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



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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.



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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.




— 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.




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


— Type 1 Diabetes TrialNet <>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 <> 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) <> study is examining methods to treat the disease and prevent complications.


Additionally, CDC’s NEXT-D study <> 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.


Drug Approved to Treat Tardive Dyskinesia


Tardive dyskinesia is a neurological disorder characterized by repetitive involuntary movements, usually of the jaw, lips and tongue, such as grimacing, sticking out the tongue and smacking the lips. Some affected people also experience involuntary movement of the extremities or difficulty breathing. Tardive dyskinesia is a serious side effect sometimes seen in patients who have been treated with antipsychotic medications, especially the older medications, for long periods to treat chronic conditions, such as schizophrenia and bipolar disorder. Tardive dyskinesia can also occur in patients taking antipsychotic medications for depression and certain medications for gastrointestinal disorders and other conditions. It is unclear why some people who take these medications develop tardive dyskinesia yet others do not.


The FDA has approved Ingrezza (valbenazine) capsules to treat adults with tardive dyskinesia. This is the first drug approved by the FDA for this condition. The efficacy of Ingrezza was shown in a clinical trial of 234 participants that compared Ingrezza to placebo. After six weeks, participants who received Ingrezza had improvement in the severity of abnormal involuntary movements compared to those who received placebo. Ingrezza may cause serious side effects including sleepiness and heart rhythm problems (QT prolongation). Its use should be avoided in patients with congenital long QT syndrome or with abnormal heartbeats associated with a prolonged QT interval. Those taking Ingrezza should not drive or operate heavy machinery or do other dangerous activities until it is known how the drug affects them.


The FDA granted Neurocrine Biosciences, Inc. Fast Track, Priority Review and Breakthrough Therapy designations for this program.


Another Holiday Dessert: White Chocolate/Marzipan with a Cashew Kiss Inside

First I ordered the little candy flowers, you see above, from Amazon and then stored in back of fridge. I knew I would think of a use for them. When Spring arrived to Manhattan and hardy little flowers started peeping through the soil, I thought of the stored decorations; they seemed to call out for white chocolate rather than dark. Gradually, this recipe fell into place. The concept and preparation were fun and easy to do. Naturally, I then wanted to share the results with you. ©Joyce Hays, Target Health Inc.


This is a perfect holiday dessert. If you wanted a different garnish like cashew crumbs or tiny pieces of shaved chocolate, or whatever you have around the house, that would work also. With this batch, because Spring had arrived, I liked the little flowers. ©Joyce Hays, Target Health Inc.


A little bite of heaven. ©Joyce Hays, Target Health Inc.



Filling Ingredients


1 and 1/2 cups toasted salt-free cashews (bought at

3 Tablespoons Grade A or B maple syrup (bought at

1/2 teaspoon bourbon vanilla extract (bought at

pinch of salt

3 Tablespoons white chocolate chips (FreshDirect)


Coating & Dipping Ingredients


3.5 ounces of a white chocolate brick (bought at Whole Foods)

1 can marzipan (bought online at

Use any type of garnish you want like: crumbs of cashew, tiny pieces of shaved dark chocolate, teeny candy flowers, rainbow sprinkles (buy in a small bottle), rum soaked pieces of cherry


Online buying, makes life so easy. For these ingredients, I went to three websites: FreshDirect, Amazon and ©Joyce Hays, Target Health Inc.




1. Take out a plate or small platter, and put parchment paper on the plate. You will put little dough balls on this plate and into the fridge for 60 minutes.

2. Plan your garnish and have it ready to sprinkle over the melted chocolate before it hardens. It’s too late to do this, once the chocolate has hardened.


Garnish is ready. ©Joyce Hays, Target Health Inc.



3. In a blender, combine all filling ingredients, except white chocolate chips, until cashews are broken down into a batter which holds together when pressed. Pulse for 30 seconds or more, if needed. Remove the batter to a bowl.


The cashews are in the food processor, with maple syrup, vanilla extract and pinch of salt. ©Joyce Hays, Target Health Inc.


Now, keep pulsing until the cashews, vanilla, maple syrup, salt, turn into a batter. ©Joyce Hays, Target Health Inc.



4. After scraping all of the batter into a bowl, now, stir in the white chocolate chips.


With a spatula, scrape out of your food processor, every last bit of the cashew dough into a regular mixing bowl (not with electric beaters). Add the white chocolate bits to the dough and mix them into the dough, with your hands. ©Joyce Hays, Target Health Inc.



5. Using your hands roll the dough into 13 to 15 half-inch balls, and place on a parchment lined plate.


Here is what a cashew dough ball looks like. (with white chocolate chips) ©Joyce Hays, Target Health Inc.


More cashew dough balls on parchment, eventually going into fridge for 60 minutes. ©Joyce Hays, Target Health Inc.



6. Put in freezer for at least 30 to 60 minutes.

7. While dough is freezing, roll out the can of marzipan. Using a cookie cutter or small round glass or cup, press the circle into the marzipan until you have 13“ to 15“ circles, thick enough to hold the dough, but not so thin that the marzipan pouch will break when the dough is put into it. There will be little scraps of the marzipan, so save them until you have enough to make another circle. Make marzipan circles that equal the number of cashew dough balls you’ve made.

8. After 60 minutes, you will place a dough ball in the center of a marzipan circle. Then with your fingers, gather the marzipan up and over the dough ball. The marzipan is easy to manipulate, so when you’ve covered the dough ball with marzipan, simply pinch it, at the top a little, and the marzipan will be sealed. You’re now ready to dip all the balls into warm white chocolate.


Marzipan has been rolled out with a wooden rolling pin. I didn’t have any cookie cutters, so I used this round dish that I use on the table to serve little extras like more anchovies for Caesar Salad, or more salmon roe for top of baked potato. Your marzipan circle should be large enough to wrap around one cashew dough ball. ©Joyce Hays, Target Health Inc.



9. In a double boiler, or small pan, melt the white chocolate.


I like to use this tiny frying pan to melt chocolate because it’s easier to use my hands to dip the balls into. ©Joyce Hays, Target Health Inc.


Here is the one stage of this recipe that you might balk at. Now, the time has come to dip the balls into the warm melted chocolate. You can do it by putting one ball at a time, into the chocolate, with your fingers. Roll it around to get completely covered, using fingers or a fork. Then remove the wet chocolate ball with fingers or with two forks, and put it on the plate you have ready with the parchment. If you’re quick, you can do this with half of your balls, and then add the sprinkles right away, to be sure they will stick. The thing is, what do you do with your sticky chocolate fingers?     :))  Guess. That’s right.



10. After the freezing time is up, remove the dough. Put one piece of the cashew dough in the middle of a marzipan circle. With your fingers, gather the outer circle of marzipan around the dough, so that the marzipan can be pinched together at the top like a little purse.

11. Have the same plate with parchment ready.

12. Pick up each little marzipan purse or ball and dip it into the melted chocolate; roll it around so you get as much of it covered as possible, then put the cashew kiss on the plate. Use your fingers or use two forks.

13. Immediately sprinkle the white balls with whatever garnish you have ready. Do this while the chocolate is still wet. Later, the sprinkle will not stick, as well.

14. Do the dipping and sprinkling, one at a time, with each little chocolate purse, putting each one to harden on the plate. Or, as mentioned, above, do the dipping fast and get half, or all on the plate and then do your garnishing, quickly while the chocolate is still wet and not yet hardened.


This is what the wet chocolate balls look like right after being dipped and garnished. ©Joyce Hays, Target Health Inc.



15. Later, you can arrange them as you like.


You can have a little bite of heaven, without too much effort. ©Joyce Hays, Target Health Inc.



Can I crow a little about my own recipe? Okay, these petit-fours or little cakes will be like a little bit of heaven in your mouth. You won’t believe how good they are. And, as you can see from the directions, they’re very easy to make.  Enjoy, my friends!


May the Spring of 2017 bring with it, a joyful renewal of much needed hope and peace!

©Joyce Hays, Target Health Inc.



From Our Table to Yours !


Bon Appetit!