Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010 : a systematic analysis for the Global Burden of Disease Study 2010

Background Non-fatal health outcomes from diseases and injuries are a crucial consideration in the promotion and monitoring of individual and population health. The Global Burden of Disease (GBD) studies done in 1990 and 2000 have been the only studies to quantify non-fatal health outcomes across an exhaustive set of disorders at the global and regional level. Neither effort quantified uncertainty in prevalence or years lived with disability (YLDs). Methods Of the 291 diseases and injuries in the GBD cause list, 289 cause disability. For 1160 sequelae of the 289 diseases and injuries, we undertook a systematic analysis of prevalence, incidence, remission, duration, and excess mortality. Sources included published studies, case notification, population-based cancer registries, other disease registries, antenatal clinic serosurveillance, hospital discharge data, ambulatory care data, household surveys, other surveys, and cohort studies. For most sequelae, we used a Bayesian meta-regression method, DisMod-MR, designed to address key limitations in descriptive epidemiological data, including missing data, inconsistency, and large methodological variation between data sources. For some disorders, we used natural history models, geospatial models, back-calculation models (models calculating incidence from population mortality rates and case fatality), or registration completeness models (models adjusting for incomplete registration with health-system access and other covariates). Disability weights for 220 unique health states were used to capture the severity of health loss. YLDs by cause at age, sex, country, and year levels were adjusted for comorbidity with simulation methods. We included uncertainty estimates at all stages of the analysis. Findings Global prevalence for all ages combined in 2010 across the 1160 sequelae ranged from fewer than one case per 1 million people to 350 000 cases per 1 million people. Prevalence and severity of health loss were weakly correlated (correlation coefficient −0·37). In 2010, there were 777 million YLDs from all causes, up from 583 million in 1990. The main contributors to global YLDs were mental and behavioural disorders, musculoskeletal disorders, and diabetes or endocrine diseases. The leading specific causes of YLDs were much the same in 2010 as they were in 1990: low back pain, major depressive disorder, iron-deficiency anaemia, neck pain, chronic obstructive pulmonary disease, anxiety disorders, migraine, diabetes, and falls. Age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010. Regional patterns of the leading causes of YLDs were more similar compared with years of life lost due to premature mortality. Neglected tropical diseases, HIV/AIDS, tuberculosis, malaria, and anaemia were important causes of YLDs in sub-Saharan Africa. Interpretation Rates of YLDs per 100 000 people have remained largely constant over time but rise steadily with age. Population growth and ageing have increased YLD numbers and crude rates over the past two decades. Prevalences of the most common causes of YLDs, such as mental and behavioural disorders and musculoskeletal disorders, have not decreased. Health systems will need to address the needs of the rising numbers of individuals with a range of disorders that largely cause disability but not mortality. Quantification of the burden of non-fatal health outcomes will be crucial to understand how well health systems are responding to these challenges. Effective and affordable strategies to deal with this rising burden are an urgent priority for health systems in most parts of the world. Funding Bill & Melinda Gates Foundation.

Targeting ASCT2-mediated glutamine uptake blocks prostate cancer growth and tumour development

Glutamine is conditionally essential in cancer cells, being utilized as a carbon and nitrogen source for macromolecule production, as well as for anaplerotic reactions fuelling the tricarboxylic acid (TCA) cycle. In this study, we demonstrated that the glutamine transporter ASCT2 (SLC1A5) is highly expressed in prostate cancer patient samples. Using LNCaP and PC-3 prostate cancer cell lines, we showed that chemical or shRNA-mediated inhibition of ASCT2 function in vitro decreases glutamine uptake, cell cycle progression through E2F transcription factors, mTORC1 pathway activation and cell growth. Chemical inhibition also reduces basal oxygen consumption and fatty acid synthesis, showing that downstream metabolic function is reliant on ASCT2-mediated glutamine uptake. Furthermore, shRNA knockdown of ASCT2 in PC-3 cell xenografts significantly inhibits tumour growth and metastasis in vivo, associated with the down-regulation of E2F cell cycle pathway proteins. In conclusion, ASCT2-mediated glutamine uptake is essential for multiple pathways regulating the cell cycle and cell growth, and is therefore a putative therapeutic target in prostate cancer.

Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990–2013: Quantifying the epidemiological transition

Background The Global Burden of Disease Study 2013 (GBD 2013) aims to bring together all available epidemiological data using a coherent measurement framework, standardised estimation methods, and transparent data sources to enable comparisons of health loss over time and across causes, age–sex groups, and countries. The GBD can be used to generate summary measures such as disability-adjusted life-years (DALYs) and healthy life expectancy (HALE) that make possible comparative assessments of broad epidemiological patterns across countries and time. These summary measures can also be used to quantify the component of variation in epidemiology that is related to sociodemographic development. Methods We used the published GBD 2013 data for age-specific mortality, years of life lost due to premature mortality (YLLs), and years lived with disability (YLDs) to calculate DALYs and HALE for 1990, 1995, 2000, 2005, 2010, and 2013 for 188 countries. We calculated HALE using the Sullivan method; 95% uncertainty intervals (UIs) represent uncertainty in age-specific death rates and YLDs per person for each country, age, sex, and year. We estimated DALYs for 306 causes for each country as the sum of YLLs and YLDs; 95% UIs represent uncertainty in YLL and YLD rates. We quantified patterns of the epidemiological transition with a composite indicator of sociodemographic status, which we constructed from income per person, average years of schooling after age 15 years, and the total fertility rate and mean age of the population. We applied hierarchical regression to DALY rates by cause across countries to decompose variance related to the sociodemographic status variable, country, and time. Findings Worldwide, from 1990 to 2013, life expectancy at birth rose by 6·2 years (95% UI 5·6–6·6), from 65·3 years (65·0–65·6) in 1990 to 71·5 years (71·0–71·9) in 2013, HALE at birth rose by 5·4 years (4·9–5·8), from 56·9 years (54·5–59·1) to 62·3 years (59·7–64·8), total DALYs fell by 3·6% (0·3–7·4), and age-standardised DALY rates per 100 000 people fell by 26·7% (24·6–29·1). For communicable, maternal, neonatal, and nutritional disorders, global DALY numbers, crude rates, and age-standardised rates have all declined between 1990 and 2013, whereas for non–communicable diseases, global DALYs have been increasing, DALY rates have remained nearly constant, and age-standardised DALY rates declined during the same period. From 2005 to 2013, the number of DALYs increased for most specific non-communicable diseases, including cardiovascular diseases and neoplasms, in addition to dengue, food-borne trematodes, and leishmaniasis; DALYs decreased for nearly all other causes. By 2013, the five leading causes of DALYs were ischaemic heart disease, lower respiratory infections, cerebrovascular disease, low back and neck pain, and road injuries. Sociodemographic status explained more than 50% of the variance between countries and over time for diarrhoea, lower respiratory infections, and other common infectious diseases; maternal disorders; neonatal disorders; nutritional deficiencies; other communicable, maternal, neonatal, and nutritional diseases; musculoskeletal disorders; and other non-communicable diseases. However, sociodemographic status explained less than 10% of the variance in DALY rates for cardiovascular diseases; chronic respiratory diseases; cirrhosis; diabetes, urogenital, blood, and endocrine diseases; unintentional injuries; and self-harm and interpersonal violence. Predictably, increased sociodemographic status was associated with a shift in burden from YLLs to YLDs, driven by declines in YLLs and increases in YLDs from musculoskeletal disorders, neurological disorders, and mental and substance use disorders. In most country-specific estimates, the increase in life expectancy was greater than that in HALE. Leading causes of DALYs are highly variable across countries. Interpretation Global health is improving. Population growth and ageing have driven up numbers of DALYs, but crude rates have remained relatively constant, showing that progress in health does not mean fewer demands on health systems. The notion of an epidemiological transition—in which increasing sociodemographic status brings structured change in disease burden—is useful, but there is tremendous variation in burden of disease that is not associated with sociodemographic status. This further underscores the need for country-specific assessments of DALYs and HALE to appropriately inform health policy decisions and attendant actions.

Genetic studies of body mass index yield new insights for obesity biology

Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10−8), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ~2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

FTO genotype is associated with phenotypic variability of body mass index

There is evidence across several species for genetic control of phenotypic variation of complex traits1, 2, 3, 4, such that the variance among phenotypes is genotype dependent. Understanding genetic control of variability is important in evolutionary biology, agricultural selection programmes and human medicine, yet for complex traits, no individual genetic variants associated with variance, as opposed to the mean, have been identified. Here we perform a meta-analysis of genome-wide association studies of phenotypic variation using ~170,000 samples on height and body mass index (BMI) in human populations. We report evidence that the single nucleotide polymorphism (SNP) rs7202116 at the FTO gene locus, which is known to be associated with obesity (as measured by mean BMI for each rs7202116 genotype)5, 6, 7, is also associated with phenotypic variability. We show that the results are not due to scale effects or other artefacts, and find no other experiment-wise significant evidence for effects on variability, either at loci other than FTO for BMI or at any locus for height. The difference in variance for BMI among individuals with opposite homozygous genotypes at the FTO locus is approximately 7%, corresponding to a difference of ~0.5 kilograms in the standard deviation of weight. Our results indicate that genetic variants can be discovered that are associated with variability, and that between-person variability in obesity can partly be explained by the genotype at the FTO locus. The results are consistent with reported FTO by environment interactions for BMI8, possibly mediated by DNA methylation9, 10. Our BMI results for other SNPs and our height results for all SNPs suggest that most genetic variants, including those that influence mean height or mean BMI, are not associated with phenotypic variance, or that their effects on variability are too small to detect even with samples sizes greater than 100,000.

Industrial Removal Office records undated, 1899-1922

Contains Board of Directors minutes (1903, 1907), Executive Committee minutes (1907), Removal Committee minutes (1903-1917), Annual Reports (1910, 1913), Monthly Reports (1901-1919), Monthly Bulletins (1914-1915), studies of those removed, Bressler's "The Removal Work, Including Galveston," and several papers relating to the IRO and immigration. Financial papers include a budget (1914), comparative per capita cost figures (1909-1922), audits (1915-1918), receipts and expenditures (1918-1922), investment records, bank balances (1907-1922), removal work cash book (1904-1911), office expenses cash account (1903-1906), and the financial records of other agencies working with the IRO (1906). Includes also removal case records of first the Jewish Agricultural Society (1899-1900), and then of the IRO (1901-1922) when it took over its work, family reunion case records (1901-1904), and the follow-up records of persons removed to various cities (1903-1914). Contains also the correspondence of traveling agents' contacts throughout the U.S. from 1905-1914, among them Stanley Bero, Henry P. Goldstein, Philip Seman, and Morris D. Waldman.

Sermon by Jacques Judah Lyons on the death of President William Henry Harrison

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Directional dominance on stature and cognition in diverse human populations

Homozygosity has long been associated with rare, often devastating, Mendelian disorders1, and Darwin was one of the first to recognize that inbreeding reduces evolutionary fitness2. However, the effect of the more distant parental relatedness that is common in modern human populations is less well understood. Genomic data now allow us to investigate the effects of homozygosity on traits of public health importance by observing contiguous homozygous segments (runs of homozygosity), which are inferred to be homozygous along their complete length. Given the low levels of genome-wide homozygosity prevalent in most human populations, information is required on very large numbers of people to provide sufficient power3, 4. Here we use runs of homozygosity to study 16 health-related quantitative traits in 354,224 individuals from 102 cohorts, and find statistically significant associations between summed runs of homozygosity and four complex traits: height, forced expiratory lung volume in one second, general cognitive ability and educational attainment (P < 1 × 10−300, 2.1 × 10−6, 2.5 × 10−10 and 1.8 × 10−10, respectively). In each case, increased homozygosity was associated with decreased trait value, equivalent to the offspring of first cousins being 1.2 cm shorter and having 10 months’ less education. Similar effect sizes were found across four continental groups and populations with different degrees of genome-wide homozygosity, providing evidence that homozygosity, rather than confounding, directly contributes to phenotypic variance. Contrary to earlier reports in substantially smaller samples5, 6, no evidence was seen of an influence of genome-wide homozygosity on blood pressure and low density lipoprotein cholesterol, or ten other cardio-metabolic traits. Since directional dominance is predicted for traits under directional evolutionary selection7, this study provides evidence that increased stature and cognitive function have been positively selected in human evolution, whereas many important risk factors for late-onset complex diseases may not have been.

Averting biodiversity collapse in tropical forest protected areas

The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon(1-3). With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses(4-9). As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world's major tropical regions. Our analysis reveals great variation in reserve `health': about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.

Proceedings of the 1998 Science Board Symposium on The Impacts of the 1997/98 El Niño Event on the North Pacific Ocean and Its Marginal Seas

Preface [pdf, 0.01 Mb] James J. O'Brien The big picture - The ENSO of 1997-98 [pdf, 0.01 Mb] James E. Overland, Nicholas A. Bond & Jennifer Miletta Adams Atmospheric anomalies in 1997: Links to ENSO? [pdf, 0.54 Mb] Vladimir I. Ponomarev, Olga Trusenkova, Serge Trousenkov, Dmitry Kaplunenko, Elena Ustinova & Antonina Polyakova The ENSO signal in the northwest Pacific [pdf, 0.47 Mb] Robert L. Smith, A. Huyer, P.M. Kosro & J.A. Barth Observations of El Niño off Oregon: July 1997 to present (October 1998) [pdf, 1.31 Mb] Patrica A. Wheeler & Jon Hill Biological effects of the 1997-1998 El Niño event off Oregon: Nutrient and chlorophyll distributions [pdf, 1.13 Mb] William T. Peterson Hydrography and zooplankton off the central Oregon coast during the 1997-1998 El Niño event [pdf, 0.26 Mb] William Crawford, Josef Cherniawsky, Michael Foreman & Peter Chandler El Niño sea level signal along the west coast of Canada [pdf, 1.25 Mb] Howard J. Freeland & Rick Thomson The El Niño signal along the west coast of Canada - temperature, salinity and velocity [pdf, 0.49 Mb] Frank A. Whitney, David L. Mackas, David W. Welch & Marie Robert Impact of the 1990s El Niños on nutrient supply and productivity of Gulf of Alaska waters [pdf, 0.06 Mb] Craig McNeil, David Farmer & Mark Trevorrow Dissolved gas measurements at Stn. P4 during the 97-98 El Niño [pdf, 0.13 Mb] Kristen L.D. Milligan, Colin D. Levings & Robert E. DeWreede Data compilation and preliminary time series analysis of abundance of a dominant intertidal kelp species in relation to the 1997/1998 El Niño event [pdf, 0.05 Mb] S.M. McKinnell, C.C. Wood, M. Lapointe, J.C. Woodey, K.E. Kostow, J. Nelson & K.D. Hyatt Reviewing the evidence that adult sockeye salmon strayed from the Fraser River and spawned in other rivers in 1997 [pdf,0.03 Mb] G.A. McFarlane & R.J. Beamish Sardines return to British Columbia waters [pdf, 0.34 Mb] Ken H. Morgan Impact of the 1997/98 El Niño on seabirds of the northeast Pacific [pdf, 0.06 Mb] Thomas C. Royer & Thomas Weingartner Coastal hydrographic responses in the northern Gulf of Alaska to the 1997-98 ENSO event [pdf, 0.76 Mb] John F. Piatt, Gary Drew, Thomas Van Pelt, Alisa Abookire, April Nielsen, Mike Shultz & Alexander Kitaysky Biological effects of the 1997/98 ENSO in Cook Inlet, Alaska [pdf, 0.22 Mb] H.J. Niebauer The 1997-98 El Niño in the Bering Sea as compared with previous ENSO events and the "regime shift" of the late 1970s [pdf, 0.10 Mb] A.S. Krovnin, G.P. Nanyushin, M.Yu. Kruzhalov, G.V. Khen, M.A. Bogdanov, E.I. Ustinova, V.V. Maslennikov, A.M. Orlov, B.N. Kotenev, V.V. Bulanov & G.P. Muriy The state of the Far East seas during the 1997/98 El Niño event [pdf, 0.15 Mb] Stacy Smith & Susan Henrichs Phytoplankton collected by a time-series sediment trap deployed in the southeast Bering Sea during 1997 [pdf, 0.21 Mb] Cynthia T. Tynan Redistributions of cetaceans in the southeast Bering Sea relative to anomalous oceanographic conditions during the 1997 El Niño [pdf, 0.02 Mb] Akihiko Yatsu, Junta Mori, Hiroyuki Tanaka, Tomowo Watanabe, Kazuya Nagasawa, Yikimasa Ishida, Toshimi Meguro, Yoshihiko Kamei & Yasunori Sakurai Stock abundance and size compositions of the neon flying squid in the central North Pacific Ocean during 1979-1998 [pdf, 0.11 Mb] O.B. Feschenko A new point of view concerning the El Niño mechanism [pdf, 0.01 Mb] Nathan Mantua 97/98 Ocean climate variability in the northeast Pacific: How much blame does El Niño deserve? [pdf, 0.01 Mb] Vadim P. Pavlychev Sharp changes of hydrometeorological conditions in the northwestern Pacific during the 1997/1998 El Niño event [pdf, 0.01 Mb] Jingyi Wang Predictability and forecast verification of El Niño events [pdf, 0.01 Mb] (Document contains 110 pages)

John Nathan Cobb (1868–1930): Founding Director of the College of Fisheries, University of Washington, Seattle

John Nathan Cobb (1868–1930) became the founding Director of the College of Fisheries, University of Washington, Seattle, in 1919 without the benefit of a college education. An inquisitive and ambitious man, he began his career in the newspaper business and was introduced to commercial fisheries when he joined the U.S. Fish Commission (USFC) in 1895 as a clerk, and he was soon promoted to a “Field Agent” in the Division of Statistics, Washington, D.C. During the next 17 years, Cobb surveyed commercial fisheries from Maine to Florida, Hawaii, the Pacific Northwest, and Alaska for the USFC and its successor, the U.S. Bureau of Fisheries. In 1913, he became editor of the prominent west coast trade magazine, Pacific Fisherman, of Seattle, Wash., where he became known as a leading expert on the fisheries of the Pacific Northwest. He soon joined the campaign, led by his employer, to establish the nation’s first fisheries school at the University of Washington. After a brief interlude (1917–1918) with the Alaska Packers Association in San Francisco, Calif., he was chosen as the School’s founding director in 1919. Reflecting his experience and mindset, as well as the University’s apparent initial desire, Cobb established the College of Fisheries primarily as a training ground for those interested in applied aspects of the commercial fishing industry. Cobb attracted sufficient students, was a vigorous spokesman for the College, and had ambitions plans for expansion of the school’s faculty and facilities. He became aware that the College was not held in high esteem by his faculty colleagues or by the University administration because of the school’s failure to emphasize scholastic achievement, and he attempted to correct this deficiency. Cobb became ill with heart problems in 1929 and died on 13 January 1930. The University soon thereafter dissolved the College and dismissed all but one of its faculty. A Department of Fisheries, in the College of Science, was then established in 1930 and was led by William Francis Thompson (1888–1965), who emphasized basic science and fishery biology. The latter format continues to the present in the Department’s successor, The School of Aquatic Fisheries and Science.

Sketch of the Life of William Blanchard Towne

Sketch of the life of William Blanchard Towne.

The Missionary pioneer, or, A brief memoir of the life, labours, and death of John Stewart, (man of colour) founder, under God of the mission among the Wyandotts at Upper Sandusky, Ohio / Published by Joseph Mitchell.

http://www.archive.org/details/missionarypionee00stewrich