Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990�2015: a systematic analysis for the Global Burden of Disease Study 2015

Background Non-fatal outcomes of disease and injury increasingly detract from the ability of the world's population to live in full health, a trend largely attributable to an epidemiological transition in many countries from causes affecting children, to non-communicable diseases (NCDs) more common in adults. For the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015), we estimated the incidence, prevalence, and years lived with disability for diseases and injuries at the global, regional, and national scale over the period of 1990 to 2015. Methods We estimated incidence and prevalence by age, sex, cause, year, and geography with a wide range of updated and standardised analytical procedures. Improvements from GBD 2013 included the addition of new data sources, updates to literature reviews for 85 causes, and the identification and inclusion of additional studies published up to November, 2015, to expand the database used for estimation of non-fatal outcomes to 60�900 unique data sources. Prevalence and incidence by cause and sequelae were determined with DisMod-MR 2.1, an improved version of the DisMod-MR Bayesian meta-regression tool first developed for GBD 2010 and GBD 2013. For some causes, we used alternative modelling strategies where the complexity of the disease was not suited to DisMod-MR 2.1 or where incidence and prevalence needed to be determined from other data. For GBD 2015 we created a summary indicator that combines measures of income per capita, educational attainment, and fertility (the Socio-demographic Index SDI) and used it to compare observed patterns of health loss to the expected pattern for countries or locations with similar SDI scores. Findings We generated 9·3 billion estimates from the various combinations of prevalence, incidence, and YLDs for causes, sequelae, and impairments by age, sex, geography, and year. In 2015, two causes had acute incidences in excess of 1 billion: upper respiratory infections (17·2 billion, 95% uncertainty interval UI 15·4�19·2 billion) and diarrhoeal diseases (2·39 billion, 2·30�2·50 billion). Eight causes of chronic disease and injury each affected more than 10% of the world's population in 2015: permanent caries, tension-type headache, iron-deficiency anaemia, age-related and other hearing loss, migraine, genital herpes, refraction and accommodation disorders, and ascariasis. The impairment that affected the greatest number of people in 2015 was anaemia, with 2·36 billion (2·35�2·37 billion) individuals affected. The second and third leading impairments by number of individuals affected were hearing loss and vision loss, respectively. Between 2005 and 2015, there was little change in the leading causes of years lived with disability (YLDs) on a global basis. NCDs accounted for 18 of the leading 20 causes of age-standardised YLDs on a global scale. Where rates were decreasing, the rate of decrease for YLDs was slower than that of years of life lost (YLLs) for nearly every cause included in our analysis. For low SDI geographies, Group 1 causes typically accounted for 20�30% of total disability, largely attributable to nutritional deficiencies, malaria, neglected tropical diseases, HIV/AIDS, and tuberculosis. Lower back and neck pain was the leading global cause of disability in 2015 in most countries. The leading cause was sense organ disorders in 22 countries in Asia and Africa and one in central Latin America; diabetes in four countries in Oceania; HIV/AIDS in three southern sub-Saharan African countries; collective violence and legal intervention in two north African and Middle Eastern countries; iron-deficiency anaemia in Somalia and Venezuela; depression in Uganda; onchoceriasis in Liberia; and other neglected tropical diseases in the Democratic Republic of the Congo. Interpretation Ageing of the world's population is increasing the number of people living with sequelae of diseases and injuries. Shifts in the epidemiological profile driven by socioeconomic change also contribute to the continued increase in years lived with disability (YLDs) as well as the rate of increase in YLDs. Despite limitations imposed by gaps in data availability and the variable quality of the data available, the standardised and comprehensive approach of the GBD study provides opportunities to examine broad trends, compare those trends between countries or subnational geographies, benchmark against locations at similar stages of development, and gauge the strength or weakness of the estimates available. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens

Geochronology in the southern Midyan terrane: a review of constraints on the timing of magmatic pulses and tectonic evolution in a northwestern part of the Arabian Shield

© 2017 Taylor & Francis The southern Midyan terrane is a composite Tonian to Ediacaran tectonostratigraphic crustal block in the northern Arabian Shield that prior to Red Sea opening was contiguous with coeval rocks in the Eastern Desert of Egypt and Sinai. Ion microprobe (sensitive high-resolution ion microprobe [SHRIMP]) dating of 12 rock samples described here and the results of other dating programmes establish a clear timeframe for depositional, intrusive, and structural events in the region and provide a chronology of tectonism in this part of the Arabian-Nubian Shield. Deposition of Zaam and Bayda group volcanosedimentary rocks and emplacement of mafic-ultramafic complexes and TTG-type diorite, tonalite, and granodiorite denote formation of the Tonian (780–715 Ma) Zaam arc and fore-arc ophiolite above a possible west-dipping subduction system in the southern part of the Midyan terrane. Convergence with the Hijaz terrane farther south and obduction of ophiolite nappes resulted by ~700 Ma in development of the Yanbu suture. Ongoing or a new subduction system led to a ~705–660 Ma Cryogenian pulse of magmatism represented by I-type calc-alkaline diorite, granodiorite, and granite that have volcanic-arc and syn-collisional granite affinities. This was followed, after a brief end-Cryogenian hiatus, by a 635–~570 Ma period of Ediacaran magmatism marked by monzogranite, syenogranite, and minor gabbro and diorite. These rocks are reported to have within-plate to volcanic-arc and syncollision chemical characteristics but their precise tectonic setting is uncertain. Structurally, the intrusions are diapiric and were evidently emplaced in an extensional regime consistent with an overlap between intrusion and Najd faulting associated, at this time, with transpressional collision and northward extension through much of the ANS. Terminal magmatism in the southern Midyan terrane postdated cessation of Najd faulting at ~575 Ma and resulted in the emplacement of undeformed within-plate A-type alkali-feldspar granites and mafic (lamprophyre) and felsic dikes

Molecular Regulation of Contractile Smooth Muscle Cell Phenotype: Implications for Vascular Tissue Engineering

The molecular regulation of smooth muscle cell (SMC) behavior is reviewed, with particular emphasis on stimuli that promote the contractile phenotype. SMCs can shift reversibly along a continuum from a quiescent, contractile phenotype to a synthetic phenotype, which is characterized by proliferation and extracellular matrix (ECM) synthesis. This phenotypic plasticity can be harnessed for tissue engineering. Cultured synthetic SMCs have been used to engineer smooth muscle tissues with organized ECM and cell populations. However, returning SMCs to a contractile phenotype remains a key challenge. This review will integrate recent work on how soluble signaling factors, ECM, mechanical stimulation, and other cells contribute to the regulation of contractile SMC phenotype. The signal transduction pathways and mechanisms of gene expression induced by these stimuli are beginning to be elucidated and provide useful information for the quantitative analysis of SMC phenotype in engineered tissues. Progress in the development of tissue-engineered scaffold systems that implement biochemical, mechanical, or novel polymer fabrication approaches to promote contractile phenotype will also be reviewed. The application of an improved molecular understanding of SMC biology will facilitate the design of more potent cell-instructive scaffold systems to regulate SMC behavior