2015 NORD Meeting


Last week, Target Health attended the NORD annual meeting, held in Crystal City, VA and participated on a Panel entitled “The Path to Progress – Rise in Orphan Drug Approvals and Breakthrough Designations.“ The Panel was chaired by Dr. Gayatri Rao, Director Office of Orphan Products Development and Panel members included, in addition to Dr. Jules Mitchel, President of Target Health, Dr. Peter Marks, Deputy Director, CBER; Dr. Jeff Allen, Executive Director, Friends of Cancer Research and Dr. Amit Sachdev, Executive Vice President, Policy, Access and Value, Vertex Pharmaceuticals.


The meeting was attended by over 400 participants with a major presence by patients, patient advocates and FDA and was inspirational.




Quality by Design (QbD) and Risk-based Monitoring Presentation at CBI Conference


On November 5-6, 2015, at Hilton Philadelphia City Avenue, Dr. Jules Mitchel, President of Target Health will be presenting a Case Study on Risk-Based Approaches to Clinical Trial Management. Here is a summary:


The best risk-based clinical monitoring plan starts with a well-designed protocol and if followed properly, assures patient safety and data quality. Monitoring of a trial includes risk-mitigation strategies with the understanding that not all risks have equal weight. The FDA wants to know if informed consent was obtained properly. Was the protocol followed? How was the protocol monitored? Were critical safety issues reported? Was the investigational product used as instructed? This case study will show: how risk-based trial management (and monitoring) begins with the protocol and underscores the definition of quality as the absence of errors that matter and are the data fit for purpose. The case study will also analyze metrics derived from actual studies ranging from small single center studies to studies as large as 1,000 subjects at 40 clinical sites. Dr. Mitchel will present results from a recent FDA inspection of a study using RBM where sites entered data in real time into EDC, with no paper records.


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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Parkinson’s Disease: The Nose Knows – (fill in the blanks)


Dr. Les Milne and his wife Joy


Smelling Parkinson’s disease before symptoms appear


A Scottish anesthesiologist, Les Milne, who worked long hours, began emitting a subtle musky 1) ___. His wife with a keen sense of smell, Joy Milne, assumed the smell was just sweat. But with the change in scent came a growing tiredness that was explained by a devastating diagnosis six years later, of Parkinson’s disease. When Joy Milne attended a meeting for the charity, Parkinson’s UK, attended by doctors and Parkinson’s patients, she noticed that the patients in the audience, shared her husband’s musky scent, and realized that the odor might be tied to the 2) ___. She mentioned this observation to a few scientists and they decided to investigate, on new skin odor tests to detect Parkinson’s disease (PD). As a result, Parkinson’s UK and the Manchester Institute of Biotechnology are investigating new 3) ___ odor tests to diagnose Parkinson’s disease earlier.


Researchers at the University of Edinburgh gave T-shirts to six people with Parkinson’s and six people without the disease. After the subjects wore the shirts, they were passed on to Joy Milne, who then had to determine by 4) ___ whether each wearer had Parkinson’s. Her diagnoses were eerily accurate – and have potentially groundbreaking implications for people living with 5) ___ disease (PD). Milne made correct assessments for 11 out of the 12 cases. In the one case she got “wrong,“ she insisted that a T-shirt worn by a member of the control group had the warning scent. Eight months after the study was conducted, she was proven right, bringing her accuracy rate up to one hundred. The supposedly healthy individual contacted one of the doctors and informed him that he had, in fact, just been diagnosed with Parkinson’s.


“That really impressed us,“ said, Edinburgh University scientist Tilo Kunath, “We had to dig further into this phenomenon.“ Intrigued by Joy Milne’s abilities as a “super-smeller,“ scientists at the universities of Manchester, Edinburgh and London are undertaking a project to identify differences in the skin 6) ___ of people with Parkinson’s, study sponsor Parkinson’s UK announced this week. Scientists believe that people with early Parkinson’s, experience skin changes that produce a particular odor. If they find the molecular signature responsible for the smell, it may be possible to develop a diagnostic test for Parkinson’s as simple as swabbing a person’s forehead. As our understanding of it stands now, the disease is incredibly difficult to diagnose. Doctors still rely on an observational technique developed in the early 1800s. There is currently no cure for Parkinson’s, a degenerative disorder of the central 7) ___ system which causes shaking, slowness of movement and difficult walking as well as behavioral problems like dementia and depression.


Arthur Roach, the director of research at Parkinson’s UK, said in a BBC announcement this week, that in addition to having a “huge impact“ on diagnostic procedures, “The research would also make it a lot easier to identify people with the disease and to test drugs that may have the potential to slow, or even stop Parkinson’s, something no current 8) ___ can achieve.“ Source: The Washington Post, October 2015, by Yanan Wang 


Click to watch this short video


ANSWERS: 1) odor; 2) disease; 3) skin; 4) smell; 5) Parkinson’s; 6) chemicals; 7) nervous; 8) drug


James Parkinson MD (1755-1824)


Illustration of Parkinson’s disease by William Richard Gowers, which was first published in A Manual of Diseases of the Nervous System (1886)


Several early sources, including an Egyptian papyrus, an Ayurvedic medical treatise, the Bible, and Galen’s writings, describe symptoms resembling those of Parkinson’s disease (PD). After Galen there are no references unambiguously related to PD until the 17th century. In the 17th and 18th centuries, several authors wrote about elements of the disease, including Sylvius, Gaubius, Hunter and Chomel.


In 1817 an English doctor, James Parkinson, published his essay reporting six cases of paralysis agitans. An Essay on the Shaking Palsy described the characteristic resting tremor, abnormal posture and gait, paralysis and diminished muscle strength, and the way that the disease progresses over time. Early neurologists who made further additions to the knowledge of the disease include Trousseau, Gowers, Kinnier, Wilson and Erb, and most notably Jean-Martin Charcot, whose studies between 1868 and 1881 were a landmark in the understanding of the disease. Among other advances, he made the distinction between rigidity, weakness and bradykinesia. He also championed the renaming of the disease in honor of James Parkinson.


In 1912 Frederic Lewy described microscopic particles in affected brains, later named “Lewy bodies“. In 1919 Konstantin Tretiakoff reported that the substantia nigra was the main cerebral structure affected, but this finding was not widely accepted until it was confirmed by further studies published by Rolf Hassler in 1938. The underlying biochemical changes in the brain were identified in the 1950s, due largely to the work of Arvid Carlsson on the neurotransmitter dopamine and Oleh Hornykiewicz on its role on PD. In 1997, alpha-synuclein was found to be the main component of Lewy bodies by Spillantini, Trojanowski, Goedert and others.


Anticholinergics and surgery (lesioning of the corticospinal pathway or some of the basal ganglia structures) were the only treatments until the arrival of levodopa, which reduced their use dramatically. Levodopa was first synthesized in 1911 by Casimir Funk, but it received little attention until the mid-20th century. It entered clinical practice in 1967 and brought about a revolution in the management of PD. By the late 1980s deep brain stimulation introduced by Alim-Louis Benabid and colleagues at Grenoble, France, emerged as a possible treatment.


James Parkinson FGS (11 April 1755 – 21 December 1824) was an English surgeon, apothecary, geologist, paleontologist, and political activist. He is most famous for his 1817 work, An Essay on the Shaking Palsy in which he was the first to describe “paralysis agitans“, a condition that would later be renamed Parkinson’s disease by Jean-Martin Charcot. James Parkinson was born in Shoreditch, London, England. He was the son of John Parkinson, an apothecary and surgeon practicing in Hoxton Square in London. He was the oldest of three siblings, which included his brother William and his sister Mary Sedgewood. In 1784 Parkinson was approved by the City of London Corporation as a surgeon. On 21 May 1783, he married Mary Dale, with whom he subsequently had eight children; two did not survive past childhood. Soon after he was married, Parkinson succeeded his father in his practice in 1 Hoxton Square. He believed that any worthwhile surgeon should know shorthand, at which he was adept. In addition to his flourishing medical practice, Parkinson had an avid interest in geology and paleontology, as well as the politics of the day. Parkinson was a strong advocate for the under-privileged, and an outspoken critic of the Pitt-government. His early career was marred by his being involved in a variety of social and revolutionary causes, and some historians think it most likely that he was a strong proponent for the French Revolution. He published nearly twenty political pamphlets in the post-French Revolution period, while Britain was in political chaos. Writing under his own name and his pseudonym “Old Hubert“, he called for radical social reforms and universal suffrage.


Parkinson called for representation of the people in the House of Commons, the institution of annual parliaments, and universal suffrage. He was a member of several secret political societies, including the London Corresponding Society and the Society of Constitutional Information. In 1794 his membership in the organization led to his being examined under oath before William Pitt and the Privy Council to give evidence about a trumped-up plot to assassinate King George III. He refused to testify regarding his part in the popgun plot, until he was certain he would not be forced to incriminate himself. The plan was to use a poisoned dart fired from a pop-gun to bring the king’s reign to a premature conclusion. No charges were ever brought against Parkinson but several of his friends languished in prison for many months before being acquitted.




First page of Parkinson’s classical essay on shaking palsy


Parkinson turned away from his tumultuous political career, and between 1799 and 1807 published several medical works, including a work on gout in 1805. He was also responsible for early writings on ruptured appendix in English medical literature. Parkinson was also interested in improving the general health and well-being of the population. He wrote several medical doctrines that exposed a similar zeal for the health and welfare of the people that was expressed by his political activism. He was a crusader for legal protection for the mentally ill, as well as their doctors and families. In 1812 Parkinson assisted his son with the first described case of appendicitis in English, and the first instance in which perforation was shown to be the cause of death. Parkinson was the first person to systematically describe six individuals with symptoms of the disease that bears his name. In his “An Essay on the Shaking Palsy“, he reported on three of his own patients and three persons who he saw in the street. He referred to the disease that would later bear his name as paralysis agitans, or shaking palsy. He distinguished between resting tremors and the tremors with motion. Jean-Martin Charcot coined the term “Parkinson’s disease“ some 60 years later. Parkinson erroneously predicted that the tremors in these patients were due to lesions in the cervical spinal cord.




Fossilized turtle, puppigerus, found in the London Clay on the Isle of Sheppey and named for Parkinson, in a collection at Teylers Museum


Parkinson’s interest gradually turned from medicine to nature, specifically the relatively new field of geology, and paleontology. He began collecting specimens and drawings of fossils in the latter part of the eighteenth century. He took his children and friends on excursions to collect and observe fossil plants and animals. His attempts to learn more about fossil identification and interpretation were frustrated by a lack of available literature in English, and so he took the decision to improve matters by writing his own introduction to the study of fossils. In 1804, the first volume of his Organic Remains of a Former World was published. Gideon Mantell praised it as “the first attempt to give a familiar and scientific account of fossils“. A second volume was published in 1808, and a third in 1811. Parkinson illustrated each volume and his daughter Emma colored some of the plates. The plates were later re-used by Gideon Mantell. In 1822 Parkinson published the shorter “Elements of Oryctology: an Introduction to the Study of Fossil Organic Remains, especially of those found in British Strata“. Parkinson also contributed several papers to William Nicholson’s “A Journal of Natural Philosophy, Chemistry and the Arts“, and in the first, second, and fifth volumes of the “Geological Society’s Transactions“. He wrote a single volume ‘Outlines of Orytology’ in 1822, a more popularized work.


On 13 November 1807, Parkinson and other distinguished gentlemen met at the Freemasons’ Tavern in London. The gathering included such great names as Sir Humphry Davy, Arthur Aikin and George Bellas Greenough. This was to be the first meeting of the Geological Society of London. Parkinson belonged to a school of thought, Catastrophism, that concerned itself with the belief that the Earth’s geology and biosphere were shaped by recent large-scale cataclysms. He cited the Noachian deluge of Genesis as an example, and he firmly believed that creation and extinction were processes guided by the hand of God. His view on Creation was that each ‘day’ was actually a much longer period that lasted perhaps tens of thousands of years in length.


Parkinson died on 21 December 1824 after a stroke that interfered with his speech, bequeathing his houses in Langthorne to his sons and wife and his apothecary’s shop to his son, John. His collection of organic remains was given to his wife and much of it went on to be sold in 1827, a catalogue of the sale has never been found. He was buried at St. Leonard’s Church, Shoreditch. Parkinson’s life is commemorated with a stone tablet inside the church of St Leonard’s, Shoreditch, where he was a member of the congregation; the exact site of his grave is not known and his body may lie in the crypt or in the churchyard. In addition, a blue plaque at 1 Hoxton Square, marks the site of his home. Several fossils were also named after him. There is no known portrait of him: a photograph, sometimes published and identified as Dr. James Parkinson, is of a dentist of the same name. The better known, James Parkinson died before photography was invented. World Parkinson’s Dayis held each year on his birthday, 11 April.




A photograph of Jean-Martin Charcot, who made important contributions to the understanding of the disease and proposed its current name honoring James Parkinson.

Nuclear Transport Problems Linked to ALS and FTD


DNA is made up of building blocks called nucleotides. In the mutated C9orf72 gene, a sequence of six nucleotides is repeated many times more than are typical. These repetitive stretches of DNA produce RNA molecules that can interfere with proteins in the cell. The RNA also generates toxic proteins called dipeptide repeat proteins. However, until now, it was unknown what specific cellular systems were impaired by these two products of the mutation.


Both amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) are caused by the death of specific neurons. In ALS, this leads to movement difficulties and eventually paralysis, while in FTD, patients experience problems with language and decision making. Past research has connected a specific mutation in the C9orf72 gene to 40% of inherited ALS cases and 25% of inherited FTD cases, as well as nearly 10% of non-inherited cases of each disorder. Recent experiments, conducted in yeast, fruit flies, and neurons from patients, found that the mutation prevents proteins and RNA from moving between the nucleus and the cytoplasm that surrounds it.


According to an article published in Nature (25 August 2015), 3 teams of scientists supported by the National Institutes of Health showed that a genetic mutation in the C9orf72 gene may destroy neurons by disrupting the movement of materials in and out of the cell’s nucleus. The results, provide a possible strategy for treating the two diseases. Evidence that the mutation impairs nuclear transport in neurons was derived from skin cells grown from patients. One team showed that these neurons have much more RNA in the nucleus compared to those created from healthy control cells, implying that the mutation prevents RNA from leaving the nucleus. The other two groups discovered that the patient-derived neurons had trouble bringing certain proteins into the nucleus as well. One group of investigators focused on how the abnormal RNA produced by the C9orf72 mutation affects a protein called RanGAP, which is essential for transporting materials into the nucleus. Building on previous work, the group confirmed that the RNA strands bind to RanGAP in brain tissue from patients with the mutation and stop the protein from performing its function. The team then treated those cells with compounds that prevented this interference and found that this eliminated the transport defect, allowing proteins to get inside the nucleus. Similarly, increasing production of RanGAP in fruit flies reduced neuronal deterioration and motor problems caused by the mutation.


In addition to the work with the lab-grown neurons, one team explored the mutation’s effects by inserting eight, 28, or 58 copies of the repetitive DNA sequence into fruit fly neurons. By doing this it was found that additional copies caused more harm to the cells. The group then performed a genetic “screen“ in which they systematically mutated other fly genes to find ones that increased or decreased this damage. Many of the genes they found code for nuclear transport proteins, which regulate the movement of molecules in and out of the nucleus. The authors noted that they were amazed to find 18 genes that relate to nucleocytoplasmic trafficking, and that this indicated that they were on to something very important.


Taken together, the three studies suggest that therapies designed to increase nucleocytoplasmic transport may be effective for treating some forms of ALS and FTD.


PINK1 Protein Crucial for Removing Damaged Mitochondria


Cells are powered by tiny energy reactors called mitochondria. When damaged, they leak destructive molecules that can cause substantial harm and eventually kill brain cells. According to an article published in Nature (12 August 2015), it was shown that a protein called PINK1, that is implicated in Parkinson’s disease, is critical for helping cells get rid of dysfunctional mitochondria. According to the new research, PINK1 does this by triggering an intricate process called mitophagy that breaks down and removes damaged mitochondria from the cell.


Mutations in PINK1 and its partner molecule Parkin cause hereditary forms of Parkinson’s disease (PD). Moreover, the inability to remove defective mitochondria from nerve cells has been linked to numerous neurodegenerative diseases, including the more common forms of PD and amyotrophic lateral sclerosis (ALS). It was previously considered that Parkin was essential to destroy damaged mitochondria, but the new research discovered that PINK1 can initiate this process without Parkin.


Study results showed that PINK1 recruits two proteins called Optineurin and NDP52 to the surface of mitochondria. These proteins, in turn, recruit a variety of other protein molecules that mark the mitochondria for degradation. Optineurin and NDP52 are members of a group of proteins called autophagy receptors. When cells were created that contained no autophagy receptors, it was found that the cells could not dispose of malfunctioning mitochondria. However, when the function of either Optineurin or NDP52 was restored, the cells regained this ability. Reinstating other autophagy receptors had little or no effect.


According to the authors, knowing that Optineurin and NDP52 are the primary autophagy receptors involved in this process can inform about the cause of different human diseases. For example, Optineurin is mutated in ALS and also in certain forms of glaucoma, whereas NDP52 is known to be mutated in Crohn’s disease. This suggests that problems with mitophagy may be involved in those diseases.


When PINK1 accumulates on the surface of defective mitochondria, it alters a molecule called ubiquitin. The modified ubiquitin then recruits autophagy receptors as well as Parkin. Parkin promotes mitophagy by bringing more ubiquitin to the mitochondria to form long chains that flag damaged mitochondria for removal. Since PINK1 is needed to start building these ubiquitin chains, the current observations suggest a new avenue for creating drugs that treat disease by boosting the disposal of damaged mitochondria.


A number of companies are trying to develop drugs to activate this pathway and some are trying to find drugs that activate Parkin. However, this new model might suggest a different strategy where it may not be so important to activate Parkin, but more important to activate PINK1.”


FDA Approves Drug for Perinatal, Infantile and Juvenile-Onset Hypophosphatasia (HPP)


Perinatal, infantile and juvenile-onset hypophosphatasia (HPP) is a rare, genetic, progressive, metabolic disease in which patients experience devastating effects on multiple systems of the body, leading to severe disability and life-threatening complications. It is characterized by defective bone mineralization that can lead to rickets and softening of the bones that result in skeletal abnormalities. It can also cause complications such as profound muscle weakness with loss of mobility, seizures, pain, respiratory failure and premature death. Severe forms of HPP affect an estimated one in 100,000 newborns, but milder cases, such as those that appear in childhood or adulthood, may occur more frequently.


The FDA this past week approved Strensiq (asfotase alfa) as the first approved treatment for perinatal, infantile and juvenile-onset HPP. According to FDA, for the first time, the HPP community will have access to an approved therapy for this rare disease. Strensiq’s approval is an example of how the Breakthrough Therapy Designation program can bring new and needed treatments to people with rare diseases. Strensiq received a breakthrough therapy designation as it is the first and only treatment for perinatal, infantile and juvenile-onset HPP. The Breakthrough Therapy Designation program encourages the FDA to work collaboratively with sponsors, by providing timely advice and interactive communications, to help expedite the development and review of important new drugs for serious or life-threatening conditions. In addition to designation as a breakthrough therapy, the FDA granted Strensiq orphan drug designation because it treats a disease affecting fewer than 200,000 patients in the United States. Orphan drug designation provides financial incentives, like clinical trial tax credits, user fee waivers, and eligibility for market exclusivity to promote rare disease drug development. Strensiq was also granted priority review, which is granted to drug applications that show a significant improvement in safety or effectiveness in the treatment of a serious condition. In addition, the manufacturer of Strensiq was granted a rare pediatric disease priority review voucher – a provision intended to encourage development of new drugs and biologics for the prevention and treatment of rare pediatric diseases. Development of this drug was also in part supported by the FDA Orphan Products Grants Program, which provides grants for clinical studies on safety and/or effectiveness of products for use in rare diseases or conditions.


Strensiq is administered via injection three or six times per week and works by replacing the enzyme (known as tissue-nonspecific alkaline phosphatase) responsible for formation of an essential mineral in normal bone, which has been shown to improve patient outcomes. The safety and efficacy of Strensiq were established in 99 patients with perinatal (disease occurs in utero and is evident at birth), infantile- or juvenile-onset HPP who received treatment for up to 6.5 years during four prospective, open-label studies. Study results showed that patients with perinatal- and infantile-onset HPP treated with Strensiq had improved overall survival and survival without the need for a ventilator (ventilator-free survival). 97% of treated patients were alive at one year of age compared to 42% of control patients selected from a natural history study group. Similarly, the ventilator-free survival rate at one year of age was 85% for treated patients compared to less than 50% for the natural history control patients.


In the clinical trial, patients with juvenile-onset HPP treated with Strensiq showed improvements in growth and bone health compared to control patients selected from a natural history database. All treated patients had improvement in low weight or short stature or maintained normal height and weight. In comparison, approximately 20% of control patients had growth delays over time, with shifts in height or weight from the normal range for children their age to heights and weights well below normal for age. Juvenile-onset patients also showed improvements in bone mineralization, as measured on a scale that evaluates the severity of rickets and other HPP-related skeletal abnormalities based on x-ray images. All treated patients demonstrated substantial healing of rickets on x-rays while some natural history control patients showed increasing signs of rickets over time. The most common side effects in patients treated with Strensiq include injection site reactions, hypersensitivity reactions (such as difficulty breathing, nausea, dizziness and fever), lipodystrophy (a loss of fat tissue resulting in an indentation in the skin or a thickening of fat tissue resulting in a lump under the skin) at the injection site, and ectopic calcifications of the eyes and kidney.


Strensiq is manufactured by Alexion Pharmaceuticals Inc., based in Cheshire, Connecticut


Autumn Souffle


A delicious medley of flavors, just in time for Halloween or Thanksgiving dinner.  The item in the background is a piece of cauliflower cake with black sesame seeds that I’m experimenting with and will share when ready.  ©Joyce Hays, Target Health Inc.



Just out of the oven and onto the table.  Smells wonderful! ©Joyce Hays, Target Health Inc.




1 pound carrots, scrubbed but not peeled

1 sweet potato, scrubbed

1 butternut squash

1 teaspoon turmeric

1 teaspoon cumin

1 teaspoon coriander

1/2 teaspoon ginger, freshly grated

2 Tablespoons canola oil

3 Tablespoons Tofutti

3 Tablespoons sour cream

3 eggs

1 Tablespoon honey

2 Tablespoons agave

1/2 can water chestnuts, removed from can and drained on paper towel

3 Tablespoons almond flour

1 teaspoon baking powder

1 teaspoon vanilla

pinch salt (optional)

1 onion, chopped

3 garlic cloves, sliced not squeezed

1 cup golden raisins

1 Tablespoon Marsala wine

1 cup almond slivers, toasted and set aside (save ? cup for garnish)

Pinch chili flakes

Pinch black pepper




Make sure you have everything, by putting all ingredients in one spot. ©Joyce Hays, Target Health Inc.




Preheat oven to 350 degrees

Scrub then peel the carrots, sweet potato and butternut squash first. Next cut into large pieces and roast in oven until soft. Remove and let them cool down.





Roasting the veggies. ©Joyce Hays, Target Health Inc.



It was easier for me to get this aluminum container out, than dig for the baking sheet, so am toasting the almond slivers, here. No oil here. Using an oven mitt, I will take this out in 4-5 minutes and just shake it, to move the almonds around for a more even toasting. ©Joyce Hays, Target Health Inc.



Toast the almond slivers on a flat baking sheet, while roasting the veggies. After 4 minutes, stir them around just to get them evenly toasted. But keep your eye on the almonds. They will be done in about 6 to 10 minutes. You don’t want to burn them, or you’ll have to do another batch of almonds.




Chopping the onion & garlic. ©Joyce Hays, Target Health Inc.



Cooking the onion & garlic. ©Joyce Hays, Target Health Inc.


While veggies are roasting, add 1 Tablespoon of the canola oil to a pan and on a low flame, cook the onion and garlic until they get a little soft and transparent. Remove pan from heat.




About to start up the food processor. ©Joyce Hays, Target Health Inc.



So far, so good. ©Joyce Hays, Target Health Inc.



In food processor, slowly blend: first the eggs, canola oil, Tofutti, sour cream, honey, agave, almond flour, baking powder, and vanilla.




Here, we’re pulsing the orange veggies and some water chestnuts. ©Joyce Hays, Target Health Inc.



As your food processor fills up, scrape the processed ingredients, out into a large bowl




Container on top has the water chestnuts, draining, and about to be added to the food processor. The water chestnuts add a nice crunch to a recipe. As for the golden raisins and almond slivers, (which have just been toasted in the oven). Don’t add them to the food processor yet, And don’t pulse them, whatever you do. Stir them in by hand, after everything has been “pulsed.“ ©Joyce Hays, Target Health Inc.



Next, add to the food processor, the water chestnuts, Marsala, onions and garlic, the carrots, sweet potato, butternut squash and all of the spices and the ginger, while you slowly pulse the food processor. Keep pulsing until the 3 orange veggies are not quite a puree (you want to have some texture in the souffle). Before you remove the mixture, add the golden raisins and 1/2 of the toasted almond slivers and stir in, by hand. Don’t pulse these last ingredients.




This is everything scraped out of the food processor. Now, the toasted almonds and golden raisins are being stirred in, by hand. ©Joyce Hays



Re-set oven temperature down to 300 degrees.


Brush some canola oil onto a baking dish and then with a spatula, scrape all of the contents of the blender, into the baking dish.




Here, the contents of the bowl have been scraped into this oiled baking dish. About to go into the oven. ©Joyce Hays, Target Health Inc.



Just out of the oven and about to sprinkle toasted almonds on top. ©Joyce Hays, Target Health Inc.



Here’s an earlier experiment with toasted pistachios on top (also good). ©Joyce Hays, Target Health Inc.



Bake at 300 degrees for 45 minutes, or until just firm. When you insert something sharp, (long skewer) and it comes out clean, the dish is done. It’s nice to have baking dishes that can go from the oven, to table, to fridge.

Time the baking so you can serve the orange veggie souffle, when it comes, right out of the oven.

When you remove from oven, sprinkle the remaining 1/2 cup of toasted almond slivers over the top of the dish and serve.




Hall is a very well-known vineyard in Napa Valley. We like their reds much better than the whites but, hey, we drank this whole bottle, with no effort. J


He wanted red and I wanted white. His Chateauneuf du Pape was v-err-y robust with a long warm finish. But I felt like my favorite sauvignon blanc, Aveta, from Stag’s Leap Wine Cellars, floral nose, strong statement on palate and soothing finish.


We had a wonderful weekend. So much fun at a play called, Ripcord, with a talkback afterwards.

Manhattan Theatre Club, (where Target Health Inc. is a corporate patron), presents its sixth collaboration with playwright David Lindsay-Abaire, in 2015.Ripcord, the Pulitzer Prize winner’s latest work is a comedy revolving around a viscous battle of wits between two elderly women in a care home. In the lead roles of Abby and Marilyn are Emmy winner Holland Taylor (The Practice, Two and a Half Men) and Drama Desk Award winner Marylouise Burke (Fuddy Meers), while Frasier alumni David Hyde Pierce directs.


The playwright, David Lindsay-Abaire is a writer who excels in a dizzying variety of genres and forms, Lindsay-Abaire first came to the world’s attention with his 2007 play Rabbit Hole. An honest and surprisingly comic tale of grieving parents, it won its author the Pulitzer Prize for Drama. Since then, he’s produced numerous comedic and dramatic works as well as the book for Shrek The Musical. This range also stretches to his work in Hollywood, having adapted Rabbit Hole for the screen with Nicole Kidman in the lead role, but also written the screenplay for the children’s animated feature Rise of the Guardians.

Especially suited for people 49 and over, Ripcord will amuse you, startle you and even make you cry. The acting is first rate and so are the sets, sound and lighting design, not to mention fine directing. Go if you can! It’s about 2 and ? hours long.


Sunday we stuck to our exercise routine (sometimes it takes discipline) and I beat Jules in Scrabble which always makes me feel good. (He won last weekend, however.)


Hope your weekend was a good one!


From Our Table to Yours!


Bon Appetit!