Salmon-Avocado Appetizer

We love salmon in our house: sauteed salmon, baked salmon, Nova Scotia salmon (Nova), salmon mousse, salmon salad. You name it; we love it. So, it was a no-brainer to come up with this recipe. What’s amazing is that I didn’t think of it sooner. This has got to be the world’s easiest, most delicious fish recipe. It came to me, after we decided to cut calories and not have weekend bagels piled high with Tofutti (soy cream cheese) and Nova, with steaming mugs of coffee. We grind our own beans because of the influence of our son Alex and because Dean Gittleman told us we were missing out on great coffee by not doing grinding our own beans! ©Joyce Hays, Target Health Inc.

 

This recipe went from a more complex, salmon ceviche with 16 ingredients to what you see here, a two-ingredient recipe with no marinade, no seasoning, no cilantro, no sake. It eliminated all the extra work, without a loss of flavor. Who could ask for anything more? ©Joyce Hays, Target Health Inc.

 

 

Ingredients For Two People

 

6 ounces of special ahi salmon, sold especially to be eaten raw, like sushi and/or sashimi

2 ripe, but not mushy avocados

1 bag of bamboo picks, 6 inches long

 

World’s easiest appetizer with only two ingredients. Or, to be precise, if you count the bamboo picks, then three items to buy. ©Joyce Hays, Target Health Inc.

 

I got this Ahi Salmon from Whole Foods. It’s in the frozen section and is especially for eating raw salmon as in my recipe and as in making sushi and/or sashimi. You want to get the very best salmon, cut and flash frozen for the purpose of eating raw fish. ©Joyce Hays, Target Health Inc.

 

 

Directions

 

1. Cut the salmon into small pieces (cube like if possible) on a cutting board. Put on a plate.

 

If from your freezer, thaw out the salmon. Then cut it into small cube-like pieces.  Keep in mind that you want to have three cubes of salmon for about 10 to 13 bamboo picks, so try to get at least a total of 30 of these small pieces of salmon. ©Joyce Hays, Target Health Inc.

 

2. Cut the avocados in half and pull out the pit the best you can, without damaging the flesh.

3. With a knife, crisscross each avocado half, so you have little squares. Then with a knife, run the blade all around the avocado half to loosen the flesh. With a small spoon take out each cube of avocado, carefully, so it stays intact. Put on a plate.

4. Get out your bamboo picks and alternately put a piece of salmon, then avocado on each stick, so that you have a total of 3 small pieces of salmon and 3 small pieces of avocado

5. Arrange the salmon picks on a serving platter and devour.

6. I suppose you could add wedges or circles of lemon and/or lime on the serving plate, which would look lovely. I didn’t think of it when I served this the last time, but will do it next time. If you have any leftover avocado, serve that on the table, or on the serving platter.

7. A white wine (icy if possible) goes well with this recipe, including champagne or prosecco.

 

So-o colorful and inviting to serve your guests! ©Joyce Hays, Target Health Inc.

 

We had icy Pouilly Fuisse with the salmon appetizers. ©Joyce Hays, Target Health Inc.

 

Pretty and Easy, not to mention delicious. Happy Spring! ©Joyce Hays, Target Health Inc.

 

This is the beautiful high ceiling of the Metropolitan Opera, after all the Swarovski crystal chandeliers slowly, have been raised up. ©Joyce Hays, Target Health Inc.

 

The breathtakingly beautiful Metropolitan Opera chandeliers, by Swarovski from Austria. Photo source: Genista – http://www.flickr.com/photos/genista/3491661640/, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=9756704

 

We’ve seen our last opera for this season. We usually go to 10 to 12 operas each year. The MetOpera season went so fast this year, can’t believe it’s almost over. My three favorite operas this year were Bellini’s I Puritani, Verdi’s Rigoletto and Wagner’s Tristin and Isolde (yes, 5 hours). For those operas lovers reading this, I am posting one aria from each opera, for you to enjoy.

 

I Puritani: Tenor Aria, Act 1

Rigoletto: Quartet, Final Act

Tristan and Isolde: Final Act: Isolde’s aria, sung by Nina Stemme, who sang at the Met in this year’s production – an epic version. At the end of this five hour opera, I stood up with tears streaming down my face – finally looked around me – the people in front of me and those next to me, were the same, moved to tears. A transcendental experience, is what we all agreed. I will never forget this particular production and I’ve seen it several times before this. Bravo to all involved and to the audience so deeply moved.

Vladimir Horowitz plays Wagner-Liszt Isolde’s Liebestod: Editor’s note: It took the legendary pianist three separate days to record this piece to his satisfaction, and he died four days after its completion on November 5, 1989.

WAGNER – Tristan und Isolde – Prelude and Liebestod (Georg Solti – Chicago Symphony Orchestra)

 

 

From Our Table to Yours !

 

Bon Appetit!

 

New state of matter may have applications in ultrafast quantum computers

Date:
April 20, 2017

Source:
California Institute of Technology

Summary:
The first 3-D quantum liquid crystals may have applications in quantum computing, report scientists. Liquid crystals fall somewhere in between a liquid and a solid: they are made up of molecules that flow around freely as if they were a liquid but are all oriented in the same direction, as in a solid. Liquid crystals can be found in nature, such as in biological cell membranes. Alternatively, they can be made artificially — such as those found in the liquid crystal displays commonly used in watches, smartphones, televisions, and other items that have display screens.

 

These images show light patterns generated by a rhenium-based crystal using a laser method called optical second-harmonic rotational anisotropy. At left, the pattern comes from the atomic lattice of the crystal. At right, the crystal has become a 3-D quantum liquid crystal, showing a drastic departure from the pattern due to the atomic lattice alone.
Credit: Hsieh Lab/Caltech

 

 

Physicists at the Institute for Quantum Information and Matter at Caltech have discovered the first three-dimensional quantum liquid crystal — a new state of matter that may have applications in ultrafast quantum computers of the future.

“We have detected the existence of a fundamentally new state of matter that can be regarded as a quantum analog of a liquid crystal,” says Caltech assistant professor of physics David Hsieh, principal investigator on a new study describing the findings in the April 21 issue of Science. “There are numerous classes of such quantum liquid crystals that can, in principle, exist; therefore, our finding is likely the tip of an iceberg.”

Liquid crystals fall somewhere in between a liquid and a solid: they are made up of molecules that flow around freely as if they were a liquid but are all oriented in the same direction, as in a solid. Liquid crystals can be found in nature, such as in biological cell membranes. Alternatively, they can be made artificially — such as those found in the liquid crystal displays commonly used in watches, smartphones, televisions, and other items that have display screens.

In a “quantum” liquid crystal, electrons behave like the molecules in classical liquid crystals. That is, the electrons move around freely yet have a preferred direction of flow. The first-ever quantum liquid crystal was discovered in 1999 by Caltech’s Jim Eisenstein, the Frank J. Roshek Professor of Physics and Applied Physics. Eisenstein’s quantum liquid crystal was two-dimensional, meaning that it was confined to a single plane inside the host material — an artificially grown gallium-arsenide-based metal. Such 2-D quantum liquid crystals have since been found in several more materials including high-temperature superconductors — materials that conduct electricity with zero resistance at around -150 degrees Celsius, which is warmer than operating temperatures for traditional superconductors.

John Harter, a postdoctoral scholar in the Hsieh lab and lead author of the new study, explains that 2-D quantum liquid crystals behave in strange ways. “Electrons living in this flatland collectively decide to flow preferentially along the x-axis rather than the y-axis even though there’s nothing to distinguish one direction from the other,” he says.

Now Harter, Hsieh, and their colleagues at Oak Ridge National Laboratory and the University of Tennessee have discovered the first 3-D quantum liquid crystal. Compared to a 2-D quantum liquid crystal, the 3-D version is even more bizarre. Here, the electrons not only make a distinction between the x, y, and z axes, but they also have different magnetic properties depending on whether they flow forward or backward on a given axis.

“Running an electrical current through these materials transforms them from nonmagnets into magnets, which is highly unusual,” says Hsieh. “What’s more, in every direction that you can flow current, the magnetic strength and magnetic orientation changes. Physicists say that the electrons ‘break the symmetry’ of the lattice.”

Harter actually hit upon the discovery serendipitously. He was originally interested in studying the atomic structure of a metal compound based on the element rhenium. In particular, he was trying to characterize the structure of the crystal’s atomic lattice using a technique called optical second-harmonic rotational anisotropy. In these experiments, laser light is fired at a material, and light with twice the frequency is reflected back out. The pattern of emitted light contains information about the symmetry of the crystal. The patterns measured from the rhenium-based metal were very strange — and could not be explained by the known atomic structure of the compound.

“At first, we didn’t know what was going on,” Harter says. The researchers then learned about the concept of 3-D quantum liquid crystals, developed by Liang Fu, a physics professor at MIT. “It explained the patterns perfectly. Everything suddenly made sense,” Harter says.

The researchers say that 3-D quantum liquid crystals could play a role in a field called spintronics, in which the direction that electrons spin may be exploited to create more efficient computer chips. The discovery could also help with some of the challenges of building a quantum computer, which seeks to take advantage of the quantum nature of particles to make even faster calculations, such as those needed to decrypt codes. One of the difficulties in building such a computer is that quantum properties are extremely fragile and can easily be destroyed through interactions with their surrounding environment. A technique called topological quantum computing — developed by Caltech’s Alexei Kitaev, the Ronald and Maxine Linde Professor of Theoretical Physics and Mathematics — can solve this problem with the help of a special kind of superconductor dubbed a topological superconductor.

“In the same way that 2-D quantum liquid crystals have been proposed to be a precursor to high-temperature superconductors, 3-D quantum liquid crystals could be the precursors to the topological superconductors we’ve been looking for,” says Hsieh.

“Rather than rely on serendipity to find topological superconductors, we may now have a route to rationally creating them using 3-D quantum liquid crystals” says Harter. “That is next on our agenda.”


Story Source:

Materials provided by California Institute of Technology. Original written by Whitney Clavin. Note: Content may be edited for style and length.


Journal Reference:

  1. J. W. Harter, Z. Y. Zhao, J.-Q. Yan, D. G. Mandrus, D. Hsieh. A parity-breaking electronic nematic phase transition in the spin-orbit coupled metal Cd 2 Re 2 O 7. Science, 2017; 356 (6335): 295 DOI: 10.1126/science.aad1188

 

Source: California Institute of Technology. “New quantum liquid crystals may play role in future of computers: New state of matter may have applications in ultrafast quantum computers.” ScienceDaily. ScienceDaily, 20 April 2017. <www.sciencedaily.com/releases/2017/04/170420141801.htm>.

Date:
April 19, 2017

Source:
The Scripps Research Institute

Summary:
New clues to the wiring of the brain have now been uncovered by a team of researchers. They found that neurons in brain regions that store memory can form networks in the absence of synaptic activity.

 

A serial electron microscopy reconstruction of a single synaptic connection.
Credit: Image courtesy of The Scripps Research Institute

 

 

Scientists at The Scripps Research Institute (TSRI) in La Jolla have revealed new clues to the wiring of the brain. A team led by Associate Professor Anton Maximov found that neurons in brain regions that store memory can form networks in the absence of synaptic activity.

“Our results imply that assembly of neural circuits in areas required for cognition is largely controlled by intrinsic genetic programs that operate independently of the external world,” Maximov explained.

A similar phenomenon was observed by the group of Professor Nils Brose at the Max Planck Institute for Experimental Medicine in Germany. The two complementary studies were co-published as cover stories in the April 19, 2017, issue of the journal Neuron.

The “Nature vs. Nurture” Question

Experience makes every brain unique by changing the patterns and properties of neuronal connections. Vision, hearing, smell, taste and touch play particularly important roles during early postnatal life when the majority of synapses is formed. New synapses also appear in the adult brain during learning. These activity-dependent changes in neuronal wiring are driven by chemical neurotransmitters that relay signals from one neuron to another. Yet, animals and humans have innate behaviors whose features are consistent across generations, suggesting that some synaptic connections are genetically predetermined.

The notion that neurons do not need to communicate to develop networks has also been supported by earlier discoveries of synapses in mice that lacked transmitter secretion in the entire brain. These studies were performed in the laboratory of Professor Thomas Südhof, who won the 2013 Nobel Prize in Physiology or Medicine.

“We thought these experiments were quite intriguing,” Maximov said, “but they also had a major limitation: mice with completely disabled nervous systems became paralyzed and died shortly after birth, when circuitry in the brain is still rudimental.”

The TSRI team set out to investigate if neurons can form and maintain connections with appropriate partners in genetically engineered animals that live into adulthood with virtually no synaptic activity in the hippocampus, a brain region that is critical for learning and memory storage. “While the idea may sound crazy at the first glance,” Maximov continued, “several observations hinted that this task is technically feasible.” Indeed, mammals can survive with injuries and developmental abnormalities that result in a massive loss of brain tissue.

Inspired by these examples, Richard Sando, a graduate student in the Maximov lab, generated mice whose hippocampus permanently lacked secretion of glutamate, a neurotransmitter that activates neurons when a memory is formed. Despite apparent inability to learn and remember, these animals could eat, walk around, groom, and even engage in rudimental social interactions.

Working closely with Professor Mark Ellisman, who directs the National Center for Microscopy and Imaging Research at the University of California, San Diego, Sando and his co-workers then examined the connectivity in permanently inactive areas. Combining contemporary genetic and imaging tools was fruitful: the collaborative team found that several key stages of neural circuit development widely believed to require synaptic activity were remarkably unaffected in their mouse model.

The outcomes of ultra-structural analyses were particularly surprising: it turns out that neurotransmission is unnecessary for assembly of basic building blocks of single synaptic connections, including so-called dendritic spines that recruit signaling complexes that enable neurons to sense glutamate.

Maximov emphasized that the mice could not function normally. In a way, their hippocampus can be compared to a computer that goes though the assembly line, but never gets plugged to a power source and loaded with software. As the next step, the team aims to exploit new chemical-genetic approaches to test if intrinsically-formed networks can support learning.


Story Source:

Materials provided by The Scripps Research Institute. Note: Content may be edited for style and length.


Journal Reference:

  1. Richard Sando, Eric Bushong, Yongchuan Zhu, Min Huang, Camille Considine, Sebastien Phan, Suyeon Ju, Marco Uytiepo, Mark Ellisman, Anton Maximov. Assembly of Excitatory Synapses in the Absence of Glutamatergic Neurotransmission. Neuron, 2017; 94 (2): 312 DOI: 10.1016/j.neuron.2017.03.047

 

Source: The Scripps Research Institute. “Closer look at brain circuits reveals important role of genetics.” ScienceDaily. ScienceDaily, 19 April 2017. <www.sciencedaily.com/releases/2017/04/170419170259.htm>.

Date:
April 18, 2017

Source:
Karolinska Institutet

Summary:
One of the most common combined oral contraceptive pills has a negative impact on women’s quality of life but does not increase depressive symptoms. This is shown by a major randomized, placebo-controlled study.

 

Birth control pills. Both general quality of life and specific aspects like mood/well-being, self-control and energy level were affected negatively by oral contraceptives.
Credit: © Jacob Kearns / Fotolia

 

 

One of the most common combined oral contraceptive pills has a negative impact on women’s quality of life but does not increase depressive symptoms. This is shown by a major randomised, placebo-controlled study conducted by researchers at Karolinska Institutet in Sweden in collaboration with the Stockholm School of Economics. The results have been published in the scientific journal Fertility and Sterility.

“Despite the fact that an estimated 100 million women around the world use contraceptive pills we know surprisingly little today about the pill’s effect on women’s health. The scientific base is very limited as regards the contraceptive pill’s effect on quality of life and depression and there is a great need for randomised studies where it is compared with placebos,” says professor Angelica Lindén Hirschberg at the Department of Women’s and Children’s Health at Karolinska Institutet.

She has led just such a study together with Niklas Zethraeus, associate professor at the Department of Learning, Informatics, Management and Ethics, Anna Dreber Almenberg from the Stockholm School of Economics, and Eva Ranehill of the University of Zürich. 340 healthy women aged between 18 and 35 were treated randomly over the course of three months with either pills with no effect (placebos) or contraceptive pills containing ethinylestradiol and levonorgestrel, the most common form of combined contraceptive pill in Sweden and many other countries. Neither the leaders of the experiment nor the subjects knew which treatment was given to which women.

The women who were given contraceptive pills estimated their quality of life to be significantly lower than those who were given placebos. Both general quality of life and specific aspects like mood/well-being, self-control and energy level were affected negatively by the contraceptives. On the other hand, no significant increase in depressive symptoms was observed.

Since the changes were relatively small, the results must be interpreted with a certain amount of caution, the researchers emphasise. In the case of individual women, however, the negative effect on quality of life may be of clinical importance.

“This might in some cases be a contributing cause of low compliance and irregular use of contraceptive pills. This possible degradation of quality of life should be paid attention to and taken into account in conjunction with prescribing of contraceptive pills and when choosing a method of contraception,” says Niklas Zethraeus.

The type of combined contraceptive pill that was used in the study (etinylestradiol + levonorgestrel) is recommended in many countries as the first choice since it is considered to entail the least risk of thrombosis among the combined contraceptive pills. The findings from the study cannot be generalised to other kinds of combined contraceptive pills because they may have a different risk profile and side-effects.


Story Source:

Materials provided by Karolinska Institutet. Note: Content may be edited for style and length.


Journal Reference:

  1. Niklas Zethraeus, Anna Dreber, Eva Ranehill, Liselott Blomberg, Fernand Labrie, Bo von Schoultz, Magnus Johannesson, Angelica Lindén Hirschberg. A first choice combined oral contraceptive influences general well-being in healthy women – a double-blind, randomized, placebo-controlled trial. Fertility and Sterility, 2017 DOI: 10.1016/j.fertnstert.2017.02.120

 

Source: Karolinska Institutet. “Oral contraceptives reduce general well-being in healthy women.” ScienceDaily. ScienceDaily, 18 April 2017. <www.sciencedaily.com/releases/2017/04/170418094245.htm>.

Date:
April 17, 2017

Source:
Mount Sinai Health System

Summary:
The sympathetic nervous system, not white blood cells, are critically important in the regulation of energy expenditure and thermogenesis, researchers reveal in a new report.

 

While researchers had previously hypothesized that macrophages, a class of white blood cells, played a major role in thermogenesis, the new study suggests that the main driver of thermogenesis is the sympathetic nervous system, which is chiefly controlled by the brain. (Stock image)
Credit: © highwaystarz / Fotolia

 

 

A new study from the Icahn School of Medicine at Mount Sinai provides important insights into how the body regulates its production of heat, a process known as thermogenesis that is currently intensely studied as a target of diabetes and obesity treatment in humans.

While researchers had previously hypothesized that macrophages, a class of white blood cells, played a major role in thermogenesis, the new study suggests that the main driver of thermogenesis is the sympathetic nervous system, which is chiefly controlled by the brain. The results were published online in Nature Medicine.

The Mount Sinai research team led by Christoph Buettner, MD, PhD, senior author of the study and Professor of Medicine (Endocrinology, Diabetes, and Bone Disease) at the Icahn School of Medicine at Mount Sinai, focused on catecholamines, hormones released by the sympathetic nervous system to activate brown fat tissue. Brown adipose tissue is a type of fat tissue that burns energy to produce heat and keep us warm. Catecholamines can also convert white fat tissue, the more familiar kind of fat tissue that stores lipids, into a tissue that resembles brown fat. The researchers tested whether macrophages could provide an alternative source of catecholamines, as had been proposed in recent years.

“Thermogenesis is a metabolic process that receives a lot of interest as a target of drugs that allow you to burn energy and hence reduce obesity and improve diabetes. It turns out that macrophages are not that important, as they are unable to make catecholamines, but clearly the brain through the sympathetic nervous system is,” says Dr. Buettner. “Therefore, it is very important to study the role of the brain and the sympathetic nervous system when it comes to understanding metabolism.”

The ability to generate heat is critical for the survival of warm-blooded animals, including humans, as it prevents death by hypothermia. “This evolutionary pressure shaped the biology of humans and that of other warm-blooded animals, and may in part explain why humans are susceptible to developing diabetes in the environment in which we live,” says Dr. Buettner.

According to Dr. Buettner, while a lot of effort has been invested in targeting the immune system to cure diabetes and insulin resistance, as of yet there are no anti-inflammatory drugs that have been shown to work well in humans with metabolic disease. “Our study suggests that perhaps the key to combating the devastating effects of diabetes and obesity in humans is to restore the control of thermogenesis and metabolism by the brain and the autonomic nervous system,” says Dr. Buettner.


Story Source:

Materials provided by Mount Sinai Health System. Note: Content may be edited for style and length.


Journal Reference:

  1. Katrin Fischer, Henry H Ruiz, Kevin Jhun, Brian Finan, Douglas J Oberlin, Verena van der Heide, Anastasia V Kalinovich, Natasa Petrovic, Yochai Wolf, Christoffer Clemmensen, Andrew C Shin, Senad Divanovic, Frank Brombacher, Elke Glasmacher, Susanne Keipert, Martin Jastroch, Joachim Nagler, Karl-Werner Schramm, Dasa Medrikova, Gustav Collden, Stephen C Woods, Stephan Herzig, Dirk Homann, Steffen Jung, Jan Nedergaard, Barbara Cannon, Matthias H Tschöp, Timo D Müller, Christoph Buettner. Alternatively activated macrophages do not synthesize catecholamines or contribute to adipose tissue adaptive thermogenesis. Nature Medicine, 2017; DOI: 10.1038/nm.4316

 

Source: Mount Sinai Health System. “Your brain, not your white blood cells, keeps you warm, new study suggests.” ScienceDaily. ScienceDaily, 17 April 2017. <www.sciencedaily.com/releases/2017/04/170417115238.htm>.

BIOMED 2017 Conference – Tel-Aviv (May 23-25, 2017)

 

Target Health will again be attending the 16th MIXiii-BIOMED 2017 Conference and Exhibition, being held at the David Intercontinental, (May 23-25, 2017) in Tel-Aviv. This is the 16th anniversary of the conference which we have been attending since 2009. We have many clients and friends in Israel, so please let us know if you will be attending. We look forward to getting together and having a coffee.

 

For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 165). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website.

 

Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor

 

QUIZ

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Dopamine Labs May Know How To Break Your Addiction to Technology (a movement to align technology with our humanity)

Ball-and-stick model of the dopamine molecule, a neurotransmitter that affects the brain’s reward and pleasure centers. Color code: Carbon, C: black; Hydrogen, H: white; Oxygen, O: red; Nitrogen, N: blue. This file is made available under the Creative Commons CC0 1.0 Universal Public Domain Dedication

 

 

In the brain, dopamine functions as a neurotransmitter – a chemical released by 1) ___ (nerve cells) to send signals to other nerve cells. The brain includes several distinct dopamine pathways, one of which plays a major role in reward-motivated behavior. Most types of rewards increase the level of dopamine in the brain, and many addictive drugs increase dopamine neuronal activity. Other brain dopamine pathways are involved in motor 2) ___ and in controlling the release of various hormones. These pathways and cell groups form a dopamine system which is neuromodulatory. Outside the central nervous system, dopamine functions primarily as a local chemical messenger. In blood vessels, it inhibits norepinephrine release and acts as a vasodilator (at normal concentrations); in the kidneys, it increases sodium excretion and urine output; in the pancreas, it reduces 3) ___ production; in the digestive system, it reduces gastrointestinal motility and protects intestinal mucosa; and in the immune system, it reduces the activity of lymphocytes. With the exception of the blood vessels, dopamine in each of these peripheral systems is synthesized locally and exerts its effects near the cells that release it.

 

Company Overview

 

Dopamine Labs, Inc. develops and delivers an application programming interface (API) that enables developers to reinforce users for their applications. Its API enables an application to hack user engagement and retention using models from neuroscience to tell that application when to reinforce a user at that moment. Addiction to technology can be like a drug 4) ___ .It’s not an accident – it’s by design. Dopamine Labs Inc., thought leaders in the mind hijacking industry, wants to equip you with the tools to reclaim your brain. Based out of Southern California, the team of five self-described coders, machine learners, brain architects, designers and hustlers, push persuasive computing? – ?technology that shapes our behavior – ?to the limits. The company provides two apps at the opposite ends of the mind hijacking spectrum: On one end is Space, an app that helps curb compulsive checking – ?like mindlessly opening and scrolling through Facebook? – ?by delaying instant 5) ___. On the other end is Dopamine, an app that helps keep users hooked. It plugs a line of code into an existing app and doles out rewards at just the scientifically-proven right moment to encourage habit building and keep you coming back for more. If Dopamine is turning the mind hijacking knob up to eleven, Space equips people with the capacity to turn it down and regain control over their 6) ___. The apps from Dopamine Labs fulfill dual needs: Their niche knowledge of neuroscience and neuroinformatics (how the brain makes decisions) is lucrative on the marketing side. Companies, eager for this intel, want to know how to better hone their users’ behaviors and persuade them to stay engaged.

 

Recent research suggests that being constantly plugged in? – ?especially when multitasking on different gadgets, or toggling between apps – ?has a profound impact on our 7) ___. A Stanford University study published last year found that chronic media multitaskers had a harder time remembering both distant and recent events. Dopamine, on the other hand, can help app-makers vie for our already scattered attention span, while the Space app is a way of making behaviors, like automatically logging on to Instagram, more mindful. As Ramsay Brown, COO and founder of Dopamine Labs, tells Thrive Global, We built our Space app because, in the bigger picture of what can be built here in persuasive technology, we can use the same techniques, the machine learning and neuroscience, to help people start behaviors that they want to start?but also to help people sustain habits, decrease behaviors they don’t like, and help people stop things entirely. With the Space version of Snapchat, for instance, you’ll get a breathing prompt before you can enter the app. The fancy neuroscience term for this is adaptive stimulus devaluation, which basically means making something desirable (like compulsively checking Snapchat) less appealing by delaying gratification. But Space isn’t about punishing or shaming you for using your favorite apps. It’s about giving you the opportunity to consider what you really want and giving you a choice to disconnect. Creating a time delay between you and the prize makes the prize less valuable, and it quells the itch we’re scratching with social media. The crux, of course, is that itch we’re scratching is a temporary fix: odds are we’re scrolling through social 8) ___ because we’re bored or stressed, but with so many little gratification escape pods, as Brown calls them, we’re able to avoid thinking about what we really need. In other words, we get to ignore “that thing that just itched in my soul, Brown says.

 

Dopamine Labs occupies a unique, and morally hazy, role at such opposite poles of the brain-hacking spectrum. But in launching both Dopamine and Space, Brown explains that the company can set the tone for how this technology can be used, rather than tell people how to use it. We’re not interested as much in being the thought police and telling people what they should want, or what kinds of brain they should aspire to create and live inside, as much as arming them with the tools that enable them to do that just as well. Brown argues that transparency around mind hijacking, and understanding how this is already happening to us all of the time, is essential to creating more mindful relationships with technology. Even knowing that the brain is incredibly malleable, Brown, who studied neuroscience at the University of Southern California (where he met future Dopamine Labs co-founder T. Dalton Combs, then studying neuroeconomics), was surprised at how we can’t resist our favorite apps. He tells TG he knew the raw science of this, but “the skeptic in me said No, no, what about freedom and dignity and autonomy and self-determination? Our proclivity to constantly check social media isn’t because of weak willpower, Brown says. [Our brains are] changing per the design?of whatever data team at these companies are desiring you to change into. So they’re using mathematical and artificial 9) ___ techniques to control, very carefully, in an experimental manner, when and how you’re shown different things, when and how you’re given your likes.

 

In the digital world, we’re actually not the customer, Brown says. “We don’t pay for Facebook. We don’t pay for Twitter or Instagram. If you’re not paying for it, you are not the customer, he says. You’re the goods being sold. How do you like that? Repeating for emphasis: Humans are the goods being sold. Big brands are the customers while our attention span, and our consumer preferences, are the things to be auctioned off. Technology is changing faster than our brains can keep up. Being transparent about how 10) ___ changes the brain, and using tools that can help redirect this, is the first step in chipping away at unhealthy habits, ones that aren’t even of our own creation. Dopamine and Space apps are intended to help catalyze our brains’ evolution. The very same things that are troubling, like the ways technology already hijacks our brains – or how malleable our brains are to these suggestions – gives Brown hope. Technology is not a tool for crushing the human spirit, Brown says, but for lifting it up.

 

Overview by Dopamine Labs

 

Dopamine Labs

 

Short review of dopamine and serotonin

 

TED Talk by former Google ethicist: How better tech could protect us from distraction

 

Short review of how Tech becomes addictive

 

ANSWERS: 1) neurons; 2) control; 3) insulin; 4) addiction; 5) gratification; 6) minds; 7) brains; 8) media; 9) intelligence; 10) technology

 

Arvid Carlsson MD (1923 to Present) and Still Going Strong at 94!

Editor’s note: Short background

 

Kathleen Montagu (died 28 March 1966) was the first researcher to identify dopamine in human brains. Working in Hans Weil-Malherbe’s laboratory at the Runwell Hospital outside London, the presence of dopamine was identified by paper chromatography in the brain of several species, including a human brain. Her research was published in August 1957, followed and confirmed by Hans Weil-Malherbe in November 1957.

 

Nobel Prize-rewarded Arvid Carlsson to be the first researcher to identify that dopamine is a neurotransmitter. His research was published in November 1957, along with colleagues Margit Linsqvist and Tor Magnusson.

 

Arvid Carlsson (born 25 January 1923) is a Swedish neuropharmacologist who is best known for his work with the neurotransmitter dopamine and its effects in Parkinson’s disease. For his work on dopamine, Carlsson was awarded the Nobel Prize in Physiology or Medicine in 2000, along with American co-recipients Eric Kandel at Columbia University and Paul Greengard at Rockefeller. Carlsson was born in Uppsala, Sweden, son of Gottfrid Carlsson, historian and later professor of history at the Lund University, where he began his medical education in 1941. In 1944 he was participating in the task of examining prisoners of Nazi concentration camps, whom Folke Bernadotte, a member of the royal Swedish family, had managed to bring to Sweden. Although Sweden was neutral during World War II, Carlsson’s education was interrupted by several years of service in the Swedish Armed Forces. In 1951, he received his M.L. degree and his M.D. He then became a professor at the University of Lund. In 1959 he became a professor at the University of Gothenburg.

 

In 1957 Kathleen Montagu succeeded in demonstrating the presence of dopamine in the human brain; later that same year Carlsson also demonstrated that dopamine was a neurotransmitter in the brain and not just a precursor for norepinephrine. Carlsson went on to developed a method for measuring the amount of dopamine in brain tissues. He found that dopamine levels in the basal ganglia, a brain area important for movement, were particularly high. He then showed that giving animals the drug reserpine caused a decrease in dopamine levels and a loss of movement control. These effects were similar to the symptoms of Parkinson’s disease. By administering to these animals L-Dopa, which is the precursor of dopamine, he could alleviate the symptoms. These findings led other doctors to try using L-Dopa on patients with Parkinson’s disease, and found it to alleviate some of the symptoms in the early stages of the disease. L-Dopa is still the basis for most commonly used means of treating Parkinson’s disease.

 

While working at Astra AB, Carlsson and his colleagues were able to derive the first marketed selective serotonin reuptake inhibitor, zimelidine, from brompheniramine. Zimelidine preceded both Fluoxetine (Prozac) and Fluvoxamine as the first SSRI, but was later withdrawn from the market due to rare cases of Guillain-Barre syndrome.

 

Still an active researcher and speaker at over 90 years of age, Carlsson, together with his daughter Maria, is working on OSU6162, a dopamine stabilizer alleviating symptoms of post-stroke fatigue.

 

DIABETES

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Rates of New Diagnosed Cases of Type 1 and Type 2 Diabetes Rising

 

In the United States, 29.1 million people are living with diagnosed or undiagnosed diabetes, and about 208,000 people younger than 20 years are living with diagnosed diabetes.

 

Type 1 diabetes, the most common form of diabetes in young people, is a condition in which the body fails to make insulin. Causes of type 1 diabetes are still unknown. However, disease development is suspected to follow exposure of genetically predisposed people to an “environmental trigger,“ stimulating an immune attack against the insulin-producing beta cells of the pancreas. Thus, Type 1 diabetes can be considered an autoimmune disease.

 

In type 2 diabetes, the body does not make or use insulin well. In the past, type 2 diabetes was extremely rare in youth, but it has become more common in recent years.

 

According to an article published in the New England Journal of Medicine (13 April 2017), rates of new diagnosed cases of type 1 and type 2 diabetes are increasing among youth in the United States. This study is the first ever to estimate trends in new diagnosed cases of type 1 and type 2 diabetes in youth (those under the age of 20), from the five major racial/ethnic groups in the U.S.: non-Hispanic whites, non-Hispanic blacks, Hispanics, Asian Americans/Pacific Islanders, and Native Americans. However, the Native American youth who participated in the SEARCH for Diabetes in Youth study are not representative of all Native American youth in the United States. Thus, these rates cannot be generalized to all Native American youth nationwide.

 

The study found that from 2002 to 2012, incidence, or the rate of new diagnosed cases of type 1 diabetes in youth increased by about 1.8% each year. During the same period, the rate of new diagnosed cases of type 2 diabetes increased even more quickly, at 4.8%. The study included 11,244 youth ages 0-19 with type 1 diabetes and 2,846 youth ages 10-19 with type 2.

 

The study results reflect the nation’s first and only ongoing assessment of trends in type 1 and type 2 diabetes among youth and help identify how the epidemic is changing over time in Americans under the age of 20 years.

 

KEY DIABETES FINDINGS FROM THE REPORT

 

— Across all racial/ethnic groups, the rate of new diagnosed cases of type 1 diabetes increased more annually from 2003-2012 in males (2.2%) than in females (1.4%) ages 0-19.

 

— Among youth ages 0-19, the rate of new diagnosed cases of type 1 diabetes increased most sharply in Hispanic youth, a 4.2% annual increase. In non-Hispanic blacks, the rate of new diagnosed cases of type 1 diabetes increased by 2.2% and in non-Hispanic whites by 1.2% per year.

 

— Among youth ages 10-19, the rate of new diagnosed cases of type 2 diabetes rose most sharply in Native Americans (8.9%), Asian Americans/Pacific Islanders (8.5%) and non-Hispanic blacks (6.3%). Note: The rates for Native Americans cannot be generalized to all Native American youth nationwide.

 

— Among youth ages 10-19, the rate of new diagnosed cases of type 2 diabetes increased 3.1% among Hispanics. The smallest increase was seen in whites (0.6%).

 

— The rate of new diagnosed cases of type 2 diabetes rose much more sharply in females (6.2%) than in males (3.7%) ages 10-19.

 

CAUSE OF RISING DIABETES INCIDENCE UNCLEAR

 

Several NIH-funded studies are directly examining how to delay, prevent, and treat diabetes:

 

— Type 1 Diabetes TrialNet <https://www.trialnet.org/>screens thousands of relatives of people with type 1 diabetes annually and conducts prevention studies with those at highest risk for the disease.

 

— The Environmental Determinants of Diabetes in the Young (TEDDY) study seeks <https://teddy.epi.usf.edu/> to uncover factors that may increase development of type 1 diabetes.

 

— For youth with type 2 diabetes, the ongoing Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) <https://portal.bsc.gwu.edu/web/today> study is examining methods to treat the disease and prevent complications.

 

Additionally, CDC’s NEXT-D study <https://www.cdc.gov/diabetes/programs/research/nextd.html> aims to understand how population-targeted policies affect preventive behaviors and diabetes outcomes and answer questions about quantity and quality of care used, costs, and unintended consequences.

 

Gene Silencing Shows Promise for Treating 2 Fatal Neurological Disorders

 

In 1996, it was discovered that mutations in the ataxin 2 gene cause spinocerebellar ataxia type 2 (SCA2), a fatal inherited disorder that primarily damages a part of the brain called the cerebellum, causing patients to have problems with balance, coordination, walking and eye movements.

 

Mutations in ataxin 2 that are associated with SCA2 cause the gene to have polyglutamine expansions, strings of repeated copies of the three letter genetic code, CAG, which stands for the amino acid glutamine. On average, symptoms appear earlier and are more severe for patients who have longer strings. People who have only 27-33 repeats will not develop SCA2 but have an increased risk for ALS.

 

Now, in two studies of mice, reported in Nature (12 April 2017), it was shown that a drug, engineered to combat the gene that causes SCA2, might also be used to treat amyotrophic lateral sclerosis (ALS), a paralyzing and often fatal disorder. For the study, it was found that the problems associated with SCA2, could be reduced by injecting mouse brains with a drug programmed to silence the ataxin 2 gene. In the second study, it was showed that injections of the same type of drug into the brains of mice prevented early death and neurological problems associated with ALS. The type of drug used is called an antisense oligonucleotide. Like an incomplete row of teeth on a zipper, these drugs are short sequences of DNA designed to bind to a portion of a gene’s instructions carried by a molecule called messenger RNA. This stops cells from manufacturing proteins, a process known as gene silencing.

 

An antisense oligonucleotide drug has been approved by the FDA for treating spinal muscular atrophy, a hereditary disorder that causes arm and leg muscle weakness and deterioration in children. Early phase clinical trials are being conducted on the safety and effectiveness of gene silencing drugs to treat several neurological disorders, including Huntington’s disease and an inherited form of ALS.

 

The authors worked with a pharmaceutical company to develop antisense oligonucleotides that silence the ataxin 2 gene rather than the CAG repeats. They then tested oligonucleotides on two lines of mice genetically engineered to have problems associated with SCA2 by programming neurons in the cerebellum to make mutant ataxin 2. In both lines, the oligonucleotides appeared to be effective. Mice injected with the drug were able to walk on a rotating rod longer than mice that received a placebo. Electrical recordings showed the drug restored the firing patterns of neurons in the cerebellum to normal. In addition to reducing ataxin 2 gene levels, the researchers found that the drug also restored the levels of several genes that appear to be decreased by mutant ataxin 2.

 

Meanwhile, authors used different mice to test the idea of combating ALS by silencing ataxin 2. These mice were genetically modified to manufacture high levels of the human version of TDP-43, a protein that normally regulates genes. The researchers investigated these mice because neurons from ALS patients often contain toxic clusters of TDP-43. The mice rapidly develop problems with walking and die early. Previous studies on yeast and flies by Dr. Gitler’s team and his collaborators have suggested that mutant ataxin 2 may control the toxicity of TDP-43. Compared to placebo, injections of the antisense oligonucleotides into the nervous system of the newborn mice extended their median lifespan by 35 percent and improved their ability to walk, while lowering ataxin 2 gene levels in the brain and spinal cord.

 

The authors saw similar results when they eliminated ataxin 2 by crossbreeding the TDP-43 mice with mice that are genetically programmed to have no ataxin 2 gene. The offspring lived longer and walked better than the TDP-43 mice. The brains of the offspring also had fewer toxic TDP-43 clusters than the TDP-43 mice.

 

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