ACRP Blog Interviews Target Health on the Paperless Clinical Trial

 

As a followup to an ACRP Webinar on March 7, entitled: “Regulatory Concerns When Running Paperless Clinical Trials,“ presented by Jonathan Helfgott, formerly of FDA and Jules Mitchel, President of Target Health Inc., Michael Causey, of the ACRP Blog interviewed Dr. Mitchel. The interview is entitled “Paperless Clinical Trials Gain Momentum.“ We were told that this was one of the most popular webinars with over 350 attendees.

 

If you want a copy of the slides, just let us know.

 

For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 165). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website.

 

Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor

 

QUIZ

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Diabetes Gene That Causes Low and High Blood Sugar Levels

The fluctuation of blood sugar (red) and the sugar-lowering hormone insulin (blue) in humans during the course of a day with three meals. One of the effects of a sugar-rich vs a starch-rich meal is highlighted.

Graphic credit: Jakob Suckale, Michele Solimena – Solimena Lab and Review Suckale Solimena 2008 Frontiers in Bioscience PMID 18508724, preprint PDF from Nature Precedings, original data: Daly et al. 1998 PMID 9625092, CC BY 3.0, https://en.wikipedia.org/w/index.php?curid=24016521

 

 

Diabetes mellitus (DM), commonly referred to as diabetes, is a group of metabolic disorders in which there are high 1) ___ sugar levels over a prolonged period. Symptoms of high blood sugar include frequent urination, increased thirst, and increased hunger. If left untreated, diabetes can cause many complications. Acute complications can include diabetic ketoacidosis, hyperosmolar hyperglycemic state, or death. Serious long-term complications include cardiovascular disease, stroke, chronic kidney disease, foot ulcers, and damage to the eyes. Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced. There are three main types of diabetes mellitus:

 

Type 1 DM results from the pancreas’s failure to produce enough 2) ___. This form was previously referred to as “insulin-dependent diabetes mellitus“ (IDDM) or “juvenile diabetes“. The cause is unknown.

 

Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly. As the disease progresses a lack of insulin may also develop. This form was previously referred to as “non insulin-dependent diabetes mellitus“ (NIDDM) or “adult-onset diabetes“. The most common cause is excessive body 3) ___ and insufficient exercise.

 

Gestational diabetes is the third main form, and occurs when pregnant women without a previous history of diabetes develop high blood sugar levels.

 

Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco. Control of blood pressure and maintaining proper foot care are important for people with the disease. Type 1 DM must be managed with insulin injections. Type 2 DM may be treated with medications with or without insulin. Insulin and some oral medications can cause low blood sugar. Weight loss surgery in those with obesity is sometimes an effective measure in those with type 2 DM. Gestational diabetes usually resolves after the birth of the 4) ___. As of 2015, an estimated 415 million people had diabetes worldwide, with type 2 DM making up about 90% of the cases. This represents 8.3% of the world’s 5) ___ population. As of 2014, trends suggested the rate would continue to rise. Diabetes at least doubles a person’s risk of early 6) ___. From 2012 to 2015, approximately 1.5 to 5.0 million deaths each year resulted from diabetes. The global economic cost of diabetes in 2014 was estimated to be US$612 billion. In the United States, diabetes cost $245 billion in 2012.

 

A recent, perhaps hopeful, study of families with rare blood sugar conditions has revealed a new gene thought to be critical in the regulation of insulin, the key 7) ___ in diabetes. The research carried out at two British universities: Queen Mary University of London, University of Exeter and in the U.S.. Vanderbilt University, and published in the journal PNAS, could lead to the development of novel treatments for both rare and common forms of diabetes. In addition to the more common forms of diabetes (type 1 or type 2), in about 1-2 per cent of cases diabetes is due to a genetic disorder. A defective gene typically affects the function of insulin-producing cells in the pancreas, known as beta cells. The research team studied the unique case of a family where several individuals suffer from diabetes, while other family members had developed insulin-producing tumors in their pancreas. These tumors, known as insulinomas, typically cause low blood sugar levels, in contrast to diabetes which leads to high blood sugar levels. The authors were initially surprised about the association of two apparently contrasting conditions within the same families — diabetes which is associated with high blood sugar and insulinomas associated with low blood sugar. The research shows that, surprisingly, the same 8) ___ defect can impact the insulin-producing beta cells of the pancreas to lead to these two opposing medical conditions. The team also observed that males were more prone to developing diabetes, while insulinomas were more commonly found in females, but the reasons behind this difference are still unknown.

 

The researcher team identified a genetic disorder in a gene called MAFA, which controls the production of insulin in beta 9) ___. Unexpectedly, this gene defect was present in both the family members with diabetes and those with insulinomas, and was also identified in a second, unrelated family with the same unusual dual picture. This is the first time a defect in this gene has been linked with a disease. The resultant mutant protein was found to be abnormally stable, having a longer life in the cell, and therefore significantly more abundant in the beta cells than its normal version. The authors commented that they believe that this gene defect is critical in the development of the disease and that they are now performing further studies to determine how this defect can, on the one hand, impair the production of insulin to cause diabetes, and on the other, cause insulinomas. The team stated that they are committed to understanding more about the causes of all types of 10) ___ and that this research provides important insights into the impact a change in this particular gene has on insulin-producing beta cells and how this relates to the development of a rare genetic form of diabetes. It’s also a great example of how studying rarer conditions could help us learn more about more common types of diabetes.“

 

The study was funded by Diabetes UK, while co-authors also got support from the UK National Institute of Health Research (NIHR), and the US National Institutes of Health, Wellcome Trust and Royal Society. Story Sources: Queen Mary University of London: researchers: Donato Iacovazzo, Sarah E. Flanagan, Emily Walker, Rosana Quezado, Fernando Antonio de Sousa Barros, Richard Caswell, Matthew B. Johnson, Matthew Wakeling, Michael Brandle, Min Guo, Mary N. Dang, Plamena Gabrovska, Bruno Niederle, Emanuel Christ, Stefan Jenni, Bence Sipos, Maike Nieser, Andrea Frilling, Ketan Dhatariya, Philippe Chanson, Wouter W. de Herder, Bjorn Konukiewitz, Gunter Kloppel, Roland Stein, Marta Korbonits, Sian Ellard. MAFAmissense mutation causes familial insulinomatosis and diabetes mellitus. Proceedings of the National Academy of Sciences, 2018; 201712262 DOI: 10.1073/pnas.1712262115

Queen Mary University of London. “Diabetes gene found that causes low and high blood sugar levels in the same family.“ ScienceDaily.com (15 January 2018); Wikipedia)

 

ANSWERS: 1) blood; 2) insulin; 3) weight; 4) baby; 5) adult; 6) death; 7) hormone; 8) gene; 9) cells; 10) diabetes

 

Robert Daniel Lawrence MD (1892-1968)

Robert Daniel Lawrence MD

Photo credit: Unknown – http://wellcomeimages.org/indexplus/image/L0000433.html, CC BY 4.0, https://commons.wikimedia.org/w/index.php?curid=35452965

  

Dr. Robert “Robin“ Daniel Lawrence (1892 – 1968) MA, MB ChB (Hons), MD, FRCP, LLD was a British physician at King’s College Hospital, London. He was diagnosed with diabetes in 1920 and became an early recipient of insulin injections in the UK in 1923. He devoted his professional life to the care of diabetic patients and is remembered as the founder of the British Diabetic Association. Dr. Lawrence, better known as Robin Lawrence was born at 10 Ferryhill Place, Aberdeen, Scotland. He was the second son of Thomas and Margaret Lawrence. His father was a prosperous brush manufacturer, whose firm supplied all the brushes to Queen Victoria and her heirs at Balmoral.

 

At eighteen, Lawrence matriculated at Aberdeen University to take an MA in French and English. After graduation, he briefly worked in an uncle’s drapery shop in Glasgow but gave this up after just a few weeks, returning to Aberdeen where he enrolled back at Aberdeen University to study medicine. He had a brilliant undergraduate career winning gold medals in Anatomy, Clinical Medicine and Surgery and graduated ?with honors’ in 1916. During his second year, on the advice of his anatomy professor he sat and passed the primary FRCS examination in London. He gave up rugby as a student, but represented the University at both hockey and tennis. He was also President of the Students’ Representative Council. On graduation he immediately joined the RAMC and after six months home service, served on the Indian Frontier until invalided home in 1919 with dysentery and was discharged with the final rank of Captain. After a few weeks convalescing at home and fishing, he went to London and obtained the post of House Surgeon in the Casualty Department at King’s College Hospital. Six months later, now being accepted as a “King’s Man“, he became an assistant surgeon in the Ear, Nose and Throat Department. Shortly afterwards, while practicing for a mastoid operation on a cadaver, he was chiseling the bone when a bone chip flew into his right eye setting up an unpleasant infection. He was hospitalized but the infection failed to settle and he was discovered to have diabetes. At his age at this time this represented a death sentence.

 

Lawrence was initially controlled on a rigid diet and the eye infection settled but left permanently impaired vision in that eye. He abandoned thoughts of a career in surgery and worked in the King’s College Hospital Chemical Pathology Department under a Dr G A Harrison. Despite his gloomy prognosis and ill-health he managed to conduct enough research to write his MD thesis. A little later, in the expectation that he had only a short time to live, and not wishing to die at home causing upset to his family, he moved to Florence and set up in practice there. In the winter of 1922-23 his diabetes deteriorated badly after an attack of bronchitis and the end of his life seemed imminent. In early 1922, Banting, Best, Collip and Macleod in Toronto, Canada made the discovery and isolation of insulin. Supplies were initially in short supply and slow to reach the UK, but in May 1923, Harrison cabled Lawrence – “I’ve got insulin – it works – come back quick“. By this time Lawrence was weak and disabled by peripheral neuritis and with difficulty drove across the continent and reached King’s College Hospital on 28 May 1923. After some preliminary tests he received his first insulin injection on 31 May. His life was saved and he spent two months in hospital recovering and learning all about insulin. He was then appointed Chemical Pathologist at King’s College Hospital and devoted the rest of his life to the care and welfare of diabetic patients.

 

Dr. Lawrence developed one of the earliest and largest diabetic clinics in the country and in 1931 was appointed assistant physician-in-charge of the diabetic department at King’s College Hospital, becoming full physician-in-charge in 1939. He also had a large private practice. He wrote profusely on his subject and his books The Diabetic Life and The Diabetic ABC, did much to simplify treatment for doctors and patients. The Diabetic Life was first published in 1925 and became immensely popular, extending to 14 editions and translated into many languages. He published widely on all aspects of diabetes and its management, producing some 106 papers either alone or with colleagues, including important publications on the management of diabetic coma, on the treatment of diabetes and tuberculosis and on the care of pregnancy in diabetics. In 1934, he conceived the idea of an association which would foster research and encourage education and welfare of patients. To this end a group of doctors and diabetics met in the London home of Lawrence’s patient, H. G. Wells, the scientist and writer, and the Diabetic Association was formed. When other countries followed suit it became the British Diabetic Association (the BDA). Lawrence was Chairman of the Executive Council from 1934-1961 and Hon. Life President from 1962.

 

Dr. Lawrence’s enthusiasm and drive ensured the life and steady growth of this association which soon became the voice of the diabetic population and constantly sought to promote the welfare of diabetics. There are now active branches through the country. He was also a prime mover in production of “The Diabetic Journal“ (forerunner of Balance), the first issue of which appeared in January 1935. Many articles thereafter were contributed by himself anonymously. He and colleague Joseph Hoet were the main proponents in founding the International Diabetes Federation and he served as their first president from 1950-1958. At their triennial conferences, Lawrence’s appearance was always greeted with acclaim. Almost immediately after his retirement, he suffered a stroke but his spirit remained indomitable and he continued seeing private patients to the end. His last publication was an account of how hypoglycemia exaggerated the signs of his hemiparesis. Although he preached strict control of diabetes for his patients, he did not keep to a strict diet himself taking instead supplementary shots of soluble insulin as he judged he needed them. He died at home in London on 27 August 1968 aged 76.

 

Lawrence was Oliver-Sharpey lecturer at the Royal College of Physicians of London in 1946. His lecture was one of the earliest descriptions and detailed study of the rare condition now known as Lipoatrophic Diabetes. He was recipient of the Banting Medal of the American Diabetes Association the same year; Banting Lecturer of the BDA in 1949 and in 1964 Toronto University conferred on him its LLD “honoris causa.“ Charles Best, then professor of physiology in Toronto, was probably the proposer for this honor as he had met and become friendly with Lawrence when doing postgraduate research in London with Sir Henry Dale and A. V. Hill in 1925-28. They remained lifelong friends meeting regularly when in each other’s country.

 

RD Lawrence is commemorated by an annual Lawrence lecture given by a young researcher in the field of diabetes to the Medical & Scientific Section of the BDA and by the Lawrence Medal awarded to patients who have been on insulin for 60 years or more. The BDA, now Diabetes UK remains his lasting memorial.

 

Immune Cells in the Retina Can Spontaneously Regenerate

 

The retina is a thin layer of cells in the back of the eye that includes light-sensing photoreceptor cells and other neurons involved in transmitting visual information to the brain. Mixed in with these cells are microglia, specialized immune cells that help maintain the health of the retina and the function of retinal neurons. Microglia are also present in other parts of the central nervous system, including the brain. In a healthy retina, communication between neurons and microglia is important for maintaining the neuron’s ability to send signals to the brain. When the retina is injured, however, microglia have an additional role: They migrate quickly to the injury site to remove unhealthy or dying cells. However, they can also remove healthy cells, contributing to vision loss. Studies show that in degenerative retinal disorders like age-related macular degeneration (AMD) and retinitis pigmentosa (RP), inhibiting or removing microglia can help retain photoreceptors, and thus slow vision loss. But return of microglia is still important to support the retina’s neurons.

 

According to an article published online in Science Advances (21 March 2018), microglia can completely repopulate themselves in the retina after being nearly eliminated. The cells also re-establish their normal organization and function. The findings point to potential therapies for controlling inflammation and slowing progression of rare retinal diseases such as RP and AMD, the most common cause of blindness among Americans 50 and older.

 

The authors were interested in understanding what happens in the retina after microglia have been eliminated, particularly whether the cells could return to their normal arrangement and fulfill their normal functions. To test this, they depleted the microglia in the retinas of mice using the drug PLX5622 (Plexxikon), which blocks the microglial CSF-1 receptor. Microglia depend on continuous signals through this receptor for survival. Interruption of this signaling for several days caused the microglia to nearly disappear, leaving just a few cells clustered around the optic nerve — the cable-like bundle of nerve fibers that carries signals from the retina to the brain. Since loss of microglia for a short time doesn’t affect the function of neurons, removing microglia temporarily — in order to reduce inflammation for example — could potentially be useful as a therapeutic intervention for degenerative or inflammatory disorders of the retina.

 

Within 30 days after stopping the drug, the authors found that the microglia had repopulated the retina, returning to normal density after 150 days. Using a novel method for visually tracking microglial movements in the retina, they determined that the returning microglia initially grew in clusters near where the optic nerve leaves the eye. Gradually, new microglia expanded outwards towards the edges of the retina. Over time, the cells re-established an even distribution across and through the various layers of the retina.

 

To test whether the new microglia were fully functional, the authors used an injury model where photoreceptor cells are damaged by bright light. The new microglia were able to activate and migrate to the injury site normally. In addition, using electroretinography (ERG), a technique that measures the electrical signals generated by retinal neurons after being stimulated with light, the researchers tested the health of different groups of neurons. They found that the microglia were able to communicate with and fully maintain the function of neurons in the retina, especially when the depletion was short-lived.

 

Drugs that remove microglia are now administered systemically, affecting the brain and other parts of the central nervous system. According to the authors, more research is needed to find ways to administer these drugs directly to the retina, sparing off-target tissues.

 

New Genetic Mutation Link to ALS

 

KIF5A regulates part of the kinesin family of proteins that serve as tiny intracellular motors. Problems with these proteins are connected to amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, Parkinson’s disease and Alzheimer’s disease. KIF5A mutations were previously known to be connected to two other rare neurodegenerative diseases with muscle weakening, stiffening and spasticity symptoms similar to ALS: hereditary spastic paraplegia type 10 (SPG10) and Charcot-Marie-Tooth Type 2 (CMT2.) Scientists suspected KIF5A might be associated with ALS but lacked definite proof until now.

 

Now, according to an article published in Neuron (21 March 2018), Kinesin family member 5A (KIF5A), has been definitively connected to ALS. The findings identify how mutations in KIF5A disrupt transport of key proteins up and down long, threadlike axons that connect nerve cells between the brain and the spine, eventually leading to the neuromuscular symptoms of ALS.

 

According to the NIH, it took a comprehensive, collaborative effort to analyze a massive amount of genetic data to pin down KIF5A as a suspect for ALS. To zero in on KIF5A, the NIH team performed a large-scale genome-wide association study, while the University of Massachusetts team concentrated on analyzing rare variants in next generation sequence data. Over 125,000 samples were used in this study, making it by far the largest such study of ALS performed to date.

 

According to the authors, axons extend from the brain to the bottom of the spine, forming some of the longest single cellular pathways in the body, and that KIF5A helps to move key proteins and organelles up and down that axonal transport system, controlling the engines for the nervous system’s long-range “cargo trucks.“ This mutation disrupts that system, causing the symptoms we see with ALS. The authors cautioned that the discovery, while exciting, still leaves much more work to be done. The authors added that next steps for the project include further study of the frequency and location of mutations within KIF5A and determining what cargos are being disrupted.

 

Device Cleared That Senses Optimal Time to Check Intraocular Pressure

 

Elevated IOP is often associated with the optic nerve damage that is characteristic of glaucoma, the leading cause of vision loss that affects an estimated 3 million Americans.. Many patients have no symptoms until significant vision has been lost, and this loss is irreversible. intraocular pressure (IOP) varies throughout the day and may not be abnormally high when the patient is at an eye care professional’s office having an eye exam. For example, it is common for IOP to increase during sleep when the patient is lying down.

 

The FDA has allowed marketing of a one-time use contact lens that may help practitioners identify the best time of day to measure a patient’s intraocular pressure (IOP). The Triggerfish has a sensor embedded in a soft silicone contact lens that detects tiny changes or fluctuations in an eye’s volume. The device is worn for a maximum of 24 hours, transmitting data wirelessly from the sensor to an adhesive antenna worn around the eye. A portable data recorder worn by the patient receives information from the antenna and can transfer the data via Bluetooth to the clinician’s computer, which shows the range of time during the day the pressure of the eye may be increasing. The device does not actually measure IOP and is not intended to be a diagnostic tool.

 

The Triggerfish is indicated for use in adults age 22 and older under the direction and supervision of a health care professional. Clinical data supporting the marketing authorization of the Triggerfish included several studies of the safety and tolerability of the contact lenses and the effectiveness of the device measurement. The effectiveness of the device was demonstrated by showing an association between the Triggerfish device output and IOP fluctuation. The most common temporary side effects were pressure marks from the contact lens, ocular hyperemia (red eyes) and punctate keratitis (irritation of the cornea). The FDA reviewed the data for the Triggerfish through the de novo premarket review pathway, a regulatory pathway for some low- to moderate-risk medical devices that are not substantially equivalent to an already legally-marketed device.

 

The Triggerfish is manufactured by Sensimed AG of Lausanne, Switzerland.

 

Tofu with Butternut Squash Noodles, Kale, Black Beans & Peanut Sauce

It’s taken a long time to really enjoy tofu, but finally, we’re converts. Tofu should never be thought of as a meat or poultry substitute. It stands on its own. If cooked correctly and creatively it’s really delicious. And, like anything else, a good sauce enhances. I’ve been experimenting for a long time, and finally have created two tofu recipes that can be shared. This is the first. ©Joyce Hays

 

Tofu & Veggie Ingredients

1 red onion, chopped

10 garlic cloves, sliced

2 packs of firm silken tofu, cut into small (3/4“) bite-size squares. Put tofu in the freezer the night before and thaw the next day before cooking.

 

Cutting the tofu after it thaws. ©Joyce Hays, Target Health Inc.

 

1 box cremini or baby bella mushrooms, cleaned with damp cloth, then sliced

1 handful of Kale or baby spinach (wash spinach 3 times), washed well, drained, dried, chopped

Sesame oil for cooking tofu

2 eggs, beaten, for cooking tofu

2 Tablespoons Panko small size, for cooking tofu

1 box of butternut squash noodles or make your own spirals

1/2 to 1 can black beans, rinsed and drained

 

Easy to find ingredients. Use either kale or spinach. We’ve tried both and each is good. ©Joyce Hays, Target Health Inc.

  

Directions For Tofu and Veggies

 

Dip each small piece of tofu into egg, then panko and cook in sesame oil on each side for 2 minutes in a wok or skillet, Cook each side of tofu ONLY ONCE.

 

Dip each piece of tofu in beaten egg, then in Panko (smallest size) ©Joyce Hays, Target Health Inc.

  

Then with tongs, (and a very narrow spatula) turn each nugget of tofu to another side and cook for 2 minutes. Do this turning two more times until each nugget is cooked on all four sides. Do not go back and re-cook any side, or the crispy outside will start to crumble away. You want to try to get each piece of tofu nice and brown and crisp on the outside. When done, drain on paper towel on a plate and set aside.

 

Cooking the tofu in sesame oil. ©Joyce Hays, Target Health Inc.

 

In the same skillet, saute over medium flame, the onion and garlic, until both turn golden. Next add the squash noodles, black beans and kale and mix all the veggies together. When the kale has wilted down, the veggies are done. Set aside and concentrate on the peanut sauce.

 

Veggies have been cooked, put into baking/serving dish and tossed with peanut sauce. ©Joyce Hays, Target Health Inc.

 

Directions For Peanut Sauce

Preheat oven to 400 degrees

In a small bowl add 1 or 2 Tablespoons sesame oil, and let 10 fresh garlic cloves, sit in the oil for 10 to 15 minutes. With a slotted spoon, remove the garlic and put on a baking sheet. Roast in oven until soft; then remove and allow to cool down.

Save the sesame oil for cooking the tofu cubes.

 

First, when I used a food processor, it was harder to judge the quality of the sauce, which was way too thick, like lumpy. I had to add 5 Tablespoons of rice vinegar and pulsed; still too thick, so I added, slowly, 1/2 cup of cold water. The photo above is after adding the extra liquid, while pulsing. Eventually, I got it right, but whisking this sauce in a bowl the second time, was easier. Scroll down for the peanut sauce recipe. ©Joyce Hays, Target Health Inc.

  

Final Serving Veggie Combo Directions

Put the veggie combo of: squash noodles, kale, beans into a large serving (baking dish). Add half of the peanut sauce and toss the veggies with the sauce until everything is well mixed.

Add the cooked tofu on top of the mixed noodles and black beans.

Using a small spatula, scrape the other half, of the sauce out of your bowl or the food processor, and over the tofu.

Warm in the oven for about 5 to 10 minutes, depending on your oven. Keep your eye on this recipe after 5 minutes, and remove it when you feel it’s nice and warm to serve.

Consider serving with rice, pasta, polenta

 

Homemade Peanut Sauce (easy)

Ingredients

Zest of 1 lime

Juice of 1 lime

1/2 cup peanut butter

1 teaspoon curry

1 pinch chili flakes

1/2 cup water

1 Tablespoon reduced-sodium soy sauce

1 Tablespoon fresh ginger, peeled, grated, or very well minced

1 teaspoon brown sugar

1 teaspoon garlic, very well minced

1 teaspoon rice vinegar (don’t substitute white vinegar; it’s too strong; whereas the rice vinegar has a more delicate flavor that blends will with the other ingredients.

 

Directions

In a medium serving bowl, combine all of the above ingredients: peanut butter, water, soy sauce, ginger, brown sugar, minced garlic, and vinegar in a bowl, stirring with a whisk until smooth.

If you feel that the sauce is too thick, slowly add more of either rice vinegar, or plain water, whisking as you add, until you get the consistency you want.

I suppose you could put everything into a food processor, but then you have to wash that out. I’ve done both, and the hand whisk was easier and less work. Your choice.

 

The end result was delicious, healthy and relatively easy. I’m working on another tofu recipe next week. ©Joyce Hays, Target Health Inc.

 

Our custom seems to be, when we find a new wine we both like, we drink it endlessly, until we run into some other wine adventure. We’ve gone through two cases of The Vice, but we’re still enjoying it, so will order two more. ©Joyce Hays, Target Health Inc.

 

We went with our house guests to the B’way show, The Band’s Visit. The dialogue was in English, Hebrew and Arabic and so was the music. For us, this alone, was reason enough to go. The plot sounds simple (An Egyptian Band with a concert date in Israel, gets lost and ends up in the wrong Israeli town), however, it’s as simple as life itself, not.

 

This show opened last year, at one of the theater clubs we sponsor, The Atlantic Theater Company in Chelsea. After it overwhelmed audiences there in 2017, it moved uptown to the Barrymore in 2018, to rave reviews. We urge you to go. You might be interested in reading the reviews of the New York Times.

 

Have a great week everyone!

From Our Table to Yours