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Rudolph, Anja,Song, Minsun,Brook, Mark N,Milne, Roger L,Mavaddat, Nasim,Michailidou, Kyriaki,Bolla, Manjeet K,Wang, Qin,Dennis, Joe,Wilcox, Amber N,Hopper, John L,Southey, Melissa C,Keeman, Renske,Fas Oxford University Press 2018 International journal of epidemiology Vol.47 No.2
<P>Conclusions: The combined effects of the 77-SNP PRS and environmental risk factors for breast cancer are generally well described by a multiplicative model. Larger studies are required to confirm possible departures from the multiplicative model for individual risk factors, and assess models specific for ER-negative disease.</P>
Reproductive profiles and risk of breast cancer subtypes: a multi-center case-only study
Brouckaert, Olivier,Rudolph, Anja,Laenen, Annouschka,Keeman, Renske,Bolla, Manjeet K.,Wang, Qin,Soubry, Adelheid,Wildiers, Hans,Andrulis, Irene L.,Arndt, Volker,Beckmann, Matthias W.,Benitez, Javier,B BioMed Central 2017 Breast cancer research Vol.19 No.-
<P><B>Background</B></P><P>Previous studies have shown that reproductive factors are differentially associated with breast cancer (BC) risk by subtypes. The aim of this study was to investigate associations between reproductive factors and BC subtypes, and whether these vary by age at diagnosis.</P><P><B>Methods</B></P><P>We used pooled data on tumor markers (estrogen and progesterone receptor, human epidermal growth factor receptor-2 (HER2)) and reproductive risk factors (parity, age at first full-time pregnancy (FFTP) and age at menarche) from 28,095 patients with invasive BC from 34 studies participating in the Breast Cancer Association Consortium (BCAC). In a case-only analysis, we used logistic regression to assess associations between reproductive factors and BC subtype compared to luminal A tumors as a reference. The interaction between age and parity in BC subtype risk was also tested, across all ages and, because age was modeled non-linearly, specifically at ages 35, 55 and 75 years.</P><P><B>Results</B></P><P>Parous women were more likely to be diagnosed with triple negative BC (TNBC) than with luminal A BC, irrespective of age (OR for parity = 1.38, 95% CI 1.16–1.65, <I>p</I> = 0.0004; <I>p</I> for interaction with age = 0.076). Parous women were also more likely to be diagnosed with luminal and non-luminal HER2-like BCs and this effect was slightly more pronounced at an early age (<I>p</I> for interaction with age = 0.037 and 0.030, respectively). For instance, women diagnosed at age 35 were 1.48 (CI 1.01–2.16) more likely to have luminal HER2-like BC than luminal A BC, while this association was not significant at age 75 (OR = 0.72, CI 0.45–1.14). While age at menarche was not significantly associated with BC subtype, increasing age at FFTP was non-linearly associated with TNBC relative to luminal A BC. An age at FFTP of 25 versus 20 years lowered the risk for TNBC (OR = 0.78, CI 0.70–0.88, <I>p</I> < 0.0001), but this effect was not apparent at a later FFTP.</P><P><B>Conclusions</B></P><P>Our main findings suggest that parity is associated with TNBC across all ages at BC diagnosis, whereas the association with luminal HER2-like BC was present only for early onset BC.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/s13058-017-0909-3) contains supplementary material, which is available to authorized users.</P>
Lei, Jieping,Rudolph, Anja,Moysich, Kirsten B,Rafiq, Sajjad,Behrens, Sabine,Goode, Ellen L,Pharoah, Paul PD,Seibold, Petra,Fasching, Peter A,Andrulis, Irene L,Kristensen, Vessela N,Couch, Fergus J,Ham BioMed Central 2015 Breast cancer research Vol.17 No.-
<P><B>Introduction</B></P><P>Tumor lymphocyte infiltration is associated with clinical response to chemotherapy in estrogen receptor (ER) negative breast cancer. To identify variants in immunosuppressive pathway genes associated with prognosis after adjuvant chemotherapy for ER-negative patients, we studied stage I-III invasive breast cancer patients of European ancestry, including 9,334 ER-positive (3,151 treated with chemotherapy) and 2,334 ER-negative patients (1,499 treated with chemotherapy).</P><P><B>Methods</B></P><P>We pooled data from sixteen studies from the Breast Cancer Association Consortium (BCAC), and employed two independent studies for replications. Overall 3,610 single nucleotide polymorphisms (SNPs) in 133 genes were genotyped as part of the Collaborative Oncological Gene-environment Study, in which phenotype and clinical data were collected and harmonized. Multivariable Cox proportional hazard regression was used to assess genetic associations with overall survival (OS) and breast cancer-specific survival (BCSS). Heterogeneity according to chemotherapy or ER status was evaluated with the log-likelihood ratio test.</P><P><B>Results</B></P><P>Three independent SNPs in <I>TGFBR2</I> and <I>IL12B</I> were associated with OS (<I>P</I> <10<SUP>−3</SUP>) solely in ER-negative patients after chemotherapy (267 events). Poorer OS associated with <I>TGFBR2</I> rs1367610 (G > C) (per allele hazard ratio (HR) 1.54 (95% confidence interval (CI) 1.22 to 1.95), <I>P</I> = 3.08 × 10<SUP>−4</SUP>) was not found in ER-negative patients without chemotherapy or ER-positive patients with chemotherapy (<I>P</I> for interaction <10<SUP>−3</SUP>). Two SNPs in <I>IL12B</I> (r<SUP>2</SUP> = 0.20) showed different associations with ER-negative disease after chemotherapy: rs2546892 (G > A) with poorer OS (HR 1.50 (95% CI 1.21 to 1.86), <I>P</I> = 1.81 × 10<SUP>−4</SUP>), and rs2853694 (A > C) with improved OS (HR 0.73 (95% CI 0.61 to 0.87), <I>P</I> = 3.67 × 10<SUP>−4</SUP>). Similar associations were observed with BCSS. Association with <I>TGFBR2</I> rs1367610 but not <I>IL12B</I> variants replicated using BCAC Asian samples and the independent Prospective Study of Outcomes in Sporadic versus Hereditary Breast Cancer Study and yielded a combined HR of 1.57 ((95% CI 1.28 to 1.94), <I>P</I> = 2.05 × 10<SUP>−5</SUP>) without study heterogeneity.</P><P><B>Conclusions</B></P><P><I>TGFBR2</I> variants may have prognostic and predictive value in ER-negative breast cancer patients treated with adjuvant chemotherapy. Our findings provide further insights into the development of immunotherapeutic targets for ER-negative breast cancer.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/s13058-015-0522-2) contains supplementary material, which is available to authorized users.</P>
Menelisi C. Dlamini,Mbongiseni L. Dlamini,Pumza Mente,Boitumelo Tlhaole,Rudolph Erasmus,Manoko S. Maubane-Nkadimeng,John A. Moma 한국공업화학회 2022 Journal of Industrial and Engineering Chemistry Vol.111 No.-
A simplistic solvothermal process to fabricate novel amorphous TiO2-BiOBr-Bentonite (A-TiO2-BiOBr-Bt)multidimensional photocatalysts in this work is a practical and economically feasible technique for thefabrication of the reported photocatalysts as it is a one-pot process. The stickiness of the A-TiO2-BiOBr-Bt wet cake and the low drying temperature make A-TiO2-BiOBr-Bt a feasible platform compositefor the fabrication of the photoreactive inner coating of water treatment containers for photocatalytictreatment of drinking water. The A-TiO2-BiOBr-Bt photocatalyst with an A-TiO2:BiOBr:Bt mass ratio of1:1:2 (Ti1Bi1Bt2) displayed the highest BET surface area of 124.8 m2/g, a low bandgap of 2.86 eV, and sufficientlylow electron-hole recombination rate. The high number of A-TiO2-BiOBr p-n heterojunctions,and the Ti-O-Si and Bi-O-Si bonds between A-TiO2-BiOBr and Bt in Ti1Bi1Bt2 lowered its electron-holerecombination rate with enhanced visible light-harvesting ability. Within 70 min of visible light irradiation,150 mg of Ti1Bi1Bt2 gave 100% conversion of 100 mL of 20 ppm phenol with a pseudo-first-order rateconstant of 0.0322 min1 at pH 4.0. Scavenging experiments showed superoxide radicals (O2) and electrons(e) being the most dominant reactive oxidation species (ROS) responsible for the phenol photodegradationprocess while holes (h+) and hydroxyl radicals (OH) also exerted appreciableparticipation.
Characterization of hard- and softwood biochars pyrolyzed at high temperature
Jiang, S.,Nguyen, T. A.,Rudolph, V.,Yang, H.,Zhang, D.,Ok, Y. S.,Huang, L. Springer Science + Business Media 2017 Environmental geochemistry and health Vol.39 No.2
<P>A wide range of waste biomass/waste wood feedstocks abundantly available at mine sites provide the opportunity to produce biochars for cost-effective improvement of mine tailings and contaminated land at metal mines. In the present study, soft- and hardwood biochars derived from pine and jarrah woods at high temperature (700 A degrees C) were characterized for their physiochemical properties including chemical components, electrical conductivity, pH, zeta potential, cation-exchange capacity (CEC), alkalinity, BET surface area and surface morphology. Evaluating and comparing these characteristics with available data from the literature have affirmed the strong dictation of precursor type on the physiochemical properties of the biochars. The pine and jarrah wood feedstocks are mainly different in their proportions of cellulose, hemicellulose and lignin, resulting in biochars with heterogeneous physiochemical properties. The hardwood jarrah biochar exhibits much higher microporosity, alkalinity and electrostatic capacity than the softwood pine. Correlation analysis and principal component analysis also show a good correlation between CEC-BET-alkalinity, and alkalinity-ash content. These comprehensive characterization and analysis results on biochars' properties from feedstocks of hardwood (from forest land clearance at mine construction) and waste pine wood (from mining operations) will provide a good guide for tailoring biochar functionalities for remediating metal mine tailings. The relatively inert high-temperature biochars can be stored for a long term at mine closure after decades of operations.</P>
Castrodale, Louisa J.,Raczniak, Gregory A.,Rudolph, Karen M.,Chikoyak, Lori,Cox, Russell S.,Franklin, Tricia L.,Traxler, Rita M.,Guerra, Marta Occupational Safety and Health Research Institute 2015 Safety and health at work Vol.6 No.4
Background: In 2012, the Alaska Section of Epidemiology investigated personnel potentially exposed to a Brucella suis isolate as it transited through three laboratories. Methods: We summarize the first implementation of the United States Centers for Disease Control and Prevention 2013 revised recommendations for monitoring such exposures: (1) risk classification; (2) antimicrobial postexposure prophylaxis; (3) serologic monitoring; and (4) symptom surveillance. Results: Over 30 people were assessed for exposure and subsequently monitored for development of illness. No cases of laboratory-associated brucellosis occurred. Changes were made to gaps in laboratory biosafety practices that had been identified in the investigation. Conclusion: Achieving full compliance for the precise schedule of serologic monitoring was challenging and resource intensive for the laboratory performing testing. More refined exposure assessments could inform decision making for follow-up to maximize likelihood of detecting persons at risk while not overtaxing resources.
Louisa J. Castrodale,Gregory A. Raczniak,Karen M. Rudolph,Lori Chikoyak,Russell S. Cox,Tricia L. Franklin,Rita M. Traxler,Marta Guerra 한국산업안전보건공단 산업안전보건연구원 2015 Safety and health at work Vol.6 No.4
Background: In 2012, the Alaska Section of Epidemiology investigated personnel potentially exposed to a Brucella suis isolate as it transited through three laboratories. Methods: We summarize the first implementation of the United States Centers for Disease Control and Prevention 2013 revised recommendations for monitoring such exposures: (1) risk classification; (2) antimicrobial postexposure prophylaxis; (3) serologic monitoring; and (4) symptom surveillance. Results: Over 30 people were assessed for exposure and subsequently monitored for development of illness. No cases of laboratory-associated brucellosis occurred. Changes were made to gaps in laboratory biosafety practices that had been identified in the investigation. Conclusion: Achieving full compliance for the precise schedule of serologic monitoring was challenging and resource intensive for the laboratory performing testing. More refined exposure assessments could inform decision making for follow-up to maximize likelihood of detecting persons at risk while not overtaxing resources.
Healy, Kevin D.,Hodgson, Louis,Kim, Tai-Young,Shutes, Adam,Maddileti, Savitri,Juliano, Rudolph L.,Hahn, Klaus M.,Harden, T. Kendall,Bang, Yung-Jue,Der, Channing J. Wiley Subscription Services, Inc., A Wiley Company 2008 Molecular carcinogenesis Vol.47 No.5
<P>Expression of the tumor suppressor deleted in liver cancer-1 (DLC-1) is lost in non-small cell lung (NSCLC) and other human carcinomas, and ectopic DLC-1 expression dramatically reduces proliferation and tumorigenicity. DLC-1 is a multi-domain protein that includes a Rho GTPase activating protein (RhoGAP) domain which has been hypothesized to be the basis of its tumor suppressive actions. To address the importance of the RhoGAP function of DLC-1 in tumor suppression, we performed biochemical and biological studies evaluating DLC-1 in NSCLC. Full-length DLC-1 exhibited strong GAP activity for RhoA as well as RhoB and RhoC, but only very limited activity for Cdc42 in vitro. In contrast, the isolated RhoGAP domain showed 5- to 20-fold enhanced activity for RhoA, RhoB, RhoC, and Cdc42. DLC-1 protein expression was absent in six of nine NSCLC cell lines. Restoration of DLC-1 expression in DLC-1-deficient NSCLC cell lines reduced RhoA activity, and experiments with a RhoA biosensor demonstrated that DLC-1 dramatically reduces RhoA activity at the leading edge of cellular protrusions. Furthermore, DLC-1 expression in NSCLC cell lines impaired both anchorage-dependent and -independent growth, as well as invasion in vitro. Surprisingly, we found that the anti-tumor activity of DLC-1 was due to both RhoGAP-dependent and -independent activities. Unlike the rat homologue p122RhoGAP, DLC-1 was not capable of activating the phospholipid hydrolysis activity of phospholipase C-δ1. Combined, these studies provide information on the mechanism of DLC-1 function and regulation, and further support the role of DLC-1 tumor suppression in NSCLC. © 2007 Wiley-Liss, Inc.</P>