The global burden of cancer 2013 global burden of disease cancer collaboration

Importance Cancer is among the leading causes of death worldwide. Current estimates of cancer burden in individual countries and regions are necessary to inform local cancer control strategies. Objective To estimate mortality, incidence, years lived with disability (YLDs), years of life lost (YLLs), and disability-adjusted life-years (DALYs) for 28 cancers in 188 countries by sex from 1990 to 2013. Evidence Review The general methodology of the Global Burden of Disease (GBD) 2013 study was used. Cancer registries were the source for cancer incidence data as well as mortality incidence (MI) ratios. Sources for cause of death data include vital registration system data, verbal autopsy studies, and other sources. The MI ratios were used to transform incidence data to mortality estimates and cause of death estimates to incidence estimates. Cancer prevalence was estimated using MI ratios as surrogates for survival data; YLDs were calculated by multiplying prevalence estimates with disability weights, which were derived from population-based surveys; YLLs were computed by multiplying the number of estimated cancer deaths at each age with a reference life expectancy; and DALYs were calculated as the sum of YLDs and YLLs. Findings In 2013 there were 14.9 million incident cancer cases, 8.2 million deaths, and 196.3 million DALYs. Prostate cancer was the leading cause for cancer incidence (1.4 million) for men and breast cancer for women (1.8 million). Tracheal, bronchus, and lung (TBL) cancer was the leading cause for cancer death in men and women, with 1.6 million deaths. For men, TBL cancer was the leading cause of DALYs (24.9 million). For women, breast cancer was the leading cause of DALYs (13.1 million). Age-standardized incidence rates (ASIRs) per 100 000 and age-standardized death rates (ASDRs) per 100 000 for both sexes in 2013 were higher in developing vs developed countries for stomach cancer (ASIR, 17 vs 14; ASDR, 15 vs 11), liver cancer (ASIR, 15 vs 7; ASDR, 16 vs 7), esophageal cancer (ASIR, 9 vs 4; ASDR, 9 vs 4), cervical cancer (ASIR, 8 vs 5; ASDR, 4 vs 2), lip and oral cavity cancer (ASIR, 7 vs 6; ASDR, 2 vs 2), and nasopharyngeal cancer (ASIR, 1.5 vs 0.4; ASDR, 1.2 vs 0.3). Between 1990 and 2013, ASIRs for all cancers combined (except nonmelanoma skin cancer and Kaposi sarcoma) increased by more than 10% in 113 countries and decreased by more than 10% in 12 of 188 countries. Conclusions and Relevance Cancer poses a major threat to public health worldwide, and incidence rates have increased in most countries since 1990. The trend is a particular threat to developing nations with health systems that are ill-equipped to deal with complex and expensive cancer treatments. The annual update on the Global Burden of Cancer will provide all stakeholders with timely estimates to guide policy efforts in cancer prevention, screening, treatment, and palliation

Global Mortality Estimates for the 2009 Influenza Pandemic from the GLaMOR Project: A Modeling Study

Background: Assessing the mortality impact of the 2009 influenza A H1N1 virus (H1N1pdm09) is essential for optimizing public health responses to future pandemics. The World Health Organization reported 18,631 laboratory-confirmed pandemic deaths, but the total pandemic mortality burden was substantially higher. We estimated the 2009 pandemic mortality burden through statistical modeling of mortality data from multiple countries. Methods and Findings: We obtained weekly virology and underlying cause-of-death mortality time series for 2005–2009 for 20 countries covering ~35% of the world population. We applied a multivariate linear regression model to estimate pandemic respiratory mortality in each collaborating country. We then used these results plus ten country indicators in a multiple imputation model to project the mortality burden in all world countries. Between 123,000 and 203,000 pandemic respiratory deaths were estimated globally for the last 9 mo of 2009. The majority (62%–85%) were attributed to persons under 65 y of age. We observed a striking regional heterogeneity, with almost 20-fold higher mortality in some countries in the Americas than in Europe. The model attributed 148,000–249,000 respiratory deaths to influenza in an average pre-pandemic season, with only 19% in person

Effect of diet on Haflinger horses with GYS1 mutation (polysaccharide storage myopathy Type 1)

Describing the effects of a carbohydrate-rich diet (CRD) on Haflingers with R309 H glycogensynthase 1 (GYS1) mutation. Haflinger mares heterozygous positive (polysaccharide storage myopathy [PSSM] type 1, n = 7) and negative (control, n = 7) for GYS1 mutation received 6 weeks of CRD and hay only (hay), with a wash out period of two. Each diet was followed by oral glucose tolerance test (oGTF), submaximal treadmill exercise test (STET), and biopsies of semitendinosus (STm) and gluteus medius (GMm) muscles. Insulin sensitivity was evaluated by oGIT. Plasma creatine kinase, aspartate aminotransferase, lactate dehydrogenase, and lactate were measured before and after STET. Semitendinosus and GMm biopsies were evaluated for distribution of fiber types (1, 2A, and 2X), chronic myopathic changes, and complex Periodic Acid Schiff (cPAS) positive amylase resistant inclusions. One Haflinger of control group had cPAS inclusions indicating PSSM type 2; therefore, it was excluded. In PSSM1 horses, cPAS were found in every STm sample, and in 10 of 14 GMm samples, furthermore, STm samples showed a greater total myopathy score and significantly more type 2A and fewer type 2X fibers compared with controls. There were no significant differences between groups regarding enzyme levels and for oGTT. Diet had no effect on muscle enzyme levels after STET and on cPAS inclusions in PSSM1 group. Glycogensynthase 1 mutation in Haflingers was not accompanied by clinical signs, even after STET. Carbohydrate-rich diet for 6 weeks did not induce clinical signs or increase cPAS inclusions. As PSSM type 2 is a possibility in Haflingers, STm muscle biopsy and cPAS evaluation should be performed if GYS1 gene test is negative. (C) 2015 Elsevier Inc. All rights reserved