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In: Proceedings of the American Association of Zoo Veterinarians and the American Association of Wildlife Veterinarians joint conference order cheap propranolol line cardiovascular disease and exercise. Climate extremes promote fatal co-infections during canine distemper epidemics in African lions generic 80 mg propranolol fast delivery kyolic cardiovascular. Causal inference in disease ecology: investigating ecological drivers of disease emergence. Why disease management needs to appreciate the relationship between wildlife, livestock and humans, and take an ecosystem approach. A summary of proactive and reactive strategies for managing animal diseases in wetlands. The dual benefits of controlling emerging infectious diseases and invasive alien species. A brief introduction to the role of communication, education, participation and awareness in disease management. However, with wetland habitats subject to substantial and widespread modification and with such a broad variety of anthropogenic uses, diseases have emerged or re-emerged in the last few decades at a far greater frequency than previously recorded. A million dead waterbirds in an outbreak of avian botulism is a clear indication of a major health problem. However, the wetland manager must understand that disease is usually a much more subtle process affecting body systems and functions, and creating energetic costs to the host. Morbidity or mortality may be the outcome but often there will be less obvious consequences on behaviour, reproductive success, the ability to compete for resources and evade predation, and so on. Disease, therefore, acts to shape and limit populations, affecting age structures and distribution of wild species. It is strange then, that wildlife disease has been rather sidelined as an issue by many ecologists for many years. Anthropogenic activities have now affected the environment to such an extent that wildlife disease has, in effect, ‘shown itself’ to the ecologists, land managers and policy makers and has now become established as a cross cutting conservation issue. The real power for disease control and prevention is in the hands of the land managers and users. For wetland diseases, these key stakeholders are the wetland managers, local wetland users including farmers, hunters, fishers and people living in and around wetlands, and those making policies affecting wetland use. Therefore, this Manual focuses on the wetland managers and policy makers with the aim of influencing the activities and practices of all those using wetlands for their vital resources and services. Effective disease management practiced at a landscape or catchment scale can ensure that disease does not spread and/or become endemic and cause long term problems. The adage of ‘prevention is better than cure’ is fundamental to disease management. Costs of disease management must be weighed against the benefits of preventing problems, in particular long term issues negatively impacting livelihoods, public health, domestic animal production and biodiversity. The spectrum of disease management practices is broad and may entail nothing more than routine wetland management practices through to major interventions for large scale disease control operations, depending on the issue, its scale and potential impact. Disease management practices may be focused on the environment, the hosts present in the wetland and its catchment, or, in the case of infectious disease, the parasite or pathogen, or any combination thereof. The outcome of disease is dependent on the relationship between a host and its environment, and in the case of infectious disease, the pathogen also. The figure shows some of the factors (outside the circles) which influence this relationship and thus some of the factors that can be targeted for disease control. Rinderpest – eradication of a disease affecting all sectors Rinderpest, once described as “the most dreaded bovine plague known”, became the first disease of animals to be eradicated by human intervention. This acute viral disease has been responsible for the death of domestic cattle for millennia, adversely affecting livestock, wildlife and agricultural livelihoods, bringing starvation and famine. In its classical, virulent form, rinderpest infection can result in 80-95% mortality in domestic cattle, yaks, buffalo and many other wild ungulate species. The disease has had far reaching conservation impacts affecting the abundance, distribution and community structure of many species as well as becoming a source of conflict between agricultural and wildlife interests. Clinical signs include: fever, depression, loss of appetite, discharges from the eyes and nose, erosions throughout the digestive tract, diarrhoea and death. Weight loss and dehydration, caused by enteric lesions, can cause death within 10-12 days. Key Actions Taken to eradicate rinderpest included the development of vaccines, disease surveillance, diagnostic tools and community-based health delivery. Initially, mass livestock vaccination programmes were implemented followed by improved disease surveillance and focussed vaccination campaigns (containing any remaining reservoirs of disease). Disease surveillance and accreditation continued until 2011, when on June 28th the world was declared free from rinderpest. Outcomes: The benefits derived from the eradication of rinderpest are numerous and include: protected rural livelihoods, increased confidence in livestock-based agriculture, an opening of trade in livestock and their products and increased food security. Veterinary services worldwide have become more proficient as a consequence of the fight against rinderpest and the conservation of numerous African ungulates has also benefited. The socio-economic benefits of rinderpest eradication are said to surpass those of virtually every other agricultural development programme and will continue to do so. Rinderpest was successfully eradicated due to ongoing, concerted, international efforts that built on existing disease control programmes in affected countries. Only through international coordination can other such transboundary diseases be controlled and eliminated, as isolated national efforts often prove unsustainable. It is important to note that different stakeholders will likely have different ideas about when interventions are required and ideally these can be addressed within management and contingency plans in ‘peacetime’ i. It is important to understand that disease management may be thwarted by poor understanding of disease ecology and dynamics, and thus the appropriate management practices to mitigate. Inappropriate disease management practices can even result in counter-productive consequences and novel disease problems. Hence, a good evidence base is important, appreciating that this may be difficult to attain due to complexities or limitations of diagnosis, surveillance, and other knowledge gaps. As human development and livestock have encroached into wild habitats, not surprisingly infectious diseases have spread between these populations, negatively affecting all three sectors. Movements of people and extensive trade in wild and domestic animals have resulted in the global spread of a number of pathogens, causing particular problems where infectious agents are novel and new hosts are immunologically naïve. The complexities of disease dynamics in wildlife have resulted in unpredicted disease emergence. Diseases of wildlife that affect humans or their livestock have sometimes led to eradication programmes targeted at wildlife which have not necessarily resulted in reduced disease prevalence but, instead, serious long term consequences for biodiversity, public health and well- being, and food security, whilst failing to address causal problems. It has become common understanding that the world can no longer deal with diseases of people, domestic livestock and wildlife in isolation and, instead, an integrated ‘One World One Health’ approach to health has developed. Delivering integrated approaches and responses across the medical, veterinary, agricultural and wildlife sectors can be problematic given existing organisational roles and structures but demonstrating the benefits this can bring should help promote this progressive way of working. The recent global eradication of rinderpest provides an example of how one disease with impacts across all sectors requires global coordinated efforts to bring about success and benefits for all. For wetlands, which provide the ‘meeting place’ for people, livestock and wildlife, a mapping of a number of important wetland diseases, according to their hosts (Figure 2-3), illustrates clearly that more diseases are shared between these sectors than are specific to any one sector. Tackling disease in one sector is unlikely to be successful in the long term without consideration of the others. Moreover, not working at an ecosystem scale, and without integrated approaches, misses opportunities for broader positive health outcomes.

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The possible relations of early breast and bottle feeding with later cholesterol concentrations and other coronary heart disease risk factors were explored in several short-term studies and larger retrospective epide- miological studies generic propranolol 80 mg cardiovascular board review 2015, but these observations are inconsistent (Fall et al cheap propranolol generic cardiovascular disease class 3. The disparate findings may be due to confounding factors such as duration of breast feeding, since human-milk feeding for less than 3 months was associated with higher serum cholesterol concentrations in men at 18 to 23 years of age, or the type of formula fed since formula composition, especially quality of fat, which has changed dramatically in the last century (Kolacek et al. The available data do not warrant a recommendation with respect to dietary cholesterol intake for infants who are not fed human milk. How- ever, further research to identify possible mechanisms whereby early nutri- tional experiences affect the atherosclerotic process in adults, as well as the sensitive periods in development when this may occur, would be valuable. High amounts of cholesterol are present in liver (375 mg/3 oz slice) and egg yolk (250 mg/ yolk). Although generally low in total fat, some seafood, including shrimp, lobster, and certain fish, contain moderately high amounts of cholesterol (60 to 100 g/half-cup serving). One cup of whole milk contains approxi- mately 30 mg of cholesterol, whereas the cholesterol contained in 2 per- cent and skim milk is 15 and 7 mg/cup, respectively. One tablespoon of butter contains approximately 12 mg of cholesterol, whereas margarine does not contain cholesterol. Dietary Intake Based on intake data from the Continuing Survey of Food Intakes by Individuals (1994–1996, 1998), the median cholesterol intake ranged from approximately 250 to 325 mg/d for men and 180 to 205 mg/d for women (Appendix Table E-15). The meta-analysis also identified a diminishing increment of serum cholesterol with increasing baseline dietary cholesterol intake. With a baseline cholesterol intake of 0, the estimated increases in serum total cholesterol concentration for intakes from 100 to 400 mg/d of added dietary cholesterol were 0. Other predictive formulas for the effect of 100 mg/d of added dietary cholesterol, which did not consider baseline cholesterol intake and are based on compilations of studies with a variety of experimental conditions, have yielded estimates of 0. Furthermore, pooled analyses of the effects of 100 mg/d of added dietary cholesterol on plasma lipoprotein cholesterol concentrations (Clarke et al. The incremental serum cholesterol response to a given amount of dietary cholesterol appears to diminish as baseline serum cholesterol intake increases (Hopkins, 1992). There is also evidence from a number of studies that increases in serum cholesterol concentration due to dietary choles- terol are blunted by diets low in saturated fat, high in polyunsaturated fat, or both (Fielding et al. There is considerable evidence for interindividual variation in serum cholesterol response to dietary cholesterol, ranging from 0 to greater than 100 percent (Hopkins, 1992). There is increasing evidence that genetic factors underlie a substantial portion of interindividual variation in response to dietary cholesterol. An instructive case is that of the Tarahumara Indians, who in addition to consuming a diet low in cholesterol, have both low intestinal cholesterol absorption and increased transformation of cholesterol to bile acids (McMurry et al. However, with an increase in dietary cholesterol from 0 to 905 mg/d, their average plasma cholesterol concentration increased 0. Variations in several genes have been associated with altered respon- siveness to dietary cholesterol. The common E4 polymorphism of the apoE gene has been associated with increased cholesterol absorption (Kesäniemi et al. The recent finding that apoE is of importance in regulating cholesterol absorption and bile acid formation in apoE knockout mice (Sehayek et al. There are numerous other candidate genes that could modulate plasma lipid and lipoprotein response to dietary cholesterol by affecting cholesterol absorption, cellular cholesterol homeostasis, and plasma lipo- protein metabolism. Studies in animal models have generated data in support of the possibility that variations among these genes may be of importance in influencing dietary cholesterol response in humans, but to date such human data are lacking. Nevertheless, the existence of marked interindividual variability in dietary cholesterol response among and within various animal models points to the likelihood that some of the mecha- nisms underlying this variability will also apply to humans. There is compelling evidence that dietary cholesterol can induce atherosclerosis in several animal species, including rabbits, pigs, nonhuman primates, and transgenic mice (Bocan, 1998; McNamara, 2000; Rudel, 1997). However, given the existence of marked inter- and intraspecies differences in cholesterol metabolism and athero- genic mechanisms, it is not possible to extrapolate these data directly to humans. A significant relative risk was also observed in the Western Electric Study, which remained significant after adjustment for a number of covariates, including dietary fat and serum cholesterol concentration (Stamler and Shekelle, 1988). More recently, in a study of 10,802 health- conscious men and women in the United Kingdom, a univariate relation- ship of cholesterol intake to ischemic heart disease mortality was observed (Mann et al. This finding was corroborated in a European study, but after multivariate analysis adjust- ing for fiber intake, the association was no longer significant (Toeller et al. Measures of atherosclerosis using imaging techniques have also been assessed in relation to diet. Angiographically assessed coronary artery disease progression over 39 months in 50 men was weakly related to cholesterol intake in univariate, but not multivariate, analysis (Watts et al. In 13,148 male and female participants in the Atherosclerosis Risk in Commu- nities Study, carotid artery wall thickness, an index of early atherosclerosis, was significantly related to dietary cholesterol intake by univariate analyses; multivariate analysis was not performed (Tell et al. Another uncertainty relates to interpreting the effects of dietary cholesterol on blood cholesterol concentrations. Finally, the considerable interindividual variation in lipid response to dietary cholesterol may result in differing outcomes in differ- ent populations or population subgroups. Cancer As shown in Tables 9-5 through 9-8, no consistent significant associa- tions have been established between dietary cholesterol intake and cancer, including lung, breast, colon, and prostate. Several case-control studies have suggested that a high consumption of cholesterol may be associated with an increased risk of lung cancer (Alavanja et al. As reviewed above, on average, an increase of 100 mg/d of dietary cholesterol is predicted to result in a 0. This effect of added cholesterol is highly variable among individuals and is considerably attenuated at higher baseline cholesterol intakes. Epidemiological studies have limited power to detect effects of such magnitude and thus do not provide a meaningful basis for establishing adverse effects of dietary cholesterol. However, no studies have examined the effects of very small increments of dietary cholesterol in numbers of subjects suffi- ciently large enough to permit statistical treatment of the data. Because cholesterol is unavoidable in ordinary, nonvegan diets, eliminating choles- terol in the diet would require significant changes in patterns of dietary intake. Independence of the effects of cholesterol and degree of saturation of the fat in the diet on serum cholesterol in man. Andersson S-O, Wolk A, Bergström R, Giovannucci E, Lindgren C, Baron J, Adami H-O. Energy, nutrient intake and prostate cancer risk: A population- based case-control study in Sweden. Dietary fat and risk of coronary heart disease in men: Cohort follow up study in the United States. Influence of formula versus breast milk on cholesterol synthesis rates in four-month-old infants. Effect of egg yolk feeding on the concentration and composition of serum lipoproteins in man.

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While no adverse effects were reported purchase propranolol online heart disease list, it was not clear from the reports what adverse effects were examined purchase propranolol american express cardiovascular revascularization medicine, and plasma aspartic acid concentrations were not reported. Since the artificial sweetener aspartame contains about 40 percent aspartic acid, studies on the effects of oral administration of this dipeptide provide useful information on the safety of aspartic acid. Twelve normal adults were orally given 34 mg/kg of body weight of aspartame and the equimolar amount of aspartic acid (13 mg/kg of body weight) in a cross- over design (Stegink et al. No increase in plasma or erythrocyte aspartate was found during the 24 hours after dosing. Plasma phenylalanine levels doubled over fasting concentrations 45 to 60 minutes after dosing with aspartame but returned to baseline after 4 hours. Each child received a physical examination and special eye examinations before and after the study. In addition, tests for liver and renal function, hematological status, and plasma levels of phenylalanine and tyrosine were conducted. Using a similar study design and a dose of 36 mg aspartame/kg body weight/d (14 mg aspartate/kg/d) given orally to young adults (mean age 19. Dose–Response Assessment All human studies on the effects of aspartic acid involve acute expo- sures (Ahlborg et al. There are some subchronic studies on the oral administration of aspartame to humans (Frey, 1976; Stegink et al. Although some studies in experimental animals were designed to obtain dose–response data, the effects measured were usually found in all doses studied. The most serious endpoint identified in animal studies was the devel- opment of neuronal necrosis in the hypothalamus of newborn rodents after dosing with aspartic acid a few days postpartum. This is a property of dicarboxylic amino acids, since glutamic acid dosing in this animal model results in similar necrotic effects (Stegink, 1976; Stegink et al. There is still some uncertainty over the relevance to humans of the new- born rodent model for assessing the neuronal necrosis potential of aspartic acid. Neuronal necrosis in the hypothalamus was not found in newborn nonhuman primates with levels of plasma dicarboxylic amino acids 10 times those found in newborn mice with neuronal necrosis (Stegink, 1976; Stegink et al. In addition, human studies where high doses of aspartic acid or aspartame were given failed to find a significant increase in the plasma level of aspartic acid. In view of the ongoing scientific debate regarding the sensitivity of newborn animals to the consumption of supplemental dicarboxylic amino acids, it is concluded that aspartic acid dietary supplements are not advis- able for infants and pregnant women. The latter is a multienzyme system located in mitochondrial membranes (Danner et al. Men 51 through 70 years of age had the highest intakes at the 99th per- centile for leucine at 14. It should be noted, however, that in most of the animal studies reported below, it is not entirely clear that these various enzyme activities are critical determinants of the effects seen. Thus, while the animal data must be interpreted with caution, there is no well-established basis for disregarding them entirely. Leucine may affect muscle protein turnover (Elia and Livesey, 1983) and stimulate insulin release and tissue sensitivity (Frexes-Steed et al. They have also been used in parenteral nutrition of patients with sepsis and other abnormalities. Although no adverse effects have been reported in these studies, it is not clear that such effects have been care- fully monitored (Skeie et al. Additionally, the data from these studies, because they involved patients with significant and sometimes unusual disease states, are not directly relevant to the problem of assessing risks to normal, healthy humans. There have been several reports of clinical trials in which groups of healthy humans, in most cases trained athletes, were given high doses of leucine by intravenous infusion (Abumrad et al. These trials measured physical and mental performance, the impact on blood levels of other amino acids, and in one case, of insulin and glucose output. In fact, in one study glutamine output from forearm muscle was significantly increased (Abumrad et al. It should be noted, however, that possible side effects in all studies were those that might have been recognized subjectively. Thus, although this collection of studies provides no evidence of adverse effects of high doses of leucine, they are of highly limited value in assessing health risks. How- ever, these imbalances, which lead to catabolism of muscle, occur only in rats on marginally adequate protein diets (Block, 1989). Kawabe and coworkers (1996) reported on a subchronic feeding study in which L-isoleucine was administered to groups of 10 rats at dietary con- centrations of 0, 1. The amino acid caused no changes in body weights, food consumption, or hematological parameters. At the highest dietary level, increased urine volumes and rela- tive kidney weights and urine pH, together with some alterations in serum electrolytes, were clearly related to treatment. There is evidence that isoleucine acts as a promoter of urinary bladder carcinogenesis in rats (Kakizoe et al. In a follow-up study of similar design, Nishio and coworkers (1986) extended the experimental period to 60 weeks and included diets supplemented with 2 or 4 percent isoleucine or leucine. It thus appears that both leucine and isoleucine are potent promoters of bladder neoplasms in rats at dietary levels of 2 percent and above; a no-effect level was not identified in either of the above studies. There is no evidence that either amino acid is carcinogenic in the absence of an initiating agent. Persaud (1969) reported that leucine is a teratogen when it is administered by intraperitoneal injection in pregnant female rats at doses as low as 15 mg/kg of body weight. No papillomas or preneoplastic lesions were observed in the control groups or in the amino acid groups. Pregnant rats were fed a low protein (6 percent casein) diet supplemented with 5 percent leucine, isoleucine, or valine. Only 11 out of 20 possible pregnancies were maintained in rats admin- istered leucine and isoleucine (2/10 for the leucine groups and 9/10 for the isoleucine groups). No consistent effects on food intake and maternal body weight gain were observed, except for an increase in both in valine- supplemented dams. They also concurrently studied the effects of tryptophan, tyrosine, and phenylalanine supplementa- tion. Feeding of the supplemented diets commenced in both genders two weeks before mating, and continued through three generations (F1, F2, F3). In the F2 and F3 generations, however, pup brain weights were reduced at day 5 and did not recover by day 20. The concen- trations of neurotransmitters were decreased in the brain in all three generations, with the most significant decrease seen for aspartate; no func- tional measurements were made to assess the possible effects of these declines in neurotransmitter concentrations. This study involved only a single level of supplementation, so a “no-effect” level was not identified.

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There is a high likelihood that Patient 2 faces a future of escalating medical interventions purchase propranolol 80 mg with amex capillaries hydrostatic pressure, declining health generic 80mg propranolol with amex blood vessels in your nose, and increasing disability. The human, social, and economic costs associated with patients such as Patient 2 are daunting and 8 In 2010, approximately 1. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 64 distressingly typical of those seen for patients with chronic diseases throughout our aging population. The Committee’s assigned task was to “explore the feasibility and need, and develop a potential framework, for creating a ‘New Taxonomy’ of human diseases based on molecular biology. Moreover, the Committee clearly recognized that developing and implementing a Knowledge Network of Disease has the unique potential to go far beyond classification of disease to act as a catalyst that would help to revolutionize the way research is done and patients are treated. Patient 1 has a high likelihood of overcoming her life-threatening disease and going on to live a long, healthy, and productive life. These prospects are a direct result of a new ability to recognize, based on molecular analyses, the precise type of breast cancer she has and to target a rational therapy to her disease. The Committee believes that the best prospects for creating a similarly bright future for Patient 2 lies in achieving a similarly precise understanding of his disease by creating a Knowledge Network of Disease and an associated New Taxonomy. The Committee recognized two key points about its charge: first, development of an improved disease taxonomy is only one facet, albeit an important one, of the challenge of leveraging advances in biomedical research to achieve better health outcomes for patients; secondly, no single stream of activity—led by any single segment of the biomedical research community—can tackle even this limited goal on its own. Both these points suggested that we could best address our charge by framing the “new-taxonomy” challenge broadly. Many of the conclusions and recommendations could apply, as well, to other challenges in “translational research” such as evaluating and refining existing treatments and developing new ones. However, disease classification is inextricably linked to all progress in medicine, and the Committee took the view that an ambitious initiative to address this challenge—and particularly to modernize the “discovery model” for the needed research —is an excellent place to start. The Committee thinks that the key to success lies in building new relationships that must span the whole spectrum of research and patient-care activities that comprise American medicine. As discussed in Chapter 2, the Committee thinks that now is a propitious time to confront the challenge of developing a Knowledge Network of Disease and deriving a New Taxonomy from it because of changes that are sweeping across basic and translational research, information technology, drug development, public attitudes, and the health-care-delivery system. Our recommendations seek to empower stakeholder communities by providing them with informational resources—the Information Commons, the Knowledge Network, and the New Taxonomy itself—that would transform the way they work and make decisions. We make no specific promises about the benefits that would ensue as this transformation occurs but have every confidence that this initiative would be a powerful, constructive force for change throughout a large enterprise that plays an increasingly central role in science, technology, the economy, and each of our lives—and one that is notoriously difficult to reform. At the core of the Committee’s optimism is a conviction that dramatic advances in biological knowledge can be coupled more effectively than they are now to the goal of improving the health outcomes of individual patients. Biology has flourished in the 50+ years since the discovery of the molecular basis of inheritance. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 65 Genome Project, genetics is in a “golden age” of discovery. Sequence similarity between genes studied in fruit flies and those studied in humans allows nearly instant recognition of the potential medical relevance of the most basic advances in biochemistry and cell biology. Increasingly, this process also works in reverse: unusual human patients call attention to molecules and biochemical pathways whose importance in basic biology had been overlooked or was otherwise inaccessible. Indeed, there are already many areas of basic biology in which human studies are leading the way to deep new insights into the way organisms work. For the simple reason that one can ask a research subject what she sees when looking at a pattern of light—instead of having to develop a crude behavioral test to find out whether she sees anything at all—we know far more about the molecular details of light reception in humans than we could ever have learned from studying mice. Particularly as biomedical research puts an increasing emphasis on unraveling the molecular underpinnings of behavior, the advantages of starting research studies with humans, rather than model organisms, are likely to grow. Experience tells us that translation of intensifying knowledge of basic biology into clinical advances is a daunting task. Furthermore, the Committee shares the sense that basic biology is at an “inflection point” in which there is every reason to expect increasing payoffs from the large investments in basic science that have brought us to this point. However, the grand challenge of coupling basic science more effectively to medicine will require a rethinking of current practices on a scale commensurate with the challenge. The Committee regards the initiative it proposes to develop the tripartite Information Commons, Knowledge Network, and New Taxonomy, as having the potential to rise to this level. Information technology is the key contributor to the technological convergence the Committee perceives. Information technology, quite simply, has made the rise of data-intensive biology possible: molecular biology, as now practiced, could not exist without modern computing systems. In medicine, information technology offers perhaps the best hope of increasing efficiency and improving our collective learning about what works and what does not. In a mere 20 years, people have made the transition from regarding most human knowledge as locked away in the dusty backrooms of research libraries to expecting it to be at their finger tips. Understandably, the public is losing patience with barriers to the sharing and dissemination of information. The social-networking phenomenon is a particularly dramatic illustration of changing attitudes toward information and associated blurring of the line between the public and private. For all these reasons, the Committee sees powerful forces converging in a way that favors the dismantling of existing barriers—institutional, cultural, economic, and legal—between the biomedical research environment, the clinic, and the public. The Committee recognizes that some aspects of the world we envision are more readily approachable than others. As emphasized throughout this report, there are many impediments to progress along the path we outline. That is the reason the Committee recommends pilot projects of increasing scope and scale as the vehicle for moving forward. Although we consider the creation of an improved classification of disease valuable in its own right, we do not recommend a crash program to pursue this goal in isolation from the broader reforms we emphasize. We regard smaller projects on the recommended path as preferable to larger, narrower initiatives that would distract attention and resources from these reforms. We think the impediments can best be overcome and the optimum design of the Information Commons, Knowledge Network, and the New Taxonomy best emerge in the context of pilot projects of increasing scope and scale. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 66 Even some stakeholders in the health-care system who find the Committee’s basic vision compelling may ask whether or not a special, organized effort is required to achieve the Committee’s goals. In particular, some might argue that there are already enough examples— many have been cited in this report—in which data-intensive laboratory tests have such clear benefits for patients that the traditional system of test development and insurance reimbursement will allow a smooth transition to a new era of molecular medicine. Indeed, there is real risk of a backlash against premature claims of the efficacy of genomic medicine (Kolata 2011). The key to avoiding such a backlash is development of a robust system for discovering applications that have real clinical benefits and validating those claims through open processes. The Committee believes that expecting or pressuring payers in the health-care system to bear the costs of integrating data-intensive biology and medicine without clear evidence of the safety, efficacy, and economic feasibility of particular applications would fail—indeed, such an effort could easily be counter-productive. On the other hand, as some of the scenarios sketched above indicate, the Committee believes that a well planned public investment in creating the system the Committee envisions would lead relatively quickly to robust public-private partnerships that would allow all stakeholders to build on early successes. Perhaps even more importantly, the Committee believes that its approach offers the most realistic available path to ultimate sustainability of precision medicine.

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