Memorial Day Weekend


On this Memorial Day weekend, we salute the brave men and women who respond to the call and join the military, dedicating their lives to the protection of this great country. Nothing is more precious than life; therefore, nothing is a greater gift, or more heroic, than offering one’s life to defend one of mankind’s great social experiments, America, the beautiful.


Springtime in NYC


This past Friday was a beautiful day, so we decided to stroll through Central Park. The rhododendrons were flowering and if you look closely, you will see 5th Avenue in the background


Springtime in NYC – ©Target Health Inc.


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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Each person has the same set of genes – about 20,000 in all. The differences between people come from slight variations in these 1) ___. For example, a person with red hair doesn’t have the “red hair gene“ while a person with brown hair has the “brown hair gene.“ Instead, all people have genes for hair color, and different versions of these genes dictate whether someone will be a redhead or a brunette. The human 2) ___ contains 50 trillion cells, and almost every one of them contains the complete set of instructions for making an individual human. These instructions are encoded in your DNA, which is a long, ladder-shaped molecule. Each rung on the ladder is made up of a pair of interlocking units, called bases, that are designated by the four letters in the DNA alphabet – A, T, G and C. ‘A’ always pairs with ‘T’, and ‘G’ always pairs with ‘C’.


The long molecules of DNA in each cell is organized into pieces called chromosomes. Humans have 23 pairs of 3) ___. Other organisms have different numbers of pairs – for example, chimpanzees have 24 pairs. The number of chromosomes doesn’t determine how complex an organism is – bananas have 11 pairs of chromosomes, while fruit flies have only 4. Chromosomes are further organized into short segments of DNA called genes. Each gene has a list of instructions, written in the DNA alphabet: – A, T, C, and G. Each gene’s instructions tell each cell how to function and what traits to express. For example, curly hair results, because the genes inherited from parents are instructing hair follicle 4) ___ to make curly strands. Cells follow the instructions, written in genes, to make proteins. Proteins do much of the work in the cells and in the body. Some proteins give cells their shape and structure. Others help cells carry out biological processes like digesting food or carrying oxygen in the blood. Using different combinations of the As, Cs, Ts and Gs, DNA creates the different 5) ___.


Cells come in a array of types; there are brain cells and blood cells, skin cells and liver cells and bone cells. But every cell contains the same instructions in the form of DNA. Cells know whether to make an eye or a foot because of intricate systems of genetic switches. Master genes turn other genes on and 6) ___, making sure that the right proteins are made at the right time in the right cells. To make new cells, an existing cell divides in two. But first it copies its DNA so the new cells will each have a complete set of genetic instructions. Cells sometimes make mistakes during the copying process – kind of like typos. These typos lead to variations in the 7) ___ sequence at particular locations, called single nucleotide polymorphisms, or SNPs (pronounced “snips“). SNPs are the most common type of genetic variation among people. Each SNP represents a difference in a single DNA building block, called a nucleotide. Millions of SNP’s have been cataloged in the human genome. Some SNPs cause disease, like sickle cell anemia. Other SNPs are normal variations in the genome. SNPs can generate biological variation between people by causing differences in the 8) ___ for proteins that are written in genes. Those differences can in turn influence a variety of traits such as appearance, disease susceptibility or response to drugs. While some SNPs lead to differences in health or physical appearance, most SNPs seem to lead to no observable differences between people at all.


DNA is passed from parent to 9) ___. SNPs are inherited versions from parents. An individual will be a match with siblings, grandparents, aunts, uncles, and cousins because of these SNPs. Each person will have far fewer matches with distantly related people. The number of SNPs that match another person can therefore be used to tell how closely related you are. The next generation of SNP annotation webservers can take advantage of the growing amount of data in core bioinformatics resources and use intelligent agents to fetch data from different sources as needed. From a user’s point of view, it is more efficient to submit a set of SNPs and receive results in a single step, which makes meta-servers the most attractive choice. However, if SNP annotation tools deliver heterogeneous data covering sequence, structure, regulation, pathways, etc., they must also provide frameworks for integrating data into a decision algorithm(s), and quantitative confidence measures so users can assess which data are relevant and which are not.


An associated freeware computer program called Promethease, developed by the SNPedia team, allows users to compare personal genetics results against the SNPedia database, generating a report with information about a person’s attributes, such as propensity to diseases, based on the presence of specific SNPs within their genome. In May 2008 Cariaso, using Promethease, won an online contest sponsored by 23andMe to determine as much information as possible about an anonymous woman based only on her genome. Cariaso won in all three categories of “accuracy, creativity and cleverness“. In 2009, the anonymous woman (“Lilly Mendel“) was revealed to be 23andMe co-founder Linda Avey, allowing a direct comparison between her actual traits and those predicted by Promethease a year earlier.


A single 10) ___ polymorphism (SNP) is a change to a single nucleotide in a DNA sequence. The relative mutation rate for an SNP is extremely low. This makes them ideal for marking the history of the human genetic tree. SNPs are named with a letter code and a number. The letter indicates the lab or research team that discovered the SNP. The number indicates the order in which it was discovered. For example, M173 is the 173rd SNP documented by the Human Population Genetics Laboratory at Stanford University, which uses the letter M.;; Wikipedia


ANSWERS: 1) genes; 2) body; 3) chromosomes; 4) cells; 5) proteins; 6) off; 7) DNA; 8) instructions; 9) child; 10) nucleotide


Professor Thomas Hunt Morgan, Geneticist

Thomas Hunt Morgan (September 25, 1866 – December 4, 1945) was an American evolutionary biologist, geneticist, embryologist, and science author who won the Nobel Prize in Physiology or Medicine in 1933 for discoveries elucidating the role that the chromosome plays in heredity. Photo credit: Unknown –, Public Domain,; This image is one of several created for the 1891 Johns Hopkins yearbook of 1891.


Thomas Hunt Morgan received his Ph.D. from Johns Hopkins University in zoology in 1890. Following the rediscovery of Mendelian inheritance in 1900, Morgan began to study the genetic characteristics of the fruit fly Drosophila melanogaster. In his famous Fly Room at Columbia University, Morgan demonstrated that genes are carried on chromosomes and are the mechanical basis of heredity. These discoveries formed the basis of the modern science of genetics. As a result of his work, Drosophila became a major model organism in contemporary genetics. The Division of Biology which he established at the California Institute of Technology has produced seven Nobel Prize winners.


Morgan was born in Lexington, Kentucky, to Charlton Hunt Morgan and Ellen Key Howard Morgan. Part of a line of Southern planter elite on his father’s side, Morgan was a nephew of Confederate General John Hunt Morgan and his great-grandfather John Wesley Hunt had been the first millionaire west of the Allegheny Mountains. Through his mother, he was the great-grandson of Francis Scott Key, the author of the “Star Spangled Banner“, and John Eager Howard, governor and senator from Maryland. Beginning at age 16, Morgan attended the State College of Kentucky (now the University of Kentucky). He focused on science and particularly enjoyed natural history. He worked with the U.S. Geological Survey in his summers and graduated as valedictorian in 1886 with a BS degree. Following a summer at the Marine Biology School in Annisquam, Massachusetts, Morgan began graduate studies in zoology at Johns Hopkins University. After two years of experimental work with morphologist William Keith Brooks, Morgan received a master of science degree from the State College of Kentucky in 1888. The college offered Morgan a full professorship; however, he chose to stay at Johns Hopkins and was awarded a relatively large fellowship to help him fund his studies. Under Brooks, Morgan completed his thesis work on the embryology of sea spiders, to determine their phylogenetic relationship with other arthropods. He concluded that with respect to embryology, they were more closely related to spiders than crustaceans. Based on the publication of this work, Morgan was awarded his Ph.D. from Johns Hopkins in 1890, and was also awarded the Bruce Fellowship in Research. He used the fellowship to travel to Jamaica, the Bahamas and to Europe to conduct further research. Nearly every summer from 1890 to 1942, Morgan returned to the Marine Biological Laboratory to conduct research. He became very involved in governance of the institution, including serving as an MBL trustee from 1897 to 1945.


In 1890, Morgan was appointed associate professor (and head of the biology department) at Johns Hopkins’ sister school Bryn Mawr College. During the first few years at Bryn Mawr, he produced descriptive studies of sea acorns, ascidian worms and frogs. In 1894 Morgan was granted a year’s absence to conduct research in the laboratories of Stazione Zoologica in Naples, where Wilson had worked two years earlier. There he worked with German biologist Hans Driesch, whose research in the experimental study of development piqued Morgan’s interest. Among other projects that year, Morgan completed an experimental study of ctenophore (commonly known as comb jellies, that live in marine waters worldwide. At the time, there was considerable scientific debate over the question of how an embryo developed. Following Wilhelm Roux’s mosaic theory of development, some believed that hereditary material was divided among embryonic cells, which were predestined to form particular parts of a mature organism. Driesch and others thought that development was due to epigenetic factors, where interactions between the protoplasm and the nucleus of the egg and the environment could affect development. Morgan was in the latter camp and his work with Driesch demonstrated that blastomeres isolated from sea urchin and ctenophore eggs could develop into complete larvae, contrary to the predictions (and experimental evidence) of Roux’s supporters.


When Morgan returned to Bryn Mawr in 1895, he was promoted to full professor. Morgan’s main lines of experimental work involved regeneration and larval development; in each case, his goal was to distinguish internal and external causes to shed light on the Roux-Driesch debate. He wrote his first book, The Development of the Frog’s Egg (1897). He began a series of studies on different organisms’ ability to regenerate. He looked at grafting and regeneration in tadpoles, fish and earthworms; in 1901 he published his research as Regeneration. Beginning in 1900, Morgan started working on the problem of sex determination, which he had previously dismissed when Nettie Stevens discovered the impact of the Y chromosome on gender. He also continued to study the evolutionary problems that had been the focus of his earliest work. In 1904, E. B. Wilson invited Morgan to join him at Columbia University. This move freed him to focus fully on experimental work. When Morgan took the professorship in experimental zoology, he became increasingly focused on the mechanisms of heredity and evolution. He had published Evolution and Adaptation (1903); like many biologists at the time, he saw evidence for biological evolution (as in the common descent of similar species) but rejected Darwin’s proposed mechanism of natural selection acting on small, constantly produced variations. Embryological development posed an additional problem in Morgan’s view, as selection could not act on the early, incomplete stages of highly complex organs such as the eye. The common solution of the Lamarckian mechanism of inheritance of acquired characters, which featured prominently in Darwin’s theory, was increasingly rejected by biologists. Around 1908 Morgan started working on the fruit fly Drosophila melanogaster, and encouraging students to do so as well. In a typical Drosophila genetics experiment, male and female flies with known phenotypes are put in a jar to mate; females must be virgins. Eggs are laid in porridge which the larva feed on; when the life cycle is complete, the progeny are scored for inheritance of the trait of interest. With Fernandus Payne, he mutated Drosophila through physical, chemical, and radiational means. Morgan began cross-breeding experiments to find heritable mutations, but they had no significant success for two years. Castle had also had difficulty identifying mutations in Drosophila, which were tiny. Finally, in 1909, a series of heritable mutants appeared, some of which displayed Mendelian inheritance patterns; in 1910 Morgan noticed a white-eyed mutant male among the red-eyed wild types. When white-eyed flies were bred with a red-eyed female, their progeny were all red-eyed. A second generation cross produced white-eyed males – a gender-linked recessive trait, the gene for which Morgan named white. Morgan also discovered a pink-eyed mutant that showed a different pattern of inheritance. In a paper published in Science in 1911, he concluded that (1) some traits were gender-linked, the trait was probably carried on one of the Y or X chromosomes, and (3) other genes were probably carried on specific chromosomes as well. Morgan proposed that the amount of crossing over between linked genes differs and that crossover frequency might indicate the distance separating genes on the chromosome. The later English geneticist J. B. S. Haldane suggested that the unit of measurement for linkage be called the morgan. Morgan’s student Alfred Sturtevant developed the first genetic map in 1913.


Morgan’s fly-room at Columbia became world-famous, and he found it easy to attract funding and visiting academics. In 1927 after 25 years at Columbia, and nearing the age of retirement, he received an offer from George Ellery Hale to establish a school of biology in California. Morgan moved to California to head the Division of Biology at the California Institute of Technology in 1928. In 1933 Morgan was awarded the Nobel Prize in Physiology or Medicine. As an acknowledgement of the group nature of his discovery he gave his prize money to Bridges’, Sturtevant’s and his own children. Morgan declined to attend the awards ceremony in 1933, instead attending in 1934. The 1933 rediscovery of the giant polytene chromosomes in the salivary gland of Drosophila may have influenced his choice. Until that point, the lab’s results had been inferred from phenotypic results, the visible polytene chromosome enabled them to confirm their results on a physical basis. Morgan’s Nobel acceptance speech entitled “The Contribution of Genetics to Physiology and Medicine“ downplayed the contribution genetics could make to medicine beyond genetic counselling. In 1939 he was awarded the Copley Medal by the Royal Society.


Morgan eventually retired in 1942, becoming professor and chairman emeritus. George Beadle returned to Caltech to replace Morgan as chairman of the department in 1946. Although he had retired, Morgan kept offices across the road from the Division and continued laboratory work. In his retirement, he returned to the questions of sexual differentiation, regeneration, and embryology. Morgan had throughout his life suffered with a chronic duodenal ulcer. In 1945, at age 79, he experienced a severe heart attack and died from a ruptured artery.


Below is Thomas Hunt Morgan’s Drosophila melanogaster genetic linkage map. This was the first successful gene mapping work and provides important evidence for the chromosome theory of inheritance. The map shows the relative positions of allelic characteristics on the second Drosophila chromosome. The distance between the genes (map units) are equal to the percentage of crossing-over events that occurs between different alleles.


Thomas Hunt Morgan’s Drosophila melanogaster genetic linkage map. This was the first successful gene mapping work and provides important evidence for the Boveri-Sutton chromosome theory of inheritance. The map shows the relative positions of allelic characteristics on the second Drosophila chromosome. The distance between the genes (map units) are equal to the percentage of crossing-over events that occurs between different alleles. This gene linkage map shows the relative positions of allelic characteristics on the second Drosophila chromosome. The alleles on the chromosome form a linkage group due to their tendency to form together into gametes. The distance between the genes (map units) are equal to the percentage of crossing-over events that occurs between different alleles. This diagram is also based on the findings of Thomas Hunt Morgan in his Drosophila cross. Graphic credit: Twaanders17 – Own work, CC BY-SA 4.0,


Source:; Wikipedia


Severe Atopic Eczema and Long Term Risk of Cardiovascular Disease


According to an article published online in the British Medical Journal (23 May 2018), a population-based matched cohort study was performed to investigate whether adults with atopic eczema are at an increased risk of cardiovascular disease and whether the risk varies by atopic eczema severity and condition activity over time. For the study, data were obtained from 1) UK electronic health records from the Clinical Practice Research Datalink, Hospital Episode Statistics, and 2) data from the Office for National Statistics, 1998-2015.


Study participants included adults with a diagnosis of atopic eczema, matched (on age, gender, general practice, and calendar time), and patients without atopic eczema. The main outcome measures were cardiovascular outcomes as measured by myocardial infarction, unstable angina, heart failure, atrial fibrillation, stroke, and cardiovascular death).


The study obtained data from a total of 387,439 patients with atopic eczema were matched to 1,528,477 patients without atopic eczema. The median age was 43 at cohort entry and 66% were female. Median follow-up was 5.1 years. Evidence of a 10% to 20% increased hazard for the non-fatal primary outcomes for patients with atopic eczema was found by using Cox regression stratified by matched set. Results showed a strong dose-response relation with severity of atopic eczema. Patients with severe atopic eczema had a 20% increase in the risk of stroke (hazard ratio 1.22, 99% confidence interval 1.01 to 1.48), 40% to 50% increase in the risk of myocardial infarction, unstable angina, atrial fibrillation, and cardiovascular death, and 70% increase in the risk of heart failure (hazard ratio 1.69, 99% confidence interval 1.38 to 2.06). Patients with the most active atopic eczema (active >50% of follow-up) were also at a greater risk of cardiovascular outcomes. Additional adjustment for cardiovascular risk factors as potential mediators partially attenuated the point estimates, though associations persisted for severe atopic eczema.


According to the authors, severe and predominantly active atopic eczema are associated with an increased risk of cardiovascular outcomes and that targeting cardiovascular disease prevention strategies among these patients should be considered.


Gut Microbiome Controls Antitumor Immune Function in the Liver


The microbiome is the collection of bacteria and other microorganisms that live in or on the body. In humans, the greatest proportion of the body’s total microbiome is in the gut. Despite extensive research into the relationship between the gut microbiome and cancer, the role of gut bacteria in the formation of liver cancer has remained poorly understood. According to an article published online in Science (24 May 2018), a connection has been found between bacteria in the gut and antitumor immune responses in the liver. The study showed that bacteria found in the gut of mice affect the liver’s antitumor immune function. The findings have implications for understanding the mechanisms that lead to liver cancer and for therapeutic approaches to treat them.


To investigate whether gut bacteria affect the development of tumors in the liver, the authors used three mouse models of liver cancer. Results showed that when the gut bacteria were depleted using an antibiotic “cocktail,“ the mice that had the antibiotics developed fewer and smaller liver tumors and had reduced metastasis to the liver. The authors then studied the immune cells in the liver to understand how the depletion of gut bacteria suppressed tumor growth in the liver of the antibiotic-treated mice. Results showed that antibiotic treatment increased the numbers of a type of immune cell called NKT cells in the livers of the mice. Further experiments showed that, in all three mouse models, the reduction in liver tumor growth that resulted from antibiotic treatment was dependent on these NKT cells. Next, it was found that the accumulation of the NKT cells in the liver resulted from an increase in the expression of a protein called CXCL16 on cells that line the inside of capillaries in the liver. The authors than asked why do mice treated with antibiotics have more CXCL16 production in these endothelial cells? The authors added that ended up being the critical point, when they found that bile acids can control the expression of CXCL16. They then did further studies, and found that if the mice were treated with bile acids, it can change the number of NKT cells in the liver, and thereby the number of tumors in the liver.


Finally, the investigators found that one bacterial species, Clostridium scindens, controls metabolism of bile acids in the mouse gut  — and ultimately CXCL16 expression, NKT cell accumulation, and tumor growth in the liver. The authors explained that while many studies have shown an association between gut bacteria and immune response, this study is significant in that it identifies not just a correlation, but a complete mechanism of how bacteria affect the immune response in liver. In the same study, the authors found that bile acids also control the expression of the CXCL16 protein in the liver of humans and wrote that, although these results are preliminary, the novel mechanism described in this study could potentially apply to cancer patients.


FDA Approves a New Treatment for PKU


Phenylketonuria (PKU) is rare and serious genetic disease that affects about 1 in 10,000 to 15,000 people in the United States. Patients with PKU are born with an inability to break down phenylalanine (Phe), an amino acid present in protein-containing foods and high-intensity sweeteners used in a variety of foods and beverages. If untreated, PKU can cause chronic intellectual, neurodevelopmental and psychiatric disabilities. Lifelong restriction of phenylalanine intake through the diet is needed to prevent buildup of Phe in the body, which can cause long-term damage to the central nervous system.


The FDA has approved Palynziq (pegvaliase-pqpz) for adults with PKU. Palynziq is a novel enzyme therapy for adult PKU patients who have uncontrolled blood Phe concentrations on current treatment. The safety and efficacy of Palynziq were studied in two clinical trials in adult patients with PKU with blood phenylalanine concentrations greater than 600 ?mol/L on existing management. Most PKU patients in the Palynziq trials were on an unrestricted diet prior to and during the trials. The first trial was a randomized, open-label trial in patients treated with increasing doses of Palynziq administered as a subcutaneous injection up to a target dose of either 20 mg once daily or 40 mg once daily. The second trial was an 8-week, placebo-controlled, randomized withdrawal trial in patients who were previously treated with Palynziq. Patients treated with Palynziq achieved statistically significant reductions in blood phenylalanine concentrations from their pre-treatment baseline blood Phe concentrations.


The most common adverse events reported in the Palynziq trials included injection site reactions, joint pain, hypersensitivity reactions, headache, generalized skin reactions lasting at least 14 days, pruritus (itchy skin), nausea, dizziness, abdominal pain, throat pain, fatigue, vomiting, cough and diarrhea. Hypersensitivity reactions occurred in most patients, likely due to formation of antibodies to the product. The most serious adverse reaction in the Palynziq trials was anaphylaxis, which occurred most frequently during upward titration of the dose within the first year of treatment. Because of this serious risk, the labeling for Palynziq includes a Boxed Warning and the product is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the Palynziq REMS Program. Notable requirements of the Palynziq REMS Program include the following:


1. Prescribers must be certified by enrolling in the REMS program and completing training

2. Prescribers must prescribe auto-injectable epinephrine with Palynziq

3. Pharmacies must be certified with the program and must dispense only to patients who are authorized to receive Palynziq

4. Patients must enroll in the program and be educated about the risk of anaphylaxis by a certified prescriber to ensure they understand the risks and benefits of treatment with Palynziq

5. Patients must have auto-injectable epinephrine available at all times while taking Palynziq


The FDA granted approval of Palynziq to BioMarin Pharmaceutical Inc.


Spring Asparagus Cheese Pie

Experimented with many times, this version of the asparagus pie has the onion/garlic mixture on the bottom. ©Joyce Hays, Target Health Inc.


This entree size slice of the asparagus cheese pie, has no onions in the bottom layer. ©Joyce Hays, Target Health Inc.


This entree slice does have a bottom layer of onions, garlic and mushrooms. ©Joyce Hays, Target Health Inc.


Here is a brunch slice of the asparagus cheese pie, with a smoked salmon layer. You can’t see the hot home brewed coffee made with freshly ground (French roasted) coffee beans. ©Joyce Hays, Target Health Inc.


Another brunch scene at our house. ©Joyce Hays, Target Health Inc.


Appetizer size: a delicious way to start any dinner. The garnish on this version, is crunshed Nori. ©Joyce Hays, Target Health Inc.



9 or 10 asparagus, washed, dried, stalks trimmed

1 cup ricotta

4 eggs

1/4 cup sour cream

1/4 cup plain Greek yogurt

1 onion, chopped

1 scallion, chopped (white part in recipe, green for garnish)

10 cloves garlic, sliced

1 anchovy fillet, well chopped (instead of salt)

1 jalapeno, seeds removed, chopped well

1 pinch black pepper

1 Tablespoon black mustard seeds

Zest of 1 fresh lemon

Juice of 1 fresh lemon

1 cup sharp cheddar, grate it at home

1 cup gruyere, grate it at home

1 cup buffalo mozzarella, shred or grate it at home




1. Do all cutting, slicing, chopping, grating

It’s a little extra work, but try to do all of your grated cheese at home. Although, it’s not found on each label, most store-bought cheese has a little something extra added to keep it fresher longer. ©Joyce Hays, Target Health Inc.


2. Preheat oven to 350 degrees.

3. Oil a pie baking dish

4. In a skillet, cook the onion, garlic, scallions, jalapeno, mustard seeds, anchovy mashed.

Just starting to cook the onions, garlic, scallions, mustard seeds, jalapeno. ©Joyce Hays, Target Health Inc.


5. In a small bowl, add the ricotta and beat eggs, one egg at a time, into the ricotta. Stir to combine well.

Beat in the eggs to the ricotta, one egg at a time. ©Joyce Hays, Target Health Inc.


6. In a skillet, cook the onion, garlic, scallions, jalapeno, mustard seeds, anchovy mixture, seasoning, lemon zest, lemon juice. Cook until garlic is golden.

7. In a large bowl, mix all cheeses, including the ricotta/eggs, yogurt and sour cream

Mixing all the cheeses with the ricotta & egg. ©Joyce Hays, Target Health Inc .


8. In the oiled baking dish, with a spatula, scrape everything out of the skillet and into the baking dish. Smooth this out.

9. Pour all of the cheese mixture, over the onion mixture.

Pouring the cheeses & eggs mixture over the onions & garlic. ©Joyce Hays, Target Health Inc.


10. Place all of the asparagus, in a circle, on top of the cheese mixture.

The final touch: Adding 10 fresh asparagus on top and in a circle. ©Joyce Hays, Target Health Inc.


11. Bake until cheese is golden and asparagus tender, 20 to 30 minutes.

Just out of the oven. You should allow this pie to cool down for about 15 to 30 minutes or the cheesy custard will not have time to set. ©Joyce Hays, Target Health Inc.


12. Remove from oven and let the pie cool down for15 to 30 minutes. When we tried to cut slices, too soon, the cheese mixture did not hold its shape. You need to wait for the cheese/egg mixture to solidify as it cools down.

One of many options: Serve with a garden salad and maybe fish, like salmon, or not. Maybe, fillet of sole sauteed with garlic butter and green grapes


We had the asparagus cheese pie as the centerpiece of dinner and also served fresh broccoli sauteed with extra virgin olive oil and garlic slices. ©Joyce Hays, Target Health Inc.


In addition to the broccoli we had a new recipe I’m experimenting with, stuffed mushrooms. Will share when ready. ©Joyce Hays, Target Health Inc.


This is a light and luscious entree. Not sure which is better, with or without the more savory bottom layer. ©Joyce Hays, Target Health Inc.


Simply delicious and so pretty for Springtime! ©Joyce Hays, Target Health Inc.


Louis Jadot produces a consistently delicious Pouilly-Fuisse, which we serve over and over again. If you’ve never tried it, go ahead. Perfect for Spring and Summer. ©Joyce Hays, Target Health Inc.


This weekend, we saw a beautifully acted, highly stimulating play, Dan Cody’s Yacht. It’s playing at the Manhattan Theater Club on West 55th Street, one of the theater clubs where Target Health is a Patron. We recommend this play because it is fine theater.


Have a great week everyone!

From Our Table to Yours

Bon Appetit!