The Increasing Burden of Imported Chronic Hepatitis B — United States, 1974–2008

Without intervention, up to 25% of individuals chronically infected with hepatitis B virus (HBV) die of late complications, including cirrhosis and liver cancer. The United States, which in 1991 implemented a strategy to eliminate HBV transmission through universal immunization, is a country of low prevalence. Approximately 3,000-5,000 U.S.-acquired cases of chronic hepatitis B have occurred annually since 2001. Many more chronically infected persons migrate to the United States yearly from countries of higher prevalence. Although early identification of chronic HBV infection can reduce the likelihood of transmission and late complications, immigrants are not routinely screened for HBV infection during or after immigration.To estimate the number of imported cases of chronic hepatitis B, we multiplied country-specific prevalence estimates by the yearly number of immigrants from each country during 1974-2008.During 1974-2008, 27.9 million immigrants entered the U.S. Sixty-three percent were born in countries of intermediate or high chronic hepatitis B prevalence (range 2%-31%). On average, an estimated 53,800 chronic hepatitis B cases were imported to the U.S. yearly from 2004 through 2008. The Philippines, China, and Vietnam contributed the most imported cases (13.4%, 12.5%, and 11.0%, respectively). Imported cases increased from an estimated low of 105,750 during the period 1974-1977 to a high of 268,800 in 2004-2008.Imported chronic hepatitis B cases account for approximately 95% of new U.S. cases. Earlier case identification and management of infected immigrants would strengthen the U.S. strategy to eliminate HBV transmission, and could delay disease progression and prevent some deaths among new Americans

Attributing Illness to Food

Identification and prioritization of effective food safety interventions require an understanding of the relationship between food and pathogen from farm to consumption. Critical to this cause is food attribution, the capacity to attribute cases of foodborne disease to the food vehicle or other source responsible for illness. A wide variety of food attribution approaches and data are used around the world, including the analysis of outbreak data, case-control studies, microbial subtyping and source tracking methods, and expert judgment, among others. The Food Safety Research Consortium sponsored the Food Attribution Data Workshop in October 2003 to discuss the virtues and limitations of these approaches and to identify future options for collecting food attribution data in the United States. We summarize workshop discussions and identify challenges that affect progress in this critical component of a risk-based approach to improving food safety

Large Coherence Area Thin-Film Photonic Stop-Band Lasers

We demonstrate that the shift of the stop band position with increasing oblique angle in periodic structures results in a wide transverse exponential field distribution corresponding to strong angular confinement of the radiation. The beam expansion follows an effective diffusive equation depending only upon the spectral mode width. In the presence of gain, the beam cross section is limited only by the size of the gain area. As an example of an active periodic photonic medium, we calculate and measure laser emission from a dye-doped cholesteric liquid crystal film

Quantifying mesoscale-driven nitrate supply: a case study

The supply of nitrate to surface waters plays a crucial role in maintaining marine life. Physical processes at the mesoscale (~10-100?km) and smaller have been advocated to provide a major fraction of the global supply. Whilst observational studies have focussed on well-defined features, such as isolated eddies, the vertical circulation and nutrient supply in a typical 100-200?km square of ocean will involve a turbulent spectrum of interacting, evolving and decaying features. A crucial step in closing the ocean nitrogen budget is to be able to rank the importance of mesoscale fluxes against other sources of nitrate for surface waters for a representative area of open ocean. While this has been done using models, the vital observational equivalent is still lacking.To illustrate the difficulties that prevent us from putting a global estimate on the significance of the mesoscale observationally, we use data from a cruise in the Iceland Basin where vertical velocity and nitrate observations were made simultaneously at the same high spatial resolution. Local mesoscale nitrate flux is found to be an order of magnitude greater than that due to small-scale vertical mixing and exceeds coincident nitrate uptake rates and estimates of nitrate supply due to winter convection. However, a non-zero net vertical velocity for the region introduces a significant bias in regional estimates of the mesoscale vertical nitrate transport. The need for synopticity means that a more accurate estimate can not be simply found by using a larger survey area. It is argued that time-series, rather than spatial surveys, may be the best means to quantify the contribution of mesoscale processes to the nitrate budget of the surface ocean

Observed multivariable signals of late 20th and early 21st century volcanic activity

The relatively muted warming of the surface and lower troposphere since 1998 has attracted considerable attention. One contributory factor to this “warming hiatus” is an increase in volcanically induced cooling over the early 21st century. Here we identify the signals of late 20th and early 21st century volcanic activity in multiple observed climate variables. Volcanic signals are statistically discernible in spatial averages of tropical and near-global SST, tropospheric temperature, net clear-sky short-wave radiation, and atmospheric water vapor. Signals of late 20th and early 21st century volcanic eruptions are also detectable in near-global averages of rainfall. In tropical average rainfall, however, only a Pinatubo-caused drying signal is identifiable. Successful volcanic signal detection is critically dependent on removal of variability induced by the El Nino–Southern Oscillation.National Science Foundation (U.S.) (Grant AGS-1342810

Associations of vomiting and antiemetic use in pregnancy with levels of circulating GDF15 early in the second trimester: A nested case-control study.

Background: Although nausea and vomiting are very common in pregnancy, their pathogenesis is poorly understood. We tested the hypothesis that circulating growth and differentiation factor 15 (GDF15) concentrations in early pregnancy, whose gene is implicated in hyperemesis gravidarum, are associated with nausea and vomiting. Methods: Blood samples for the measurement of GDF15 and human chorionic gonadotrophin (hCG) concentrations were obtained early in the second trimester (median 15.1 (interquartile range 14.4-15.7) weeks) of pregnancy from 791 women from the Cambridge Baby Growth Study, a prospective pregnancy and birth cohort. During each trimester participants completed a questionnaire which included questions about nausea, vomiting and antiemetic use. Associations with pre-pregnancy body mass indexes (BMI) were validated in 231 pregnant NIPTeR Study participants. Results: Circulating GDF15 concentrations were higher in women reporting vomiting in the second trimester than in women reporting no pregnancy nausea or vomiting: 11,581 (10,977-12,219) (n=175) vs. 10,593 (10,066-11,147) (n=193) pg/mL, p=0.02). In women who took antiemetic drugs during pregnancy (n=11) the GDF15 levels were also raised 13,157 (10,558-16,394) pg/mL (p =0.04). Serum GFD15 concentrations were strongly positively correlated with hCG levels but were inversely correlated with maternal BMIs, a finding replicated in the NIPTeR Study. Conclusions: Week 15 serum GDF15 concentrations are positively associated with second trimester vomiting and maternal antiemetic use in pregnancy. Given GDF15's site of action in the chemoreceptor trigger zone of the brainstem and its genetic associations with hyperemesis gravidarum, these data support the concept that GDF15 may be playing a pathogenic role in pregnancy-associated vomiting.This work was supported by the Wellcome Trust [100574; Strategic Award]; and an unrestricted award from the Novo Nordisk Foundation (International Prize for Excellence in diabetes research) (both SOR). The Cambridge Baby Growth Study has been funded by the Medical Research Council (7500001180) (CLA), European Union Framework 5 (QLK4-1999-01422) (IAH), the Mothercare Foundation (RG54608) (IAH), Newlife Foundation for Disabled Children (07/20) (IAH), and the World Cancer Research Fund International (2004/03) (DBD). It is also supported by the National Institute for Health Research Cambridge Biomedical Research Centre. KKO and JRB are supported by the Medical Research Council (Unit Programme MC_UU_12015/2). The NIPTeR study was in part supported by an AMC-VUMC Alliance grant

Evidence of a Causal Association Between Insulinemia and Endometrial Cancer: A Mendelian Randomization Analysis.

BACKGROUND: Insulinemia and type 2 diabetes (T2D) have been associated with endometrial cancer risk in numerous observational studies. However, the causality of these associations is uncertain. Here we use a Mendelian randomization (MR) approach to assess whether insulinemia and T2D are causally associated with endometrial cancer. METHODS: We used single nucleotide polymorphisms (SNPs) associated with T2D (49 variants), fasting glucose (36 variants), fasting insulin (18 variants), early insulin secretion (17 variants), and body mass index (BMI) (32 variants) as instrumental variables in MR analyses. We calculated MR estimates for each risk factor with endometrial cancer using an inverse-variance weighted method with SNP-endometrial cancer associations from 1287 case patients and 8273 control participants. RESULTS: Genetically predicted higher fasting insulin levels were associated with greater risk of endometrial cancer (odds ratio [OR] per standard deviation = 2.34, 95% confidence internal [CI] = 1.06 to 5.14, P = .03). Consistently, genetically predicted higher 30-minute postchallenge insulin levels were also associated with endometrial cancer risk (OR = 1.40, 95% CI = 1.12 to 1.76, P = .003). We observed no associations between genetic risk of type 2 diabetes (OR = 0.91, 95% CI = 0.79 to 1.04, P = .16) or higher fasting glucose (OR = 1.00, 95% CI = 0.67 to 1.50, P = .99) and endometrial cancer. In contrast, endometrial cancer risk was higher in individuals with genetically predicted higher BMI (OR = 3.86, 95% CI = 2.24 to 6.64, P = 1.2x10(-6)). CONCLUSION: This study provides evidence to support a causal association of higher insulin levels, independently of BMI, with endometrial cancer risk.This study was supported by MRC grant MC_UU_12015/1 and by the Innovative Medicines Initiative Joint Undertaking under EMIF grant agreement n° 115372 (contributions from the European Union's Seventh Framework Programme (FP7/2007-2013) and EFPIA companies). ANECS recruitment was supported by project grants from the National Health and Medical Research Council of Australia (ID#339435), The Cancer Council Queensland (ID#4196615) and Cancer Council Tasmania (ID#403031 and ID#457636). SEARCH recruitment was funded by a programme grant from Cancer Research UK [C490/A10124]. Case genotyping was supported by the National Health and Medical Research Council (ID#552402). Control data was generated by the Wellcome Trust Case Control Consortium (WTCCC), and a full list of the investigators who contributed to the generation of the data is available from the WTCCC website. We acknowledge use of DNA from the British 1958 Birth Cohort collection, funded by the Medical Research Council grant G0000934 and the Wellcome Trust grant 068545/Z/02. Funding for this project was provided by the Wellcome Trust under award 085475. Recruitment of the QIMR controls was supported by the National Health and Medical Research Council of Australia (NHMRC). The University of Newcastle, the Gladys M Brawn Senior Research Fellowship scheme, The Vincent Fairfax Family Foundation, the Hunter Medical Research Institute and the Hunter Area Pathology Service all contributed towards the costs of establishing the Hunter Community Study. K.T.N. was supported by the Gates Cambridge Trust. R.K.S. is supported by the Wellcome Trust (grant number WT098498). A.B.S. is supported by the National Health and Medical Research Council (NHMRC) Fellowship Scheme. D.F.E. is a Principal Research Fellow of Cancer Research UK. A.M.D is supported by the Joseph Mitchell Trust.This is the final version of the article. It first appeared from Oxford University Press via http://dx.doi.org/10.1093/jnci/djv17

Causes of differences in model and satellite tropospheric warming rates

In the early twenty-first century, satellite-derived tropospheric warming trends were generally smaller than trends estimated from a large multi-model ensemble. Because observations and coupled model simulations do not have the same phasing of natural internal variability, such decadal differences in simulated and observed warming rates invariably occur. Here we analyse global-mean tropospheric temperatures from satellites and climate model simulations to examine whether warming rate differences over the satellite era can be explained by internal climate variability alone. We find that in the last two decades of the twentieth century, differences between modelled and observed tropospheric temperature trends are broadly consistent with internal variability. Over most of the early twenty-first century, however, model tropospheric warming is substantially larger than observed; warming rate differences are generally outside the range of trends arising from internal variability. The probability that multi-decadal internal variability fully explains the asymmetry between the late twentieth and early twenty-first century results is low (between zero and about 9%). It is also unlikely that this asymmetry is due to the combined effects of internal variability and a model error in climate sensitivity. We conclude that model overestimation of tropospheric warming in the early twenty-first century is partly due to systematic deficiencies in some of the post-2000 external forcings used in the model simulations