Mixing the reactive with the personal: Opportunities for end-user programming in personal information management

The transition of personal information management (PIM) tools off the desktop to the Web presents an opportunity to augment these tools with capabilities provided by the wealth of real-time information readily available. In this chapter, we describe a personal information assistance engine that lets end-users delegate to it various simple context- and activity-reactive tasks and reminders. Our system, Atomate, treats RSS/ATOM feeds from social networking and life-tracking sites as sensor streams, integrating information from such feeds into a simple unified RDF world model representing people, places and things and their time-varying states and activities. Combined with other information sources on the web, including the user's online calendar, web-based e-mail client, news feeds and messaging services, Atomate can be made to automatically carry out a variety of simple tasks for the user, ranging from context-aware filtering and messaging, to sharing and social coordination actions. Atomate's open architecture and world model easily accommodate new information sources and actions via the addition of feeds and web services. To make routine use of the system easy for non-programmers, Atomate provides a constrained-input natural language interface (CNLI) for behavior specification, and a direct-manipulation interface for inspecting and updating its world model

Oral health and human papillomavirus-associated head and neck squamous cell carcinoma

BACKGROUND: Indicators of poor oral health, including smoking, have been associated with increased risk of head and neck squamous cell carcinoma, especially oropharyngeal squamous cell carcinoma (OPSCC), yet few studies have examined whether this association is modified by human papillomavirus (HPV) status. METHODS: Data from interviews and tumor HPV status from a large population-based case-control study, the Carolina Head and Neck Cancer Study (CHANCE), were used to estimate the association between oral health indicators and smoking among 102 HPV-positive patients and 145 HPV-negative patients with OPSCC and 1396 controls. HPV status was determined by p16INK4a (p16) immunohistochemistry. Unconditional, multinomial logistic regression was used to estimate odds ratios (ORs) for all oral health indictors adjusting for important covariates. RESULTS: Routine dental examinations were associated with a decreased risk of both HPV-negative OPSCC (OR, 0.52; 95% confidence interval [CI], 0.35-0.76) and HPV-positive OPSCC (OR, 0.55; 95% CI, 0.36-.86). Tooth mobility (a proxy for periodontal disease) increased the risk of HPV-negative disease (OR, 1.70; 95% CI, 1.18-2.43) slightly more than the risk for HPV-positive disease (OR, 1.45; 95% CI, 0.95-2.20). Ten or more pack-years of cigarette smoking were strongly associated with an increased risk of HPV-negative OPSCC (OR, 4.26; 95% CI, 2.85-6.37) and were associated less with an increased risk of HPV-positive OPSCC (OR, 1.62; 95% CI, 1.10-2.38). CONCLUSIONS: Although HPV-positive and HPV-negative HNSCC differ significantly with respect to etiology and tumorigenesis, the current findings suggest a similar pattern of association between poor oral health, frequency of dental examinations, and both HPV-positive and HPV-negative OPSCC. Future research is required to elucidate interactions between poor oral health, tobacco use, and HPV in the development of OPSCC. Cancer 2017;71–80. © 2016 American Cancer Society

Evaluation of pathologic staging using number of nodes in p16-negative head and neck cancer

Objectives: The 8th edition AJCC staging guidelines for head and neck squamous cell carcinoma (HNSCC) recently introduced pathologic staging criteria for nodal disease among p16-positive patients. In this study we evaluate pathologic staging in p16-negative HNSCC. Materials and Methods: We compared pathologic staging to the 7th and 8th edition AJCC staging systems using a statewide population-based cohort. All M0 p16-negative surgical patients were included. The outcome was five-year overall survival. Results: Of 304 patients identified, 113 were N0, 157 had 1–4 positive nodes, and 34 had ≥4 nodes. Survival was 71% (95% CI 61–78%) with no nodes, 48% (36%−60%) for 1–4 nodes, and 24% (11 – 39%) for > 4 nodes. When compared to the AJCC systems, the pathologic staging yielded a larger total survival gradient, more montonic survival, better consistency across primary sites, and a slightly lower Bayesian information criterion (1510 vs 1538). After adjusting for disease characteristics, demographics, and tobacco use, hazard ratios for survival were similar using pathologic and AJCC criteria. Conclusion: In this cohort, pathological staging was more prognostic than AJCC staging. This is the first study to evaluate pathologic staging in p16-negative cancer; if these findings are verified, a universal nodal staging system could be introduced

Socioeconomic status, access to care, risk factor patterns, and stage at diagnosis for head and neck cancer among black and white patients

Background: Little is known about how factors combine to influence progression of squamous cell carcinoma of the head and neck (HNSCC). We aimed to evaluate multidimensional influences of factors associated with HNSCC stage by race. Methods: Using retrospective data, patients with similar socioeconomic status (SES), access to care (travel time/distance), and behavioral risk factors (tobacco/alcohol use and dental care) were grouped by latent class analysis. Relative frequency differences (RFD) were calculated to evaluate latent classes by stage, race, and p16 status. Results: We identified three latent classes. Advanced T-stage was higher for black (RFD = +20.2%; 95% CI: −4.6 to 44.9) than white patients (RFD = +10.7%; 95% CI: 2.1–19.3) in the low-SES/high-access/high-behavioral risk class and higher for both black (RFD = +29.6%; 95% CI: 4.7–54.5) and white patients (RFD = +23.9%; 95% CI: 15.2–32.6) in the low-SES/low-access/high-behavioral risk class. Conclusion: Results suggest that SES, access to care, and behavioral risk factors combine to underly the association with advanced T-stage. Additionally, differences by race warrant further investigation

Genome‐wide association study of INDELs identified four novel susceptibility loci associated with lung cancer risk

Genome‐wide association studies (GWAS) have identified 45 susceptibility loci associated with lung cancer. Only less than SNPs, small insertions and deletions (INDELs) are the second most abundant genetic polymorphisms in the human genome. INDELs are highly associated with multiple human diseases, including lung cancer. However, limited studies with large‐scale samples have been available to systematically evaluate the effects of INDELs on lung cancer risk. Here, we performed a large‐scale meta‐analysis to evaluate INDELs and their risk for lung cancer in 23,202 cases and 19,048 controls. Functional annotations were performed to further explore the potential function of lung cancer risk INDELs. Conditional analysis was used to clarify the relationship between INDELs and SNPs. Four new risk loci were identified in genome‐wide INDEL analysis (1p13.2: rs5777156, Insertion, OR = 0.92, P = 9.10 × 10−8; 4q28.2: rs58404727, Deletion, OR = 1.19, P = 5.25 × 10−7; 12p13.31: rs71450133, Deletion, OR = 1.09, P = 8.83 × 10−7; and 14q22.3: rs34057993, Deletion, OR = 0.90, P = 7.64 × 10−8). The eQTL analysis and functional annotation suggested that INDELs might affect lung cancer susceptibility by regulating the expression of target genes. After conducting conditional analysis on potential causal SNPs, the INDELs in the new loci were still nominally significant. Our findings indicate that INDELs could be potentially functional genetic variants for lung cancer risk. Further functional experiments are needed to better understand INDEL mechanisms in carcinogenesis

First -decay spectroscopy of and new -decay branches of

19 pags., 14 figs., 3 tabs.The  decay of the neutron-rich and was investigated experimentally in order to provide new insights into the nuclear structure of the tin isotopes with magic proton number above the shell. The -delayed -ray spectroscopy measurement was performed at the ISOLDE facility at CERN, where indium isotopes were selectively laser-ionized and on-line mass separated. Three -decay branches of were established, two of which were observed for the first time. Population of neutron-unbound states decaying via rays was identified in the two daughter nuclei of and , at excitation energies exceeding the neutron separation energy by 1 MeV. The -delayed one- and two-neutron emission branching ratios of were determined and compared with theoretical calculations. The -delayed one-neutron decay was observed to be dominant -decay branch of even though the Gamow-Teller resonance is located substantially above the two-neutron separation energy of . Transitions following the  decay of are reported for the first time, including rays tentatively attributed to . In total, six new levels were identified in on the basis of the coincidences observed in the and decays. A transition that might be a candidate for deexciting the missing neutron single-particle state in was observed in both  decays and its assignment is discussed. Experimental level schemes of and are compared with shell-model predictions. Using the fast timing technique, half-lives of the , and levels in were determined. From the lifetime of the state measured for the first time, an unexpectedly large transition strength was deduced, which is not reproduced by the shell-model calculations.M.P.-S. acknowledges the funding support from the Polish National Science Center under Grants No. 2019/33/N/ST2/03023 and No. 2020/36/T/ST2/00547 (Doctoral scholarship ETIUDA). J.B. acknowledges support from the Universidad Complutense de Madrid under the Predoctoral Grant No. CT27/16- CT28/16. This work was partially funded by the Polish National Science Center under Grants No. 2020/39/B/ST2/02346, No. 2015/18/E/ST2/00217, and No. 2015/18/M/ST2/00523, by the Spanish government via Projects No. FPA2017-87568-P, No. RTI2018-098868-B-I00, No. PID2019-104390GB-I00, and No. PID2019-104714GB-C21, by the U.K. Science and Technology Facilities Council (STFC), the German BMBF under Contract No. 05P18PKCIA, by the Portuguese FCT under the Projects No. CERN/FIS-PAR/0005/2017, and No. CERN/FIS-TEC/0003/2019, and by the Romanian IFA Grant CERN/ISOLDE. The research leading to these results has received funding from the European Union’s Horizon 2020 research and innovation programme under Grant Agreement No. 654002. M.Str. acknowledges the funding from the European Union’s Horizon 2020 research and innovation program under Grant Agreement No. 771036 (ERC CoG MAIDEN). J.P. acknowledges support from the Academy of Finland (Finland) with Grant No. 307685. Work at the University of York was supported under STFC Grants No. ST/L005727/1 and No. ST/P003885/1

Genetically Determined Height and Risk of Non-hodgkin Lymphoma

Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00\u20131.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01\u20131.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes

Fine-Scale Mapping of the 5q11.2 Breast Cancer Locus Reveals at Least Three Independent Risk Variants Regulating MAP3K1

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