By S. Arakos. Bluefield State College.
A key ﬁnding is that heart disease accounts for a large fraction of excess female mortality discount 80mg super levitra. In developing countries super levitra 80 mg mastercard, women simply die of cardiovascular disease at a rate closer to that of men purchase 80mg super levitra overnight delivery. It could be genetic: for instance discount 80 mg super levitra otc, the recently discovered “heart disease gene” so prevalent in South Asia (Dhandapany et al. Or it may truly be lack of “similar care”: women seek or receive medical care less often in developing countries, or may be subject to greater stress. Understanding why women appear to be at a particular disadvantage from cardiovascular disease is important work for future research. It is beyond the scope of this paper to disentangle the role of direct gender discrimination from other factors—biological, social, environmental, behavioural, or economic—in explaining the pervasive phenomenon of excess female mortality. By moving away from (while not abandoning) recent literature that highlights the importance of the sex ratio at birth as a key determinant of missing women, we have taken a preliminary step towards a uniﬁed study of a much broader set of issues. Schistosomiasis—infection by a parasitic worm—affects millions in sub-Saharan Africa. See Nikiforov and Mamaev (1998) for a historical perspective on gender imbalances in cardiovascular disease in now-developed countries. Even in rural areas of India, chronic diseases (primarily coronary) are now the leading cause of death (see Joshi et al. There is a large literature aimed at explaining differential mortality patterns by gender in developed countries; see, e. Stocks and ﬂows Unlike several of the central papers we have cited, such as Sen (1990) and Coale (1991), our paper discusses annual “ﬂows” of missing women, rather than the existing “stock” at any point of time. To understand the issues involved in converting ﬂows to stocks, consider the difference between the actual female death rate and the corresponding reference rate: w w (a) ≡ d (a) − u (a). In computing the ﬂow of missing women at age a, we multiply (a) by the female population at age a, as we have already done. However, the impact of (a) on the overall stock of missing women is more far-reaching: it affects every cohort of women currently older than a. M ore precisely, a cohort of age a is diminished at an earlier age a by an amount that depends on the value of (a) that prevailed a − a years ago. In general, we lack data on this value and this creates a serious difﬁculty in converting the ﬂow numbers to stocks. We could make the “steady state” assumption that all age-speciﬁc death rates have remained constant over several years, but it would have to be defended, and that is beyond the scope of this paper. However, it is worth noting that, no matter how we resolve this issue, a given proportional ﬂow at an earlier age must be more important than the same ﬂow at a later age. It will simply affect more women, and must therefore translate into larger stocks. Simply as an example, we report our tentative estimates under the assumption of time-invariance of. W eﬁnd approximately 20 million missing women in India, 58 million missing women in China, and 8 million missing women in sub-Saharan Africa. Look at the enormous difference between China and the other two regions (in ﬂows all three regions were about the same). This comes from the fact that excess female deaths in China are clustered at age 0. We reiterate, though, that these estimates must be treated with a great deal of caution. It is misleading because different countries have different fertility and death rates, and (in particular) different age distributions. They may also have different sex ratios at birth for genetic or environmental reasons that have nothing to do with missing females. The procedure is also uninformative: we cannot tell at what ages the missing women are clustered, or what diseases are responsible. Thus, we cannot begin to ask about the various channels: discrimination, biology, social norms, and so on. By unpacking missing women by age and disease, our paper takes a limited and preliminary step in this direction. First, once we control for natural variations in the sex ratio at birth, sub-Saharan Africa has as many missing women as India and China: signiﬁcantly more as a percentage of the female population. Sub-Saharan Africa has no missing females at birth, while the corresponding proportion for India is under 11%. For instance, excess female mortality up to age 15 does not account for more than a third of the total in India or sub-Saharan Africa. Our study of excess female deaths by age and disease yields the following ﬁndings. For developing countries today, the epidemiological transition—the changing composition of dis- ease—explains very little of excess female mortality. Cardiovascular deaths are an overwhelmingly strong source of missing women at older ages in India and dominate all other sources of excess female mortality. Finally, congenital deaths at infancy, as well as Injuries, account for a suspiciously large total of excess female deaths in India. In sub-Saharan Africa, missing girls also die prematurely from preventable diseases: malaria is a primary killer. That said, there are excess female deaths in childhood which are due to respiratory and perinatal causes. To us, these are warning signs that active female discrimination in China possibly stretches beyond the prenatal. Indeed, a large chunk of missing women in China, as well as in India, are found after the age of 45. In China, these excess deaths from Group 2 diseases account for close to 40% of the ﬂow of all missing women. These numbers point to the importance of studying the conditions of elderly women in India and China. As a ﬁnal note, we observe some similarities between age-speciﬁc percentages of missing women in the historical United States (ca. Our exercise cannot disentangle the role of direct gender discrimination from other factors (biological, social, environmental, behavioural, or economic) in explaining “missing women”. But it allows us to seek out potential pathways of inﬂuence, and to assess the comparative contributions made by various categories to overall excess female mortality. In this context, observe that “category” need not be circumscribed by just age and disease. For instance, inspired by the work of Das Gupta (1987), Muhuri and Preston (1991), and others on family composition and female mortality, we could—in principle—assess the contribution of the category “girls aged 0–5 with female siblings” to overall excess female mortality. We could compare this category with something entirely different, such as “Injuries”.
Enteric secretomotor reﬂexes cannot act in isolation super levitra 80 mg fast delivery, they must be modulated to take into account whole body ﬂuid balance order super levitra 80 mg free shipping. This control is exerted through blood volume and blood pressure detectors that change the activity of two sympathetic pathways cheap super levitra 80 mg, vasoconstrictor pathways and secretomotor inhibitory pathways (Fig buy super levitra 80 mg line. In mild cases, this stimulates diarrhea that helps expel the pathogens and their toxic products. The ﬁnal secretomotor neuron of reﬂexes that play an essential role in balancing local ﬂuid ﬂuxes and in whole body water and electrolyte balance is illustrated. Large volumes of ﬂuid are absorbed from the lumen with nutrients, such as glucose. The absorption of nutrients with ﬂuid activates enteric secretomotor reﬂex pathways that impinge on the secretomotor neurons. It is important that the balance of this ﬂuid exchange is modulated by sympathetic vasoconstrictor and secretomotor inhibitory pathways. Activity in these sympathetic pathways, which inhibit secretion and reduce local blood ﬂow, is determined by whole body ﬂuid status, which includes sensory detection through blood volume detectors, baroreceptors and osmoreceptors. Oxford: Blackwell 2006 However, when there are high levels of pathogens or toxins, the intestine is overwhelmed and a pathological, life-threatening hypersecretion can ensue. These intestinofugal neurons are in the afferent limbs of entero-enteric reﬂexes, that pass from distal to proximal regions through sympathetic ganglia, where intestinofugal neurons form synapses [27, 164, 165]. Distension of segments of intestine activates the reﬂex pathways, causing sympathetic inhibition of motility in more proximal regions. In the case of the stomach, acid or hypertonic solution in the lumen of the upper small intestine causes inhibition of gastric motility and emptying into the duodenum through entero-enteric reﬂexes [166, 167]. The entero-enteric reﬂex that is initiated by fat in the distal intestine and slows transit in the proximal small intestine is referred to as the ileal brake . Thus the reﬂexes arise in distal regions and regulate more proximal regions, so that luminal contents that arrive at more distal regions are adequately processed proximally. The major efferent connections of sympathetic pathways are to myenteric ganglia, through which gastrointestinal movements are inhibited, to submucosal ganglia, through which ﬂuid movement into the lumen is inhibited, and to intramural arteries that are constricted by sympathetic nerve activity. The efferent pelvic nerves convey the outputs of the lumbosacral defecation centers. The enteric nervous system consists of many thousands of interconnected ganglia that extend from the upper esophagus to the internal anal sphincter. Motor neurons in the enteric ganglia supply all major effectors in the gastrointestinal tract. This is necessary because of the very large ﬂuid load that is contributed to by water and electrolyte movement that is associated with nutrient digestion and absorption. Thus the digestive tract is controlled through integrating centers in the brainstem, spinal cord, sympathetic ganglia and gut wall that are extensively interconnected through conventional afferent and efferent pathways and via the intestinofugal neurons. Schemann M, Grundy D (1992) Electrophysiological identiﬁcation of vagally innervated enteric neurons in guinea pig stomach. Filogamo G, Gabella G (1970) Effects of extrinsic denervation on the synapses of myenteric plexus. Neurosci Lett 57:125–130 3 The Enteric Nervous System and Gastrointestinal Innervation: Integrated. Neural and neuro-immune mechanisms of visceral hyper- sensitivity in irritable bowel syndrome. Larsson M, Arvidsson S, Ekman C, Bayati A (2003) A model for chronic quantitative studies of colorectal sensitivity using balloon distension in conscious mice – effects of opioid receptor agonists. Lynn P, Zagorodnyuk V, Hennig G, Costa M, Brookes S (2005) Mechanical activation of rectal intraganglionic laminar endings in the guinea pig distal gut. Gonella J, Bouvier M, Blanquet F (1987) Extrinsic nervous control of motility of small and large intestines and related sphincters. Di Nardo G, Blandizzi C, Volta U, Colucci R, Stanghellini V, Barbara G et al (2008) Review article: molecular, pathological and therapeutic features of human enteric neuropathies. Brehmer A, Rupprecht H, Neuhuber W (2010) Two submucosal nerve plexus in human intestines. Prog Neurobiol 72:143–164 3 The Enteric Nervous System and Gastrointestinal Innervation: Integrated. Timmermans J-P, Hens J, Adriaensen D (2001) Outer submucous plexus: an intrinsic nerve network involved in both secretory and motility processes in the intestine of large mammals and humans. Pfannkuche H, Reiche D, Sann H, Schemann M (1998) Different subpopulations of cholin- ergic and nitrergic myenteric neurones project to mucosa and circular muscle of the guinea- pig gastric fundus. Ito S, Ohga A, Ohta T (1988) Gastric relaxation and vasoactive intestinal peptide output in response to reﬂex vagal stimulation in the dog. Am J Physiol 272:G4–G9 3 The Enteric Nervous System and Gastrointestinal Innervation: Integrated. Chiocchetti R, Mazzuoli G, Albanese V, Mazzoni M, Clavenzani P, Lalatta-Consterbosa G et al (2008) Anatomical evidence for ileal Peyer’s patches innervation by enteric nervous system: a potential route for prion neuroinvasion? Ichikawa S, Eda N, Uchino S (1992) Close association of peptidergic nerves with lympho- cytes in canine and monkey ileal villi. Jean A (2001) Brain stem control of swallowing: neuronal network and cellular mechanisms. Kuramoto H, Kato Y, Sakamoto H, Endo Y (1996) Galanin-containing nerve terminals that are involved in a dual innervation of the striated muscles of the rat esophagus. Wu M, Majewski M, Wojtkiewicz J, Vanderwinden J-M, Adriaensen D, Timmermans J-P (2003) Anatomical and neurochemical features of the extrinsic and intrinsic innervation of the striated muscle in the porcine esophagus: evidence for regional and species differences. Izumi N, Matsuyama H, Ko M, Shimizu Y, Takewaki T (2003) Role of intrinsic nitrergic neurones on vagally mediated striated muscle contractions in the hamster oesophagus. Kelling G (1903) Untersuchungen uber die Spannungszustande der Bauchwand, der Magen-¨ ¨ und der Darmwand. Abrahamsson H, Jansson G (1969) Elicitation of reﬂex vagal relaxation of the stomach from pharynx and esophagus in the cat. Abrahamsson H (1973) Vagal relaxation of the stomach induced from the gastric antrum. Beani L, Bianchi C, Crema A (1971) Vagal non-adrenergic inhibition of guinea-pig stomach. J Physiol 556:557–569 3 The Enteric Nervous System and Gastrointestinal Innervation: Integrated. Sjovall¨ H, Abrahamsson H, Westlander G, Gillberg R, Redfors S, Jodal M et al (1986) Intestinal ﬂuid and electrolyte transport in man during reduced circulating blood volume. Kuntz A, Saccomanno G (1944) Reﬂex inhibition of intestinal motility mediated through decentralized prevertebral ganglia. Neurogastroenterol Motil 22:7–18 Chapter 4 Intestinal Barrier Function and the Brain-Gut Axis Carmen Alonso, Marıa Vicario, Marc´ Pigrau, Beatriz Lobo, and Javier Santos Abstract The luminal-mucosal interface of the intestinal tract is the ﬁrst relevant location where microorganism-derived antigens and all other potentially immuno- genic particles face the scrutiny of the powerful mammalian immune system. Upon regular functioning conditions, the intestinal barrier is able to effectively prevent most environmental and external antigens to interact openly with the numerous and versatile elements that compose the mucosal-associated immune system.
While most people who use the steps in this book to overcome their fears will do quite well over the long term trusted super levitra 80mg, there are some factors that may increase the likelihood of your fear reemerging after treatment has ended discount 80 mg super levitra fast delivery. It’s important to make yourself aware of these potential pitfalls so that you can recognize and combat them if needed: 7 Doing too little exposure after treatment has ended 7 Returning to old habits of avoidance 7 Experiencing increased life stress (for example super levitra 80 mg line, being under a deadline at work generic 80 mg super levitra mastercard, experiencing 134 overcoming medical phobias conflict in a personal relationship, or having to cope with news of a serious illness of a good friend or relative) 7 Confronting a new situation not previously faced on your exposure hierarchy 7 Having a traumatic experience during an exposure 7 Having an unexpected fear reaction during an exposure We’ll discuss each of these pitfalls and also provide some tips on dealing with each one so as to minimize the possibility of your fear returning. It’s important that you continue to expose yourself to the feared object or situation occasionally, even after you’re better. You can even look for opportunities to accom- pany family members on dental visits. If your fear was directed toward needles or injections, become a regular staying well 135 blood donor. If you feared medical settings, look for oppor- tunities to visit or even volunteer in a hospital. Hang on to some of the exposure items you used to overcome your fear, such as videotapes, pictures, Web sites, needles, syringes, alcohol swabs, or anything else you used during your exposure exercises. You might consider putting a screen saver of a feared image on your computer at home or at work. Put up pictures of feared images or place feared objects around your home in plain sight so that they become a part of your day-to-day life. Carry a feared object or image in your purse or briefcase or keep one in your drawer at work. Before treatment, avoidance of certain feared situations or objects was prob- ably common for you. You may have become so used to avoiding that you didn’t recognize it when it was happen- ing. When treatment of your phobia ends, it’s important to ensure that you don’t slip back into old patterns of avoid- ance. In particular, you need to be alert to the subtle ways avoidance can start to creep back into your life. Minor avoidance of fearful situations may make your day-to-day life a little less stressful, but you now know that this 136 overcoming medical phobias short-term relief will result in more anxiety over the long term. Small instances of avoidance can grow into larger ones, and avoidance strengthens fear. You may start to put off medical checkups or dental visits without really think- ing about it. Be on the lookout for minor instances of avoidance and address them right away, before they become larger. Or your spouse may offer to take the kids to the dentist when checkup time rolls around, instead of you. All of these are examples of subtle ways that others may make it easier for you to avoid your fears. These well-intentioned but not so helpful acts need to be stopped when identified. For example, ask your friends and family to stop warning you about images or items that they worry might scare you. If you’re fearful of blood, ask them to stop buying the meat at the butcher counter and offer to do it yourself. If you’re afraid of nee- dles, ask them to include you in the community blood donor drive. If you fear medical situations, ask them to staying well 137 stop avoiding conversations on medical topics when you’re around. Every opportunity you can find to con- front your phobia means that your phobia will become that much weaker. Life stresses such as marital conflict, job pressures, financial problems, or parenting pressures can increase your baseline level of anxiety. In turn, a situation that would provoke a minimal fear response at times of low stress could cause a much more intense fear response at times of high stress. If you find that your fear seems to be returning, survey your life for any possible stresses. Look for ways to relax through such activities as exercise, medita- tion, listening to quiet music, or talking to a good friend. Also, keep in mind that during stressful times you may have to increase the frequency of your exposures to counterbalance the negative effect of the stress. Luckily, once the life stress subsides, your fear will probably return to its prestress level. You may have gotten to the point of having very little anxiety in all the practice situa- tions you confronted, and it may seem that you are com- pletely over your fear of needles. You know this will involve use of a small scalpel followed by a few stitches—something that hadn’t been a part of your initial exposure hierarchy. It may feel that you’re right back where you started, and this can be discouraging. Thinkofthe various objects or situations you could expose yourself to as you confront this new fear. Begin to expose yourself to this new situation using the same methods as in chapter 5. Review the cognitive challenges you wrote about in your journal when working through the exercises in chap- ter 7. The great thing about exposure therapy is that once you understand the basics of it, it can be applied to almost any feared situation. If you find that new, fearful situations emerge fre- quently, it might be a good idea to review your initial exposure hierarchy to make certain that it was as com- plete as you could make it. Make sure it was as varied as possible and that you tackled all of the steps on your staying well 139 hierarchy. Sometimes, as people approach their more dif- ficult hierarchy steps, they seem to convince themselves that they’ve come far enough and don’t really need to go any further. By this we mean that exposing yourself to situa- tions that might cause anxiety even in people without phobias can give you a good buffer (especially if you expe- rience any slight regressions in your improvement), as well as a great sense of accomplishment and the confi- dence to face any future challenges that arise. For example, let’s suppose you conquered your fear of needles but later find yourself having blood drawn by an inexperi- enced lab technician who has to make five attempts to get the needle into your vein, causing a lot of distress and pain. Your fear of needles may be rekindled, and your ini- tial impulse may be to start avoiding needles again. In this case, you need to remind yourself that avoidance will only serve to strengthen your fear. It’s essential that you make every attempt to get back into the situation as soon as pos- sible. If it’s too difficult to return to that exact situation, look at your hierarchy and begin practicing in situations that are more manageable. Remember, you have all the tools you need to treat this fear before it gets out of hand. You arranged to have some dental work done over four different appoint- ments in order to give yourself frequent exposure opportu- nities. The first three appointments went well and you’ve managed your anxiety successfully. You then go to your fourth appointment and, for whatever reason (maybe you skipped breakfast that morning, or perhaps you’re out of breath from taking the stairs instead of the elevator), you begin to feel faint in the chair.
The World Bank buy super levitra 80 mg mastercard, the World Health Organization purchase super levitra 80 mg on-line, and the Fogarty International Center of the National Institutes of Health do not guarantee the accuracy of the data included in this work 80mg super levitra with amex. The boundaries order super levitra 80 mg with visa, colors, denominations, and other information shown on any map in this work do not imply any judgement on the part of The World Bank, the World Health Organization, or the Fogarty International Center of the National Institutes of Health concerning the legal status of any territory or the endorsement or acceptance of such boundaries. Copying and/or transmitting portions or all of this work without permission may be a violation of applicable law. The International Bank for Reconstruction and Development / The World Bank encourages dissemination of its work and will normally grant permission to reproduce portions of the work promptly. For permission to photocopy or reprint any part of this work, please send a request with complete infor- mation to the Copyright Clearance Center Inc. This book is dedicated to the memory of Sir Richard Doll, Fellow of the Royal Society (born Hampton, United Kingdom, October 28, 1912; died Oxford, United Kingdom, July 24, 2005). It is entirely fitting that an assessment of world health at the end of the 20th century should be dedicated to the memory of a man whose work did so much to improve it. Preston xv Preface xvii Editors xix Advisory Committee to the Editors xxi Contributors xxiii Disease Control Priorities Project Partners xxv Acknowledgments xxvii Abbreviations and Acronyms xxix Chapter 1 Measuring the Global Burden of Disease and Risk Factors, 1990–2001 1 Alan D. Lopez, Stephen Begg, and Ed Bos Regional Demographic Characteristics 18 Changes in Mortality, 1990–2001 21 Trends in Causes of Child Death, 1990–2001 28 Discussion 32 Conclusions 35 Annex 2A: Key Demographic Indicators, by Country/Therritory, 1990 and 2001 36 Acknowledgments 43 Notes 43 References 43 vii Chapter 3 The Burden of Disease and Mortality by Condition: Data, Methods, and Results for 2001 45 Colin D. Lawn, and Jelka Zupan Stillbirths and Neonatal Mortality in the Context of the Global Burden of Disease 428 The Burden of Disease Resulting from Events Near the Time of Birth 431 Conclusions 442 Annex 6A: Flexible Functional Forms for the Acquisition of Life Potential 442 Annex 6B: Supplementary Tables 445 Annex 6C: Causes of Neonatal Mortality: Comparison of Numbers from the Global Burden of Disease with those from the Child Health Epidemiology Reference Group 461 Acknowledgments 462 References 462 List of Boxes Box 1. Calculated to Include Stillbirths (Valued the Same as Newborn Deaths) 452 Table 6B. The picture that it paints is not only updated; it Before 1990, the global disease landscape was perceived is also more precise. The small minority of the world’s population residing in countries measurement instrument has also been improved. Nowhere were estimates of dis- notably, a critical new layer of physical risk factors and their ease incidence, prevalence, survival, and disabling sequelae distribution has been added, providing valuable new tools for consistently combined into population-level profiles of mor- policy makers. This second application of the global burden of disease Publication of the Global Burden of Disease (1990) was a framework permits an analysis of trends observed since the watershed event in the assessment of health and disease. The volume is appropriately cautious in draw- ed a comprehensive portrait of diseases, injuries, and causes of ing inferences about disease-specific trends because of changes death. It dealt creatively and carefully with the hundreds of in data sources and, in some instances, improvements in issues that had to be addressed to develop useful, broadly approaches to measurement. These included establishing terms The volume also contains a valuable and admirably frank of trade among disabling conditions, among age groups and chapter on the sensitivity of estimates to various sources of generations, and between the living and the dead. Some estimates are found to that offered tempting shortcuts, the authors decided in favor of have wide bands of uncertainty. Like national income would be much greater without the heroic efforts reflected in accounts, it connected parts to a whole and measured the whole this volume. As a sophisticated measuring My congratulations to the authors and the sponsoring device, it could not be ignored by any serious student of epi- agencies. One might have experimented with its calibrations, but the device itself was irreplaceable. In 2002, a number of organizations—the Fogarty The review generated findings about the comparative cost- International Center of the U. National Institutes of Health, effectiveness of interventions for most diseases important in the World Bank, the World Health Organization, and the Bill & developing countries. This consistency constraint led to downward one dealing with deaths and the disease burden by cause and revision of the estimates of deaths from many diseases. In addition, the because health system activities, including the choice of inter- World Bank invested in generating improved estimates of ventions, depend partly on the magnitude of health problems, deaths and the disease burden by age, cause, and region for and because assessment of the burden of diseases, injuries, and 1990. Results of this initial assessment of the global burden of risk factors includes important methodological and empirical disease appeared both in the World Development Report 1993 dimensions. Organization has also invested in improving the conceptual, During 1999–2004, the authors of this volume and many methodological, and empirical basis of burden of disease collaborators from around the world worked intensively to assessments and the assessment of the disease and injury assemble an updated, comprehensive assessment of the global xvii burden of disease and its causes. New York: Oxford University conditions of the world’s population at the beginning of Press. Quantification of Health Risks: The Global and Regional Burden of New York: Oxford University Press. Prior to joining the World Health Organization health and Head of the School of Population Health at the in 2000, he worked for the Australian Institute of Health and University of Queensland, Australia. Prior to joining the uni- Welfare for 13 years in technical and senior managerial posts. Mathers has published widely on population health Health Organization in Geneva, where he held a series of tech- and mortality analysis; on inequalities in health, health nical and senior managerial posts, including chief epidemiolo- expectancies, and burden of disease; and on health system gist in the Tobacco Control Program (1992–5), manager of costs and performance. He developed the first set of the Program on Substance Abuse (1996–8), director of the Australian health accounts mapping health expenditures by Epidemiology and Burden of Disease Unit (1999–2001), and age, sex, and disease and injury causes (1998) and carried out senior science adviser to the director-general (2002). At the World Health Organization, he played a key role and causes of death, including the impact of the global tobacco in the development of comparable estimates of healthy life epidemic, and on the global descriptive epidemiology of major expectancy for 192 countries, in the reassessment of the global diseases, injuries, and risk factors. He is the coauthor of the burden of disease for the years 2000–2, and in the develop- seminal Global Burden of Disease Study (1996), which has ment of software tools to support burden of disease analysis at greatly influenced debates about priority setting and resource the country level. He has been awarded major research global, regional, and country mortality and burden of disease grants in epidemiology, health services research, and popula- from 2002 to 2030. Mathers graduated with an honors degree and university Queensland; and is a member of Australia’s Medical Services medal in physics from the University of Sydney in 1975 and was Advisory Committee. His principal research interests are the measure- ematics from the University of Western Australia in 1973 and a ment and reporting of population health and its determinants, master of science degree in statistics from Purdue University in burden of disease methods and applications, measurement of the United States. His He has collaborated with leading researchers throughout the principal research interests are analysis of mortality data; bur- world on issues relating to the development and applications of den of disease methods and applications; and quantification of summary measures of population health. He has collaborated extensively with leading researchers Majid Ezzati is an assistant professor of international health at throughout the world on these issues, particularly at Harvard the Harvard School of Public Health. He holds bachelor’s and and Oxford universities, and he holds an adjunct appointment master’s degrees in engineering from McMaster and McGill at Harvard University as professor of population and interna- Universities and a Ph. Ezzati’s research interests center around understanding the causal determinants Colin D. Mathers is a senior scientist in the Evidence and of health and disease, especially as they change in the process of Information for Policy Cluster at the World Health social and economic development and as a result of technolog- Organization in Geneva. World Health Organization’s Epidemiology and Burden of xix His current research focuses on two main areas. Murray is the Richard Saltonstall professor of area is the relationship among energy, air pollution, and health public policy, professor of social medicine, and director of the in developing countries, on which he conducts field research Harvard Initiative for Global Health. This research has led to university, for five years he led the World Health Organization’s the identification and design of technological interventions for Evidence and Information for Policy Cluster, which was dedi- reducing exposure to indoor air pollution from household cated to building the evidence base and fostering a culture of evi- energy use. His second area of research is major health risk fac- dence to inform health decision making. The cluster was respon- tors and their role in the current and future disease burden sible for work on epidemiology and the burden of disease, the globally and in specific countries and regions. His research on World Health Survey,cost-effectiveness analysis,national health risk factors focuses on environmental risks, smoking, and accounts, catastrophic health spending, responsiveness, health nutritional risks. He was the lead scientist for the World Health financing policy, human resources for health systems, coverage Organization’s Comparative Risk Assessment Project, which of health interventions, quality of care and patient safety, stew- was reported in the World Health Report 2002: Reducing Health, ardship of health systems,assessment of health system perform- Promoting Healthy Life.