Feasibility of snapshot GNSS carrier phase amendment based on LAMBDA ratio tests

This research was funded by Albora Technologies and Universitat Politècnica de Catalunya with industrial PhD grant number DI 082 from the Generalitat de Catalunya; This research was partially funded by the Spanish Ministry of Science and Innovation project RTI2018-094295-B-I00. P.C. has been partially supported by the NSF under Awards CNS-1815349 and ECCS-1845833.Peer ReviewedPostprint (author's final draft

A Method to determine secondary codes and carrier phases of short snapshot signals

Recently, the Snapshot Real-Time Kinematic (SRTK) technique was demonstrated, which aims at achieving high accuracy navigation solutions with a very short signal collection. The main challenge in implementing SRTK is the generation of valid carrier-phase measurements, which relies on a data bit ambiguity (DBA) resolution process. For pilot signals, this step is equivalent to the correct selection of secondary code indexes (SCIs) from the ambiguous sets obtained from a multi-hypotheses (MH) acquisition process. Currently, SCI ambiguities are solved independently for each satellite. However, this method is ineffective when the snapshot signal is relatively short. In order to tackle this problem, this article proposes a new method that makes use of assistance data and processes information from all satellites to jointly solve the DBA issue. This new method is shown to be more effective in determining the correct SCI and enabling valid snapshot carrier-phase measurements, largely expanding the scope of high-accuracy snapshot positioning.This research was supported by the Albora Technologies and Universitat Politècnica de Catalunya with industrial PhD grant number DI 082 from the Generalitat de Catalunya and the project RTI2018-094295-B-I00 funded by the MCIN/AEI 10.13039/501100011033 which is co-funded by the FEDER programme. P.C. has been partially supported by the NSF under Awards CNS-1815349 and ECCS-1845833.Peer ReviewedPostprint (published version

Accounting for error due to misclassification of exposures in case–control studies of gene–environment interaction

We consider analysis of data from an unmatched case–control study design with a binary genetic factor and a binary environmental exposure when both genetic and environmental exposures could be potentially misclassified. We devise an estimation strategy that corrects for misclassification errors and also exploits the gene–environment independence assumption. The proposed corrected point estimates and confidence intervals for misclassified data reduce back to standard analytical forms as the misclassification error rates go to zero. We illustrate the methods by simulating unmatched case–control data sets under varying levels of disease–exposure association and with different degrees of misclassification. A real data set on a case–control study of colorectal cancer where a validation subsample is available for assessing genotyping error is used to illustrate our methods. Copyright © 2007 John Wiley & Sons, Ltd.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/58640/1/3044_ftp.pd

Cloud-based single-frequency Snapshot RTK positioning

With great potential for being applied to Internet of Things (IoT) applications, the concept of cloud-based Snapshot Real Time Kinematics (SRTK) was proposed and its feasibility under zero-baseline configuration was confirmed recently by the authors. This article first introduces the general workflow of the SRTK engine, as well as a discussion on the challenges of achieving an SRTK fix using actual snapshot data. This work also describes a novel solution to ensure a nanosecond level absolute timing accuracy in order to compute highly precise satellite coordinates, which is required for SRTK. Parameters such as signal bandwidth, integration time and baseline distances have an impact on the SRTK performance. To characterize this impact, different combinations of these settings are analyzed through experimental tests. The results show that the use of higher signal bandwidths and longer integration times result in higher SRTK fix rates, while the more significant impact on the performance comes from the baseline distance. The results also show that the SRTK fix rate can reach more than 93% by using snapshots with a data size as small as 255 kB. The positioning accuracy is at centimeter level when phase ambiguities are resolved at a baseline distance less or equal to 15 km.This research was funded by Albora Technologies and Universitat Politècnica de Catalunya with industrial PhD grant number DI 082 from the Generalitat de Catalunya; This research was partially funded by the Spanish Ministry of Science and Innovation project RTI2018-094295-B-I00. P.C. has been partially supported by the NSF under Awards CNS-1815349 and ECCS-1845833Peer ReviewedPostprint (published version

A rewiring model of intratumoral interaction networks.

Intratumoral heterogeneity (ITH) has been regarded as a key cause of the failure and resistance of cancer therapy, but how it behaves and functions remains unclear. Advances in single-cell analysis have facilitated the collection of a massive amount of data about genetic and molecular states of individual cancer cells, providing a fuel to dissect the mechanistic organization of ITH at the molecular, metabolic and positional level. Taking advantage of these data, we propose a computational model to rewire up a topological network of cell-cell interdependences and interactions that operate within a tumor mass. The model is grounded on the premise of game theory that each interactive cell (player) strives to maximize its fitness by pursuing a rational self-interest strategy, war or peace, in a way that senses and alters other cells to respond properly. By integrating this idea with genome-wide association studies for intratumoral cells, the model is equipped with a capacity to visualize, annotate and quantify how somatic mutations mediate ITH and the network of intratumoral interactions. Taken together, the model provides a topological flow by which cancer cells within a tumor cooperate or compete with each other to downstream pathogenesis. This topological flow can be potentially used as a blueprint for genetically intervening the pattern and strength of cell-cell interactions towards cancer control

Polymorphisms in GSTT1, GSTZ1, and CYP2E1, Disinfection By-products, and Risk of Bladder Cancer in Spain

Background: Bladder cancer has been linked with long-term exposure to disinfection by-products (DBPs) in drinking water.Objectives: In this study we investigated the combined influence of DBP exposure and polymorphisms in glutathione S-transferase (GSTT1, GSTZ1) and cytochrome P450 (CYP2E1) genes in the metabolic pathways of selected by-products on bladder cancer in a hospital-based case–control study in Spain. Methods: Average exposures to trihalomethanes (THMs; a surrogate for DBPs) from 15 years of age were estimated for each subject based on residential history and information on municipal water sources among 680 cases and 714 controls. We estimated effects of THMs and GSTT1, GSTZ1, and CYP2E1 polymorphisms on bladder cancer using adjusted logistic regression models with and without interaction terms. Results: THM exposure was positively associated with bladder cancer: adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were 1.2 (0.8–1.8), 1.8 (1.1–2.9), and 1.8 (0.9–3.5) for THM quartiles 2, 3, and 4, respectively, relative to quartile 1. Associations between THMs and bladder cancer were stronger among subjects who were GSTT1 +/+ or +/– versus GSTT1 null (pinteraction = 0.021), GSTZ1 rs1046428 CT/TT versus CC (pinteraction = 0.018), or CYP2E1 rs2031920 CC versus CT/TT (pinteraction = 0.035). Among the 195 cases and 192 controls with high-risk forms of GSTT1 and GSTZ1, the ORs for quartiles 2, 3, and 4 of THMs were 1.5 (0.7–3.5), 3.4 (1.4–8.2), and 5.9 (1.8–19.0), respectively. Conclusions: Polymorphisms in key metabolizing enzymes modified DBP-associated bladder cancer risk. The consistency of these findings with experimental observations of GSTT1, GSTZ1, and CYP2E1 activity strengthens the hypothesis that DBPs cause bladder cancer and suggests possible mechanisms as well as the classes of compounds likely to be implicated.This work was funded by the Intramural Research Program of the National Institutes of Health, National Cancer Institute (N02-CP-11015), the Fondo de Investigación Sanitaria (00/0745, G03/174, G03/160, C03/09, and C03/90), and the Instituto de Salud Carlos III, Spanish Health Ministry (CP06/00341

LINE-1 methylation in leukocyte DNA, interaction with phosphatidylethanolamine N-methyltransferase variants and bladder cancer risk

BACKGROUND: Aberrant global DNA methylation is shown to increase cancer risk. LINE-1 has been proven a measure of global DNA methylation. The objectives of this study were to assess the association between LINE-1 methylation level and bladder cancer risk and to evaluate effect modification by environmental and genetic factors. METHODS: Bisulphite-treated leukocyte DNA from 952 cases and 892 hospital controls was used to measure LINE-1 methylation level at four CpG sites by pyrosequencing. Logistic regression model was fitted to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). Interactions between LINE-1 methylation levels and environmental and genetic factors were assessed. RESULTS: The risk of bladder cancer followed a nonlinear association with LINE-1 methylation. Compared with subjects in the middle tertile, the adjusted OR for subjects in the lower and the higher tertiles were 1.26 (95% CI 0.99–1.60, P=0.06) and 1.33 (95% CI 1.05–1.69, P=0.02), respectively. This association significantly increased among individuals homozygous for the major allele of five single-nucleotide polymorphisms located in the phosphatidylethanolamine N-methyltransferase gene (corrected P-interaction<0.05). CONCLUSIONS: The findings from this large-scale study suggest that both low and high levels of global DNA methylation are associated with the risk of bladder cancer

Cancer Informatics for Cancer Centers (CI4CC): Building a Community Focused on Sharing Ideas and Best Practices to Improve Cancer Care and Patient Outcomes.

Cancer Informatics for Cancer Centers (CI4CC) is a grassroots, nonprofit 501c3 organization intended to provide a focused national forum for engagement of senior cancer informatics leaders, primarily aimed at academic cancer centers anywhere in the world but with a special emphasis on the 70 National Cancer Institute-funded cancer centers. Although each of the participating cancer centers is structured differently, and leaders' titles vary, we know firsthand there are similarities in both the issues we face and the solutions we achieve. As a consortium, we have initiated a dedicated listserv, an open-initiatives program, and targeted biannual face-to-face meetings. These meetings are a place to review our priorities and initiatives, providing a forum for discussion of the strategic and pragmatic issues we, as informatics leaders, individually face at our respective institutions and cancer centers. Here we provide a brief history of the CI4CC organization and meeting highlights from the latest CI4CC meeting that took place in Napa, California from October 14-16, 2019. The focus of this meeting was "intersections between informatics, data science, and population science." We conclude with a discussion on "hot topics" on the horizon for cancer informatics

Disinfection By-Products in Drinking Water and Bladder Cancer:Evaluation of Risk Modification by Common Genetic Polymorphisms in Two Case-Control Studies

BACKGROUND: By-products are formed when disinfectants react with organic matter in source water. The most common class of disinfection by-products, trihalomethanes (THMs), have been linked to bladder cancer. Several studies have shown exposure–response associations with THMs in drinking water and bladder cancer risk. Few epidemiologic studies have evaluated gene–environment interactions for total THMs (TTHMs) with known bladder cancer susceptibility variants. OBJECTIVES: In this study, we investigated the combined effect on bladder cancer risk contributed by TTHMs, bladder cancer susceptibility variants identified through genome-wide association studies, and variants in several candidate genes. METHODS: We analyzed data from two large case–control studies—the New England Bladder Cancer Study ([Formula: see text] cases/1,162 controls), a population-based study, and the Spanish Bladder Cancer Study ([Formula: see text] cases/772 controls), a hospital-based study. Because of differences in exposure distributions and metrics, we estimated effects of THMs and genetic variants within each study separately using adjusted logistic regression models to calculate odds ratios (ORs) and 95% confidence intervals (CI) with and without interaction terms, and then combined the results using meta-analysis. RESULTS: Of the 16 loci showing strong evidence of association with bladder cancer, rs907611 at 11p15.5 [leukocyte-specific protein 1 (LSP1 region)] showed the strongest associations in the highest exposure category in each study, with evidence of interaction in both studies and in meta-analysis. In the highest exposure category, we observed [Formula: see text] (95% CI: 1.17, 2.34, [Formula: see text]) for those with the rs907611-GG genotype and [Formula: see text]. No other genetic variants tested showed consistent evidence of interaction. DISCUSSION: We found novel suggestive evidence for a multiplicative interaction between a putative bladder carcinogen, TTHMs, and genotypes of rs907611. Given the ubiquitous exposure to THMs, further work is needed to replicate and extend this finding and to understand potential molecular mechanisms. https://doi.org/10.1289/EHP989