WASHINGTON (Reuters) - Using a bright orange electrocardiogram machine attached with suction cups to the body of a blue whale, scientists for the first time have measured the heart rate of the world's largest creature and came away with insight about the renowned behemoth's physiology.

The blue whale, which can reach up to 100 feet (30 meters) long and weigh 200 tons, lowers its heart rate to as little as two beats per minute as it lunges under the ocean surface for food, researchers said on Monday.

The maximum heart rate they recorded was 37 beats per minute after the air-breathing marine mammal returned to the surface from a foraging dive.

"The blue whale is the largest animal of all-time and has long fascinated biologists," said Stanford University marine biologist Jeremy Goldbogen, who led the study published in the journal Proceedings of the National Academy of Sciences.

"In particular, new measures of vital rates and physiological rates help us understand how animals work at the upper extreme of body mass," Goldbogen added. "What is life like and what is the pace of life at such a large scale?"

Generally speaking, the larger the animal, the lower the heart rate, minimizing the amount of work the heart does while distributing blood around the body.

The normal human resting heart rate ranges from about 60 to 100 beats per minute and tops out at about 200 during athletic exertion. The smallest mammals, shrews, have heart rates upwards of a thousand beats per minute.

The researchers created a tag device, encased in an orange plastic shell, that contained an electrocardiogram machine to monitor a whale's heart rhythm swimming in the open ocean. The device had four suction cups to enable them to attach it to the whale non-invasively.

The researchers obtained nine hours of data from an adult male whale about 72 feet (22 meters) long encountered in Monterey Bay off California's coast.

"First we have to find a blue whale, which can be very difficult because these animals range across vast swaths of the open ocean. By combining many years of field experience and some luck, we position a small, rigid-hulled, inflatable boat on the whale's left side," Goldbogen said.

"We then have to deploy the tag using a six-meter (20-foot) long carbon-fiber pole. As the whale surfaces to breathe, we tag the whale in a location that we think is closest to the heart: just behind the whale's left flipper," Goldbogen added.

Baleen whales such as blue whales, despite their immense size, feed on tiny prey. As filter-feeders, they take huge amounts of water into their mouths and strain out prey including shrimp-like krill and other zooplankton using baleen plates made of keratin, the same material found in fingernails.

During feeding dives, the whale exhibited extremely low heart rates, typically of four to eight beats per minute and as low as two. After surfacing to breathe following foraging dives, the whale had heart rates of 25 to 37 beats per minute.

(Reporting by Will Dunham; Editing by Sandra Maler)

Reuters

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First-Ever Measurement of a Blue Whale's Heartbeat Reveals Surprising Extremes - ScienceAlert

Wednesday, 27 November 2019, 9:43 amPress Release: University of Waikato

27 November 2019

Leading Plant PhysiologistProfessor Margaret Barbour welcomed as Dean of Science atUniversity of Waikato

Professor Margaret Barbour commencedher position as Dean of Science at the University of Waikatoon 18 November. She was previously Professor of PlantPhysiology in the School of Life and Environmental Sciencesat the University of Sydney.

Vice-Chancellor, ProfessorNeil Quigley says, We are delighted to welcome ProfessorBarbour back to the University of Waikato where she startedher tertiary education. Professor Barbour is a leadingexpert in her scientific field, and will be an asset inleading the School of Science into the future.

Experimental plant physiology is the focus of ProfessorBarbours research, and she is an internationallyrecognised expert in stable isotope effects duringphotosynthesis, respiration and transpiration of higherplants. She pioneered novel stable isotope techniques tomeasure isofluxes between plants and the atmosphere, as wellas developing an underlying theory to explain variation.

These techniques and theory have allowed newunderstanding of plant regulation of carbon and waterdynamics, with applications in crop production, plantecological physiology and paleoclimatic reconstruction fromtree rings.

Professor Barbour completed her Bachelor andMaster of Science from the University of Waikato, beforeheading overseas to complete her PhD in plant physiologyfrom the Australian National University (ANU).

Followingher PhD, Professor Barbour spent time at Landcare Researchin New Zealand, before moving back over the Tasman to takeup an Australian Research Council Fellowship at theUniversity of Sydney, and then more recently as AssociateDean of Research for the Faculty of Science.

I amdelighted to be back in my personal heartland, and excitedto contribute to the future of the University of Waikato,says Professor Barbour.

In this age of publicquestioning of scientific evidence, it is important that wescientists find new ways to connect our understanding withthat from other disciplines, with policy makers, and withthe public. I look forward to helping build theseconnections.

ENDS

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New Dean of Science at University of Waikato - Scoop.co.nz

From the cells in our bodies and the cell phones in our pockets, to the structure of the entire universe, the research honored by this years Nobel Prizes covers a lot of ground.

But, as is always the case at the University of Delawares annual Nobel Symposium, faculty members were able to use their own expertise to share insights into the prize-winning work with an audience of UD and community members.

As a bonus, the audience at this years event also learned about two scandals involving the prize for literature.

The symposium on Tuesday, Nov. 19, hosted by the College of Arts and Sciences in Harker Lab, featured seven short talks about this years laureates and their work, as well as a special tribute to novelist Toni Morrison, who won the Nobel Prize in Literature in 1993 and died in August.

The following are the prizes highlighted at the symposium.

Physiology or Medicine

Just as a candle needs oxygen to burn cleanly, cells need oxygen, to convert food into energy, Ramona Neunuebel, assistant professor of biological sciences, said at the symposium. But too much oxygen is deadly, and too little is deadly.

Neunuebel explained the Nobel Prize in Physiology or Medicine, which was awarded to William G. Kaelin Jr., Sir Peter J. Ratcliffe and Gregg L. Semenza for discovering how cells are able to sense and then adjust their oxygen levels. Oxygen levels can vary, depending on elevation or injury, for example, and scientists have long been puzzled by how cells are able to adapt.

The three laureates put the puzzle together by looking at different aspects of the molecular process that regulates the activity of genes. Together, they found the pathway, Neunuebel said.

She noted that, based on these discoveries, drugs are being developed to target anemia, kidney disease, cancer and other serious conditions.

Economics

Jim Berry, associate professor of economics, began his talk by pointing out that, despite billions of dollars spent each year on aid to developing countries, the question, Does this aid actually work? has been complex and difficult to answer.

But, he said, thanks to the work by this years winners of the Nobel Prize in economic sciences, a much more reliable, experimental approach has been developed. The laureates Abhijit Banerjee, Esther Duflo and Michael Kremer are all relatively young, and Duflo is only the second woman to win the economics prize, Berry said.

Their approach, which Berry termed, Start small, then go big, breaks down the factors involved in each aspect of aid. In seeking to improve education, for example, a researcher might start with the question of whether providing more textbooks to an impoverished school would make a difference in the students achievements and then randomly assign schools in the area being studied to receive or not receive more books.

(The answer? Using teaching methods that are responsive to students needs, not the quantity of textbooks, is what makes a real difference.)

This is an approach thats similar to a medical trial, Berry said. By doing more and larger randomized experiments of this type, researchers can much more accurately identify strategies that are effective, and donors can then target aid to those initiatives.

The research conducted by this years laureates has considerably improved our ability to fight global poverty, the Nobel Prize organization said in announcing the award.

Physics

Sarah Dodson-Robinson, associate professor of physics and astronomy, discussed this years Nobel Prize in Physics, awarded to three scientists, one whose work led to a new understanding of the universes history and two who discovered the first exoplanet orbiting a solar-type star.

This is all about looking for other worlds and understanding the universe, Dodson-Robinson told the audience.

James Peebles won his share of the prize for 50 years of work that is now the basis for our understanding of the universe, the Nobel organization said. His work moved cosmology [the study of the origin of the universe] from pencil and paper to science, Dodson-Robinson said.

The other recipients, Michel Mayor and Didier Queloz, made the first discovery of an exoplanet, a planet outside our Solar System, that is orbiting a solar-type star. They made the discovery in 1995, and since then, Dodson-Robinson said, Weve gone from one planet to thousands. Its been a real revolution in astronomy.

Peace

When Ethiopian Prime Minister Abiy Ahmed Ali was awarded the 2019 Nobel Peace Prize, the announcement also specifically recognized all the stakeholders working for peace and reconciliation in Ethiopia and in the East and Northeast African regions.

At UDs Nobel Symposium, Wunyabari Maloba, professor and department chair of Africana studies and professor of history, noted that the Peace Prize is intended to honor the recipient but also to encourage other leaders to undertake reforms.

Abiy took office in April 2018 and worked with Eritrean President Isaias Afwerki to resume peace talks between the two nations in their long-running border conflict. The two leaders worked out the principles of an agreement, warfare ended and the border between the two countries was reopened.

Although there have been setbacks since then, the prize should be seen as an encouragement for the reforms Abiy has implemented, Maloba said. Something to celebrate here is that half of his cabinet is composed of women, Maloba added.

The hope, he said, is that the Peace Prize will inspire other leaders to demonstrate the courage and daring to bring about peace and stability.

Chemistry

Lithium-ion batteries play a role in every part of our lives, including the battery thats in your pocket right now powering your mobile phone, said Eric Bloch, assistant professor of chemistry and biochemistry.

He explained this years Nobel Prize in Chemistry, which recognized the research conducted by John Goodenough, M. Stanley Whittingham and Akira Yoshino. The three worked separately on different aspects of building a better battery, with the result being the lightweight, rechargeable and powerful lithium-ion battery thats now used in phones, laptops and electric vehicles.

Calling the recognition overdue, Bloch said the battery will continue to play a key role in the future, especially as a means to store energy generated by wind and solar power.

If were going to transition away from fossil fuel lithium-ion batteries are how were going to do it, Bloch said. And we have these three [laureates] to thank.

Literature (2018 and 2019)

No prize was awarded last year in the literature category, after a sexual assault and financial scandal disrupted the Swedish Academys awards committee. The organization regrouped after several resignations and this year awarded two prizes.

Viet Dinh, assistant professor of English, discussed both writers who were honored Olga Tokarczuk, a Polish author who won the delayed 2018 prize, and Peter Handke of Austria, who was awarded the 2019 Nobel. The two authors, Dinh said, provide interesting counterpoints to each other, with different styles and bodies of work.

Not all of Tokarczuks books have been translated into English, and Dinh focused on those that have. He described her 2007 work, Flights, as a fascinating book composed of 116 vignettes. The extremely short stories, he said, mix fiction and fact, jump forward and back in time and can each stand alone, but together they form a constellation of themes focused on the concept of travel.

Dinh also spoke about Tokarczuks Drive Your Plow Over the Bones of the Dead, which he said has a narrower focus than the expansive Flights. The author takes a story that could be a classic whodunit mystery and transforms it into a kind of fable, he said.

While Tokarczuks body of work is smaller and has an outward focus, Handkes is much larger and more diverse, Dinh said. Hes written novels, essays, dramatic works and screenplays over more than 50 years, including The Goalkeepers Anxiety at the Penalty Kick, Offending the Audience and Wings of Desire.

The Nobel organization called him one of the most influential writers in Europe since World War II, but his controversial selection for this years prize has created another scandal. His 1996 book A Journey to the Rivers: Justice for Serbia, depicted Serbia as the victim of the 1990s Yugoslav conflict, and in 2006 he spoke at the funeral of Serbian nationalist leader Slobodan Milosevic, who died while on trial for war crimes.

The dilemma, Dinh said, is, How do you approach a work of art when the artist is known to hold [offensive or controversial] views? He suggested that, instead of ignoring the views or refusing to engage with the artists work, readers should consider also reading works by other writers that offer context and different points of view.

Special presentation honoring Toni Morrison

A. Timothy Spaulding, associate professor of English and of Africana studies, gave a tribute to 1993 laureate Toni Morrison, who is the only black woman to have won the Nobel Prize in Literature.

Calling her prose luminous and poetic, Spaulding said, It is impossible to read a Toni Morrison novel without deep feeling or contemplation.

He praised the vitality of Morrisons language and the way in which her work speaks so clearly and unflinchingly about the horrors of slavery and the legacy of racism. Even while writing about such topics, Spaulding said, Morrisons beautiful and eloquent use of language creates compelling contradictions and paradoxes.

Her work, he said, is intensely rooted in the black experience but also has a broad reach that speaks to all readers.

Morrison published her first novel, The Bluest Eye, in 1970, and went on to publish 10 other acclaimed works of fiction, including Sula, Song of Solomon and Beloved, which won the 1988 Pulitzer Prize.

This article includes information from the Nobel Prize organization.

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Illuminating the Nobels | UDaily - UDaily

Reportage in a Chinese medicine practice in Lyon, France Acupuncture session. (Photo by: ... [+] BSIP/Universal Images Group via Getty Images)

Sometimes I'm not sure whether the best response to pseudoscience is to ignore it, or to patiently try to explain why it's wrong, or to get mad.

This week I'm mad.

My anger and frustration was triggered bya tweetfrom Memorial Sloan-Kettering's Integrative Medicine account, shown here:

Image captured by the author

For those who don't know,Memorial Sloan-Kettering Cancer Centeris one of the world's leading cancer centers, both for treatment and research. If you are diagnosed with cancer, MSK is one of the best places to go.

But not everything at MSK is world class. Unfortunately, they have an"integrative medicine"center that offers a mixture of therapies ranging from helpful to benign to useless. One of their biggest activities is acupuncture, which they claim offers a wide range of benefits to cancer patients.

The MSK tweet shown here was boasting abouta new, $3.7 million studyfunded by NIH to study the effect of acupuncture on pain that cancer patients experience from chemotherapy and bone-marrow transplants.

Here's why I'm mad: cancer patients are extremely vulnerable, often suffering the most frightening and difficult experience of their lives. They are completely dependent on medical experts to help them. When a place like MSK suggests a treatment, patients take it very seriouslyas they should. But they really have no choice: a cancer patient cannot easily look for a second opinion, or switch hospitals or doctors. Even if they have the money (and cancer treatment is extremely expensive), switching hospitals might involve a long interruption with no treatment, during which they could die, and it might also involve traveling far from their home.

Offering these patients ineffective treatments based on pseudoscienceand make no mistake, that's what acupuncture isis immoral. Now, I strongly suspect that the MSK's "integrative medicine" doctors sincerely believe that acupuncture works. Their director, Jun Mao, is clearly a true believer, as explained inthis profile of himon the MSK website. But that doesn't make it okay.

I've written about acupuncture many times before (here,here,here, andhere, for example), but let me explain afresh why it is nonsense.

Acupuncture is based on a pre-scientific notion, invented long before humans understood physiology, chemistry, neurology, or even basic physics, which posits that a mysterious life force, called "qi," flows through the body on energy lines called meridians. As explainedin this article by MSK's Jun Mao:

"According to traditional Chinese medicine ... interruption or obstruction of qi was believed to make one vulnerable to illness. The insertion of needles at specific meridian acupoints was thought to regulate the flow of qi, thus producing therapeutic benefit."

Today we know that none of this exists. There is no qi, and there are no meridians. In that same article, Jun Mao continued by admitting that

"the ideas of qi and meridians are inconsistent with the modern understanding of human anatomy and physiology."

And yet this is what they offer to patients at MSK.

Just to be certain, I readone of the latest studies from MSK, published early this year, which claims to show that acupuncture relieves nausea, drowsiness, and lack of appetite in multiple myeloma patients who were going through stem cell transplants.

It's a mess: totally unconvincing, and a textbook case of p-hacking (ordata dredging). The paper describes a very small study, with just 60 patients total, in which they measured literally dozens of possible outcomes: overall symptom score at 3 different time points, a different score at 3 time points, each of 13 symptoms individually, and more. I counted 24 different p-values, most of them not even close to significant, but they fixated on the 3 that reached statistical significance. The two groups of 30 patients weren't properly balanced: the sham acupuncture group started out with more severe symptoms according to their own scoring metric, andFigure 2in the paper makes it pretty clear that there was no genuine difference in the effects of real versus sham acupuncture.

But they got it published (in a mediocre journal), so now they point to it as "proof" that acupuncture works for cancer patients. This study, bad as it is, appears to be the basis of the $3.7 million NIH grant that they're now going to use, they say, in "a larger study in 300 patients to confirm these previous findings."

And there you go: the goal of the new study,according to the scientists themselves, is not to see if the treatment works, but to confirm their pre-existing belief that acupuncture works. Or, asone scientist remarked on Twitter, "they already have a result in mind, the whole wording of this suggests that they EXPECT a positive outcome. How did this get funded exactly?"

Good question.

So I'm mad. I'm mad that NIH is spending millions of dollars on yet another study of a quack treatment (acupuncture) that should have been abandoned decades ago, but that persists because people make money off it. (And, as others have explained in detail, acupuncture is actually a huge scam that former Chinese dictator Mao Zedong foisted on his own people, because he couldn't afford to offer them real medicine. For a good expos of Chairman Mao's scam,see this 2013 Slate piece.)

But I'm even more upset that doctors at one of the world's leading cancer centers are telling desperately ill patients, who trust them with their lives, that sticking needles into their bodies at bogus "acupuncture points" will relieve the pain and nausea of chemotherapy, or help them with other symptoms of cancer. I'm willing to bet that most MSK doctors don't believe any of this, but they don't want to invest the time or energy to try to stop it.

(I am somewhat reassured by the fact that MSK'sTwitter accounthas nearly 75,000 followers, while it's integrative medicine Twitter account has just 110.)

Or perhaps they are "shruggies": doctors who don't believe in nonsense, but figure it's probably harmless so they don't really object. To them I suggest this:read Dr. Val Jones's accountof how she too was a shruggie, until she realized that pseudoscience causes real harm.

And finally, let me point tothis study inJAMA Oncologyfrom last year,by doctors from Yale, which looked at the use of so-called complementary therapies among cancer patients. They found that

"Patients who received complementary medicine were more likely to refuse other conventional cancer treatment, and had a higher risk of death than no complementary medicine."

And also seethis 2017 studyfrom the Journal of the National Cancer Institute, which found that patients who used alternative medicine were 2.5 times more likely to die than patients who stuck to modern medical treatments.

That's right,Memorial Sloan-Kettering: patients who use non-traditional therapies are twice as likely to die. Thats why Im mad. This is not okay.

Read the original post:
Prestigious NY Cancer Center Will Spend $3.7M To Study Bogus Cancer Treatment - Forbes

If youre anything like me, the memory of your very first CrossFit WOD is burned into your lungs.

From the moment that the clock started running until the very last rep of the workout, you likely sucked wind harder than at any previous point in your life. As you fell to the ground afterwards in a heap of exhaustion, a love/hate relationship with the sport of fitness developed right on the chalk stained and sweat soaked spot.

What many of us were experiencing was an introduction to metabolic conditioning. This newly coined term describes a high intensity training model designed to, in the words of CrossFit founder Greg Glassman, increase the storage and delivery of energy for any activity.

In a 2003 Crossfit Journal article, Glassman shared his position on the importance of metabolic conditioning to avoid specificity of adaptation allowing for first wave cardiovascular and respiratory adaptations.

Its been 16 years since that original journal article was written.

16 years of thrusters, wall-balls and those ever elusive airdyne calories. 16 years of sweat, grit, commitment, and community. A lot of memories and training milestones can be packed into a 16 year time frame.

There are a lot of cardiovascular and respiratory adaptations that can be made as well. One of the greatest physiological adaptations that an athlete can make, however, remains largely untapped in the sports training community.This leaves the door to progress wide open, despite how seasoned and experienced a CrossFit athlete you may be. It is the adaptation that determines how the process of delivering energy for any activity that Glassman spoke about 16 years ago actually occurs.

Its our ability to utilise oxygen more efficiently and more effectively.

Understanding how oxygen is directly related to energy production may mark the next major paradigm shift in human health, fitness and sports performance.

When CrossFit first began, anaerobic output was a glaring weak link in the athletic chain for many athletes. The sport has evolved to the point where this statement might not be true anymore.

Past Games events have demonstrated the effectiveness of CrossFits ability to increase work capacity over short duration. High intensity workouts showcase a collective need to perform more aerobic capacity training.

But, what is aerobic capacity? Does it mean just putting in more LSD (long, slow distance) efforts or is it changing the way that our body utilises oxygen to fuel the release of ATP to power muscular activity.

It is possible to put in hours of focused endurance work each week while never making the critical adaptation which allows this process of more effective energy delivery to take place: that process is an increased tolerance to carbon dioxide and must be trained specifically in order to be improved.

Take the following test from the book The Oxygen Advantage by Patrick McKeown to determine whether your breathing is a buried weakness or a hidden strength.

Note: This is not a test of willpower or a test of how long you can hold your breath. Once you get the first urge to breathe stop the timer and you will have the information that you need to assess your C02 tolerance.

Was it 10 seconds? 20 seconds? 40 seconds or more?

If you were in a large room filled with athletes performing this test you would find that C02 scores would run the gamut from less than 10 seconds to more than 40 seconds.

What does your score mean, and how does it affect your athletic performance?

A score below 20 seconds indicates a comparatively high level of sensitivity to carbon dioxide which will require you to rely on a higher volume of oxygen during training while needing to offload more C02.

This is an athletic disadvantage when compared to an athlete who can work at higher intensities with an increased ability to utilise C02 for more efficient oxygen transport, instead of ridding the body of C02 prematurely and suffering the cost of gassing out as a result.

For every 5 second increase in your C02 tolerance score you can expect to feel more energy, increased stamina, and less fatigue in your aerobic training.

When you exhale and pinch your nose, carbon dioxide levels begin to rise. Your sensitivity to rising carbon dioxide will determine how you will need to breathe during a difficult workout which, in turn, determines your ability to use available oxygen to power those hard working muscles when you need it most.

I strongly believe that the ability to extract and utilisethese basic physiological principles will separate the pack in the seasons to come.

Although variance is a key tenet to the CrossFit training methodology, the WOD is written clearly on the board prior to each training session or competition along with the implicit energy system demands and estimated workout duration for all competitors to study.

A rudimentary understanding of energy consumption and energy demands allows each competitor to make basic decisions about pace prior to the workout beginning. Unlike a sport such as mixed martial arts where the energy demands may be directly dependant on the tactics and approach of your opponent, or a team sport such as basketball where a dynamic interplay between players dictates the pace of the game, CrossFit offers a strategic opportunity that is akin to understanding the basics of accounting.

Oxygen Is Currency. Movement is Expensive.

If you have a $1,000 budget for a 5 day vacation, you would be unlikely to spend $900 of it on the first day. Equally, if you saw a 21 minute workout on the whiteboard you would be unlikely to approach it as if it were a 400m sprint.

Understanding the aerobic and anaerobic demands of each workout beforehand allows you to approach each effort with a heightened level of athletic intelligence.

An understanding of how breathing impacts aerobic and anaerobic performance and that you can not only control your breathing but significantly improve it allows you to gain a competitive advantage in your next WOD despite the specific time demands of the workout.

Simple Breathing Techniques to Improve your Crossfit Performances

The process of cellular respiration is a complex one. Fortunately, even the most basic understanding of how oxygen fuels muscular activity can provide a distinct advantage in terms of pacing yourself during workouts as well as in the development of stronger breathing muscles and an increased tolerance to carbon dioxide: the secret ingredient when it comes to utilising oxygen effectively and efficiently.

The next time you find yourself bent over with hands-on-knees after a tough set of thrusters, struggling to get air into your lungs, keep the following in mind:

There is no shortage of available oxygen in the atmosphere.

It is your internal environment that has changed due to the intensity of the workout. More specifically, your ability to get oxygen from your bloodstream and into muscles has been diminished.

Thats because the key to unlocking oxygen from the bloodstream is C02 and big breaths taken while exhaling through your mouth are offloading C02 from the body at too high a rate to make efficient oxygen utilisation possible.

Heres an easy way to remember this next time that you train:

The amount of Co2 that you lose is the amount of oxygen that you cant use.

The knowledge of this basic physiological process becomes a competitive advantage for any athlete willing to train the following respiratory adaptations in order to master their breathing and improve their aerobic capacity:

You happen to have access to the most powerful and effective breathing machine ever created: the human nose.

The nose is designed for the purpose of up-taking oxygen, removing harmful particles from the atmosphere, warming air prior to entering the body and creating a highly pressurised flow of oxygen directly into the lungs and diaphragm. It also induces the release of nitric oxide, a potent vasodilator that widens the walls of your blood vessels creating a more effective pathway for oxygen rich blood to make it to muscles.

It may be smaller than the mouth, but thats the athletic advantage. If getting more oxygen into our bodies were the solution to avoid gassing out in workouts we would simply take bigger breaths. However, oxygen is in no short supply.

The ability to use available oxygen i.e, extract it from the hemoglobin in the bloodstream, which is the job of carbon dioxide, is the challenge that we face when training.

Nasal breathing allows us to increase our oxygen utilisation while decreasing the amount of C02 that we offload while training.

Keep in mind that C02 is not simply a waste gas, it is like oxygens teammate in a partner WOD. They work together and if one bales out, the others performance suffers.

Breathing through the nose can initially be difficult for many athletes. Therein lies the advantage for those willing to train the adaptation.

After a few weeks of consistent training, many athletes can perform at upwards of 90% max heart rate with nasal-only breathing. They uptake oxygen faster and more effectively and delay premature transitions into anaerobic respiration which come at the cost of increased metabolic waste to buffer.

They also remain fresh so that, if they do decide to shift to mouth breathing near the end of a workout in order to sprint to the finish, they are positioned for a powerful finish.

Use an assault bike, rower or ski erg and try the following 4 minute warm-up.

EMOM for 4 minutes:

Nasal breathing only. Put out as much wattage as the prescribed breathing cadence allows.

Before long you will be able to increase the wattage while sticking to the prescribed warm-up breathing pattern.

This is akin to doing pull-ups and push-ups for your breathing muscles while making the physiological adaptations to carbon dioxide that help separate you from the pack and break through those PR plateaus that weve all experienced.

Additional Training Tips

How you breathe post-workout will affect how quickly your heart rate returns to baseline levels as well as how effective your post-workout mobility session will be (you cant relax a body that is still in a high-stress state).

Your ability to recover more effectively sets you up for success in your next training session. This simple post-workout breathing exercise can help you optimise your recovery and get the most from your hard work:

As a CrossFit athlete, you train your body and you push it hard. Youve most likely already made nutritional changes to support your training and youve worked to prioritise sleep to support your recovery. Youve looked at the various pieces that make up the training puzzle and youve worked hard to put each one in place.

It just so happens that one of the most important puzzle pieces may have been right underneath our noses the whole time

Training comes down to getting oxygen to the body when it needs it most. No amount of willpower or dedication can outweigh the most basic and essential demands of our physiology. The more effective we become at using oxygen to fuel our athleticism, the higher we can raise the ceiling of our own performances potential.

David Bidler is a writer, speaker, and performance-breathing coach living in Portland, Maine. David owns The Distance Project: Strength and Conditioning. Follow him @the_distance_project on Instagram.

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Breathe to Perform: Improve Your Breathing To Unlock Hidden Athletic Potential - BOXROX

Daniel Dankovich

EAST LIVERPOOL Dr. Daniel Dankovich, lecturer-biology at Kent State East Liverpool, received the 2019 Outstanding Teaching Award from the University Teaching Council at Kent State. This is the universitys highest honor for nontenure-track faculty.

Dankovich began teaching part-time for Kent State in 2010, teaching on the Salem, Twinsburg, Burton and East Liverpool campuses. He became a full time faculty member on the East Liverpool Campus in 2018, teaching human biology and anatomy/physiology.

Now living in Canfield, Dankovich graduated from Austintown Fitch High School in 1980. He received two bachelors degrees (in biology and psychology) from the Ohio State University in 1984, before earning his Doctor of Chiropractic degree from the National College of Chiropractic in 1989.

Dan is not satisfied with simply being really good, noted Dr. David Dees, dean and CAO for the Kent State Columbiana County campuses. Over the last several years, he has dedicated himself to finding even better ways to teach. Dan has dedicated himself to focusing more on student learning, rather than just his lecturing style.

Individuals who are the best at their profession are never satisfied with just being good. These individuals are on a path to find greatness and Dan represents this in the area of college teaching.

Dankovich also took the initiative to create a food pantry for students on the East Liverpool Campus and created a student leadership council that helps manage the food distributions.

Like all great educators, Dr. Dankovich understands that being a professor is about more than just what goes on in the classroom, Dees continued. Dan always volunteers and/or takes the lead on important projects. His passion for helping students is in everything he does and he role models for his colleagues the best practices in higher education.

The Outstanding Teaching Award is presented annually to faculty members who consistently showcase astounding skills in classroom teaching. Award winners are formally recognized at the annual University Teaching Council Conference on the Kent Campus.

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2019 Outstanding Teaching Award | News, Sports, Jobs - The Review

Before European settlers arrived in North America, there were millions of wild turkeys spread across what are now 39 U.S. states. But by the 1930s, wild turkeys had disappeared from at least 20 states and their total population had dropped to 30,000.

Over the next few decades, a series of reforms, conservation efforts and demographic changes helped bring wild turkeys back from the brink of extinctionmaking them one of the United States biggest wildlife success stories.

Wild turkey populations started declining in the 17th century as Euorpean colonists hunted them and displaced their habitats. By the time President Abraham Lincoln made Thanksgiving an official U.S. holiday in 1863, wild turkeys had disappeared completely from Connecticut, Vermont, New York and Massachusetts. Within a couple decades, they also disappeared from states farther west like Kansas, South Dakota, Ohio, Nebraska and Wisconsin. In an 1884 issue of Harpers Weekly, one writer predicted wild turkeys would soon become as extinct as the dodo.

Illustration for a 1908 Thanksgiving postcard.

Jim Heimann Collection/Getty Images

Wild turkeys, or Meleagris gallopavo, were not the only native U.S. species that were in danger. By 1889, there were only 541 American bison left. By the 1930s, when wild turkey populations hit their lowest, the passenger pigeon had already become extinct. The crisis in native species populations galvanized conservationists, who helped pass the Federal Aid in Wildlife Restoration Act of 1937, also known as the Pittman-Robertson Act. This act placed a tax on hunting guns and ammunition to pay for wildlife restoration efforts.

The 1930s also saw a major shift among the U.S. population that would end up benefiting wild turkeys, albeit unwittingly. The Great Depression forced many families to abandon their farms, leaving the land open for wild turkeys to expand into. As these farms slowly reverted to native grasses, shrubs, and trees, wild turkey habitat began to emerge, according to the National Wild Turkey Federations website.

READ MORE: What Life Was Like in the Great Depression

E. Donnall Thomas Jr., author of How Sportsmen Saved the World: The Unsung Conservation Effort of Hunters and Anglers, says the decline of cotton farms in particular may have helped wild turkeys rebound in states like Texas.

Thomas father, who won the Nobel Prize in physiology or medicine in 1990, recalls that there was nothing but raccoons, opossums and other small game to hunt growing up in Mart, Texas during the 1930s. But when Thomas traveled back to the area with his father around the 1960s, his father was absolutely astounded to see how wild turkey had flourished.

When he grew up there, all the land was planted in cotton, Thomas says. Cotton is terrible wildlife habitatnothing can eat it, it doesnt provide good escape coverand he was quite sure thats the reason that species like deer and turkeys werent there during the 1930s. When we went back, cotton was gone.

These changes in the 1930s provided good habitats for wild turkeys. However, their numbers didnt really start to rebound until the 1950s, because until then, conservationists couldnt figure out a good way to relocate wild turkeys to these habitats.

The conservation movement started bringing various species back around the turn of the century, says Jim Sterba, author of Nature Wars: The Incredible Story of How Wildlife Comebacks Turned Backyards Into Battlegrounds. But wild turkeys were [one of] the last species that got brought back because they couldnt figure out how to do it.

Finally, in the 1950s, conservationists realized they could safely relocate wild turkeys with rocket or cannon nets. These are nets that shoot out and trap animals. Because of relocation efforts, there are now millions of wild turkeys across dozens of states.

A wild turkey spotted along the highway in 1975, believed to be one of several wild turkeys once planted along the South Platte River in northeastern Colorado.

John G. White/The Denver Post/Getty Images

Thomas speculates that one of the reasons wild turkeys are able to thrive in Montana, the state he lives in, is because of a change in ranching habits that also took place around the 1930s. During this time, cattle ranchers began to bring their cows into feedlots near their ranch houses during the winter. The change in ranching habits had absolutely nothing to do with turkeys, but ended up providing them with a reliable food source to survive the winter.

Turkeys can eat cow manure, Thomas explains. They love to dig through manure, pick out undigested seeds and bits of corn and whatever the cattle have been eating In the winter, when theres snow, its not unusual to see 100 wild turkeys gathered around at a little feedlot next to a ranch building.

Although the food source is most important during the winter, when cattle are concentrated in one area, wild turkeys also eat cow manure in warmer seasons when the cattle are more spread out. Its very, very common to see wild turkeys in the spring flipping over cow turds, he says, adding, that food source wouldnt be here if the cattle werent here.

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How the Great Depression Helped Spare Wild Turkeys From Extinction - History

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Science teacher Jeffery Underwood with a student from his first period class. Due to limited facilities, Weiss must use Underwoods classroom during class labs.

(NICOLE KHUDYAKOV / EYE OF THE TIGER)

Science teacher Jeffery Underwood with a student from his first period class. Due to limited facilities, Weiss must use Underwoods classroom during class labs.

(NICOLE KHUDYAKOV / EYE OF THE TIGER)

(NICOLE KHUDYAKOV / EYE OF THE TIGER)

Science teacher Jeffery Underwood with a student from his first period class. Due to limited facilities, Weiss must use Underwoods classroom during class labs.

One week prior to the start of the 2018-2019 school year, physiology teacher Oliver Weiss learned he would now be teaching fourth period physiology, a lab-based science course, in a room that lacked the necessary materials found in a traditionally equipped lab-classroom.

This is part of a larger trend where students enrollment in lab-based science courses outnumber available lab classrooms, requiring teachers to share.

We have more science teachers than we have classrooms, so we know theres going to be some kind of shifting around, Weiss said. Its just a matter of how do we do it in such a way that its equitable for everybody.

According to the master schedule developed last spring, Weiss was initially set to teach the course in Darcee Durhams classroom, which has lab equipment available. However, last minute scheduling changes initiated the move to history teacher Carol Crabtrees social science classroom, which lacks the space, chemical showers, sinks, outlets for microscopes, and other basic equipment necessary to perform dissections and labs.

(MICHAEL LEEMAN / EYE OF THE TIGER)Science teacher Oliver Weiss helps a student in his fourth period physiology class.

Crabtree was initially informed of this change a few days prior to the start of the school term through her colleagues. Assistant principal Matt Pipitone later confirmed the switch.

Im going to assume it was a last minute decision, because I was told at the last minute, Crabtree said.

The unplanned change meant this was the first time in his teaching career that Weiss wouldnt have immediate access to a science classrooms with lab equipment for his physiology course.

In order to accommodate for the lack of space and equipment, Weiss has been altering his curriculum plans to adhere to his new constraints.

Thus far, this includes adjusting labs and class projects to occur outside and scheduling to borrow other science teachers lab classrooms if necessary.

His flexibility extends to AP environmental science Jeffery Underwood, who is willing to lend out his room for dissections and other necessary physiology labs that are meant to be at the core of the curriculum, thereby simultaneously displacing his own students from their fourth period classroom.

(NICOLE KHUDYAKOV / EYE OF THE TIGER)Science teacher Jeffery Underwood with a student from his first period class. Due to limited facilities, Weiss must use Underwoods classroom during class labs.

Underwoods own experience with mobile classrooms taught him that there are budgetary and spacial limits that force RHS science teachers to continue sharing lab-spaces.

Outfitting a classroom is very expensive, Underwood said. For science classrooms, its expensive to make sure that youve got your water and your gas and all those things that are needed to teach a science class.

On days when physiology stays in room 903, Crabtree, who no longer has full access to her classroom during her fourth period prep, relegates herself to the hallway in the lower level of the 900 west building. The teacher nook, located near the bathrooms, faces foot traffic and noise from in-session classes. It is also one of the few available teacher work spaces with a computer, which Crabtree uses to more comfortably complete her work.

Obviously its not an ideal situation, but its really the only place [to get work done], Crabtree said. The inconvenience is much worse for science teachers who are being displaced.

Crabtree frequently sees other teachers working under similar circumstances in the hallway throughout the day.

As physics teachers, Leslie Kalmer and JoAnne Cook also share classrooms with one another, though their shared subject allows them to have constant access to all equipment necessary for their labs, demonstrations and other class-wide projects.

Sharing classrooms is cumbersome, Cook said. [But] I would rather share a classroom because I think its better for the students.Kalmer believes that even Weiss willingness to be flexible in his lesson plans isnt enough to fully counteract the absence of basic equipment.

He was put in a situation that is very difficult that I wouldnt want to do, Kalmer said. Having to teach a science class, especially so lab-oriented, is almost impossible to do. He cant possibly do it the way he wants.

Weiss plans his schedule around his labs and class-wide activities. His ultimate goal is to avoid interfering with his lessons plans too drastically and noticeably impacting the students learning experience.

Im just going to focus on what I can do for my students instead of what I cant do, Weiss said.

Despite his efforts, students are aware of the limitations of their classroom. Senior Julia Barnes feels restricted by the lack of readily available equipment.

It sucks, Barnes said. I feel like we arent getting as much out of our lessons as we normally would.

See original here:
Classroom availability limited - Eye of the Tiger

This transcript has been edited for clarity.

Michelle L. O'Donoghue, MD, MPH: Hi. I'm Dr Michelle O'Donoghue, reporting from the American Heart Association Scientific Sessions in Philadelphia. Joining me today is Dr Jacqueline Tamis-Holland from Mt Sinai in New York, as well as Dr Rasha Al-Lamee from Imperial College in London. We're going to be talking about the ISCHEMIA trial. Obviously there has been a lot of talk about the results of this study. Perhaps you'd like to lead off and walk us through the study design and the top-line findings.

Rasha K. Al-Lamee, MBBS, MA, PhD: This was a landmark international study with over 38 countries taking part. For study design, they looked at patients with stable coronary artery disease who had moderate to severe ischemia as assessed by exercise testing, nuclear scanning, stress echocardiography, and MRI. Patients went on to have a CT to rule out left main stem in particular and were randomized to either an invasive or conservative arm, with optimal medical therapy given to both groups. This was an unblinded trial, so patients were aware of their treatment allocation as were the physicians. They evaluated hard endpoints between the two groups and then also symptomatic secondary endpoints. The primary outcome included death, myocardial infarction (MI), hospitalization for unstable angina, resuscitated cardiac arrest, and hospitalization for heart failure.

O'Donoghue: I think many people thought about ISCHEMIA as a "sequel" to the COURAGE trial. You hit on a very important point that within the ISCHEMIA cohort, everybody did undergo a coronary CT angiography (CTA), so you did have a sense of their coronary anatomy prior to their entering the study. Similarly with COURAGE, the patient population had all undergone coronary angiography before being randomized.

Al-Lamee: What really stood out for this trial was the fact that they randomized them ahead of a coronary angiogram. Hopefully we got away from one of the criticisms that COURAGE received, which was that patients with proximal left anterior descending (LAD) disease would never make it to trial; they would never be randomized, so there was some selection bias. I think some of that was minimized by this very groundbreaking trial design.

O'Donoghue: What do you view as the top-line results that you want viewers to walk away with?

Jacqueline E. Tamis-Holland, MD: The most important thing to me is the fact that their mortality was incredibly low and that the event rate was relatively low. These patients, with the exception of those who might have left main disease, have a relatively good outcome regardless of what we do in the initial setting. I'm comfortable saying that we can take our time deciding what we want to do. We don't have to rush to the cath lab that evening after their stress test, and we can have a conversation with them.

O'Donoghue: I was really quite struck by the fact that this was a patient population where a lot of them had proximal LAD diseasethings that would give us pause in a clinical setting. Yet the event rate was quite low. Do we think that optimal medical therapy is what is making a big difference in the backdrop for these patients?

Tamis-Holland: I definitely think it's helpingno doubt about it. It makes a difference in our outcome compared to what we used to do many years ago, where you saw different degrees of aggressiveness. It does help contribute to that.

Al-Lamee: The investigators published a paper in Circulation: Cardiovascular Quality and Outcomes a week ago looking at the level to which they delivered that medical therapy. They tried very hard to deliver optimal medical therapy. Patients were judged in terms of their adherence; nonadherent patients were not even included in the trial. They tried very hard to get to target on lipids and to target on blood pressure, and also give them some pretty decent antianginal therapy, which we have not necessarily seen in some of the trials that preceded it and we're not so good at doing in clinical practice.

Tamis-Holland: Although the percentage of patients who actually were optimal was really not that high.

Al-Lamee: And they didn't change so much within the trial. But it's hard to do that with such an international trial. Even at the point when they realized that some sites were not going to target, they went back out to those sites and tried to reeducate them to do some extra strategies to make it better.

O'Donoghue: Perhaps even more remarkable is that even though medical therapy was not fully optimized, there still was not any clear benefit of stenting these patients in terms of mortality reduction or net MI reduction.

Al-Lamee: These stable patients probably have a very different disease than the acute patients that come to our cath labs. We very rarely have patients for whom we perform primary percutaneous coronary intervention (PCI) who tell us they have had angina over the past few weeks. Often this is the first time they presented with it. There must be a very different disease process going on between these two groups.

O'Donoghue: It's always important to underscore that this was a stable patient population. There was discussion that when you stent a patient, there seems to be a little bit of early hazard in terms of earlier risk for MI, many of those probably periprocedural. And a little bit of a benefit was emerging late in terms of MI reduction on the late side. But this was overall sort of offset by that early hazard.

Tamis-Holland: We still have to wait to see the manuscript regarding the clinical relevance, although they met the criteria and they had very strict criteria for postprocedure MI. I would be curious to know how clinically relevant those postprocedure MIs were. More importantly, I would like to know more about the spontaneous MIs, which were clearly higher in the group of patients who got conservative care.

Al-Lamee: Once we saw those curves cross, seeing the 5-year data is going to be key to see whether things change and we suddenly have a reversal in the primary endpoints essentially over time.

O'Donoghue: Perhaps you'd like to talk about the symptomatology piece and whether you feel that ISCHEMIA demonstrated a reduction in overall anginal symptoms. How do we put that in the context of ORBITA?

Al-Lamee: I guess the good-news story from ISCHEMIA is that there does seem to be a significant improvement in symptoms for those patients who have the invasive strategy. I do caveat that with the fact that this was an unblinded trialbut the follow-up goes out to 36 months. You would expect placebo to attenuate over time, although in the later myocardial revascularization trials, we saw that the placebo effect can last out to 30 months. That is hard to tell. Having said that, symptom improvement in terms of freedom from angina was actually quite similar to ORBITA. In our secondary analysis, patients were 20% more likely to have freedom from angina if they got angioplasty. And there, too, the rates were quite similar. They do kind of tie up. We recently published our stress echostratified analysis looking at all patients stratified on the basis of their burden of stress echo ischemia. Patients with the highest stress echo ischemia at pre-randomization benefited the most in terms of symptom reduction on angina frequency with PCI versus placebo. I would say that the two studies are quite in parallel.

O'Donoghue: As I think back to COURAGE, it seemed like the improvement in symptoms started to wane over time. It started to close between the treatment arms.

Tamis-Holland: BARI 2D showed the same thingthat initial improvement was seen and then over time they converged. I feel very strongly that it is a definite improvement in symptoms as opposed to a placebo because of the fact that the two trials similar to this did show an attenuation in the difference in ischemia and it did stay out to 3 years.

Al-Lamee: Symptoms are important to our patients, right? They want quality-of-life differences. Yes, some of that may have been placebo, but there is probably some definitive improvement.

O'Donoghue: The point made yesterday during the discussion was that ISCHEMIA reassures us that we can go that route for a patient who is appropriate for initial medical management. If they continue to have intractable symptoms or it's really interfering with their quality of life, ISCHEMIA also gives us some reassurance that there is no clear net harm from going ahead and stenting patients in that situation. There might be the early hazard, and that is a conversation we need to have with our patients beforehand. But nonetheless, it ends up being net-neutral in terms of the hard outcomes of death or risk for MI.

Tamis-Holland: It reflects back to where we started, which is that regardless of the degree of ischemia, you can comfortably say that if you are taking care of a patient, you are doing it to try to improve their quality of life or symptoms. So if you need to do a revascularization procedure to help make them feel better, it's still fine. It was fine before [ISCHEMIA] and it's still fine.

Al-Lamee: Sometimes I use an analogy with orthopedic surgery: You don't do a total hip replacement or knee replacement to save someone's life; you do it to improve their quality of life. And those patients still want that procedure. Maybe that is the place for angioplasty in stable coronary artery disease.

Tamis-Holland: But it's surgery too.

Al-Lamee: Absolutely. That is key. You make a great point. A quarter of these patients had coronary artery bypass grafting (CABG). It's revascularization as a whole, I suppose.

O'Donoghue: It's not just a stenting trial. It's a little bit different from COURAGE that way because coronary anatomy was not known upfront.

O'Donoghue: Let's say that people watching this are thinking, How am I going to evaluate the next patient who comes in to my clinic who has been having anginal symptoms? Maybe you do or do not yet have a stress test. Even though it was part of ISCHEMIA, is the stress test going to modify your thinking, necessarily? And do we need to have knowledge of their coronary anatomy once you're aware of the fact that they have moderate to severe ischemia in any given distribution? When do we say, "I'll give medical therapy; I don't need to know any more." Or do we need to investigate a little bit further?

Tamis-Holland: Before we can extrapolate the results of the trial to our patient in the office who comes to us with an abnormal stress test, I think we do need to define the anatomy, whether by protocol with CT scan or whether they are taken to the lab to understand whether this patient with this degree of ischemia would have met the criteria to be enrolled. Otherwise, if they had severe left main, they would not have been included.

I think that is important, but I'm also not really sure. I'm curious to know what your feelings are, of where you think the role of stress testing versus just defining the anatomy comes in. I still feel that functional testing is sometimes helpful in those 75-year-olds who are going to have incidental coronary disease anyway. What do you do with that?

Al-Lamee: The pathway in the United Kingdom is really quite different to the United States. Our gatekeeper has become the CT. This was National Institute for Health and Care Excellence (NICE) guidance a while ago. In fact, when I do the rapid-access chest pain clinic, the majority of patients have a CT.

Tamis-Holland: If they are abnormal, do you then follow it with a functional test?

Al-Lamee: I check their CTs, and if they have very significant symptoms which I think are cardiac, the predominant strategy has been to get these guys to the lab. Then I go for coronary angiogram, and at that point we do invasive physiology on the majority.

Tamis-Holland: What if they are 75 years old and they get short of breath or tired after two blocks? Not really angina symptoms.

Al-Lamee: Or you see kind of moderate disease on CT. For those patients I do functional testing. But the predominant strategy has been CT for us. And then when we see very significant disease, it's very heavily calcified and you can't define it any further, or it may be triple vessel or left main, we send those patients straight to the lab. I don't know if that is the right strategy, but that has been our strategy.

O'Donoghue: In some ways, you're now exposing them to double the contrast load and extra radiation. I suppose you could argue certainly for the three-vessel disease or left main, where it's going to definitively change your management. But what if you saw a 90% proximal LAD lesion on the coronary CTA? Would you feel the need to bring them back to the cath lab to confirm that?

Al-Lamee: I find it really tricky. We had a bunch of patients with proximal LADs in ORBITA and they clearly had a load in ISCHEMIA too. I still feel like that 50-year-old guy with that proximal LAD wants that fixed, and I want to fix it. The reality is that we don't necessarily have the evidence that you change that person's hard outcomes. I still find it uncomfortable to leave those patients alone. I don't know what to say.

O'Donoghue: A lot of interventional cardiologists would say the same thing.

Al-Lamee: I ran ORBITA and I'm saying that. To be honest, I have become much more conservative in patients with circumflex lesions and right coronary lesions, and I often start with medicine and see where it goes.

Tamis-Holland: I would agree with that. I'm still perplexed about the severe triple or the very proximal LAD. I would like to really see a drill-down of the data. I know that they said there was no difference. I believe that one of the interactions was proximal LAD versus not, and there was no difference.

I'd be especially curious about the breakdown of the CABG patients to see whether there was a difference in outcome between patients who had enough disease to undergo CABG compared with those whose disease just required PCI.

Al-Lamee: Definitely. And also even for the quality-of-life data. My sense is that the quality of life is quite different for those having had a CABG versus PCI. I would be interested to see if CABG patients have exactly the same quality-of-life improvement or whether having had that big procedure makes a difference going forward.

O'Donoghue: You raise concerns about the "oculostenotic reflex" when they are in the cath lab. On some level, the beauty of doing a coronary CTA is that it might make it easier to make a decision or have a conversation with the patient first before thinking about stenting them.

Al-Lamee: It is important when we discuss it with them now that we do not scare the patient. In the United Kingdom there is a waiting list for coronary angiography, and sometimes you have these patients asking whether they should be paying for this to happen privately so they can have it quickly. I don't think there's any need for that now. I think we can calm them down. We can say it's okay to get them on the right meds and then wait until the cath to see.

O'Donoghue: One of the comments you are making about bringing them to the cath lab is about getting a better sense of the severity of the stenosis. One topic that has been much discussed after ORBITA was the concept of fractional flow reserve (FFR). How much should FFR and instantaneous wave-free ratio (iFR) be guiding our decision-making in this situation? What are your thoughts?

Al-Lamee: It's tricky because the problem with the invasive physiology data and FFR data is that the ischemic threshold for FFR was much lower than the critical threshold we are now using; 0.75 was the initial threshold. And when we looked at the ORBITA dataset in terms of FFR and iFR stratification, we found a really distinct relationship between FFR and iFR burden at pre-randomization. The lower the FFR, the lower the iFR, the more likely it was that angioplasty versus placebo would have an impact on stress echo ischemia or reduction ischemia. But we didn't find any impact on symptoms or exercise time. That may be because we were underpowered. It may also be over time because from our stress echo dataset, we've seen something different. We've seen a relationship between stress echo and symptoms. I'm starting to wonder if the FFR and iFR really tell us about the burden of disease and myocardial mass that is actually affected by that stenosis. Maybe an iFR of 0.4 in the circumflex is quite a different thing to an iFR of 0.4 in an LAD. So, I don't know. I'm still using physiology a lot and I will continue to use physiology a lot because I believe the data. I believe that it's important. But I am slightly starting to change my threshold of treatment. And I don't suddenly think that with a 0.79 on FFR I need to get on and treat. I'm trying to think about the patient more.

Tamis-Holland: I agree. To be honest with you, most of the data on FFR is really for the intermediate stenosis. It's definitely helpful in the symptomatic patient with intermediate disease. For the asymptomatic patient with severe disease, I'm not sure I would necessarily use that entirely as a marker of whether I intervene or not, especially now. So I take them to the lab or it's okay to intervene because the FAME study would show a benefit with an FFR that is abnormal. I don't know if I would have that same approach. In fact, the FAME study only included symptomatic patients. I'd be careful about asymptomatic patients.

Al-Lamee: The other thing with FAME 2 for me is that those urgent revascularization rates in FAME 2 have never been replicated in another trial again. They had urgent revascularization rates of over 20%. That is a little bit crazy to me because when we see the hospitalization for unstable angina in ISCHEMIA, it's much lower, and in ORBITA we didn't have these patients suddenly presenting with acute coronary syndrome or needing to be taken to the cath lab. It didn't happen. So, it speaks likely to the design of the trial, I think. And since it's not been reproducible, I'm a bit wary about FAME 2.

O'Donoghue: There was no clear indication that death or MI is modified.

Tamis-Holland: It's entirely driven by revascularization.

O'Donoghue: Which many would consider to be a softer outcome.

Tamis-Holland: Particularly when a physician and patient know of a lesion that has never been taken care of.

Al-Lamee: One thing that I was really pleased with was how [the ISCHEMIA investigators] defined hospitalization for unstable angina and they adjudicated it. You had to have more than just chest pain. You had to have ECG changes, you had to have troponin checked. They didn't do this in FAME 2, which meant that the vast majority of the revascularizations just happened for a chest pain presentation, troponin negative, ECG negative. And that could have been affected by unblinding, potentially.

O'Donoghue: One observation I heard somebody make yesterday was that, not surprisingly, for those patients who ended up having revascularization, at least PCI, there was a higher usage of dual antiplatelet therapy (DAPT) in that setting. I've heard some people postulate that some of that later MI benefit may in fact be some of those differences in therapy rather than the stent itself. It may be some additional benefit of having a P2Y12 inhibitor on board. Any thoughts on that?

Al-Lamee: We need to know more about that. It's possible that there is a definite contribution. It would make sense that the DAPT might make a contribution. Perhaps this is a dual effectsome of it from the revascularization, some of it the medications.

Tamis-Holland: I agree completely. This was not a trial on bleeding versus ischemic events in patients on DAPT. So that whole issue of bleeding events, which would be adjudicated in a trial that was looking specifically at that, is not. So you are getting, in a sense, the "DAPT trial" benefits of long-term DAPT without looking at the bleeding risk. We know from the CAPRIE trial that a single antiplatelet with a P2Y12 inhibitor is superior to aspirin alone in the vascular disease patients. One would think that it's a similar kind of situation.

O'Donoghue: It will be interesting to see whether this is something we should be considering for our patients with stable coronary disease who are being medically managed without a stent. Should we be thinking about a P2Y12 inhibitor for those patients? Obviously, it has been a little harder to demonstrate net clinical benefit in the past. Nonetheless, thinking about how best to optimize medical therapies is most important.

Al-Lamee: That is a trial we need.

Tamis-Holland: I was just going to say that. I was thinking we need to plan a trial.

O'Donoghue: That is the perfect place to wrap up. We'll start working on our trial designs. Thank you both for joining me today to discuss this very exciting topic.

Tamis-Holland: Thank you for having me.

Al-Lamee: Thank you.

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Managing the SIHD Patient in a Post-ISCHEMIA World - Medscape

Clyde Wayne Bardin, an endocrinologist known for his work on birth control devices such as Norplant and Mirena, died at home last month (October 10). He was 85.

Bardin was a giant in the field of endocrinology who contributed substantially to our knowledge of reproductive physiology, the development of unique methods of contraception and the clinical care of patients with disorders of reproduction, write five leading endocrinologists, including three of his former students, in the Endocrine Societys Endocrine News. His legacy includes not only his research contributions but also his leadership and service to the endocrine community.

Born in 1934 in McCamey, Texas, Bardin grew up with a love of opera and football. He studied biology at Rice University, graduating in 1957, and went on to earn an MD in 1962 from Baylor Universitys medical college (now Baylor College of Medicine).

During the 1960s, Bardin received further medical training at Cornell University and then at the National Cancer Institute, where he became interested in the role of hormones in disease. He took a position as the head of Penn State Universitys division of endocrinology in 1970, and later as vice president of the Population Council, a nonprofit launched by John D. Rockefeller III that researches biomedicine, social science, and public health.

It was during the late 1970s that Bardin started developing new methods of contraception for women that could provide long-lasting effects, as an alternative to the daily contraceptive pill introduced in the US in the early 1960s.

COURTESY OF THE ENDOCRINE SOCIETY

One approach was the development of implants that would release small amounts of the hormone progestin under the skin over several years. An early version of the technology, called Norplant, was introduced to the US market in 1991, although side effects and bad press led to the device being withdrawn from the market in 2002.

Bardin was also involved in the creation of Mirena, an intrauterine device (IUD) that releases the synthetic progesterone-like hormone levonorgestrel, and was approved as a contraceptive device by the US Food and Drug Administration (FDA) in 2000. He additionally helped promote the development of other synthetic hormones for contraceptive purposes, and encouraged researchers to work on contraceptives for men as well as for women.

There has been a lot of skepticism around whether men would ever use a contraceptive, James Sailer, the executive director of the Population Councils Center for Biomedical Research in New York City, tells The New York Times, but Dr. Bardin saw it as an obvious unmet need.

In addition to publishing hundreds of scientific articles and book chapters during his career, Bardin worked to promote the success of the endocrinology community as a whole. He acted as president of the Endocrine Society from 1993 to 1994, mentored many students who went on to become endocrinologists themselves, and later in his career became a consultant for companies trying to develop new contraceptive agents.

The endocrinologists writing for Endocrine News note that Bardin was especially capable when it came to juggling his research and clinical practicethough he still found time to keep up his lifelong interest in opera with visits to the New York Metropolitan Opera House and to spend time with his family.

C. Wayne Bardin can be considered one of the Giants of Endocrinology over the last 40 years, they write, as well as a great human being, and an inspiration to those who follow in his footsteps.

Bardin is survived by his wife, Beatrice, as well as two daughters, three stepchildren, and six grandchildren, the Times reports.

Catherine Offord is an associate editor atThe Scientist. Email her atcofford@the-scientist.com.

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Endocrinologist and Reproductive Physiologist Wayne Bardin Dies - The Scientist