDMO) Patheon, for $7.2 billion.

Originally posted here:

Thermo Fisher Launches CRISPR and TALEN Genome-Editing Workshops - Genetic Engineering & Biotechnology News (press release)

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Merck has been granted its first CRISPR technology patent by the Australian Patent Office.

On Wednesday, June 14, Merck issued a press release explaining that the office had granted it patent rights over the use of CRISPR in a genomic integration method for eukaryotic cells.

The patent covers chromosomal integration (or cutting of the chromosomal sequence of eukaryotic cells, such as mammalian and plant cells, and insertion of an external or donor DNA sequence into those cells using CRISPR).

Merck has patent filings for its insertion CRISPR method in Brazil, Canada, China, Europe, India, Israel, Japan, Singapore, South Korea and the US.

Udit Batra, member of the Merck executive board and CEO of life science, said: Merck has developed an incredible tool to give scientists the ability to find new treatments and cures for conditions for which there are limited options, including cancer, rare diseases and chronic conditions, such as diabetes.

In May this year, Merck revealed that it had developed an alternative CRISPR genome-editing method called proxy-CRISPR.

According to Merck, the proxy-CRISPR technique can cut previously unreachable cell locations, making CRISPR more efficient, flexible and specific, and giving researchers more experimental options.

Several patent applications have been filed on this technology.

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Merck granted its first CRISPR patent in Australia - Life Sciences Intellectual Property Review (subscription)

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June 15, 2017

Patients with severe and end-stage heart failure have few treatment options available to them apart from transplants and "miraculous" stem cell therapy. But a new Tel Aviv University study finds that stem cell therapy may, in fact, harm heart disease patients.

The research, led by Prof. Jonathan Leor of TAU's Sackler Faculty of Medicine and Sheba Medical Center and conducted by TAU's Dr. Nili Naftali-Shani, explores the current practice of using cells from the host patient to repair tissueand contends that this can prove deleterious or toxic for patients. The study was recently published in the journal Circulation.

"We found that, contrary to popular belief, tissue stem cells derived from sick hearts do not contribute to heart healing after injury," said Prof. Leor. "Furthermore, we found that these cells are affected by the inflammatory environment and develop inflammatory properties. The affected stem cells may even exacerbate damage to the already diseased heart muscle."

Tissue or adult stem cells"blank" cells that can act as a repair kit for the body by replacing damaged tissueencourage the regeneration of blood vessel cells and new heart muscle tissue. Faced with a worse survival rate than many cancers, many heart failure patients have turned to stem cell therapy as a last resort.

"But our findings suggest that stem cells, like any drug, can have adverse effects," said Prof. Leor. "We concluded that stem cells used in cardiac therapy should be drawn from healthy donors or be better genetically engineered for the patient."

Hope for improved cardiac stem cell therapy

In addition, the researchers also discovered the molecular pathway involved in the negative interaction between stem cells and the immune system as they isolated stem cells in mouse models of heart disease. After exploring the molecular pathway in mice, the researchers focused on cardiac stem cells in patients with heart disease.

The results could help improve the use of autologous stem cellsthose drawn from the patients themselvesin cardiac therapy, Prof. Leor said.

"We showed that the deletion of the gene responsible for this pathway can restore the original therapeutic function of the cells," said Prof. Leor. "Our findings determine the potential negative effects of inflammation on stem cell function as they're currently used. The use of autologous stem cells from patients with heart disease should be modified. Only stem cells from healthy donors or genetically engineered cells should be used in treating cardiac conditions."

The researchers are currently testing a gene editing technique (CRISPER) to inhibit the gene responsible for the negative inflammatory properties of the cardiac stem cells of heart disease patients. "We hope our engineered stem cells will be resistant to the negative effects of the immune system," said Prof. Leor.

Explore further: Adult stem cell types' heart repair potential probed

More information: Nili Naftali-Shani et al, Left Ventricular Dysfunction Switches Mesenchymal Stromal Cells Toward an Inflammatory Phenotype and Impairs Their Reparative Properties Via Toll-Like Receptor-4Clinical Perspective, Circulation (2017). DOI: 10.1161/CIRCULATIONAHA.116.023527

Journal reference: Circulation

Provided by: Tel Aviv University

New University of Otago research is providing fresh insights into how a patient's adult stem cells could best be used to regenerate their diseased hearts.

Genetically engineered human cardiac stem cells helped repair damaged heart tissue and improved function after a heart attack, in a new animal study.

Scientists use mathematical modeling to simulate human mesenchymal stem cell delivery to a damaged heart and found that using one sub-set of these stem cells minimises the risks associated with this therapy. The study, published ...

An international team of researchers, funded by Morris Animal Foundation, has shown that adipose (fat) stem cells might be the preferred stem cell type for use in canine therapeutic applications, including orthopedic diseases ...

A*STAR researchers and colleagues have developed a method to isolate and expand human heart stem cells, also known as cardiac progenitor cells, which could have great potential for repairing injured heart tissue.

(HealthDay)A new method for delivering stem cells to damaged heart muscle has shown early promise in treating severe heart failure, researchers report online July 27 in Stem Cells Translational Medicine.

Researchers at Karolinska Institutet in Sweden have obtained the first 3D snapshots of a sperm protein attached to a complementary egg coat protein at the beginning of fertilisation. The study, which reveals a common egg ...

As we bask in the summer heat, it is easy to take for granted that humans are also prepared for the cold of winter, with overcoats in the closet and home heating systems ready to be fired up as an added assurance against ...

Organs-on-Chips (Organ Chips) are emerging as powerful tools that allow researchers to study the physiology of human organs and tissues in ways not possible before. By mimicking normal blood flow, the mechanical microenvironment, ...

Monash University's Biomedicine Discovery Institute (BDI) researchers have collaboratively developed a therapeutic approach that dramatically promotes the growth of muscle mass, which could potentially prevent muscle wasting ...

As a molecular biologist, Kaori Noridomi gets an up-close view of the targets of her investigations. But when she began studying the molecular structures of a rarely diagnosed autoimmune disorder, myasthenia gravis, she decided ...

Researchers from Imperial College London and colleagues have found a potential way to target the receptors that specifically control appetite in mouse brains, potentially without causing other side effects.

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Cardiac stem cells from heart disease patients may be harmful - Medical Xpress

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Russias Progress 67 (67P) cargo craft is orbiting Earth and on its way to the International Space Station Friday morning carrying over three tons of food, fuel and supplies. Meanwhile, the three member Expedition 52 crew researched a variety of space science on Thursday while preparing for the arrival of the 67P.

Commander Fyodor Yurchikhin and Flight Engineer Jack Fischer will monitor the automated docking of the 67P to the Zvezda service module Friday at 7:42 a.m. EDT. NASA TV will broadcast live the resupply ships approach and rendezvous beginning at 7 a.m. The 67Ps docking will mark four spaceships attached to the space station.

Fischer spent the morning photographing mold and bacteria samples on petri dishes as part of six student-led biology experiments that are taking place inside a NanoRacks module. In the afternoon, he removed protein crystal samples from a science freezer, let them thaw and observed the samples using a specialized microscope.

Flight Engineer Peggy Whitson tended to rodents Thursday morning cleaning their habitat facilities and restocking their food. In the afternoon, she moved to human research swapping out samples for the Cardiac Stem Cells study that is exploring why living in space may accelerate the aging process.

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Station Crew Researches Mold, Rodents and Stem Cells as Cargo Ship Chases Station - Space Fellowship

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Back to Browse Journals International Journal of Women's Health Volume 9

Ahmed Badawy,1 Mohamed A Sobh,2 Mohamed Ahdy,3 Mohamed Sayed Abdelhafez1

1Department of Obstetrics and Gynecology, 2Department of Internal Medicine, 3Department of Clinical Pharmacology, Mansoura University, Mansoura, Egypt

Objective: Attempting in vivo healing of cyclophosphamide-induced ovarian insufficiency in a mouse model using bone marrow mesenchymal stem cells (BMMSCs). Methods: Female BALB/c white mice were used to prepare a model for premature ovarian failure by single intraperitoneal injection of cyclophosphamide (80 mg/kg). Ten mice were injected with BMMSCs and then sacrificed after 21 days for morphometric evaluation of the ovaries. Hormonal profile was evaluated while mice were being sacrificed. Another 10 mice were left for natural breeding with male mice, and 5 of these were injected with BMMSCs. Oocyte-like structures were obtained from 3 mice and were subjected to in vitro fertilization/intracytoplasmic sperm injection. Results: Morphometric analysis of the ovaries demonstrated the presence of newly formed primordial follicles. Contribution of MSCs to the formation of these follicles was proven by a labeling technique. There was a drop in estradiol and rise in follicle-stimulating hormone levels, followed by resumption of the hormonal levels to near normal 21 days after MSCs therapy. The 5 mice that were injected with MSCs became pregnant after natural breeding. Fertilization and further division was reported in 5 oocytes subjected to intracytoplasmic sperm injection, but division did not continue. Conclusion: From this proof-of-concept trial, we can say that healing of damaged ovaries after chemotherapy in mice is possible using in vivo therapy with BMMSCs. This should open the gate for a series of animal studies that test the possibility of in vitro maturation of germinal epithelium of the ovary into mature oocytes.

Keywords: cyclophosphamide, stem cell, POF, ovarian insufficiency

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Bone marrow mesenchymal stem cell repair of cyclophosphamide-induced ovarian insufficiency in a mouse model - Dove Medical Press

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Newswise You might think stem cells only exist inside a fetus, but your adult body has a stockpile of stem cells, armed and ready to respond. These remarkable cells can develop into any other type of cell, like muscle or bone or nerve cells.

Researchers know heart attacks and strokes summon these cells. They flock to your heart or brain from all over your body to help you stay alive.

But, scientists did not realize other injuries, like a torn ACL of the knee, could command the army of stem cells to deploy.

Kevin Baker, Ph.D., Beaumont director of Orthopedic Research, conducted a study with Beaumont orthopedic surgeon Kyle Anderson, M.D., and others that revealed ACL tears send a signal to stem cells throughout our body.

After an ACL tear, Dr. Baker and his colleagues found a six-fold increase in stem cells circulating around the knee, similar to the bodys response to a major, life-threatening event like a stroke or heart attack.

However, when the stem cells arrive to help regenerate and repair the injured ligament, they get stuck. They cant get through the thick membrane that surrounds the knee joint.

We think this discovery will help us to understand how the body responds to an ACL injury, and also how post-traumatic osteoarthritis develops after a joint injury, Dr. Anderson said.

Post-traumatic osteoarthritis is a form of arthritis that develops after a knee injury. Its a common injury that affects veterans, athletes and anyone who puts stress and strain on their knees. But, until now, little was known about how the body attempts to heal these injuries.

As we age, the number of stem cells in our body declines. This could explain why your knee joint doesnt heal as well after a trauma when you are older, Dr. Baker said.

Osteoarthritis affects more than 30 million adults in the United States, according to the Centers for Disease Control and Prevention, and many of these cases occur after trauma to a joint. Its also a leading cause of disability.

The next step of our research will be finding methods to get the stem cells inside the joint. If the stem cells can get through the membrane around the knee, they could help speed up the healing process and perhaps delay or prevent arthritis, Dr. Baker added.

The study, funded in part by the American Orthopedic Society of Sports Medicine, is entitled, Acute mobilization and migration of bone marrow-derived stem cells following anterior cruciate ligament rupture. The authors believe it is the first study of its kind to reveal the bodys systemic stem cell response to an ACL injury.

Dr. Baker and Dr. Andersons research will appear in an upcoming edition of the journal Osteoarthritis and Cartilage. Other members of the research team are Perry Altman, M.D., Beaumont orthopaedic surgery resident, as well as Asheesh Bedi, M.D., and Tristan Maerz, Ph.D., of the University of Michigan.

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Researchers Discover Body's Stem Cell Army Hits a Wall When Responding to an ACL Injury - Newswise (press release)

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Scientists have used artificial skin grafts grown from induced pluripotent stem cells to cover the developing spines of rat fetuses while still in the womb.

Asian Scientist Newsroom | June 14, 2017 | In the Lab

AsianScientist (Jun. 14, 2017) - Researchers from Japan have developed a stem cell-based therapy to treat a severe congenital bone defect known as myelomeningocele. Their findings have been published in Stem Cell Reports.

Myelomeningocele is the most serious and common form of spina bifida, a condition in which the backbone and spinal canal do not close before birth, leaving parts of the spinal cord and nerves exposed.

A baby born with this disorder typically has an open area or a fluid-filled sac on the mid to lower back. Most children with this condition are at risk of brain damage because too much fluid builds up in their brains. They also often experience symptoms such as loss of bladder or bowel control, loss of feeling in the legs or feet, and paralysis of the legs.

To develop a minimally invasive treatment to cover large myelomeningocele defects earlier during pregnancy, the researchers first generated artificial skin from human induced pluripotent stem cells (iPSCs), and then successfully transplanted the skin grafts into rat fetuses with the condition.

We provide preclinical proof of concept for a fetal therapy that could improve outcomes and prevent lifelong complications associated with myelomeningoceleone of the most severe birth defects, said senior study author Professor Akihiro Umezawa of Japan's National Research Institute for Child Health and Development.

Since our fetal cell treatment is minimally invasive, it has the potential to become a much-needed novel treatment for myelomeningocele.

The human iPSCs were generated from fetal cells taken from amniotic fluid from two pregnancies with severe fetal disease (Down syndrome and twin-twin transfusion syndrome). The researchers then used a chemical cocktail in a novel protocol to turn the iPSCs into skin cells and treated these cells with additional compounds such as epidermal growth factor to promote their growth into multi-layered skin.

In total, it took approximately 14 weeks from amniotic fluid preparation to 3D skin generation, which would allow for transplantation to be performed in humans during the therapeutic window of 28-29 weeks of gestation.

Next, the researchers transplanted the 3D skin grafts into 20 rat fetuses through a small incision in the uterine wall. The artificial skin partially covered the myelomeningocele defects in eight of the newborn rats and completely covered the defects in four of the newborn rats, protecting the spinal cord from direct exposure to harmful chemicals in the external environment.

Moreover, the engrafted 3D skin regenerated with the growth of the fetus and accelerated skin coverage throughout the pregnancy period. Notably, the transplanted skin cells did not lead to tumor formation, but the treatment significantly decreased birth weight and body length.

We are encouraged by our results and believe that our fetal stem cell therapy has great potential to become a novel treatment for myelomeningocele, Umezawa said. However, additional studies in larger animals are needed to demonstrate that our fetal stem cell therapy safely promotes long-term skin regeneration and neurological improvement.

The article can be found at: Kajiwara et al. (2017) Fetal Therapy Model of Myelomeningocele with Three-dimensional Skin Using Amniotic Fluid Cell-derived Induced Pluripotent Stem Cells.

Source: Cell Press; Photo: Kazuhiro Kajiwara. Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.

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3D Artificial Skin Used To Treat Spina Bifida In Rats - Asian Scientist Magazine

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Paul Levine, a resident of West Tisbury, former professor at Harvard, and visiting professor at Stanford University, writes occasionally about scientific research taking place today, along with profiles of the Islands scientists and their work and facts of scientific note on the Island. This week, he follows up on his gene-editing column from six weeks ago, which described the genetics research that has led to CRISPR, which stands for clustered regularly interspaced short palindromic repeats. If youre wondering what that is, read on.

In this, the second column on the subject of gene editing, imagine a world in which many human genetic disorders have been eliminated, no children are born with cystic fibrosis, Tay-Sachs disease, sickle cell anemia, or other genetic disorders. Welcome to the world of CRISPR, an acronym for clustered regularly interspaced short palindromic repeats of the DNA of a gene. CRISPR can locate a defective gene and, along with an enzyme called Cas9, can, like a pair of scissors, snip out the unwanted gene and suture a desirable gene in its place. It is a technique of genetic editing that is more precise, efficient, and affordable than anything that has come before. What I describe below is specific to the Vineyard (the elimination of Lyme disease) and relevant to society as a whole for the potential for great good, but also for possible misuse use of the technology, which has raised questions of ethics and safety.

CRISPR-Cas9 as a tool for genetic editing has a history that goes back to a 2011 scientific conference at which microbiologist Emmanuelle Charpentier, now the director of the Max Planck Institute for Infection Biology in Berlin, met Jennifer Doudna, professor of chemistry and molecular and cell biology at the University of California, Berkeley. They talked about CRISPR-Cas9, and what follows is the story of one of the most significant achievements in genetics since the discovery of the structure and function of DNA. It is a story that involves brilliant scientists, competition, big egos, patent disputes, and the possibility of a Nobel Prize, not to mention the immense financial gain by biotech, agribusiness, and pharmaceutical companies.

Prior to todays application of CRISPR to edit genes, it was known that it was a means by which bacteria protected themselves from infection by viruses by recognizing and binding to viral DNA and destroying it with enzymes. Charpentier and Doudna wondered whether the technique could be applied to other things than the detection and destruction of viral DNA. If it could, it might lead to a way to snip out bad genes and possibly replace them with good ones. They began a collaborative research project with bacteria, and developed a technique for cutting out and replacing bacterial genes with CRISPR and an enzyme, Cas9. In other words, it was now possible to edit the bacterial genome by cutting and pasting genes. Doudna and Charpentier published their research in the journal Science in 2012. Aware of the great potential that the ability to edit genomes presented, the University of California patented their discovery.

At about the same time, Feng Zhang at the Broad Institute of MIT and Harvard was working with Cas9, and discovered that CRISPR-Cas9 could also be applied to edit the genes of animals and plants. His discovery was published a few months after the publication of the work of Doudna and Charpentier.

The Broad Institute applied for and received a patent based on the results of Zhangs research. However, prior to their filing, the University of California, Berkeley, had filed for and received a patent based on Doudnas and Charpentiers research.

In a patent dispute, it was ruled that the Broad Institutes patent took precedent over the University of California patent because it applies to animal and plant cells. The University of California, Berkeley, has asserted that although their patent involves bacteria, it includes all forms of life.

Unfortunately, a consequence of the dispute is the enmity that has developed between some of the parties involved.

It was not long before life scientists throughout the world began to develop the technique in order to advance progress in human genetic engineering to cure some of the 6,000 human genetic disorders.

With respect to applications of CRISPR-Cas9 to edit human genes, research is underway to use it to control insect- and spider-borne disease; for example, mosquitoes that carry the malaria parasite and the viruses that cause dengue, West Nile, and Zika fever. The object of the research is to produce sterile female mosquitoes by using CRISPR-Cas9 to edit out the genes required for their fertility, and distribute the sterile females in areas around the world where mosquito-borne diseases occur. This approach has been met with some success at the laboratory level.

Another research effort which might be familiar to you is to eliminate Lyme disease by distributing white-footed mice that have been manipulated with gene-editing techniques to effectively be immune to the bacteria which causes Lyme, all using CRISPR-Cas9. This would break the transmission cycle of the bacteria (see MV Times, Scientist proposes genetic attack on M.V. ticks, July 20, 2016).

I havent mentioned possible commercial applications of CRISPR-Cas9, and the great profits to be made by Monsanto and other agribusiness companies by the production of genetically modified plants and domestic animals. The technology is also appealing to Big Pharma. Its worth looking at the highly controversial and ethical questions that accompany the use of CRISPR-Cas9. In contrast with noninheritable somatic cell human gene editing described above, there is another technique called germ line gene editing, which makes gene changes at the level of human eggs, sperm, and embryos that would be heritable. Experiments on human embryos have been carried out by scientists in China and the U.K. that have raised concern that CRISPR-Cas9 could lead to the production of designer babies parents choosing the traits they want their children to have. Designer babies are a vast topic, too vast to bring up here, but there is an excellent discussion of the subject in Roger Gosdens The Brave New World of Reproductive Technology.

Jennifer Doudna, at U.C. Berkeley, and Feng Zhang at MIT, the principal developers and promoters of gene editing, appear to be at odds over the ethical questions surrounding the technology. Doudna is concerned with the ethics and the publics perception of CRISPR-Cas9, but Zhang appears less so, and prefers to drive the research to cure genetic disorders, putting aside the possibility of the production of designer babies.

If you want to explore CRISPR-Cas9 and come to an opinion regarding one of the most significant developments in genetics in this century, I urge you to read Robert Kolkers 2016 article in Bloomberg BusinessWeek, How Jennifer Doudnas Gene Editing Technique Will Change the World. It can be found at bit.ly/CRISPRdoudna. Listen to Doudnas TED Talk here: bit.ly/TEDdoudna.

Finally, I should mention that a two-act play named Gene Play, about the story of recDNA and CRISPR-Cas9, will be read by a cast of actors at the Vineyard Playhouse on June 19.

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Science and Scientists on the Vineyard: Genes at play with CRISPR - Martha's Vineyard Times

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The Southern California weight loss surgery clinic notes that defeating obesity is always healthful, but rarely simple.

Los Angeles, California (PRWEB) June 14, 2017

A June 8th article on Madame Noire offers a list of alleged compliments that can actually be taken as insults by people who have successfully managed to lose a significant amount of weight. While many of these observations can be made with the most benign intentions, the article notes that the complexities of weight loss make saying something like "Look how much weight she lost! Doesn't she look great?" can place undue attention on people who, generally speaking, just want to be left alone and accepted for who they are. Weight loss surgery specialists Dr. Feiz & Associates notes the article points up the reality that weight loss, with or without a surgical procedure, is more than just a physical change. It's a very personal matter that involves a complex interplay between physiological and psychological factors.

Dr. Feiz & Associates notes that many people assume weight loss surgery is an almost semi-magical procedure which actually causes fat to disappear on its own. In reality, such procedures as a sleeve gastrectomy work by creating physical changes that have psychological impacts. Specifically, the procedure removes approximately 75-85% of the stomach. The impact is twofold because the small stomach makes overeating physically uncomfortable but, perhaps more importantly, it also reduces the production of a hormone called ghrelin, which "tells" the brain that it's time to eat. The substance is believed to be largely responsible for creating the nagging hungry feelings that drives overweight people to continue eating, even when they know for a fact that they have consumed more than enough food; worse, ghrelin production tends to increase as individuals lose weight. Dr. Feiz & Associates says that, while sleeve gastrectomies do make weight loss a great deal easier, patients still have to muster the psychological energy to permanently change their approach to food and eating.

Dr. Feiz & Associates notes that the challenges involved with obesity and weight loss can lead to sensitivities that may well linger even after the additional weight has gone. They add that, for patients, this means realizing that they will have to address these matters, perhaps with the help of a coach or therapist, and develop a new relationship not only with food, but with their body. For friends and family of people who appear to be successfully dealing with their obesity, it means that a certain amount of sensitivity will be required, says the weight loss clinic.

Readers who would like to learn more about Dr. Feiz & Associates and if weight loss surgery might be right for them are invited to call (800) 868-5946. They can also the visit the clinic via the web at http://www.DrFeiz.com.

For the original version on PRWeb visit: http://www.prweb.com/releases/2017/06/prweb14415093.htm

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List of Weight Loss "Compliments" to Avoid Highlights the Complexities of Weight Loss, Says Dr. Feiz & Associates - Benzinga

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Addressing baldness in women

The sight of hair loss can be very worrying for a woman, at times making her lose confidence. Greater the stress, greater the hair loss. Pattern baldness is a serious concern amongst women.Dr Premalatha, DermatologistofHairline International Hair & Skin Clinictalks about hormone induced hair loss in women and the myths surrounding hair transplants.

It concerns changes in the level of androgens, the male hormones and alteration in female hormone levels.In PCOD(polycystic ovarian disease),women find hair on their head getting thinner while hair on their face gets coarser. Too much androgen brings in abnormal new hair growth, such as on the face, between the belly button and pubic area. One can see these signs by observing changes in menstrual periods. Another sign would be new acne formations. Procedures such as scalp analysis andblood tests can diagnose the cause ofhair loss in women. Another factor leading to hair loss is too much or too little of Thyroid hormone. The danger associated with female pattern baldness is that hair loss is permanent if not treated.

Q. Can you comment about the condition of hair in women during the time of pregnancy and delivery? After pregnancy and delivery, a phenomenon known as Telogen Effluvium is observed. It occurs due to many other reasons as well, like drastic weight loss, major surgery or high levels of stress.This phenomenon involves shedding of large amounts of hair each day, during shampooing, styling or brushing.Women experiencing the phenomenon witness large amounts of hair being shed usually 6 weeks to 3 months after a stressful event, like a pregnancy. At the peak of this condition, handfuls of hair may be lost. In order to find evidence to diagnose someone with Telogen Effluvium, doctors may look for small club-shaped bulbs on the fallen hair roots. The presence of the bulbs indicates that the hair has gone through a complete cycle of growth, suggesting the cycle may have sped up due to stress, because of pregnancy. The only thing one can do when experiencing Telogen Effluvium is wait until the hair loss slows down. Also other contributing factors such as stress related problems can be tackled by reducing anxiety through meditation and other recommended ways.

Q. The obvious answer to patterned chronic hair loss here is hair transplant. Can you tell us a bit about how it works? Both medical and surgical line of management should be considered.Hair transplant is a method of hair redistribution wherein hair is removed from areas on the scalp and placed on areas which are balding. Minor scars may appear on the areas where hair is removed, but the end result is permanent. Other solutions such as a change in hairstyle, or hair weaving, can also be utilized to improve appearance.Very few people however have the courage to undergo the treatment, even though latest researches show that market for hair transplantation is growing rapidly. Many myths surround this treatment, preventing people suffering from pattern balding from giving it a try.

Q. Can we discuss some of them? The method of hair transplant is holistic and all round yields good results. But people have false notions about it. A common myth is that old people cannot undergo treatment, preventing old people from undergoing it. Age has nothing to do with it. The texture and quality of your existing hair determines whether or not you are suitable for it.

Also, some people believe hair transplant is only possible at the initial stages of hair loss. On the contrary, it is actually the opposite. It is in fact more difficult to predict in the initial stages the extent of hair loss and whether you require treatment. It makes more sense to go to the physician when hair loss gets stable.The treatment does not give immediate results. The patient generally sees results after about 8 months, and the head filling with hair within 9-12 months.

Another myth is that surgery affects the brain. There is no connection whatsoever. Surgery involves only the skin of your scalp. There is no contact with any part of the brain.Lastly, a common misconception is that surgery leaves no scars. This is untrue. Every hair restoration technique leaves scars on the scalp. Surgery however reduces these scars to a formation of multiple dots. However, scarring is minimal and almost invisible even if you are completely bald.

Q. Concerns exist on affordability of the surgery. What is your comment?

Cost of surgery depends on a number of factors, especially the number of grafts to be transplanted. It can be a little costly, but definitely affordable. Most hair transplant clinics offer options of paying in instalments.

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Addressing baldness in women - Ibcworldnews

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