Radiation hardness of the LHCb Outer Tracker van Eijk, D.; Bachmann, S.; Bauer, Th ...
Nuclear instruments & methods in physics research. Section A, Accelerators, spectrometers, detectors and associated equipment,
09/2012, Letnik:
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This paper presents results on the radiation hardness of the LHCb Outer Tracker (OT) during LHC operation in 2010 and 2011. Modules of the OT have shown to suffer from ageing effects that lead to ...gain loss, after irradiation in the laboratory. Under irradiation at moderate intensities an insulating layer is formed on the anode wire of the OT straw cells. This ageing effect is caused by contamination of the counting gas due to outgassing of the glue used in the construction of the OT modules. Two methods to monitor gain stability in the OT are presented: module scans with radioactive sources and the study of hit efficiency as a function of amplifier threshold. No gain loss is observed after receiving 1.3fb−1 of integrated luminosity corresponding to an integrated charge of 0.055C/cm in the hottest spot of the detector.
The LHCb Outer Tracker is a gaseous detector covering an area of 5x6 m2 with 12 double layers of straw tubes. The detector with its services are described together with the commissioning and ...calibration procedures. Based on data of the first LHC running period from 2010 to 2012, the performance of the readout electronics and the single hit resolution and efficiency are presented. The efficiency to detect a hit in the central half of the straw is estimated to be 99.2%, and the position resolution is determined to be approximately 200 um. The Outer Tracker received a dose in the hottest region corresponding to 0.12 C/cm, and no signs of gain deterioration or other ageing effects are observed.
The persistent environmental contaminants perfluoroalkyl substances (PFASs) have gained attention due to their potential adverse health effects, in particular following early life exposure. ...Information on human fetal exposure to PFASs is currently limited to one report on first trimester samples. There is no data available on PFAS concentrations in fetal organs throughout all three trimesters of pregnancy.
We measured the concentrations of perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnA), and perfluorohexane sulfonic acid (PFHxS) in human embryos and fetuses with corresponding placentas and maternal serum samples derived from elective pregnancy terminations and cases of intrauterine fetal death. A total of 78 embryos and fetuses aged 7–42 gestational weeks were included and a total of 225 fetal organs covering liver, lung, heart, central nervous system (CNS), and adipose tissue were analyzed, together with 71 placentas and 63 maternal serum samples. PFAS concentrations were assayed by liquid chromatography/triple quadrupole mass spectrometry.
All evaluated PFASs were detected and quantified in maternal sera, placentas and embryos/fetuses. In maternal serum samples, PFOS was detected in highest concentrations, followed by PFOA > PFNA > PFDA = PFUnA = PFHxS. Similarly, PFOS was detected in highest concentrations in embryo/fetal tissues, followed by PFOA > PFNA = PFDA = PFUnA. PFHxS was detected in very few fetuses. In general, PFAS concentrations in embryo/fetal tissue (ng/g) were lower than maternal serum (ng/ml) but similar to placenta concentrations. The total PFAS burden (i.e. the sum of all PFASs) was highest in lung tissue in first trimester samples and in liver in second and third trimester samples. The burden was lowest in CNS samples irrespective of fetal age. The placenta:maternal serum ratios of PFOS, PFOA and PFNA increased across gestation suggesting bioaccumulation in the placenta. Further, we observed that the ratios were higher in pregnancies with male fetuses compared to female fetuses.
Human fetuses were intrinsically exposed to a mixture of PFASs throughout gestation. The compounds were detected in all analyzed tissues, suggesting that PFASs reach and may affect many types of organs. Collectively, our results demonstrate that PFASs pass the placenta and deposit to embryo and fetal tissues, calling for risk assessment of gestational exposures.
•PFASs were detected in maternal serum, placenta and fetal organs throughout pregnancy.•PFASs concentrations in fetal tissues were similar to placenta levels.•Fetal PFAS levels were highest in liver and lung and lowest in central nervous system.•PFOS, PFOA, and PFNA accumulated in placenta across gestation.•PFOA accumulated more in placentas with male fetuses compared to female fetuses.
Hepatocellular carcinoma (HCC) development entails changes in liver metabolism. Current knowledge on metabolic perturbations in HCC is derived mostly from case‐control designs, with sparse ...information from prospective cohorts. Our objective was to apply comprehensive metabolite profiling to detect metabolites whose serum concentrations are associated with HCC development, using biological samples from within the prospective European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (>520 000 participants), where we identified 129 HCC cases matched 1:1 to controls. We conducted high‐resolution untargeted liquid chromatography‐mass spectrometry‐based metabolomics on serum samples collected at recruitment prior to cancer diagnosis. Multivariable conditional logistic regression was applied controlling for dietary habits, alcohol consumption, smoking, body size, hepatitis infection and liver dysfunction. Corrections for multiple comparisons were applied. Of 9206 molecular features detected, 220 discriminated HCC cases from controls. Detailed feature annotation revealed 92 metabolites associated with HCC risk, of which 14 were unambiguously identified using pure reference standards. Positive HCC‐risk associations were observed for N1‐acetylspermidine, isatin, p‐hydroxyphenyllactic acid, tyrosine, sphingosine, l,l‐cyclo(leucylprolyl), glycochenodeoxycholic acid, glycocholic acid and 7‐methylguanine. Inverse risk associations were observed for retinol, dehydroepiandrosterone sulfate, glycerophosphocholine, γ‐carboxyethyl hydroxychroman and creatine. Discernible differences for these metabolites were observed between cases and controls up to 10 years prior to diagnosis. Our observations highlight the diversity of metabolic perturbations involved in HCC development and replicate previous observations (metabolism of bile acids, amino acids and phospholipids) made in Asian and Scandinavian populations. These findings emphasize the role of metabolic pathways associated with steroid metabolism and immunity and specific dietary and environmental exposures in HCC development.
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Changes in liver function precede the development of hepatocellular carcinoma (HCC). Many of these changes can be detected in the blood, as can biomarkers related to lifestyle or environmental exposures that may affect HCC risk. In this study, based on a large, prospective observational cohort, the authors used high resolution mass spectrometry‐based metabolomics to identify alterations in circulating levels of 92 metabolites associated with HCC risk, 14 of which could be annotated with high confidence and some of which were observed up to 10 years prior to diagnosis. These results offer insight into early metabolic perturbations and mechanisms leading to this deadly cancer.
Several studies on pregnancy-associated cancers have suggested an association with congenital anomalies in offspring. Previous studies have included maternal cancers diagnosed up to 2 years after ...pregnancy; however, long latency periods of some cancers mean that cancers diagnosed many years postpartum might have been present during pregnancy in a preclinical state. This paper considers the association between maternal cancers diagnosed from 2 years prior to pregnancy until the mother reaches 50 years of age, and congenital anomalies, as diagnosed at birth or within the first year of life. The current population-based study looks at associations of cancers in mothers with congenital anomalies in their children. Children were followed up from birth to diagnosis of a congenital anomaly, death, emigration or end of follow-up (whichever occurred first). A total of 56,016 children (2.6%) were considered exposed to a maternal cancer of any type; and they had a hazard ratio (HR) of 1.04 (95% confidence interval CI: 1.00, 1.09) compared with unexposed children. The greatest HR was seen among children whose mothers had been diagnosed with cancers before or during pregnancy (HR: 1.37, 95% CI: 1.07, 1.75). Similar results were seen when paternal cancers were used as a 'negative control'. Statistically significant associations were seen for some specific congenital anomalies of organ systems (congenital anomalies of the musculoskeletal system HR: 1.13, 95% CI: 1.02, 1.25) and for some specific types of maternal cancer (leukaemia HR: 1.31, 95% CI: 1.01, 1.61, The results of the main analyses suggest a small increase in risk of congenital anomalies in offspring of mothers diagnosed with cancer from 2 years before pregnancy, until the mother reaches 50 years of age; with the greatest increase seen for exposure in the pre-pregnancy and pregnancy period. These results may reflect shared causes for some cancers and some congenital anomalies. The similar results seen for paternal cancers indicate that the cause may be genetic or related to the families' social and environmental conditions.
Modeling the behavior of crown fires is challenging due to the complex set of coupled processes that drive the characteristics of a spreading wildfire and the large range of spatial and temporal ...scales over which these processes occur. Detailed physics-based modeling approaches such as FIRETEC and the Wildland Urban Interface Fire Dynamics Simulator (WFDS) simulate fire behavior using computational fluid dynamics based methods to numerically solve the three-dimensional, time dependent, model equations that govern, to some approximation, the component physical processes and their interactions that drive fire behavior. Both of these models have had limited evaluation and have not been assessed for predicting crown fire behavior. In this paper, we utilized a published set of field-scale measured crown fire rate of spread (ROS) data to provide a coarse assessment of crown fire ROS predictions from previously published studies that have utilized WFDS or FIRETEC. Overall, 86% of all simulated ROS values using WFDS or FIRETEC fell within the 95% prediction interval of the empirical data, which was above the goal of 75% for dynamic ecological modeling. However, scarcity of available empirical data is a bottleneck for further assessment of model performance.
Persistent organic pollutants (POPs) are industrial chemicals with long half-lives. Early life exposure to POPs has been associated with adverse effects. Fetal exposure is typically estimated based ...on concentrations in maternal serum or placenta and little is known on the actual fetal exposure. We measured the concentrations of nine organochlorine pesticides (OCPs), ten polychlorinated biphenyl (PCB) congeners, and polybrominated diphenyl ether (PBDE) congeners by gas chromatography – tandem mass spectrometry in maternal serum, placenta, and fetal tissues (adipose tissue, liver, heart, lung and brain) in 20 pregnancies that ended in stillbirth (gestational weeks 36–41). The data were combined with our earlier data on perfluoroalkyl substances (PFASs) in the same cohort (Mamsen et al. 2019). HCB, p,p’-DDE, PCB 138 and PCB 153 were quantified in all samples of maternal serum, placenta and fetal tissues. All 22 POPs were detected in all fetal adipose tissue samples, even in cases where they could not be detected in maternal serum or placenta. Tissue:serum ratios were significantly higher in later gestations, male fetuses, and pregnancies with normal placental function. OCPs showed the highest tissue:serum ratios and PFAS the lowest. The highest chemical burden was found in adipose tissue and lowest in the brain. Overall, all studied human fetuses were intrinsically exposed to mixtures of POPs. Tissue:serum ratios were significantly modified by gestational age, fetal sex and placental function. Importantly, more chemicals were detected in fetal tissues compared to maternal serum and placenta, implying that these proxy samples may provide a misleading picture of actual fetal exposures.
•OCPs, PCBs, and PBDEs were detected in maternal serum, placenta, and fetal tissues.•All chemicals were found in fetuses even when not detected in maternal serum/placenta.•Tissue:serum ratios were higher in pregnancies with male fetuses and normal placenta.•Tissue:serum ratios differed by chemical type: OCP > PCB > PFAS.•Chemicals in maternal serum and placenta are not reliable proxies of fetal exposure.
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