What Does Target Health Inc. Do For a Living?


Several times a year we are asked what Target Health Inc. does for a living. So here is a brief summary.


In 2013, Target Health will celebrate its 20th year as a New York City-based, full-service e*CRO with full-time staff dedicated to all aspects of the “paperless clinical trial” complementing our expertise in:


1. Drug and Device Strategic Development Planning

2. All aspects of Regulatory Affairs including eCTD submissions

3. Clinical Research Management

4. Biostatistics

5. Data Management

6. Internet-based clinical trials (Target e*CRF®)

7. Medical Writing


In addition to Target e*CRF, we also provide fully validated software for clinical trials including:


1. Target e*CTR® (eSource eClinical Trial Record; fully integrated with Target e*CRF )

2. Target Encoder®(coding MedDRA and WHODrug)

3. Target e*Pharmacovigilance™ (Form 3500A and CIOMS1; fully integrated with Target e*CRF)

4. Target Document® (eTMF)

5. Target e*CTMS® (Clinical Trial Management System)

6. Target Monitoring Reports (fully integrated with Target e*CRF)

7. Target Newsletter™ (fully integrated with Target e*CRF)


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

Ray Kurzweil Teams Up With Google to Tackle Artificial Intelligence


Ray Kurzweil



Think we’ll have artificial intelligence by 2029?  Ray Kurzweil does. He is simultaneously idolized and infamous for saying so. And now he will put his ideas to the test. Last Friday, Kurzweil announced he’s accepted a position with technology giant 1) ___ as Director of Engineering. Like all things exponential, the new relationship is on the fast track. Singularity Hub reached out to Kurzweil to learn what he and Google aim to accomplish. He told us, “We hope to combine my 2) ___ years of experience in thinking about thinking with Google scale resources (in everything—engineering, computing, communications, data, users) to create truly useful AI that will make all of us smarter.”


It’s not surprising Google is interested in Kurzweil’s services. A few years back, Google cofounder Larry Page told Esquire, “We have some people at Google who are trying to build artificial 3) ___, and to do it at a large scale. I don’t think it’s that far off.” In his latest book, How to Create a Mind, Kurzweil says humans can reverse engineer the brain to create artificial intelligence – and similarly says we’ll do it much sooner than anyone thinks. A good match, no?


Kurzweil specializes in machine learning and language processing and will focus on new projects at Google involving both. Some of those skills may help further hone Google’s learning search algorithm, language translation application, and 4) ___ recognition software. But Google has plenty of talent already well versed in those technologies and the firm is known to invest in more ambitious undertakings. The special projects team, Google X, is working on self-driving cars, augmented-reality glasses, and a slew of projects outside the public’s purview. Kurzweil says he will work on AI, and one imagines that may include an attempt to reverse 5) ___ the brain.


It’s a bold objective but not unprecedented. We’ve often written here at Singularity Hub about other similar undertakings. These include Blue Brain Project, IBM SyNAPSE, and Spaun. Fascinating projects, worthy of attention one and all. But imagine what’s possible with Google’s formidable resources – dollars and talent – behind one of AI’s best known and most vocal advocates. Might such a collaboration bump the quest for 6) ___ intelligence up a few years? It can’t hurt.


Scientists Create Artificial Brain With 2.3 Million Simulated Neurons


Another computer is setting its wits to perform 7) ___ tasks. But this computer is different. Instead of the tour de force processing of Deep Blue or Watson’s four terabytes of facts of questionable utility, Spaun attempts to play by the same rules as the human brain to figure things out. Instead of the logical elegance of a CPU, Spaun’s computations are performed by 2.3 million simulated 8) ___ configured in networks that resemble some of the brain’s own networks. It was given a series of tasks and performed pretty well, taking a significant step toward the creation of a simulated brain.


Spaun stands for Semantic Pointer Architecture: Unified Network. It was given 6 different tasks that tested its ability to recognize digits, recall from memory, add numbers and complete patterns. Its cognitive network simulated the prefrontal 9) ___ to handle working memory and the basal ganglia and thalamus to control movements. Like a human, Spaun can view an image and then give a motor response; that is, it is presented images that it sees through a camera and then gives a response by drawing with a robotic arm.


Will AI brains of the future look more like Watson or Spaun?


And its performance was similar to that of a human brain. For example, the simplest task, image recognition, Spaun was shown various numbers and asked to draw what it sees. It got 94% of the numbers correct. In a working memory task, however, it didn’t do as well. It was shown a series of random numbers and then asked to draw them in order. Like us with human brains, Spaun found the pattern recognition task easy, the working memory task not quite as easy.


The important thing here is not how well Spaun performed on the tasks – your average 10) ___ could find ways to perform much better than Spaun. But what’s important is that, in Spaun’s case, the task computations were carried out solely by the 2.3 million artificial neurons spiking in the way real neurons spike to carry information from one neuron to another. The visual image, for example, was processed hierarchically, with multiple levels of neurons successively extracting more complex information, just as the brain’s visual system does. Similarly, the motor response mimicked the brain’s strategy of combining many simple movements to produce an optimal, single movement while drawing.


Chris Eliasmith, from the University of Waterlook in Ontario, Canada and lead author of the study is happy with his cognitive creation. He said, “It’s not as smart as monkeys when it comes to categorization “but it’s actually smarter than monkeys when it comes to recognizing syntactic patterns, structured patterns in the input, that monkeys won’t recognize.” One thing Spaun can’t do is perform tasks in real-time. Every second you saw Spaun performing tasks in the video actually requires 2.5 hours of numbers crunching by its artificial brain. The researchers hope to one day have it perform in real-time. It’s important to note that Spaun isn’t actually learning anything by performing these tasks. Its neural nets are hardwired and are incapable of the modifications that real neurons undergo when we learn. But producing complex behavior from a simulated neuronal 11) ___ still represents an important initial step toward building an artificial brain.


Christian Machens, a neuroscientist at the Champalimaud Neuroscience Programme in Lisbon and was not involved in the study, wrote that the strategy for building a simulated brain is “to not simply incorporate the largest number of neurons or the greatest amount of detail, but to reproduce the largest amount of functionality and behavior.” We’re still a long way from artificial intelligence that is sentient and self-aware. And there’s no telling if the 12) ___ of the future will have brains that look like ours or if entirely different solutions will be used to produce complex behavior. Whatever it looks like, Spaun is a noble step in the right direction.


Interview with Ray Kurzweil


ANSWERS: 1) Google; 2) fifty; 3) intelligence; 4) speech; 5) engineer; 6) artificial; 7) human; 8) neurons; 9) cortex; 10) computer; 11) network; 12) robots

A New Look at Einstein’s Brain May Answer Why He Was So Smart


Thanks to work of pathologist Thomas Harvey to preserve Albert Eisntein’s brain decades ago, we can continue to busy ourselves today with trying to figure out what made Albert Einstein so smart. Knowing the world would want to scrutinize the brain of one of the most brilliant persons to ever live, Harvey took photographs of the brain then cut it into tissue slices which he mounted onto slides and distributed to some of the world’s most prominent neuropathologists who hoped to find an anatomical clue as to how Einstein achieved his startling genius.


The initial analyses didn’t turn up much, except for the fact that Einstein’s brain, counterintuitively, was actually smaller than average. And early tissue studies showed the normal hallmarks of aging, biomarkers that were expected for someone who lived to the age of 76. So Harvey put the brain fragments in a formalin-filled jar, stuck the jar inside a cider box and kept the box under a beer cooler in his office. The fabled brain was pulled out decades later, when, in 1985 a study showed that two parts of Einstein’s brain contained higher amounts of glia, the cells that surround and support neurons. And another study published in the nineties concluded that a groove was missing in one part of the cortex. What was interesting was the area missing the groove is thought to process visuo-spacial information and be important for mathematical skills. The scientists speculated that the missing groove might have enhanced neuronal connections, partially explaining why Einstein’s visuo-spatial and mathematical skills were mindbogglingly enhanced.


Is the key to Einstein’s genius in the folds and grooves of his brain, or did he just do more with what he had?


Now more scientists are revisiting the six decades long curiosity. Dean Falk and her fellow anthropologists at Florida State University in Tallahassee analyzed 14 of Harvey’s original photographs that had only recently been found. Some of the photographs were taken at angles not seen in photos previously studied, offering new views of Einstein’s brain. They compared his brain anatomy to that of 85 brains which had been previously described in two other studies. They found that Einstein’s prefrontal cortex was “highly convoluted” compared to the average amount of convolutions observed in the other brains. The prefrontal cortex is important in higher level, abstract thought. It’s possible that the increased number of folds and fissures in Einstein’s prefrontal cortex contributed to his ability to carry out his famous thought experiments, such as imagining himself traveling alongside a beam of light. The photos also showed a part of Einstein’s right somatosensory cortex was enlarged. The area, which processes sensory information from the left hand, is thought to have overdeveloped due to his extensive violin playing.


Humans, the most intelligent species on the planet, owe their acumen to the evolutionary enlargement of the brain as well as the coincident reorganization of the brain’s connections occurring over time. Regarding intelligence, the most important reorganization is generally accepted to be the increased specialization of the neocortex, the part of the brain responsible for carrying out higher brain functions. One has to wonder, though, about the true power of nature over nurture. Does the secret to Einstein’s genius really lie in the folds and fissures of his brain? Did his extra-specialized prefrontal cortex really give us the special theory of relativity? Currently we cannot definitively answer these questions, but it’s certainly fun to try.


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Genetic Mystery of Behcet’s Disease Unfolds Along the Ancient Silk Road


According to an article published online in Nature Genetics (6 January 2013), four new regions on the human genome associated with Behcet’s disease have been identified.


Named for the Turkish physician who described it in 1937, Behcet’s (pronounced BET’-chets) disease is triggered by complex genetic and environmental factors, and causes inflammation of blood vessels in various parts of the body. Common symptoms include painful mouth and genital sores, and eye inflammation that can lead to blindness. In some cases, it can be life-threatening, affecting blood vessels in the brain, lungs, and other vital organs. About 1 in 250 people in Turkey have Behcet’s disease; others with the disease are found largely in regions along the Silk Road. For nearly 2,000 years, traders used this 4,000-mile network linking the Far East with Europe to exchange goods, culture and, in the case of the Silk Road disease, genes.


Genetic factors are thought to play a role in susceptibility to Behcet’s disease, with the human leukocyte antigen (HLA) B-51 gene region of the genome, accounting for about 20% of genetic risk for the disease. Researchers have been aware of the HLA B-51 association for about 40 years. Two years ago, the authors identified gene associations at two other specific chromosome locations, or loci.


“The current study represents an important advance because it dramatically broadens the spectrum of genetic loci associated with Behcet’s disease,” said Dan Kastner, M.D., Ph.D., scientific director of the Intramural Research Program at the National Human Genome Research Institute and senior author of the study. “These newly discovered genetic associations provide a link between Behcet’s disease and other more common illnesses, and thereby suggest new therapies for Behcet’s disease. In addition, two of the newly discovered genes provide an intriguing link between genes and the microbes in our environment.”


The investigation was a genome-wide association study (GWAS) that enrolled 1,209 Turkish people affected by Behcet’s disease and 1,278 unaffected Turkish people-all residents of the country. The study looked at many points on the human genome called single-nucleotide polymorphisms (SNPs), with each SNP representing a difference in a single DNA building block, called a nucleotide. SNP differences were then compared between people with and without disease. Results showed that from nearly 800,000 SNPs, detected and mapped a small number that are found in those who have Behcet’s disease at a significantly higher rate than in those without the disease, suggesting that the variant or another one nearby contributes to the disease.


Each of the four newly identified gene regions is already known to play a role in immune regulation. The genetic associations have helped classify Behcet’s disease with more common inflammatory conditions such as psoriasis, inflammatory bowel disease and a form of spinal arthritis called ankylosing spondylitis. Among the newly identified regions:


1. An important association was found between Behcet’s disease and a gene called ERAP1. ERAP1 codes for a molecule that processes microbial proteins in white blood cells. Variants of this protein can lead to more or less efficient processing of microbial proteins before they are loaded onto HLA molecules for presentation to the immune system. The variants of ERAP1 identified in this study increase the risk of Behcet’s disease, but only in those individuals with one specific HLA type, HLA-B51, which has previously been associated with Behcet’s disease. Dr. Kastner speculates that the ERAP1 variant associated with Behcet’s disease processes microbial proteins in such a way that they can be loaded onto the HLA-B51 molecule to trigger an abnormal immune response. The very same variant of ERAP1 that is associated with Behcet’s disease is protective for ankylosing spondylitis and psoriasis, but only in people with the HLA types associated with those diseases.


2. A significant association of Behcet’s disease with variants near the CCR1 gene. Proteins coded by this gene help infection-fighting blood cells migrate to sites of invading microorganisms. When this function is defective, the microorganisms can trigger a persistent inflammatory response.


3. An association of the disease with variants in the KLRC4 gene. The function of the receptor protein coded by this gene is not well understood, but the authors suggest that it may be important to investigate further because it is located within the genomic region with the strongest evidence for linkage to a disease gene in a study of Turkish family health histories in which members sometimes have a rare familial form of Behcet’s disease.


4. An association with the STAT4 gene, in which different variants in the same vicinity of the genome increase risk for autoimmune diseases, including rheumatoid arthritis and lupus.

New Gene Affects Clearance of Hepatitis C Virus


Chronic infection with hepatitis C virus is a cause of liver cirrhosis and liver cancer. Up to 80% of people who are acutely infected with hepatitis C fail to clear the virus and develop chronic hepatitis C infection, and of these, approximately 5% develop liver cancer. Individuals of African ancestry do not respond as well to current treatments of hepatitis C infection compared to patients of European or Asian ancestry.


Previously, results from genome-wide association studies (GWAS) identified common inherited genetic markers that were associated with response to hepatitis C virus treatment and spontaneous clearance of the infection. Those markers are located on chromosome 19 near a known interferon gene, IFNL3. However, molecular investigations into IFNL3 did not explain the GWAS association with spontaneous virus clearance or treatment response.


According to an article published online in Nature Genetics (6 January 2013), a gene was discovered that interferes with the clearance of hepatitis C virus infection. The study also identified an inherited variant within this gene, Interferon Lambda 4 (IFNL4), that predicts how people respond to treatment for hepatitis C infection.


The study found that the IFNL4 region harbors a variant that is found in two alternative forms. One form, called deltaG, results in a deletion in one of the four bases that comprise DNA. The change creates an alteration known as a frameshift, which produces the IFNL4 protein, while the form without the deletion does not produce IFNL4. By analyzing data from hepatitis C-infected African-Americans and European-Americans participating in clinical studies, the authors found that the presence of the IFNL4 protein is associated with poorer clearance and response to treatment than the form that does not produce IFNL4. The deletion variant is more common in people of African ancestry, which helps partially explain why African-Americans have a lower response to current hepatitis C treatments than patients of Asian and European ancestry.


The new gene belongs to what is now a family of four interferon-lambda protein-encoding genes, three of which were discovered more than ten years ago (IFNL1, IFNL2 and IFNL3) The mechanism by which the IFNL 4 protein impairs hepatitis C virus clearance remains unknown. Further studies will explore molecular function of this novel protein in normal and disease conditions.

Variant of TREM2 Associated with the Risk of Alzheimer’s Disease


Sequence variants, including the e4 allele of apolipoprotein E, have been associated with the risk of the common late-onset form of Alzheimer’s disease (AD). Few rare variants affecting the risk of late-onset Alzheimer’s disease have been found. In order to address this issue, a study published in the New England Journal of Medicine (2013;368:107-116) obtained the genome sequences of 2,261 Icelanders and identified sequence variants that were likely to affect protein function. These variants were imputed into the genomes of patients with AD and control participants and then tested for an association with AD. Replication tests were performed using case-control series from the United States, Norway, the Netherlands, and Germany. One of the controls included a genetic association with cognitive function in a population of unaffected elderly persons.


Results showed that a rare missense mutation (rs75932628-T) in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2), which was predicted to result in an R47H substitution, was found to confer a significant risk of Alzheimer’s disease in Iceland (odds ratio, 2.92). The mutation had a frequency of 0.46% in controls 85 years of age or older. It was also found that carriers of rs75932628-T between the ages of 80 and 100 years without AD had poorer cognitive function than noncarriers (P=0.003).


According to the authors, the findings strongly implicate variant TREM2 in the pathogenesis of AD, and given the reported antiinflammatory role of TREM2 in the brain, the R47H substitution may lead to an increased predisposition to AD through impaired containment of inflammatory processes.

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


FDA is Requiring Lower Recommended Dose for Zolpidem (Ambien)


The FDA has announced it is requiring the manufacturers of Ambien, Ambien CR, Edluar and Zolpimist, widely used sleep drugs that contain the active ingredient zolpidem, to lower current recommended doses. Ambien and Ambien CR are also available as generics. New data show that zolpidem blood levels in some patients may be high enough the morning after use to impair activities that require alertness, including driving.


Using lower doses of zolpidem means less of the drug will remain in the blood in the morning hours. Since women eliminate zolpidem from their bodies more slowly than men, the FDA has notified the manufacturers that the recommended dose should be lowered for women and that the labeling should recommend that health care professionals consider a lower dose for men. Data show the risk for next-morning impairment is highest for patients taking the extended-release forms of these drugs. The FDA urges health care professionals to caution all patients (men and women) who use these products about the risks of next-morning impairment for activities that require complete mental alertness, including driving.


The FDA has informed the manufacturers that the recommended dosage of zolpidem for women should be lowered from 10 milligrams (mg) to 5 mg for immediate-release products (Ambien, Edluar, and Zolpimist) and from 12.5 mg to 6.25 mg for extended-release products (Ambien CR). For men, the FDA has informed the manufacturers that the labeling should recommend that health care professionals consider prescribing these lower doses (5 mg for immediate-release products and 6.25 mg for extended-release products). These products are currently available on the market in both the higher and lower dosages.


In a Drug Safety Communication, the FDA also reminded the public that morning impairment is not limited to zolpidem. Drowsiness is listed as a common side effect in the labels of all insomnia drugs, along with warnings that people may still feel drowsy the next day after taking one of these products. Moreover alertness can be impaired even in people who do not feel drowsy.


People who are currently taking the higher doses (10 mg or 12.5 mg) of zolpidem-containing insomnia medicines should continue taking the prescribed dose as directed until discussing with their health care professional how to safely continue to take the medicine. Each patient and situation is unique, and the appropriate dose should be discussed with a health care professional. Patients should read the Medication Guide that comes along with their medication for additional information on the benefits and risks of these products.


The labeling change is based on findings in driving simulation and laboratory studies showing that, in some individuals, zolpidem blood levels the morning after use appear capable of impairing driving to a degree that increases the risk of a motor vehicle accident.

Garlic Roasted Salmon & Brussels Sprouts with Black Beans


Eat for a sharper mind with brain foods like salmon, avocado, black beans, to boost brain power. Adding omega-3-rich ingredients, such as oily fish, to your diet, as well as iron-rich foods, such as beans, and water-rich foods, such as leafy salad greens, can support healthy cognitive function.




  1. 14 large cloves garlic
  2. 1/4 cup extra-virgin olive oil
  3. 1/3 cup chopped fresh cilantro
  4. 1 teaspoon Kosher salt (optional)
  5. 3/4 teaspoon black pepper, or to your taste
  6. 6 cups Brussels sprouts, trimmed and sliced
  7. 3/4 cup white wine, preferably Chardonnay (never use store-bought cooking wine)
  8. 2 pounds wild-caught salmon fillet, skinned, cut into 6 portions
  9. Lemon wedges
  10. Black beans (canned if you don’t want to make them), well rinsed in cold water (drained) before using




  1. Preheat oven to 450°F.
  2. Mince 2 of the garlic cloves and combine in a small bowl with the oil, 1 tablespoon cilantro, 1/2 teaspoon salt and 1/4 teaspoon pepper.
  3. Cut the remaining garlic cloves in half and put in a large roasting pan, with all of the cut Brussels sprouts and 3 Tablespoons from your mixture of oil and garlic with seasonings.
  4. Roast the sprouts, stirring once, for 15 minutes.
  5. Meanwhile, add the Chardonnay wine to your remaining oil & garlic mixture.
  6. Remove the pan from oven, stir black beans in with the sprouts, for health, as well as for color, as many as you would like, and place the salmon fillet on top of the veggies.
  7. Drizzle the wine mixture over the salmon and sprinkle it with the remaining 1 tablespoon cilantro and (optional) pinches of salt and pepper.
  8. Bake until the salmon is just cooked through, 5 to 10 minutes more (less time if you like it rare)
  9. Serve with lemon wedges.


Roasting salmon on top of Brussels sprouts, a few black beans and garlic, flavored with wine and fresh cilantro, is simple enough for a weeknight meal yet delicious enough to serve to company on the weekend. This recipe should be enough for 4 to six people. Serve with whole-wheat couscous or jasmine rice, your favorite warm bread and a nice tossed salad with avocados. As for the wine, you guessed it, a beautiful chilled Chardonnay.



Brainy Theater – “The Other Place”


Laurie Metcalf  brilliantly  portrays a drug-company scientist who believes she has a brain tumor
Photo: Sara Krulwich/The New York Times



By Joyce Hays, Target Health Inc.  –  We rarely recommend places to go to in our home town, the Big Apple, but this past Thursday, a theatrical event opened in Manhattan, about the pharmaceutical industry and disease, that is such a perfectly crafted play, superbly acted and directed, that we would be negligent to our readers, if we did not recommend it.

The play is, “The Other Place” by Sharr White.


We include the New York Times review by Charles Isherwood, a controversial and caustic theater critic, known for his sometimes excessive harshness, who does give this play, “The Other Place,” an excellent review.


Feel free to give your own thoughts about this profound and stimulating play.


Watchful Waiting


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



The elections are over, the Affordable Care Act’s Constitutionality has been affirmed by the Supreme Court and the political oxygen has been consumed by the budget negotiations (of which we’ve almost certainly seen only Part 1 of what promises to be a continuing saga). We have, it seems, at least for the moment, little energy remaining for health matters.


The undoubtedly transient calm offered by this artificial respite affords the chance, with unusual dispassion, to simply observe as key elements of the ACA are implemented (or not) over the coming months. We can collectively assess how the complex interactions among politics, money, power, and even (cynicism acknowledged) some modest concern for the welfare of their constituents, influence politicians as they make critical decisions about implementing the ACA.


Key elements to watch include the decisions by the various States to create their own insurance exchanges or default to those crafted and managed by the Federal Government. There is clearly resistance among the States; the Kaiser Family Foundation suggests that as of January 2013 twenty-five (25) states had elected the default (e.g. Federal) option. Also in play as a consequence of the Supreme Court is each State’s decision so accept (or not) the Federal incentive offered to expand access to their individual Medicaid programs. This original requirement to expand Medicaid, readers may recall, was the key element of the Act struck down by the Supreme Court. The ACA originally required States to expand Medicaid access or forfeit all Medicaid matching funds, a financial penalty deemed by the Supremes to be extreme and therefore unconstitutionally coercive. Therefore, States will now have the chance to reject the Medicaid expansion funds while retaining the current Federal matching support for their Medicaid recipients; they can, therefore, maintain the ‘status-quo’ and elect not to expand their Medicaid roles. To the extent States take this course, clearly, they potentially undermine one of the key ACA goals, expanding coverage. Of course, the Supreme Court set the bad example for the states, in the first place.


Based upon the States’ responses Medicaid expansion, like the exchanges, is receiving mixed support; the Advisory Board reports that 15 States have declared themselves as either ‘leaning toward’ not, or definitely not participating in the expansion. Given that in the short term (often the politically relevant timeframe) funding for the expansion is generous, it seems something other than a straightforward financial calculation may be at play.


Finally, there are remaining court challenges including, unsurprisingly, objections to the inclusion of contraception as an essential health benefit with mandated coverage.


So, whatever one’s views of the ACA, it is clear that we are far from finished with healthcare; instead we seem to have just begun traveling down a lengthy and likely contentious path. Perhaps though, with the passage and pending implementation of a now constitutionally cleared ACA we are (channeling Churchill) at ‘the end of the beginning’.


At the very least, there shall be plenty of material for On-Target.


Editors note:  The ACA is the law of the land and is here to stay.  It was written, in the first place, as a highly flexible, inclusive, elastic document, able to handle many trials and errors over the years, until it reaches the point where all Americans have health coverage at a much lower cost to the country, and to its citizens.