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Cambridge, MA, United States

Harvard University is a private Ivy League research university in Cambridge, Massachusetts, established in 1636. Its history, influence and wealth have made it one of the most prestigious universities in the world.Established originally by the Massachusetts legislature and soon thereafter named for John Harvard , Harvard is the United States' oldest institution of higher learning, and the Harvard Corporation is its first chartered corporation. Although never formally affiliated with any denomination, the early College primarily trained Congregation­alist and Unitarian clergy. Its curriculum and student body were gradually secularized during the 18th century, and by the 19th century Harvard had emerged as the central cultural establishment among Boston elites. Following the American Civil War, President Charles W. Eliot's long tenure transformed the college and affiliated professional schools into a modern research university; Harvard was a founding member of the Association of American Universities in 1900. James Bryant Conant led the university through the Great Depression and World War II and began to reform the curriculum and liberalize admissions after the war. The undergraduate college became coeducational after its 1977 merger with Radcliffe College.The University is organized into eleven separate academic units—ten faculties and the Radcliffe Institute for Advanced Study—with campuses throughout the Boston metropolitan area: its 209-acre main campus is centered on Harvard Yard in Cambridge, approximately 3 miles northwest of Boston; the business school and athletics facilities, including Harvard Stadium, are located across the Charles River in the Allston neighborhood of Boston and the medical, dental, and public health schools are in the Longwood Medical Area. Harvard has the largest financial endowment of any academic institution in the world, standing at $32.3 billion as of June 2013.Harvard is a large, highly residential research university. The nominal cost of attendance is high, but the University's large endowment allows it to offer generous financial aid packages. It operates several arts, cultural, and scientific museums, alongside the Harvard University Library which is the world's largest academic and private library system, comprising 79 individual libraries with over 18 million volumes.It has many eminent alumni. Eight U.S. presidents and several foreign heads of state have been graduates. It is also the alma mater of 62 living billionaires and 335 Rhodes Scholars, both the most in the country. To date, some 150 Nobel laureates have been affiliated as students, faculty, or staff. Wikipedia.

Willett W.,Harvard University
Nutritional Epidemiology

This book is about the complex relationships between diet and risks of important diseases, such as cancer and cardiovascular disease. The book starts with an overview of research strategies in nutritional epidemiology - still a relatively new discipline that combines the vast knowledge compiled by nutritionists during this century with the methodologies developed by epidemiologists to study the determinants of diseases with multiple etiologies and long latent periods. A major section is devoted to the methods of dietary assessment using data on food intake, biochemical indicators of diet, and measures of body composition and size. The reproducibility and validity of each approach and the implications of measurement error are considered in detail. The analysis, presentation, and interpretation of data from epidemiologic studies of diet and disease are explored in depth. Particular attention is paid to the important influence of total energy intake on findings in such studies. To illustrate methodological issues in nutritional epidemiology, the relationships of dietary factors to the incidence of lung and breast cancer, heart disease, and birth defects are examined in depth. This new edition, in addition to updating existing chapters, includes new chapters on assessment of physical activity, nutrition, and genetic epidemic ology, and the role of nutritional epidemiology in policy. © 2013 by Oxford University Press. All rights reserved. Source

Samocha K.E.,Harvard University
Nature Genetics

Spontaneously arising (de novo) mutations have an important role in medical genetics. For diseases with extensive locus heterogeneity, such as autism spectrum disorders (ASDs), the signal from de novo mutations is distributed across many genes, making it difficult to distinguish disease-relevant mutations from background variation. Here we provide a statistical framework for the analysis of excesses in de novo mutation per gene and gene set by calibrating a model of de novo mutation. We applied this framework to de novo mutations collected from 1,078 ASD family trios, and, whereas we affirmed a significant role for loss-of-function mutations, we found no excess of de novo loss-of-function mutations in cases with IQ above 100, suggesting that the role of de novo mutations in ASDs might reside in fundamental neurodevelopmental processes. We also used our model to identify ∼1,000 genes that are significantly lacking in functional coding variation in non-ASD samples and are enriched for de novo loss-of-function mutations identified in ASD cases. Source

Recent studies have revealed that multiple intracellular signaling proteins may assemble into structured, yet sometimes infinite, higher-order signaling machines for transmission of receptor activation information to cellular responses. These studies advance our understanding of cell signaling and implicate new molecular mechanisms in proximity-driven enzyme activation, threshold behavior, signal amplification, reduction of biological noise, and temporal and spatial control of signal transduction. © 2013 Elsevier Inc. Source

Background Body-mass index (BMI) and diabetes have increased worldwide, whereas global average blood pressure and cholesterol have decreased or remained unchanged in the past three decades. We quantified how much of the effects of BMI on coronary heart disease and stroke are mediated through blood pressure, cholesterol, and glucose, and how much is independent of these factors. Methods We pooled data from 97 prospective cohort studies that collectively enrolled 1·8 million participants between 1948 and 2005, and that included 57 161 coronary heart disease and 31 093 stroke events. For each cohort we excluded participants who were younger than 18 years, had a BMI of lower than 20 kg/m2, or who had a history of coronary heart disease or stroke. We estimated the hazard ratio (HR) of BMI on coronary heart disease and stroke with and without adjustment for all possible combinations of blood pressure, cholesterol, and glucose. We pooled HRs with a random-effects model and calculated the attenuation of excess risk after adjustment for mediators. Findings The HR for each 5 kg/m2 higher BMI was 1·27 (95% CI 1·23-1·31) for coronary heart disease and 1·18 (1·14-1·22) for stroke after adjustment for confounders. Additional adjustment for the three metabolic risk factors reduced the HRs to 1·15 (1·12-1·18) for coronary heart disease and 1·04 (1·01-1·08) for stroke, suggesting that 46% (95% CI 42-50) of the excess risk of BMI for coronary heart disease and 76% (65-91) for stroke is mediated by these factors. Blood pressure was the most important mediator, accounting for 31% (28-35) of the excess risk for coronary heart disease and 65% (56-75) for stroke. The percentage excess risks mediated by these three mediators did not differ significantly between Asian and western cohorts (North America, western Europe, Australia, and New Zealand). Both overweight (BMI ≥25 to <30 kg/m2) and obesity (BMI ≥30 kg/m2) were associated with a significantly increased risk of coronary heart disease and stroke, compared with normal weight (BMI ≥20 to <25 kg/m2), with 50% (44-58) of the excess risk of overweight and 44% (41-48) of the excess risk of obesity for coronary heart disease mediated by the selected three mediators. The percentages for stroke were 98% (69-155) for overweight and 69% (64-77) for obesity. Interpretation Interventions that reduce high blood pressure, cholesterol, and glucose might address about half of excess risk of coronary heart disease and three-quarters of excess risk of stroke associated with high BMI. Maintenance of optimum bodyweight is needed for the full benefits. Source

Mathis D.,Harvard University
Cell Metabolism

Chronic, low-grade inflammation of visceral adipose tissue, and systemically, is a critical link between recent strikingly parallel rises in the incidence of obesity and type 2 diabetes. Macrophages have been recognized for some time to be critical participants in obesity-induced inflammation of adipose tissue. Of late, a score of other cell types of the innate and adaptive arms of the immune system have been suggested to play a positive or negative role in adipose tissue infiltrates. This piece reviews the existing data on these new participants; discusses experimental uncertainties, inconsistencies, and complexities; and puts forward a minimalist synthetic scheme. © 2013 Elsevier Inc. Source

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