Target Health Partners in South America with LAT Research in EDC and DM


Target Health is pleased to announce that we are collaborating with our South American partner CRO LAT Research on a very exciting project in Chagas Disease. LAT Research is managing the study in South America and Target Health is providing EDC and data management services. With a nod to nostalgia: Dr. Mitchel taught Tropical Medicine at Weill Cornell where he was the “expert“ on mosquito control.


LAT is a private Contract Research Organization founded in Argentina with the advantages of an agile company. LAT offers Clinical Drug Development and Consulting Services in emerging countries across Latin and South America with focus on quality and deliverables. LAT’s team is specialized in conducting all phases of clinical trials (I – IV) and has expertise in managing clinical research in a broad range of therapeutic areas. Please contact Warren Pearlson (212-681-2100 ext. 104) at Target Health to explore this opportunity for your company.


Other current international partners include Technostat Ltd. (Israel) and LSK Global Pharma Services Co. (Korea).


2015 DIA Annual Meeting in Washington, DC


Please stop by and see us at Booth 2527. As always, we will have our comfortable couches.



Our incomparable office manager, Neil Lassalle, organizing the THI Booth at DIA.


Also, on June 16, 2015, at the DIA Annual Meeting in Washington, DC, between 3:30- 5:00, Dr. Jules T. Mitchel, PhD, MBA, President of Target Health Inc., will be chairing a symposium on How Risk-Based Monitoring and eSource Methodologies Are Impacting Clinical Sites, Patients, Regulators and Sponsors. This symposium will show how risk-based monitoring and eSource methodologies are impacting the way clinical trials are being conducted and managed. Specific topics include:


The Time Is Now for Risk-Based Monitoring: Frances E. Nolan, Medidata Solutions Worldwide,

Overcoming Clinical Trial Data Collection Challenges with eSource Solutions and Leveraging Mobile Technologies: Avik Kumar Pal, CliniOps

Using eSource to Maximize Clinical Development Productivity and Efficiency: Edward Stephen Seguine, Clinical Ink


Springtime in NY – The Birds are Back – Can You identify It


If you can identify this water bird, send us a note.



Can you identify this Manhattan Central Park bird?


ON TARGET is the newsletter of Target Health Inc., a NYC-based, full-service, contract research organization (eCRO), providing strategic planning, regulatory affairs, clinical research, data management, biostatistics, medical writing and software services to the pharmaceutical and device industries, including the paperless clinical trial.


For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. 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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Glucagon Receptor Blockade Lowers Blood Glucose in Animals


Novel monoclonal antibody lowered glucose levels in mice and monkeys


Congratulations to our friends and colleagues at Regeneron.


Blockade of the glucagon receptor (GCGR) protein could prove to be an effective strategy for treating 1) ___ and other conditions characterized by hyperglycemia, researchers reported in the latest issue of the journal Endocrinology. Researchers from the biotech company Regeneron Pharmaceuticals reported the development of a fully human monoclonal antibody — REGN1193 — that blocks the glucagon receptor and was found to lower blood 2) ___ levels in both transgenic- and diet-induced-diabetic mice. In a series of experiments in diabetic and nondiabetic monkeys, REGN1193 normalized blood glucose in the diabetic animals without inducing 3) ___ in nondiabetic monkeys, researcher Haruka Okamoto, PhD, of Regeneron in Tarrytown, N.Y., and colleagues noted. Okamoto added that “REGN1193 normalized blood glucose in spontaneously hyperglycemic cynomolgus monkeys for 7 days and that the profound efficacy and prolonged half-life of REGN1193 and other GCGR blocking antibodies are in line with or superior to other classes of antihyperglycemic agents currently approved for diabetes.”


Glucagon is secreted in the 4) ___, and it is involved in stimulating hepatic glucose production as well as regulating lipid metabolism, energy balance, adipose tissue mass, and food intake. The protein’s effects are mediated through the glucagon receptor, which is highly expressed in the liver and at lower levels in kidney, intestinal smooth muscles, brain, and adipose tissue. Antagonizing glucagon action represents an attractive therapeutic option for reducing hepatic glucose production in settings of hyperglycemia where glucagon excess plays a key pathophysiological role. The research in the mice and monkeys suggested that REGN1193 primarily lowers glucose through inhibition of hepatic glucose output, but the experiments also suggested that the monoclonal antibody impacts glucose levels by decreasing body 5) ___ and increased glucagon-like peptide 1 (GLP-1) secretion. According to the authors, “It is well established that persistent activation of the GLP-1 pathway provides the best improvements in glycemic control and that GCGR inhibition induced increase in plasma GLP-1 results from increased production in the pancreatic alpha cells. In GCGR knockout mice, FGF21 expression is also increased. However, our FGF21 knockout mouse data suggest that FGF21 does not contribute to the improved glycemic control in the presence of REGN1193.


A single administration of the monoclonal antibody to diabetic cynomolgus monkeys normalized fasting blood glucose and glucose tolerance and increased circulating levels of glucagon and amino 6) ___, but 8 weeks of REGN1193 exposure did not cause hypoglycemia or increase pancreatic alpha cell area in normoglycemic monkeys. These data suggest that REGN1193 may provide a valuable therapeutic candidate to test the possibility that GCGR blockade could offer benefits to patients with either acute or chronic hyperglycemia. The research was funded by Regeneron Pharmaceuticals, Tarrytown, N.Y. Sources: Regeneron; (Salynn Boyles); Reference: Okamoto H, et al “Glucagon receptor blockade with a human antibody normalizes blood glucose in diabetic mice and monkeys” Endocrin 2015; DOI: 10.1210/en.2015-1011.


ANSWERS: 1) diabetes; 2) glucose; 3) hypoglycemia; 4) pancreas; 5) weight; 6) acids


Medical Ethics: The Monster Study


Blessed are the pure in heart. These UK children are participating in a recent happiness test, which attempts to measure happiness levels in young children – the opposite of the Monster Study


The Monster Study is the name given to a stuttering experiment performed on 22 orphan children in Davenport, Iowa in 1939. It was conducted by Wendell Johnson at the University of Iowa. Johnson chose one of his graduate students, Mary Tudor, to conduct the experiment, and he supervised her research. After placing the children in control and experimental groups, Tudor gave positive speech therapy to half of the children, praising the fluency of their speech, and negative speech therapy to the other half, belittling the children for every speech imperfection and telling them they were stutterers. Many of the normal speaking orphan children who received negative therapy in the experiment suffered negative psychological effects and some retained speech problems for the rest of their lives. Dubbed the “Monster Study“ by some of Johnson’s peers, who were horrified that he would experiment on orphan children to prove a hypothesis, the experiment was kept hidden for fear Johnson’s reputation would be tarnished in the wake of human experiments conducted by the Nazis during World War II. Because the results of the study were never published in any peer-reviewed journal, Tudor’s dissertation is the only official record of the details of the experiment.


The University of Iowa publicly apologized for the Monster Study in 2001. Patricia Zebrowski, University of Iowa assistant professor of speech pathology and audiology, stated, “The body of data that resulted from Johnson’s work on children who stutter and their parents is still the largest collection of scientific information on the subject of stuttering onset. Although new work has determined that children who stutter are doing something different in their speech production than non-stutterers, Johnson was the first to talk about the importance of a stutterer’s thoughts, attitudes, beliefs, and feelings. We still don’t know what causes stuttering, but the ?Iowa’ way of approaching study and treatment is still heavily influenced by Johnson, but with an added emphasis on speech production.“


The research began with selection of twenty-two subjects from a veterans’ orphanage in Iowa. None were told the intent of her research, and they believed that they were to receive speech therapy. Tudor was trying to induce stuttering in healthy children and to see whether telling stutterers that their speech was fine would produce a change. Included among the twenty-two subjects were ten orphans whom teachers and matrons had marked as stutterers before the study began. Tudor and five other graduate students who agreed to serve as judges listened to each of the children speak, graded them on a scale from 1 (poor) to 5 (fluent) and concurred with the school’s assessment. Five were assigned to Group IA, the experimental set, and would be told that their speech was fine. The five in Group IB, the control group, would be told that their speech is “as bad as people say“. The remaining 12 children were chosen at random from the population of normally fluent orphans. Six of these were assigned to IIA. These children, ranging in age from 5 to 15, were to be told that their speech was not normal at all, that they were beginning to stutter and that they must correct this immediately. The final six children in Group IIB, similar in age to those in IIA, were normal speakers who were to be treated as such and given compliments on their nice enunciation. On the first visit, Tudor tested each child’s I.Q. and identified whether they were left-handed or right-handed. A popular theory at the time held that stuttering was caused by a cerebral imbalance. If, for example, a person was born left-handed but was using their right hand, their nerve impulses would misfire, affecting their speech. Johnson did not believe the theory, but still suggested Tudor test each child’s handedness. She had them draw on chalkboards and squeeze the bulb of the dynamometer. Most were right-handed, but left-handed children were present in all the groups. There was no correlation between handedness and speech in this subject crop. During this period, they assigned numbers to the children, such as “Case No 15 Experimental Group IIA.“ The experimental period lasted from January until late May 1939, and the actual intervention consisted of Tudor driving to Davenport from Iowa City every few weeks and talking with each child for about 45 minutes. She followed an agreed-upon script. In her dissertation, she reported that she talked to the stuttering youngsters who were going to be told that they did not stutter. She said to them, in part, “You’ll outgrow [the stuttering], and you will be able to speak even much better than you are speaking now. Pay no attention to what others say about your speaking ability for undoubtedly they do not realize that this is only a phase.“


To the non-stuttering youngsters in IIA, who were to be branded stutterers, she said: “The staff has come to the conclusion that you have a great deal of trouble with your speech. You have many of the symptoms of a child who is beginning to stutter. You must try to stop yourself immediately. Use your will power. Do anything to keep from stuttering. Don’t ever speak unless you can do it right. You see how [the name of a child in the institution who stuttered severely] stutters, don’t you? Well, he undoubtedly started this very same way.“ The children in IIA responded immediately. After her second session with a 5-year-old, Tudor wrote, “It was very difficult to get her to speak, although she spoke very freely the month before.“ Another in the group was a 9-year-old who “practically refuses to talk,“ a researcher wrote in his final evaluation. “Held hand or arm over eyes most of the time.“ A 15-year-old who was the oldest in her group, became “much more conscious of herself, and she talked less,“ Tudor noted. The 15-year-old also began to interject and to snap her fingers in frustration. She was asked why she said ‘a’ so much. “Because I’m afraid I can’t say the next word.“ “Why did you snap your fingers?“ “Because I was afraid I was going to say ‘a.’“ All the children’s schoolwork fell off. One of the boys began refusing to recite in class. The other, an 11-year-old, started anxiously correcting himself. “He stopped and told me he was going to have trouble on words before he said them,“ Tudor reported. She asked him how he knew. He said that the sound “wouldn’t come out. Feels like it’s stuck in there.“ The sixth orphan, a 12-year-old, grew withdrawn and fractious. During their sessions, Tudor asked whether her best friend knew about her ‘stuttering,’ the child muttered, “No.“ “Why not?“ “I hardly ever talk to her.“ Two years later, she ran away from the orphanage and eventually ended up at the rougher Industrial School for Girls – simultaneously escaping her human experimentation.


Mary Tudor herself wasn’t untouched. Three times after her experiment had officially ended she returned to the orphanage to voluntarily provide follow-up care. She told the IIA children that they didn’t stutter after all. The impact, however well-meaning, was questionable. She wrote to Johnson about the orphans in a slightly defensive letter dated April 22, 1940, “I believe that in time they will recover, but we certainly made a definite impression on them.“ The results of the study were freely available in the library of the University of Iowa, but Johnson did not seek publication of the results. The experiment became national news in the wake of a series of articles conducted by an investigative reporter at the San Jose Mercury News in 2001, and a book was written to provide an impartial scientific evaluation. The panel of authors in the book consists mostly of speech pathologists who fail to reach any consensus on either the ethical ramifications or scientific consequences of the Monster Study. Richard Schwartz concludes in Chapter 6 of the book that the Monster Study “was unfortunate in Tudor and Johnson’s lack of regard for the potential harm to the children who participated and in their selection of institutionalized children simply because they were easily available. The deception and the apparent lack of debriefing were also not justifiable.“ Other authors concur claiming the orphan experiment was not within the ethical boundaries of acceptable research. Others, however, felt that the ethical standards in 1939 were different from those used today. Some felt the study was poorly designed and executed by Tudor, and as a result the data offered no proof of Johnson’s subsequent hypothesis that “stuttering begins, not in the child’s mouth but in the parent’s ear“ — i.e., that it is the well-meaning parent’s effort to help the child avoid what the parent has labeled “stuttering“ (but is in fact within the range of normal speech) that contributes to what ultimately becomes the problem diagnosed as stuttering.


On 17 August 2007, six of the orphan children were awarded $925,000 by the State of Iowa for lifelong psychological and emotional scars caused by six months of torment during the Iowa University experiment. The study learned that although none of the children became stutterers, some became self-conscious and reluctant to speak. A spokesman for the University of Iowa called the experiment “regrettable“ and added: “This is a study that should never be considered defensible in any era. In no way would I ever think of defending this study. In no way. It’s more than unfortunate.“ Before her death, Mary Tudor expressed deep regret about her role in the Monster Study and maintained that Wendell Johnson should have done more to reverse the negative effects on the orphan children’s speech. Despite Wendell Johnson’s role in the creation of the Monster Study, Tudor still felt she had made many positive contributions to speech pathology and stuttering research.


The lawsuit was an outgrowth of a San Jose Mercury News article in 2001 conducted by an investigative reporter. The article revealed that several of the orphans had long-lasting psychological effects stemming from the experiment. The state tried unsuccessfully to have the lawsuit dismissed but in September 2005, the Iowa’s Supreme Court justices agreed with a lower court in rejecting the state’s claim of immunity and petition for dismissal. Many of the orphans testified that they were harmed by the “Monster Study“ but outside of Mary Tudor, who testified in a deposition on November 19, 2002, there were no actual eyewitnesses to the events. The advanced age of the three surviving former orphans on the plaintiff’s side helped expedite a settlement with the state. The Iowa attorney general’s office said in a press release on August 17, 2007, that the settlement of $925,000 was fair and appropriate, although the state refused to accept liability for any potential harm caused to the orphans. “For the plaintiffs, we hope and believe it will help provide closure relating to experiences from long ago and to memories going back almost 70 years. For all parties, it ends long-running, difficult and costly litigation that only would have run up more expenses and delayed resolution to plaintiffs who are in their seventies and eighties.“ (DM Register)


Despite the settlement, the debate remains contentious over what harm, if any, the Monster Study caused the orphan children. [Nicholas Johnson], the son of the late Wendell Johnson, has vehemently defended his father. He and some speech pathologists have argued that Wendell Johnson did not intend to harm the orphan children and that none of the orphans were actually diagnosed as “stutterers“ at the end of the experiment. Other speech pathologists have condemned the experiment and said that the orphans’ speech and behavior was adversely affected by the negative conditioning they received. Letters between Mary Tudor and Wendell Johnson that were written shortly after the experiment ended showed that the children’s speech had deteriorated significantly. Mary Tudor returned to the orphanage three times to try to reverse the negative effects caused by the experiment but lamented the fact that she was unable to provide enough positive therapy to reverse the deleterious effects. (Ethics and Orphans. San Jose Mercury News). Today, the American Speech-Language-Hearing Association prohibits experimentation on children when there exists a significant chance of causing lasting harmful consequences. It may be unfair, however, to judge the study by the formal ethical standards that were only created later. The negative consequences of this study appear minor when compared with ethical violations in human subjects, research in other fields, conducted throughout the second half of the 20th century. These latter cases, reviewed, approved and funded in major research institutions, sometimes resulted in the death of subjects.


The study was “suppressed“ in the sense that Wendell Johnson made no attempt to pursue publication of his results, reportedly on the advice of colleagues, who warned him that the experiment could tarnish his career. However, the thesis was bound, cataloged, and made available in the university’s library in identical fashion to all other masters theses. It was often checked out over the years. It was referred to in academic and general publications. Within the profession of speech pathology, there is to this day no single, agreed-upon hypothesis of stuttering – either as to its cause or a single, most appropriate therapy. (This statement is consistent with what is attributed to Patricia Zebrowski, above).


Prediction of Perinatal Depression from Adolescence and Before Conception


Perinatal depression is a neglected global health priority, affecting 10-15% of women in high-income countries and a greater proportion in low-income countries. Outcomes for children include cognitive, behavioral, and emotional difficulties and, in low-income settings, perinatal depression is associated with stunting and physical illness. According to an article published online in The Lancet (10 June 2015), a study was performed to assess the extent to which women with perinatal depressive symptoms had a history of mental health problems before conception.


The investigation derived data from the Victorian Intergenerational Health Cohort Study (VIHCS), a follow-up study of participants in the Victorian Adolescent Health Cohort Study (VAHCS), which was initiated in August, 1992, in the state of Victoria, Australia. In VAHCS, participants were assessed for health outcomes at nine timepoints (waves) from age 14 years to age 29 years. Depressive symptoms were measured with the Revised Clinical Interview Schedule and the General Health Questionnaire. Enrolment to VIHCS began in September, 2006, during the ninth wave of VAHCS; depressive symptoms at this timepoint were measured with the Composite International Diagnostic Interview. Study participants were contacted women every 6 months (from age 29 years to age 35 years) to identify any pregnancies. Perinatal depressive symptoms were measured using the Edinburgh Postnatal Depression Scale (EPDS) by computer-assisted telephone interview at 32 weeks of gestation, 8 weeks after birth, and 12 months after birth. The authors defined perinatal depression as an EPDS score of 10 or more.


For the study design, from a stratified random sample of 1,000 female participants in VAHCS, 384 women with 564 pregnancies were enrolled. 253 (66%) of these women had a previous history of mental health problems at some point in adolescence or young adulthood. Results showed that 117 women with a history of mental health problems in both adolescence and young adulthood had 168 pregnancies, and perinatal depressive symptoms were reported for 57 (34%) of these pregnancies, compared with 16 (8%) of 201 pregnancies in 131 women with no preconception history of mental health problems (adjusted odds ratio 8.36). Perinatal depressive symptoms were reported at one or more assessment points in 109 pregnancies; a preconception history of mental health problems was reported in 93 (85%) of these pregnancies.


According to the authors, perinatal depressive symptoms are mostly preceded by mental health problems that begin before pregnancy, in adolescence or young adulthood. Women with a history of persisting common mental disorders before pregnancy are an identifiable high-risk group, deserving of clinical support throughout the childbearing years. Furthermore, the window for considering preventive intervention for perinatal depression should extend to the time before conception.


Diabetes Mellitus, Obesity, and Diagnosis of Amyotrophic Lateral Sclerosis


Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disorder. Several vascular risk factors have been associated with decreased risk for ALS. Although diabetes is also a risk factor for vascular disease, the few studies of diabetes and ALS have been inconsistent. Cardiometabolic health is a measure of a person’s risk for diabetes and heart disease, and is determined by a set of conditions that include weight, blood glucose levels and cholesterol. Although prior studies have suggested a role of cardiometabolic health on pathogenesis of amyotrophic lateral sclerosis (ALS), the association with diabetes mellitus has not been widely examined.


As a result, a study published online in JAMA Neurology (1 June 2015), was performed to examine the association between diabetes and obesity, each identified through International Statistical Classification of Diseases, Eighth or Tenth Revision codes in a hospital registry, and ALS using data from the Danish National Registers. The investigation was a population-based nested case-control study of 3,650 Danish residents diagnosed as having ALS between January 1, 1982, and December 31, 2009, and 365,000 controls (100 for each ALS case) matched on age and gender. The analysis was conducted in September and October 2014 with the main outcomes and measures being the adjusted odds ratio for ALS associated with diabetes or obesity diagnoses at least 3 years prior to the ALS diagnosis date.


Results showed that when considering diabetes and the obesity indicator together, the estimated odds ratio for ALS was 0.61 for diabetes and 0.81 for obesity. There was no observed effect modification on the association with diabetes by gender. The authors did find a significant modification by age at ALS diagnosis and age at first mention of diabetes in the hospital registers. The protective association was stronger with increasing age at ALS diagnosis (P?=?.01), and the odds ratio for first mention of diabetes was 1.66 before age 40 years but 0.52 for older ages. These results are consistent with different associations for type 1 vs. type 2 diabetes.


FDA Approves Brain Implant to Help Reduce Parkinson’s Disease and Essential Tremor Symptoms


According to the NIH, an estimated 50,000 Americans are diagnosed with Parkinson’s disease (PD) each year, and about one million Americans have the condition. The neurological disorder typically occurs in people over age 60, when cells in the brain that produce a chemical called dopamine become impaired or die. Dopamine helps transmit signals between the areas of the brain that produce smooth, purposeful movement — like eating, writing and shaving. In its early stages, PD typically affects one side of the body and starts as problems with movement, stiffness, and mild tremors. Gradually, the symptoms can affect both sides of the body and medications may become less effective. People with late stage PD have many symptoms including: trouble walking, impaired posture and balance, muscle stiffness and tremors in the arms and hands that make it difficult to perform everyday tasks.


Essential tremor affects several million people and usually occurs in those over age 40. Essential tremor most often affects the hands and arms and can be slowly progressive, starting on one side of the body but eventually affecting both sides. Hand tremor is the most common symptom, but tremors can also affect movement in the head, arms, voice, tongue, legs, and trunk. About half of essential tremor cases result from a genetic mutation. For the remainder of cases, the cause is unknown.


There are no cures for PD or essential tremor, but finding better ways to manage symptoms is essential for patients.


The FDA has approved the Brio Neurostimulation System, an implantable deep brain stimulation device to help reduce the symptoms of PD and essential tremor, a movement disorder that is one of the most common causes of tremors. The Brio Neurostimulation System can help some patients when medication alone may not provide adequate relief from symptoms such as walking difficulties, balance problems, and tremors. The Brio Neurostimulation System consists of a small (1.9in x 2.1in x 0.4in) battery-powered, rechargeable electrical pulse generator implanted under the skin of the upper chest and wire leads that attach to electrodes placed within the brain at specific locations depending on whether the device is being used to treat PD or essential tremor. The electrical pulse generator continuously delivers low intensity electrical pulses to target areas in the brain. Health care providers make adjustments to the pulse generator to optimize the effects of the Brio Neurostimulation System.


Data supporting the safety and effectiveness of the device system included two clinical studies. One study included 136 patients with Parkinson’s disease and the other included 127 patients with essential tremor. In both studies, patients had symptoms, including tremors, that were not adequately controlled with drug therapy. The Brio Neurostimulation System was used in addition to medication for patients with PD and the majority of patients with essential tremor who used the device were able to control their symptoms without the need for medications. Researchers implanted the Brio Neurostimulation System in all patients and assessed effectiveness for PD patients at three months and essential tremor patients at six months.  Results showed that both groups demonstrated statistically significant improvement on their primary effectiveness endpoint when the device was turned on compared to when it was turned off. Serious adverse events included intracranial bleeding, which can lead to stroke, paralysis or death. Other device-related adverse events included infection and dislocation of the device lead under the skin. The Brio Neurostimulation System is manufactured by St. Jude Medical in St. Paul, Minnesota.


Brio Neurostimulation System is the second device approved by the FDA for Parkinson’s and essential tremor. The first device, Medtronic’s Activa Deep Brain Stimulation Therapy System, was approved in 1997 for tremor associated with essential tremor and Parkinson’s disease. In 2002, the indications were expanded to include the symptoms of Parkinson’s disease.


Baked Kale Gratin with Turkey Sausage


Just coming out of the oven, a whopping success! ©Joyce Hays, Target Health Inc.




3 Tablespoons olive oil

1 pound turkey sausage

1/3 cup dry white wine

2 bunches (about 1 pound) kale, stemmed and torn into large pieces

2 shallots, chopped

2 garlic cloves, minced

2 Pinches chili flakes

Pinch black pepper (or grind to your taste)

1 stick butter (for the roux)

1/3 cup chickpea flour

2 cups milk

8 ounces fresh goat cheese

1 cup freshly grated Parmigiano-Reggiano

1 cup Panko (large size)

3 Tablespoons melted butter (for the Panko topping)

2 Tablespoons minced fresh herbs (such as a combination of cilantro, parsley, oregano and basil)




Wonderful fresh ingredients from Whole Foods, which recently opened one block from our home. But, I still like FreshDirect. ©Joyce Hays, Target Health Inc.




1. Wash the kale well, so all the sand and grit is removed. Then dry on paper towels

2. Heat the oven to 350 degrees.

3. In a large, heavy-bottom saute pan, heat the olive oil over medium-high heat. Stir in the sausage, shallots and garlic and cook until browned on all sides and cooked through, about 5 minutes.




Browning the sausage all over. Delicious aroma of the sausage cooking with the shallots and garlic. Almost ready to add the wine. ©Joyce Hays, Target Health Inc.


4. Add the wine and cook, scraping the flavoring from the bottom of the pan. Continue to cook until the wine reduces and is mostly evaporated, 1 to 2 minutes. Decrease the heat to medium.





Beautiful fresh kale from Whole Foods. ©Joyce Hays, Target Health Inc.



Adding the kale pieces one handful at a time, to the sausage skillet. ©Joyce Hays, Target Health Inc.


5. Stir in the kale, one handful at a time. Cook the kale, stirring it in with the sausage, until it begins to wilt and turn a bright green. Continue adding kale by the handful until it is all added to the saute pan and is just wilted. Do not overcook the kale. Cut the cooked sausage in bite size pieces and stir together with the kale. Remove from heat and set the pan aside.

6. In a large saucepan, melt one-half cup (1 stick) butter over medium heat. Whisk in the flour to form a roux. Slowly add the milk, whisking constantly to get rid of any lumps. Bring the mixture to a simmer, whisking frequently. Reduce the heat to a gentle simmer and cook for 10 minutes.




Adding the goat cheese to the roux (butter & flour mixture). ©Joyce Hays, Target Health Inc.


7. Crumble the goat cheese to the sauce and whisk until the cheese is melted and the sauce is smooth, then stir in the sausage and kale. Remove from heat.

8. Spoon the mixture into a shallow, 2-quart gratin dish.





I couldn’t stop sniffing the fragrance of this fresh cilantro, also from Whole Foods. ©Joyce Hays, Target Health Inc.



Making the topping with Panko, parmesan, herbs & butter. ©Joyce Hays, Target Health Inc.


9. In a medium bowl, combine the Parmigiano-Reggiano, Panko and minced fresh herbs. Pour over the 3 Tablespoons melted butter and stir until the butter is evenly distributed to form the topping.

10. Sprinkle the topping evenly over the sausage and kale mixture.




Going into the oven to bake for 30 minutes. I baked this for an extra 10 minutes to get the topping a crispier golden brown. ©Joyce Hays, Target Health Inc.


11. Bake the gratin until the topping is golden-brown and the filling is bubbly, about 30 minutes.

12. Cool slightly before serving.




Mmm smells so good. On the top ten list of yummy comfort foods. ©Joyce Hays, Target Health Inc.



A perfect one dish meal, with icy Stag’s Leap sauvignon blanc. A red would be good with this dish also. ©Joyce Hays, Target Health Inc.



Everything is right about this fabulous Sterling “cab.“ ©Joyce Hays, Target Health Inc.



Rainier fresh cherries for dessert. ©Joyce Hays, Target Health Inc.



Last Saturday, my horse won the coveted Triple Crown race at Belmont Stakes. (American Pharoah the winning horse, jockey was Vincent Espinoza). We splurged and celebrated with fifteen year old Sterling Cabernet Sauvignon. Fabulous full wine with long robust finish! ©Joyce Hays, Target Health Inc.


My father (Mother also) was born and bred in Manhattan. As a teenager at the Horace Mann School, he would occasionally slip out and join his NY lawyer, uncle, at the race track. The Belmont track was around then. They both loved horse racing and I inherited my love of this sport from my father. There is nothing more beautiful than these gorgeous animals galloping their hearts out, as keenly competitive as the jockeys, trainers, owners, viewers (and bettors like me). Interesting tidbit: My father swam with friends in the Hudson River in the 1920s and came down with polio. His physician father, knew about the disease and reacted quickly, wrapping my father in warm wet cloths, which got changed as soon as they cooled. This went on constantly until my father recovered. Any delay of treatment could have resulted in paralysis. Very lucky to have a smart physician for father. (and grandfather).


Anyway, long live horse racing!




Here are the three amazing races of a truly magnificent horse!


Victor Espinoza is the jockey riding American Pharoah in the 2015 Belmont Stakes – Triple Crown Winner


2015 Belmont Stakes, American Pharoah Wins Triple Crown


2015 Preakness Winner, American Pharoah Wins Victor Espinoza, jockey


2015 Kentucky Derby, American Pharoah Wins Victor Espinoza, jockey


From Our Table to Yours!


Bon Appetit!