Growth at Target Health – Expanding to New Jersey
Target Health Inc., established in 1993, is expanding to New Jersey. Our software programming department, headed by Senior Director, Joonhyuk Choi, will be located near the Meadowlands, not far from New York City. Our executive offices and clinical, data management, statistics and business development departments will remain on the 23 and 24th floors at 261 Madison Avenue.
Abstract Expressionist and Master Nature Photographer
Our friend and colleague, James Farley, Clinical Data Manager at TransTech Pharma LLC and subscriber to ON TARGET newsletter, is sharing another great photo, this time a gorgeous view of the pier – just after Sunset – at Holden Beach, NC.
Sunset at Holden Beach, NC, 2015 ©JFarleyPhotography.com
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
Scientists Reprogram Fat Cells to Increase Fat Burning
Scientists have now discovered how fat cells can be reprogrammed to burn fat instead of storing it. By analyzing molecular processes, scientists have described for the first time how white fat cells are converted into brown fat cells.
Cells responsible for storing 1) ___ can be converted into cells that burn fat and keep you thinner and healthier. Scientists have now discovered how this conversion happens. We’ve mapped the fat cells’ genomes and identified a protein which activates specific 2) ___ that reprogram the fat cells to burn fat instead of storing it, says Professor S. Mandrup from the department of biochemistry and molecular biology at the University of Southern Denmark (SDU). The study’s findings, recently published the January 2015 journal, Genes & Development, are a crucial step on the way to developing 3) ___ that can make the body transform fat into energy instead of storing it.
Our body contains three different types of fat cells: White cells, which store fat derived from food so that you put on weight if you eat too much; 4) ___ fat cells, which convert fat into energy instead of storing it; Brite fat cells are beige/brownish in color (brite is short for brown-in-white). Like brown cells they convert fat into heat. Scientists have long been interested in brite fat cells because it has been shown that white fat cells can be browned and turned into brite so that they burn fat instead of storing it. Studies show that overweight people have a lot of white cells in their fatty 5) ___. We’ve known for a long time that exposure to the cold, for example, can cause the body to produce more brite fat cells which produce heat, although we have not known much about which molecular mechanisms are at play.
Anti-Diabetic Medication Browns Cells
In order better to understand how fat-storing white cells can become fat-burning brite cells, scientists at SDU have grown white cells in the laboratory and added a medication previously used to increase the insulin sensitivity of 6) ___ patients. The medication known as rosiglitazone (Avandia) makes the fat cells turn brown thus making them brite — but exactly what effect the drug has on the cells at the molecular level has been unclear until now. To study this, the scientists used advanced gene sequencing technology to map and analyze the genome of both the white and brite cells in order to find out which genes are active when the 7) ___ cells turn brite.
A Specific Protein Activates Genes
Their analyses did not only show where in the fat cells’ genome there is activity when white cells are converted to brite cells, but also that a specific 8) ___, known as KLF11, has to be present for the cells to be reprogrammed to burn fat instead of storing it. It’s clear that KLF11 finds the genes in the cells which are active when white fat cells are being converted into brite cells. KLF11 is already known as a protein important to the functionality of insulin-producing beta-cells in the pancreas, but with our study we have demonstrated, for the first time that the protein is also necessary for white fat cells to be reprogrammed to brite fat cells.
White fat cells have been known about for many years, but it was not until 2009 that scientists discovered that adult human beings also have so-called brown fat tissue. The fatty tissue is referred to as brown because of its reddish-brown color when viewed through a microscope. The brown color occurs because the cells contain many mitochondria and 9) ___ vessels. Over the past decade it was also discovered that humans have brite fat cells. Brite fat cells burn fat just like the brown ones. In other words: the more brite and brown fat cells you have the more 10) ___ you burn. Unlike the entirely brown fat cells, brite cells are produced from already-existing white fat tissue of the kind we have most of in our body. Scientists still have a lot to learn about brite fat cells. They do not know, for instance, whether we can cause more brite fat cells to be produced, e.g. by eating specific foods. It is not known, either, whether brite cells can only be produced by converting white cells, or whether the body can produce its own new brite fat cells. In the long term, it will be possible to use the discovery to develop new medication which can impact on precisely those areas in the fat cells’ genome. This will make it possible to prevent overweight people from developing insulin intolerance and diabetes or other diseases related to 11) ___. We know more about which buttons we have to push to increase specific processes in the cells which activate the browning process. KLF11 is just one of the factors that determines which genes are active, researchers are certain there are many others.
Jacob B. Hansen, an associate professor at the Department of Biology of the University of Copenhagen, who studies brown fat cells, says that the new results represent an important step towards understanding how fat cell conversion takes place in humans. The molecular understanding of how brite is produced and much of what we do know comes from experiments on mice, however, this study is entirely based on 12) ___ cell material. Experiments on mice have shown that KFL11 can regulate parts of the biology of brown fat cells, but in this study, the scientists used advanced methods which enabled them to characterize the browning process in great detail. This was much more elegant than the work previously done on mice because they’ve observed all the genes in one go and found the areas in the genome of the cells which KLF11 binds to. Pills against obesity are closer to reality. The result certainly is a step in the direction of a cure which e.g. can reduce the risk of people developing type 2 diabetes and countering other health issues related to being overweight. The potential is interesting, because the better we understand the biology of fat cells, the closer we’ll get to being able to design medication which can cause the body to produce more beige and brown fat cells, which experiments on mice have shown effective to improve glucose tolerance. But this doesn’t mean that in five years will have a magic pill against obesity, Hansen says. The work done at SDU is basic science, which improves our knowledge of the process known as browning, but a lot more research will have to be done before we fully understand the process and its significance. The genome of white adipocytes, has been investigated and is reprogrammed during browning using advanced genome sequencing technologies. Browning has been stimulated in human white adipocytes by a drug used to treat type II diabetes and compared to white and brite fat cells. This comparison showed that 13) ___ fat cells have distinct gene programs which, when active, make these cells particularly energy-consuming. By identifying the areas of the genome that are directly involved in the reprogramming, an important factor has been identified in the process — the gene regulatory protein KLF11 (Kruppel Like Factor-11), which is found in all fat cells, is required for the reprogramming to take place. This research has been a long process, taking four years to get the results being published. The discovery of the brite fat cell mechanisms and the specific regulatory areas brings scientists closer to understanding how reprogramming of white fat cells takes place. This knowledge potentially means, that in the future drugs can be 14) ___to activate the genomic regions and browning factors like KLF11 in the treatment of obesity.
ANSWERS: 1) fat; 2) genes; 3) drugs; 4) brown; 5) tissue; 6) diabetes; 7) white; 8) protein; 9) blood; 10) energy; 11) obesity; 12) human; 13) brite; 14) targeted
The Ob(Lep) Gene and Weight Loss
Structure of the obese protein leptin-E100
The Ob(Lep) gene (Ob for obese, Lep for leptin) is located on chromosome 7 in humans. Human leptin is a 16 kDa protein of 167 amino acids. Leptin should not to be confused with Lectin or Lecithin.
Leptin (from Greek meaning thin), the satiety hormone, is a hormone made by fat cells which regulates the amount of fat stored in the body. It does this by adjusting both the sensation of hunger, and adjusting energy expenditures. Hunger is inhibited (satiety) when the amount of fat stored reaches a certain level. Leptin is then secreted and circulates through the body, eventually activating leptin receptors in the arcuate nucleus of the hypothalamus. Energy expenditure is increased both by the signal to the brain, and directly via leptin receptors on peripheral targets. The effect of leptin is opposite to that of ghrelin, the hunger hormone. Ghrelin receptors are on the same brain cells as leptin receptors, so these cells receive competing satiety and hunger signals. Leptin and ghrelin, along with many other hormones, participate in the complex process of energy homeostasis. Although regulation of fat stores is deemed to be the primary function of leptin, it also plays a role in other physiological processes, as evidenced by its multiple sites of synthesis other than fat cells, and the multiple cell types beside hypothalamic cells which have leptin receptors. Many of these additional functions are yet to be defined.
Leptin was approved in the United States in 2014 for use in congenital leptin deficiency and generalized lipodystrophy.
An analog of human leptin metreleptin (trade name Myalept) was first approved in Japan in 2013, and in the United States (US) in February 2014. In the US it is indicated as a treatment for complications of leptin deficiency, and for the diabetes and hypertriglyceridemia associated with congenital or acquired generalized lipodystrophy. Leptin is known to interact with amylin, a hormone involved in gastric emptying and creating a feeling of fullness. When both leptin and amylin were given to obese, leptin-resistant rats, sustained weight loss was seen. Due to its apparent ability to reverse leptin resistance, amylin has been suggested as possible therapy for obesity.
Historically, the existence of a hormone regulating hunger and energy expenditure was hypothesized based on studies of mutant obese mice that arose at random within a mouse colony at the Jackson Laboratory in 1950. Mice homozygous for the ob mutation (ob/ob) ate voraciously and were massively obese. In the 1960s, a second mutation causing obesity and a similar phenotype was identified by Douglas Coleman, also at the Jackson Laboratory, and was named diabetes (db), as both ob/ob and db/db were obese. Rudolph Leibel and Jeffrey M. Friedman reported the mapping of the ob gene in 1990. Consistent with Coleman’s and Leibel’s hypothesis, several subsequent studies from Leibel’s and Friedman’s labs and other groups confirmed that the ob gene encoded a novel hormone that circulated in blood and that could suppress food intake and body weight in ob and wild type mice, but not in db mice.
In 1994, with the ob gene isolated, Friedman reported the discovery of the gene. In 1995, Caro’s laboratory provided evidence that the mutations present in the mouse ob gene did not occur in humans. Furthermore the ob gene expression was increased in human obesity, which led to postulate the concept of leptin resistance. At the suggestion of Roger Guillemin, Friedman named this new hormone leptin from the Greek lepto meaning thin. Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encodes the leptin receptor and that it is expressed in the hypothalamus, a region of the brain known to regulate the sensation of hunger and body weight.
Coleman and Friedman have been awarded numerous prizes acknowledging their roles in discovery of leptin, including the Gairdner Foundation International Award(2005), the Shaw Prize (2009), the Lasker Award, the BBVA Prize and the King Faisal International Prize. The discovery of leptin has been documented in a series of books including Fat: Fighting the Obesity Epidemic by Robert Pool, The Hungry Gene by Ellen Ruppel Shell, and Rethinking Thin: The New Science of Weight Loss and the Myths and Realities of Dieting by Gina Kolata.Fat: Fighting the Obesity Epidemic and Rethinking Thin: The New Science of Weight Loss and the Myths and Realities of Dieting review the work in the Friedman laboratory that led to the cloning of the ob gene.
A mutant leptin was first described in 1997, and subsequently six additional mutations were described. All of those affected were from Eastern countries; and all had variants of leptin not detected by the standard immunoreactive technique. The most recently described eighth mutant reported in January2015 is unique in that it is detected by the standard immunoreactive technique, indicating that leptin levels are elevated but the leptin is nonfunctional. These eight mutations all cause extreme obesity in infancy, with hyperphagia. Leptin is produced primarily in the adipocytes of white adipose tissue. It is also produced by brown adipose tissue, placenta (syncytiotrophoblasts), ovaries, skeletal muscle, stomach (the lower part of the fundic glands), mammary epithelial cells, bone marrow, pituitary, liver, gastric chief cells and P/D1 cells. Leptin circulates in blood in free form, bound to proteins and leptin levels vary exponentially, not linearly, with fat mass. Leptin levels in blood are higher between midnight and early morning, perhaps suppressing appetite during the night. The diurnal rhythm of blood leptin levels can be modified by meal-timing. In humans, many instances are seen where Leptin dissociates from the strict role of communicating nutritional status between body and brain and no longer correlates with body fat levels:
1. Leptin level is decreased after short-term fasting (24-72 hours), even when changes in fat mass are not observed.
2. Leptin plays a critical role in the adaptive response to starvation.
3. In obese patients with obstructive sleep apnea, leptin level is increased, but decreased after the administration of continuous positive airway pressure. In non-obese individuals, however, restful sleep (i.e., 8-12 hours of unbroken sleep) can increase leptin to normal levels.
4. Serum level of leptin is reduced by sleep deprivation.
5. Leptin level is increased by perceived emotional stress.
6. Leptin level is decreased by increases in testosterone levels and increased by increases in estrogen levels.
7. Leptin level is chronically reduced by physical exercise training.
8. Leptin level is increased by dexamethasone.
9. Leptin level is increased by insulin.
10. Leptin levels are paradoxically increased in obesity.
Brain Recalls Old Memories Via New Pathways
Shift in fear retrieval circuitry eyed in anxiety disorders – NIH-funded studies
People with anxiety disorders, such as post traumatic stress disorder (PTSD), often experience prolonged and exaggerated fearfulness. Now, an animal study suggests that this might involve disruption of a gradual shifting of brain circuitry for retrieving fear memories. Researchers funded by the National Institutes of Health have discovered in rats that an old fear memory is recalled by a separate brain pathway from the one originally used to recall it when it was fresh.
Results of the study, published online in the journal Nature (19 January 2015) showed that after rats were conditioned to fear a tone associated with a mild shock, their overt behavior remained unchanged over time, but the pathway engaged in remembering the traumatic event took a detour, perhaps increasing its staying power. Immediately after fear conditioning, a circuit running from the prefrontal cortex, the executive hub, to part of the amygdala, the fear hub, was engaged to retrieve the memory. But several days later, the authors discovered that retrieval had migrated to a different circuit – from the prefrontal cortex to an area in the thalamus, called the paraventricular region (PVT). The PVT, in turn, communicates with a different central part of the amygdala that orchestrates fear learning and expression. The authors used a genetic/laser technique called optogenetics to spot the moving memory. This technique can activate or silence specific pathways to tease them apart. The authors hypothesized that the PVT may serve to integrate fear with other adaptive responses, such as stress, thereby strengthening the fear memory, and that people with anxiety disorders, any disruption of timing-dependent regulation in retrieval circuits might worsen fear responses occurring long after a traumatic event.
In the same issue of Nature, Bo Li, Ph.D. and Mario Penzo, Ph.D. of Cold Spring Harbor Laboratory in New York, and colleagues, reveal how the long-term fear memory circuit works in mice to translate detection of stress into adaptive behaviors. These authors independently discovered the same shift in memory retrieval circuitry occurring, over time, after fear conditioning in mice. Using powerful genetic-chemical, as well as optogenetic, methods to experimentally switch pathways on and off, they showed conclusively that neurons originating in the PVT regulate fear processing by acting on a class of neurons that store fear memories in the central amygdala area. This article traced this activity in the PVT to the action of a messenger chemical, brain-derived neurotrophic factor (BDNF), which has previously been implicated in mood and anxiety disorders. For example, altered BDNF expression has been linked to PTSD. BDNF from the PVT, working via a specific receptor, activated the memory-storing amygdala neurons. Simply infusing BDNF into the central amygdala area caused mice to freeze in fear, suggesting that it not only enables the formation of fear memories, but also the expression of fear responses.
Registering Eye Movements During Reading in Alzheimer’s Disease
Reading requires the fine integration of attention, ocular movements, word identification, and language comprehension, among other cognitive parameters. Several of the associated cognitive processes such as working memory and semantic memory are known to be impaired by Alzheimer’s disease (AD). As a result, a study published online in the Journal of Clinical and Experimental Neuropsychology (28 February 2014) analyzed eye movement behavior of 18 patients with probable AD and 40 age-matched controls during Spanish sentence reading.
Results showed that controls focused mainly on word properties and considered syntactic and semantic structures. In addition, the controls’ knowledge and prediction about sentence meaning and grammatical structure were quite evident when considering some aspects of visual exploration, such as word skipping, and forward saccades. Saccades are quick, simultaneous movements of both eyes between two phases of fixation in the same direction. By contrast, in the AD group, the predictability effect of the upcoming word was absent, visual exploration was less focused, fixations were much longer, and outgoing saccade amplitudes were smaller than those in controls.
According to the authors, the altered visual exploration and the absence of a contextual predictability effect might be related to impairments in working memory and long-term memory retrieval functions and that these eye movement measures demonstrate considerable sensitivity with respect to evaluating cognitive processes in AD. As a result, these measures could provide a user-friendly marker of early disease symptoms and of its posterior progression.
FDA Clears First System of Mobile Medical Apps for Continuous Glucose Monitoring
Diabetes is a serious, chronic metabolic condition where the body is unable to convert glucose into the energy needed to carry out daily activities. An estimated 25.8 million people in the U.S. – about 215,000 of them under age 20 – have diabetes. If left untreated, high blood glucose levels (hyperglycemia) can lead to serious long-term problems such as stroke, heart disease, and damage to the eyes, kidneys and nerves.
A continuous glucose monitor (CGM) is a device that includes a small, wire-like sensor inserted just under the skin that provides a steady stream of information about glucose levels in the fluid around the cells (interstitial fluid). CGMs are worn externally and continuously display an estimate of blood glucose levels, and the direction and rate of change of these estimates. When used along with a blood glucose meter, CGM information can help people with diabetes detect when blood glucose values are approaching dangerously high and dangerously low levels.
The FDA has cleared for marketing the first set of mobile medical apps that allow people with diabetes to automatically and securely share data from a CGM with other people in real-time using an Apple mobile device such as an iPhone. The Dexcom Share Direct Secondary Displays system’s data-sharing capability allows caregivers to a person with diabetes to monitor that individual’s blood sugar levels remotely through a legally marketed device that is available on mobile devices. Devices like the Dexcom Share were previously available through open source efforts, but were not in compliance with regulatory requirements. The Dexcom Share system is the first of its kind to offer a legally marketed solution for real-time remote monitoring of a patient’s CGM data.
The Dexcom Share system displays data from the G4 Platinum CGM System using two apps: one installed on the patient’s mobile device and one installed on the mobile device of another person. Using Dexcom Share’s mobile medical app, the user can designate people (followers) with whom to share their CGM data. The app receives real-time CGM data directly from the G4 Platinum System CGM receiver and transmits it to a Web-based storage location. The app of the follower can then download the CGM data and display it in real-time.
The FDA reviewed data for the Dexcom Share system through the de novo classification process, a regulatory pathway for low- to moderate-risk medical devices that are novel and not substantially equivalent to any legally marketed device. Data provided by the device maker showed the device functions as intended and transmits data accurately and securely.
Because the device is low to moderate risk, a regulatory concept when classifying devices not requiring a Pre-Market Approval (PMA) application, the FDA has classified the device as class II exempt from premarket submissions. In the future, manufacturers wishing to market devices like the Dexcom Share system will not need premarket clearance by the FDA prior to marketing, but they will still need to register and list their device with the agency, as well as follow other applicable laws and regulations.
Alberto Gutierrez, PhD, Director of the Office of In Vitro Diagnostics and Radiological Health in the FDA’s Center for Devices and Radiological Health said that Exempting devices from premarket review is part of the FDA’s effort to ensure these products provide accurate and reliable results while still encouraging the development of devices that meet the needs of people living with diabetes and their caregivers.
The Dexcom Share system does not replace real-time continuous glucose monitoring or standard home blood glucose monitoring. It is also not intended to be used by the patient in place of a primary display device. Additionally, CGM values alone are not approved to determine dosing of diabetes medications. CGMs must be calibrated by blood glucose meters, and treatment decisions, such as insulin dosing, should be based on readings from a blood glucose meter.
The Dexcom Share system is manufactured by Dexcom, Inc., located in San Diego, California.
Salmon Cakes – Jules Mitchel Style
Delicious and easy to make – ©Joyce Hays, Target Health Inc.
2 salmon fillets (remove any bones and skin)
1 cup Panko, plus extra Panko if you want to roll the cakes in it before cooking
1 large clove of garlic, juiced
1 teaspoon turmeric/black pepper (MegaFood)
1/2 cup fresh dill, chopped
1 pinch chili flakes (or cayenne)
Lemon zest from 1/2 fresh lemon (no juice)
Coconut oil only for frying
Lemon and lime slices, only for garnish on the serving dish
Consider serving with an easy homemade tartar sauce (recipe below)
This is the diced salmon and the salmon paste, together – ©Joyce Hays, Target Health Inc.
1. Dice one of the salmon fillets, and put into a medium mixing bowl.
2. Into a food processer, put the other salmon fillet and pulse until you get a smooth paste.
3. Using a spatula, get all of this salmon paste into the same mixing bowl.
The color of the salmon will change color when you add the other ingredients.
In this photo, all ingredients were added together, mixed and placed in fridge for 2 hours. Now, I’m ready to make the salmon cakes. Notice, how the color of the salmon has changed slightly – ©Joyce Hays, Target Health Inc.
To the mixing bowl, add the remaining ingredients, mix well, cover, and put in the refrigerator for 2 hours, so ingredients will blend well.
Just before cooking, (optional) you can roll the cakes in Panko.
Heat the coconut oil in a frying pan, shape the mixture into small patties (roll into a ball and then squash it in the pan), and fry for one or two minutes on each side, (depending on the thickness of your patties) until they are golden and springy to the touch. You should be able to make 6+ out of the ingredients.
Keeping one of the salmon fillets chunky gives these fishcakes a great texture
Quick n’ Easy Tartar Sauce
Creamy and delicious ©Joyce Hays, Target Health Inc.
1. 1-1/2 Cup Kraft mayonnaise (my favorite store bought mayo) (you choose: regular, low-fat or no-fat mayo)
2. 1 large dill pickle, well chopped (I like Polish pickles best)
3. 1/2 sweet onion, chopped
4. 1/2 teaspoon dry mustard
5. 2 teaspoons fresh parsley, well chopped
6.1/8 teaspoon paprika
7. 1/2-1 teaspoon fresh-squeezed lemon juice (to taste)
Mix all ingredients in a bowl. Cover and place in refrigerator for 2 hours, so ingredients blend well. Serve this tartar sauce, with the JULES MITCHEL STYLE Salmon Patties, NOT THE THAI STYLE CAKES.
Jules Mitchel ©Joyce Hays, Target Health Inc.
So, what d’ya do with a husband, so used to getting most things his way? This is not a trick question – LOL
Earlier in the week, I created a recipe that I thought was wonderful. I called it Salmon Cakes Thai Style. He ate 1/2 of one of the Thai salmon cakes and stubbornly refused to eat anymore. I couldn’t believe it. He was so recalcitrant, simply refused. I decided to overcome my own stubborn streak, because of the possibility that readers of the newsletter, might feel the same way. I therefore, adapted my Thai recipe and called the new one, Salmon Cakes Jules Mitchel Style, which is the recipe for this week, and my way of ribbing my hub a little.
Here, below, is the Thai Style Recipe, so that if you’re in a Thai state of mind, you can try this as well. I loved it!
Salmon Cakes Thai Style
2 salmon fillets (remove any bones and skin)
1 cup Panko plus extra Panko if you want to roll the cakes in it before cooking
1 Tablespoon ginger puree (bought on Amazon)
1 Tablespoon lemongrass paste (bought on Amazon)
2 large cloves of garlic, chopped well
1 teaspoon ground cumin
1 teaspoon turmeric/pepper mixed spice
1 teaspoon coriander
1 teaspoon cardamom
2/3 cup fresh cilantro, chopped
1 pinch chili flakes (or cayenne)
1 Tablespoon fish sauce (FreshDirect)
1 Tablespoon soy/tamari sauce (Amazon or FreshDirect)
Juice of 1/2 lime
Coconut oil (or ghee) only for frying
Taking the skin off fish and ingredients ©Joyce Hays, Target Health Inc.
Cooking the Salmon Thai Cakes ©Joyce Hays, Target Health Inc.
The directions for Thai Cakes are exactly the same as the Jules Mitchel Style Salmon Cakes.
Salmon Cakes Thai Style, served with Iranian rice.©Joyce Hays, Target Health Inc.
I served both types of Salmon Cakes with a fennel, pear, grape, Sumo tangerine, salad, tossed with some toasted sesame seeds, a few flaked almonds and a lemon or lime dressing. Also, one of my rice recipes made with Iranian rice, (above) that I bought online at Amazon.
This is the only Turmeric (from Amazon) I’m using for cooking, these days. The proportions of Turmeric to black pepper, are just right.
Cloudy Bay Sauvignon Blanc, chilled, worked well with this dinner. ©Joyce Hays, Target Health Inc.
With the Jules Mitchel Salmon Cakes, I served Moroccan Ratatouille, another of my creations, that I’m trying out on my dearest guinea pig husband. He gave this a thumbs-up. Very soon, I will share this recipe in a future newsletter.
From Our Table to Yours!