Incorporating a Hyperspectral Direct-Diffuse Pyranometer in an Above-Water Reflectance Algorithm

In situ hyperspectral remote-sensing reflectance (Rrs(λ)) is used to derive water quality products and perform autonomous monitoring of aquatic ecosystems. Conventionally, above-water Rrs(λ) is estimated from three spectroradiometers which measure downwelling planar irradiance(Ed(λ)), sky radiance (Ls(λ)), and total upwelling radiance (Lt(λ)), with a scaling of Ls(λ)/Ed(λ)used to correct for surface-reflected radiance. Here, we incorporate direct and diffuse irradiance,(Edd(λ)) and Eds(λ)), from a hyperspectral pyranometer (HSP) in an Rrs(λ) processing algorithm from a solar-tracking radiometry platform (So-Rad). HSP measurements of sun and sky glint (scaled Edd(λ)/Ed(λ) and Eds(λ)/Ed(λ)) replace model-optimized terms in the 3C (three-glint component) Rrs(λ) algorithm, which estimates Rrs(λ) via spectral optimization of modelled atmospheric and water properties with respect to measured radiometric quantities. We refer to the HSP-enabled method as DD (direct-diffuse) and compare differences in Rrs(λ) and Rrs(λ) variability (assessed over 20 min measurement cycles) between 3C and DD as a function of atmospheric optical state using data from three ports in the Western Channel. The greatest divergence between the algorithms occurs in the blue part of the spectrum where DD has significantly lower Rrs(λ) variability than 3C in clearer sky conditions. We also consider Rrs(λ) processing from a hypothetical two-sensor configuration (using only the Lt(λ) spectroradiometer and the HSP and referred to as DD2) as a potential lower-cost measurement solution, which is shown to have comparable Rrs(λ) and Rrs(λ) variability to DD in clearer sky conditions. Our results support that the HSP sensor can fulfil a dual role in aquatic ecosystem monitoring by improving precision in Rrs(λ) alongside its primary function to characterize aerosols

A solution to the trilemma of the moist Charney-Phillips staggering

This is the author accepted manuscript. The final version is available from the Royal Meteorological Society via the DOI in this recordThe Charney-Phillips grid, used in many numerical models of the atmosphere, involves vertically staggering the nodes of the density variable with the nodes of the entropy-type variable. When moisture is included in such a model, it is either co-located with density so that moisture can be transported conservatively and consistently with dry mass, or with the entropy-type variable so that the coupling between moisture and temperature can be represented well. Both properties are desirable, yet at first it appears difficult to obtain both simultaneously. Here we present a framework to resolve this problem, by co-locating the moisture mixing ratio with potential temperature but formulating its transport as that of a density on a vertically-shifted mesh. Within this framework, particular choices of the operators involved provide the desired conservation and consistency properties of the moisture transport. The framework is described in the context of a finite element approach. We also present an explicit Runge-Kutta time stepping scheme that is appropriate for use within this framework. This approach is then illustrated through numerical tests, which demonstrate that it does indeed have the desired conservation and consistency properties.Natural Environment Research Council (NERC

Broad changes in body mass index between age 10 and adulthood are associated with type 2 diabetes risk independently of adult body mass index

 This is the author accepted manuscript. The final version is available from Elsevier via the DOI in this record Diabetes Research and Wellness FoundationDiabetes UKEuropean Foundation for the Study of Diabete

CONSISE statement on the reporting of Seroepidemiologic Studies for influenza (ROSES-I statement): an extension of the STROBE statement

published_or_final_versio

Population-calibrated Multiple Imputation for a Binary/categorical Covariate in Categorical Regression Models

Multiple imputation (MI) has become popular for analyses with missing data in medical research. The standard implementation of MI is based on the assumption of data being missing at random (MAR). However, for missing data generated by missing not at random mechanisms, MI performed assuming MAR might not be satisfactory. For an incomplete variable in a given data set, its corresponding population marginal distribution might also be available in an external data source. We show how this information can be readily utilised in the imputation model to calibrate inference to the population by incorporating an appropriately calculated offset termed the "calibrated-δ adjustment." We describe the derivation of this offset from the population distribution of the incomplete variable and show how, in applications, it can be used to closely (and often exactly) match the post-imputation distribution to the population level. Through analytic and simulation studies, we show that our proposed calibrated-δ adjustment MI method can give the same inference as standard MI when data are MAR, and can produce more accurate inference under two general missing not at random missingness mechanisms. The method is used to impute missing ethnicity data in a type 2 diabetes prevalence case study using UK primary care electronic health records, where it results in scientifically relevant changes in inference for non-White ethnic groups compared with standard MI. Calibrated-δ adjustment MI represents a pragmatic approach for utilising available population-level information in a sensitivity analysis to explore potential departures from the MAR assumption

Grouping of tooth surfaces by susceptibility to caries: a study in 5–16 year-old children

BACKGROUND: The decline in caries has slowed and this may be indicative of variation in the susceptibility of differing teeth to caries. This study tests the hypothesis that in children, there are groups of tooth sites that exhibit differences in caries susceptibility. METHODS: Probit analysis of caries data collected from a 4-year longitudinal study of 20,000 schoolchildren aged between 5 and 16 years in 10 differing locations in the United States. RESULTS: The development of dental caries within the mouth followed a fixed hierarchy indicating that tooth surfaces show variation in caries susceptibility. Certain teeth and tooth sites have similar susceptibilities and can be grouped, the sizes of the groups vary. The most susceptible group consists of six tooth surfaces: the buccal pits and occlusal fissured surfaces of the first molar teeth. The second group consisted of 12 sites on the second molar and premolar teeth. The group formed by the least susceptible sites included the largest number of tooth surfaces and consists of the majority of the lower anterior teeth and canines. CONCLUSION: Variation in the caries susceptibility of tooth surfaces exists. Surfaces can be grouped according to caries susceptibility. An effect that reduces the cariogenic challenge of one of the sites within a group is likely to affect all the other sites within the particular group

Genetic evidence that higher central adiposity causes gastro-oesophageal reflux disease: a Mendelian-randomization study

Background: Gastro-oesophageal reflux disease (GORD) is associated with multiple risk factors but determining causality is difficult. We used a genetic approach [Mendelian randomization (MR)] to identify potential causal modifiable risk factors for GORD. Methods: We used data from 451 097 European participants in the UK Biobank and defined GORD using hospital-defined ICD10 and OPCS4 codes and self-report data (N = 41 024 GORD cases). We tested observational and MR-based associations between GORD and four adiposity measures [body mass index (BMI), waist-hip ratio (WHR), a metabolically favourable higher body-fat percentage and waist circumference], smoking status, smoking frequency and caffeine consumption. Results: Observationally, all adiposity measures were associated with higher odds of GORD. Ever and current smoking were associated with higher odds of GORD. Coffee consumption was associated with lower odds of GORD but, among coffee drinkers, more caffeinated-coffee consumption was associated with higher odds of GORD. Using MR, we provide strong evidence that higher WHR and higher WHR adjusted for BMI lead to GORD. There was weak evidence that higher BMI, body-fat percentage, coffee drinking or smoking caused GORD, but only the observational effects for BMI and body-fat percentage could be excluded. This MR estimated effect for WHR equates to a 1.23-fold higher odds of GORD per 5-cm increase in waist circumference. Conclusions: These results provide strong evidence that a higher waist-hip ratio leads to GORD. Our study suggests that central fat distribution is crucial in causing GORD rather than overall weight.This article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.S.E.J. is funded by the Medical Research Council (grant: MR/M005070/1). A.R.W., T.M.F and H.Y. are supported by the European Research Council grants: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC and 323195. H.Y. is also funded by the Diabetes UK RD Lawrence fellowship (grant: 17/0005594). R.N.B. is funded by the Wellcome Trust and Royal Society, grant 104150/Z/14/Z. J.T. is supported by an Academy of Medical Sciences (AMS) Springboard award, which is supported by the AMS, the Wellcome Trust, GCRF, the Government Department of Business, Energy and Industrial strategy, the British Heart Foundation and Diabetes UK (SBF004\1079). N.A.K. declares personal fees from Falk, Takeda and Pharmacosmos; other fees from Janssen; and non-financial support from Janssen, AbbVie and Celltrion outside the submitted work. J.R.G. received honoraria from Falk, AbbVie and Shield therapeutics, outside the submitted work for unrelated topics. T.A. reports grants from AbbVie, MSD, Napp Pharmaceuticals, Celltrion, Pfizer, Janssen and Celgene during this study; personal fees and non-financial support from Immunodiagnostik; personal fees and non-financial support from Napp Pharmaceuticals, AbbVie and MSD; personal fees from Celltrion and Pfizer; grants and personal fees from Takeda; and grants and non-financial support from Tillotts, outside the submitted work.published version, accepted version (12 month embargo), submitted versio

Simulated distributions from negative experiments highlight the importance of the body mass index distribution in explaining depression–body mass index genetic risk score interactions

This is the final version. Available on open access from Oxford University Press via the DOI in this record. Data availability: All data from UK Biobank are publicly available; the negative experiments algorithm can be found here https://github.com/drar wood/gags.Abstract. Background: Depression and obesity are complex global health problems. Recent studies suggest a genetic predisposition to obesity might be accentuated in people with depression, but these analyses are prone to bias. Here, we tested the hypothesis that depression accentuates genetic susceptibility to obesity and applied negative control experiments to test whether any observed interactions were real or driven by confounding and statistical biases. Methods: We used data from upto 378,000 Europeans in UK Biobank, a 73 variant Body Mass Index (BMI) genetic risk score, 2 depression measures (depressive symptoms (DS), major depression (MD)) and an antidepressant usage variable available. We tested whether a) depression and b) antidepressant treatment accentuated genetic susceptibility to obesity. Finally, we performed negative control experiments by sampling individuals at random so that they had BMI distributions identical to depression cases and controls. Results: Depression was associated with an accentuation of an individuals genetic risk of obesity with evidence of interactions for both DS and MD (Pinteraction=7x10-4 and 7x10-5 respectively). Antidepressant usage within DS cases accentuated genetic obesity risk (Pinteraction=9x10-4), but not for MD (Pinteraction=0.13). Negative control experiments suggested that the observed interactions for MD (empirical-P =0.067) may be driven by statistical biases or confounding factors but were not possible with the larger DS groups. Antidepressant usage interaction also appears to be driven by statistical artefacts (empirical-P=0.510 using MD and 0.162 using DS). Conclusion: We have highlighted the importance of running negative experiments to confirm putative interactions in gene-environment studies. We provide some tentative evidence that depression accentuates an individual’s genetic susceptibility to higher BMI but demonstrated that the BMI distributions within cases and controls might drive these interactions.Academy of Medical SciencesEuropean Research Council (ERC

Trim17, novel E3 ubiquitin-ligase, initiates neuronal apoptosis

Accumulating data indicate that the ubiquitin-proteasome system controls apoptosis by regulating the level and the function of key regulatory proteins. In this study, we identified Trim17, a member of the TRIM/RBCC protein family, as one of the critical E3 ubiquitin ligases involved in the control of neuronal apoptosis upstream of mitochondria. We show that expression of Trim17 is increased both at the mRNA and protein level in several in vitro models of transcription-dependent neuronal apoptosis. Expression of Trim17 is controlled by the PI3K/Akt/GSK3 pathway in cerebellar granule neurons (CGN). Moreover, the Trim17 protein is expressed in vivo, in apoptotic neurons that naturally die during post-natal cerebellar development. Overexpression of active Trim17 in primary CGN was sufficient to induce the intrinsic pathway of apoptosis in survival conditions. This pro-apoptotic effect was abolished in Bax(-/-) neurons and depended on the E3 activity of Trim17 conferred by its RING domain. Furthermore, knock-down of endogenous Trim17 and overexpression of dominant-negative mutants of Trim17 blocked trophic factor withdrawal-induced apoptosis both in CGN and in sympathetic neurons. Collectively, our data are the first to assign a cellular function to Trim17 by showing that its E3 activity is both necessary and sufficient for the initiation of neuronal apoptosis. Cell Death and Differentiation (2010) 17, 1928-1941; doi: 10.1038/cdd.2010.73; published online 18 June 201