| 1. |
- Adcox, K, et al.
(författare)
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PHENIX detector overview
- 2003
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Ingår i: Nuclear Instruments & Methods in Physics Research. Section A: Accelerators, Spectrometers, Detectors, and Associated Equipment. - 0167-5087. ; 499:2-3, s. 469-479
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Tidskriftsartikel (refereegranskat)abstract
- The PHENIX detector is designed to perform a broad study of A-A, p-A, and p-p collisions to investigate nuclear matter under extreme conditions. A wide variety of probes, sensitive to all timescales, are used to study systematic variations with species and energy as well as to measure the spin structure of the nucleon. Designing for the needs of the heavy-ion and polarized-proton programs has produced a detector with unparalleled capabilities. PHENIX measures electron and muon pairs, photons, and hadrons with excellent energy and momentum resolution. The detector consists of a large number of subsystems that are discussed in other papers in this volume. The overall design parameters of the detector are presented. (C) 2002 Elsevier Science B.V. All rights reserved.
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| 2. |
- Adler, SS, et al.
(författare)
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PHENIX on-line systems
- 2003
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Ingår i: Nuclear Instruments & Methods in Physics Research. Section A: Accelerators, Spectrometers, Detectors, and Associated Equipment. - 0167-5087. ; 499:2-3, s. 560-592
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Tidskriftsartikel (refereegranskat)abstract
- The PHENIX On-Line system takes signals from the Front End Modules (FEM) on each detector subsystem for the purpose of generating events for physics analysis. Processing of event data begins when the Data Collection Modules (DCM) receive data via fiber-optic links from the FEMs. The DCMs format and zero suppress the data and generate data packets. These packets go to the Event Builders (EvB) that assemble the events in final form. The Level-1 trigger (LVL1) generates a decision for each beam crossing and eliminates uninteresting events. The FEMs carry out all detector processing of the data so that it is delivered to the DCMs using a standard format. The FEMs also provide buffering for LVL1 trigger processing and DCM data collection. This is carried out using an architecture that is pipelined and deadtimeless. All of this is controlled by the Master Timing System (MTS) that distributes the RHIC clocks. A Level-2 trigger (LVL2) gives additional discrimination. A description of the components and operation of the PHENIX On-Line system is given and the solution to a number of electronic infrastructure problems are discussed. (C) 2002 Elsevier Science B.V. All rights reserved.
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| 3. |
- Giele, Walter, et al.
(författare)
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The QCD / SM working group: Summary report
- 2002
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Ingår i: Physics at TeV colliders. Proceedings, Euro Summer School, Les Houches, France, May 21-June 1, 2001. ; , s. 275-426, s. 275-426
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 4. |
- Khan, A, et al.
(författare)
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Long-term leptin treatment of ob/ob mice improves glucose-induced insulin secretion
- 2001
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Ingår i: International Journal of Obesity. - : Springer Science and Business Media LLC. - 1476-5497 .- 0307-0565. ; 25:6, s. 816-821
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Previous studies have demonstrated that leptin inhibits glucose-stimulated insulin secretion from isolated islets, although a lack of leptin effect on insulin secretion has also been reported. The effect of long term in vivo leptin treatment of insulin secretion has, however, not been established. Therefore, in the present study, we have evaluated the effect of long term in vivo treatment of leptin on glucose-induced insulin secretion in ob/ob mice. METHODS: After 7 days' treatment of leptin (100 microg daily s.c.), insulin release was measured in isolated islets by batch incubation followed by radioimmunoassay. Glucose utilization and oxidation were measured by measuring the formation of (3)H(2)O and (14)CO(2) from [5-(3)H] and [U-(14)C] glucose, respectively. Glucose-6-phosphatase activity was measured by measuring the conversion of (14)C-glucose-6-P to (14)C-glucose. In addition, immunohistochemistry of pancreatic specimens was undertaken for study of expression of insulin, GLUT-2 and hormone-sensitive lipase (HSL). RESULTS: Leptin treatment significantly improved insulin secretion both at 5.5 mM (by 15%; P<0.05) and 16.7 mM (by 85%; P<0.001) glucose, compared to vehicle-treated controls. Furthermore, whereas leptin treatment did not affect islet insulin or DNA contents, a significant decrease in islet triglyceride content and glucose-6-phosphatase activity was observed. Moreover, the immunocytochemical data revealed an increased immunostaining for insulin, GLUT-2 and hormone-sensitive lipase (HSL) in islets from leptin-treated ob/ob mice. CONCLUSION: The results suggest that long-term leptin treatment of ob/ob mice improves glucose-stimulated insulin secretion in parallel with reduced glucose-6-phosphatase activity, increased HSL and decreased triglyceride levels in islets. These perturbations may explain the improvement of glucose-stimulated insulin secretion induced by leptin.
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| 5. |
- Neumann, Patrick, et al.
(författare)
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Trunk posture: reliability, accuracy, and risk estimates for low back pain from a video based assessment method
- 2001
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Ingår i: International Journal of Industrial Ergonomics. - 0169-8141. ; 28, s. 355-365
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Tidskriftsartikel (refereegranskat)abstract
- It has been recently reported that both dynamic movement characteristics, as well as the duration of postures adopted during work, are important in the development of low back pain (LBP). This paper presents a video-based posture assessment method capable of measuring trunk angles and angular velocities in industrial workplaces. The interobserver reliability, system accuracy, and the relationship of the measured exposures to the reporting of low back pain are reported. The video analysis workstation consisted of a desktop computer equipped with digital video capture and playback technology, a VCR, and a computer game type joystick. The operator could then use a joystick to track trunk flexion and lateral bending during computer-controlled video playback. The joystick buttons were used for binary input of twisting. The inter-observer reliability for peak flexion and percentage of time spent in posture category variables were excellent (ICC>0.8). Lower reliability levels were observed for peak and average velocity and movement related variables. The video analysis system time series data showed very high correlation to the criterion optoelectronic imaging system (r ¼ 0:92). Root mean square errors averaged 5.81 for the amplitude probability distribution function data. Trunk flexion variables including peak level, peak velocity, average velocity indicators, and percent time in flexion category indicators all showed significant differences between cases and controls in the epidemiological study. A model consisting of the measures peak trunk flexion, percent time in lateral bend and average lateral bending velocity emerged after multivariable analysis for relationship to low back pain.
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| 6. |
- Swietlicki, Erik, et al.
(författare)
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Hygroscopic properties of aerosol particles in the northeastern Atlantic during ACE-2
- 2000
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Ingår i: Tellus. Series B: Chemical and Physical Meteorology. - : Stockholm University Press. - 0280-6509 .- 1600-0889. ; 52:2, s. 201-227
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Tidskriftsartikel (refereegranskat)abstract
- Measurements of the hygroscopic properties of sub-micrometer atmospheric aerosol particles were performed with hygroscopic tandem differential mobility analysers (H-TDMA) at 5 sites in the subtropical north-eastern Atlantic during the second Aerosol Characterization Experiment (ACE-2) from 16 June to 25 July 1997. Four of the sites were in the marine boundary layer and one was, at least occasionally, in the lower free troposphere. The hygroscopic diameter growth factors of individual aerosol particles in the dry particle diameter range 10-440 nm were generally measured for changes in relative humidity (RH) from <10% to 90%. In the marine boundary layer, growth factors at 90% RH were dependent on location, air mass type and particle size. The data was dominated by a unimodal growth distribution of more-hygroscopic particles, although a bimodal growth distribution including less-hygroscopic particles was observed at times, most often in the more polluted air masses. In clean marine air masses the more-hygroscopic growth factors ranged from about 1.6 to 1.8 with a consistent increase in growth factor with increasing particle size. There was also a tendency toward higher growth factors as sodium to sulphate molar ratio increased with increasing sea-salt contribution at higher wind speeds. During outbreaks of European pollution in the ACE-2 region, the growth factors of the largest particles were reduced, but only slightly. Growth factors at all sizes in both clean and polluted air masses were markedly lower at the Sagres, Portugal site due to more proximate continental influences. The frequency of occurrence of less-hygroscopic particles with a growth factor of ca. 1.15 was greatest during polluted conditions at Sagres. The free tropospheric 50 nm particles were predominately less-hygroscopic, with an intermediate growth factor of 1.4, but more-hygroscopic particles with growth factors of about 1.6 were also frequent. While these particles probably originate from within the marine boundary layer, the less-hygroscopic particles are probably more characteristic of lower free tropospheric air masses. For those occasions when measurements were made at 90% and an intermediate 60% or 70% RH, the growth factor G(RH) of the more-hygroscopic particles could be modelled empirically by a power law expression. For the ubiquitous more-hygroscopic particles, the expressions G(RH) = (1 - RH/100)-0.210 for 50 nm Aitken mode particles and G(RH) = (1 - RH/100)-0.233 for 166 nm accumulation mode particles are recommended for clean marine air masses in the north-eastern Atlantic within the range 0 < RH < 95%, and for wind speeds for which the local sea-salt production is small (< ca. 8 m s-1).
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| 7. |
- Valle, M., Zavialov, A., Li, W., Stagg, S.M., Sengupta, J., Nielsen, R., Nissen, P., Harvey, S., Ehrenberg, M. and Frank, J.
(författare)
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Incorporation of aminoacyl-tRNA in the ribosome as seen by cryo-EM.
- 2003
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Ingår i: Nature Structural Biology. ; 10, s. 899-906
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Tidskriftsartikel (refereegranskat)
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| 8. |
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| 9. |
- Arsura, Marcello, et al.
(författare)
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Transient activation of NF-kappaB through a TAK1/IKK kinase pathway by TGF-beta1 inhibits AP-1/SMAD signaling and apoptosis : implications in liver tumor formation.
- 2003
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Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 0950-9232 .- 1476-5594. ; 22:3, s. 412-425
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Tidskriftsartikel (refereegranskat)abstract
- NF-kappaB has been implicated in the regulation of apoptosis, a key mechanism of normal and malignant growth control. Previously, we demonstrated that inhibition of NF-kappaB activity by TGF-beta1 leads directly to induction of apoptosis of murine B-cell lymphomas and hepatocytes. Thus, we were surprised to determine that NF-kappaB is transiently activated in response to TGF-beta1 treatment. Here we elucidate the mechanism of TGF-beta1-mediated regulation of NF-kappaB and induction of apoptosis in epithelial cells. We report that TGF-beta1 activates IKK kinase, which mediates IkappaB-alpha phosphorylation. In turn, the activation of IKK following TGF-beta1 treatment is mediated by the TAK1 kinase. As a result of NF-kappaB activation, IkappaB-alpha mRNA and protein levels are increased leading to postrepression of NF-kappaB and induction of cell death. Inhibition of NF-kappaB following TGF-beta1 treatment increased AP-1 complex transcriptional activity through sustained c-Jun phosphorylation, thereby potentiating AP-1/SMADs-mediated cell killing. Furthermore, TGF-beta1-mediated upregulation of Smad7 appeared independent of NF-kappaB. In hepatocellular carcinomas of TGF-beta1 or TGF-alpha/c-myc transgenic mice, we observed constitutive activation of NF-kappaB that led to inhibition of JNK signaling. Overall, our data illustrate an autocrine mechanism based on the ability of IKK/NF-kappaB/IkappaB-alpha signaling to negatively regulate NF-kappaB levels thereby permitting TGF-beta1-induced apoptosis through AP-1 activity.
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| 10. |
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