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- Abazov, V. M., et al.
(författare)
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Determination of the strong coupling constant from the inclusive jet cross section in pp collisions at s=1.96 TeV
- 2009
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Ingår i: PHYS REV D. - 1550-7998 .- 1550-2368. ; 80, s. 111107-
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Tidskriftsartikel (refereegranskat)abstract
- We determine the strong coupling constant alpha(s) and its energy dependence from the p(T) dependence of the inclusive jet cross section in pp collisions at s=1.96 TeV. The strong coupling constant is determined over the transverse momentum range 50 < p(T)< 145 GeV. Using perturbative QCD calculations to order O(alpha(3)(s)) combined with O(alpha(4)(s)) contributions from threshold corrections, we obtain alpha(s)(M-Z)=0.1161(-0.0048)(+0.0041). This is the most precise result obtained at a hadron-hadron collider.
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- Alonso-Fernandez, Fernando, et al.
(författare)
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Iris Recognition Based on SIFT Features
- 2009
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Ingår i: 2009 First IEEE International Conference on Biometrics, Identity and Securit. - 9781424452767 ; , s. 1-8
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Konferensbidrag (refereegranskat)abstract
- Biometric methods based on iris images are believed to allow very high accuracy, and there has been an explosion of interest in iris biometrics in recent years. In this paper, we use the Scale Invariant Feature Transformation (SIFT) for recognition using iris images. Contrarily to traditional iris recognition systems, the SIFT approach does not rely on the transformation of the iris pattern to polar coordinates or on highly accurate segmentation, allowing less constrained image acquisition conditions. We extract characteristic SIFT feature points in scale space and perform matching based on the texture information around the feature points using the SIFT operator. Experiments are done using the BioSec multimodal database, which includes 3,200 iris images from 200 individuals acquired in two different sessions. We contribute with the analysis of the influence of different SIFT parameters on the recognition performance. We also show the complementarity between the SIFT approach and a popular matching approach based on transformation to polar coordinates and Log-Gabor wavelets. The combination of the two approaches achieves significantly better performance than either of the individual schemes, with a performance improvement of 24% in the Equal Error Rate.
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- Maynard, Christa J., et al.
(författare)
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Accumulation of ubiquitin conjugates in a polyglutamine disease model occurs without global ubiquitin/proteasome system impairment
- 2009
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Ingår i: Proceedings of the National Academy of Sciences. - : Proceedings of the National Academy of Sciences. - 1091-6490 .- 0027-8424. ; 106:33, s. 13986-13991
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Tidskriftsartikel (refereegranskat)abstract
- Aggregation-prone proteins have been suggested to overwhelm and impair the ubiquitin/proteasome system (UPS) in polyglutamine (polyQ) disorders, such as Huntington's disease (HD). Overexpression of an N-terminal fragment of mutant huntingtin (N-mutHtt), an aggregation-prone polyQ protein responsible for HD, obstructs the UPS in cellular models. Furthermore, based on the accumulation of polyubiquitin conjugates in brains of R6/2 mice, which express human N-mutHtt and are one of the most severe polyQ disorder models, it has been proposed that UPS dysfunction is a consistent feature of this pathology, occurring in both in vitro and in vivo models. Here, we have exploited transgenic mice that ubiquitously express a ubiquitin fusion degradation proteasome substrate to directly assess the functionality of the UPS in R6/2 mice or the slower onset R6/1 mice. Although expression of N-mutHtt caused a general inhibition of the UPS in PC12 cells, we did not observe an increase in the levels of proteasome reporter substrate in the brains of R6/2 and R6/1 mice. We show that the increase in ubiquitin conjugates in R6/2 mice can be primarily attributed to an accumulation of large ubiquitin conjugates that are different from the conjugates observed upon UPS inhibition. Together our data show that polyubiquitylated proteins accumulate in R6/2 brain despite a largely operative UPS, and suggest that neurons are able to avoid or compensate for the inhibitory effects of N-mutHtt.
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