Archive for July, 2017

Willow Cannan

OCEAN SPRINGS, Miss. Imagine that you are the parent of an adorable, healthy, curious and loving baby girl.

As she grows, you realize she is not meeting her developmental milestones, but your doctor assures you that she will catch up to the rest of the children eventually. She doesnt speak, is slow to walk and while this in itself is not alarming, your pediatrician refers you to a neurologist.

You wait weeks for the results and the doctor confirms your deepest fears with a devastating diagnosis your baby girl has a rare and fatal genetic condition for which there is no known medication or cure.

In May 2016, Tom Cannan and Amber Olsens daughter Willow was diagnosed with Multiple Sulfatase Deficiency (MSD), a rare type of lysosomal storage disorder. She was born with a mutation of the SUMF1 gene, which means that her body does not create sulfatase enzymes.

This prevents her body from breaking down and recycling natural cellular waste. It is a fatal condition that affects the entire body.

Over the next few years, Willows body will slowly break down, she will lose her vision, and her brain will eventually shut downlikely all before she reaches her tenth birthday.

At just three years old, Willow now walks with a walker, has trouble sitting or eating on her own, and has never spoken.

The doctors told us to go home and spend time with our daughter that there was nothing we could do besides be with her and make her comfortable. We found research online that a treatment was close but lacked funding. We realized we had to develop a plan and put it in action, so we created the United MSD Foundation to raise money for a cure. Our campaign is called Warriors for Willow. We will fund the work needed to develop a clinical trial, we just hope it is in time for Willow, says Willows mother Amber.

While less than 50 children worldwide have been diagnosed with Willows specific condition, lysosomal storage disorders are believed to have an estimated frequency of one in every 5,000 live births. A cure for MSD could potentially result in the cure for multiple conditions, saving thousands of children.

Theres been a resurgence of new types of treatments for these rare inherited disorders like MSD, says Director of UNC Gene Therapy Center, Dr. Steven Gray. Gene therapy has been at the forefront of this resurgence and has proven to have outstanding results in many cases. Because we know whats wrong and what genes are missing, I have high hopes that a cure can be identified. However, it all comes down to funding.

The United MSD Foundations goal is to raise $210,000 by October 1, 2017, to fund the next stage of research. As a rare condition, Multiple Sulfatase Deficiency has not attracted research funding from pharmaceutical companies, which leaves families like Willows to fight for a cure on their own. The United MSD Foundation aims to ensure that this devastating condition receives the research attention it requires and deserves.

In the beginning, we hoped that finding a cure for MSD would save our daughter, says Willows father Tom. We just wanted her to live. But now we are fighting for all of the families worldwide whose lives have been devastated by this condition. We have to give them hope.

To see a video of Willows story or to donate to the United MSD Foundation, click here.All donations will help fund research and clinical testing to identify a cure for MSD.

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Ocean Springs parents fight to save 3-year-old daughter from fatal genetic condition - WGNO

Great Ormond Streets position was outlined in court documents:

At the first hearing in Charlies case in March, GOSHs position was that every daythat passed was a day that was not in his best interests. That remains its view of his welfare. Even now, Charlie shows physical responses to stressors that some of those treating him interpret as pain and when two international experts assessed him last week, they believed that they elicited a pain response. In GOSHs view there has been no real change in Charlies responsiveness since January. Its fear that his continued existence has been painful to him has been compounded by the Judges finding, inApril, that since his brain became affected by RRM2B, Charlies has been an existence devoid of all benefit and pleasure. If Charlie has had a relationship with the world around him since his best interests were determined, it has been one of suffering.

Throughout, his parents hopes have been sustained by advice received from overseas. Mitochondrial disorders comprise a specialised and small international field. The experts in that field meet, collaborate and exchange ideas on a very regular basis and it is that valued collaboration that allows progress to be made and patients to be provided with the best possible care. Professor Hirano (the Professor), whose laboratory research has an international reputation, is very well known to the experts at GOSH and he communicated with them about NBT treatment for Charlie at the very end of December. In January, GOSH invited the Professor to come and see Charlie. That invitation remained open at all times but was not taken up until 18 July after being extended, once again, this time by the Court.

In the months between January and July, the Professor provided written and oral evidence for the best interests hearing in April and, after the Court decided that NBT was not in Charlies best interests, he went on to provide further written evidence for the Court of Appeal and the Supreme Court. Most recently, on 6 July, he co-signed the letter indicating that he had new information that changed the picture for Charlie, that brought this case back before the High Court.

When the hospital was informed that the Professor had new laboratory findings causing him to believe NBT would be more beneficial to Charlie than he had previously opined,GOSHs hope for Charlie and his parents was that that optimism would be confirmed. It was, therefore, with increasing surprise and disappointment that the hospital listened to the Professors fresh evidence to the Court. On 13 July he stated that not only had he not visited the hospital to examine Charlie but in addition, he had not read Charlies contemporaneous medical records or viewed Charlies brain imaging or read all of the second opinions about Charlies condition (obtained from experts all of whom had taken the opportunity to examine him and consider his records) or even read the Judges decision made on 11 April. Further, GOSH was concerned to hear the Professor state, for the first time, whilst in the witness box, that he retains a financial interest in some of the NBT compounds he proposed prescribing for Charlie. Devastatingly, the information obtained since 13 July gives no cause for optimism. Rather, it confirms that whilst NBT may well assist others in the future, it cannot and could not have assisted Charlie.

In the months ahead, all at GOSH will be giving careful thought to what they can learnfrom this bruising court case that might enrich the care it provides to its most vulnerable patients and families. It is hoped that those who, like the Professor, have provided the opinions that have so sustained Charlies parents, their hopes and thus this protracted litigation with its many consequences, will also find much upon which to reflect.

GOSH is a tertiary referral centre and a centre of research excellence. It celebrates and enthuses about gene therapy and experimental treatment of all types. But it also believes in its patients as people. The hospital strives to work with children and parents to strike a balance of treatment benefits and burdens that combines evidence and compassion.

Where that balance falls ethically in favour of pioneering treatment, GOSH shares each familys excitement at the journey that follows. GOSH believes that novel therapies are best provided in the context of formal clinical trials. The hospital does not treat its most vulnerable children simply because it can and on no account does it treat them purely because novel treatment furthers GOSHs research.

All of GOSHs thoughts go with Charlie and his mother and father the hospital wishes each of them peace in their hearts at the end of this day and each day to come.

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US doctor who wanted to treat Charlie Gard had 'financial interest' says Great Ormond Street - Metro

So it was that Eos, goddess of the dawn, fell in love with Tithonus, a handsome young prince of Troy and, beguiling him with her beauty, brought him to her palace on Mount Olympus.

They lived happily for many years but, being mortal, age eventually overtook Tithonus. In her despair, Eos beseeched Zeus to grant her love immortality. Moved to pity, he granted her request but even the king of Olympus could not bestow eternal youth on a human for that would make him as one of the gods.

As one age passed into the next, Tithonus, withered and shrunken, cried incessantly for release from his torment but Zeus could not undo a wish once granted. It was Eos who eventually provided her poor lover a measure of relief by transforming him into a cicada. Now each summer he emerges from the ground with a fresh body to sing in eternal praise of his beauteous goddess. Or is it rather a lament over his crusted, hollow shell of a body?

Many of the myths and stories we have long told ourselves are cautionary tales against the dangers of hubris, our overconfident pride and arrogance before the gods. Divinity will mete out retribution to those who forget their place in the natural scheme of things. Chief among these absolutes of the human condition is our mortality; we all must die and woe betide any who would seek to have it otherwise.

But consider this statement from the website of the California Life Co. (Calico), a biotechnology firm established in 2013:

Calico is a research and development company whose mission is to harness advanced technologies to increase our understanding of the biology that controls lifespan. We will use that knowledge to devise interventions that enable people to lead longer and healthier lives. Executing on this mission will require an unprecedented level of interdisciplinary effort and a long-term focus for which funding is already in place.

The company is a subsidiary of Alphabet Inc., whose most famous other subsidiary goes by the name of Google. By 2016, Larry Page, Alphabets CEO (and co-founder of Google) had committed the company to contributing $240 million to Calico, with an additional $490 million should it be needed.

Calico is by no means the only Silicon Valley outfit investing big dollars in the life extension sciences field. SENS (Strategies for Engineered Negligible Senescence) Research Foundation, founded in 2009, and Human Longevity Inc., founded in 2014, are two of its better-funded competitors but there are others.

Whats going on here? Lets start with some data. Since 1900, the average human life span has increased by 30 years. But with this, so have the rates of age-related health issues such as cancer, heart disease, stroke, diabetes and dementia. In the U.S., up to age 44 the leading causes of death are accidents and violence. From there to age 65, its cancer and heart disease after that.

Medical advances are making significant inroads on each of these diseases and they may be conquered within your childrens lifetime. What then? Well, epidemiologists suggest a cure for cancer would only add 3.3 years to the average lifespan while the prevention of heart disease would tack on another four years. The elimination of all disease likely would only extend life into the mid-90s.

To go further, the aging process itself must be slowed. Even in the absence of disease, our bodies senesce as our organs, tissues, cells and macromolecules accumulate damage at an ever-increasing rate. Eric Verdin of the Buck Institute for Research on Aging has observed that if you just kept aging at the rate you age between 20-30, youd live to a thousand. But at 30, everything starts to change. Thereafter your risk of mortality doubles every seven years.

Most longevity scientists are health spanners, seeking a healthier life with a compressed morbidity (i.e., a quick and painless death). But immortalists like SENS Research founder Aubrey de Grey and futurist Ray Kurzwell believe science can carry us much further. If aging is encoded in the DNA of our genes, they argue, there should be no technological reason why we couldnt identify and address those parts of our genomes that are responsible for senescence.

Like so much else in modern biology, medical research is increasingly becoming an information science. To find the genetic correlates of aging will entail the compilation and analysis of an almost unthinkable mass of biotechnical data. Who has the big-data skillset and financial resources to back such an undertaking?

Silicon Valley.

But what about the economics, ethics and religious implications of an immortality united with youthful vigor? Should aging be viewed as a medical disease to be treated as any other or are we just asking for it with such hubristic thinking?

Ken Baker is a scientist and a retired biology professor. If you have a natural history topic youd like the author to consider for an upcoming column, email your idea to rweaver@advertiser-tribune.com.

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It is estimated that genetics are a contributing factor in up to 10 percent of couples who experience infertility or recurrent pregnancy loss, so it stands to reason that genetic testing has the potential to help many of those couples in their quest to have a family.

Genetic testing examines DNA, which has been called the chemical database that carries instructions for the bodys functions and can reveal gene changes that may cause illness or disease, including infertility. Since both men and women can have fertility issues, they can all benefit from genetic testing.

Identifying a genetic cause for your infertility can help you make the right decision on how to proceed by choosing the treatments that are most likely to help.

Additionally, genetic testing is advised before you have children if you or your partner has a family history of a genetic disorder, such as sickle cell anemia, Tay-Sachs disease or cystic fibrosis. Such testing can reveal if either or both of you carry a copy of an altered gene that would put a child at risk of developing the disorder.

A Board-Certified Reproductive Endocrinologist would make suggestions as to what blood tests should be ordered, which in most cases will follow the American College of Obstetrics and Gynecology (ACOG)'s recommendations.

If youre interested in learning more about genetic testing, contact us.

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Genetic Testing: Finding the cause of your infertility ...

Paula Ward scrolls through the website for 23andMe which was recently approved for direct-to-consumer genetic tests for health risks. KOMO photo

One of the top sellers on Amazon Prime Day this year has nothing to do with electronics. It's a $200 test for personal ancestry and genetic health risks.

The health risk part of that test has a lot of people asking : How much do you really want to know?

As a two year breast cancer survivor, Paula Ward knows she has some degree of cancer risk. But she wonders what other possible health risks might lurk in her DNA.

"My grandmother did have Parkinson's," Ward said. "Alzheimer's is also a concern because I did have a great aunt that had that, on my mother's side."

Ward likes the idea of going online to order a genetic test to learn more.

23andMe is the first genetic testing lab to get FDA approval for marketing health risk tests directly to consumers. Customers receive a kit in the mail that includes a sterile tube to collect and send back a sample of your saliva.

The results do not tell whether or not you'll get a particular disease, only if you're genetically predisposed.

23andMe is approved to test for 10 diseases but right now only tests for four: Late-onset Alzheimer's Disease, Parkinson's Disease, Hereditary Thrombophilia, linked to an increase tendedancy for blood clots, and Alpha 1 Antitrypsin Deficiency, an inherited condition linked to lung and liver disease.

"But it's really important to know that it's not diagnosing disease or health condition," explained 23andMe Medical Associate Stacey Detweiler.

On it's website, 23andMe emphasizes that its health risks reports are not for diagnosis. They only tell whether you carry certain markers associated with risks for certain health conditions.

The company says other genetic factors not covered by its tests can also pay a role in your overall health risks. So can different factors specific to your own environment and lifestyle.

"It's not giving that diagnosis," Detwiler said. "But it's kind of like another tool that you can use working with your physician, for working towards just overall general good health."

But Geneticist Dr. Gail Jarvik,head of the the Medical Genetics division at the University of Washington, urges caution.

"We have had a number of people contact us after 23andme started testing again for risk of disease," Jarvik said. "And one particular patient has a 40% risk of Alzheimers disease and is extremely concerned and would like to know what can be done. And there's very little you can do to modify your risk of Alzheimers disease using that information, that the rest of us shouldn't be doing anyway. Better diet, and better exercise, most of us would benefit from."

Critcs fear some people are not emotionally prepared for the potential results of the test, especially when many genetic diseases have no remedy.

"We don't have really good, specific ways of modifying risks of Alzheimers and Parkinsons, which are part of this test," Jarvik said. "And people should think about that before they order the test, do I want to know ths information? Will it improve my quality of life? Or just make me very worried?"

"We do highlight that this is information that once you learn it, you can't unlearn it,so to really be confident that this is information that you do want to know," Detweiler said.

"It's just a tool," said Leanne Spaulding, who plans to discuss taking the test with her family. Spaulding knows her family has a history of dementia and diabetes.

"If there's anything else that runs in my family that I don't know about, I'd just as soon know, and be able to do something about it, and be able to make plans around it," Spaulding said

Paula Ward agrees that having her potential health risk information might be an added tool for long-term planning, lifestyle changes or discussing your health with your family. Ward's advice: Before you decide on a genetic health test, do your homework, and be very honest with yourself.

"You know how you are," Ward said. "If you stress over little things, then maybe that's something you don't need to know."

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Mail order genetic tests for health risks. How much do you want to ... - KOMO News

USA TODAY High School Sports has a weekly column on the college recruiting process. Here, youll find practical tips and real-world advice on becoming a better recruit to maximize your opportunities to play at the college level. Joe is a former college-athlete and coach at the NAIA level, where he earned an NAIA National Championship. Joe is just one of many former college and professional players, college coaches, and parents who are part of the Next College Student Athleteteam. Their knowledge, experience, and dedication along with NCSAs history of digital innovation, and long-standing relationship with the college coaching community have made NCSA the largest and most successful athletic recruiting network in the country.

Imagine if there was a scientific way to discover whether or not your child is destined to be an elite athlete. Sounds like pure science fiction, right? Some companies, however, believe that they have the secret. The answers are in your genes.

Genetic testing is one of the newer trends to sweep through the sports and fitness world. Companies claim that, with a simple genetic test, they can tell who has what it takes to be an elite soccer player, football player, sprinter, endurance athlete and more. They can also determine athletes who are more prone to certain injuries. And the tests can help trainers understand the type of workout plan an athletes body will respond to best.

You might be wondering if these genetic tests are too good to be true (so were we), and if you need to take them to stay competitive in your college athletic recruiting. We looked at the data to better understand the how, when, where and why behind genetic testing for athletes.

Scientists have studied the genetic code of some elite and pro athletes, finding a few similar genes among these top competitors. To gauge aspiring athletes potential, companies look into their genetic codeusing a saliva sampleto see if they also contain those performance-enhancing genes that are present in the code of elite athletes.

Some companies primarily look for one particular gene: ACTN3. This gene is associated with the presence of a specific protein that helps muscles powerfully contract at high speeds. They claim that, depending on the variation of a persons ACTN3 gene, an individual is more genetically inclined to excel in either power or endurance sports. In fact, Atlas Sports Genetics president, Kevin Reilly, told Scientific Americanthat the genetic tests are more useful than physical tests to determine a childs athletic abilities before they turn 9.

Similarly, Soccer Genomicsexplains that with just one saliva sample, it can tell you if you have the genetic makeup required to excel in soccer. The Soccer Genomics website claims that their proprietary method checks an athletes speed, flexibility mobility, endurance, risk of injury, strength and nutrition. Soccer Genomics also provides athletes with a full report so they can understand their genetic strengthsand weaknesses.

Baylor Universitys football teamhas joined the genetic testing bandwagon, using the technology to build personalized training programs for each athlete. To do so, Baylor University hired Athletigen, which claims it uses cutting edge sports science to help athletes reach their highest levels of performance.

Were all trying to climb a mountain, and theres an infinite number of ways we can do so, Dr. Jeremy Koenig, the CEO of Athletigen, told USA Today. In knowing that information, you can optimize an athletes training plan or nutrition plan, based on their needs and also based on their goals.

While all of this is amazing technology, scientists around the world are stepping up to say, Not so fast! Experts claim that we simply dont know enough about the genetic code and how it affects athletic performance to be able to predict if an individual is predisposed to be an elite athlete.

Stephen Roth, an assistant professor of exercise physiology, aging, and genetics at the University of Maryland in College Park, pointed out in Scientific American that there are some 20,000 genes in the entire genome. So far, about 200 have been identified to have a positive association with fitness-related performance. However, we are only just scratching the surface on these 200, and there could be many more genes yet that play a critical role in athletic performance. He adds, Most research suggests that genetics contribute significantly to sports performance, buts very hard to put a number on it.

Furthermore, researchers explain that genetic testing companies tend to pick out data that better supports their claim and use studies that are simply too small to be relevant. Harvard geneticist Dr. Robert Green told Stat News, The notion that [athletic genetic testing companies] are somehow tailoring recommendations on the basis of your DNA is nonsense.

This new craze in fitness and sports will certainly continue to get refined over the years as we learn more about how genetics affect athletic ability. While the research isnt there yet to make genetic testing for athletes foolproof, there might still be some merit in sending in your saliva for testing. Maybe youre just interested in learning more about how your genetic code could affect your potential athletic performance. Perhaps a genetics-focused work out plan will benefit you in the long run.

As with all fitness and sports fads, however, its important to take it all with a grain of salt. Can you get genetically tested? Of course! Do you have to in order to get recruited? Definitely not.

Coaches dont need to see your genetic makeup to know if youre a good fit for their roster. They want to see your athletic ability, your potential, your work ethic and your character. Theres nothing wrong with using something like genetic testing to get an edge on the competition. But at the end of the day, you just need to be able to prove to coaches why youre a great fit for their team.

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Genetic testing: The new way to identify and train elite athletes? - USA TODAY High School Sports

Genetic counsellor Bruce Hopper, along with some members of the local genetics team, will Be at Taree City Centre on Jeans for Genes Day, Friday August 4.

Genetic counsellor Bruce Hopper and his team will be at Taree City Centre on Jeans for Genes said. It is also an opportunity for people to have a quick conversation with Bruce about the developments in genetics research.

Each year as Jeans for Genes Day places the focus on how our genes may impact our health, we marvel at the technological advances in genetic testing that occur year after year.

Bruce Hopper, genetic counsellor at Hunter New England Local Health District, said this year the very effective panel testing for multiple genes is now an extra option for clinicians helping families.

Panel testing allows us to now test multiple genes at once, at a much cheaper price than we could have even four months ago,Mr Hopper said.

The new technology has led us to be able to change from testing one gene at a time, to now being able to test multiple genes at once.

This has led to us in the clinical setting to assist individuals and families by testing for additional genes not logistically possible up until a few months ago,he said.

This technology has already been used for a number of patients with a family history of cancer as well as some families with cardiac conditions.

Jeans for Genes Day, an initiative of the Childrens Medical Research Institute, based at Westmead Hospital, undertakes research into attempting to establish why, children specifically, are born with certain genetic conditions.

Following identification of a genetic cause the focus is then on tailoring a specific treatment for that child.

Mr Hopper, along with some members of the local genetics team, will be at Taree City Centre on Jeans for Genes Day, Friday August 4,with merchandise and badges.

It is also an opportunity for people to have a quick conversation with Mr Hopper about the developments in genetics research.

To make an appointment to see a genetic counsellor and discuss genetic concerns, individuals first need to speak with their GP and discuss a referral to the genetic service both in Taree, Forster and the surrounds.

A number of shops in the Lower Mid-North Coast Region will be wearing jeans and selling badges as will the staff at Manning Hospital.

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Jeans for Genes Day stall at Taree City Centre - Gloucester Advocate

Five years ago, Alice Collins Plebuch made a decision that would alter her future or really, her past.

She sent away for a "just-for-fun DNA test." When the tube arrived, she spit and spit until she filled it up to the line, and then sent it off in the mail. She wanted to know what she was made of.

Plebuch, now 69, already had a rough idea of what she would find. Her parents, both deceased, were Irish-American Catholics who raised her and her six siblings with church Sundays and ethnic pride. But Plebuch, who had a long-standing interest in science and DNA, wanted to know more about her dad's side of the family. The son of Irish immigrants, Jim Collins had been raised in an orphanage from a young age, and his extended family tree was murky.

After a few weeks during which her saliva was analyzed, she got an email in the summer of 2012 with a link to her results. The report was confounding.

About half of Plebuch's DNA results presented the mixed British Isles bloodline she expected. The other half picked up an unexpected combination of European Jewish, Middle Eastern and Eastern European. Surely someone in the lab had messed up. It was the early days of direct-to-consumer DNA testing, and Ancestry.com's test was new. She wrote the company a nasty letter informing them they'd made a mistake.

But she talked to her sister, and they agreed she should test again. If the information Plebuch was seeing on her computer screen was correct, it posed a fundamental mystery about her very identity. It meant one of her parents wasn't who he or she was supposed to be and, by extension, neither was she.

Eventually, Plebuch would write to Ancestry again. You guys were right, she'd say. I was wrong.

We are only just beginning to grapple with what it means to cheaply and easily uncover our genetic heritage.

Over the past five years, as the price of DNA testing kits has dropped and their quality has improved, the phenomenon of "recreational genomics" has taken off. According to the International Society of Genetic Genealogy, nearly 8 million people worldwide, but mostly in the United States, have tested their DNA through kits, typically costing $99 or less, from such companies as 23andMe, Ancestry.com and Family Tree DNA.

The most popular DNA-deciphering approach, autosomal DNA testing, looks at genetic material inherited from both parents and can be used to connect customers to others in a database who share that material. The results can let you see exactly what stuff you're made from as well as offer the opportunity to find previously unknown relatives.

For adoptees, many of whom can't access information about their birthparents because of closed adoption laws, DNA testing can let them bypass years, even decades, of conventional research to find "DNA cousins" who may very well lead them to their families.

But DNA testing can also yield uncomfortable surprises. Some testers, looking for a little more information about a grandparent's origins, or to confirm a family legend about Native American heritage, may not be prepared for results that disrupt their sense of identity. Often, that means finding out their dad is not actually their dad, or discovering a relative that they never knew existed perhaps a baby conceived out of wedlock or given up for adoption.

In 2014, 23andMe estimated that 7,000 users of its service had discovered unexpected paternity or previously unknown siblings a relatively small fraction of overall users. The company no longer provides data on surprise results. However, its customer base has more than doubled since 2014, and now contains more than 2 million people and as more people get involved with recreational genomics, bloodline surprises are certain to become a more common experience. The 2020s may turn out to be the decade that killed family secrets, for better and for worse.

"We see it every day," says CeCe Moore, a genetic genealogist and consultant for the PBS series "Finding Your Roots." She runs a 54,000-person Facebook group, DNA Detectives, that helps people unravel their genetic ancestries. "You find out that a lot of things are not as they seem, and a lot of families are much more complex than you assume."

Alice Plebuch found herself in this place in the summer of 2012. To solve the mystery of her identity, she needed more help than any DNA testing company could offer. After all, genetic testing gives you the what, but not the why.

Plebuch would turn out to be uniquely suited to the role of private eye in her own detective story. Now living in the suburbs of Vancouver, Washington, she worked as an IT manager for the University of California before her retirement. "I did data processing most of my life, and at a fairly sophisticated level," she says. Computers do not intimidate her, and neither do big questions that require the organization and analysis of complex information. She likes to find patterns hidden in the chaos.

Just the skills necessary to solve a very old puzzle.

After the initial shock of her test results, Plebuch wondered if her mother might have had an affair. Or her grandmother, perhaps? So, she and her sister, Gerry Collins Wiggins, both ordered kits from DNA testing company 23andMe.

The affair scenario seemed unlikely certainly out of character for her mom, and besides, all seven Collins children had their father's hooded eyes. But she couldn't dismiss it. "My father, he was in the Army and he was all over the world, and it was just one of those fears that you have when you don't know," she says.

As they waited for their results, they wondered. If the Ancestry.com findings were right, it meant one of Plebuch's parents was at least partly Jewish. But which one?

They had a gut sense that it was unlikely to be their mother, who came from a large family, filled with cousins Plebuch and her siblings all knew well. Dad, who died in 1999, seemed the likelier candidate. Born in the Bronx, Jim Collins was a baby when his mother died. His longshoreman father, John Collins, was unable to care for his three children and sent them to live in orphanages. He died while Jim was still a child, and Jim had only limited contact with his extended family as an adult.

But still, the notion Jim could somehow be Jewish seemed far-fetched. His parents had come to the United States from Ireland, and that history was central to Jim's sense of himself. "He was raised in an orphanage; he didn't have anything else," Plebuch says. "He had his Irish identity."

She plunged into online genealogy forums, researching how other people had traced their DNA and educating herself about the science. She and her sister came up with a plan: They would persuade two of their first cousins to get tested their mother's nephew and their father's nephew. If one of those cousins was partly Jewish, they'd know for sure which side of the family was contributing the mysterious heritage.

The men agreed. The sisters sent their kits and waited.

Then Plebuch's own 23andMe results came back. They seemed consistent with her earlier Ancestry.com test, indicating lots of Ashkenazi Jewish ancestry from areas such as Belarus, Russia, Ukraine and Lithuania. She also discovered that her brother Bill had recently taken a 23andMe test. His results were a relief sort of.

"No hanky-panky," as Plebuch puts it. They were full siblings, sharing about 50 percent of the relevant DNA, including the same mysterious Jewish ancestry. This knocked out another theory they had considered that Plebuch might have been adopted.

Plebuch found a feature on 23andMe's website showing what segments along her chromosomes were associated with Ashkenazi Jews. Flipping back and forth, comparing her DNA to her brother's, she had a sudden insight.

There was a key difference between the images, lurking in the sex chromosomes. Along the X chromosome were blue segments indicating where she had Jewish ancestry, which could theoretically have come from either parent because females inherit one X from each. But males inherit only one X, from their mothers, along with a Y chromosome from their fathers, and when Plebuch looked at her brother's results, "darned if Bill's X chromosome wasn't lily white." Clearly, their mother had contributed no Jewish ancestry to her son.

"That was when I knew that my father was the one," Plebuch says.

The next day, her sister Gerry Wiggins's results came back: She, too, was a full sibling who also displayed significant Jewish ancestry. Then, Plebuch got an email from a retired professor known for his skill at interpreting ancestry tests, to whom she'd sent hers. "What you are is 50 percent Jewish," he wrote. "This is in fact as solid as DNA gets, which in this case is very solid indeed."

But how could their father have been Jewish? Could Jim Collins's parents have been secret Irish Jews? Or maybe Jews from Eastern Europe who passed themselves off as Irish when they came to the country as immigrants?

Now they really needed the data from the cousin on their father's side. If he also had Jewish ancestry, Plebuch figured, that could point to a family secret buried in Europe.

They waited for months, through a series of setbacks problems in the lab, problems with the mail. Meanwhile, the sisters emailed back and forth.

Plebuch asked her younger sister: Did this revelation about their father's ethnicity unnerve her? They'd been so certain of their family roots, and "now we know nothing," she wrote.

"It is the first thing I think about when I wake up in the morning," Wiggins replied, "and the last thing I think about as I drift off to sleep."

At last, Plebuch was alerted that her cousins' results were ready. The data from their mom's nephew revealed that he was a full first cousin, as expected sharing about 12.5 percent of his DNA with Plebuch.

But the results from her dad's nephew, Pete Nolan, whose mother was Jim Collins' sister, revealed him to be a total stranger, genetically speaking. No overlap whatsoever with Plebuch or, by extension, with her father.

In other words, Plebuch's cousin wasn't actually her cousin.

And her dad's sister wasn't actually his sister.

Plebuch was devastated. This finding knocked out the secret-Jews theory but if it put Plebuch closer to the truth, she still felt unmoored. She was deeply fond of Nolan, with whom she shared a birthday. "I was afraid he was going to reject me because we were no longer biological cousins."

She called Nolan to share the results of his DNA test. "He was sad," Plebuch says, "but he also told me I was the best cousin he ever had."

Plebuch and Wiggins came to the stunned conclusion that their dad was somehow not related to his own parents. John and Katie Collins were Irish Catholics, and their son was Jewish.

"I really lost all my identity," Plebuch says. "I felt adrift. I didn't know who I was you know, who I really was."

For Wiggins, the revelation confirmed a long, lingering sense that something was amiss with her father's story. Studying the family photographs on her wall, she'd thought for years that their paternal grandfather looked like no one in her immediate family. Visiting Ireland in 1990, she had searched the faces for any resemblance to her 5-foot-4, dark-haired father. "There was nobody that looked like my dad," Wiggins says.

The sisters set about methodically pursuing several theories. With Jim Collins and his parents long dead, Plebuch knew she needed to unravel his story through the living. She signed up to take a class in Seattle on how to use DNA to find her father's relatives.

If the woman Jim called his sister was not his sister, was there evidence of an actual sibling out there somewhere? Might that sibling have children? Might Plebuch and her siblings have first cousins they'd never known about?

---

The dystopian novelistMargaret Atwood is fond of saying that all new technologies have a good side, a bad side, and a "stupid side you hadn't considered." Doing DNA testing for fun can carry consequences few of us might anticipate. It requires little investment at the outset, but it has the potential to utterly change our lives.

After researching her family history, Laurie Pratt decided five years ago to enhance her genealogical knowledge by testing herself and her parents. This was how she discovered that her dad was not related to her.

Pratt, 52, an airline ground operations supervisor in Orange County, California, went to her mother, who at first said the results were "impossible." But over time, her mother divulged hazy memories of a short-lived relationship during a period when she and her husband were briefly separated.

Her mother couldn't recall a name before she died. The man who raised Pratt also died; she never told him he was not, biologically speaking, her father.

She searched over several years, eventually identifying a potential candidate within the family tree of previously unknown cousins she found through DNA matching. She sent this man a letter and days later, in February of this year, he suddenly popped up in the Ancestry.com database, identified by a saliva test as her biological father.

The man called her, and they spoke briefly on the phone. Though he was unmarried when Pratt was conceived, he fretted over the idea that he had abandoned a baby without knowing it. Pratt asked if they could meet, and the man agreed, but asked if he could take some time first to process the news and tell his wife and daughter.

Two days later, Pratt logged onto Ancestry.com and discovered that the man's test had been deleted.

Reactions to DNA testing surprises vary dramatically. Moore, the genetic genealogist, says that, in her experience, even those who are initially dismayed end up glad that "they learned about the truth of themselves."

But seekers may be a self-selecting bunch, and those who find the truth thrust upon them by someone else's quest are not always happy about it. Gaye Sherman Tannenbaum, an adoptee who spent decades searching for her birthparents and now helps others on their quests, says in some instances, people are "outright hostile" when they learn of a newly discovered relative.

The reaction is understandable: DNA surprises often imply extramarital affairs, out-of-wedlock births and decades-old secrets.

Researchers from theUniversity of Leuven in Belgium recently examined the English-language websites of 43 direct-to-consumer DNA testing companies and found that few companies warn consumers about the possibility of discovering "misattributed paternity."

23andMe is unusual in offering multiple warnings. ("Unexpected relationships may be identified that could affect you and your family.") "We are as transparent as possible," says Kate Black, the privacy officer for 23andMe, brought on in 2015after the company was criticized for failing to prepare consumers for such surprises. "We try to educate and inform people in every tool."

Still, consumers may skim those warnings, or refuse to believe such surprises might lurk within their own families. Jennifer Utley, the director of research at Ancestry.com, says that even though she had seen many cases of surprise relatives in her work, she still found herself in "complete shock" when she tested her own DNA and discovered a first cousin she hadn't known existed.

"I had no idea who this person was," says Utley, who has since learned that her cousin was the product of a teenage relationship, raised by an adoptive family. Of her family, she now concludes: "We're the best secret-keepers on the planet."

Pratt says she doesn't regret testing her DNA. She found herself both "devastated and curious" after the initial discovery about her genetic heritage. But, of course, that discovery was not hers alone, because her genes are not hers alone. Cases of unexpected paternity and secret adoptions implicate other people.

"I think this jars him," she says of her biological father. "He goes to bed the good guy he's always been very religious, very Catholic. And he wakes up, he's Mick Jagger. He has a baby. It blew his mind a little bit."

In late April, Pratt sent the man another letter. She had "no desire to push myself into your family," she wrote, nor make a financial claim. What she sought were stories about him and his family, to help her build a sense of where she came from. Just one meeting, a few hours, was all she asked.

She still hasn't heard back.

By early 2013, the Collins children were hot on the trail of a hundred-year-old mystery.

They had their father's birth certificate, indicating that he'd been born on Sept. 23, 1913. They wrote to his orphanage and learned that their dad had been sent there by the New York Society for the Prevention of Cruelty to Children.

Plebuch wondered if Jim Collins, just a baby at the time, had somehow been confused with another child when he was taken from his father's home.

She found a forensic artist said to be skilled in understanding how faces change over time. She sent her a picture of her dad sitting on his father's lap when he was about 11 months, along with photos of him as an adult. Were these of the same person?

Probably, the forensic artist ruled. The ears hadn't changed, and the mouth, chin and facial proportions seemed the same.

If the mystery of their father didn't begin with his parents' life in Ireland, nor with his own time in the orphanage, Plebuch and her sister concluded it must have happened shortly after Jim was born. Unusually for the era, his mother gave birth not at home but at Fordham Hospital in the Bronx.

Could something have happened there?

Wurts Bros./Museum of the City of New York

By this time, the sisters were using techniques developed by Moore and others to help adoptees try to find relatives in a vast universe of strangers' spit. Every time a site like 23andMe informed them of what Plebuch calls a "DNA cousin" on their Jewish side someone whose results suggested a likely cousin relationship they would ask to see that person's genome. If the person agreed, the site would reveal any places where their chromosomes overlapped.

The idea, Plebuch explains, was to find patterns in the data. A group of people who share segments on the same chromosome probably share a common ancestor. If Plebuch could find a group of relatives who all shared the same segment, she might be able to use that along with their family trees, family surnames, and ancestors' home towns in the old country to trace a path into her father's biological family.

The work was slow and painstaking, complicated by the fact that Ashkenazi Jews frequently marry within the group and often are related in multiple ways. This can make distant relatives look like a closer match than they actually are. But the sisters forged on, sending at least 1,000 requests for genome-sharing to DNA cousins through 23andMe. It became Plebuch's full-time job.

Some ignored their overtures, while others were drawn in by the saga and devoted their own efforts to helping the sisters untangle it. It was as if the Collins sisters had plugged into a larger family, a web of strangers who wanted to help because generations before, their ancestors had shared soup, shared heartache, slept in the same bed.

One DNA cousin made a clever suggestion: Why not search for evidence of a baby born around the same time under a common Jewish surname, Cohen? He reasoned that the nurses, perhaps relying on an alphabetical system, might have confused a Collins baby with a Cohen baby. CeCe Moore was by now volunteering to advise Plebuch, and with additional help from Tannenbaum and the New York City Birth Index of 1913, Plebuch found a Seymour Cohen born in the Bronx on Sept. 23. DNA cousins fanned out on the Internet, tracking down a descendant of Seymour's sister.

Plebuch wrote to the woman, a professor in North Carolina, and offered to pay for her test kit if she'd contribute something completely free and absolutely priceless: her saliva. The woman agreed.

Weeks later, the results came back. No relation.

After that red herring, Plebuch decided to dive deeper into the 1913 birth index, to find babies who were in the hospital at the same time as her father. It was no easy task: The list of children born in the Bronx in 1913 ran 159 pages, was not ordered by date, and didn't distinguish hospital births from home births. But she manage to isolate all the male children born on Sept. 23, as well as the day after and the day before. She further narrowed the list to names that sounded either Jewish or ethnically neutral 30 babies in all.

Her hope was that one of those babies would share a surname with one of the people that the DNA matching sites identified as a likely relative. So she searched methodically.

"Appel" nothing. "Bain" nothing. "Bamson" nothing.

It was another dead end.

The sisters went back to the chromosome segment matching, both at 23andMe and Family Tree DNA, where they had also uploaded their genetic data. They bought at least 21 DNA test kits for themselves, relatives and strangers suspected of being relations. Plebuch found she and her siblings matched to 6,912 likely DNA relatives, with 311,467 "segment matches" among them segments along the chromosomes that overlapped with those of the Collins children. Which is to say, 311,467 potential clues.

The data they had kept on spreadsheets quickly became overwhelming, so their brother Jim, a retired software and systems engineer who had worked on NASA supercomputers, designed an iPad app called DNAMatch to help them and other seekers keep their data straight.

Plebuch was determined, and unusually well suited to the task of solving a puzzle hidden in big data. She and Wiggins searched this way for two and a half years. But she was having no luck finding someone closely related to her father's biological family they simply weren't in the system.

Perhaps they didn't know about DNA testing, or couldn't afford it, or weren't interested.

All the sisters could do was keep working and waiting, hoping the DNA testing revolution would make its way to strangers who shared their blood.

---

Ultimately, the crack in the case came not through Plebuch's squad of helpful DNA cousins, but through a stranger with no genetic connection.

It was Jan. 18, 2015, a Sunday, and Plebuch was feeling down. She was writing an email to her cousin Pete Nolan the beloved relative it turned out she wasn't really related to to update him on her stalled search.

As administrator of his 23andMe account, she had permission to check the list of his DNA relatives yet rarely did so, since new relatives rarely showed up. But she decided to check it this day and this time, there was a new person. A stranger had just had her saliva processed, and she showed up as a close relative of Nolan.

Plebuch emailed the woman and asked if she would compare genomes with Nolan. The woman agreed, and Plebuch could see the segments where her cousin and the stranger overlapped. Plebuch thanked her, and asked if her results were what she expected.

"I was actually expecting to be much more Ashkenazi than I am," the woman wrote. Her name was Jessica Benson, a North Carolina resident who had taken the test on a whim, hoping to learn more about her Jewish ethnicity. Instead, she wrote, she had discovered "that I am actually Irish, which I had not expected at all."

Plebuch felt chills. She wrote back that her father had been born at Fordham Hospital on Sept. 23, 1913. Had anyone in the Benson family been born on that date?

Jessica replied. Her grandfather, Phillip Benson, might have been born around that date, she wrote.

Plebuch began to cry.

She started combing through her list of baby names from the 1913 Index. No "Benson" born that day in the Bronx. But then, well after midnight, she found it:

The New York City Birth Index had a "Philip Bamson," born Sept. 23 one of the names she had searched among her DNA cousins. This had to be Phillip Benson, his name misrecorded on his birth certificate.

Read the rest here:
She thought she was Irish until a DNA test opened a 100-year-old mystery - Chicago Tribune

Ok I managed to get them done. Woooh.

They are NON DEFAULT skins so you will need Rez Delnavas UI mod in order to use them.They come in Faces only OR the full set which includes my anatomical skins.They come in all base flesh tones and I added a bonus rainbow tone slider.

DOWNLOAD

FACES ONLY mediafire / 4shared

FULL FACE & BODY SET mediafire / 4sharedThese come with my child/toddler bodies and my busty st claire and male muscular bodies.

I hope you like them. If you think I can fix anything let me know and I will keep it in mind for v2. Let me know if I stuffed anything up as well

<3

Here are those full non-default packages you requested.I edited the male faces slightly to suit the female ones.

Let me know if I borked anything.

SILK / 4shared includes females faces, male silk faces, busty st claire and muscular bodies, Jack & Jill faces and bodies, Ladybug faces and bodies.

VELVET / 4shared includes females faces, male velvet faces, busty st claire and muscular bodies, Jack & Jill faces and bodies, Ladybug faces and bodies.

<3

Hey guys, here are the new faces Ive been working on. I started these because I wanted an alternative to my current Naughty & Nice face skins. The nose on those is rather defined in the tip area which makes very nice button noses but not much else. I also wanted to take the time to fix a few other issues on the originals. The eyelids were bothering me, for example, among other things.

So I came up with Silk, its a smoother, more highlighted less shaded version of my original faces. The entire nose length is smooth and highlighted and I have muted a lot of the shaded areas on the face, for example the eye socket area, undereyes and the cheeks. The lip texture was smoothed and softened and the eyelid area was neatened up with the tear-ducts scaled down slightly.

Here is Silk:

From then I started playing with the nostril area and I ended up with a face that had a more defined nostril. I couldnt decide which I preferred and I knew that some of you would like silk whilst others would like velvet, so I decided to publish both.

Here is Velvet:

Here is a comparison of the three skins:

The elder face skins were also smoothed out a little to match the Silk & Velvet YA skins. The noses were changed accordingly.

Both faces come in Default and Non-Default and will match up with my Naughty & Nice and my Busty St Clair body skins.They also have custom sliders which have the names printed on them. The dots are black & white and the sliders come in a range of colours.

DOWNLOAD:

Silk Non Default Mediafire / 4sharedSilk Default Mediafire / 4sharedVelvet Non Default Mediafire / 4sharedVelvet Default Mediafire / 4shared

If you have previously downloaded the full set of Default Naughty & Nice Face/Body skins and wish to use one of these faces instead, then I suggest you remove the Naughty & Nice full set and just install the bodies instead then you can choose which faces you like.

You can download one of these faces as your default if you wish, and you can also have the other as a non-default. At the moment I have my Naughty & Nice faces installed, my Busty st Claire bodies and I have Silk and Velvet as non-defaults.

Enjoy <3

Credits:Escands Oh My EyesCmarNYCs SkininatorRez Delnavas UI Mod needed for Non-Defaults

Read the original here:
Genetics LadyFrontbum

We females always knew we could have sex when asleep, not that we want to, and that men can't. It turns out the same applies to fruit flies.

A vast international study by multiple institutions one can't have too many studying woo-woo in fruit flies has concluded that when male Drosophila are sleep-deprived, their interest in courtship disappears.

When the female is bushed, nothing happens to their mating behavior.

One way to deprive a fruit fly of sleep, would seem to be to offer it sex. The team also realized that aroused male Drosophilae got little sleep. Sexually aroused females slept fine.

Given the nature of the beasts, animals have to choose between sex and sleep. At least, the males do they can't do both at the same time. Now scientists have found how the choice is regulated, at least in the fruit fly.

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"An organism can only do one thing at a time," states the team, with Prof. Michael Nitabach of Yale, an expert on molecular physiology and genetics, in Nature Communications. "What we have discovered is a neuronal connection that regulates the interplay between courtship and sleep."

What Nitabach and his colleagues from the Howard Hughes Medical Institute, the Southeast University in China, and the University of San Diego, did is to study the neuronal activity involved in sex and sleep. They found that sleep-deprived male flies lost interest in courtship, but the females' mating behavior was unaffected.

Darwin would be proud

The evolutionary explanation they offer is a trivial one. The males' behavior is easily explained as adaptive: Falling asleep during sex is not a good way to pass on your genes, they stated.

But, they wondered, why are females still receptive to male advances when sleepy? One possibility is that as the recipient, they can afford to be. Another, postulated by Nitabach, is that the females can't afford to pass up an eligible suitor. But there are a lot of fruit flies out there. Ostensibly, the females would seem to be spoiled for choice.

The team also found functional connections between the different nervous centers that mediate sex and sleep, they say. Nitabach's conclusion is that whichever behavior has the highest biological drive at a given moment physiologically suppresses the yen for the other behavior. Thus, when a boy fly wants sleep badly enough, it depresses his sex drive, and vice versa.

So, is the human drive for sex and the human desire for sleep also controlled by our neurons? Probably, at least to some degree. Just like the fruit fly, there are other factors in play.

Read the rest here:
When the male fruit fly gets a headache - Haaretz

WILLIAMSTOWN, Mass. Two grants from the National Science Foundation (NSF) will support ongoing research by Luana Maroja, associate professor of biology at Williams College, into evolutionary genetics. The grants, totaling $137,315, were recently approved by the NSF.

The grants will support two projects Maroja is working on related to speciation and genetics. The first grant, for $91,173, will support collaborative research Maroja and her students are undertaking with Cornell University on the importance of sex chromosomes in speciation, specifically looking at whether genes that do not transfer genetic information from one species to another during hybridization are concentrated on the X chromosome. The project will provide important insights into the genomic architecture of speciation, the role of the X chromosome in reproductive isolation and divergent adaptation, and will contribute to ongoing debates about how differentiation accumulates in genomes over time.

As part of the project, Maroja and her students will develop evolution workshops aimed to help educate middle and high school students.

The second grant of $46,142 will support a project in collaboration with Union College to understand processes that cause speciation. The project will test if chromosomal rearrangements (CRs) are involved in speciation using three distinct races of fruit flies. Maroja and her students will genetically map speciation phenotypes, male courtship song and female mating preferences for male song between two pairs of fruit fly races to determine certain traits are shared across the species. The project also will test whether CRs act to reduce gene exchange between nascent species by comparing patterns of genomic divergence inside CRs.

As part of this project, Maroja will develop evolution lab workshops aimed to help educate middle and high school students in Williamstown. She also will continue to develop workshops and labs for underserved girls and minorities in a partnership with the Flying Cloud Institute.

Maroja has taught at Williams since 2010. She has a bachelor's and master's degree from the Universidade Federal do Rio de Janeiro, and in 2008 she received a Ph.D. from Cornell.

View post:
Williams Professor Wins Grants to Study Evolutionary Genetics - iBerkshires.com

Grace D'ArcyAssistant News Editor

A landmark study by Trinity researchers has revealed a little more of the history of the Iberian people, giving more clarity to the impact migration had on the genetic makeup and culture of early Portuguese settlers.

This is the first time researchers have studied the impact of these migrations on this specific area of Europe and the the work by the two Trinity staff, in collaboration with colleagues in Portugal, enables scientists to examine the threads of European history and explain variations and similarities between geographic areas today.

Previous genome studies have found that it was often technological innovations in pre-history that were associated with profound population change. But this new research from Trinity sheds light on how these advancements influenced changes in the population at the edge of the Atlantic, revealing the key role of migration.

The genomes of individuals who lived on the Iberian Peninsula in the Bronze Age had minor genetic input from Steppe invaders, suggesting that these migrations played a smaller role in the genetic makeup and culture of Iberian people, compared to other parts of Europe. This likely had implications for the spread of culture, language and technology, with the relative lack of invasion possibly explaining why a pre-European language Euskera still exists in Iberia today.

Trinitys Prof Daniel Bradley and Prof Rui Martiniano worked with Ana Maria Silva of the University of Coimbra, Portugal, in developing the research. In a press statement, Bradley, the Professor of Population Genetics at Trinity, said: Unlike further north, a mix of earlier tongues and Indo-European languages persist until the dawn of Iberian history, a pattern, he said, that resonates with the real but limited influx of migrants around the Bronze Age.

Between the 4,200-3,500 BC and the Middle Bronze Age, central and northern Europe received a massive influx of people from the Steppe regions of Eastern Europe and Asia. Archaeological digs in Iberia have uncovered changes in culture and funeral rituals during this time, but no one had looked at the genetic impact of these migrations in this part of Europe before.

The researchers sequenced the genomes of 14 individuals who lived in Portugal during the Neolithic and Bronze Ages and compared them to other ancient and modern genomes. In contrast with other parts of Europe, they detected only subtle genetic changes between the Portuguese Neolithic and Bronze Age samples resulting from small-scale migration. However, these changes are more pronounced on the paternal lineage, which indicates a strong bias towards male migration in ancient times.

In a press statement, Martiniano, said: It was surprising to observe such a striking Y chromosome discontinuity between the Neolithic and the Bronze Age, such as would be consistent with a predominantly male-mediated genetic influx.

The researchers also estimated height from the samples, based on relevant DNA sequences, and found that European hunter-gatherers are significantly taller than their early Neolithic farming counterparts. Genetic input from Neolithic migrants decreased the height of Europeans, which subsequently increased steadily through later generations, due to increased interaction between populations.

Originally posted here:
Trinity Researchers Lead Analysis of Portugal and Spain's Genetic History - The University Times

The biggest history news stories of the week, including two pioneering genome studies that have shed fascinating new light on humanitys ancient past and its echoes in the present.

Present day Lebanese are descendants of Biblical Canaanites

A new genome study of ancient remains from the Near East suggests that present day Lebanese people are direct descendants of the Biblical Canaanites.

The research, which has been published in the American Journal of Human Genetics, sequenced the entire genomes of 4,000 year-old Canaanites who inhabited the region during the Bronze Age, and compared them to other ancient and present day populations.

Despite the Canaanites creating the first alphabet and establishing colonies throughout the Mediterranean, historians and archaeologists only have a limited knowledge of them. They are mentioned several times in the Bible, as well as in ancient Greek and Phoenician texts, but experts know little about their genetic identity, who their ancestors were, and if they have any descendants today.

The study by the researchers from the Wellcome Trust Sanger Institute determined that more than 90% of present Lebanese ancestry is likely to be from the Canaanites, with a small proportion coming from a different Eurasian population. The researchers estimate that new Eurasian people mixed with the Canaanite population about 2,200 to 3,800 years ago at a time when there were many conquests of the region from outside.

Details about the Canaanites own ancestry have also been revealed. The study claims that they were a mixture of local people who settled in farming villages during the Neolithic period and eastern migrants who arrived in the area around 5,000 years ago.

For the first time we have genetic evidence for substantial continuity in the region, from the Bronze Age Canaanite population through to the present day. Dr Claude Doumet-Serhal, co-author of the study and Director of the Sidon excavation site in Lebanon, said.

These results agree with the continuity seen by archaeologists. Collaborations between archaeologists and geneticists greatly enrich both fields of study and can answer questions about ancestry in ways that experts in neither field can answer alone.

Meanwhile, Dr. Chris Tyler-Smith, lead author from the Wellcome Trust Sanger Institute, said: Genetic studies using ancient DNA can expand our understanding of history, and answer questions about the likely origins and descendants of enigmatic populations like the Canaanites, who left few written records themselves.

Now we would like to investigate the earlier and later genetic history of the Near East, and how it relates to the surrounding regions.

Bronze Age Iberia spared the brunt of Steppe invaders

New DNA analysis of people who lived in the Iberian Peninsula during the Bronze Age has revealed that they received only minor genetic input from Steppe invaders, suggesting the Steppe migrations played less of a role in the cultural and genetic makeup of Iberian people than they did in populations elsewhere in Europe.

Between the Middle Neolithic (4200-3500 BCE) and the Middle Bronze Age (1740-1430 BCE), Central, Northwestern and Northern Europe received a massive influx of people from the Steppe regions of Eastern Europe and Asia. Archaeological digs have gained insights into some of the impacts of these influxes on Iberia, in the form of changing cultural practices and funeral rituals, but the genetic effect has remained hitherto unexamined.

The genomes of fourteen people who lived in Portugal in the Neolithic and Bronze Age were sequenced for the study, which has been published in the journal PLOS Genetics. These genomes were then compared with other ancient and modern genetic data, revealing only subtle changes between the Portuguese Neolithic and Bronze Age DNA, suggesting a minor genetic influence from the Steppe. Surprisingly, the changes were significantly more pronounced in paternal lineage.

It was surprising to observe such a striking Y chromosome discontinuity between the Neolithic and the Bronze Age, such as would be consistent with a predominantly male-mediated genetic influx says first author Rui Martiniano. Height was also estimated from the samples, based on relevant DNA sequences, revealing that genetic input from Neolithic migrants decreased the height of Europeans, which subsequently increased steadily through later generations.

By showing that migration into the Iberian Peninsula occurred on a much smaller scale than elsewhere in Europe, the study raises questions about the impact this had on language, culture and technology. For example, the fact that the Basque region of Spain speaks a pre-Indo-European language could be explained by these findings. The discovery also supports a theory which says Indo-European languages spread through Europe from the Steppe heartland.

The study was carried out by Daniel Bradley and Rui Martiniano of Trinity College Dublin, in Ireland, and Ana Maria Silva of University of Coimbra, Portugal.

New project aims to highlight importance of The Indian Army in the First World War

In the UK, The Soldiers of Oxfordshire (SOFO) Museum and Oxford Universitys History Faculty have received a 12,000 grant from the Arts & Humanities Research Council Voices of War & Peace WWI Engagement Centre, for their project titled: The Indian Army in the First World War: An Oxfordshire & Buckinghamshire Perspective.

The project aims to shed new light on the British Indian Armys role in the war on the Eastern Front in Iraq through an outreach programme and touring exhibition. Sikhs, Muslims and Hindus of all ages in the local community are being called upon to engage with researchers by sharing stories, experiences and memorabilia. The touring exhibition will then showcase the findings in November.

Photographs that have never been displayed before will explore the experiences of British and Indian soldiers in the conflict, as well as the Iraqi prisoners.

Featured image: Archaeological remains of individual MC337 excavated from the site of Hipogeu de Monte Canelas I, Portugal, and analysed by the archaeologist Rui Parreira and the anthropologist Ana Maria Silva. Courtesy of Rui Parreira

Link:
History News of the Week: The Biblical Canaanites' Modern Descendants - New Historian

A startling new review of sperm production finds that men throughout most of the industrialized world have seen, in aggregate, a 52 percent decline in sperm count over the last generation and a half with exposure to endocrine-disrupting environmental pollution the probable cause.

A sweeping meta-analysis of data from nearly 200 individual studies, the research does not directly attribute the decline to any particular cause, and it notes that many factors are capable of driving down sperm production, especially in the short term.

However, it lists environmental pollution particularly so-called endocrine disruptors, which can act like estrogen in males as the most prominent explanation for this widespread, 38-year-long decline, which one expert is calling a death spiral of infertility in men.

The team, led by Hagai Levine of Hadassah-Hebrew University in Jerusalem, reviewed more than 2,500 articles reporting primary data on sperm counts in men around the world. After excluding research on men selected for study because they were known to have fertility problems, or factors specifically associated with lower sperm production, they assembled for meta-analysis a set of 185 studies of nearly 43,000 men who gave samples between 1973 and 2011.

From these results, they calculate that sperm counts declined by 50 to 60 percent among men in North America, Europe, Australia and New Zealand. Men in South America, Africa and Asia did not show comparable declines, but the authors explain that data for these regions was not comparable in quantity or quality, especially before 1985.

In addition to the obvious problem of reduced fertility, their paper notes that lowered sperm counts are associated with a variety of medical conditions, pointing to a likelihood of diminished health and a shorter lifespan.

As for the probable causes of such a steep decline, the authors say

While the current study is not designed to provide direct information on the causes of the observed declines, sperm count has been plausibly associated with multiple environmental and lifestyle inuences, both prenatally and in adult life. In particular, endocrine disruption from chemical exposures or maternal smoking during critical windows of male reproductive development may play a role in prenatal life, while lifestyle changes and exposure to pesticides may play a role in adult life. Thus, a decline in sperm count might be considered as a canary in the coal mine for male health across the lifespan. Our report of a continuing and robust decline should, therefore, trigger research into its causes, aiming for prevention.

The sheer scope of the data gathered for analysis here would seem to address neatly the objections of some skeptics of sperm-count decline including, for one recent example, the cancer epidemiologist Geoffrey Kabat, writing in Forbes a few months ago that sperm-count studies are too small or narrow to reliably factor out the normal variability that occurs from place to place and time to time, in response to all kinds of environmental influences and individual behaviors.

Published on Tuesday in the journal Human Reproduction Update, the study follows by one week another study which apparently and amazingly is the first to test for cumulative endocrine-disruption effects from chemical exposure across successive generations.

The study looked at sperm production and abnormalities of the reproductive tracts in male mice. Its chilling conclusion: The impacts are worse in the second generation than the first, and worse still in the next, with some third-generation mice producing no sperm at all.

Though potentially more significant, in my view, this paper has gotten far less attention than the Levine research; I first saw it referenced in Environmental Health News in a piece by Pete Myers, a Ph.D. biologist who co-wrote the early and influential book on endocrine disruption, Our Stolen Future, published in 1996.

Myers is the founder and chief scientist at EHN, a daily online publication that does original reporting on environmental health science while aggregating, annotating and critiquing reporting done elsewhere. In his view, the two studies taken together mean you should be worried and your kids should be terrified.

The intergenerational study was published last Thursday in the journal PLOS Genetics, and looked at abnormalities in the reproductive tracts of male mice and two generations of their male offspring. It aimed to answer what lead researcher Tegan Horan, a doctoral student at Washington State University told Myers she saw as a simple question with real-world relevance that had simply never been addressed."

Here is Myers terse summary of the research context:

Since World War II, successive generations of people have been exposed to a growing number and quantity of environmental estrogens chemicals that behave like the human hormone estrogen. Thousands of papers published in the scientific literature (reviewed here) tie these to a wide array of adverse consequences, including infertility and sperm count decline.

This phenomenon exposure of multiple generations of mammals to endocrine disrupting compounds had never been studied experimentally, even though that's how humans have experienced EDC exposures for at least the last 70 years. That's almost three generations of human males.

More than a dozen papers have now been published on "trans-generational epigenetic inheritance," where exposure in a great-grandmother causes adverse effects in great-grandson without further exposures and without changes in DNA sequence. But crucially these experiments typically only expose one generation the first rather induce ongoing exposures across generations, which is the reality of human experience.

Reaction to the Levine study has been positive, both on the quality of its findings and their importance, with many in the scientific community endorsing its tentative attribution of the problem to environmental exposure.

Allen Pacey, an andrologist at Britains Sheffield University, told the BBC that "I've never been particularly convinced by the many studies published so far claiming that human sperm counts have declined in the recent past. However, the study today by Dr Levine and his colleagues deals head-on with many of the deficiencies of previous studies."

Frederick vom Saal, Curators Distinguished Professor Emeritus of Biological Sciences at the University of Missouri, told Myers that "the study is a wakeup that we are in a death spiral of infertility in men."

And Enrique Schisterman of the National Institutes of Health, where he serves as chief of the epidemiology branch at the National Institute of Child Health and Human Development, told Time magazine that Levines work represented a significant advance and pointed to a serious problem.

I think there is a consensus in the scientific community that if the results are real, it has to be an environmental factor. Genetics would not explain such a rapid decline.

* * *

Both papers can be read and downloaded without charge; the Levine paper on sperm counts is here and the Horan paper on reproductive abnormalities in successive generations is here.

Read more from the original source:
Falling sperm counts are linked to endocrine-disrupting chemicals - MinnPost

Illustration by Luisa Rivere/Yale E360

The worldwide effort to return islands to their original wildlife, by eradicating rats, pigs, and other invasive species, has been one of the great environmental success stories of our time.Rewilding has succeeded on hundreds of islands, with beleaguered species surging back from imminent extinction, and dwindling bird colonies suddenly blossoming across old nesting grounds.

But these restoration campaigns are often massively expensive and emotionally fraught, with conservationists fearful of accidentally poisoning native wildlife, and animal rights activists having at times fiercely opposed the whole idea. So what if it were possible to rid islands of invasive species without killing a single animal? And at a fraction of the cost of current methods?

Thats the tantalising but also worrisome promise of synthetic biology, aBrave New Worldsort of technology that applies engineering principles to species and to biological systems. Its genetic engineering, but made easier and more precise by the new gene editing technology called CRISPR, which ecologists could use to splice in a DNA sequence designed to handicap an invasive species, or to help a native species adapt to a changing climate. Gene drive, another new tool, could then spread an introduced trait through a population far more rapidly than conventional Mendelian genetics would predict.

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Synthetic biology, also called synbio, is already a multi-billion dollar market, for manufacturing processes in pharmaceuticals, chemicals, biofuels, and agriculture. But many conservationists consider the prospect of using synbio methods as a tool for protecting the natural world deeply alarming. Jane Goodall, David Suzuki, and others havesigned a letterwarning that use of gene drives gives technicians the ability to intervene in evolution, to engineer the fate of an entire species, to dramatically modify ecosystems, and to unleash large-scale environmental changes, in ways never thought possible before.The signers of the letter argue that such a powerful and potentially dangerous technology should not be promoted as a conservation tool.

Environmentalists and synthetic biology engineers need to overcome what now amounts to mutual ignorance, a conservationist says.

On the other hand, a team of conservationbiologists writing early this yearin the journalTrends in Ecology and Evolutionran off a list of promising applications for synbio in the natural world, in addition to island rewilding:

Transplanting genes for resistance to white nose syndrome into bats, and for chytrid fungus into frogs and other amphibians.

Giving corals that are vulnerable to bleaching carefully selected genes from nearby corals that are more tolerant of heat and acidity.

Using artificial microbiomes to restore soils damaged by mining or pollution.

Eliminating populations of feral cats and dogs without euthanasia or surgical neutering, by producing generations that are genetically programmed to be sterile, or skewed to be overwhelmingly male.

And eradicating mosquitoes without pesticides, particularly in Hawaii, where they are highly destructive newcomers.

Kent Redford, a conservation consultant and co-author of that article, argues that conservationists and synbio engineers alike need to overcome what now amounts to mutual ignorance. Conservationists tend to have limited and often outdated knowledge of genetics and molecular biology, he says.Ina 2014 articleinOryx, he quoted one conservationist flatly declaring, Those were the courses we flunked. Stanford Universitys Drew Endy, one of the founders of synbio, volunteers in turn that 18 months ago he had never heard of the IUCN the International Union for Conservation of Nature or its Red List of endangered species.In engineering school, the ignorance gap is terrific, he adds.But its symmetric ignorance.

At a major synbio conference he organised last month in Singapore, Endy invited Redford and eight other conservationists to lead a session on biodiversity, with the aim, he says, of getting engineers building the bioeconomy to think about the natural world ahead of time My hope is that people are no longer merely nave in terms of their industrial disposition.

Likewise, Redford and the co-authors of the article inTrends in Ecology and Evolution, assert that it would be a disservice to the goal of protecting biodiversity if conservationists do not participate in applying the best science and thinkers to these issues. They argue that it is necessary to adapt the culture of conservation biologists to a rapidly-changing reality including the effects of climate change and emerging diseases.Twenty-first century conservation philosophy, the co-authors conclude, should embrace concepts of synthetic biology, and both seek and guide appropriate synthetic solutions to aid biodiversity.

Through gene drive technology, mice, rats or other invasive species can theoretically be eliminated from an island without killing anything.

The debate over synthetic biodiversity conservation, as theTrends in Ecology and Evolutionauthors term it, had its origins in a2003 paperby Austin Burt, an evolutionary geneticist at Imperial College London.He proposed a dramatically new tool for genetic engineering, based on certain naturally occurring selfish genetic elements, which manage to propagate themselves in as much as 99 percent of the next generation, rather than the usual 50 percent. Burt thought that it might be possible to use these super-Mendelian genes as a Trojan horse, to rapidly distribute altered DNA, and thus to genetically engineer natural populations. It was impractical at the time.Butdevelopmentof CRISPR technology soon brought the idea close to reality, and researchers have since demonstrated the effectiveness of gene drive, as the technique became known, in laboratory experiments on malaria mosquitoes, fruit flies, yeast, and human embryos.

Burt proposed one particularly ominous-sounding application for this new technology: It might be possible under certain conditions, he thought, that a genetic load sufficient to eradicate a population can be imposed in fewer than 20 generations. And this is, in fact, likely to be the first practical application of synthetic biodiversity conservation in the field. Eradicating invasive populationsis of coursethe inevitable first step in island rewilding projects.

The proposed eradication technique is to use the gene drive to deliver DNA that determines the gender of offspring.Because the gene drive propagates itself so thoroughly through subsequent generations, it can quickly cause a population to become almost all male and soon collapse.The result, at least in theory, is the elimination of mice, rats, or other invasive species from an island without anyone having killed anything.

Research to test the practicality of the method including moral, ethical, and legal considerations is already under way through a research consortium ofnonprofitgroups, universities, and government agencies in Australia, New Zealand, and the United States.At North Carolina State University, for instance, researchers have begun working with a laboratory population of invasive mice taken from a coastal island.They need to determine how well a wild population will accept mice that have been altered in the laboratory.

The success of this idea depends heavily,according togene drive researcher Megan Serr, on the genetically modified male mice being studs with the island lady mice Will she want a hybrid male that is part wild, part lab? Beyond that, the research programme needs to figure out how many modified mice to introduce to eradicate an invasive population in a habitat of a particular size. Other significant practical challenges will also undoubtedly arise.For instance,a study early this yearin the journalGeneticsconcluded that resistance to CRISPR-modified gene drives should evolve almost inevitably in most natural populations.

Political and environmental resistance is also likely to develop.In an email, MIT evolutionary biologist Kevin Esvelt asserted that CRISPR-based gene drives are not suited for conservation due to the very high risk of spreading beyond the target species orenvironment. Even a gene drive systemintroduced toquickly eradicate an introduced population from an island, he added, still is likely to have over a year to escape or be deliberately transported off-island. If it is capable of spreading elsewhere, that is a major problem.

Even a highly contained field trial on a remote island is probably a decade or so away, said Heath Packard, of Island Conservation, a nonprofit that has been involved in numerous island rewilding projects and is now part of the research consortium.We are committed to a precautionary step-wise approach, with plenty of off-ramps, if it turns out to be too risky or not ethical.But his group notes that 80% of known extinctions over the past 500 or so years have occurred on islands, whicharealso home to 40% of species now considered at risk of extinction. That makes it important at least to begin to study the potential of synthetic biodiversity conservation.

Even if conservationists ultimately balk at these new technologies, business interests are already bringing synbio into the field for commercial purposes.For instance, a Pennsylvania State University researcher recently figured out how to use CRISPR gene editing to turn off genes that cause supermarket mushrooms to turn brown.The USDepartment of Agriculturelast year ruledthat these mushrooms would not be subject to regulation as a genetically modified organism because they contain no genes introduced from other species.

With those kinds of changes taking place all around them, conservationists absolutely must engage with the synthetic biology community, says Redford, and if we dont do so it will be at our peril. Synbio, he says, presents conservationists with a huge range of questions that no one is paying attention to yet.

This article originally appeared on Yale Environment 360 and is republished here with permission.

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Should genetic engineering be used as a tool for conservation? - chinadialogue

A group of scientists in Oregon has successfully modified the genes of embryos using CRISPR, a cut-and-paste gene-editing tool.

The experiments, which have not yet been subject to peer review, were conducted by biologist Shoukhrat Mitalipov and colleagues at Oregon Health & Science University in Portland, MIT Technology Review reported. Mitalipov conducted the experiments on dozens of single-celled embryos, which were discarded before they could progress very far in development, according to Technology Review. This is the first time that scientists in the United States have used this approach to edit the genes of embryos.

The CRISPR/Cas9 gene-editing system is a simple "cut and replace" method for editing precise spots on the genome. CRISPRS are long stretches of DNA that are recognized by molecular "scissors" called Cas9; by inserting CRISPR DNA near target DNA, scientists can theoretically tell Cas9 to cut anywhere in the genome. Scientists can then swap a replacement gene sequence in the place of the snipped sequence. The replacement sequence then gets automatically incorporated into the genome by natural DNA repair mechanisms.

In 2015, a group in China used CRISPR to edit several human embryos that had severe defects, though none were allowed to gestate very long before being discarded. If rumors are to be believed, the new results are more promising than those earlier efforts, according to Technology Review. The Chinese technique led to genetic changes in some, but not all of the cells in the embryos, and CRISPR sometimes snipped out the wrong place in the DNA. According to Technology Review, the new technique was used in dozens of embryos that were created for in vitro fertilization (IVF), using the sperm of men who had severe genetic defects.

In general, editing the germ line meaning sperm, eggs or embryos has been controversial, because it means permanently changing the DNA that is passed on from one generation to the next. Some scientists have called for a ban on germ-line editing, saying the approach is incredibly risky and ethically dubious.

However, a National Academy of Sciences report published earlier this year suggested that embryo editing could be ethical in the case of severe genetic diseases.

Originally published on Live Science.

Link:
Scientists Use CRISPR to Edit Human Embryos - Live Science

For the first time, scientists in the US have successfully edited the DNA of viable human embryos using the powerful gene-editing tool CRISPR, according to a report by MIT Technology Review. Gaining the ability to edit human DNA is the first step toward one day allowing scientists to prevent babies from being born with incurable diseases or disabilities. But further success with this kind of research is likely to raise the heated discussion on the ethical implications of genetically altering human embryos.

The research which has yet to be published was led by Shoukhrat Mitalipov of Oregon Health and Science University. It involved editing a large number of viable embryos and effectively correcting disease-causing genes, according to MIT Technology Review. (Its unclear exactly how many embryos were edited, or which genes.) The embryos were developed for only a few days and were not implanted. Without implantation, embryos cannot develop into babies.

Human embryos have been edited with CRISPR before, only in China. In the US, this kind of research is much more controversial: theres even a ban on using National Institutes of Health funding for research using gene-editing technologies in human embryos. In February, however, a committee created by the National Academy of Sciences and the National Academy of Medicine endorsed the use of genetic engineering on human embryos when there isnt a reasonable alternative available, and only to eliminate serious diseases.

There are many concerns around genetically engineering humans. CRISPR is a very precise gene-editing tool, but it can sometimes lead to editing errors. So some fear that small mistakes could lead to permanent problems in the human gene pool. There are also ethical concerns: bioethicists fear that gene-editing will lead to a world where parents will be able to customize their own designer baby, complete with specific traits.

These super-baby concerns could be worked out easily, says Arthur Caplan, a bioethicist at New York University. If you dont want eugenics, you just draw a line and stop there, Caplan tells The Verge. Scientists and bioethicists should agree on rules on what should and should not be done, and then make sure that editors of scientific journals enforce them. Research into how to create designer babies should not be published. Or you could have the National Academy of Sciences work with industry and Congress to lay out a review committee and permit funding.

If America were to take the lead both in terms of working with journals, working with private foundations, with patient groups, and working with state and federal government, I think youd get collaboration from the rest of the world, Caplan says.

Engineered humans are still far away into the future. But Mitalipovs research is getting us closer: he and his team were able to edit the embryos precisely, with very few editing errors, according to STAT. They also avoided another problem: in experiments in China, the desired DNA changes were picked up only by some cells, not all the cells of an embryo an effect called mosaicism. That makes gene-editing unsafe. But Mitalipov was able to significantly reduce mosaicism, according to MIT Technology Review.

Some in the field questioned just how groundbreaking the research is. Hank Greely, a law professor and bioethicist at Stanford University, tweeted that the real breakthrough will be when someone actually implants the human embryos, so they can develop into human beings.

Regardless, the research shows just how far gene editing has come and makes the prospect of engineered, disease-free humans more science fact than science fiction.

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Human embryos reportedly edited for first time in the US using CRISPR - The Verge

An artists conception of the DNA-cutting enzyme Cas9.

By Jon CohenJul. 26, 2017 , 9:00 AM

The University of California (UC) has fired another legal salvo in the prolonged patent battle over CRISPR, the revolutionary gene-editing technology that has spawned a billion-dollar industry.

UC leads a group of litigants who contend that the U.S. Patent Trial and Appeal Board (PTAB) wrongly sided with the Broad Institute in Cambridge, Massachusetts, and two partnersHarvard University and the Massachusetts Institute of Technology in Cambridgein February when it ruled that the Broad group invented the use of CRISPR in eukaryotic cells. After that ruling, UC moved the battleground to the U.S. Court of Appeals for the Federal Circuit. In a 25 July brief to the Federal Circuit, the UC group contends that PTAB ignored key evidence and made multiple errors.

The UC litigants indisputably first showed in 2012 that CRISPR could work in DNA of simpler organisms, and soon after filed a patent application on the gene-editing technique. They claim the Broad group learned from that disclosed invention and applied CRISPR to eukaryotic cells. The essential legal question is whether the Broads patent application is a novel, patentable invention, or whether it was obvious in the sense that anyone skilled in the artin other words, any trained molecular biologistwould have a reasonable expectation of success of using the CRISPR system to edit genes in eukaryotic cells.

The UC group contends PTAB ignored key decisions on these general questions made by the U.S. Supreme Court and the Federal Circuit. It reiterated its long-held claim that applying CRISPR to eukaryotic cells was so obvious that six different labs did it in the same time frame, which it complains the PTAB essentially dismissed as irrelevant. And its brief notes that patent examiners rejected similar eukaryotic cell CRISPR patent applications from Sigma-Aldrich and ToolGenfiled before the Broads patent applicationbecause it made claims that were non-novel or obvious in light of UCs disclosed work.

Jacob Sherkow,an intellectual property attorney at the New York Law School in New York City who has closely followed each round in the fierce battle, says the UC groups brief at times overplays these mistakes relative to the PTAB's analysis. He notes that the PTABs decision was thorough and the standards to overturn its decisions are high. While there were some interesting chestnuts in its briefsuch as UC pointing out that the PTAB virtually ignored some important patents pending at the time [the Broad] patent was filedI don't think that's going to be enough to win the day [for] UC, he says.

In a statement, the Broad Institutesuggested the UC will not prevail in its challenge:

Notably, the [UC]brief hinges on its argument that, although [UC]s work simply involved characterizing a purified enzyme in a test tube, it rendered obvious that genome editing could be made to work in living mammalian cells.

This is inaccurate, as the PTAB noted repeatedly in its decision.

Updated, 7/26/2017, 12:33 p.m.: Statement from the Broad Institute added.

View original post here:
Ding, ding, ding! CRISPR patent fight enters next round | Science ... - Science Magazine

Mike Feibus/ Special for USA Today Published 9:00 a.m. ET July 24, 2017

Humans had better be ready to play God. Because weve now got the tools to do just that.

Credit the recent discovery of CRISPR-Cas9, a powerful gene-editing tool that gives scientists the ability to make precise edits of single strands of DNA. Other so-called molecular scissors had already been developed, but they were very costly and time-consuming to implement. The emergence of CRISPR has put genomics exploration into overdrive with quick, precise and cheap tools, sending science on a fast track to new discoveries.

CRISPR could be used to erase and replace mutations that make some susceptible to a wide range of conditions, from AIDS to the Zika virus. Healthier, more resilient farm animals, pets, fruits and vegetables are also in the hopper.

Billions of dollars are being poured into CRISPR research, precisely because the possibilities are seemingly endless. Start-ups have sprouted around CRISPR pioneers, including CRISPR Therapeutics, Editas Medicine, eGenesis, Intellia Therapeutics and Synthego. Last year, three of them went public, each IPO resulting in valuations in excess of $500 million.

Earlier this month, Harvard University researchers revealed that they actually used CRISPR to etch a motion GIF of a galloping horse into the DNA of living bacteria. Not exactly a cure for cancer, to be sure. Though it does raise some intriguing possibilities for using DNA to store non-genetic data, like a built-in human flash drive. As well, the demonstration does serve as a good illustration for just how much editing prowess CRISPR affords.

Laboratory fun aside, keeping a lid on CRISPR will be paramount, as it is just as potent a tool for evil as it is for good. CRISPR could potentially pave the way for bad actors on the world stage to develop, say, chemical weapons alongside super-soldiers resistant to them.

Such doomsday scenarios keep some scientists up at night, in much the same way that Albert Einstein fretted over the shape of our future in a nuclear world and former Intel CEO Andy Grove feared for our privacy and security in the early days of the Internet boom.

Indeed, with the global WannaCry ransomware attack and North Koreas ever-present march to intercontinental nuclear attack capability as a backdrop, effectively locking down CRISPR technology to prevent catastrophe could become as crucial to our own survival as the cures it spawns.

And we havent even touched on the ever-present fear of the unintended consequences of going where no man has gone before. What if, say, the Harvard researchers inadvertently created a deadly, drug-resistant, mother-of-all mutant bacteria with their artistic demonstration? That issue came to the fore in late May not with horses, but with mice.

Two blind mice, in fact. In 2015, researchers successfully restored the mices sight using CRISPR to repair a gene mutation that causes blindness. In a follow-up study, disclosed May 30in a letter to the editor of a health journal, researchers found hundreds of unintended mutations throughout the mices genome. The researchers noted that the mice did not exhibit any ill effects as a result.

The news spooked investors, who sent shares of the publicly-traded CRISPR stocks downward. As well, it also spurred some observers to wonder aloud whether we are ready to handle our newfound godlike powers.

The news didnt concern many scientists, however. Most of them understand the process of discovery is rarely a straight line. And bumps in the road like the errant mutations found in the follow-up study are all part of the journey. Some even assert that many of the mutations wouldnt occur today, because the circa-2015 CRISPR tools the researchers used are as outmoded as VCRs. They feel confident that, by the time you head to the doctor for some gene-editing to wipe away your ailments, theyll have it all ironed out.

Lets hope so. Because if not, Galloping Horse Syndrome would be the least of our problems.

Mike Feibus is principal analyst at FeibusTech, a Scottsdale, Ariz., market strategy and analysis firm focusing on mobile ecosystems and client technologies. Reach him atmikef@feibustech.com. Follow him on Twitter @MikeFeibus.

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CRISPR gene editing tool: Are we ready to play God? - USA TODAY

Those who keep track of current science news, scientists and nonscientists alike, have probably found themselves asking aloud very often is there anything CRISPR cant do? So far, it would seem the answer to that question is "no" as a team of investigators from Schepens Eye Research Institute of Massachusetts Eye and Ear have found a new area for CRISPR interventionangiogenesis of the retina. The scientists were able to prevent the development of angiogenesis in mice, which often causes vision loss and blindness and is a feature of several degenerative eye conditions, including proliferative diabetic retinopathy (PDR), wet age-related macular degeneration (AMD), and retinopathy of prematurity (ROP).

Findings from the new studypublished recently in Nature Communications in an article entitled Genome Editing Abrogates Angiogenesis In Vivocould potentially lead to the development of new therapies for eye conditions marked by pathological intraocular angiogenesis.

"We know that vascular endothelial growth factor receptor 2 (VEGFR2) plays an essential role in angiogenesis," explained senior study investigator Hetian Lei, Ph.D., assistant professor of ophthalmology at Harvard Medical School and assistant scientist at Schepens Eye Research Institute of Massachusetts Eye and Ear. "The CRISPR/Cas9 system can be utilized to edit the VEGFR2 gene, preventing intraocular pathological angiogenesis."

Even with the success of several VEGF-inhibiting agents in reducing neovascular growth and lessening vascular leakage in retinal diseases such as PDR and AMD, several therapeutic challenges remainnamely a need for sustained treatment and a modality to treat the sizeable number of patients who do not respond to anti-VEGF therapies.

Clinically, many vision disorders present when blood vessels within the retina begin to grow new, abnormal blood vessels on the surface of the retina. As the damage progresses, these vessels can leak, rupture, or cause retinal detachment, leading to impaired vision. In the current study, the investigators decided to use the CRISPR/Cas9 system to target the VEGFR2 gene in mice, with the hope of preventing the start of angiogenesis.

...we report that a system of adeno-associated virus (AAV)-mediated clustered regularly interspaced short palindromic repeats (CRISPR)-associated endonuclease (Cas)9 from Streptococcus pyogenes (SpCas9) is used to deplete VEGFR2 in vascular endothelial cells (ECs), whereby the expression of SpCas9 is driven by an endothelial-specific promoter of intercellular adhesion molecule 2, the authors wrote. We further show that recombinant AAV serotype 1 (rAAV1) transduces ECs of pathologic vessels, and that editing of genomic VEGFR2 locus using rAAV1-mediated CRISPR/Cas9 abrogates angiogenesis in the mouse models of oxygen-induced retinopathy and laser-induced choroid neovascularization.

Amazingly, the research team was able to prevent retinal angiogenesis in the preclinical models using only a single injection of the AAV/CRISPR therapy. The investigators were excited by their findings and are optimistic that their study will lead to future strategies using genome-editing tools to vision loss disorders.

"As this genomic editing gains traction in virtually all medical fields, we are cautiously optimistic that this powerful tool may present a novel therapy to prevent vision loss in eye disease marked by intraocular pathological angiogenesis," Dr. Lei concluded. "While further study is needed to determine safety and efficacy of this approach, our work shows that the CRISPR/Cas9 system is a precise and efficient tool with the potential to treat angiogenesis-associated diseases."

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CRISPR Prevents Beginning Stage of Vision Loss - Genetic Engineering & Biotechnology News

I walked into Camp East Woods in Oyster Bay, Long Island, about twenty minutes before class started. Dozens of kids, from four years old to sophomores in high school, were trying to figure out where their friends were, checking different rooms to see who had arrived. It smelled like sunscreen and sweat.

I was there for the Serious Science program, where kids of all ages get to explore everything from biochemistry to engineering. The syllabus included CRISPR, the powerful gene editing technology that allows you to cut out and change specific sections of DNA. Researchers are using it to battle things like HIV, blindness, and malaria, just to name a few.

CRISPR is all the rage in the scientific community, and I was curious how Jane Powel, who leads the program, planned to teach this crucial subject to young kids. When new science makes its way into mainstream conversations, especially powerful science like CRISPR, those discussions can suffer when there's a significant gap in knowledge between researchers and the public. Without everyone at the table, conversations can become tainted with confusion, fear, and impulsive decisions. And that education has to start pretty early.

At the classroom that day, I expected such a complicated experiment and nuanced topic would require a very structured day, a really clear plan, and lots of guidance. I was wrong.

Students discussing the CRISPR experiment with Powel. Image: Michael Fairchild

Once class started, Powel quickly dove into a discussion of CRISPR, introducing it with a frequently used metaphor that compares it to the process of deleting and replacing a mistake that you've typed on the computer. There were a couple dozen or so kids in the room, all listening closely, and they jumped to answer any questions Powel posed to them.

While they named different things that you might want to cut from a genomelike genes that lead to higher risks of cancer or those that cause muscular dystrophyPowel asked the students if there were any potential issues with CRISPR that scientists might want to consider alongside all of the good that might come of it. A nine-year-old named Evan immediately raised his hand to point out that it's possible other parts of DNA could be damaged aside from the region you're trying to fix.

"Sometimes it sounds like a great idea to cut and paste and edit DNA, and other times it sounds like it might have a bad consequence that we weren't even thinking of," Powel agreed.

After the discussion, the classroom broke into groups and the students went off to do their activities. Some wanted to fly drones, helicopters, hovercrafts, and remote control airplanes. Others were going to drive an electric car that a student's uncle had built and lent to the camp. Another group went to pick flowers, dissect them, and look at their parts under a microscope.

I sat down with the group getting ready to perform the CRISPR experiment, which would involve them transforming a harmless bacteria's DNA to make it resistant to an antibiotic. Five girls were at the table. There was Despina, a soft-spoken sophomore in high school who got interested in genetics from a biology class in school. And three 11-year-oldsAvery, Cristabella, and Darshini. Nine-year-old Brinley was the youngest of the group.

A student mixes agar to be poured into plates. Image: Mallory Locklear

In the day's experiment, the campers would grow cultures of E. coli, bacteria that are usually susceptible to the antibiotic Streptomycin. And the following day, they would take that fresh bacteria and treat it with chemicals that would allow the CRISPR/Cas9 complex to enter the bacterial cells, and then cut out and replace the part of the E. coli DNA that binds to Streptomycin. If successful, the E.coli should then be able to grow on plates treated with the antibiotic instead of being killed, something it normally can't do.

As the students got into the nitty gritty of the day's work, Powel broached the ethics conversation again. "Everybody's excited about this, but people are worried about it too," she said, "Because just as Evan said, sometimes you can think you're doing a good thing and you're really not. Or there are some people who want to do bad things."

Some of the concerns with CRISPR tap into questions surrounding consent, reach, and unintended effects. For example, knocking malaria out of an entire mosquito population sounds like a net positive, but could also make those insects more susceptible to carrying other disease. Additionally, making changes to DNA with CRISPR impacts not only the organism or person, but its progeny as well.

That also brings up the issue of consent. Sure, someone may not have any issues with having their own disease-causing genes snipped out while they were in the womb, but going beyond that and making changes that aren't survival-related, what about the choices of the individual and their descendants?

Plates of bacteria. Image: Mallory Locklear

"Now you have this very powerful tool, so that's why it's so important that you guys learn about this and use it for good," Powel said. "And know what's going on when you hear news and be able to think critically."

Educators across the country are starting to incorporate CRISPR, and these lessons in genetic literacy, into their teachings. Michael Hirsch, who teaches science to 6th to 8th graders at the Acera School in Massachusetts, introduced CRISPR into his curriculum this past year. He also brought up its ethical aspects with his students.

"No one in the class seemed to have any objections to removing potentially hazardous and dangerous diseases from the genome," he said, "But it ran the gamut from, we shouldn't decide [whether parents will conceive a] boy or girl, to we can't decide [a baby's] hair color. Then again, some were like, well, I do want my baby to be born with a certain hair color so"

It seems to help that both Hirsch and Powel have unconventional teaching methods. "I've always wanted to cater my classroom science experience, and give students the same sort of struggles and highs and lows in doing research as I experienced in the lab," says Hirsch, who studied molecular biology in college and worked in the biotech industry before becoming a teacher.

When he teaches, he sets students up as they would be if they were scientists in a lab. "There's some sort of problem and there has to be either mystery in how you get to the solution or mystery in the starting materials and what you end up with. It can't all be cookbook," he says, "Give them as little information as possible to keep them going."

A student's CRISPR notes at the camp. Image: Mallory Locklear

Back on Long Island, the CRISPR group was joined by two boys discussing how getting negatively charged DNA through the bacteria's negatively charged cell wall is a problem they would have to surmount in order to transform their bacteria's DNA. One of the boys, John Michael, jumped up and grabbed two magnets from a drawer to give a visual.

As they talked about what helps solve this particular problema buffer with three chemicals that will neutralize the negative DNA charge and make the bacteria's cell wall permeablethey began setting up their bacterial cultures and then expertly streaked their sample across a number of plates they'd put together earlier in the day. Their culture would have to sit overnight before they could do the next steps.

Throughout the day, some students showed hesitation when working through some of the steps, always short-lived. They mixed and poured agar, labeled plates, and pipetted reagents with very little help from Powel.

Teaching CRISPR to kids is about bringing science to the public and bringing the public into discussions about how to implement it. It's hard to have meaningful conversations about CRISPR or the ethics of using it if people don't understand what it is. So, the only way to implement safeguards or boundaries that aren't driven by misunderstanding or fear is to make CRISPR accessible to everyonescientists, non-scientists, even kids.

At the very beginning of class, one student summed up something Powel has been instilling in her students all summer and what scientific understanding and education is so often about, "It's about seeing things in a new way."

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These Kids Are Learning CRISPR At Summer Camp - Motherboard

Researchers in Portland, Oregon have, for the first time, edited a human embryo in the US.

This work adds to the promise of CRISPR, and it stands as an important step toward the birth of the first genetically modified humans.

By now, most of us know what CRISPR gene editing is. At the very least, we have heard of this revolutionary technology that allows us to alter DNA - the source code of life itself.

One day, CRISPR could allow us to delete genes in order to eradicate genetic diseases, add in new genes in order to vastly improve various biological functions, or even genetically modify human embryos in order to create an entirely new class of humans of super humans.

But first, we have a lot of research to do.

And that brings us to today. Reports from MIT were just released which assert that the very first attempt at creating genetically modified human embryos in the United States has been carried out by a team of researchers in Portland, Oregon.

"So far as I know this will be the first study reported in the US," Jun Wu, who played a role in the project and is a collaborator at the Salk Institute, said to MIT.

According to MIT, the work was led by Shoukhrat Mitalipov, who comes from the Oregon Health and Science University.

Although details are scarce at this point, sources familiar with the work assert that the research involved changing the DNA of one-cell embryos using CRISPR gene-editing.

Further, Mitalipov is believed to have broken records in two notable ways:

This is notable because, despite the fact that it has been around for several years now, CRISPR is still an incredibly new tool - one that could have unintended consequences.

As previous work published in the journal Nature Methods revealed, CRISPR-Cas9 could lead to unintended mutations in a genome.

However, the work was later reviewed by researchers at another institution and the findings were brought into question.

It remains to be seen whether the original study will be corrected or retracted, but this development highlights the importance of peer review in science.

In this regard, Mitalipov's work brings us further down the path to understanding exactly how CRISPR works in humans, and reveals that is it possible to avoid both mosaicism (changes that are taken up not by only some of the cells of an embryo, as opposed to all of them) and ;off-target' effects.

It is important to note that none of the embryos were allowed to develop for more than a few days, and that the team never had any intention of implanting them into a womb.

However, it seems that this is largely due to ongoing regulatory issues, as opposed to issues with the technology itself.

In the United States, all efforts to turn edited embryos into a baby - to bring the embryo to full term - have been blocked by Congress, which added language to the Department of Health and Human Services funding bill that forbids it from approving any such clinical trials.

Yet, the potential of the CRISPR-Cas9 system as a gene editing technology is undeniable.As previously mentioned, it has seen success in developing possible cancer treatments, in making animals disease-resistant, and it has even shown promise in replacing antibiotics altogether.

This new work adds to the promise of CRISPR, and stands as an important step toward the birth of the first genetically modified humans.

This article was originally published by Futurism. Read the original article.

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Scientists Have Used CRISPR to Edit a Human Embryo in The US For The First Time - ScienceAlert

Malfunctioning glial cells that keep nerve cells from forming working communication networks may be the basis of the wiring problems in the brains of people with schizophrenia, new research suggests.

The inability of these cells to do their jobappears to be a primary contributor to the disease.

When researchers transplanted human brain cells generated from individuals diagnosed with childhood-onset schizophrenia into mice, the animals nerve cell networks did not mature properly and the mice exhibited the same antisocial and anxious behaviors seen in people with the disease.

The findings of this study argue that glial cell dysfunction may be the basis of childhood-onset schizophrenia, says neurologist Steve Goldman, co-director of the Center for Translational Neuromedicine at the University of Rochester Medical Center (URMC) and lead author of the study.

The inability of these cells to do their job, which is to help nerve cells build and maintain healthy and effective communication networks, appears to be a primary contributor to the disease.

Glia are an important family of support cells found in the brain and play a critical role in the development and maintenance of the brains complex interconnected network of neurons. Glia includes two major types: astrocytes and oligodendrocytes.

Astrocytes are the brains principal support cells, while oligodendrocytes are responsible for producing myelin, the fatty tissue that, like the insulation on electrical wires, wraps the axons that connect different nerve cells. The source of both these cells is another cell type called the glial progenitor cell (GPC).

Astrocytes perform several functions in the brain. During development, astrocytes colonize areas of the brain and establish domains in which these cells help direct and organize the network of connections between nerve cells.

Individual astrocytes also send out hundreds of long fibers that interact with synapsesthe junction where one neurons axon meets anothers dendrite. The astrocytes help facilitate the communication between neurons at the synapses by regulating the flow of glutamate and potassium, which enable neurons to fire when they are communicating with each other.

In the new study, the researchers obtained skin cells from individuals with childhood-onset schizophrenia and reprogrammed the cells to create induced pluripotent stem cells (iPSC) which, like embryonic stem cells, are capable of giving rise to any cell type found in the body. Next, the team manipulated the iPSCs to create human GPCs.

The human GPCs were then transplanted into the brains of neonatal mice. These cells out-competed the animals own native glia, resulting in mice with brains comprised of animal neurons and human GPCs, oligodendrocytes, and astrocytes.

The researchers observed that human glial cells derived from schizophrenic patients were highly dysfunctional. The development of oligodendrocytes was delayed and the cells did not create enough myelin-producing cells, meaning signal transmission between the neurons was impaired.

The development of astrocytes was similarly tardy so that the cells were not present when needed and were thus ineffective in guiding the formation of connections between neurons. The astrocytes also did not mature properly, resulting in misshapen cells that could not fully support the signaling functions of the neurons around them.

The astrocytes didnt fully mature and their fibers did not fill out their normal domains, meaning that while they provided control to some synapses, others had no coverage, says Martha Windrem, also with the Center for Translational Neuromedicine and first author of the study. As a result, the neural networks in the animals became desynchronized and uncoordinated.

The researchers also subjected the mice to a series of behavioral tests. They observed that the mice with human glial cells from individuals diagnosed with schizophrenia were more fearful, anxious, anti-social, and had a variety of cognitive deficits compared to mice transplanted with human glial cells obtained from healthy people.

The studys authors point out that the new research provides scientists with a foundation to explore new treatments for the disease. Because schizophrenia is a unique to humans, until now scientists have been limited in their ability to study the disease. The new animal model developed the by the researchers can be used to accelerate the process of testing drugs and other therapies in schizophrenia.

The study also identifies a number of glial gene expression flaws that appear to create chemical imbalances that disrupt communication between neurons. These abnormalities could represent targets for new therapies.

Additional coauthors of the study are from the University of Rochester, the University of Copenhagen, George Washington University, Johns Hopkins University, and Case Western University.

The study appears in the journal Cell. Funding from National Institute of Mental Health, the National Institute of Neurological Disorders and Stroke, the G. Harold and Leila Y. Mathers Charitable Foundation, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, and the Novo Nordisk and Lundbeck Foundations supported the research.

Source: University of Rochester

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Glial cells botch wiring in childhood schizophrenia - Futurity: Research News

Over the past twenty years, Jamie Sherrill has become one of the most in-demand skincare gurus in Hollywood. But you may not know her name--she goes by the moniker Nurse Jamie, which is also the name of her line of cult-favorite beauty tools and potions, as well as her Los Angeles spa, Nurse Jamie Beauty Park. Before you ask--yes, Sherrill is, in fact, a nurse, but she's also a certified aesthetician, which means she can offer her devoted clients, who range from Jessica Alba to Ruby Rose, a wide-range of services that promise flawless skincare through some very unique methods that can be done both at home and in the office. "At Nurse Jamie Beauty Park, our vision is simple to offer not only the best non-surgical beauty solutions available on the market, but also a customized combination of the most cutting-edge technical advances in anti-aging, skincare and beauty today," Sherrill explains. "High-tech tools, devices and home-based care are a big part of my regiment and I make everyone participate."

Here, Sherrill offers insight into the most in-demand celebrity beauty desires, and offers tips on improving your complexion at home.

You have a wide range of high profile clients, all unique with their own concerns and skincare regimens. What are the most common concerns you hear?Celebrities come in all shapes, sizes and ages, so everyone is going to have a different treatment plan. This year body sculpting is big from banning the bra strap fat to firming the tush, while laser hair removal, Botox, fillers and glowing skin are year round trends. Those requests never go out of style.

What types of treatments are most requested before a red carpet appearance?Some are genetically blessed and don't really do more than an oxygen facial and an electric facial"to be fully red carpet ready. But that said--we start to lose collagen production and skin elasticity starting at 25, so we will typically use a range of key technologies in lasers for skin texture and complexion.TheACELLeratorat home beauty tool is idealto help serums and product be absorbed for a lifting and tightening effect, and has a great anti-inflammatory property. You can use every day but specifically just before an event for a more open eye look or more defined cheek even if you just flew in!This works well for the face and body, so it helps with stretch marks and skin smoothing for waistline, hips and thighs. Trust me this is acelebsecret. If you don't believe me, do one side of your face for just one minute then look into a mirror.

But don't forget red carpet prep needs to happen every day, too. Eat well, sleep well on the right pillow, take off make-up at night and use good quality products with the best raw ingredients. Home care matters as much as in office does.

When your clients are on location for months at a time, what tips do you give them?Think maintain, not reclaim and always try to be preventative.Think of the rules of eating that are good for your body; most apply to your skin as well. It is the largest organ of the body so treat it like one.Be consistent with taking off makeup nightly and never with a washcloth. Use a hypoallergenic and antibacterial surface to cleanse your skin. Exfoliate regularly, manually or with a tool, but gently and consistently.

Invest in a beautytool to help increase absorption of products like my Instant Uplift or ACELLerator Ultra. Just like the machines we have in office, they increase absorption and efficacy of your products while helping to improve and maintain tone. Also, wear sunscreen.It seems basic, but all helps. At-home devices are the future of beauty -- you can have the best raw ingredients in the world, but as skin is the largest organ of the body its main function is to protect. The number one cause of aging is UV damage, the number two is smoking, and the third is sleeping on a traditional pillow.Use satin only and a shape that will help you train to sleep on your back, so that the most delicate areas around the eyes, cheeks and neck do not form permanent wrinkles.

It's the middle of summer. Other than sunscreen and hats, what other advice do you have for fending off skin discoloration?Use good quality products with the best raw ingredients. Old school skincare was to use aggressive products that caused chemical cell turnover reaction, which can make you more susceptible to sun damage. (Retin-A is so 1980s!) My opinion is to use retinol ingredients sparingly. Epidermal Growth Factor (EGF) - causes cell turnover and has significant effects on delaying the aging process - including preserving skins cells and skins overall vitality and radiance, without leaving you red, flaky, and shiny. I hate the shiny face -it kills meovertime I see I can spot theglare from across the room.The Nurse Jamie tools that you incorporate into your treatments seem to have a loyal following of their own. Like the Beauty Stamp, for example. How does that work?The Beauty Stamp may very well be the best investment anyone can make. A small pad features a cross section of micro needles in a grid that helps with micro exfoliation, opens channels for product delivery and efficacy and aids in the body process of collagen andelastinproduction. It is my triple threat. For day of events you need to focus on complexion and texture in a non-invasive way or only protocols with no downtime and no risk. Don't try something new with a high risk to low reward for the day of an event. Nothing worse than redness or inflammation when you are dressed to impress and need your face to match! How about the Accelerator Ultra?TheACELLeratorat home beauty tool is ideal for a daily regimentto help serums and product be absorb lifting and tightening effect and has a great anti-inflammatory property.You can use every day but specifically just before an event for a more open eye look or more defined cheek--even if you just flew in! This works well for face and body so it helps with stretch marks and skin smoothing for waistline, hips and thighs, too. Trust me, this is acelebsecret dont believe me? Do one side of your face for just one minute then look into a mirror.What is your top selling tool?UpLift Massaging Beauty Roller. It has a huge celebrity following.Are there any foods or vitamins that you recommend for vibrant skin?A B12 Energy Shot. Close to a decade ago I injected Paris Hilton and Nicole Richie with it right in their bums on national television forThe Simple Life,and in turn injectable vitamins became one of our most popular treatments...

What are the biggest skincare mistakes people make?Side sleeping and over exfoliating. We need to treat our skin like a silk fabric not a piece of leather. When youoverexfoliate(physically and chemically) and withtoo much frequency it destroys the protective barrier that your skin has - once it is removed or compromised you are you exposing your skin to environmental toxins, sun damage pre-mature aging, acne, etc. It's very common.

What is your personal daily skin routine?Taking off my make-up--I can't go to bed with my make-up on. Period. The UpLift Facial Massaging Beauty Roller, EGF Stem Cell Complex--I dont go anywhere without this cream. I would bathe in it if I could--and I use my ACELLerator for 10 minutes each night on both sides of my face while I sit in bed.I practice what I preach.That way I can give them my best face - and tell them it is what I do and mean it! Ive dedicated my life to skin and created my line for products that I felt that were missing in the marketplace. As a busy working mom of three toddlers Im proud to say that Im my own client.

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Celebrity Skincare Guru Nurse Jamie on Why At-Home Beauty Tools Are the Future - W Magazine

Zion Market Research, the market research group announced the analysis report titled 'Hormone Replacement Therapy Market: Global Industry Analysis, Size, Share, Growth, Trends, and Forecasts 20162024'

This press release was orginally distributed by SBWire

Sarasota, FL -- (SBWIRE) -- 07/27/2017 -- Global Hormone Replacement Therapy Market: Overview

The medical treatment where the patients receive hormones to substitute the naturally occurring hormones with the other hormones or to add naturally occurring hormones that are absent is known as hormone replacement therapy. In the females that are at the stage of menopause, hormone replacement therapy is used to restore female hormone levels, so that the body functions normally.

Request Free Sample Report @ https://www.zionmarketresearch.com/sample/hormone-replacement-therapy-market

Global Hormone Replacement Therapy Market: Segmentation

The global hormone replacement therapy is fragmented into therapy type, distribution channel, and application. On the basis of a therapy type, the global market is segregated into estrogen replacement therapy, thyroid hormone replacement, and growth hormone replacement. The thyroid hormone replacement segment is further sub-segmented into tablets, injections, and capsules. The growth hormone replacement segment is sub-categorized into somatostatin analogs and dopamine agonist. On the basis of the distribution channel, the market is categorized into e-commerce, retail pharmacies and drugstores, hospital pharmacies, compounding pharmacies, and others. On the basis of application, the market is divided into hypothyroidism, menopause, cancer, hypopituitarism, and others.

Global Hormone Replacement Therapy Market: Growth Factors

The key factors that are driving the hormone replacement therapy market are enlarged demand for the regenerative medicines which include reproductive-cycle boosting and anti-aging. The market is being positively impacted due to the increasing demand from other therapeutic areas which include thyroid hormone therapy and growth hormone therapy as the hormone replacement therapy is comparatively safe and efficient method and is cost effective. The other benefits that are associated with the hormone replacement therapy include minimum risk incidence of cardiovascular disease, osteoporosis, and vasomotor symptoms are also reduced thus expecting to fuel the growth of hormone replacement therapy market. The limitations of the hormone replacement therapy market include the side effects that are involved in this therapy such as fluid retention, indigestion, headache, and depression thus hindering the popularity of the therapeutic area.

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Global Hormone Replacement Therapy Market: Regional Analysis

Regional diversification of the hormone replacement therapy market is given as follows Asia Pacific, Latin America, the Middle East & Africa, Western Europe, Eastern Europe, and North America. The region that is dominating the hormone replacement therapy market is North America, which is due to the fact that the U.S has the largest market owing to the popularity of the therapy among the patients that are aged 35 years and above. The factors that are contributing to the market growth in this region are increasing disposable income, early aging, and the availability of compounded drugs. In the coming years, the hormone replacement therapy market will grow speedily in Asia Pacific region owing to the increasing awareness among the people. The emerging nations such as India, Japan, and China will contribute largely to the market growth.

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Global Hormone Replacement Therapy Market: Competitive Players

The key market players that are involved in the hormone replacement therapy market include Pfizer, BioSante Pharmaceuticals and Amgen, Noven Pharmaceuticals, Bayer AG, Merck & co., and QuatRx Pharmaceuticals.

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About Zion Market ResearchZion Market Research is an obligated company. We create futuristically, cutting edge, informative reports ranging from industry reports, a company reports to country reports. We provide our clients not only with market statistics unveiled by avowed private publishers and public organizations but also with Vogue and newest industry reports along with pre-eminent and niche company profiles. Our database of market research reports comprises a wide variety of reports from Cardinal industries. Our database is been updated constantly in order to fulfill our clients with prompt and direct online access to our database. Keeping in mind the client's needs, we have included expert insights on global industries, products, and market trends in this database. Last but not the least, we make it our duty to ensure the success of clients connected to usafter allif you do well, a little of the light shines on us.

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Hormone Replacement Therapy Market: Global Industry Analysis, Size, Share, Growth, Trends, and Forecasts 2016 ... - Digital Journal