Conference on Rare Diseases and Orphan Products

 

Target Health will attend & exhibit at the US Conference on Rare Diseases and Orphan Products, October 22-24, 2012 at the Capitol Hilton in Washington, DC. Warren Pearlson will be representing Target Health at our table top exhibit. If you attend, please stop by and say hello.

 

Orphan Product Designations

 

1.  Alagille Syndrome

2.  Burn progression in hospitalized patients

3.  Caries prevention, head and neck cancer

4.  Cushing’s syndrome secondary to ectopic ACTH secretion

5.  Debridement in hospitalized patients with 3rd degree burns

6.  Edema-related effects in hospitalized patients with 3rd degree burns

7.  Gaucher Disease

8.  Hereditary angioedema

9.  Osteonecrosis of the jaw

10. Scleroderma (FDA/EMA)

 

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 at www.targethealth.com

Tuberculosis

 

 

According to WHO and CDC, in 2008, there were 8.8 million new cases of tuberculosis (TB) reported worldwide. In 2011, there were 10,521 new cases in the US. Tuberculosis (TB) is a potentially fatal contagious disease that can affect almost any part of the body but is mainly an infection of the 1) ___. It is caused by a bacterial microorganism, the tubercle bacillus or Mycobacterium tuberculosis. Although TB can be treated, cured, and can be prevented if persons at risk take certain drugs, scientists have never come close to wiping it out globally. Few diseases have caused so much distressing illness for centuries and claimed so many lives.

 

TB was popularly known as 2) ___ for a long time. Scientists know it as an infection caused by M. tuberculosis. In 1882, the microbiologist Robert Koch discovered the tubercle bacillus, at a time when one of every seven deaths in Europe was caused by TB. Because antibiotics were unknown, the only means of controlling the spread of infection was to isolate patients in private sanitoria or hospitals limited to patients with TB – a practice that continues to this day in many countries. The net effect of this pattern of treatment was to separate the study of tuberculosis from mainstream medicine. Entire organizations were set up to study not only the disease as it affected individual patients, but its impact on the society as a whole. At the turn of the twentieth century more than 80% of the population in the United States were infected before age 20, and tuberculosis was the single most common cause of 3) ___. By 1938 there were more than 700 TB hospitals in this country.

 

Tuberculosis spread much more widely in Europe when the industrial revolution began in the late nineteenth century. The disease became widespread somewhat later in the United States, because the movement of the population to large cities made overcrowded housing so common. When streptomycin, the first 4) ___ effective against M. tuberculosis, was discovered in the early 1940s, the infection began to come under control. Although other more effective anti-tuberculosis drugs were developed in the following decades, the number of cases of TB in the United States began to rise again in the mid-1980s. This upsurge was in part again a result of overcrowding and unsanitary conditions in the poor areas of large cities, prisons, and homeless shelters. Infected visitors and immigrants to the United States have also contributed to the resurgence of TB. An additional factor is the AIDS epidemic. AIDS patients are much more likely to develop tuberculosis because of their weakened 5) ___ systems. There still are an estimated 8-10 million new cases of TB each year worldwide, causing roughly 3 million deaths.

 

TB spreads by droplet infection. This type of transmission means that when a TB patient exhales, coughs, or sneezes, tiny droplets of fluid containing tubercle bacilli are released into the 6) ___. This mist, or aerosol as it is often called, can be taken into the nasal passages and lungs of a susceptible person nearby. Tuberculosis is not, however, highly contagious compared to some other infectious diseases. Only about one in three close contacts of a TB patient, and fewer than 15% of more remote contacts, are likely to become infected. As a rule, close, frequent, or prolonged contact is needed to spread the disease. Of course, if a severely infected patient emits huge numbers of bacilli, the chance of transmitting infection is much greater. Unlike many other infections, TB is not passed on by contact with a patient’s clothing, bed linens, or dishes and cooking utensils. The most important exception is pregnancy. The fetus of an infected mother may contract TB by inhaling or swallowing the bacilli in the 7) ___ fluid.

 

Once inhaled, tubercle bacilli may reach the small breathing sacs in the lungs (the alveoli), where they are taken up by cells called 8) ___. The bacilli multiply within these cells and then spread through the lymph vessels to nearby lymph nodes. Sometimes the bacilli move through blood vessels to distant organs. At this point they may either remain alive but inactive (quiescent), or they may cause active disease. Actual tissue damage is not caused directly by the tubercle bacillus, but by the reaction of the person’s tissues to its presence. In a matter of weeks the host develops an immune response to the bacillus. Cells attack the bacilli, permit the initial damage to heal, and prevent future disease permanently.

 

Infection does not always mean disease; in fact, it usually does not. At least nine of ten patients who harbor M. tuberculosis do not develop symptoms or physical evidence of active disease, and their x-rays remain negative. They are not contagious; however, they do form a pool of infected patients who may get sick at a later date and then pass on TB to others. It is thought that more than 90% of cases of active tuberculosis come from this pool. In the United States this group numbers 10-15 million persons. Whether or not a particular infected person will become ill is impossible to predict with certainty. An estimated 5% of infected persons get sick within 12-24 months of being infected. Another 5% heal initially but, after years or decades, develop active tuberculosis either in the lungs or elsewhere in the 9) ___. This form of the disease is called reactivation TB, or post-primary disease. On rare occasions a previously infected person gets sick again after a later exposure to the tubercle bacillus.

 

Pulmonary tuberculosis is TB that affects the lungs. Its initial symptoms are easily confused with those of other diseases. An infected person may at first feel vaguely unwell or develop a 10) ___ blamed on smoking or a cold. A small amount of greenish or yellow sputum may be coughed up when the person gets up in the morning. In time, more sputum is produced that is streaked with blood. Persons with pulmonary TB do not run a high 11) ___, but they often have a low-grade one. They may wake up in the night drenched with cold sweat when the fever breaks. The patient often loses interest in food and may lose weight. Chest pain is sometimes present. If the infection allows air to escape from the lungs into the chest cavity (pneumothorax) or if fluid collects in the pleural space (pleural effusion), the patient may have difficulty breathing. If a young adult develops a pleural effusion, the chance of tubercular infection being the cause is very high. The TB bacilli may travel from the lungs to lymph nodes in the sides and back of the neck. Infection in these areas can break through the skin and discharge pus. Before the development of effective antibiotics, many patients became chronically ill with increasingly severe lung symptoms. They lost a great deal of weight and developed a wasted appearance. This outcome is uncommon today – at least where modern treatment methods are available.

 

Although the lungs are the major site of damage caused by tuberculosis, many other organs and tissues in the body may be affected. The usual progression is for the disease to spread from the lungs to locations outside the lungs (extrapulmonary sites).

 

In the United States, for example, the incidence of newly reported cases of TB has fallen steadily since 1992 to its lowest level ever, and in 2002 (last report) was 5.2/100,000 population, a stunning public 12) ___ accomplishment. Such impressive progress, however, is found only in rich (industrialized) nations, although problems remain in many of their marginalized inner-city communities; moreover, the reverse is occurring in many poor (developing) countries, which is where the great majority, 86%, of the world’s total population live. And not only are these destitute regions home to 95% of all the world’s cases of active tuberculosis and 98% of the nearly 2 million deaths from the disease each year, exactly the same countries are now being ravaged by the pandemic of human immunodeficiency virus (HIV) infection – the most powerful factor ever known to favor the development of tuberculosis.

 

ANSWERS: 1) lungs; 2) consumption; 3) death; 4) antibiotic; 5) immune; 6) air; 7) amniotic; 8) macrophages; 9) body; 10) cough; 11) fever; 12) health

 

Medicine at the Time of John Keats (1795-1821)

 

19th century painting of John Keats, who never got nearer to a university classroom than the front door, became in his quarter-century of life both a physician and one of the great English poets

 

 

There is general agreement that consumption, the common name for tuberculosis (TB) in its early days, increased dramatically in Europe and North America during the 17th and 18th centuries and then began to decline. Death rates from TB peaked in the year 1800, a phenomenon linked to the socioeconomic conditions (overcrowding, poor nutrition, lack of hygiene and sanitation, dearth of medical care) that prevailed during the early years of the unfolding industrial revolution (1750-1850). Mortality from TB was colossal: one of every four deaths recorded in parish registries from England at the end of the eighteenth century was attributed to this disease TB affected those who had been poorly fed and were under nourished. It also affected those who lived in dirty and damp homes. TB can be spread by a person breathing in the exhaled sputum of someone who already has the disease. In the overcrowded tenements of the industrial cities, one infected person could spread the disease very easily. Though accurate records are difficult to acquire, it is believed that TB killed one-third of all those who died in Britain between 1800 and 1850.

 

In April 1804, when Keats was eight, his father died. The cause of death was a skull fracture suffered when he fell from his horse while returning from a visit to John and his brother George at school. Thomas Keats died intestate. Keat’s mother, Frances, remarried two months later, but left her new husband soon afterwards, and the four children went to live with their grandmother, Alice Jennings, in the village of Edmonton. In March 1810, when Keats was 14, his mother died of TB, leaving the children in the custody of their grandmother. That autumn, Keats left Clarke’s school to apprentice with Dr. Thomas Hammond, a surgeon and apothecary who was a neighbor and the doctor of the Jennings family. Keats lodged in the attic above the surgery at 7 Church Street until 1813. Cowden Clarke, who remained a close friend of Keats, described this period as “the most placid time in Keats’s life.”

 

Having finished his apprenticeship with Dr. Hammond, Keats registered as a medical student at Guy’s Hospital (now part of King’s College London) and began studying there in October 1815. Within a month of starting, he was accepted as a dresser at the hospital, assisting surgeons during operations, the equivalent of a junior house surgeon today. However, Keats’s training took up increasing amounts of his writing time, and he was increasingly ambivalent about his medical career. He felt that he faced a stark choice. Keats’s first surviving poem, “An Imitation of Spenser,” had been written in 1814, when he was 19. Now, strongly drawn by ambition, inspired by fellow poets such as Leigh Hunt and Lord Byron, and beset by family financial crises, he suffered periods of depression. His brother George wrote that John “feared that he should never be a poet, & if he was not he would destroy himself”. In 1816, Keats received his apothecary’s license, which made him eligible to practice as an apothecary, physician, and surgeon, but before the end of the year he announced to his guardian that he was resolved to be a poet, not a surgeon.

 

Although he continued his work and training at Guy’s Hospital in London, Keats devoted more and more time to the study of literature, experimenting with verse forms, particularly the sonnet. In May 1816, Leigh Hunt, well known publisher, agreed to publish the sonnet “O Solitude” in his magazine The Examiner, a leading liberal magazine of the day. It was the first appearance in print of Keats’s poetry. However, later that year, he committed himself for further study in order to become a member of the Royal College of Surgeons.

 

Keats changed publishers to Taylor and Hessey because they were highly enthusiastic about his work. Within a month of the publication of Poems they were planning a new Keats volume and had paid him an advance. Hessey became a steady friend to Keats and made the company’s rooms available for young writers to meet. Their publishing lists eventually included, in addition to Keats, Coleridge, Hazlitt, Clare, Hogg, Carlyle and Lamb.

 

‘Beauty is truth, truth beauty’ – that is all / you know on earth, and all ye need to know”. In early December, under the heady influence of his artistic friends, Keats had decided to give up medicine in favor of poetry. Having left his training at the hospital, suffering from a succession of colds, and unhappy with living in damp rooms in London, Keats moved with his brothers into rooms at 1 Well Walk in the village of Hampstead in April 1817.

 

On September 21, 1819, John Keats wrote to his brother George that he was “scarcely content to write the best verses for the fever they leave behind. I want to compose without this fever.” The fever is no metaphor. In another letter dated that same day, he had sent a friend a copy of his poem “To Autumn,” written just then, one of the greatest poems in the English language and the last of Keats’s great odes. For Keats, poetry was never emotion recollected in tranquility, as it was for Wordsworth. It was often tranquility refigured by his fevered mind.

 

A portrait of John Keats by his friend Joseph Severn. Credit:Hulton Archive/Getty Images

 

 

The mental fever of making poems was, for Keats, a medical issue. When he fell ill, beginning in 1817, the doctors always tried to stop him from writing poetry. One physician kept dosing Keats with mercury, hoping to cure his recurring sore throat and perhaps a case of venereal disease, for which mercury, a dangerous substance, was a standard treatment at the time. And every doctor – even Keats himself, who had medical training – advised the use of laudanum, a tincture of opium in alcohol. Keats had given it to his brother Tom in late 1818 to ease his pain and suppress his tubercular cough when he was dying, and Keats had used it to help himself sleep during that terrible time. For someone as ill as Keats would be, it was a palliative, not a hallucinogen. That he used it makes no difference at all to our estimate of the man or his poems.

 

As Nicholas Roe writes in his new biography of Keats, “it is difficult to appreciate how commonplace an opium habit was in Keats’s lifetime.” Opium was dispensed “as a matter of course, and for a simple reason: it was the only painkiller that worked.” Keats had seen opium used regularly during his medical training, and there is no question that he took laudanum as early as 1818.

 

Having left his training at the hospital, suffering from a succession of colds, and unhappy with living in damp rooms in London, Keats moved with his brothers into rooms at 1 Well Walk in the village of Hampstead in April 1817. Both John and George nursed their brother Tom, who was suffering from TB. In July 1817, while on the Isle of Mull, Keats caught a bad cold and “was too thin and fevered to proceed on the journey.”After his return south in August, Keats continued to nurse Tom, exposing himself to infection. Some biographers suggest that this is when John Keats succumbed to TB, his “family disease.” His brother Tom Keats died on 1 December 1818.

 

During 1820 Keats displayed increasingly serious symptoms of TB, suffering two lung hemorrhages in the first few days of February. Hunt nursed him in London for much of the following summer. At the suggestion of his doctors, he agreed to move to Italy. On 13 September, they left for Gravesend and four days later boarded the sailing brig “Maria Crowther”, where he made the final revisions of “Bright Star”. The journey was a minor catastrophe: storms broke out followed by a dead calm that slowed the ship’s progress. When they finally docked in Naples, the ship was held in quarantine for ten days due to a suspected outbreak of cholera in Britain. Keats reached Rome on 14 November, by which time any hope of the warmer climate he sought had disappeared.

 

Keats wrote his last letter on 30 November 1820 to Charles Armitage Brown; “Tis the most difficult thing in the world to me to write a letter. My stomach continues so bad, that I feel it worse on opening any book – yet I am much better than I was in Quarantine. Then I am afraid to encounter the proing and conning of any thing interesting to me in England. I have an habitual feeling of my real life having past, and that I am leading a posthumous existence.”

 

Keats moved into a villa on the Spanish Steps, today the Keats-Shelley Memorial House museum. Despite care, his health rapidly deteriorated, and the medical attention he received may have hastened his death.In November 1820, Keats was placed on a starvation diet of an anchovy and a piece of bread a day, hoping to reduce the blood flow to his stomach. On 10 December 1820, Keats began to cough and then vomit blood. Clark was summoned and promptly bled him. The loss of blood dizzied and confused Keats. When Clark left, Keats got out of his bed, stumbled around the rooms, and said to Severn, “This day shall be my last.” Severn feared a suicide attempt and hid any sharp object he could find as well as the laudanum prescribed by Clarke. Keats was delirious for the rest of the day, until a violent hemorrhage and bleeding weakened him into calm. Over the next nine days he suffered five severe hemorrhages and continued bleedings by Clark. The doctor visited constantly and put him on a strict diet, mostly fish. Keats begged for food, believing he was being starved. Clark held no hope of recovery and admitted as much to Keats. The poet’s thoughts turned again to suicide and he begged Severn for the laudanum, at first appealing to Severn’s self-interest, but he was refused. Keats became angry; he raged at Severn for keeping him alive against his will. When Severn, not trusting himself, gave the bottle to Clark, Keats turned on the doctor asking “How long is this posthumous life of mine to last?”

 

The first months of 1821 marked a slow and steady decline into the final stage of TB. Keats was coughing up blood and covered in sweat. Severn nursed him devotedly and observed in a letter how Keats would sometimes cry upon waking to find himself still alive. Severn writes,

“Keats raves till I am in a complete tremble for him about four, the approaches of death came on. [Keats said] ‘Severn-I-lift me up-I am dying-I shall die easy; don’t be frightened—be firm, and thank God it has come.’ I lifted him up in my arms. The phlegm seem’d boiling in his throat, and increased until eleven, when he gradually sank into death, so quiet, that I still thought he slept.”

 

John Keats died in Rome on 23 February 1821

 

Editor’s bit of trivia: While researching John Keats and his environment of London and the English countryside, I discovered the Village of Bo Peep, near the town of Hastings. I smiled in recognition that everyone’s childhood poem of “Little Bo Peep” was based in the reality of a mapped location.

Sources: The New York Times, Nicholas Roe’s new biography of Keats, Wikipedia

Healthy Diet Linked to Reduced Type 2 Diabetes Risk Post-Pregnancy

 

The body uses insulin, produced in the pancreas, to move the sugar glucose from the blood and into the cells. In people with type 2 diabetes, cells do not respond appropriately to insulin, and, if untreated, blood sugar reaches high levels. Complications of diabetes include heart disease, stroke, kidney disease, blindness and amputation.

 

Research has shown that, among the general population, healthy eating can reduce the risk of developing type 2 diabetes and that before they conceive, women who follow a diet low in cholesterol and animal fat, low in sugar sweetened beverages, but high in fiber, and who are physically active have a reduced risk of gestational diabetes.

 

In about 5% of U.S. pregnancies, women who do not have diabetes before becoming pregnant develop high blood sugar levels in pregnancy. This condition, called gestational diabetes, raises a woman’s risk of developing type 2 diabetes later in life up to sevenfold, compared to pregnant women who don’t have gestational diabetes. Little is known about the role healthy lifestyle factors may have in preventing progression from gestational diabetes to type 2 diabetes later in life.

 

According to an article published online in the Archives of Internal Medicine (9 October 2012), by sticking to a healthy diet in the years after pregnancy, women who develop diabetes during pregnancy can greatly reduce their risk of developing type 2 diabetes. Previously, it was not known how much the risk for type 2 diabetes in these women could be lowered through adhering to healthy diet.

 

The study found the greatest reductions in type 2 diabetes risk were for women who followed diets rich in whole grains, fresh fruits, vegetables, and legumes, and included poultry, seafood, and nuts, with limiting intake of red and processed meats. Those who followed this type of diet in the years after having gestational diabetes consistently reduced their risk by about half that of women who did not.

 

This study included 4,413 women who developed gestational diabetes between 1991 and 2001. The women were taking part in a long-term study of nurses called the Nurses’ Health Study II. As part of the ongoing study, the nurses filled out questionnaires every other year on lifestyle and health. They completed a questionnaire every four years about their intake of several common food items during the previous year. The researchers ranked the women’s responses in terms of how closely they adhered to three widely studied diets: < >

 

1        Mediterranean-style diet

2        Dietary Approaches to Stop Hypertension — or DASH diet

3        Healthy Eating Index, a measure of how closely an individual follows the healthy eating guidelines developed by the United States Department of Agriculture.

 

All three diets promote eating fruits, vegetables, nuts, legumes and whole grains.

 

Of the women in the study, 491 later developed type 2 diabetes. The researchers found that women who adhered most closely to these diets (scores in the top 25%) lowered their risk for type 2 diabetes considerably when compared to the least compliant group (lowest 25%):

 

Mediterranean Diet (40% lower risk)

Dash Diet (46% lower risk)

Healthy Eating Index pattern (57% lower risk)

 

On average, these women developed type 2 diabetes about 14 years after they had experienced gestational diabetes.

Detailed View of Brain Protein Structure

 

Binding of neurotensin initiates a series of reactions in nerve cells. Previous studies have shown that neurotensin may be involved in Parkinson’s disease, schizophrenia, temperature regulation, pain, and cancer cell growth.

 

X-ray crystallography is a technique in which scientists shoot X-rays at crystallized molecules to determine a molecule’s shape and structure. The X-rays change directions, or diffract, as they pass through the crystals before hitting a detector where they form a pattern that is used to calculate the atomic structure of the molecule. These structures guide the way scientists think about how proteins work.

 

Neurotensin receptors and other GPCRs belong to a large class of membrane proteins which are activated by a variety of molecules, called ligands. Previous X-ray crystallography studies showed that smaller ligands, such as adrenaline and retinal, bind in the middle of their respective GPCRs and well below the receptor’s surface.

 

According to a paper published online in Nature (10 October 2012), the first highly detailed description of how neurotensin, a neuropeptide hormone which modulates nerve cell activity in the brain, interacts with its receptor has been identified. Their results suggest that neuropeptide hormones use a novel binding mechanism to activate a class of receptors called G-protein coupled receptors (GPCRs).

 

The study used X-ray crystallography to show what the receptor looks like in atomic detail when it is bound to neurotensin. The results provide the most direct and detailed views describing this interaction which may change the way scientists develop drugs targeting similar neuropeptide receptors.

GENETICS

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Sugar-Sweetened Beverages and Genetic Risk of Obesity

 

Temporal increases in the consumption of sugar-sweetened beverages have paralleled the rise in obesity prevalence, but whether the intake of such beverages interacts with the genetic predisposition to adiposity is unknown.

 

As a result, a study published in the New England Journal of Medicine (2012; 367:1387-1396) was performed to the interaction between genetic predisposition and the intake of sugar-sweetened beverages in relation to body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) and obesity risk in 6934 women from the Nurses’ Health Study (NHS) and in 4,423 men from the Health Professionals Follow-up Study (HPFS) and also in a replication cohort of 21,740 women from the Women’s Genome Health Study (WGHS). The genetic-predisposition score was calculated on the basis of 32 BMI-associated loci. The intake of sugar-sweetened beverages was examined prospectively in relation to BMI.

 

Results showed in the NHS and HPFS cohorts, that the genetic association with BMI was stronger among participants with higher intake of sugar-sweetened beverages than among those with lower intake. In the combined cohorts, the increases in BMI per increment of 10 risk alleles were 1.00 for an intake of less than one serving per month, 1.12 for one to four servings per month, 1.38 for two to six servings per week, and 1.78 for one or more servings per day (P<0.001 for interaction). For the same categories of intake, the relative risks of incident obesity per increment of 10 risk alleles were 1.19, 1.67, 1.58, and 5.06 (P=0.02 for interaction). In the WGHS cohort, the increases in BMI per increment of 10 risk alleles were 1.39, 1.64, 1.90, and 2.53 across the four categories of intake (P=0.001 for interaction); the relative risks for incident obesity were 1.40, 1.50, 1.54, and 3.16, respectively (P=0.007 for interaction).

 

According to the authors, the genetic association with adiposity appeared to be more pronounced with greater intake of sugar-sweetened beverages.

TARGET HEALTH excels in Regulatory Affairs. Each week we highlight new information in this challenging area

 

FDA Statement on Fungal Meningitis Outbreak

 

On October 6, 2012, the New England Compounding Center (NECC), following an earlier recommendation by FDA that none of the firm’s compounded products be used, announced a voluntary recall of all products currently in circulation that were compounded at and distributed from its facility in Framingham, Massachusetts.

 

FDA is working closely with the CDC and state partners to investigate an outbreak of meningitis among patients who had received an epidural steroid injection. Investigation into the exact source of the outbreak is still ongoing, but the outbreak is associated with a potentially contaminated medication. That product is preservative-free methylprednisolone acetate (80mg/ml), an injectable steroid produced and distributed by New England Compounding Center (NECC) in Framingham, Massachusetts. CDC’s interim data show that all infected patients received injection with this product. As of Oct 3, 2012, NECC has voluntarily shut down.

 

FDA has observed fungal contamination by direct microscopic examination of foreign matter taken from a sealed vial of methylprednisolone acetate collected from NECC. FDA is in the process of conducting additional microbial testing to confirm the exact species of the fungus. As part of the ongoing investigation, FDA will continue to work closely with CDC and state authorities to determine whether this sample taken from the product matches the organism found in patients. We are working diligently to expedite that process.

 

Out of an abundance of caution, FDA is taking the additional step of recommending that health care professionals and consumers not use any product that was produced by NECC at this time. In addition, FDA requests that health care professionals retain and secure all remaining products purchased from NECC until FDA provides further instructions regarding the disposition of these products.

Scallops For Two From Glen Park

 

Target Health Inc. is fortunate to have many multi-talented people. In addition to our employees’ specialized skills in drug and device development, there is music, art, writing, vocal ability, carpentry, clothing design, photography, investment guru, etc. and lucky for the ON TARGET newsletter’s new Healthy Eating section, we have several serious chefs.

 

Contributed by Dr. Glen Park, Senior Director of Clinical/Regulatory Affairs, Target Health Inc.

 

 

Ingredients

 

  • 1 tbsp olive oil
  • 1 medium shallot
  • 1/2 pound shiitake mushrooms sliced
  • 1/2 bunch kale (black or lancinated preferred, but any good dark green would be good) rinsed, with ribs removed and the leaves cut cross-wise into 1/4 in strips. Do not dry completely. In the bowl, massage the leaves gently for 2-3 minutes to soften them.
  • 1/4 pound cherry tomatoes sliced in half
  • 1/4 cup Chicken stock
  • 2 tbsp Cream
  • 1 tbsp canola oil
  • Sea scallops – 6-12 good sized fresh scallops (depending on whether this is a primo or a secondo)
  • Salt and pepper to season

 

 Directions

  • Over medium heat, add the olive oil to a warm pan and sauté the shallot to soften, but not brown.
  • Increase the heat and add the mushrooms and stir, cooking until they have released their water and are browning on the edges.
  • Add the kale to the pan – the residual water on the leaves from rinsing will provide some moisture to steam.
  • Continue to cook, stirring occasionally until the kale is wilted.
  • Add the tomatoes, cover and cook over low heat until tomatoes start to soften.
  • Meanwhile, dry the scallops with a paper towel and generously season with salt and pepper.
  • Place a sauté pan over high heat and heat until the canola oil is shimmering hot. Carefully place the scallops in the pan separated so they do not touch. Cook for 2-3 minutes on one side, until the scallop releases from the pan with a good sear.
  • Turn over and cook for another 2-3 minutes until seared on the second side, but still soft and slightly translucent in the center (do not overcook).
  • While the scallops are searing, uncover the kale and increase the heat back to high. Add the cream and bring to a boil to thicken.
  • To serve, arrange a bed of kale on the plate and top with scallops.

 

Editor’s note: We have eaten Glen Park’s glorious creations and know that you will want to sop up his sauce/juice with warm bread, so have that on hand. Only because a wine was not included with his scallop recipe, we suggest a Medoc, a light Cabernet, or a rose. And, btw, serve the new Keats “Hippocrene” cocktail, before diving into the amazing scallops.

 

Cheers!

Libation Homage to Keats

 

 

John Keats in a miniature from 1819

What would Keats drink?

 

Last Thursday, at a celebration in Chicago honoring the centenary of Poetry magazine, guests raised a cocktail created especially for the occasion. Named the Hippocrene – the mythological source of poetic inspiration – it is the work of Brian West, a web developer at Columbia College Chicago and cocktail enthusiast, and is primarily inspired by John Keats’s “Ode to a Nightingale.”

 

Mr. West became interested in mixology during the three and a half years he worked as Web producer for the Poetry Foundation, which publishes the magazine. When he was asked to create the drink, he said in an e-mail, he looked at the myth around the Hippocrene spring and the Pegasus, but also at a few lines from “Ode to a Nightingale.” As the tale goes, Pegasus – the winged horse that has long been the symbol of Poetry magazine – struck the mythical Mount Helicon, a peak sacred to the muses, and out gushed the Hippocrene.

 

The fountain is invoked in many poems, including “Ode to a Nightingale.” The lines Mr. West focused on came from the second stanza:

 

O, for a draught of vintage! that hath been
Cool’d a long age in the deep-delved earth,
Tasting of Flora and the country green,
Dance, and Provençal song, and sunburnt mirth!
O for a beaker full of the warm South,
Full of the true, the blushful Hippocrene,
With beaded bubbles winking at the brim,
And purple-stained mouth;
That I might drink, and leave the world unseen,
And with thee fade away into the forest dim:

 

“It was obvious that we needed a sparkling wine,” said Mr. West, pointing to those “beaded bubbles winking” in the stanza’s seventh line. “I was also inspired by the line, ‘Tasting of Flora and the country green,’ to add some herbal notes with gin, mint, ginger and basil,” he said.

 

He found both Prosecco and Korbel Extra Dry performed nicely as the sparkling wine in his concoction, and for the gin – given Keats’s British heritage, what other base spirit would have been appropriate? – Mr. West thinks Ransom Old Tom Gin, Farmer’s Gin and Small’s Gin work best. The ginger in the drink comes in the form of ginger liqueur, and the mint arrives as mint tea. The drink also includes lemon juice, grapefruit juice and grapefruit bitters. (With so many glories of the garden in this concoction, surely Wordsworth would have joined Keats in a glassful.)

 

The event, where the cocktail will be unveiled, will also commemorate the publication of “The Open Door,” an anthology of 100 poems collected from Poetry’s archives, published by the University of Chicago Press. The magazine was founded in Chicago in 1912 by Harriet Monroe.

 

Recipe for “The Hippocrene” (created by Brian West)

 

Ingredients

  • 1 1/4 ounces gin
  • 3/4 ounce ginger liqueur (domaine de canton)
  • 1/2 ounce fresh grapefruit juice
  • 1/4 ounce fresh lemon juice
  • 1 tablespoon mint tea (brewed at double strength) and chilled
  • 2 ounces dry, sparkling wine
  • Fresh basil, for garnish
  • Dash or two grapefruit bitters

 

Method

  • Single glass preparation:
  • Combine all ingredients except sparkling wine, basil, and bitters (if using) in a mixing glass over ice. Stir and strain into a glass and top with remaining ingredients.
  • Punch preparation:
  • Combine all ingredients (in greater quantities) except sparkling wine, basil and bitters in an adequately sized serving bowl, along with some large blocks of ice. It’s best to let this mixture chill and dilute a little while before adding everything else, but if time is short, it could be refrigerated beforehand and water (sparkling or still) can be added along with the rest of the ingredients at service time. The basil should still be added directly to the glass, as it is the aroma and not necessarily the flavor that you’re after. It would also be nice to garnish the mixing bowl with some citrus slices, for color and a generally vigorous appearance.

 

Adapted from The New York Times. Source: Brian West, article by Robert Simonson

The Compounding Conundrum

 

By Mark L. Horn, MD, MPH, Chief Medical Officer, Target Health Inc.

 

Despite the almost overwhelming temptation to comment upon the just completed first presidential debate, this week it is sadly necessary to address a current and ongoing health crisis, a crisis directly related and of profound importance to our industry.

 

As this piece is written the CDC has confirmed 14 deaths and 156 sick individuals in a spreading contagion of aspergillus meningitis now impacting patients in ten states. The source of the infections is suspected to be a contaminated injectable steroid preparation (methylprednisolone acetate) sourced from a single compounding pharmacy in Massachusetts. Over 13,000 individuals may have been exposed. We could all feel a bit better about this if we could innocently ask, ‘how could this happen’; sadly, we cannot. Not only do we know how these events can happen, we can reasonably posit why they happen, are aware that they have occurred before, and most critically, we know that, absent reform, they will almost certainly happen again.

 

Compounding pharmacies serving large markets apparently occupy an imprecisely defined space in the regulatory scheme, somewhere between acknowledged, identified (and federally regulated) manufacturers and pharmacies individualizing medicines for specific patients who may need atypical doses or formulations for unique clinical reasons. As is often so the case in health care these days, the fundamental drivers seem to be financial. Compounders evidently provide cheaper formulations of established medicines intended to treat large numbers of typical patients.

 

What is especially frightening about the current example is that the compounded medicine, an injectable corticosteroid, seems readily available and not especially expensive. Another recent example of infection secondary to compounding included several cases of infectious endophthalmitis attributed to the unlabeled use of a compounded version of bevacizumab to treat age related macular degeneration (AMD). In this instance, the medicine was used as an alternative to an approved, similarly acting and significantly more expensive agent, ranibizumab. In this example, the difference in cost was (and remains) significant.

 

Irrespective of the potential cost savings and the associated criticisms of manufacturers’ designing development, marketing, and pricing strategies to maximize revenue, it seems evident that the current oversight and regulation of compounding pharmacies is inadequate. Whatever one’s philosophical view of government, large scale compounding seems an area where thoughtful and transparent regulation coupled with clear lines of responsibility would potentially eliminate significant morbidity, and sadly now, mortality.

 

So far, in this episode, 14 people are dead, 156 critically sick, and somewhere in the range of 13,000 others can’t be sure if their headache or stiff neck is due to stress and anxiety or is instead the precursor of a potentially deadly illness.

 

It is simply unacceptable, given this event, the recent history of other similar episodes and the likelihood that without change additional episodes will occur, that the ‘status quo’ be allowed to continue.