DIA Meeting 2015: Target Health to Chair a Symposium on eSource and Risk-based Monitoring
Target Health Inc. is pleased to announce that at the annual meeting of the DIA, being held in Washington DC (June 14-18, 2015), Dr. Jules T. Mitchel will chair a Symposium entitled: How Risk-Based Monitoring and eSource Methodologies are Impacting Clinical Sites, Patients, Regulators and Sponsors.
The Symposium will show how risk-based monitoring and eSource methodologies are impacting the way clinical trials are being conducted and managed. Using results and experience from completed and ongoing clinical trials, the speakers will identify how eSource and risk-based monitoring methodologies are impacting the clinical research enterprise including clinical research sites, patients, regulators, quality assurance, CRAs, and project, safety and data managers.
In addition to Dr. Mitchel, speakers include:
- Ed Seguine, MBA, (CEO, Clinical Ink) who will discuss eClinical and eSource: Global Regulatory Challenges and Opportunities
- Frances Nolan, MBA (Vice President, Quality and Regulatory Affairs, Medidata Solutions Worldwide) who will discuss Overcoming Clinical Trial Data Collection Challenges with eSource Solution and Leveraging Mobile Technologies
- Avik Pal, MBA, (CEO, CliniOps) who will discuss Innovation by Design: Using eSource to Maximize Clinical Development Productivity and Efficiency
Sunrise From the 24th Floor Offices of Target Health Inc.
Sunrise from the 24th Floor © Target Health Inc.
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
Exercise and Your Heart
The benefits of exercise have been known since antiquity. Marcus Cicero, around 65 BCE, stated: It is exercise alone that supports the spirits, and keeps the mind in vigor. However, the link between physical health and 1) ___ (or lack of it) was only discovered in 1949 and reported in 1953 by a team led by Jerry Morris. Dr. Morris noted that men of similar social class and occupation (bus conductors versus bus drivers) had markedly different rates of heart attacks, depending on the level of exercise they got: bus drivers had a sedentary occupation and a higher incidence of heart disease, while bus conductors were forced to move continually and had a lower incidence of heart disease. This link had not previously been noted and was later confirmed by other researchers. Just one day of exercise can protect the heart against a heart 2) ___, and this protection is upheld with months of exercise, making exercise one of the few sustainable preconditioning stimuli (Journal of Applied Physiology, September 2011). Wow.
Heart attacks occur when a plaque suddenly breaks off from the walls of an artery supplying blood to the heart. The plaque travels down the ever-narrowing artery until it completely blocks the flow of blood to a part of the heart’s muscle. The heart’s muscle must receive oxygen from the bloodstream all the time. When a part of the heart muscle is suddenly deprived of oxygen, it dies and you suffer a heart attack. The dying heart muscle usually causes severe pain, in the chest, back or left arm. Heart attacks are not caused by progressive narrowing of an artery. Lack of oxygen is the ultimate cause of heart muscle damage. Anything that increases the ability of the heart muscle to survive oxygen deprivation or increases 3) ___ supply to the heart muscle helps to prevent heart attacks.
Exercise helps to prevent heart attacks, and the more intensely you exercise, the greater the protection. Researchers in Norwaytreated recovering heart attack victims with the same intense training methods used by competitive athletes (American Heart Journal). They supervised them as they ran on a treadmill very fast for a few seconds, rested and then repeated their intense intervals. For example, some of the patients ran fast for 30 seconds every five minutes. The interval-training heart attack victims were able to use more oxygen maximally (VO2max) and had their heart rates return toward normal faster than other heart attack victims who did slower continuous training. This advantage persisted for 30 months after the patients completed their 12-week rehabilitation program.
Intense training is not accepted as a treatment for heart attack victims, particularly those who have chest pain with exercise or excessive shortness of 4) ___. Intense exercise can precipitate heart attacks in people with blocked arteries. The exercise sessions are usually supervised by trained technicians using electrocardiograms, at least in the beginning. Intense exercise does not damage healthy hearts. All known tests for heart function show no damage from intense exercise. Post-exercise electrocardiograms and echocardiograms are normal, as are blood levels of heart-specific enzymes, creatine kinase and creatine kinase MB, and myoglobin (Medicine and Science in Sports and Exercise).
Exercise increases the size and number of mitochondria in the 5) ___ of mice (American Journal of Physiology, September 2011). The mice ran on a treadmill for an hour a day, six days a week, for eight weeks. This could explain how exercise improves memory, treats depression, and makes people feel better and helps them to think more clearly. Until now, the leading theory to explain how exercise improves memory and treats depression was that exercise causes the brain to release endorphins, morphine-like compounds that can improve mood. However, endorphins would not explain the improvement in memory and brain function associated with a regular exercise program Mitochondria are tiny chambers in 6) ___ that turn food into energy more efficiently than any other process in your body. Scientists have known for years that exercise enlarges and increases the number of mitochondria in muscle cells, to increase strength, speed and endurance; but this is the first research paper to offer a plausible explanation why exercise improves memory and relieves depression. The increase in brain mitochondria could also explain how training for sports increases endurance by making the brain resistant to fatigue. It also could explain how exercise treats mental disorders, delays aging, and improves certain types of nerve damage.
People who exercise regularly are far less likely to suffer dementia and had less than half the risk of death during the 17-year study period, compared to those who do not exercise (Medicine & Science in Sports & Exercise, February, 2012). Researchers followed 45,000 men and 15,000 women, ages 20 to 88 years, in the United States for an average of 17 years. Six times as many people in the low fitness group suffered from dementia, compared to those who exercised regularly. While deaths in the United States associated with heart disease, breast cancer and stroke have declined in recent years, deaths related to dementia and Alzheimer’s disease rose 46 percent between 2002 and 2006. Another exciting study, from Japan, shows that many of the benefits that exercise provides to muscles are also provided to your brain (The Journal of Physiology, February, 2012;590 (Pt 3):607-16).
THE STUDY: Adult male rats exercised to exhaustion at moderate intensity on a treadmill. Glycogen, sugar stored in muscles, was depleted by 82-90 percent. One day later, the rats’ muscles could store 43-46 percent more than they could originally, In a like manner, brain glycogen levels decreased by 50-64 percent with exhaustive exercise, and were able to store 29-63 percent more on the next day. The greater the depletion of sugar in muscles and brain, the greater the ability to store more sugar after the rats were fed. The brain filled with sugar before the muscles did and after four weeks of training, the rats’ brains could store significantly more glycogen.
EXPLANATION: Sugar is the most efficient source of 7) ___ for your muscles during intense exercise. Sugar is the most efficient source of energy for your brain ALL the time. When you exercise regularly, you increase the ability of your muscles to store sugar so you can move faster and longer. This study suggests that exercise also increases the energy supply to your brain, which will help you to think and reason better.
Arthritis is classified into three types: inflammatory, degenerative, and traumatic. Your doctor first checks to see if you have a history of trauma that damaged your joint. If you don’t, he does a host of blood tests looking for a source of inflammation (an overactive immunity): various diseases, infections or the deposition of crystals in the joint fluid. If your doctor finds none of these, your doctor announces to you that you have osteoarthritis, which means that he/she doesn’t have the foggiest idea what is causing your joint pain. He/she then does X rays and MRIs. If the cartilage is gone and a bone at the joint touches the end of the opposing bone, your doctor may recommend a joint replacement. If the cartilage is intact, the major treatment is exercise (Current Pain and Headache Reports, December 2011: 15(6):423-30). Regardless of the cause of your joint pain, inactivity will increase damage to the joint. If you don’t move that joint, you can expect it to degenerate to the point where the joint loses its ability to move through its full range of motion. When you stop using a joint, the muscles around it grow weak and the tendons stiffen. This leads to further joint damage and lack of mobility. Of course, you should not pound on, or apply too much force on damaged joints because too much force can break more cartilage, leading to a joint replacement. Do not run with arthritis in knees or hips. Running is almost always contraindicated if you have joint 8) ___ in the legs, hips or lower back because during running, your foot hits the ground with a force that is transmitted up your leg all the way to your back. The faster you run, the greater and more damaging the force of your foot strike. If you want to run with joint pain, you must run very slowly, and even then, you are still transmitting the foot strike force up your leg and into your back. The safest sports for people with painful joints are those that do not involve foot strike force. Cycling is done in a smooth rotary motion. Swimming helps protect your joints because of the buoyancy of the water. Exercise equipment such as elliptical trainers or stair steppers will allow you to move your joints without pounding on your feet. Any of these activities help you to strengthen the muscles around the damaged joints and keep the tendons flexible. Whatever sport you choose, the same rules of training that athletes use apply to you:
Start out by pedaling, walking or swimming very 9) ___ and stop if your muscles feel heavy or hurt. Stop even if you have just started your workout for that day. When you can pedal, walk or swim for 30 minutes a day without increasing your joint pain, you are ready to start training. If you do not exercise intensely enough to feel some burning in your muscles, your muscles will not get stronger. You have to work hard enough to damage muscles because healing strengthens them. Athletes take a harder workout on one day in which they feel a burning in their muscles. When you exercise hard enough to feel sore on the next day, you should go slowly for as many days as it takes for the muscles to heal and the soreness to go away. The normal soreness you feel 8 to 24 hours after you have taken an intense workout is called Delayed Onset Muscle Soreness (DOMS). The difference between DOMS and an injury: DOMS is symmetrical; you feel the same soreness on both sides of your body. Also, DOMS does not worsen with easy exercise. Stop exercising immediately if the pain does not improve as you continue to move. If your discomfort increases as you exercise, you have an injury or are headed for an injury. If your joint pain is so severe that you cannot exercise, you need to find some way to have your joints moved for you. Go to a physical 10) ___ who will move your joints for you and use massage, heat, cold or electrical stimulation to help you regain the ability to move the joints. Allowing your joints to stay in one position without daily movement will cause further joint damage and make your arthritis pain worse.
ANSWERS: 1) exercise; 2) attack; 3) oxygen; 4) breath; 5) brains; 6) cells; 7) energy; 8) damage; 9) slowly; 10) therapist
Jackie Gleason, An Unhealthy Life Worth Living (1916-1987)
1961 as Minnesota Fats, in The Hustler
As Ralph Kramden, the brash, blustering, uncouth and bumbling fool in the TV sitcom, The Honeymooners, Jackie Gleason was probably the most famous television character of his day. He portrayed similar personality disorders in movies with characters such as Minnesota Fats in the The Hustler and Buford T. Justice in the Smokey and the Bandit series. Although his public image was that of a buffoon, he was very smart with money. He came from severe poverty but he made incredible amounts of money from just about everything he did. The 39 episodes of The Honeymooners ran live on television for only two years, 1955 and 1956, but supplied him and his heirs with many millions of dollars from reruns that are still shown today. He couldn’t read or write a note of music, but he would hum tunes to seasoned musicians who would write them down and sell his songs that still bring royalties. The characters he played on the screen used many of the same personality traits he developed or observed, early in life.
Gleason was born at 364 Chauncey Street in the Bushwick, section of Brooklyn. He grew up nearby, at 328 Chauncey (an address he later used for Ralph and Alice Kramden on The Honeymooners). Originally named Herbert Walton Gleason Jr., he was baptized John Herbert Gleason. His parents were Mae Maisie (nee Kelly), a subway change-booth attendant and Herbert Walton Herb Gleason, insurance auditor. His mother was from Farranree, Cork, Ireland, and his father was Irish American. Gleason was one of their two children; his brother Clemence died of spinal meningitis at age 14. At age nine, Gleason’s father abandoned the family. Gleason remembered his father having beautiful handwriting, as Herbert Gleason often worked at the family’s kitchen table writing policies in the evenings. The night before his disappearance, Gleason’s father disposed of any family photos he was pictured in; just after noon on December 15, 1925, he collected his hat, coat, and paycheck, leaving the insurance company and his family permanently. When it was evident he was not coming back, Mae went to work for the Brooklyn-Manhattan Transit Corporation (BMT).
Jackie spent his youth hanging out with a local gang and playing pool. He never finished high school. He supported himself by telling jokes in a theater for four dollars a night, and working in pool halls and carnivals. His mother died when he was 19. He got jobs as a comedian in night clubs and he spent money as fast as he made it. When he was 24, Jack Warner of Warner Brothers saw his comedy routine at a night club and offered him his first movie role. At age 33, he became Chester A. Riley in the television production The Life of Riley. At age 36, he starred in The Jackie Gleason Show as a series of characters who screamed instead of speaking, and were unable to speak correct English. At age 49, he took the role of Ralph Kramden, a bus driver who was married toAlice in the Honeymooners. He bullied her and they fought in every show. He was so mean that it was funny, and they always made up at the end of every show. Today a life-size statue of bus driver Ralph Kramden stands in the Port Authority Bus Terminal in New York City.
At age 20, Jackie wed a vaudeville dancer, Genevieve Halford, but they had a very stormy marriage because he refused to come home after his night club jobs. He must have come home at least twice because they had two daughters. They separated in 1941, but got back together in 1948, and separated again in 1951. In 1954, while he was still married, he broke his leg. His wife came to visit him in the hospital and found Marilyn Taylor, a dancer on his television show, in his room. Everyone in the entire hospital got to hear them fight, after which she filed for divorce. It took 16 years for the divorce to become final. In 1970, ten days after his divorce from his first wife, Gleason married Beverly McKittrick a secretary whom he had met two years earlier. Four years later, while he was still married to Beverly, he went back to seeing Marilyn Taylor, who was now a widow with a young son. He filed for divorce from his second wife, married Taylor and stayed with her for the rest of his life.
Gleason’s lifestyle was so self-destructive that it is amazing that he lived to be as old as 71. He was morbidly obese, often weighing in at close to 300 pounds. He was famous for being able to drink every other actor under the table, and smoked more than four packs of Marlboro cigarettes a day. His favorite food was red meat, he loved rich desserts and hated vegetables. He did not exercise, even after he moved to Miami where his home had an exercise room that was larger and better-equipped than many commercial gyms. His lifestyle caused horrible diseases and prevented him from really enjoying his fame and financial successes. In 1978, at age 62, he had chest pains while playing the lead role in the play Sly Fox and was treated and released from the hospital. The following week his pain was so bad that he could not perform and had to have triple-bypass surgery. In 1986, at age 70, while he was acting in his last film, Nothing in Common, he was diagnosed with colon cancer that had spread to his liver. He was also diagnosed with diabetes, from which he had probably suffered for many years. If that wasn’t enough, he was afflicted with very painful clotted hemorrhoids. During the filming, he told his daughter: I won’t be around much longer. In 1987, he died at his beautiful Miami mansion. On the base of the statue at his grave are the words And Away We Go.
The same lifestyle factors that increase risk for heart attacks also increase risk for diabetes, dementia, impotence, and several types of cancer. Jackie Gleason’s lifestyle increased his risk for colon cancer, metastatic cancer to his liver, diabetes, heart attacks and a young death. There is a stronger association between red meat and colon cancer than with any other cancer. At any age, you can reduce your risk for these diseases by changing your lifestyle. Cancer survivors have been shown to live longer when they adopt a healthful lifestyle, and many heart attack patients and diabetics can reverse much of the damage they have caused when they eat healthfully and get plenty of exercise. Source: Wikipedia; Gabe Mirkin MD
Chromosome Region Linked to Gigantism
Gigantism, a rare disorder that causes excessive childhood growth, results from a defect in the pituitary, a pea-sized gland at the base of the brain that makes growth hormones and controls the activity of other glands in the body. Some people with gigantism have a tumor in the pituitary that secretes extra hormone; others just have an oversized pituitary. People with this condition are abnormally tall and may have delayed puberty, large hands and feet, and double vision. Gigantism is often treated by removing the tumor, or even the entire pituitary, but can sometimes be treated with medication alone.
According to an article published online in the New England Journal of Medicine (3 December 2014), researchers at the NIH have found a duplication of a short stretch of the X chromosome in some people with Gigantism. According to the NIH, in theory, the causes of overgrowth and undergrowth in children should be regulated by the same mechanisms, and understanding how children grow is extraordinarily important, as an indicator of their general health and their future well-being.
The research started with a family who came to the NIH Clinical Center for treatment in the mid-1990s. A mother who had been treated for gigantism had two sons who were also growing rapidly. A second family, with an affected daughter, came to NIH from Australia. The girl had the same duplication the researchers saw in the first family.
For the current study, the investigators used whole-genome analysis to find major changes in the DNA in 43 people with gigantism. Results showed that every person in the study who had gigantism as an infant or a toddler had the same defect, a duplication of a stretch of the X chromosome. Family members without gigantism did not have the duplication. Next the investigators sought to identify which gene might be responsible for the excessive growth. While the length of the DNA duplication varied among the patients, the same four genes were found to be duplicated in all of the patients. After testing the genes, the most likely suspect was a gene called GPR101. GPR101’s activity was up to 1,000 times stronger in the pituitaries of children with the duplication than in the pituitaries of typically developing children. The investigators also looked at samples from the pituitary tumors of 248 people with acromegaly, a condition in which adults produce excess growth hormone. None of the patients had the duplication that was seen in people with gigantism. However, 11 of the acromegaly patients did have a mutation in GPR101, suggesting that the gene also may play a role in that condition as well.
Figuring out exactly how the protein derived from GPR101 works is the next frontier and it is hoped that these discoveries will lead to new treatments for gigantism in children as well as in insights into undergrowth.
Mouse Study Reveals Potential Clue to Extra Fingers or Toes
Polydactyly, a birth defect involving extra fingers on the hand or extra toes on the feet is estimated to occur in roughly 1 of every 500 to 1,000 births. The condition appears to result from a mutation in any of a number of genes. Polydactyly may involve only one extra finger or toe, or it may include multiple extra digits. The condition may also appear as part of a larger disorder having other organ abnormalities, some of which may be serious or life- threatening.
According to a study published online in Cell Reports (21 November 2014), it was found that a mouse version of polydactyly results from a malfunction of the cellular machinery that processes one of the cell’s internal transportation vehicles. The authors found that a mouse form of polydactyly appears to result from an error in a single gene out of a group containing the information needed to make a protein complex. The protein complex is called Endosomal Sorting Complex Required for Transport II — ESCRT-II, for short. Endosomes ferry molecules from the cell’s surface to the cell’s interior. When it functions normally, ESCRT-II processes endosomes for eventual disassembly within the cell. The mutation impairs the functioning of ESCRT-II, endosomes cannot be processed properly. As a result, an excess of a hormone known as fibroblast growth factor accumulates on the cell’s surface.
According to the authors, since this congenital defect appears both in isolation and in conjunction with other abnormalities, gaining fundamental knowledge of these genetic pathways is vital to developing effective genetic diagnostic screens and directed therapies.
The Fibroblast Growth Factors are a Family of Proteins Known as Cell Signaling Molecules
At top left: After a fibroblast growth factor binds to a cell, it triggers two potential sequences of events. Under typical conditions, it sets off a cascade of chemical reactions that eventually cause cells to divide, and even to differentiate into tissues and organs. In the other, shown in the image at the above left, it’s processed and then marked for eventual disassembly. With this internal breakdown process, the cell achieves a balance — once the cell acquires a critical mass of a fibroblast growth factor, the excess is marked for elimination. The process begins with the fibroblast growth factor (FGF) attaching to a special site, or receptor, on the cell surface, something like the way a key fits into a lock. The receptor changes shape, setting off the reactions that trigger the cell into such actions as dividing or giving rise to an organ or tissue type. At some point, sufficient FGF has bound to receptors on the cell surface. In response, pocket-like structures form on the cell’s surface. The cell surface changes shape — it involutes, like the surface of a water-filled balloon with a finger in it. This sunken-in structure contains many such FGF-receptor pairs. Eventually, this involution pinches off inside the cell, forming a spherical structure known as an endosome. Like a bathysphere ferrying ocean researchers to the sea depths, the endosome conveys the FGF-receptor duplexes deep into the cell. During their journey, the endosomes encounter a protein complex, called Endosomal Sorting Complex Required for Transport II — ESCRT-II, for short. When it’s functioning normally, ESCRT-II processes the endosome, reducing it in size. The details of just how ESCRIT-II processes the endosome aren’t fully understood. Once this processing takes place, the endosome fuses with another cellular body, called a lysosome. The lysosome disassembles the endosome, degrading it and its contents — FGF and its receptor.
At bottom left: The researchers discovered that, in the mouse strain they bred for the study, a mutation in a gene for a key subunit of ESCRT-II impairs the ability of ESCRT-II to do its job. This gene contains the information needed to make vacuolar protein sorting protein 25, or Vps25. The mutant Vps25 protein interferes with ESCRT-II’s ability to do its job. Because the endosomes aren’t sufficiently processed, the lysosomes have trouble breaking them apart. As a result, endosomes accumulate inside the cell. Fewer endosomes form at the cell surface, and FGF-receptor pairs accumulate on the surface because they can’t be removed rapidly enough. This situation creates an imbalance – increasing the amount of FGF bound to receptors on the cell surface. The end result in the mice with the Vps25 mutation is polydactyly.
NIH Takes Step to Speed the Initiation of Clinical Research by Ensuring Use of Single IRB
Institutional review boards (IRBs) play a critical role in assuring the ethical conduct of clinical research, and studies must be reviewed and approved by an IRB before they can begin. When the regulations for protection of human subjects were first published, most clinical research was conducted at a single institution. Since then, the research landscape has evolved, and many studies are carried out at multiple sites and within large networks. Studies that go beyond a single site are often able to recruit more individuals from diverse populations. These multi-site studies can often generate important results in less time. However, working through IRB review at each site can add delay without increasing the protections for the research participants in the study.
The National Institutes of Health (NIH) has issued a draft policy to promote the use of a single IRB in multi-site clinical research studies. The draft NIH policy proposes that all NIH-funded, multi-site studies carried out in the United States, whether supported through grants, contracts, or the NIH intramural program, should use a single IRB. Exceptions to the policy would be allowed if local IRB review is necessary to meet the needs of specific populations or where it is required by federal, state or tribal laws or regulations. Wider use of single IRB review in multi-site studies will help achieve greater efficiencies in the initiation of studies across NIH’s entire clinical research portfolio.
A number of NIH institutes and centers have been supporting the use of a single IRB in multi-site studies, and their experiences have shown the benefits and feasibility of the single IRB review model. Examples include the National Cancer Institute’s (NCI) Central Institutional Review Board, which has been in place for the review of NCI-sponsored clinical trials since 1999. The National Institute of Neurological Disorders and Stroke has also incorporated the use of a single IRB for its Network for Excellence in Neuroscience Clinical Trials’ (NeuroNEXT) and its stroke research network, NIH StrokeNET.
NIH is seeking public comments on the draft policy through a 60 day comment period closing Jan. 29, 2015 and comments may be submitted by any of the following methods:
— Email: SingleIRBpolicy@mail.nih.gov
— Fax: 301-496-9839
— Mail/hand delivery/courier: Office of Clinical Research and Bioethics Policy, Office of Science Policy, National Institutes of Health, 6705 Rockledge Drive, Suite 750, Bethesda, MD 20892.
Kale and Cheese Stuffed Potatoes
This is a delicious recipe and easy to make. ©Joyce Hays, Target Health Inc.
Clearing up the feast, for our (visiting) son the lawyer. The kale and cheese stuffed potatoes are on the far left.
Kale and Cheese Stuffed Potatoes
(Kale for Brunch, Lunch or Dinner)
3 russet potatoes about 10 oz. each (long and flat)
1 bunch Tuscan kale
1 Tablespoon olive oil
1 Tablespoon butter
1 large leek
1 cup coarsely grated cheddar, gruyere or comte
3/4 cup sour cream
Pinch black pepper
3 fresh garlic cloves, minced
Get all ingredients together ©Joyce Hays, Target Health Inc.
Heat oven to 400oF.
- Cook potatoes the first time:Gently scrub potatoes but do not peel. Pierce all over with a fork so that steam escapes. If you don’t poke some holes, you could have a potato explosion followed by a mess. Bake 1 hour to 1 hour 15 minutes or until potatoes are tender when pierced in center. Leave oven on.
- While potatoes cook, prepare stuffing: Tear kale leaves off the stems, and wash leaves in cold water to remove any dirt. Don’t dry. Tear leaves into large pieces. Heat a pan over medium-high and add the kale and a pinch of salt. Cook in the pan with just the water clinging to the leaves until they wilt down. Remove from pan and transfer to a colander and when cool enough to handle, wring out any extra moisture. I use either paper toweling or a clean kitchen towel. On a cutting board, finely chop greens. There should be about a cup of well-chopped greens; more or less.
- Trim leek down to the yellow and pale green part. Halve lengthwise and wash in cold water to remove any dirt, then pat dry. Cut leek halves the long way, again, so they’re in quarter-stalks, and thinly slice.
In a bowl, mixing the cooked kale, garlic and leeks ©Joyce Hays, Target Health Inc.
- Heat a large skillet over medium heat; add butter and oil. When both are warm, add leek and reduce heat to medium-low. Cook until mostly tender and sweet, about 10 to 15 minutes, stirring. Avoid letting it brown. Add the minced garlic and chopped kale back to pan and warm up with leeks, for about 1 minute. Transfer mixture to a bowl.
Potatoes, leeks, kale have been mashed, sour cream and 3/4 grated cheese have been stirred in. Mixture is ready to heap into the baked shells of the potato. ©Joyce Hays, Target Health Inc.
- Prepare potatoes: When potatoes are cool enough to handle, halve lengthwise and scoop out all but the last 1/4-inch thickness of skin and potato (you want the potato shell to remain strong enough to hold all the stuffing). Now add the potato insides, to bowl with leeks and greens. Arrange the potato shells on a baking sheet. Mash potatoes, leeks and kale together until smooth. Stir in the sour cream, 3/4 of cheese and more salt and pepper (optional). Now, heap the kale/potato mixture into the potato skins. Sprinkle with remaining 1/4 of cheese.
Going in oven for second time ©Joyce Hays, Target Health Inc.
- Bake potatoes a second time, 20 to 30 minutes, until golden brown and crispy. Serve while still nice and warm
We opened some of this bottled red satin, which we were saving for a special occasion. One of our sons was visiting so we had a blast of a feast with this excellent Napa Valley Cab. (you can’t see the third glass). This is a well-known vineyard putting forth, year after year, only excellent wines. You can’t go wrong drinking it now or investing in futures.
Friday night, we started by toasting with this delicious (from start to finish), full bodied cab, and a salad with fresh ripe tomatoes, cut up avocados, green olives, mini thin-skinned cucumbers, endive and a fresh lemon juice/olive oil dressing. Then came the unbelievably tender center-cut fillet mignon with marsala/mushroom sauce, the (recipe above) kale/cheese stuffed potatoes, some cauliflower fritters with pomegranate arils (will post my recipe soon), some sweet potato/date patties with chopped pistachios (will post another of my recipes soon) and more wine. For dessert, the rest of last week’s recipe, my persimmon custard cake.
We saw the just-opened B’way play, The Real Thing, and enjoyed it immensely as well as stimulating discussions afterwards. A wonderful weekend was had by all. We look forward to many more visits, now that our monster renovation is nearly over.
From Our Table to Yours!