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Better Buy: Myriad Genetics, Inc. vs. Opko Health, Inc. – Motley Fool

It's been a rough 12 months for Myriad Genetics (NASDAQ:MYGN) and Opko Health (NASDAQ:OPK). Myriad lost nearly half of its market cap during the period, while Opko stock is down around 20%.

Could better days be ahead for these two stocks? And which is the better pick for long-term investors? Here's how Myriad Genetics and Opko Health stack up against each other.

Image source: Getty Images.

There are three primary arguments in favor of buying Myriad Genetics stock. The company is a leader in the U.S. hereditary cancer screening market and is poised to expand its lead. Myriad is quickly growing its non-hereditary cancer business. The company also has significant opportunities in international markets.

How does Myriad plan to grow its U.S. hereditary cancer business? The greatest potential lies in expanding testing beyond breast cancer patients. A key to achieving this objective is with Myriad's myRisk, a single comprehensive DNA test that screens for breast cancer, ovarian cancer, colon cancer, uterine cancer, melanoma, pancreatic cancer, prostate cancer, and gastric cancer.

In Myriad Genetics' fiscal year 2013, only 1% of total testing volume stemmed from non-hereditary cancer screening. The company expects to report that figure is roughly 67% for fiscal year 2017. One primary product making this growth possible is GeneSight, a genomic test used to help physicians prescribe the correct psychiatric medications for patients. Myriad picked up GeneSight with its acquisition last year of Assurex Health.

As for international growth, Myriad is looking over the short term to expand primarily in the Canadian and major European markets. Over the longer term, though, the company plans to grow significantly in Japan, China, and Brazil.

Myriad's management team thinks the company can grow revenue at an average annual rate of more than 10% with an operating margin of at least 30%. The stock is up so far in 2017, thanks to a string of good news for the company -- including positive coverage decisions for Myriad's EndoPredict breast cancer test by multiple Blue Cross Blue Shield plans.

There are two key things to look at with Opko Health: the company's current products and services and its pipeline prospects. Opko currently gets over 80% of its revenue from services provided by Bio-Reference Labs, which it acquired in 2015. Bio-Reference generates solid cash flow and helps Opko market its 4Kscore prostate cancer DNA test.

Opko also has two drugs on the market. Varubi, which is used to treat chemotherapy-induced nausea and vomiting (NINV), is licensed to Tesaro. Rayaldee won U.S. regulatory approval in June 2016 for thetreatment of secondary hyperparathyroidism (SHPT) in adults with stage 3 or 4 chronic kidney disease (CKD). Although it's still relatively early in the commercial launch of Rayaldee, the potential for the drug appears to be quite promising. CKD is the ninth leading cause of death, with most CKD patients dying from cardiovascular disease precipitated by SHPT. There aren't any great options for treating SHPT other than Rayaldee.

Opko has several pipeline candidates. The most eagerly anticipated product is human growth hormone hGH-CTP that Opko is developing in partnership withPfizer. Opko reported disappointing results from a late-stage study of hGH-CTP.However, the company saw some outliers in the clinical data that gave hope that the hormone could potentially still win regulatory approval. Opko and Pfizer are working to advance to a regulatory filing based on an additional statistical analysis of the data.

Unlike Myriad Genetics, Opko isn't turning a profit right now. The company reported a net loss in 2016 of $25 million. However, its bottom line has improved and should get a big boost if Rayaldee picks up steam.

Quite frankly, both of these stocks are risky. Myriad Genetics faces intense competition in the DNA screening business. It's also at the mercy of payers' reimbursement decisions. Opko Health could be derailed if its hGH-CTP doesn't win approval or if Rayaldee sales don't meet expectations.

Personally, my risk tolerance isn't enough for me to buy either of these stocks. However, I thinkOpko gets the nod as the better choice between the two. The basis of my decision was on the opportunity that Opko has if things go its way. Granted, that might not happen. But if the company enjoys some good luck, the stock could soar.

Keith Speights owns shares of Pfizer. The Motley Fool has no position in any of the stocks mentioned. The Motley Fool has a disclosure policy.

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Better Buy: Myriad Genetics, Inc. vs. Opko Health, Inc. - Motley Fool

Tennessee Bird Flu Shares Name, Not Genetics, Of Feared China Strain – Huffington Post

The strain of bird flu that infected a chicken farm in Tennessee in recent days shares the same name as a form of the virus that has killed humans in China, but is genetically distinct from it, U.S. authorities said on Tuesday.

The U.S. Department of Agriculture identified the strain in Tennessee as H7N9, following a full genome sequencing of samples from the farm. It said all eight gene segments of the virus had North American wild bird lineage.

On Sunday, the USDA confirmed the farm in Tennessee was infected with highly pathogenic bird flu, making it the first case in a commercial U.S. operation in more than a year.

In China, at least 112 people have died from H7N9 bird flu this winter, Xinhua news agency said on Friday.

However, that virus has Eurasian lineage, U.S. flu experts said.

Even though the numbers and the letters are the same, if you look at the genetic fingerprint of that virus, it is different, said Dan Jernigan, director of the influenza division at the National Center for Immunization and Respiratory Diseases at U.S. Centers for Disease Control and Prevention.

Jernigan said the risk to humans from the virus found in Tennessee is low. Genome sequencing shows the H7N9 virus did not have genetic features present in the virus in China that make it easier for humans to become infected, he said.

The virus found in Tennessee likely mutated to become highly pathogenic from a less dangerous, low pathogenic form, he said.

Disease experts fear a deadly strain of bird flu could mutate into a form that could be passed easily between people and become a pandemic.

Multiple outbreaks of the virus have been reported in poultry farms and wild flocks across Europe, Africa and Asia in the past six months. Most involved strains that were low risks for human health, but the sheer number of different types, and their simultaneous presence in so many parts of the world, has increased the risk of viruses mixing and mutating - and possibly jumping to people, according to disease experts.

Chinas Center for Disease Control and Prevention has said the majority of people infected by H7N9 in China reported exposure to poultry, especially at live markets.

Identifying the viruses in Tennessee and China both as H7N9 is similar to having two cars from different states with the same license plate number, said Carol Cardona, avian flu expert at the University of Minnesota.

The strain in Tennessee is NOT the same as the China H7N9 virus that has impacted poultry and infected humans in Asia, the USDA emphasized in a statement.

While the subtype is the same as the China H7N9 lineage that emerged in 2013, this is a different virus and is genetically distinct from the China H7N9 lineage, the USDA added.

U.S. officials are working to determine how the Tennessee farm, which was a supplier to Tyson Foods Inc, became infected. All 73,500 birds there were killed by the disease or suffocated with foam to prevent its spread.

Tyson, the worlds biggest chicken company, is hopeful this is an isolated incident, spokesman Worth Sparkman said.

Authorities have not identified the name of the farm or the town in Lincoln County, Tennessee, where it is located.

(Editing by Matthew Lewis and Bernard Orr)

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Tennessee Bird Flu Shares Name, Not Genetics, Of Feared China Strain - Huffington Post

Genetics and cancer: why testing can aid prevention – WRVO Public Media

No one wants to talk about cancer. A disease that has taken the lives of so many, even the word itself has an ominous connotation. But as much as we dont want to talk about it, new genetic technology suggests that starting the conversation about your familys cancer history might be in everyones best interest.

In her new book, "A Cancer in the Family: Take Control of your Genetic Inheritance," Dr. Theodora Ross addresses how our familys medical history plays a role in our health. To shed some light on the genetics of cancer, as well as genetic counseling, Ross spoke with Take Care to explain the importance of knowing your family history. Ross, a cancer geneticist, is director of University of Texas Southwestern Medical Centers cancer genetics program.

First and foremost, Ross says that while you may feel theres nothing you can do about an impending cancer diagnosis, knowing is always better than not knowing. Ross herself was hesitant to find out about her own genetics, even though she's a cancer expert and has a family history of the disease, including a sister with breast cancer. But when she developed a melanoma in 2004, she decided it was time to talk to a geneticist and a genetic counselor.

Ross attributes her hesitation to truthiness, which occurs when we want something to be true. Often when it comes to health, we ignore or deny potential problems. We dont go to doctors when were healthy, we dont want to believe there could be a problem, and so we dont look.

But Ross says knowing the family history of a patient is an important step in prevention, and helps not only the patient, but researchers too. Genetic counselors can go to physicians and obtain medical records, which gives researchers more data to work with, and gives patients an accurate understanding of their family history.

According to Ross, the most common genetically inherited cancer syndrome is Lynch syndrome, which occurs when there is a mutation in mismatched repaired genes. This mutation will lead to a predisposition to colon, endometrial, ovarian, pancreatic, and other cancers. The kicker? Only 5 percent of people with this syndrome actually know they have it, and its common. About one in 300 have it, says Ross. And if they knew, they could carry out preventative measures such as frequent colonoscopies and check-ups.

Comprehensive genetic testing is becoming cheap enough, according to Ross, for people to seek out this information at a reasonable cost. Genetic counselors, she says, have an incredible ability to connect with their patients while providing them with the information they need to make the most of their genetic history. Talking about cancer in the family can be a scary conversation, but its crucial, says Ross, to aid in our efforts towards prevention.

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Genetics and cancer: why testing can aid prevention - WRVO Public Media

ACC 2017: CVD Outcomes for Evolocumab, Intermediate-Risk TAVR, Coronary Physiology Tests, and More – TCTMD

Returning to their own backyard again this year, the American College of Cardiology (ACC) 2017 Scientific Sessions kick off next Friday with high hopes of giving the world some headlines to compete with other news coming out of the nations capital. Among the hot-ticket items on this years roster are a large, cardiovascular outcomes trial for a market-approved PCSK9 inhibitor, a randomized comparison of a non-vitamin K antagonist oral anticoagulant (NOAC) against aspirin in acute coronary syndromes, and 2-year outcomes from ABSORB III, the pivotal randomized trial that led to US approval of the first bioresorbable scaffold in 2016.

According to the ACC 2017 program chairs, who spoke with media via a telebriefing last week, this years conference attracted over 2,600 abstracts, of which 114 were late-breaking clinical trial (LBCT) submissions. A full 23 of these were selected as late breakers, and an additional 17 submissions are grouped in the featured clinical research sessions. There are a total of five LBCT sessions and three featured clinical research sessions distributed throughout the 3-day congress, which runs from Friday, March 17, through Sunday, March 19.

Were incredibly excited about this upcoming meeting, Jeffrey Kuvin, MD (Dartmouth-Hitchcock Medical Center, Manchester, NH), enthused during the telebriefing. Were confident there will be numerous practice-changing science presentations.

Chief among those is shaping up to be FOURIER, the 27,500-patient cardiovascular outcomes trial testing the PCSK9 inhibitor evolocumab on top of statin therapy against statins alone for the prevention of cardiovascular death, nonfatal MI, nonfatal stroke, hospitalization for angina, or coronary revascularization. As previously reported by TCTMD, the company announced in February that the trial had met its primary and secondary endpoints, but full details on those will be released in the opening LBCT session at ACC.

This is undoubtedly going to be a widely noted study and has the potential to be truly game changing, Kuvin said

Fleshing out Fridays opening LBCT session are the SPIRE I and II results looking at cardiovascular outcomes with a second PCSK9 inhibitor, bococizumab. These trials were stopped early in late 2016 after trial monitors noticed an unanticipated attenuation of LDL cholesterol lowering over time combined with an increase in immunogenicity and injection-site reactions.

The third trial in what the ACC has dubbed its opening showcase is SURTAVI, the pivotal trial testing the CoreValve transcatheter valve (Medtronic) in intermediate-risk patients with severe symptomatic aortic stenosis. The trial, which was initially launched outside the United States and then extended to include US patients, is anticipated to pave the way for an expanded US Food and Drug Administration (FDA)-approved indication later this year.

Day two of ACC 2017 includes two LBCT sessions, the first of which is jointly hosted by the Journal of the American College of Cardiology and the Journal of the American Medical Association.

During the telebriefing, Kuvin highlighted EBBINGHAUS, a cognitive function substudy from FOURIER, as well as two NOAC studies in that session. The first of these, EINSTEIN CHOICE, is looking at rivaroxaban versus aspirin for extended treatment of venous thromboembolism, while the second, GEMINI-ACS-1, is comparing rivaroxaban and aspirin on top of P2Y12 inhibition for patients post-ACS.

ACC 2017 Vice Chair Andrew Kates, MD (Washington University in St. Louis, MO), also speaking on the media telebriefing, took over from Kuvin to list some of the highlights of the remaining two LBCT sessions. Topping Kates list was ABSORB III. When the primary results of the study were released in 2015, the Absorb BVS (Abbott Vascular) was noninferior to DES at 1 year, Kates noted, adding that severalbut not allstudies have pointed to an increased rate of scaffold thrombosis with the bioresorbable device after 1 year. What were excited about at ACC 17 is well be hearing the interval data between years 1 and 2 [as well as the] the 2-year data in this session, Kates said, adding, Certainly its going to be important data that were looking forward to hearing.

Kates highlighted a number of other key trials throughout the program. These included LEVO-CTS looking at the use of levosimendan in patients with LV systolic dysfunction undergoing cardiovascular surgery with cardiopulmonary bypass, part of Sundays LBCT IV session co-hosted by JACC and the New England Journal of Medicine. Also in LBCT IV, Kates noted, is a trial testing a cerebral protection device during cardiac surgery.

While using embolic protection devices is safe and does capture embolic material, Kates said, its really not clear whether these devices really do anything to prevent strokes, or if they may reduce cognitive decline after surgery. This is certainly a very important topic that we all care about.

Finally, from LBCT V, Kates highlighted two heart rhythm studies, RE-CIRCUIT and ARISTOTLE. The first is looking at a relatively new drug, dabigatran (Pradaxa, Boehringer Ingelheim), used without interruption during ablation for atrial fibrillation. The second is looking at an old drug, digoxin, in A-fib patients with and without heart failure.

For Interventionalists: TAVR and FFR/iFR

Interventionalists attending ACC 2017 will find plenty of other late breakers relevant to their subspecialty. Updates from transcatheter valve studies are dotted throughout the LBCT and featured clinical research sessions, including, in LBCT IV, an MRI analysis of microbleeds during TAVR and two studies looking at subclinical leaflet thrombosis in surgical and transcatheter valve prostheses. Saturdays featured clinical research session is focused on interventions and comparisons of SAVR and TAVR; transcatheter valve replacement for native versus failed surgical bioprostheses; and TAVR for bicuspid versus tricuspid valve disease. The same session also has a presentation addressing 1-year outcomes with the MitraClip (Abbott) in the US following FDA approval.

Coronary disease is also front and center, particularly in LBCT IV. This session includes a trial of culprit lesion versus complete revascularization in STEMI, plus two randomized trials of fractional flow reserve (FFR) versus instantaneous wave-free ratio (iFR): DEFINE-FLAIR and iFR-SWEDEHEART. These two large CV outcomes trials will determine how the physiologic information provided by iFR compares with the usefulness of FFR in guiding treatment.

Research and Practice

Beyond the late breakers and featured research, this years ACC has11 learning pathways including one on special topics spanning everything from malpractice minefields to public reporting. There are also seven keynote lectures, including one by Janet S. Wright, MD, executive director of the joint Centers for Disease Control/Centers for Medicare & Medicaid Services Million Hearts initiative, now perilously close to its deadline of preventing 1 million heart attacks and strokes by the end of 2017. Another keynote will be delivered by NEJM Editor-in-Chief Jeffrey Drazen, MD, speaking on data sharing in clinical trials. Drazen famously penned a controversial editorial in the journal poking holes in the Open Data proposal set forth in draft form by the International Committee of Medical Journal Editors and referring to the risk of research parasites, a position he revised in a second editorial days later.

The entire TCTMD editorial teamCaitlin Cox, Yael Maxwell, Laura McKeown, Todd Neale, Michael ORiordan, and me, Shelley Wood, will be on the ground at ACC 2017. Follow us on Twitter for breaking news and find our in-depth stories on our conference coverage page.

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ACC 2017: CVD Outcomes for Evolocumab, Intermediate-Risk TAVR, Coronary Physiology Tests, and More - TCTMD

The Neuroscience of Seeing an Ex – Discover Magazine

When I arrived at the wine bar, there was only one open table dimly lit and intimate. The booze, music and candlelight felt like a callback to our first kiss 15 years before, almost to the day.

There was no sign of him, so I ordered a chardonnay and two small plates, and tried to focus on the novel I brought with me, ironically titled What She Knew. Instead, I found myself flashing back to the last time I saw him.

We had just returned from a trip to Napa to scout wedding venues. After a heated kiss, I drove to my apartment 95 miles away.

Days later, I learned hed been cheating on me, and I ended our six-year relationship the best of my life up to that point with a two-line email. He fired back with a litany of messages, which began with profanity and culminated in pleas.

PLEASE DONT LEAVE ME. . . YOU ARE MY EVERYTHING, he screamed through the screen.

He sent texts, letters, roses, and initiated countless hang-up calls.

I never responded. I never told him a mutual friend confirmed my suspicions. I never considered reconciling.

Over the years, we corresponded intermittently, but not about anything deep and never to revisit our history. But when work took me to his hometown of Santa Barbara, I reached out and asked if hed like to meet.

Im happily married with kids. Hes engaged. Whats the harm?

Apparently my urge to reconnect with an ex makes sense. The brain develops pathways based on learned patterns, says love expert Helen Fisher, a senior research fellow at the Kinsey Institute, Indiana University. So, if you laid down a powerful pattern that this person was your life partner, your brain can retain traces of that circuitry, even after youve bonded with someone new.

Nevertheless, I struggled to understand why, even though its certainly not the case for everyone especially those who have had toxic relationships I felt so comfortable sitting across the table from someone who pulled the rug out from under me. So down the rabbit hole I went to find out what happens in our brains when we reunite with an old love.

Laying Down a Template I met Ben (not his real name) when we were both 26. We had a sweet, albeit star-crossed romance. He was an irrepressible free spirit, a dreamer, a romantic. I was an ambitious type A who played it safe. Like peanut butter and jelly, we complemented each other.

He was the first to make me dinner, teach me to surf in ice-cold waters and unlock the seemingly impenetrable fortress of my body. Together, we formed our identities and defined what love meant. In the process, he ingrained himself into my psyche.

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The Neuroscience of Seeing an Ex - Discover Magazine

CHI St. Vincent Moves Neuroscience Institute to North Campus – Arkansas Business Online

by Arkansas Business Staff on Thursday, Mar. 9, 2017 1:07 pm

CHI St. Vincent in Little Rock announced on Wednesday that is renovating its CHI St. Vincent North campus in Sherwood for $10 million over the next 18 months to move its Arkansas Neuroscience Institute there.

The renovations include finishing out the third floor, renovating the operation space to accomodate ANI's specialized equipment and adding a helipad.

The health care system said it will also build a $4 million state-of-the-art ANI education and research center adjacent to the renovated space. That center will have a 250-seat auditorium, lab facilities, a conference room and a space to accomodate future growth.

CHI St. Vincent is seeking support in the form of philanthropic gifts for the new building.

According to a news release, the move will also aldlow the program to expand its staff and services, to include epilepsy surgery and surgery for movement disorders.

"Creating a destination Neuroscience Institute at our north campusin central Arkansas allows us to better serve a full spectrum of neurological disorders and treat the growing number of patients ANI serves from all 75 counties in Arkansas, 37 states and other countries around the world," CEO Chad Aduddell said in the news release.

ANI has five neurosurgeons, each having a different subspecialty, and Dr. Ali Krisht, is its director. They perform more than 1,000 surgeries per year.

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CHI St. Vincent Moves Neuroscience Institute to North Campus - Arkansas Business Online

Creepy mouse experiment helps scientists understand contagious behavior – Ars Technica

A mouse watches a video of another mouse scratching and becomes itchy. This means contagious scratching isn't based on smells or being familiar with the itchy mouse.

Humans and other social animals suffer from something called contagious itching. It's when you see somebody else scratching and suddenly need to scratch yourself, too. Now, a group of scientists led by Zhou-Feng Chen at the Center for the Study of Itch at Washington University in St. Louis have discovered that mice have the same problem. In the process, the scientists may have identified what causes some contagious behaviors.

Once Chen and his colleagues had established that mice have contagious itching just like other mammals, they wanted to know more. How did such behavior arise in the neurocircuitry of mouse brains? One possibility was that it was a kind of empathetic reaction to mice they knew well or that it was a response to smelling or touching an itchy mouse. But they found that mice could catch itches from strange miceand even from mice they saw on video (see video above). So clearly all they needed was to see another itchy mouse to get itchy themselves.

Chen and his team then dove straight into the neurobiology of the mice. Brain scans of the scratching mice revealed activity in a region called the suprachiasmatic nucleus, whose neurons emitted a chemical called gastrin-releasing peptide (GRP). By switching GRP on and off in mouse brains, the researchers discovered that it governed only contagious scratching. Mice with blocked GRP still got itchy, but they didn't start scratching when they saw other scratching mice.

The researchers used optogenetics, or light stimulation, to trigger activity in the suprachiasmatic nucleus, where social scratching is processed. At first the mouse in this video seems nonplussed, then it starts scratching frantically.

Then the researchers wondered if they could induce contagious scratching even when there were no other mice nearby to catch it from. So they injected GRP directly into their subjects' brains and also used brain implants that stimulated electrical signaling in the suprachiasmatic nucleus. Both types of treatment caused the mice to engage in frantic scratching, as if they had just seen one of their fellow rodents scratching themselves. In a paper for Science, Chen and his colleagues suggest that this means contagious scratching is a kind of involuntary response, hardwired into the brain.

University of Sussex neuroscientist Anil Seth, who was not involved in the research, told The Guardian that "very deep and evolutionary ancient mechanisms might be involved."

What kind of evolutionary pressures would create such a fundamental process in the brain? "It's possible that when a lot of mice are scratching, maybe it warns other mice that this is a place that has a lot of insects, and you'd better start scratching before it is too late," Chen told Live Science.

He and his colleagues write that their work also "may have implications for our understanding of neural circuits that control socially contagious behaviors." In other words, it's possible that there are other socially contagious activities in animals that could be induced by brain implants.

It's hard to deny that this sounds like the first step toward some kind of Matrix-like dystopia, where brain implants fool us into thinking we're eating tasty steaks. But that's unlikely. Human behavior is far more complex than what we see in mice. Still, this research has revealed something fascinating about how mammal brains work. With a little neurochemical intervention, scientists can induce social reflexes in mice who are entirely alone.

Science, 2017. DOI: 10.1126/science.aak9748

Listing image by Science

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Creepy mouse experiment helps scientists understand contagious behavior - Ars Technica

The Future of Human-Centered Robotics – Electronic Design

Luis Sentis will lead a session, A Developers Primer for Coding Human Behavior in Bots, at SXSW on Sunday, March 12, 2017.

Human-centered robotics hold a special place in the robotics field because they both mimic human sensing and cognitive behavior, and are designed to assist humans for safety and productivity. To explore human-centered robotics is to explore human beings and how we sense the world, analyze complex and often conflicting information, and act upon our findings, modifying perception, understanding, and action as new information is available.

Such machines could be of great practical benefit to humans on long space flights to Mars, for instance, or as human proxies in hazardous environments such as a chemical spill or even ordinary circumstances like education or elder care.

Obviously, creating human-centered robots poses many challenges in conception, design, and the hardware and software that support them. My own work in this burgeoning field focuses on designing high-performance series elastic actuators for robotic movements, embedded control systems, motion planning for dynamic locomotion, and real-time optimal control for human-centered robots.

Once we have a platform for human-centered robotics, and once we can create the hardware and software and the logic to drive them, we can turn to its real-world applications, which are many.

Most readers probably have only a passing acquaintance with human-centered robotics, so allow me to use this brief blog to introduce a few ideas about this topic and its challenges.

Humanoid and Human-Centered

Since perhaps the 1950s, television and the movies have often portrayed humanoid robotsrobots that take roughly human formentertaining us with how closely they mimic humans or by how far they fall short. Sometimes, in a dramatic plot turn, a humanoid robot becomes malevolent or uncontrollable by humans.

I prefer the term human-centered robot, because it most closely describes my field of endeavor: How to create a robot that is focused on assisting a human being; sometimes guided by a human, but also learning on its own what action or behavior would be most helpful to that human.

In my view, we do not yet have sufficient evidence to say that humanoid robots are most effective when interacting with humans. They may well be, but we do not have definitive data on the question.

However, it appears anecdotally true that humanoid robots fire the human imagination and that has its benefits. In addition to their portrayal in popular media, I have found that humanoid robots draw the most, well, human interest. Soon after creating one we named Dreamer in 2013, in the Human Centered Robotics Lab (HCRL) at the Cockrell School of Engineering at the University of Texas at Austin, we generally received more attention from curious students, engineers, investors andwouldnt you know itmovie producers. (Dreamer eventually had a bit part in Transformers 4 in 2014.) If humanoid robots help draw attention and interest to human-centered robotics, so be it.

Applications and Productivity

The more important aspect of this field is how to create human-centered robotics that sense their surroundings and either respond to human directions or intuit what actions would best serve their human counterpart.

Ive mentioned the possible robotic applications of space travel, perhaps as a companion to astronauts on a space walk, as a human proxy in hazardous environments or as a caregiver to an elderly person. In each case, the notion of productivity is different.

If you think of productivity for robotics generally in a manufacturing setting, it can be measured in terms of hours of work performed and profits earned. But in a long space journey to Mars, productivity will be measured instead in terms of the astronauts enhanced safety and ability to accomplish difficult tasks. In a hazmat spill, productivity might be measured in terms of human lives saved. In elder care, how well did a robot perform in changing bandages or applying ointment to a sore, preserving the persons health?

Robot Knows Best

Another quest in human-centered robotics is to create the ability of a robot to not just predict human behavior, but to perform what I call intervention. Whatever its level of complexity, can we build a robot with logic that assesses a situation for optimal actions, whether directed by a human or not? This translates to a robots ability to say to itself, Well, the human is operating the system in such a way. We could do better if computationally I have a hypothesis about what would be best for the human and intervene with that particular behavior.

This ability requires pairing social cognitive theories with mathematics. And I have found that advances are possible for what I call self-efficacy, which is basically the self-confidence to achieve a certain behavior.

At this point, self-efficacy can be achieved in very simple scenarios. One potential application is to use a human-centered robot to motivate students to solve problems by sensing and reacting to students level of engagement, then producing an interaction that motivates the student and enhances learning. I hope to demonstrate this and give attendees a chance to code such behavior in a human-centered robot at SXSW.

Touch and Whole Body Sensing

One major way in which humans interact is through touch. We place a hand on a shoulder or grasp someones forearm to gain their attention. Robotsparticularly humanoid ones with mobilityare likely to be large and quick, so touch becomes an important element in the safety of their human counterparts. We do not want a robot that runs into an astronaut on a space walk or pins someone to a wall. Thus, we are developing what I call whole body sensing. Though some in this field are pursuing something known as sensory skin, at the HCRL we have taken a more economical approach to minimize the amount of electronics needed.

We use a distributed sensor array on the robots surface, but they number in the dozens, not the thousands employed in sensory skin. Instead, we combine different sensing modalities internal to the robot, such as accelerometers, which aid stabilization, and vibration sensors that enable the machine to triangulate information on whats happening in the immediate environment. This enables the robot to respond to human touch, but within the context of other information it is receiving from its environment. We call this whole-body contact awareness, a combination of internal and external sensing and awareness.

Spin-offs

I hope this mere glimpse into the world of human-centered robotics piques your curiosity. It may serve to attract those who wish to work in the field. But the general public should also understand that advances in this field will eventually make their way into human-centered robotics in our homes, our businesses, manufacturing, agriculture, smart cities, the Internet of Things, you name it. Well have systems somedaywe already do, with limited abilitiesto sense human behaviors and intervene to produce optimal conditions based on an understanding of whats best for the people involved in a particular situation.

Today, we have smart thermostats that learn our preferences for heating and cooling our homes. Tomorrow, we may have human-centered robotic systems that optimize our cities.

Luis Sentis is an Assistant Professor in the Department of Aerospace Engineering at the University of Texas (UT) at Austin. He also leads UT Austins Human Centered Robotics Laboratory and is co-founder of Apptronik Systems Inc., a contractor for NASA's Johnson Space Center.

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The Future of Human-Centered Robotics - Electronic Design

Researchers discover genetic bases of Opitz C syndrome – News-Medical.net

March 10, 2017 at 1:31 PM

Opitz C syndrome is a genetic disease that causes severe disabilities in patients and has been diagnosed in three people in the Iberian Peninsula, and sixty people in the world. A team led by the professors Daniel Grinberg and Susana Balcells, from the Group on Human Molecular Genetics of the University of Barcelona and the Biomedical Research Networking Center of Rare Diseases (CIBERER) has now identified a gene that causes the Opitz C syndrome in the only patient in Catalonia diagnosed with this severe congenital disease. This new scientific advance is a first step to discover the genetic bases of this syndrome which, so far, does not offer treatment possibilities, prenatal diagnosis or genetic counseling.

The new study, published in the journal Scientific Reports, has the participation of several researchers at the CRG, including members of the Genomic and Epigenomic Variation in Disease laboratory, the genomics unit, and the bioinformatics unit. It also had the participation of John M. Opitz (University of Utah, United States), Giovanni Neri (Catholic University of the Sacred Heart, Italy) and experts at the Department of Clinical and Molecular Genetics of the University Hospital Vall d'Hebron (VHIR).

Opitz C syndrome: rare but not invisible

The genetic bases of this ultra-minority disease, described for the first time in 1969 by John M. Opitz, are still unknown. It is generally thought that its origin is caused by the apparition of dominant -maternally silenced- novo mutations. At the moment, the diagnose is clinical and it is based on the symptomatology presented on patients with different degrees (trigonocephaly, learning disability, psychomotor disability, etc.) and which, in lots of cases, coincides with similar minority pathologies such as the syndromes of Schaaf-Yang, Bohring-Opitz and Prader-Willi.

In the new study, the experts described for the first time, the existence of a novo mutation -p.Q638*- located in the gene MAGEL2 of the only diagnosed person with Opitz C syndrome in Catalonia. Identifying this mutation, found in the Prader-Willi Region on chromosome 15, widens the knowledge horizons on genetics and the possibilities for a diagnosis on these rare diseases.

"The p.Q638* mutation, identified in the gene MAGEL2, coincides with the one described concurrently and independently in a patient with Schaaf-Yang syndrome, a new minoritary disease affecting fifty people in the world. The first cases were described on a scientific bibliography in 2013 by the team of Professor Christian Schaaf, from the Baylor College of Medicine, Houston", says Professor Daniel Grinberg, member of the Institute of Biomedicine of the University of Barcelona (IBUB), the Research Institute of Sant Joan de Du (IRSJD) and CIBERER.

"Consequently, from a genetic diagnosis perspective -says DanieL Grinberg- this patient initially diagnosed with Opitz C in Catalonia would correspond to the group of patients with Schaaf-Yang syndrome"

Genetics will define the limits of rare diseases

Identifying the genes that cause a disease is a breakpoint to understand the pathology and set new future therapeutic approaches that improve the quality of life of the patients. In the new study, the teams of the UB and the CRG applied techniques of DNA massive sequencing (exome and genome), a powerful methodology that allows identifying altered genes in each patient.

According to Luis Serrano, director of CRG, "projects like this one show the important role of genomics in the future of medicine and the way on which we diagnose and treat diseases. To understand the diseases and offering not only a diagnosis but also approaches to possible treatments is very relevant in minority diseases. It is a satisfaction for the CRG to contribute with our knowledge and advanced technologies in a project that gives hope to a vulnerable collective" concluded the researcher.

Susana Balcells, tenured lecturer at the UB and also member of IBUB and CIBERER, added "what we can see from a clinical symptomatology view in these kinds of diseases which are so hard to study and diagnose, is far from the initial molecular defect that generates the disease".

"All these clinical doubts -continued Balcells- will be solved with genetics, which will define the limits of these rare diseases and will ease the scientific consensus on the diagnosis and genetic causes that create them".

Crowdfunding: when society supports scientific research

The members of the Group of Human Molecular Genetics of the University of Barcelona and the CRG are currently in contact with the team of Professor Schaaf and three families of patients diagnosed with Schaaf-Yang syndrome in the Iberian Peninsula.

In December 2026, the first author of the study published in Scientific Reports, Roser Urreitzi, researcher of CIBERER and lecturer at the UB, coordinated the meeting between the experts and the affected families. The meeting took place at the Faculty of Biology of the University of Barcelona and was a new encouragement for the collaboration of researchers and affected families in future projects with the participation of the UB, CRG and CIBERER Biobank, in Valencia. This cooperation has also allowed the three patients to be examined by the same clinical expert: the pediatrician Dr Anna M. Cueto, assistant doctor and clinical geneticist at the Department of Clinical and Molecular Genetics of the University Hospital Vall d'Hebron in Barcelona. This is clearly a new progress in the field of ultra-minority diseases.

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Researchers discover genetic bases of Opitz C syndrome - News-Medical.net

Saving GINA: Is Genetic Privacy Imperiled? – PLoS Blogs (blog)

A bill that passed its first hurdle yesterday in Congress threatens to take away genetic privacy protections put in place with the Genetic Information Nondiscrimination Act(GINA) of 2008.H.R.1313, the Preserving Employee Wellness Programs Act, might instead be called the telling on relatives ruling.

GINA

According to GINA, employers cant use genetic information to hire, fire, or promote an employee, or require genetic testing, and health insurers cant require genetic tests nor use results to deny coverage. The law clearly defines genetic tests DNA, RNA, chromosomes, proteins, metabolites and genetic information genetic test results and family history of a genetic condition.

GINA refers to a case,Norman-Bloodsaw v. Lawrence Berkeley Labfrom 1998, that allowed clerical and administrative workers to sue their employer for requiring testing for highly private and sensitive medical genetic information such as syphilis, sickle cell trait, and pregnancy without their consent or knowledge during a general employee health exam. Im not sure how syphilis and pregnancy got lumped in with sickle cell trait (a carrier), but requiring any such test is considered an illegal search under the Fourth Amendment. The sickle cell request also violates Title VII of the Civil Rights Act by singling out employees of African ancestry.

Yesterday the bill passed its first mark-up session, and will either head for the next markup with the Ways and Means Committee or become part of a package of health-care-related bills that goes to the House floor soon, according to Derek Scholes, PhD, the American Society of Human Genetics (ASHG) director of science policy, who attended the session.

Nancy J. Cox, PhD, ASHG president, in a letter to the U.S. House Committee on Education and the Workforce, provides a frightening overview:

If enacted, this legislation would undermine fundamentally the privacy provisions of the Genetic Information Nondiscrimination Act (GINA) and the Americans with Disabilities Act (ADA). It would allow employers to ask employees invasive questions about their and their families health, as well as genetic tests they and their families have undergone. It would further allow employers to impose stiff financial penalties on employees who choose to keep such information private, thus empowering employers to coerce their employees into providing their health and genetic information.

Single-gene diseases are unlike other health conditions or clinical findings, such as infections or high serum cholesterol readings, because a diagnosis in one person reveals risks to relatives in accordance with Mendels laws. A 24-year-old school bus driver in perfect health, for example, whose parent receives a diagnosis of Huntingtons disease, could under the new bill face queries from an employer or health insurer about the 50% risk.

ALL IS NOT WELL(NESS)

The bill isbuilt around an exception in GINA concerning genetic testing that is part of health or genetic services the employer offers, such as part of a wellness program. However, GINA stipulates that only the person and the health care provider or board certified genetic counselor can view the results. GINA also spells out that genetic testing as part of a wellness program must be entirely voluntary.

A May 16, 2016, ruling from the Equal Employment Opportunity Commissionlaid the groundwork for penalizing employees who refuse to answer questions about their or their spouses health. This could amount to thousands of dollars a year, according to a report from the Kaiser Family Foundation. H.R.1313 would make that even worse.

It would further permit workplace wellness programs to penalize much more severely employees who wish to keep their genetic and health information private, allowing penalties of up to 30 percent of the total cost of an employees health insurance, Dr. Cox writes. And the Public Health Service Act permits an increase to 50%. Penalties of this magnitude would compel Americans to choose between retaining the privacy of their health and genetic information and accessing affordable health insurance.

Is charging for the right to enjoy the genetic privacy that was once mandated by law a mechanism to underwrite the new health care plan?

REPERCUSSIONS

H.R.1313 would effectively repeal the fundamental genetic and health privacy protections in GINA and the ADA. It would allow workplace wellness programs to ask employees questions about genetic tests taken by themselves or their families, and to make inquiries about the medical history of employees, their spouses, their children, and other family members, Dr. Cox writes.

Other family members harkens back to GINA, bastardizing its protections, for the 2008 law casts a wide net for relatives, down to the fourth degree.

While first-degree relatives are a persons children, siblings, and parents, and second-degree are grandparents, grandchildren, uncles, aunts, nephews, nieces, and half-siblings, third-degree relatives extend to great-grandparents, great grandchildren, great uncles/aunts, and first cousins, and, ridiculously, fourth-degree relatives to great-great-grandparents, great-great-grandchildren, and first cousins once-removed. I remember my disappointment when I realized that the notifications of new fifth cousins pouring into my email after taking an ancestry test were pretty meaningless, since we each have more than 4,000 of them.

Also worrisome is that the new mandate reeks of genetic determinism, the idea that genotype dictates phenotype.

Genetic information alone does not a diagnosis make. Thats why a clinical diagnosis considers symptoms and results of other types of tests. And while the example of the young bus driver with a family history of HD lies at an extreme because people who inherit the mutation nearly always develop the disease, that situation of complete penetrance is unusual. Most inherited diseases are incompletely penetrant some people with a disease-associated genotype may never develop the condition due to protections from other genes (see Why do healthy people have harmful mutations?here). Another repercussion of H.R.1313 is that it might frighten people away from participating in clinical trials.

I also fear misunderstanding on the part of people charged with analyzing anyones genetic fitness, so to speak, on the basis of a list of mutations or other gene variants. Remember the sickle cell screen of the early 1970s? That was adisasterbecause many parents thought that a finding of children having sickle cell trait meant that they had or would develop the disease. I was even told off-the-record that at least one parental suicide resulted from the well-meant but widespread misinformation.

Will wellness coaches serve as the go-betweens for employees and employers, and if so, how much genetics do they know? Would a wellness coach know that the Huntingtons disease that is in the family of the active and healthy 24-year-old takes many years to develop, even after the first symptoms appear? I didnt see any hard science requirements in this job descriptionor a few others. (Im thinking of the Pilates instructors who have told me that I am lengthening my spine, but thats probably not the same thing.)

The letter from ASHG urges the committee not to support H.R.1313, and to encourage workplace wellness programs without sacrificing employees civil rights. All Americans should be free to participate in genetic research or benefit from genetics-based clinical advances without fear of genetic discrimination, Dr. Cox concludes.

As we gear up to encourage folks to participate in the Precision Medicine Initiativeby contributing their personal genome information, the direct to consumer genetic testing industryis not only alive and well but growing, and loading our genome sequences onto our smartphonesis no longer science fiction, H.R.1313 seems to be coming at a most inopportune time. Lets hope the 1313 is bad luck for its passage!

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Saving GINA: Is Genetic Privacy Imperiled? - PLoS Blogs (blog)