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We developed an efficient neural network algorithm for solving the Multiple Traveling Salesmen Problem (MTSP). A new transformation of the N-city M-salesmen MTSP to the standard Traveling Salesmen Problem (TSP) is introduced. The transformed problem is represented by an expanded version of Hopfield-Tank's neuromorphic city-position map with (N + M-1)-cities and a single fictitious salesmen. The dynamic model associated with the problem is based on the Basic Differential Multiplier Method (BDMM) [26] which evaluates Lagrange multipliers simultaneously with the problem's state variables. The algorithm was successfully tested on many problems with up to 30 cities and five salesmen. In all test cases, the algorithm always converged to valid solutions. The great advantage of this kind of algorithm is that it can provide solutions to complex decision making problems directly by solving a system of ordinary differential equations. No learning steps, logical if statements or adjusting of parameters are required during the computation. The algorithm can therefore be implemented in hardware to solve complex constraint satisfaction problems such as the MTSP at the speed of analog silicon VLSI devices or possibly future optical neural computers. 相似文献
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A design is proposed for case-control studies in which selection of subjects for full variable ascertainment is based jointly on disease status and on easily obtained "screening" variables that may be related to the disease. Recruitment of subjects follows an independent Bernoulli sampling scheme, with recruitment probabilities set by the investigator in advance. In particular, the sampling can be set up to achieve, on average, frequency matching, provided prior estimates of the disease rates or odds ratios associated with screening variables such as age and sex are available. Alternatively--for example, when studying a rare exposure--one can enrich the sample with certain categories of subject. Following such a design, there are two valid approaches to logistic regression analysis, both of which allow for efficient estimation of effects associated with the screening variables that were allowed to bias the recruitment. The statistical properties of the estimators are compared, both for large samples, based on asymptotics, and for small samples, based on simulations. 相似文献
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Maria Teresa Landi Nilanjan Chatterjee Lynn R. Goldin Melissa Rotunno Kevin Jacobs Meredith Yeager Qizhai Li Dario Consonni Sholom Wacholder Ryan Diver Jarmo Virtamo Zhaoming Wang Kimberly F. Doheny Cathy Laurie Rayjean Hung James D. McKay John McLaughlin Ming-Sound Tsao Yufei Wang Lars Vatten Egil Arnesen Christine Bouchard Tonu Vooder Kristian Välk Chu Chen Patrick Sulem Thorunn Rafnar Wiebke Sauter Heike Bickeböller Jenny Chang-Claude Kari Stefansson Christopher I. Amos Sharon A. Savage Margaret A. Tucker Neil E. Caporaso 《American journal of human genetics》2009,85(5):679-74
Three genetic loci for lung cancer risk have been identified by genome-wide association studies (GWAS), but inherited susceptibility to specific histologic types of lung cancer is not well established. We conducted a GWAS of lung cancer and its major histologic types, genotyping 515,922 single-nucleotide polymorphisms (SNPs) in 5739 lung cancer cases and 5848 controls from one population-based case-control study and three cohort studies. Results were combined with summary data from ten additional studies, for a total of 13,300 cases and 19,666 controls of European descent. Four studies also provided histology data for replication, resulting in 3333 adenocarcinomas (AD), 2589 squamous cell carcinomas (SQ), and 1418 small cell carcinomas (SC). In analyses by histology, rs2736100 (TERT), on chromosome 5p15.33, was associated with risk of adenocarcinoma (odds ratio [OR] = 1.23, 95% confidence interval [CI] = 1.13–1.33, p = 3.02 × 10−7), but not with other histologic types (OR = 1.01, p = 0.84 and OR = 1.00, p = 0.93 for SQ and SC, respectively). This finding was confirmed in each replication study and overall meta-analysis (OR = 1.24, 95% CI = 1.17–1.31, p = 3.74 × 10−14 for AD; OR = 0.99, p = 0.69 and OR = 0.97, p = 0.48 for SQ and SC, respectively). Other previously reported association signals on 15q25 and 6p21 were also refined, but no additional loci reached genome-wide significance. In conclusion, a lung cancer GWAS identified a distinct hereditary contribution to adenocarcinoma. 相似文献
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Jill Koshiol Melissa Rotunno Dario Consonni Angela Cecilia Pesatori Sara De Matteis Alisa M. Goldstein Anil K. Chaturvedi Sholom Wacholder Maria Teresa Landi Jay H. Lubin Neil E. Caporaso 《PloS one》2009,4(10)
Background
Chronic obstructive pulmonary disease (COPD) has been consistently associated with increased risk of lung cancer. However, previous studies have had limited ability to determine whether the association is due to smoking.Methodology/Principal Findings
The Environment And Genetics in Lung cancer Etiology (EAGLE) population-based case-control study recruited 2100 cases and 2120 controls, of whom 1934 cases and 2108 controls reported about diagnosis of chronic bronchitis, emphysema, COPD (chronic bronchitis and/or emphysema), or asthma more than 1 year before enrollment. We estimated odds ratios (OR) and 95% confidence intervals (CI) using logistic regression. After adjustment for smoking, other previous lung diseases, and study design variables, lung cancer risk was elevated among individuals with a history of chronic bronchitis (OR = 2.0, 95% CI = 1.5–2.5), emphysema (OR = 1.9, 95% CI = 1.4–2.8), or COPD (OR = 2.5, 95% CI = 2.0–3.1). Among current smokers, association between chronic bronchitis and lung cancer was strongest among lighter smokers. Asthma was associated with a decreased risk of lung cancer in males (OR = 0.48, 95% CI = 0.30–0.78).Conclusions/Significance
These results suggest that the associations of personal history of chronic bronchitis, emphysema, and COPD with increased risk of lung cancer are not entirely due to smoking. Inflammatory processes may both contribute to COPD and be important for lung carcinogenesis. 相似文献6.
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The kin-cohort design is a promising alternative to traditional cohort or case-control designs for estimating penetrance of an identified rare autosomal mutation. In this design, a suitably selected sample of participants provides genotype and detailed family history information on the disease of interest. To estimate penetrance of the mutation, we consider a marginal likelihood approach that is computationally simple to implement, more flexible than the original analytic approach proposed by Wacholder et al. (1998, American Journal of Epidemiology 148, 623-629), and more robust than the likelihood approach considered by Gail et al. (1999, Genetic Epidemiology 16, 15-39) to presence of residual familial correlation. We study the trade-off between robustness and efficiency using simulation experiments. The method is illustrated by analysis of the data from the Washington Ashkenazi Study. 相似文献
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Rolando Herrero Wim Quint Allan Hildesheim Paula Gonzalez Linda Struijk Hormuzd A. Katki Carolina Porras Mark Schiffman Ana Cecilia Rodriguez Diane Solomon Silvia Jimenez John T. Schiller Douglas R. Lowy Leen-Jan van Doorn Sholom Wacholder Aimée R. Kreimer for the CVT Vaccine Group 《PloS one》2013,8(7)
Background
Human papillomavirus (HPV) infection, particularly with type 16, causes a growing fraction of oropharyngeal cancers, whose incidence is increasing, mainly in developed countries. In a double-blind controlled trial conducted to investigate vaccine efficacy (VE) of the bivalent HPV 16/18 vaccine against cervical infections and lesions, we estimated VE against prevalent oral HPV infections 4 years after vaccination.Methods and Findings
A total of 7,466 women 18–25 years old were randomized (1∶1) to receive the HPV16/18 vaccine or hepatitis A vaccine as control. At the final blinded 4-year study visit, 5,840 participants provided oral specimens (91·9% of eligible women) to evaluate VE against oral infections. Our primary analysis evaluated prevalent oral HPV infection among all vaccinated women with oral and cervical HPV results. Corresponding VE against prevalent cervical HPV16/18 infection was calculated for comparison. Oral prevalence of identifiable mucosal HPV was relatively low (1·7%). Approximately four years after vaccination, there were 15 prevalent HPV16/18 infections in the control group and one in the vaccine group, for an estimated VE of 93·3% (95% CI = 63% to 100%). Corresponding efficacy against prevalent cervical HPV16/18 infection for the same cohort at the same visit was 72·0% (95% CI = 63% to 79%) (p versus oral VE = 0·04). There was no statistically significant protection against other oral HPV infections, though power was limited for these analyses.Conclusions
HPV prevalence four years after vaccination with the ASO4-adjuvanted HPV16/18 vaccine was much lower among women in the vaccine arm compared to the control arm, suggesting that the vaccine affords strong protection against oral HPV16/18 infection, with potentially important implications for prevention of increasingly common HPV-associated oropharyngeal cancer.ClinicalTrials.gov, Registry number NCT00128661相似文献10.
Safaeian M Hildesheim A Gonzalez P Yu K Porras C Li Q Rodriguez AC Sherman ME Schiffman M Wacholder S Burk R Herrero R Burdette L Chanock SJ Wang SS 《PloS one》2012,7(4):e33619