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Archive for the ‘Genetics’ Category

‘One among millions’: DNA is not the only genetic molecule – Big Think

Wednesday, November 27th, 2019

Simply put, the so-called central dogma of biology asserts that genetic information flows from DNA to RNA to proteins, and once that information is passed to a protein, it cannot be returned as DNA or RNA again. It's dubbed the central dogma because it seems to be universal amongst all living organisms. There are some exceptions to the linear flow described in the popular version of the central dogma information can be passed back and forth between RNA and DNA or between DNA and DNA or RNA and RNA, but the central players remain the same: DNA, RNA, and proteins.

But what if this didn't have to be the case? Could genetic information be stored in media other than the two nucleic acids of DNA and RNA? New research published in the Journal of Chemical Information and Modeling suggests that there might not be just a handful of alternative molecules for storing genetic information, but millions.

The central dogma of biology asserts that the genetic information is transcribed from DNA to RNA, which then translates that information into useful products like proteins. This new research, however, suggests that DNA and RNA are just two options out of millions of others.

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Analogues to nucleic acids exist, many of which serve as the foundation for important drugs for treating viruses like HIV and hepatitis as well as for treating cancers, but until recently, no one was sure of how many unknown nucleic acid analogues could be out there.

"There are two kinds of nucleic acids in biology," said co-author Jim Cleaves, "and maybe 20 or 30 effective nucleic acid-binding nucleic acid analogues. We wanted to know if there is one more to be found or even a million more. The answer is, there seem to be many more than was expected."

Cleaves and colleagues decided to conduct a chemical space analysis in essence, a sophisticated computer technique that generates all possible molecules that adhere to a set of defined criteria. In this case, the criteria were to find compounds that could serve as nucleic acid analogues and as a means of storing genetic information.

"We were surprised by the outcome of this computation," said co-author Markus Meringer. "It would be very difficult to estimate a priori that there are more than a million nucleic acidlike scaffolds. Now we know, and we can start looking into testing some of these in the lab."

Though no specific analogues were targeted in this paper, it does present a long list of candidates to be explored for use as drugs for serious diseases like HIV or cancer. A more intriguing possibility suggested by the research is that life itself may have taken its very first steps using one of these alternative compounds.

Many scientists believe that before DNA became the dominant means of storing genetic information, life used RNA to code genetic data and pass it down to offspring. In part, this is because RNA can directly produce proteins, which DNA can't do on its own, and because it's a simpler structure than DNA. Over time, life likely started to opt for using DNA for storage due to its greater stability and to rely on RNA as a kind of middleman for producing proteins. But RNA on its own is still a very complicated compound and is fairly unstable; in all likelihood, something simpler came before RNA, possibly using some of the nucleic acid analogues identified in this study.

Not only does this shed light on how life may have started on Earth, but it also has implications for alien life as well. Co-author Jay Goodwin said, "It is truly exciting to consider the potential for alternate genetic systems based on these analogous nucleosides that these might possibly have emerged and evolved in different environments, perhaps even on other planets or moons within our solar system. These alternate genetic systems might expand our conception of biology's 'central dogma' into new evolutionary directions, in response and robust to increasingly challenging environments here on Earth."

When we search for extraterrestrial life, often we're looking for signs of RNA and DNA, but this may be an excessively narrow scope. After all, if millions of alternatives exist, there would need to be something very special indeed for life to universally favor using just DNA and RNA.

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'One among millions': DNA is not the only genetic molecule - Big Think

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Collection of genetic data leads to privacy concerns – The New Economy

Wednesday, November 27th, 2019

A DNA test can reveal surprising facts about us certain genes make us more inclined to have dry earwax, for example, and others make us more likely to sneeze when we see a bright light. Some genes even result in people being more attractive targets for mosquitoes, so if youve ever felt personally singled out by the insect during the summer months, its not a cruel conspiracy its your DNA.

Innocuous facts like these were what DNA kits were used for finding out when they first became commercially available. However, as the tests have become more sophisticated, the companies behind them have shifted their marketing focus. Users of at-home DNA tests have been known to uncover deep-rooted facts about themselves, from discovering long-lost relatives to learning of their ancestors origins and their susceptibility to genetic diseases.

Finding out that you have a pre-existing health condition might not seem like the best idea for a Christmas present, but that hasnt stopped the test kits from enjoying a surge in popularity. MIT Technology Review estimates that by the start of 2019, more than 26 million people had taken an at-home ancestry test. The market is expected to be worth $45bn by 2024.

Nevertheless, despite the emerging industrys rampant growth, there have been mounting concerns that its practices could infringe on consumers rights. Whenever people fork out $100 to $200 for a DNA test, the hidden cost of that transaction is their personal data which, from then on, is held in the databases of a private company. Once these companies obtain genetic information, its very difficult for users to get it back.

By taking DNA tests at home, many have unwittingly stumbled upon long-kept family secrets. Some have seen their parents go through a bitter divorce after their test revealed they were actually conceived through an affair

Ignorance is blissLong before people were able to take DNA tests from the comfort of their own home, psychologists worried about their possible impact on peoples mental health. Ever since the Human Genome Project was started in 1990, many scholars have maintained that DNA tests should be used with caution, on the grounds that understanding ones own health risks could lead to anxiety or depression.

Conversely, a study by the Hastings Centre found that discovering an increased risk of developing Alzheimers disease did not make people more depressed or anxious. And in the event that people discover a particularly urgent health risk like a mutation of the BRCA1 or BRCA2 genes, which puts individuals at a high risk of developing cancer at a young age any adverse psychological effects are presumably worth it to obtain this life-saving information.

However, at-home DNA tests could still pose a risk to mental health, in part because they remove medical professionals from the equation. Adrian Mark Thorogood, Academic Associate at the Centre of Genomics and Policy, warned that this is far from best practice for receiving a DNA test result. Results should be communicated through a medical professional who can interpret the result in the individuals specific context, and offer a clear description of the tests limits, he told The New Economy.

Without a professionals assistance, users could be left alone to battle with a troubling revelation about their health. There is also a danger that without guidance, some people could misinterpret their test result, placing undue stress on their mental health.

There is another unpleasant discovery that people can make through a DNA test one they may be even less prepared for. By taking DNA tests at home, many have unwittingly stumbled upon long-kept family secrets. Some have seen their parents go through a bitter divorce after their test revealed they were actually conceived through an affair. Others have discovered they were conceived by rape and that their mother decided to never tell them. What began as a seemingly harmless urge to find out more about their heritage ends in psychological trauma and family breakdown.

Brianne Kirkpatrick, a genetics counsellor, is part of a growing sector of therapy specifically tailored towards helping people come to terms with receiving unexpected DNA results. One cant help but wonder whether her patients end up wishing theyd never taken the test at all.

I dont recall anyone saying they wish they could go back and not learn the truth, Kirkpatrick said. But I have had a number of people say to me they wish they had found out their shocking information from a person, rather than a computer.

While we might think wed prefer to suffer a DNA leak than a leak of our credit card details, genetic data has its own unique set of complications

The fact that virtually anyone can now find out their real parentage through a simple DNA test has wide-reaching repercussions for the accountability of paternity. Historically, men have always had a much greater ability to conceal their status as a parent, as they dont have to bear the child. The world of direct-to-consumer DNA testing blows this capacity for anonymity out of the water.

This is particularly problematic when it comes to sperm donation. Anonymity is a key selling point for many potential donors, but now all their future biological offspring has to do is swab the inside of their cheek to completely compromise that anonymity. Research suggests that we could see a drop in donor rates as a result. A 2016 study in the Journal of Law and the Biosciences found that 29 percent of potential donors would actually refuse to donate if their name was put on a registry.

The wave of parental discoveries made through direct-to-consumer DNA tests raises questions about where the responsibility of the seller sits in all this. Most health professionals recommend that individuals seek out genetics counselling once they receive DNA results. Some, like Invitae, offer counselling services but arent direct-to-consumer companies. Many of those that are including 23andMe do not offer such a service. It could be argued that this shows a certain disregard for the consequences of using their product. Unfortunately, irresponsible decisions like this have tended to characterise the industrys path to success.

Genetic Wild WestIn September 2019, 17 former employees from the Boston-based genetic testing company Orig3n accused the firm of giving consumers inaccurate results. Allegedly, if a customer took the same test twice, their results could be extremely different each time. A former lab technician produced a leaked report to Bloomberg Businessweek that revealed 407 errors like this hadoccurred over a period of three months.

Part of Orig3ns USP was that it offered advice supposedly calculated based on a consumers genetic profile. Former employees have cast doubt over the companys modus operandi by claiming that the advice they gave was in fact routinely lifted from the internet. The advice given ranged from the technically correct but uninspired to the broadly unhelpful such as telling people to eat more kale and the utterly bogus, like advising clients to eat more sugar to eliminate stretch marks.

Although Orig3n is a relatively small player in the sector, news of this scam nonetheless illustrates how little protection consumers have in this nascent market. Analysts say we are currently witnessing a Wild West period in the consumer genetics space thanks to a lack of regulation, raising concerns over whether we can trust these companies with our genetic data. While we might think wed prefer to suffer a DNA leak than a leak of our credit card details, genetic data has its own unique set of complications.

In the United States, if my social security number is stolen, that is difficult, but not impossible, to get frozen, changed, etc, said Natalie Ram, an associate professor at the University of Maryland Francis King Carey School of Law and a specialist in bioethics and criminal justice. But theres literally no way to change your genetic code.

Genetics platforms like 23andMe, AncestryDNA and FamilyTreeDNA are now sitting on a goldmine of very personal data. In 2013, a 23andMe board member told Fast Company that it wanted to become the Google of personalised healthcare. If this statement makes anything clear, its that the company wasnt planning on making its millions simply by selling DNA test kits: its mission was always to amass significant amounts of data on its users, which it could then monetise.

There is a wide range of reasons why companies might want to buy genetic data. Perhaps the most benign is medical research, which genetics platforms allow users to opt in or out of. But other companies might use your genetic data to better sell you products or, conversely, deny them to you for instance, one sector that would see a clear monetary value in obtaining genetic data is insurance. In the US, the Genetic Information Nondiscrimination Act of 2008 prevents employers and health insurers from using a persons genetic information when making decisions about hiring, firing or raising rates. However, this does not include life insurance or short or long-term disability insurance.

At first glance, it seems as if theres a simple solution: if users are concerned about these risks, they should just choose for their data to be kept anonymous. However, choosing this option is not as foolproof as it once was. As long ago as 2009, researchers demonstrated that they could correctly identify between 40 and 60 percent of all participants in supposedly anonymous DNA databases by comparing large sets of that data with public datasets from censuses or voter lists. Since that experiment, DNA databases have grown massively.

With access to four to five million DNA profiles, upwards of 90 percent of Americans of European descent will be identifiable, said Ram. Its verging on a comprehensive DNA database that no US state or jurisdiction has suggested would be appropriate.

Shaping the lawWith comforting statements like your privacy is very important to us (ancestry.co.uk) and we wont share your DNA (familytreedna.com) emblazoned on their websites, some genetics platforms seem to be making privacy their number one priority. In the US, 23andMe and Ancestry are part of the Coalition for Genetic Data Protection, which lobbies for privacy protection in the DNA space. However, while the coalition advocates genetic data privacy in a specific context, it argues for a one-size-fits-all policy concerning all data. By comparison, the EUs General Data Protection Regulation regards genetic information as personal data, which makes DNA unique from other kinds of data.

There is a fundamental legal problem with boxing genetic data in with all other varieties, including the data that social media websites collect about us. In most cases, what a person does on the internet implicates them alone genetic data is different. We share our DNA with members of our family, which means that sharing it without their consent can be problematic.

Even if I can consent to using my DNA to identify me, that should not extend to my ability to consent to using my DNA to identify my relatives, said Ram. The reason I think thats a really critical distinction is because genetic relatedness is almost always involuntarily foisted upon us. So we dont choose our parents, we dont choose how many siblings we have. Its a product of biology, not a product of choice.

The legal issues surrounding genetic relatedness were put to the test in 2018 when police discovered the true identity of the Golden State Killer, who terrorised California in the 1970s and 1980s in a homicidal spree. Law enforcement officials were able to convict him only because they had succeeded in connecting the DNA of the suspect with that of a family relative on GEDmatch, a genetic database in the public domain. Across the US and around the world, people celebrated the arrest of a notorious criminal. The only problem was that the means of capturing him was not necessarily legal.

Prior to the case, GEDmatchs site policy made no explicit reference to the potential use of consumers data by law enforcement. However, the company defended itself by saying that users should have assumed it could be put to that use.

While the database was created for genealogical research, it is important that GEDmatch participants understand the possible uses of their DNA, including identification of relatives that have committed crimes or were victims of crimes, said GEDmatch operator Curtis Rogers in a statement.

Some genes even result in people being more attractive targets for mosquitoes, so if youve ever felt personally singled out by the insect during the summer months, its not a cruel conspiracy its your DNA

However, privacy advocates like Ram argue that users consent for law enforcement to look at their data should not have been assumed. At least from a constitutional perspective in the United States, individuals ought to be recognised to have whats called an expectation of privacy in their genetic data, even if they use one of these services, she told The New Economy.

After the case, genetics platforms updated their policies to clarify their position on law enforcements use of peoples data. Interestingly, they took very different stances. While 23andMe and Ancestry said they would not allow law enforcement to search through their genetic genealogy databases, FamilyTreeDNA updated its policy to say it would give up data to officials, but only in the investigation of violent crimes. Users didnt know it at the time, but FamilyTreeDNAs policy update was already too little too late: in January 2019, it was revealed that the company had been secretly working with the FBI for nearly a year to solve serious crimes, without informing its users.

The Golden State Killer case exposed how little protection consumers really had in the direct-to-consumer genetics market. It showed that genetics platforms were capable of suddenly changing or contradicting their own policies and even, in the case of FamilyTreeDNA, betraying the trust of consumers.

Some might argue that this infringement on genetic privacy is simply the price we must pay to catch dangerous criminals. Of course, without the use of a genealogy database, the Golden State Killer may never have been caught. But the fact that genetic data can be harnessed to solve very serious crimes should not justify law enforcements unbridled access to such databases. Abuses of power do happen and, in the context of direct-to-consumer DNA tests, they already have: in 2018, for example, Canadian immigration officials compelled a man to take a DNA test and upload his results to FamilyTreeDNAs website. They then used the website to find and contact some of his relatives in the UK to gather more evidence in order to deport him.

Todays consumers are continually adjusting to shrinking levels of privacy. From the introduction of video surveillance and the mapping of residential areas on Google Earth to the revelation that Facebook harvests vast amounts of user data, we have seen the public react in the same way again and again: there is an initial public outcry, and then consumers simply adjust to the new level of diminished privacy. Our response to the rise of genetics platforms risks the issue being consigned to the same fate.

It is up to regulators to protect individuals right to privacy. While our genetic data may be something of a genie out of the bottle, that should not give the companies that collect it free rein over who sees it and what they choose to do with it.

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Collection of genetic data leads to privacy concerns - The New Economy

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Genetic testing IVF embryos doesn’t improve the chance of a baby – The Conversation AU

Wednesday, November 27th, 2019

If youre going through IVF, you may be offered a test to look at your embryos chromosomes.

Pre-implantation genetic testing for aneuploidy (chromosome abnormalities), known as PGT-A, is an add on used to help choose embryos with the right number of chromosomes. Its promoted by IVF clinics as a way to increase the chance of success, especially for women over 35.

But the evidence shows that in most cases, PGT-A doesnt improve the chance of a baby.

Read more: The business of IVF: how human eggs went from simple cells to a valuable commodity

Human cells usually contain 46 chromosomes. Aneuploidy is a term that describes a chromosome number that is different from 46 either too many or too few chromosomes.

In human embryos, most aneuploidies are lethal, resulting in miscarriage, or do not result in pregnancy at all.

The chance of aneuploidy increases with the age of the woman; by the time a woman reaches age 40, approximately 80% of her embryos are aneuploid.

All couples produce some aneuploid embryos, whether they conceive naturally or with IVF. The idea behind PGT-A is that if the aneuploid embryos can be identified they can be discarded, so that only embryos capable of producing a healthy pregnancy are used.

PGT-A involves the woman having fertility drugs to produce several eggs. When they are mature, they are retrieved and mixed with sperm to create embryos.

Embryos are grown in the laboratory for five to six days. At this time, two types of cells are distinguishable: the cells that will develop into the placenta and the cells that will become the baby.

Read more: Considering using IVF to have a baby? Here's what you need to know

A few cells are removed from the future placenta for testing and the embryos are frozen until test results are available.

If the test shows there are normal embryos, one is thawed and transferred to the womans uterus. Any remaining normal embryos will be kept frozen for transfer later if the first transfer is unsuccessful.

Importantly, PGT-A doesnt correct chromosomally abnormal embryos, it simply allows couples to avoid transferring them.

Many clinics recommend PGT-A for women over 35 (more than half of women who have IVF) and those who have had repeated miscarriages or failed IVF treatments. This is because women over 35 and women with previous losses are more likely to produce aneuploid embryos.

While the theory behind PFT-A makes sense, randomised controlled trials (the gold standard evidence to tell us if an intervention makes a difference) have not demonstrated a clear benefit.

Of the two most recent trials of PGT-A, one reported fewer embryo transfers and fewer miscarriages in the PGT-A group but neither showed benefits in terms of improving the live-birth rate.

PGT-A actually has the potential to reduce the chance of a baby. It can do this in two ways.

First, PGT-A is not 100% accurate. This means that inevitably, some embryos that have the capacity to form a healthy baby will be discarded.

The most common reason for these false positive results is that a proportion of embryos are mosaic they have a mix of normal and abnormal cells. Surprisingly, mosaic chromosome abnormalities are quite common in early human embryos, and do not seem to prevent the embryo developing into a healthy baby.

However, if abnormal cells are removed and tested, the embryo will be misclassified as abnormal and discarded a lost opportunity for a healthy pregnancy.

Read more: Fertility miracle or fake news? Understanding which IVF 'add-ons' really work

Many healthy babies have been born to people who have elected to have mosaic embryos transferred because they were the only embryos they had.

In a recent study of 98 women who had mosaic embryos, 32 (33%) elected to have at least one transferred. Of these, 11 (34%) had a successful pregnancy with apparently healthy babies born.

Second, while the risk is small, embryos can be damaged in the biopsy procedure and some embryos dont survive the freezing and thawing process.

PGT-A costs around A$700 per embryo which adds up to A$2,800 if there are four embryos to test.

While doctors likely offer their patients detailed and individualised information about different treatment options, information about the possible benefits of PGT-A on clinic websites can be difficult to interpret.

Thats why independent information about the pros and cons of PGT-A is needed to help people make informed decisions. The Victorian Assisted Reproductive Treatment Authority (VARTA) has developed a downloadable resource about the current state of knowledge about PGT-A.

Some clinics are now offering a less invasive technique where, rather than removing cells from the embryo, they test the fluid that the embryo is grown in to determine if the embryo has the right number of chromosomes. Time will tell of this will improve the chance of having a baby with IVF.

In the meantime, it may help to ask the five questions recommended by Choosing Wisely:

And in the case of IVF: how will this improve my chance of a live birth?

Read more: Your questions answered on donor conception and IVF

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Genetic testing IVF embryos doesn't improve the chance of a baby - The Conversation AU

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German shepherd stuck in ‘perpetual puppyhood’ due to rare genetic condition – Fox News

Friday, November 22nd, 2019

A purebred German shepherd will forever be the size of a pupdue to a rare genetic condition.

Ranger, 2, has pituitary dwarfism, a genetic condition that primarily affects German shepherds, but can also affect such breeds as the Saarloos wolfdog and the Karelian bear dog.

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Ranger the German Shepherd with pituitary dwarfism. (SWNS)

Rangers owner, Shelby Mayo, told British news agencySWNS that she knew the dog mightend up smaller than other German shepherds; he was apparentlythe runt of his litter.

When we originally got Ranger from the breeder, he was smaller than all his other littermates, but we figured that was because he had a parasite called Coccidia, said Mayo, of Phoenix.

Ranger was treated for the parasite, but he later contracted another parasite Giardia and developed an infectionon his neck.

''During this time Ranger remained very small, the vet had suspected that he may have pituitary dwarfism, a genetic mutation, she said. But we were still skeptical as this condition is very rare.

A few months later, Ranger was neutered,after which time we started to see big changes, Mayo said. Ranger began to suffer from weight and hair loss, as well as dry and flaky skin more signs of the condition, as dogs with pituitary dwarfism often experience skin and hair abnormalities, per ScienceDirect.

One of Rangers nearly 70,000 followers on Instagram who also has a German shepherd with dwarfism warned the owner that the dog may be suffering from low thyroid levels,not uncommon in dogs with the condition.

NEW JERSEY DOGS, INCLUDING 3-MONTH-OLD PITBULL, BURNED WITH BLOWTORCH, ANIMAL RESCUERS SAY

So our vet checked his thyroid levels and sure enough he was low. This can cause hair loss and a loss of appetite, said Mayo, noting that medication and a special soap remedied the condition.

Though dogs with pituitary dwarfism are more prone to health issues andtypically have shortened lifespans,Mayo told SWNS that Ranger ishealthy and happy as can be as of now and enjoys playing with her two other dogs, Hazel and Jessie.

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German shepherd stuck in 'perpetual puppyhood' due to rare genetic condition - Fox News

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This Mom Is Buying Mutant Mice From China To Find A Cure For Her Sons Rare Genetic Disease – BuzzFeed News

Friday, November 22nd, 2019

When Amber Freed first told doctors her baby boy wasnt able to move his hands, they said that wasnt possible.

Freed had given birth to twins in March 2017. While her baby girl, Riley, squirmed and babbled and crawled through the first year of her life, her fraternal twin, Maxwell, was different. He didnt crawl or babble like Riley did. I would fill out their baby books each month, and Riley had met all of these milestones. Maxwell didnt reach one, she said. Most alarmingly, however, Freed noticed that he never moved his hands.

She knew the news was going to be bad when they sent her to the sad room at the hospital, a featureless conference space filled with grim-faced doctors, to hear the diagnosis.

You take your baby to the doctor and you say, He cant move his hands. And they look at you and they say, Of course he can, said Freed.

Then they look for themselves, and you can see from the look on their faces that they have never seen anything like this.

On June 14, 2018, at the Children's Hospital Colorado in Denver, Maxwell was diagnosed with a genetic disease called SLC6A1. The diagnosis explained why the infant hadnt moved his hands or learned how to speak for the first year of his life, while Riley was thriving. But it didnt explain much else: All the doctors who diagnosed Maxwell knew about the genetic disease came from a single five-page study published in 2014, the year of its discovery. It was too rare to even have a name, she was told, so the doctors just called it by the name of the affected gene: SLC6A1.

Now her 2-year-old son is at the center of a multimillion-dollar race against time, one thats come to include genetics researchers whom Freed personally recruited, paid for by $1 million that Freed and her husband, Mark, have raised themselves. At the center of their research will be specially crafted mutant mice that Freed paid scientists in China to genetically alter to have the same disease as Maxwell. The four mice are scheduled to arrive stateside next week, but Freed said shes prepared to smuggle them into the US disguised as pets if there are any problems.

In total, Amber and Mark will need to raise as much as $7 million to test a genetic treatment for their child. And unless they can find and fund a cure, SLC6A1 will condemn Maxwell to severe epileptic seizures, most likely starting before he turns 3. The seizures may trigger developmental disabilities for a lifetime, often accompanied by aggressive behavior, hand flapping, and difficulty speaking.

And the Freeds will have to do it largely alone there are only an estimated 100 other people diagnosed with SLC6A1 in the world. This is the rarest of the rare diseases, pediatric geneticist Austin Larson of the Children's Hospital Colorado told BuzzFeed News.

SLC6A1 is just one of thousands of untreatable rare diseases, and the perilous path it has set up for Freed, half science quarterback and half research fundraiser, is one that few parents can follow. My dream is to create a playbook of how I did this for those that come after me, said Freed. I never want there to be another family that has suffered like this.

You can think of SLC6A1 as a vacuum cleaner in the brain, genetic counselor Katherine Helbig of the Childrens Hospital of Philadelphia, told BuzzFeed News. Helbig will speak at the first conference on the gene at the American Epilepsy Society meeting in Baltimore on Dec. 5, an effort organized by Freed.

The protein made by the gene acts as a stop sign to message-carrying chemicals in the brain, halting them by vacuuming them up once they reach their destination brain cell, Helbig explained.

When one of the two copies of the SLC6A1 gene in every brain cell is damaged, like in Maxwells case, too little of its protein is available to perform its vacuuming duties, leading to miscommunication between cells, developmental disorders, autism-like symptoms, and, often, severe epileptic seizures.

Maxwell is about the age when epileptic seizures typically start in kids with the genetic disease, said Helbig, adding, There probably are many more children out there who have it, but they just havent had the right test to find it. At least 100 similar genetic defects cause similar kinds of epilepsy, afflicting about 1 in 2,000 kids, she said.

I was the one who presented this diagnosis to Amber, said Larson of the Children's Hospital Colorado. There was no medicine or diet or any other treatment for SLC6A1. It wasnt an easy conversation. Most of the time when we present a diagnosis for a genetic condition, there is not a specific treatment available.

At that moment, it was just vividly clear that the only option was for me to create our own miracle, said Freed. Nobody else was going to help.

Half the battle with a rare genetic disease is getting researchers interested, said Helbig.

At that moment, it was just vividly clear that the only option was for me to create our own miracle. Nobody else was going to help.

So that is what Freed set out to do. She quit her job as a financial analyst and started making phone calls to scientists, calling 300 labs in the first three months. For those who didnt respond, she sent them snacks via Uber Eats.

Her search, and a rapid-fire education on genetic diseases, led her to conclude the best hope for helping Maxwell was an experimental technique called gene therapy.

All the roads zeroed in on one scientist: Steven Gray of the University of Texas Southwestern Medical Center in Dallas. In 2018, a team headed by Gray reported the first human experiments of gene transfer by spinal injection, conducted in 5 to 10 children with mutations in a gene called GAN that causes swelling in brain cells.

The GAN gene transfer in that experiment, first tested in mice, attached a corrected version of the damaged gene to a harmless virus. Viruses reproduce by infecting cells and hijacking their DNA machinery to reproduce their own genes, making more viruses. The gene therapy virus in turn leaves behind a corrected gene in the DNA of cells they infect. Injected into the spinal cord, Grays virus can travel straight to the brain, leaving behind the corrected gene after the virus has run its course.

I gave him my 30-second equity analyst pitch. I told him why Maxwell was a good patient, that we would raise $4 million to $7 million, and quarterback every step of the research, she said. And it worked. He agreed to make it a priority if we could raise the money.

The SLC6A1 researchers with the Freeds at a science meeting. From left: Terry Jo Bichell, Frances Shaffo, Amber Freed, Katty Kang, and Mark Freed.

Less than a month after meeting Gray, Freed contacted a lab at Tongji University in Shanghai that was also researching SLC6A1. The lab agreed to develop a mouse with Maxwells specific mutation for less than $50,000, using a gene modification technology called CRISPR that has revolutionized genetic engineering in the lab. CRISPR mice are much more expensive in the US, and this lab had experience with the gene, said Freed.

By July of this year, an experiment with a gene therapy virus that corrects SLC6A1 was tested on normal lab mice, which showed no sign of a toxic response, an encouraging sign. And by September, a line of CRISPR mice with Maxwells exact genetic mutation had been created at Tongji University.

It is the literal mouse version of him, said Freed. Testing a therapy in this mouse is as close as science can get to testing in my son directly.

To pay for all this, Maxwells family started fundraising last November and organized the first medical symposium on SLC6A1 in New Orleans that same month. They opened a GoFundMe account, which has raised $600,000, and held 35 fundraisers, which raised an additional $400,000 by October. In one charity competition, Larson from the Colorado Childrens Hospital, who diagnosed Maxwell, personally helped her raise $75,000.

It is the literal mouse version of him. Testing a therapy in this mouse is as close as science can get to testing in my son directly.

That money is helping to pay for the next step getting the CRISPR mice to Grays lab to test the SLC6A1-correcting virus on them. But its not as simple as putting the mice in a box and shipping them by mail. The mice will be transferred through a lab at Vanderbilt University headed by Katty Kang, an expert on the neurotransmitter disrupted by Maxwells mutation.

Amber is helping us to advance science, and everyone is making this a priority because of the young lives at stake not just Maxwell, but other children this could help, Kang told BuzzFeed News.

Once the four mice arrive, they will spend several weeks in quarantine, be tested to make sure they have Maxwells specific point mutation in the SLC6A1 gene, and breed with normal lab mice to produce generations of mixed-inheritance mice to serve as controls in future experiments. The mutant mice will be closely monitored before they head to UT Southwestern to make sure that they demonstrate the same problems and genetics as human patients with SLC6A1 and can therefore be used in any future clinical trials of gene therapy.

Right now at UT Southwestern, results from a safety test of the gene therapy virus conducted by Grays lab on young, normal lab mice is awaiting publication. If that works out, once the Chinese mice are sent over, they will also receive the gene-correcting virus. His team will see if their symptoms improve and to what extent their brain cells accept the corrected gene.

Maxwell's brain cells seen through a microscope (left), and a sample of his cells in a petri dish.

And then, Freed just needs another $5.5 million. Half a million dollars will go to test the virus in a second SLC6A1 animal model, likely a rat, as another safety step. Two million dollars will go toward creating more of the gene-correcting virus for a human safety study if that proves to be safe. And finally, if all that works out, $3 million will be needed to conduct the experiment on Maxwell and other children next year, following the path of the GAN clinical trial led by Gray.

Its a really horrible realization that the only thing standing in the way of a cure for your 2-year-old is money, said Freed.

Freed acknowledges that she has only been able to pursue a cure for Maxwell because her family has the resources to do so which she would never have had growing up in small towns in Texas, Montana, and Colorado in a poor family affected by alcoholism. I grew up visiting my parents in rehab and knew what to say to put a family member on a 72-hour psychiatric hold by age 12, she said. She dug herself out to build a career in finance, and hoped her kids would never have to experience the struggles she did growing up.

Even so, the fight hasnt been easy on them or on Maxwells sister, Riley.

Freed worries her daughter is growing up in doctors' waiting rooms, waiting on treatments for her brother to end. Maxwells disease has progressed, causing him to constantly clench his fingers, and sometimes pull his sisters hair. His 3-year-old sister will gently remind him, Soft hands, Maxie.

Families like the Freeds are at the forefront of efforts to turn diagnoses of rare genetic ailments, which often used to be the stopping point for medicine, into treatments. A similar case saw the family of a 3-year-old girl, Mila Makovec, raise $3 million for gene therapy to cure her Batten disease, a deadly genetic brain disease that affects 2 to 4 of every 100,000 children born in the US.

In a New England Journal of Medicine editorial on that case published in October, FDA officials questioned how high the agency should set the safety bar for such treatments, meant for severe diseases affecting so few people. In these cases, parents are often collaborators in developing treatments, and might not want to stop efforts that come with high risks. Even in rapidly progressing, fatal illnesses, precipitating severe complications or death is not acceptable, so what is the minimum assurance of safety that is needed? wrote senior FDA officials Janet Woodcock and Peter Marks.

This is way beyond what anyone expects of families.

Finally, Woodcock and Marks wrote, finding sustainable funding for such interventions may prove challenging, because the cost of production can be quite substantial, particularly for gene therapies.

In our era of financial inequality, the specter of wealthy parents buying custom genetic treatments for their childrens ailments while other parents desperately resort to GoFundMe accounts, or else do nothing looms as a possibility.

This is way beyond what anyone expects of families, said Larson. The pathway has been opened up by the brave new world of improved genetic diagnoses, and the coming of age of rapid genetic engineering tools like CRISPR.

But only 20 years ago, an experimental gene therapy that relied on a harmless virus killed an 18-year-old volunteer, Jesse Gelsinger, in a research misconduct case that brought gene therapy to a standstill. Now more than 2,500 gene therapy clinical trials have been conducted, and more than 370 are underway. The human genome was not sequenced until 2000; today, mapping an entire human gene map costs around $700. In this new era, customized treatments for rare genetic diseases like Maxwells are suddenly possible.

What I hope is that we are paving the way for other parents to help their children, said Freed.

Families of children with rare genetic diseases are also working together to make treatments like the one Freed is spearheading possible, said Larson.

They support each other and work together, he said. The best example might be the families of children with cystic fibrosis, who through the Cystic Fibrosis Foundation and the discovery of the gene responsible for the disease in 1989 have pushed for the discovery of new drug treatments. In October, the FDA approved a breakthrough pharmaceutical that could treat 90% of cases.

It is easier working with FDA on this kind of approach rather than starting from scratch, Gray told BuzzFeed News by email. After all, he said, its easier to follow a path that youve already walked down.

Similarly, Freed hopes the SLC6A1 Connect advocacy group she started can lead to similar treatments for other children with genetic epilepsies caused by the gene.

I dont think any parent should be expected to single-handedly cure his or her childs rare disease, said Helbig. Amber is a very tenacious and persistent person, and she will fight tooth and nail for her kids. But a lot of people dont have the resources and they shouldnt have to.

Helbig says that cautious optimism is appropriate on the chances of research yielding a genetic therapy for children like Maxwell. For SLC6A1, its really too early to say whether this is going to work.

But if it works, it might lead many more parents to get genetic tests for children that will reveal undiagnosed problems, she said. Many doctors discourage extensive genetic tests, thinking they wont find anything helpful. In the absence of known treatments, insurers are also reluctant to pay for such tests, discouraging all but the most fortunate and resourceful parents. Even for them, there are no guarantees.

The other tough reality is the possibility this treatment wont be completed in time to help Maxwell, said Freed. I love him with every ounce of my being, and I want him to know that I did everything humanly possible to change his outcome.

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Genetic Resistance to Devastating Ash Tree Disease Discovered and It Could Help Save the Species – EcoWatch

Friday, November 22nd, 2019

From 2010 to 2017, the U.S. unintentionally played middleman to somewhere between 650 and 772 tons of shark fin exports, accounting for as many as 1.29 million sharks. (The exact number of sharks is difficult to determine, since most of the records NRDC managed to obtain expressed shipment size by weight, not individual parts, and different conditions translate into different weights per piece. Frozen fins weigh more than dried fins, for example).

"When we let these shark fin shipments pass through our borders without monitoring them, the U.S. becomes a weak link," says report coauthor Elizabeth Murdock, director of the NRDC's Pacific Oceans Initiative.

It doesn't have to be this way. The U.S. has a stronger legal framework and more regulatory resources than most of the world. If anything, we should be one of the strongest links in the fight against a black market trade that threatens marine biodiversity.

Back in 2000, the U.S. banned shark finning, the practice of cutting a shark's fins off and then dumping the animal back into the ocean. But it is still legal in many states to catch a shark, bring it back to shore, and cut it up into parts including fins, steaks, and other marketable items. (Possessing or selling shark fins is not always illegal just when the fins come from species protected by the Endangered Species Act or the Convention on International Trade in Endangered Species of Wild Fauna and Flora).

Each year, tens of millions of sharks wind up on hooks and in nets, many of which belong to Americans. According to NRDC's report, the number of sharks we land each year makes us the seventh-largest shark-fishing nation in the world. Still, scientists seem to agree that the U.S. is doing a pretty good job of managing its shark populations. A study published in 2017 in the journal Current Biology listed America's Alaskan skate, blacktip shark, and spiny dogfish fisheries (among others) as "bright spots of sustainable shark fishing." Indeed, countries such as the U.S., Australia, Canada, and New Zealand are leading the world when it comes to harvesting sharks in ways that don't drive them toward extinction. However, the unfortunate fact remains that the vast majority (91 percent) of the world's shark fisheries are unsustainable.

Silky shark. NOAA / Teachers at Sea Program

As cargo, shark fins are not required to route through one of those 17 ports if they are not "unloaded." If that's the case, those fins can move along without a second glance. At the same time, products that qualify as "seafood" are also exempt from special port inspection unless the species involved requires a permit under the Endangered Species Act (which lists only the two hammerhead species mentioned above) or CITES (which lists only 14 of the more than 400 shark species known to science). The hammerhead fins in Hong Kong were listed as "dried seafood," which is one of the reasons why they were able to pass through Houston without closer inspection.

Murdock says sharks slip through a legal loophole because they qualify as both wildlife and seafood. This makes shark products even more difficult to regulate than, say, elephant ivory or rhino horn. "It's not a new problem," says environmental consultant David Shiffman, a marine conservation biologist at Arizona State University, "but it's one that doesn't get a lot of attention."

"One of the things is just how it's coded," Shiffman says. "In some countries shark is counted as 'seafood, frozen,' and in some cases it's 'shark fins,' and in some cases it's shark fins from a particular species. But it's not consistent from country to country, and it's not necessarily consistent from year to year, and that makes it really hard to keep track of this stuff."

So how do we help close these loopholes? Murdock says routing all shark fin shipments through the ports where officials have capacity to inspect them properly should become standard operating procedure. (This measure alone wouldn't stop every illegal wildlife shipment; Houston, after all, is one of those ports). A full-on federal ban against the shark fin trade wouldn't hurt either, she says. (Twelve states, such as Texas and California, have so far banned the shark fin trade within their borders). Other recommendations from the report are more international in scope, including ratcheting up the existing CITES resolutions; improving enforcement of fishing laws in nations where the shark products typically originate; and generally more, more, and still more partnerships between countries.

"It's clear that it's only going to get solved through international collaboration, because some of the countries from which these shipments are coming have a lot less capacity for law enforcement and inspections and monitoring than the United States does," says Murdock. So by stepping up efforts on our own shores, we can also help keep things on the up-and-up all over the world.

Shiffman says the report "has some excellent recommendations of what we should do about this," but he'd really like to see more data on how prevalent the problem is. And so would Murdock. She and her colleagues have had to scratch and claw for roughly two years to bring as many cases to the surface as they have.

"We're confident that this is just the tip of the iceberg," says Murdock. "It's just hard to know how big the iceberg is."

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A Rare Genetic Disorder Turned These Siblings’ Blood ‘Milky’ White – Livescience.com

Friday, November 22nd, 2019

A rare genetic disorder caused three siblings' blood to flood with fat and turn "milky" white, according to a new report of the unusual case.

The three siblings consisted of one set of fraternal twins (a daughter and son) and an older son, all born to a first-cousin couple in a Pennsylvania Dutch family. In their teens and early 20s, all three siblings experienced mysterious symptoms, including bouts of abdominal pain. They had all been diagnosed with hypertriglyceridemia, a fairly common disorder that causes fatty molecules called triglycerides to build up in the blood.

Now in their 50s, the siblings recently underwent genetic testing and learned that they have a condition that's much more rare, affecting only 1 in every million people, according to the case report, published today (Nov. 18) in the journal Annals of Internal Medicine.

Those with the ultrarare disorder, known as familial chylomicronemia syndrome (FCS), may accumulate more than 1,000 milligrams of triglycerides per deciliter (mg/dL) of blood. For comparison, normal blood levels of the fat should fall below 150 mg/dL, and 500 mg/dL would be considered "very high" in a healthy person, according to the National Institutes of Health.

Indeed, in people with FCS, blood fat levels are so high that the normally crimson fluid turns the color of milk. (FCS is not the only condition that can cause milk-colored blood; the symptom may also appear in people with severe hypertriglyceridemia.)

Related: The Color of Blood: Here Are Nature's Reddest Reds (Photos)

The three siblings had long struggled to keep their triglyceride levels under control and suffered frequent inflammation of the pancreas, also known as pancreatitis a serious condition that can cause abdominal pain, fever and vomiting. At the hospital, the male twin's triglyceride levels reached as high as 5,000 mg/dL, while the other brother's levels peaked at around 6,000 mg/dL. The female twin's triglyceride levels soared highest of all, reaching 7,200 mg/dL at maximum.

The siblings hoped their doctors could help subdue those aggressive symptoms.

To confirm the sibling's rare diagnosis, the doctors looked to their patients' genes. Triglycerides typically build up in the blood due to multiple malfunctioning genes and other related health conditions, such as diabetes or high-blood pressure, according to the Journal of the American Board of Family Medicine. But when doctors probed the siblings' genetic code, the researchers spotted only one mutated gene that was key for breaking down triglycerides in the body.

In healthy people, the gene contains instructions to build a protein called lipoprotein lipase (LPL), which typically coats the blood vessels that run through muscles and fatty tissues in the body, according to the Genetics Home Reference. LPL breaks down fats carried in the blood; without an adequate supply, the siblings' blood plasma ran thick with excess triglycerides.

Related: How to Speak Genetics: A Glossary

Each sibling carried two copies of the mutated LPL gene, meaning both their parents passed down the mutated genetic code to the children, the case report noted. What's more, the particular genetic mutation in the siblings had never been seen before, the authors said. The doctors placed the siblings on a fat-restricted diet, which successfully stabilized their triglyceride levels and quelled their bouts of pancreatitis. Sometimes, when triglyceride levels spike, doctors must manually replace the fat-filled blood of their patients with healthy blood from donors, Live Science previously reported. Thankfully, the siblings' condition could be curtained with diet alone.

Originally published on Live Science.

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Camel Milk and Autism: Connecting the Genetic Dots | DNA Science Blog – PLoS Blogs

Friday, November 22nd, 2019

After reading Christina Adamss new book Camel Crazy: A Quest for Miracles in the Mysterious World of Camels(New World Library), I may have a new favorite animal (sorry, cats and hippos).

Most of us know camels as curiosities at zoos. As beasts of burden highly adapted to hot and dry climates, theyve served the trade routes that helped build civilizations, and may indeed flourish in our increasingly hot and dry world. We value their hide, meat, and especially their milk.

Camels are unusual, biologically speaking. And that may be why their milk can alleviate some aspects of autism.

Camel milk sounds weird to American ears, but camels are a domestic fact of life elsewhere. Although the US classifies them as exotic animals, they actually have early origins here; fossils have been found in Los Angeles. But the true reservoir of knowledge on camels is found in rural cultures and universities in the Middle East, Asia, and Africa, Christina told me.

Got Camel Milk?

In 2005, Christina met a camel at a childrens book fair in Orange County CA. Rather than hauling kids around, the animal was standing near a display of lotions and soaps made with camel milk. When the owner started to tell Christina how the milk is hypoallergenic and helps premature babies in the Middle East, she glanced over at 7-year-old Jonah. Hed already had four years of costly treatments for autism.

Might it help reboot my sons immune system and help his autism symptoms? she recalls thinking, aware of a link to immune dysfunction. Cow milk and cheese made him hand-flap and walk in circles, which he described as feeling like having dirt in my brain. Vegan substitutes like rice, nut, or soy increased his allergic response.

Camel Crazy details Christinas two-year journey to find the milk. Once she started giving it to Jonah, four ounces at a time, mixed in with food like cereal, his behavior changed quickly.

He became calm. Inquisitive. Caring. His language became more emotional and focused. He held his head straight instead of rolling it. Eating became neat, not a mess fest. He dressed himself and began making eye contact. He even got his shoes and backpack on and was calmer in the car going to school.

By the third dose, Jonah was sleeping through the night. He became more fluid, social, and attuned. Within days he could cross the street without me holding on to him. Within weeks his skin grew smoother. The milk also reversed his skin irritation, agitation, mental distraction, hyperactivity, and stomach pain, Christina recalled.

So she did research and spread the word, first in an article Got Camel Milk? that went viral, then in a peer-reviewed case report, Autism Spectrum Disorder Treated With Camel Milk, published in Global Advances in Health and Medicine. After describing Jonahs early difficulties, she wrote on October 10, 2007, two weeks before my sons tenth birthday, he drank his first half cup (4 oz) of thawed raw unheated camel milk. The case report documents Jonahs sustained symptom improvements associated with drinking half a cup a day from 2007 to 2013.

Christina then began traveling the world, giving presentations on camel milk and autism, and consulting with scientists and vets. Camel Crazy details her immersion into the world of camels and cameleers, from Tuareg, Amish and Somali people in America to herders in India, Dubai and Abu Dhabi. She serves on the editorial board of the new International Journal of Camel Science.

I was a beta reader for Camel Crazyand loved it. Being a nerd I searched for the science, and wasnt disappointed. The milk indeed has some startling differences from other milks, yet tastes, Christina says, like cows milk.

Camels drink a lot, pee a little, exhale minimal vapor, have insulating coats, and their red blood cells balloon and shrink as the water content in the bloodstream shifts. Natural selection has favored persistence of these traits that provide adaptation to heat, aridity, and exposure to intense ultraviolet radiation and choking dust. Body temperature ranges from 93.2-104F (3440C).

Being specifically a genetics nerd, I delved deeper into the DNA that encodes the unusual versions of proteins that might explain the magic of camel milk, as well as other details of the physiology. Much of the info below comes from the article Desert to Medicine: A Review of Camel Genomics and Therapeutic Products, from three researchers at United Arab Emirates University.

Fighting an Opioid Released from Casein Breakdown

The first technical paper Christina found was The etiology of autism and camel milk as therapy, from Ben Gurion University researchers Reuven Yagil and Yosef Shabo. Parent reports inspired their work.

They zeroed in on an opiate-like effect. Casein, the most abundant milk protein, breaks down into peptide pieces. And one of them, beta-casomorphin-7, is an opioid. It can slip through the leaky gut of a person with autism and enter the brain. Could an opiate bathing the brain affect social interactions and lack of interest in surroundings?

Other breakdown peptides of casein (-casein and no -lactoglobulin), which are more abundant in cows milk, may spike milk allergies.

Upping Anti-Oxidants

Camel milk delivers potent anti-oxidants that might temper autism symptoms, wrote King Saud University researchers Laila Al-Ayadhi and Nadra Elyass Elamin in a2013 report. People with autism are more sensitive to oxidative stress, which is damage from unstable forms of oxygen called oxygen free radicals.

The researchers measured levels of three anti-oxidants in the blood of 60 kids with autism: superoxide dismutase, myeloperoxidase, and an enzyme needed to make glutathione. Over a two-week period, 24 children drank raw camel milk, 25 drank boiled camel milk, and 11 drank cows milk. The trial was double-blinded and randomized, but it wasnt a crossover, in which each child would have had all three milk experiences. Nevertheless, raw camel milk was superior in anti-oxidant levels and a behavioral rating scale.

Special Tiny Antibodies

Camels share with only their camelid brethren (llamas, alpacas, vicunas, and guanacos) tiny antibodies in milk, called nanobodies. Most antibodies have one or more Y-shaped subunits; a nanobody is one arm of one Y, the variable region that distinguishes species. A student discoveredcamel nanobodies in a lab course at the University of Brussels in 1993, analyzing a dromedarys blood serum. Camels make large antibodies too.

Nanobodies can squeeze into places more bulbous antibodies cannot, vanquishing a wider swath of viruses and bacteria. They look strikingly like monoclonal antibodies, and so have become darlings of pharma, particularly in cancer drug discovery.

A camels streamlined nanobodies arose from a mutation that removed the hinges that connect the Y-shaped arms of more conventional antibodies. Sometimes a mutation is a good thing!

Further infection protection comes from the milk protein lactoferrin, which fights hepatitis C.

Tolerating High Blood Sugar

A camel-herding people in India, the Raika, drink camel milk and dont get diabetes. Thats because camels tolerate high blood glucose levels, and some of that ability seeps into their milk.

P. Agrawal, at the SP Medical College, Bikaner, India and colleagues have conducted clinical trialsthat show that camel milk decreases blood glucose and hemoglobin A1c (a three-month-measure of blood glucose), and, in people with type 1 diabetes, reduces the insulin requirement by up to 30 percent .

How can camels have high blood sugar yet low HbA1C? In most animals, the beta chains of hemoglobin bind glucose at several points, upping HbA1C. This doesnt happen in camels. If glucose binding to hemoglobin in us is like Velcro, then in camels, its like contact between a boot and slippery ice.

Conserving Water

Milk requires water, and camels are masters at conserving it. A self-contained cooling system, as Christina describes it, cycles body water from a camels nostrils to its mouth. The multi-layered eyelids and double row of eyelashes keep out blowing sand. Their unique oval blood cells compress as camels safely dehydrate, then swell up again as they refill with water, keeping their blood flowing in extreme conditions.

Camels dont dry out in the desert, as we would, thanks to variants of the genes that encode the cytochrome P450 (CYP) enzymes. They enable camels to resorb lots of water while tolerating high salt conditions, without their blood pressure spiking. Their kidneys are keenly attuned to taking back water.

Camel milk is also high in the calming neurotransmitter GABA, low in lactose, and has more vitamin C than cows milk.

Beyond Milk

The astonishing adaptations of the camel arent restricted to its milk. Here are a few more that have their roots in the animals genes.

Variations on the Camel Theme

About 94% of the worlds 35 million camels are the domesticated, one-humped dromedaries (Camelus dromedaries) of northern and eastern Africa, the Arabian Peninsula, and southwest Asia. A feral branch lives in Australia. Wild dromedaries are extinct and are in a separate genus, Camelops hesternus. They dwelled in western North America.

About 2 million two-humped domesticated Bactrian (Camelus bactrianus) camels live on the steppes of central Asia, and each weighs about 1,000 pounds. Fewer than 100 wild Bactrian camels remain; they split from a shared ancestor about 700,000 years ago. Today they live in Mongolia and in northwest Chinas Xinjiang Province, in an area that was a nuclear testing site for 45 years. In 2008 the wild Bactrians were designated a distinct species, Camelus ferus.

When bactrian and dromedary camels interbreed, most offspring have one hump, some with a dip in the middle.

Camel Genomics

Camel genomes are remarkably diverse with many mutations, perhaps because people havent controlled their breeding. Doing so is challenging.

The jelly-like consistency of camel semen complicates both freezing and using artificial insemination. Still, researchers from Oman and France recently published a report about possible genetic improvements: selecting for traits that ease of using milking machines, provide resistance to infections, improve racing ability, and enhance beauty. Camels are, after all, gorgeous creatures.

The first camel genome sequence, published in 2012, revealed 20,821 genes splayed out among 37 chromosome pairs. Some 2,730 genes have evolved faster in camels than in their cattle relatives, many involved in carbohydrate and lipid metabolism. Perhaps the unusual variants contribute to the camels ability to conserve water.

Researchers from Kuwait University report in PLOS Onethat they analyzed DNA from the blood, spit, and hair of nine camels, concluding that tail hair follicle DNA is the best tissue source to create a biobank.The International Camel Consortium for Genetic Improvement and Conservation promotes camel genetic conservation.

Bring on the Camel Fro-Yo!

The milk isnt cheap. Camel Milk Cooplists $36.99 for a weeks supply. And as Christinas book explains, theres little to no incentive to conduct a clinical trial or to attempt to replicate natures magical mix of milk ingredients. Camel Crazy includes a users guide and directory of global sources.

The milk is available in liquid, frozen, and powdered form. Camel-milk-containing products include skin cream, cheeses, ice cream pops, chocolate milk, and a delectable-looking sweet called barfi, which means snow in Persian (not vomit).

When will camel milk come to Starbucks?

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Myriad Genetics Announces Regulatory Approval of the BRACAnalysis Diagnostic System in Japan for Breast Cancer Patients – BioSpace

Friday, November 22nd, 2019

SALT LAKE CITY, Nov. 21, 2019 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (NASDAQ: MYGN), a leader in molecular diagnostics and precision medicine, announced that Japans Ministry of Health, Labour and Welfare (MHLW) has approved the BRACAnalysis Diagnostic System (i.e., BRACAnalysis) to help physicians determine which women with breast cancer have Hereditary Breast and Ovarian Cancer (HBOC) syndrome and qualify for additional medical management. BRACAnalysis is a genetic test that identifies germline mutations in the BRCA1/2 genes.

We are excited that the MHLW has approved the BRACAnalysis Diagnostic System for HBOC risk assessment in patients with breast cancer, said Seigo Nakamura, M.D., Ph.D., Professor and Chairman, Department of Surgery, Division of Breast Surgical Oncology and Director, Breast Center of Showa University Hospital in Tokyo and president of the Japanese Organization of Hereditary Breast and Ovarian Cancer (JOHBOC). Our goal is to use the BRACAnalysis test to identify patients with BRCA mutations and determine who will benefit from more advanced medical care.

Under the MHLW decision, physicians may use BRACAnalysis to test for BRCA mutations in women with breast cancer who meet the genetic testing guidelines defined by JOHBOC. Those patients who test positive for a deleterious BRCA mutation will be eligible to receive advanced medical management, such as prophylactic surgery or targeted therapies.

Myriads BRACAnalysis test is the gold standard for BRCA testing. The approval of BRACAnalysis for HBOC risk assessment in Japan is further validation of the quality and utility of our pioneering genetic test, said Gary A. King, executive vice president of International Operations, Myriad Genetics. We look forward to working with our commercial partners in Japan to ensure that BRACAnalysis is available to patients.

Myriad has an exclusive partnership with SRL Inc., a subsidiary of Miraca Group, to commercialize the BRACAnalysis Diagnostic System in Japan.

Todays announcement follows two prior regulatory approvals for the BRACAnalysis Diagnostic System in Japan. In February 2019, BRACAnalysis was approved as a companion diagnostic for Lynparza (olaparib) in women with ovarian cancer, and in March 2018, it was approved as a companion diagnostic for Lynparza in patients with metastatic inoperable or recurrent breast cancer.

About the BRACAnalysis Diagnostic SystemBRACAnalysis is a diagnostic system that classifies a patients clinically significant variants (DNA sequence variations) in the germline BRCA1 and BRCA2 genes. Variants are classified into one of the five categories; Deleterious, Suspected Deleterious, Variant of Uncertain Significance, Favor Polymorphism, or Polymorphism. Once the classification is completed, the results are sent to medical personnel in Japan for determining the eligibility of patients for treatment with Lynparza.

About SRLSince the establishment in 1970, SRL, Inc., a member of the Miraca Group, Japan-based leading healthcare group, has been providing comprehensive testing services as the largest commercial clinical laboratory in Japan. SRL carries out nearly 400,000,000 tests per year, covering a wide range of testing services including general/emergency testing, esoteric/research testing, companion diagnostics tests, genomic analysis, and etc. For more information, please visit https://www.srl-group.co.jp/english/.

About Myriad GeneticsMyriad Genetics Inc., is a leading precision medicine company dedicated to being a trusted advisor transforming patient lives worldwide with pioneering molecular diagnostics. Myriad discovers and commercializes molecular diagnostic tests that: determine the risk of developing disease, accurately diagnose disease, assess the risk of disease progression, and guide treatment decisions across six major medical specialties where molecular diagnostics can significantly improve patient care and lower healthcare costs. Myriad is focused on five critical success factors: building upon a solid hereditary cancer foundation, growing new product volume, expanding reimbursement coverage for new products, increasing RNA kit revenue internationally and improving profitability with Elevate 2020. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BART, BRACAnalysis, Colaris, Colaris AP, myPath, myRisk, Myriad myRisk, myRisk Hereditary Cancer, myChoice, myPlan, BRACAnalysis CDx, Tumor BRACAnalysis CDx, myChoice CDx, EndoPredict, Vectra, GeneSight, riskScore, Prolaris, ForeSight and Prequel are trademarks or registered trademarks of Myriad Genetics, Inc. or its wholly owned subsidiaries in the United States and foreign countries. MYGN-F, MYGN-G.

Lynparza is a registered trademark of AstraZeneca.

Safe Harbor StatementThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to Japans Ministry of Health, Labour and Welfare (MHLW) marketing approval of the companys BRACAnalysis Diagnostic System to identify patients with breast cancer who would be eligible for additional medical management; the Company working with commercial partners in Japan to ensure that BRACAnalysis is available to patients; and the Company's strategic directives under the caption "About Myriad Genetics." These "forward-looking statements" are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by forward-looking statements. These risks and uncertainties include, but are not limited to: the risk that sales and profit margins of our molecular diagnostic tests and pharmaceutical and clinical services may decline; risks related to our ability to transition from our existing product portfolio to our new tests, including unexpected costs and delays; risks related to decisions or changes in governmental or private insurers reimbursement levels for our tests or our ability to obtain reimbursement for our new tests at comparable levels to our existing tests; risks related to increased competition and the development of new competing tests and services; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and pharmaceutical and clinical services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and pharmaceutical and clinical services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and pharmaceutical and clinical services and any future tests and services are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating our laboratory testing facilities and our healthcare clinic; risks related to public concern over genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to our ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we license or acquire; risks related to our projections about our business, results of operations and financial condition; risks related to the potential market opportunity for our products and services; the risk that we or our licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying our tests; the risk of patent-infringement claims or challenges to the validity of our patents or other intellectual property; risks related to changes in intellectual property laws covering our molecular diagnostic tests and pharmaceutical and clinical services and patents or enforcement in the United States and foreign countries, such as the Supreme Court decision in the lawsuit brought against us by the Association for Molecular Pathology et al; risks of new, changing and competitive technologies and regulations in the United States and internationally; the risk that we may be unable to comply with financial operating covenants under our credit or lending agreements; the risk that we will be unable to pay, when due, amounts due under our credit or lending agreements; and other factors discussed under the heading "Risk Factors" contained in Item 1A of our most recent Annual Report on Form 10-K for the fiscal year ended June 30, 2019, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

Media Contact: Ron Rogers(801) 584-3065rrogers@myriad.com

Investor Contact:Scott Gleason(801) 584-1143sgleason@myriad.com

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Ash dieback: Genetic resistance offers new hope over unstoppable disease expected to kill 70 per cent of species – The Independent

Friday, November 22nd, 2019

A devastating fungal disease, the cause of ash dieback, is on course to decimate Europes ash trees, with 70 million in the UK currently expected to perish over the coming years, costing the economy an estimated 15bn.

But in some pockets of woodland, resistance to the sickness has been detected, offering a glimmer of hope that ash trees will not be permanently erased from the landscape.

Scientists sequenced whole genomic DNA from 1,250 ash trees in 31 different areas in order to identify the inherited genes associated with ash dieback resistance.

Sharing the full story, not just the headlines

The study, published in the journal Nature Ecology & Evolution, shows resistance is controlled by several genes, offering hope survivors could be used to restore diseased woodlands, either by natural regeneration or selective breeding.

Professor Richard Nichols, author of the study from Queen Mary University of London, said: We found that the genetics behind ash dieback resistance resembled other characteristics like human height, where the trait is controlled by many different genes working together, rather than one specific gene.

Overall winner of the competition

Csaba Daroczi/NPOTY 2019

Winner in the Underwater category

Alexey Zozulya/NPOTY 2019

Finalist in the Mammals category

Jose Juan Hernandez/NPOTY 2019

Finalist in the Man and Nature category

Tom Svensson/NPOTY 2019

Finalist in the Mammals category

Marcio Cabral/NPOTY 2019

Winner of the Youth category

Giacomo Redaelli/NPOTY 2019

Finalist in the Man and Nature category

Britta Jaschinski/NPOTY 2019

Finalist in the Other Animals category

Wei Fu/NPOTY 2019

Finalist in the Landscapes category

Brandon Yoshizawa/NPOTY 2019

Finalist in the Man and Nature category

Pedro Narra/NPOTY 2019

Overall winner of the competition

Csaba Daroczi/NPOTY 2019

Winner in the Underwater category

Alexey Zozulya/NPOTY 2019

Finalist in the Mammals category

Jose Juan Hernandez/NPOTY 2019

Finalist in the Man and Nature category

Tom Svensson/NPOTY 2019

Finalist in the Mammals category

Marcio Cabral/NPOTY 2019

Winner of the Youth category

Giacomo Redaelli/NPOTY 2019

Finalist in the Man and Nature category

Britta Jaschinski/NPOTY 2019

Finalist in the Other Animals category

Wei Fu/NPOTY 2019

Finalist in the Landscapes category

Brandon Yoshizawa/NPOTY 2019

Finalist in the Man and Nature category

Pedro Narra/NPOTY 2019

Now we have established which genes are important for resistance we can predict which trees will survive ash dieback. This will help identify susceptible trees that need to be removed from woodlands, and provide the foundations for breeding more resistant trees in future.

Samples were collected from ash trees in a Forest Research mass screening trial, which comprises 150,000 trees across 14 sites in southeast England.

The researchers screened for resistance genes using a rapid approach where the DNA of diseased and unaffected trees was separated.

Many of the genes found to be associated with ash dieback resistance were similar to those previously shown to be involved in disease or pathogen responses in other species.

Ash dieback is a major threat to the UK landscape. According to the Woodland Trust, the effects will be staggering.

It will change the landscape forever and threaten many species which rely on ash, the trust has warned.

The fungus Hymenoscyphus fraxineusaffects ash trees of any age and in the UK between 70 and 95 per cent of ash trees are expected to succumb.

The 15bn economic impact is expected to be greater than that of the 2001 foot-and-mouth disease outbreak which led to more than 6 million cattle and sheep being exterminated, according to an assessment this year by a team from Oxford University.

The predicted costs include clearing up dead and dying trees, but also lost benefits provided by the trees, including water and air purification and carbon sequestration.

The loss of these services is expected to be the biggest cost to society, while millions of ash trees also line Britains roads and urban areas, and clearing up dangerous trees will cost billions of pounds.

The disease has spread throughout Europes ash populations, and was first recorded in the UK in 2012.

Professor Richard Buggs, senior research leader in plant health at the Royal Botanic Gardens, Kew and lead author of the paper, said: There is no cure for ash dieback and it threatens to kill over half of the 90 million ash trees in the UK. This will have huge impacts on the British landscape.

Our new findings of the genetic basis of natural resistance found in a small minority of British ash trees help us to predict how ash populations will evolve under ash dieback. While many ash trees will die, our findings are encouraging from a long-term perspective and reassure us that ash woodlands will one day flourish again.

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Ash dieback: Genetic resistance offers new hope over unstoppable disease expected to kill 70 per cent of species - The Independent

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An American company will test your embryos for genetic defects. But designer babies aren’t here just yet – The Conversation AU

Friday, November 22nd, 2019

Designer baby, anyone? A New Jersey startup company, Genomic Prediction, might be able to help you.

Genomic Prediction claims to be able to use DNA testing to predict disease risk in an embryo. The idea is to study hundreds or thousands of small variations in DNA, known as genetic markers, and use sophisticated computer algorithms to correlate these with diseases such as type 1 and type 2 diabetes, breast cancer and intellectual disability.

If the companys recent research is any guide, it may move on to predicting other traits such as height and even educational attainment.

But the connections between genetic variations and differences in real human beings are far from straightforward. And even if we can make these connections, should we?

In my own field, forensic genetics, we have a similar goal: to produce a molecular photofit or DNA mugshot of the perpetrator of a crime, using DNA left at a crime scene. At first, there was great optimism.

Only six genetic markers were required to predict blue or brown eye colour with reasonable accuracy. However, prediction of intermediate eye colours (green, hazel, light brown) was less accurate. Testing for hair colour soon followed (24 markers) and, most recently, skin colour (41 markers).

Eye, hair and skin colour are all largely controlled by a small number of genes related to the pigment melanin. There are two types of melanin, a dark and a light form, and between them they give rise to the spectrum of eye, hair and skin colours.

Read more: World's first genetically modified human embryo raises ethical concerns

High doses of the light pigment are found only in individuals with European ancestry, particularly northern European. Prediction systems have really only been developed and tested rigorously on Europeans and North Americans.

This is the case with many large genome-wide association studies (GWAS) and data sets, including some of those used by Genomic Prediction. Individuals without European ancestry are poorly represented, and the associations between genetic markers and traits dont always replicate in populations that dont have European ancestry.

Since these first few pigmentation prediction systems, progress has been slow in forensic genetics. This is because most traits even ones that are strongly influenced by genetics are very polygenic, which means they are influenced by many different genes.

For example, height and educational attainment are both highly heritable. But they are under the influence of hundreds, if not thousands, of genetic markers, each with a very small effect on the trait.

Further, the marker variants with the largest influence are generally the rarest ones. For example, the variants with the largest influence on height each account for only one or two centimetres and are present in no more than 0.2% of the population. More common variants each account for height differences of mere millimetres or even less.

Polygenic scores add up all the tiny effects of these multiple marker variants to give an overall prediction. But there are several caveats.

First, they dont take account of genetic synergies (epistasis). The effects of two (or more) different markers may not add up in any simple way.

Second, they completely ignore environmental effects: the nurture part of nature versus nurture. For example, although both are highly heritable, height is affected by nutrition, and educational attainment is influenced by educational expectations and parental education. So, really, what is being predicted is the genetic potential for a particular trait.

Assuming Genomic Prediction can predict these potentials accurately, will they all be found in one embryo?

Lets say you want a tall, brown-eyed, high educational achiever with a low risk of breast cancer. The odds of finding all of these potentials in one embryo is very low, like throwing dozens of dice and having them all come up with sixes.

Even if you are lucky with your roll of the genetic dice, are you sure your designer baby will thank you when they grow up? Your idea of the perfect trait might not be theirs. You are, in effect, choosing their DNA without their consent.

Read more: 3-parent IVF could prevent illness in many children (but it's really more like 2.002-parent IVF)

Are you ready to see a prediction of what your baby might look like as an adult, or a photo-board from which to choose your future offspring? Companies are already offering to produce molecular photofits of unknown donors of crime-scene DNA. Its not a giant leap to designer babies.

At US$1,000 per case and an additional US$400 per screened embryo for expanded pre-implantation genomic testing (EPGT is Genomic Predictions flagship product), designer babies will inevitably be more available to wealthier parents. There are valid concerns that this could lead to genetic advantage and disadvantage along socio-economic lines.

Genetic screening is already common practice, especially for chromosomal disorders. Like many others, my own daughter received a nuchal fold thickness assessment as a standard ultrasound screen for Down syndrome.

Screening for genetic risks is just one more step along this continuum. But how many steps should we take? Once we start selecting for desirable characteristics, its easy to see the moral slope becoming very slippery.

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iOmx Therapeutics’ iOTarg Genetic Screening Platform Featured in Podium Presentation at PEGS Europe 2019 – PRNewswire

Friday, November 22nd, 2019

MARTINSRIED, Germany and MUNICH, Nov. 21, 2019 /PRNewswire/ -- iOmx Therapeutics AG (iOmx), a biopharmaceutical company developing cancer therapeutics based on novel immune checkpoint targets, announced today that its Vice President, Antibody Development, Stefanie Urlinger, PhD, delivered a podium presentation highlighting the discovery of IGSF11, a novel immune checkpoint molecule on tumor cells, using its iOTarg discovery platform at the 11th PEGS Europe Protein & Antibody Engineering Summit (PEGS Europe 2019) in Lisbon, 12-18 November, 2019.

The podium presentation, titled, "A Comprehensive Screening Platform to Identify the Next Generation of Cancer Immunotherapy Targets," reports the identification of IGSF11, a postulated VISTA interaction partner, as an important immune checkpoint molecule on tumor cells using iOTarg, the company's proprietary, high-throughput target discovery platform. In an MC38 murine colon adenocarcinoma mouse model, CRISPR knockout of IGSF11 resulted in a >70% reduction in tumor growth, independently validating the target. Interestingly, patients refractory to anti-PD1 or anti-CTLA4 therapies overexpress IGSF11 and exhibit poor progression-free survival.

Based on these findings, iOmx is developing a novel anti-IGSF11 antibody as monotherapy in patients with solid tumor indications that are resistant to PD-1/PD-L1 therapies. The company presented data showcasing their IGSF11-specific antibodies which block the interaction to VISTA and exhibit strong immune lysis of tumor cells in vitro. Additionally, beyond IGSF11, iOTarg resulted in the identification of other novel immune checkpoint targets and unique immune evasion biologies against which iOmx is pursuing first-in-class drug development projects - all in the pre-clinical stage.

"Current limitation of the approved immune checkpoint inhibitors to induce response in majority of cancer patients requires us to identify and drug additional key vulnerabilities in refractory tumors," said Nisit Khandelwal, Ph.D., co-founder and Senior Vice President of iOmx Therapeutics. "PEGS Europe 2019 Summit is an ideal event to showcase the ability of iOmx' iOTarg genetic screening platform to systematically identify novel and druggable immune checkpoint targets, such as IGSF11, that are expressed by PD-L1 non-responsive tumors. Based on our findings, we have initiated pre-clinical development of a first-in-class IGSF11-targeting antibody that eliminates tumor induced immune suppression, especially in anti-PD-1 refractory tumors. Furthermore, we continue to investigate new immuno-oncology targets with our unique iOTarg discovery engine."

About iOmx TherapeuticsiOmx (www.iomx.com) focuses on the development of first-in-class cancer therapeutics addressing novel immune checkpoints hijacked by cancer cells. The company's proprietary platform, iOTarg, systematically screens tumor cells for expression of immune checkpoint modulators, that, when knocked-down, increase T cell immunity against cancer cells. iOmx is building a pipeline of promising cancer immunotherapeutics based on novel, proprietary targets with a known mode of action. Founded in 2016 based on the work of its scientific founders Philipp Beckhove and Nisit Khandelwal conducted at the German Cancer Research Center, the company has been funded by MPM Capital (both its BV2014 and UBS Oncology Impact Funds), Sofinnova Partners, Wellington Partners and Merck Ventures and is based in Martinsried / Munich, Germany.

Contact:Investor / Media Contacts: Miriam Miller / Jason Rando Tiberend Strategic Advisors, Inc. 212-375-2694 / 2665 mmiller@tiberend.com jrando@tiberend.com

SOURCE iOmx Therapeutics AG

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Scientists reveal why we feel so tired in the morning – Yahoo Sports

Sunday, November 17th, 2019

If youre the type of person who snoozes your alarm every morning or cant function before (or even after) yourmorning coffee, there might be a genetic reason for that.

New research by DNA testing company,23andMe, has discovered that genetic programming plays a part in our wake up time.

The research studied over 1,500 British people to determine that 7.55am was the UKs average genetic wake up time.

This means that the average Brit willwake upnaturally just before 8am each day.

READ MORE: Drinking tea or coffee has no impact on sleep, according to study

Many people set their alarms for much earlier than that, hence our feelings of tiredness and lack of productivity.

Interrupting your bodys circadian rhythm (which is the official term for our body clock) can leave us feeling out of sorts at the beginning of the day.

If you dont feel tired first thing, it doesnt mean youre immune to these feelings. Many people have tiredness slumps at different points in the day.

READ MORE: Parents can buy children anti-nightmare mist

TheNHShas found that one in five of us get unusually tired and have suggested some good ways to wake yourself up when the slump sets in.

Exerciseis cited as one of the key ways to bolster your energy reserve. Aside from the psychological benefits of exercise, it alsolowers your risk of early death by 30%.

Cutting down oncaffeineis another recommended way to beat the tiredness. As a nation of tea drinkers, we are all at risk of being over-stimulated by the affects of caffeine. Switching to decaffeinated tea and coffee could make all the difference.

Getting into a routine of having daytime naps may also interrupt your bodys circadian rhythm. If you go to sleep every time you feel a bout of tiredness, you may struggle to get to sleep at night, so says the NHS.

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Should this deer be culled? The answer may not be what you think. – Clarion Ledger

Sunday, November 17th, 2019

Mississippi has produced some giant bucks and even a world record. Here are the top six deer on record in Mississippi by category. Brian Broom

Studies show genetics can't be controlled in wild deer populations

It's a common debate on social media.

A hunter gets a photo on a game camera that shows a deer with a spike on one side and a normal antler on the other and asks if the deer should be removed.

Many will say the buck needs to be taken to prevent the continuation of its genesinto future generations, but biologists say that's probably not the correct answer.

Many hunters feel a buck with a spike on one side should be removed from the herd to improve genetics, but biologists say that's not the case.(Photo: Special to Clarion Ledger)

"That's almost always related to some kind of injury," said Kip Adams, Quality Deer Management Association director of conservation. "It's usually not genetic.

"Most of those are injury-related. Deer just aren't genetically built to have crazy antlers like that. Most of the time, if the animal is allowed to live, he'll drop those antlers and you won't see it in future years."

However, there are times when a malformed antler caused by injury will return after antlers are shed.

"It could," Adams said. "It could be an injury to the base. If the injury is right at the base of the antler, it could recur in future years."

Adams said a serious injury to the body can also cause a recurring abnormal antler.

"Again, none of that is genetic-related," Adams said. "So, it's not passed on.

"If you remove them you're not doing anything to change the genetics of the deer herd. The only gain you're making is providing more food for the rest of the herd by removing them."

One of the causes of pedicle, or antler base damage, that seems to be more common is what has been called "dirty sheds."

Gabriel Karns, who is currently avisiting assistant professor in the School of Environment and Natural Resources at Ohio State University, wrote an article published by QDMA about his work examining skulls of bucks with spikes on one side.

"Most commonly, it appeared that antlers had failed to cleanly separate from the pedicles, as in normally shed antlers,and that the antler base had fractured off portions of the pedicle and sometimes even the surrounding cranium those dirtysheds I mentioned earlier," Karns wrote."Although the antlerogenic periosteum tries to heal itself in advance of the next antler growing season, the integrity of the pedicle is compromised and becomes a messy combination of intact pedicle and callus tissue.

"Picture how water flows out of the end of a garden hose, then picture what happens when you partially block the nozzle with your thumb. The blood supply and nutrient flow necessary for normal antler development is impeded leading to stunted growth and irregular antler configurations due to the animals prior injury. Complicating the issue once initial damage occurs, subsequent antler cycles tend to re-aggravate the injury, resulting in repetitive abnormal antlers."

So, a spike on one side or otherwise deformed antler is likely caused by injury, but what if it isn't? What if it really is a genetic trait? Shouldn't the buck be harvested to prevent passing along that genetic trait? You can remove him, but you're not doing anything other than putting meat in the freezer.

"It's been shown over and over that you can't alter genetics in the wild," Adams said. "A buck with big antlers can sire a buck with small antlers and vice-versa. Those antler traits aren't 100 percent inheritable."

Adams' statement is backed by a study in Texas. Wild bucks were captured andmicrochipped. Samples of DNA were taken from them and they were released. Family trees of bucks were developed through DNA samples taken over a number of years. What the researchers discovered isin the wild there is no correlation between a buck's antler size and that of its offspring.

"Don't think you're making an improvement in the deer herd from a genetic standpoint," Adams said. "Hunters don't need to concern themselves or worry about it."

Deer hunting: 'It just made a good day that much better.' Father and son double down on big bucks

Win big money: You can win a share of $1,500 in the Big Bucks Photo Contest sponsored by Van's

Please, shoot them: 12 bucks on MSU Deer Lab's most wanted list. Here's why.

ContactBrian Broomat 601-961-7225 orbbroom@gannett.com. FollowClarion LedgerOutdoors on Facebookand @BrianBroom onTwitter.

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The genetic basis of Peruvians’ ability to live at high altitude – Ars Technica

Friday, November 15th, 2019

Enlarge / Many Peruvians are well adapted to high-altitude life in the Andes.

Eric Lafforgue/Art in All of Us

Sherpas are physiologically adapted to breathing, working, and living in the thin air of the Himalayas, enabling them to repeatedly schlep stuff up and down Mount Everest. The Quechua, who have lived in the Andes for about 11,000 years, are also remarkably capable of functioning in their extremely high homes. New work suggests that these adaptations are the result of natural selection for particular genetic sequences in these populations.

Both populations live above 14,000 feet (4,267m), under chronic hypoxialack of oxygenthat can cause headaches, appetite suppression, inability to sleep, and general malaise in those not habituated to altitude. Even way back in the 16th century, the Spaniards noted that the Inca tolerated their thin air amazingly well (and then they killed them).

Metabolic adaptations give these highlanders a notably high aerobic capacity in hypoxic conditionsthey get oxygenated blood to their muscles more efficiently. But the genetic basis for this adaptation has been lacking. Genome Wide Association Studies, which search the entire genome for areas linked to traits, had found tantalizing clues that one particular gene might be a site of natural selection in both Andeans and Tibetans. It encodes an oxygen sensor that helps cells regulate their response to hypoxia.

This new work looked for genetic variants that were more common in the Quechua population compared to white lowlanders from Syracuse, New York. The researchers then tried to correlate the variants with the Quechuas high aerobic capacity at altitude. But none of the genetic differences showed a significant association with high aerobic capacity, probably because the sample size429 Quechua and 94 lowlanderswas too small to detect one.

So the researchers subjected the data to a more sensitive statistical analysis. This analysis found five variants of the gene that were significantly associated with the Quechuas adaptive high aerobic capacity in hypoxic conditions; they also appeared significantly more frequently in the Quechua population than in lowlanders. This observation was buttressed by analysis of a second, independent cohort of Quechua compared to global populations from the 1000 Genomes Project.

All of the adaptive variants were in the regulatory region of the geneDNA that controls when and where the gene is active. None were in the part of the gene that encodes a protein. So, the location and timing of the protein's activity seems to be more important than the protein itself in the Quechua.

A number of conditions must be met to claim that a population is genetically adapted to specific conditions. First, there must in fact be an adaptation: in this case, enhanced aerobic capacity under hypoxia. Check. Next, that adaptation must be associated with a genetic variant, and that variant must occur in the population of interest at rates indicating that it is being selected for. Thats what this most recent work did.

But it has not shown that the adaptation has increased the groups fitness, in terms of improving fertility and/or limiting mortality. And it is not absolutely certain that aerobic capacity is the trait being selected for; it is possible that this gene does something else oxygen-related that is really the trait being selected for, and the observed enhanced aerobic capacity is just a bonus side-effect.

Tibetans have alterations to the protein encoded by this gene, which is intriguing. Even more intriguing is that the Tibetan variants are not associated with high aerobic capacity in hypoxia, but with low hemoglobin. Counterintuitively, this seems to help Tibetans at altitude by increasing their blood flow to an extent that compensates for the fact that the blood carries less oxygen.

PNAS, 2019. DOI: 10.1073/pnas.1906171116 (About DOIs).

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A new study hopes to prevent disease before it starts through genetics – KSL.com

Friday, November 15th, 2019

HURRICANE What would life be like if you knew you would get cancer one day, but could prevent it beforehand? Clinicians in Utah are hoping to accomplish just that through a new study.

One St. George man said he's participating for the health of his posterity.

Durward Wadsworth, 76, grew up on a farm in Southern Utah. He worked alongside his family tending to the fruits trees, horses, and other animals.

"We had to milk cows and bring hay in," he said.

The farm has remained, but things have changed.

"I have a brother that passed away. I have a sister that passed away, Wadsworth said.

They both died from cancer. Wadsworth was also diagnosed with colon cancer and finished chemo only a year ago.

It's not a fun treatment, he said. He went to the Dixie Regional Cancer Center for 12 rounds of chemo.

As a teenager Wadsworth was exposed to radiation during nuclear testing at the Nevada National Security Site.

"As kids, we didn't know any different, so we would go up on the hill and watch when one would explode and you could actually see the mushroom and hear the boom, he said.

Both his family history of cancer and heart disease, and his exposure to radiation, had him concerned.

His son encouraged him to participate in Intermountain Healthcare's HerediGene population study. Clinicians hope this study, in collaboration with deCODE Genetics of Iceland, will help them better understand the human genome.

Dr. Lincoln Nadauld, Chief of Precision Health at Intermountain Healthcare, said the study is unprecedented. He said it looks at the link between genes and human disease.

"This study is the largest of its kind. It's an attempt to map the genomes of 500,000 people over the next five years, Nadauld said. There is no genetic study in health care that has ever been reported or ever attempted that compares in size or scope.

Nadauld said this study will impact generations to come.

(It) will allow us and subsequent generations to better understand health and the origins of disease and health care-related issues, he said. It's going to change the way that we deliver health care for the better.

Nadauld hopes the study will help doctors better predict and prevent disease before someone is ill.

So let's intervene with either a medicine or a lifestyle change so that you never have to experience heart failure or heart attack or a stroke, he explained.

While this type of precision genomics started in oncology, Nadauld said his team has applied it to all of their medical disciplines, including cardiovascular and neurodegenerative disorders, metabolic issues and even mental illness.

This study could uncover the link between mental illness and genes, and could identify new treatments for mental illness, he said.

Even though Wadsworth still has a lot of life to live, he knows he probably won't personally benefit from the study by the time its completed. "But, you know, my posterity will benefit, he said.

That's enough motivation for him. Wadsworth said he doesn't want his five children and 18 grandchildren to suffer through cancer like he did.

"We want the best health care for them, he said. He also hopes they'll carry on the family farm.

Nadauld said the study isn't just for people who have been sick, but will include mostly healthy individuals.

He said it just takes a simple blood draw to participate. Nadauld said by the end of the year there will be 25 different walk-in clinics across the entire state.

Nadauld said he anticipates a very small percentage of the participants will be informed of a health issue, in which doctors and patients need to take action.

We expect that will happen in about 3% of our participants, he said.

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Genetics may be the reason why you hate vegetables, study shows – Yahoo Food

Friday, November 15th, 2019

Cant stand the taste of vegetables? Your genes may be to blame.

Preliminary newresearchpresented at the American Heart Association (AHA) Scientific Sessions shows that a specific gene makes certain foods especially, broccoli, cauliflower, cabbage, and Brussels sprouts taste extremely bitter to some people.

The gene in question is calledTAS2R38. Everyone inherits two copies of this taste gene, but which variant of the gene you get makes all of the difference. According to the AHA: People who inherit two copies of the variant called AVI arent sensitive to bitter tastes from certain chemicals. Those with one copy of AVI and another called PAV perceive bitter tastes of these chemicals; however, individuals with two copies of PAV, often called super-tasters, find the same foods exceptionally bitter.

In the study, researchers analyzed questionnaires from 175 men and women about how often they ate certain foods and found that those with the PAV form of the gene who are more sensitive to bitter tasting foods were more than two and a half times as likely to eat the least amount of vegetables.

For super-tasters, the bitterness they taste in vegetables goes beyond being mildly annoying. A super-taster is a person who experiences a bitter taste with a much greater intensity than others,Tina Sindher, MD, an allergist and immunologist with Stanford Health Care, tells Yahoo Lifestyle, noting that super-tasters have many more visible taste papillae (bumps on the tongues surface) with more taste receptor cells compared to others.

Or as the lead author of the study,Jennifer L. Smith, PhD, RN, put it to theAHA: Were talking a ruin-your-day level of bitter when they tasted the test compound.

Super-tasters have the hardest time eating brassica vegetables broccoli, cauliflower, Brussels sprouts, cabbage, turnips, collards, kale, bok choy along with spinach, coffee, and tart citrus flavors. Studies show that bitter tasters eat fewer soy products and drink less green tea, and rated these foods to be more bitter than non-tasters, says Sindher.

That bitterness is getting in the way of super-tasters eating their vegetables, which may mean losing out on some health benefits. An overall healthy diet thats rich in vegetables and fruits may reduce the risk ofheart disease, including heart attack andstroke, according to theU.S. Department of Agriculture. Vegetables are also a good source ofdietary fiber, which helps reduce blood cholesterol levels and may lower risk of heart disease.

And in case you were wondering, just because you hate cilantro doesnt mean youre a super-taster. Disgust with that particular herb, which some find smells like soap, is a combination of two genetic variants (one of which is tied to sensing odors), according toNature. Cilantros aroma is created by several substances, which include fragments of fat molecules called aldehydes the same (or similar) aldehydes youll find in soap and lotions, according to aNew York Timesreport.

Super-tasters are individuals who are sensitive to specific bitter compounds, none of which are found in cilantro, explains Sindher. In fact, an aversion to cilantro occurs due to genetic variants associated with sensing smells and sensitivity to the aldehyde chemicals that give cilantro its distinctive flavor.

But for true super-tasters, how can they make sure to eat their vegetables? Unfortunately, theres no obvious way to disguise the bitter taste, explains Sindher. However, some strategies may be to sprinkle some sweetness to help mask bitter flavors, she says. Spices can help enhance flavor. Adding a little fat can also decrease bitterness.

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Genetic study reveals the family secrets of people in the 1800s – New Scientist News

Friday, November 15th, 2019

By Michael Le Page

Celebrating the Birth by Jan Steen, 1664. The Wallace Collection, London

In the 19th century, poorer families living in cities in Europe had a higher rate of children who werent biologically related to their legal fathers. This is according to a genetic study that looked at how this rate differs for different socio-economic groups.

It is widely assumed many men arent the biological fathers of their children. The rate of extra-pair paternity, as this is called, has been claimed to be as high as 30 per cent today. They look just like the milkman, goes the popular joke that no parent finds funny.

However, over the past two decades DNA studies in several countries have shown the average rate is low around 1 per cent. Maarten Larmuseau at KU Leuven in Belgium, who authored one of these studies, wondered whether there was a difference between groups.

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He suspected, for example, that the rate was higher among aristocrats in the 17th century, as there was often a large age gap between husband and wife. Extra-pair paternity is depicted in the 1664 painting Celebrating the Birth by Jan Steen, which shows a wealthy Dutch father holding his newborn child. But behind him a man is making the sign of the cuckolds horns, meaning the child was fathered by another.

Larmuseaus team identified 500 pairs of men in Belgium and the Netherlands where, according to genealogical records, each pair descended from the same male ancestor through a male lineage. Half of these ancestors were born before 1840 and the oldest was from 1315.

The men in each pair should have inherited their shared ancestors Y chromosome, as it comes from the father. When DNA testing revealed a mismatch, the team tested other male descendants to narrow down when a son had been fathered by someone other than the husband. All the men were volunteers and the team didnt test close relatives to avoid uncovering recent cases.

What we found was completely the opposite to what we expected, says Larmuseau.

The rate of extra-pair paternity among farmers and more well-to-do craftsmen and merchants was about 1 per cent, rising to 4 per cent among labourers and weavers and nearing 6 per cent among working class people who lived in densely populated cities in the 19th century. This was in comparison to a rate of around 0.5 per cent among the more well-off.

What the study cannot reveal is why people were more likely to be in this situation. We cannot give an explanation, Larmuseau says. We cannot interview them.

One possibility is that poorer women in cities were more vulnerable to male sexual violence and exploitation.

The overall rate was still low, at 1.6 per cent per generation. But that still means a very large number of people alive today may not be aware of their biological parentage. Larmuseau says 30 million people worldwide have done ancestry tests, which suggests up to 500,000 could have made a shocking discovery about their father. Companies offering these tests dont provide any counselling, he says.

Journal reference: Current Biology, DOI: 10.1016/j.cub.2019.09.075

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Endangered birds leave genetic clues in their drinking water – Cosmos

Friday, November 15th, 2019

By Natalie Parletta

Australian researchers have worked out how to trace an endangered bird species by analysing water samples from its drinking holes.

Using environmental DNA (eDNA), a team led by Karen Gibb from Charles Darwin University identified the movements of the stunning rainbow-coloured Gouldian finch (Erythrura gouldiae), a species native to tropical savanna woodlands in Australias north.

Once numbering in the millions, there are now just 2500 adults as a result of the illegal bird trade, altered habitat, predators and wildfires, and the species is listed as endangered.

eDNA is used to detect the locations and numbers of rare and threatened species from water samples and to date has mostly been applied to freshwater animals.

Gibbs and team, including colleagues from the University of Western Australia, saw an opportunity to track the Gouldian finch using water sample analysis, as it needs to drink several times a day.

To do this, they developed a test that can identify estrildid finches from a fragment of mitochondrial DNA, and a probe specifically designed to detect Gouldian finch DNA.

This was necessary to distinguish the colourful finches from masked finches (Poephila personata) and long-tailed finches (P. acuticauda) other estrildid species that often flock together at the same waterholes.

Its a much more accurate test, says Gibb. By having primers that pick up other finches it tells us the eDNA is good enough quality to be amplified. If the Gouldian test is then negative, we can be confident that the eDNA test worked, but there just werent Gouldian finches at that site.

First, they piloted it in wildlife park aviaries before doing field trials at the Yinberrie Hills in the Northern Territory, where scientists and rangers had good observation data to validate the tests.

With a 200-millilitre water sample they could successfully detect Gouldian finch eDNA from waterholes the birds had visited in the previous 48 hours, and where there were lots of birds, it was still measurable from the samples two weeks later.

When it worked in the real world at the waterholes, even where the water was poor quality in places where it was hot and looked a bit oily we were really excited, says Gibb.

The study opens new options for rangers and scientists to keep track of the birds movements by simply collecting small water samples during their explorations, which will help inform conservation efforts.

People who are travelling around will be able to put a cup of water into an appropriate container and then into a car fridge, and be able to take a lot of samples, Gibbs says. We can cover a much larger area.

The study is published in the journal Endangered Species Research.

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Endangered birds leave genetic clues in their drinking water - Cosmos

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Aversion to Broccoli May Have Genetic Roots – Scientific American

Friday, November 15th, 2019

If you have heart disease, your doctor might tell you, eat more vegetables. A tactic that haslimited success.

Getting people to change their diets is actually pretty hard. These are lessons I would give over and over again. And I would think, Why is this so hard to do?

Jennifer L. Smith is a nurse researcher at the University of Kentucky who now has a preliminary answer about why change is so hard: it might depend on your genes. Specifically, whether or not youre genetically predisposed to perceive bitternessand therefore bitter veggies.

So broccoli is definitely one of them. They tend to be cruciferous vegetables, like broccoli, cauliflower, cabbage, brussels sprouts, asparagus."

If you ever took that test in science class where you put a piece of paper on your tongue to see if it tastes bitter, you might already know your bitter status.

Smith took saliva samples from 175 adults known to be at risk of cardiovascular disease. She then did a genetic test to determine whether they had a copy of a bitter-taste gene variant. She also had them fill in a questionnaire about their eating habits.

After controlling for factors like age, gender, income, and so on, Smith found that people with a copy of the bitter-sensitive gene variant were just 40 percent as likely to report eating a lot of veggies as were the folks without the gene variant.

Shes presenting the results this week at the American Heart Association Scientific Sessionsin Philadelphia. [Jennifer L. Smith et al., TAS2R38 haplotype predicts vegetable consumption in community dwelling adults at risk for cardiovascular disease]

If these findings hold up to more testing, Smith says, perhaps doctors could advise patients with this gene variant to avoid the most offensively bitter veggies but to try the others. Or perhaps certain herbs and spices might counteract the bitterness, she says.

Of course, chefs already figured this outwith cheesy broccoli. But for heart patients, the better flavor might not be a favor.

Christopher Intagliata

[The above text is a transcript of this podcast.]

Go here to see the original:
Aversion to Broccoli May Have Genetic Roots - Scientific American

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