Solving inverse problems of unknown contaminant source in groundwater-river integrated systems using a surrogate transport model based optimization

The paper presents a new approach to identify the unknown characteristics (release history and location) of contaminant sources in groundwater, starting from a few concentration observations at monitoring points. An inverse method that combines the forward model and an optimization algorithm is presented. To speed up the computation, the transfer function theory is applied to create a surrogate transport forward model. The performance of the developed approach is evaluated on two case studies (literature and a new one) under different scenarios and measurement error conditions. The literature case study regards a heterogeneous confined aquifer, while the proposed case study was never investigated before, it involves an aquifer-river integrated flow and transport system. In this case, the groundwater contaminant originated from a damaged tank, migrates to a river through the aquifer. The approach, starting from few concentration observations monitored at a downstream river cross-section, accurately estimates the release history at a groundwater contaminant source, even in presence of noise on observations. Moreover, the results show that the methodology is very fast, and can solve the inverse problem in much less computation time in comparison with other existing approaches

LLM: Realizing Low-Latency Memory by Exploiting Embedded Silicon Photonics for Irregular Workloads

As emerging workloads exhibit irregular memory access patterns with poor data reuse and locality, they would benefit from a DRAM that achieves low latency without sacrificing bandwidth and energy efficiency. We propose LLM (Low Latency Memory), a codesign of the DRAM microarchitecture, the memory controller and the LLC/DRAM interconnect by leveraging embedded silicon photonics in 2.5D/3D integrated system on chip. LLM relies on Wavelength Division Multiplexing (WDM)-based photonic interconnects to reduce the contention throughout the memory subsystem. LLM also increases the bank-level parallelism, eliminates bus conflicts by using dedicated optical data paths, and reduces the access energy per bit with shorter global bitlines and smaller row buffers. We evaluate the design space of LLM for a variety of synthetic benchmarks and representative graph workloads on a full-system simulator (gem5). LLM exhibits low memory access latency for traffics with both regular and irregular access patterns. For irregular traffic, LLM achieves high bandwidth utilization (over 80% peak throughput compared to 20% of HBM2.0). For real workloads, LLM achieves 3 × and 1.8 × lower execution time compared to HBM2.0 and a state-of-the-art memory system with high memory level parallelism, respectively. This study also demonstrates that by reducing queuing on the data path, LLM can achieve on average 3.4 × lower memory latency variation compared to HBM2.0

A generalized quantum nonlinear oscillator

We examine various generalizations, e.g. exactly solvable, quasi-exactly solvable and non-Hermitian variants, of a quantum nonlinear oscillator. For all these cases, the same mass function has been used and it has also been shown that the new exactly solvable potentials possess shape invariance symmetry. The solutions are obtained in terms of classical orthogonal polynomials

Non-homologous end-joining pathway associated with occurrence of myocardial infarction: gene set analysis of genome-wide association study data

<p>Purpose: DNA repair deficiencies have been postulated to play a role in the development and progression of cardiovascular disease (CVD). The hypothesis is that DNA damage accumulating with age may induce cell death, which promotes formation of unstable plaques. Defects in DNA repair mechanisms may therefore increase the risk of CVD events. We examined whether the joints effect of common genetic variants in 5 DNA repair pathways may influence the risk of CVD events.</p> <p>Methods: The PLINK set-based test was used to examine the association to myocardial infarction (MI) of the DNA repair pathway in GWAS data of 866 subjects of the GENetic DEterminants of Restenosis (GENDER) study and 5,244 subjects of the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) study. We included the main DNA repair pathways (base excision repair, nucleotide excision repair, mismatch repair, homologous recombination and non-homologous end-joining (NHEJ)) in the analysis.</p> <p>Results: The NHEJ pathway was associated with the occurrence of MI in both GENDER (P = 0.0083) and PROSPER (P = 0.014). This association was mainly driven by genetic variation in the MRE11A gene (PGENDER = 0.0001 and PPROSPER = 0.002). The homologous recombination pathway was associated with MI in GENDER only (P = 0.011), for the other pathways no associations were observed.</p> <p>Conclusion: This is the first study analyzing the joint effect of common genetic variation in DNA repair pathways and the risk of CVD events, demonstrating an association between the NHEJ pathway and MI in 2 different cohorts.</p&gt

Sex differences in the risk of coronary heart disease associated with type 2 diabetes:a Mendelian Randomization analysis

OBJECTIVE Observational studies have demonstrated that type 2 diabetes is a stronger risk factor for coronary heart disease (CHD) in women compared with men. However, it is not clear whether this reflects a sex differential in the causal effect of diabetes on CHD risk or results from sex-specific residual confounding. RESEARCH DESIGN AND METHODS Using 270 single nucleotide polymorphisms (SNPs) for type 2 diabetes identified in a type 2 diabetes genome-wide association study, we performed a sex-stratified Mendelian randomization (MR) study of type 2 diabetes and CHD using individual participant data in UK Biobank (251,420 women and 212,049 men). Weighted median, MR-Egger, MR-pleiotropy residual sum and outlier, and radial MR from summary-level analyses were used for pleiotropy assessment. RESULTS MR analyses showed that genetic risk of type 2 diabetes increased the odds of CHD for women (odds ratio 1.13 [95% CI 1.08–1.18] per 1-log unit increase in odds of type 2 diabetes) and men (1.21 [1.17–1.26] per 1-log unit increase in odds of type 2 diabetes). Sensitivity analyses showed some evidence of directional pleiotropy; however, results were similar after correction for outlier SNPs. CONCLUSIONS This MR analysis supports a causal effect of genetic liability to type 2 diabetes on risk of CHD that is not stronger for women than men. Assuming a lack of bias, these findings suggest that the prevention and management of type 2 diabetes for CHD risk reduction is of equal priority in both sexes

Measurement of the cross-section and charge asymmetry of WW bosons produced in proton-proton collisions at s=8\sqrt{s}=8 TeV with the ATLAS detector

This paper presents measurements of the $W^+ \rightarrow \mu^+\nu$ and $W^- \rightarrow \mu^-\nu$ cross-sections and the associated charge asymmetry as a function of the absolute pseudorapidity of the decay muon. The data were collected in proton--proton collisions at a centre-of-mass energy of 8 TeV with the ATLAS experiment at the LHC and correspond to a total integrated luminosity of 20.2~\mbox{fb^{-1}}. The precision of the cross-section measurements varies between 0.8% to 1.5% as a function of the pseudorapidity, excluding the 1.9% uncertainty on the integrated luminosity. The charge asymmetry is measured with an uncertainty between 0.002 and 0.003. The results are compared with predictions based on next-to-next-to-leading-order calculations with various parton distribution functions and have the sensitivity to discriminate between them.Comment: 38 pages in total, author list starting page 22, 5 figures, 4 tables, submitted to EPJC. All figures including auxiliary figures are available at https://atlas.web.cern.ch/Atlas/GROUPS/PHYSICS/PAPERS/STDM-2017-13

Search for chargino-neutralino production with mass splittings near the electroweak scale in three-lepton final states in √s=13 TeV pp collisions with the ATLAS detector

A search for supersymmetry through the pair production of electroweakinos with mass splittings near the electroweak scale and decaying via on-shell W and Z bosons is presented for a three-lepton final state. The analyzed proton-proton collision data taken at a center-of-mass energy of √s=13  TeV were collected between 2015 and 2018 by the ATLAS experiment at the Large Hadron Collider, corresponding to an integrated luminosity of 139  fb−1. A search, emulating the recursive jigsaw reconstruction technique with easily reproducible laboratory-frame variables, is performed. The two excesses observed in the 2015–2016 data recursive jigsaw analysis in the low-mass three-lepton phase space are reproduced. Results with the full data set are in agreement with the Standard Model expectations. They are interpreted to set exclusion limits at the 95% confidence level on simplified models of chargino-neutralino pair production for masses up to 345 GeV

Genome-wide association scan meta-analysis identifies three Loci influencing adiposity and fat distribution.

To identify genetic loci influencing central obesity and fat distribution, we performed a meta-analysis of 16 genome-wide association studies (GWAS, N = 38,580) informative for adult waist circumference (WC) and waist-hip ratio (WHR). We selected 26 SNPs for follow-up, for which the evidence of association with measures of central adiposity (WC and/or WHR) was strong and disproportionate to that for overall adiposity or height. Follow-up studies in a maximum of 70,689 individuals identified two loci strongly associated with measures of central adiposity; these map near TFAP2B (WC, P = 1.9x10(-11)) and MSRA (WC, P = 8.9x10(-9)). A third locus, near LYPLAL1, was associated with WHR in women only (P = 2.6x10(-8)). The variants near TFAP2B appear to influence central adiposity through an effect on overall obesity/fat-mass, whereas LYPLAL1 displays a strong female-only association with fat distribution. By focusing on anthropometric measures of central obesity and fat distribution, we have identified three loci implicated in the regulation of human adiposity