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- Aaron, F. D., et al.
(författare)
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Measurement of the inclusive e(+/-) p scattering cross section at high inelasticity y and of the structure function F-L
- 2011
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Ingår i: European Physical Journal C. Particles and Fields. - : Springer Science and Business Media LLC. - 1434-6044. ; 71:3
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Tidskriftsartikel (refereegranskat)abstract
- A measurement is presented of the inclusive neutral current e(+/-) p scattering cross section using data collected by the H1 experiment at HERA during the years 2003 to 2007 with proton beam energies E-p of 920, 575, and 460 GeV. The kinematic range of the measurement covers low absolute four-momentum transfers squared, 1.5 GeV2 < Q(2) < 120 GeV2, small values of Bjorken x, 2.9 . 10(-5) < x < 0.01, and extends to high inelasticity up to y = 0.85. The structure function F-L is measured by combining the new results with previously published H1 data at E-p = 920 GeV and E-p = 820 GeV. The new measurements are used to test several phenomenological and QCD models applicable in this low Q(2) and low x kinematic domain.
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| 5. |
- Nimmo, K., et al.
(författare)
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A burst storm from the repeating FRB 20200120E in an M81 globular cluster
- 2023
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Ingår i: Monthly Notices of the Royal Astronomical Society. - : Oxford University Press (OUP). - 0035-8711 .- 1365-2966. ; 520:2, s. 2281-2305
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Tidskriftsartikel (refereegranskat)abstract
- The repeating fast radio burst (FRB) source FRB 20200120E is exceptional because of its proximity and association with a globular cluster. Here we report 60 bursts detected with the Effelsberg telescope at 1.4 GHz. We observe large variations in the burst rate, and report the first FRB 20200120E 'burst storm', where the source suddenly became active and 53 bursts (fluence ≥0.04 Jy ms) occurred within only 40 min. We find no strict periodicity in the burst arrival times, nor any evidence for periodicity in the source's activity between observations. The burst storm shows a steep energy distribution (power-law index α = 2.39 ± 0.12) and a bimodal wait-time distribution, with log-normal means of 0.94+0.07−0.06 s and 23.61+3.06−2.71 s. We attribute these wait-time distribution peaks to a characteristic event time-scale and pseudo-Poisson burst rate, respectively. The secondary wait-time peak at ∼1 s is ∼50 × longer than the ∼24 ms time-scale seen for both FRB 20121102A and FRB 20201124A - potentially indicating a larger emission region, or slower burst propagation. FRB 20200120E shows order-of-magnitude lower burst durations and luminosities compared with FRB 20121102A and FRB 20201124A. Lastly, in contrast to FRB 20121102A, which has observed dispersion measure (DM) variations of ΔDM > 1 pc cm−3 on month-to-year time-scales, we determine that FRB 20200120E's DM has remained stable (ΔDM < 0.15 pc cm−3) over >10 months. Overall, the observational characteristics of FRB 20200120E deviate quantitatively from other active repeaters, but it is unclear whether it is qualitatively a different type of source.
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| 10. |
- Marazioti, Antonia, et al.
(författare)
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KRAS signaling in malignant pleural mesothelioma
- 2022
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Ingår i: EMBO Molecular Medicine. - : EMBO. - 1757-4684 .- 1757-4676. ; 14:2
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Tidskriftsartikel (refereegranskat)abstract
- Malignant pleural mesothelioma (MPM) arises from mesothelial cells lining the pleural cavity of asbestos-exposed individuals and rapidly leads to death. MPM harbors loss-of-function mutations in BAP1, NF2, CDKN2A, and TP53, but isolated deletion of these genes alone in mice does not cause MPM and mouse models of the disease are sparse. Here, we show that a proportion of human MPM harbor point mutations, copy number alterations, and overexpression of KRAS with or without TP53 changes. These are likely pathogenic, since ectopic expression of mutant KRASG12D in the pleural mesothelium of conditional mice causes epithelioid MPM and cooperates with TP53 deletion to drive a more aggressive disease form with biphasic features and pleural effusions. Murine MPM cell lines derived from these tumors carry the initiating KRASG12D lesions, secondary Bap1 alterations, and human MPM-like gene expression profiles. Moreover, they are transplantable and actionable by KRAS inhibition. Our results indicate that KRAS alterations alone or in accomplice with TP53 alterations likely play an important and underestimated role in a proportion of patients with MPM, which warrants further exploration.
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