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Freedman, Arnold

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Freedman

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Arnold

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Freedman, Arnold
Author's Publications: search.filters.isAuthorOfPublication.9ceb0305-4524-4c5e-965c-5faab8477d43

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    Atmospheric Chemistry and the Biosphere: General Discussion
    (Royal Society of Chemistry (RSC), 2017) Archibald, Alexander; Freedman, Arnold; Bejan, Lustian; Brown, Steven; Brüggemann, Martin; Carpenter, Lucy; Collins, John; Evans, Mathew; Finlayson-Pitts, Barbara; George, Christian; Hastings, Meredith; Heard, Dwayne; Hewitt, Christopher; Isaacman-VanWertz, Gabriel; Kalberer, Markus; Keutsch, Frank; Kiendler-Scharr, Astrid; Knopf, Daniel; Lelieveld, Jos; Marais, Eloise; Petzold, Andreas; Ravishankara, A.; Reid, Jonathan; Rovelli, Grazia; Scott, Catherine; Sherwen, Tomás; Shindell, Drew; Tinel, Liselotte; Unger, Nadine; Wallington, Timothy J.; Wahner, Andreas; Williams, Jonathan; Young, Timothy; Zelenyuk, Alla; Wallington, Timothy
    Lucy Carpenter opened discussion of the paper by Christian George: Your previous work has emphasised the abiotic production of VOCs from surface ocean processes, mainly from photosensitized chemistry of surfactants. Does this work indicate that decay of microbial cells is the really dominant source of these VOC-producing surfactants and photosensitizers, and if so - does this really mean this is an abiotic process? Christian George responded: As shown in our paper, VOC emissions increased drastically when the microbial cells were dying. Moreover, the highest VOC production was observed for the cellular fraction of the biofilms, i.e. intracellular material and cellular debris.
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    Genetic Variation in DNA Repair Pathways and Risk of Non-Hodgkin's Lymphoma
    (Public Library of Science, 2014) Rendleman, Justin; Antipin, Yevgeniy; Reva, Boris; Adaniel, Christina; Przybylo, Jennifer A.; Dutra-Clarke, Ana; Hansen, Nichole; Heguy, Adriana; Huberman, Kety; Borsu, Laetitia; Paltiel, Ora; Ben-Yehuda, Dina; Brown, Jennifer; Freedman, Arnold; Sander, Chris; Zelenetz, Andrew; Klein, Robert J.; Shao, Yongzhao; Lacher, Mortimer; Vijai, Joseph; Offit, Kenneth; Kirchhoff, Tomas
    Molecular and genetic evidence suggests that DNA repair pathways may contribute to lymphoma susceptibility. Several studies have examined the association of DNA repair genes with lymphoma risk, but the findings from these reports have been inconsistent. Here we provide the results of a focused analysis of genetic variation in DNA repair genes and their association with the risk of non-Hodgkin's lymphoma (NHL). With a population of 1,297 NHL cases and 1,946 controls, we have performed a two-stage case/control association analysis of 446 single nucleotide polymorphisms (SNPs) tagging the genetic variation in 81 DNA repair genes. We found the most significant association with NHL risk in the ATM locus for rs227060 (OR = 1.27, 95% CI: 1.13–1.43, p = 6.77×10−5), which remained significant after adjustment for multiple testing. In a subtype-specific analysis, associations were also observed for the ATM locus among both diffuse large B-cell lymphomas (DLBCL) and small lymphocytic lymphomas (SLL), however there was no association observed among follicular lymphomas (FL). In addition, our study provides suggestive evidence of an interaction between SNPs in MRE11A and NBS1 associated with NHL risk (OR = 0.51, 95% CI: 0.34–0.77, p = 0.0002). Finally, an imputation analysis using the 1,000 Genomes Project data combined with a functional prediction analysis revealed the presence of biologically relevant variants that correlate with the observed association signals. While the findings generated here warrant independent validation, the results of our large study suggest that ATM may be a novel locus associated with the risk of multiple subtypes of NHL.