| 1. |
- Abelev, B., et al.
(author)
-
Production of inclusive gamma(1S) and gamma(2S) in p-Pb collisions at, root S-NN=5.02 TeV
- 2015
-
In: Physics Letters. Section B: Nuclear, Elementary Particle and High-Energy Physics. - : Elsevier BV. - 0370-2693. ; 740, s. 105-117
-
Journal article (peer-reviewed)abstract
- We report on the production of inclusive gamma(1S) and gamma(2S) in p-Pb collisions at root S-NN = 5.02 TeV at the LHC. The measurement is performed with the ALICE detector at backward (-4.46 < ycms < 2.96) and forward (2.03 < ycms <3.53) rapidity down to zero transverse momentum. The production cross sections of the gamma(1S) and gamma(2S) are presented, as well as the nuclear modification factor and the ratio of the forward to backward yields of gamma(1S). A suppression of the inclusive gamma(1S) yield in p-Pb collisions with respect to the yield from pp collisions scaled by the number of binary nucleon-nucleon collisions is observed at forward rapidity but not at backward rapidity. The results are compared to theoretical model calculations including nuclear shadowing or partonic energy loss effects. (C) 2014 The Authors. Published by Elsevier B.V.
|
|
| 2. |
- Abelev, B., et al.
(author)
-
Suppression of Upsilon(1S) at forward rapidity in Pb-Pb collisions at root s(NN)=2.76 TeV
- 2014
-
In: Physics Letters. Section B: Nuclear, Elementary Particle and High-Energy Physics. - : Elsevier BV. - 0370-2693. ; 738, s. 361-372
-
Journal article (peer-reviewed)abstract
- We report on the measurement of the inclusive Upsilon(1S) production in Pb-Pb collisions at root s(NN) = 2.76 TeV carried out at forward rapidity (2.5 < y < 4) and down to zero transverse momentum using its mu(+)mu(-) decay channel with the ALICE detector at the Large Hadron Collider. Astrong suppression of the inclusive Upsilon(1S) yield is observed with respect to pp collisions scaled by the number of independent nucleo-nnucleon collisions. The nuclear modification factor, for events in the 0-90% centrality range, amounts to 0.30 +/- 0.05(stat) +/- 0.04(syst). The observed Upsilon(1S) suppression tends to increase with the centrality of the collision and seems more pronounced than in corresponding mid-rapidity measurements. Our results are compared with model calculations, which are found to underestimate the measured suppression and fail to reproduce its rapidity dependence. (C) 2014 The Authors. Published by Elsevier B. V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/3.0/). Funded by SCOAP(3).
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Wang, Li-San, et al.
(author)
-
Rarity of the Alzheimer Disease-Protective APP A673T Variant in the United States.
- 2015
-
In: JAMA neurology. - : American Medical Association (AMA). - 2168-6157 .- 2168-6149. ; 72:2
-
Journal article (peer-reviewed)abstract
- Recently, a rare variant in the amyloid precursor protein gene (APP) was described in a population from Iceland. This variant, in which alanine is replaced by threonine at position 673 (A673T), appears to protect against late-onset Alzheimer disease (AD). We evaluated the frequency of this variant in AD cases and cognitively normal controls to determine whether this variant will significantly contribute to risk assessment in individuals in the United States.
|
|
| 7. |
|
|
| 8. |
- Van Deerlin, Vivian M, et al.
(author)
-
Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP-43 inclusions
- 2010
-
In: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 42:3, s. 234-239
-
Journal article (peer-reviewed)abstract
- Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). FTLD-TDP is frequently familial, resulting from mutations in GRN (which encodes progranulin). We assembled an international collaboration to identify susceptibility loci for FTLD-TDP through a genome-wide association study of 515 individuals with FTLD-TDP. We found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM106B. Three SNPs retained genome-wide significance following Bonferroni correction (top SNP rs1990622, P = 1.08 x 10(-11); odds ratio, minor allele (C) 0.61, 95% CI 0.53-0.71). The association replicated in 89 FTLD-TDP cases (rs1990622; P = 2 x 10(-4)). TMEM106B variants may confer risk of FTLD-TDP by increasing TMEM106B expression. TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism.
|
|
| 9. |
- Bohmer, Sylvia-Annette, et al.
(author)
-
Association of the Protein-Tyrosine Phosphatase DEP-1 with Its Substrate FLT3 Visualized by In Situ Proximity Ligation Assay
- 2013
-
In: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:5, s. e62871-
-
Journal article (peer-reviewed)abstract
- Protein-tyrosine phosphatases (PTPs) are important regulators of signal transduction processes. Essential for the functional characterization of PTPs is the identification of their physiological substrates, and an important step towards this goal is the demonstration of a physical interaction. The association of PTPs with their cellular substrates is, however, often transient and difficult to detect with unmodified proteins at endogenous levels. Density-enhanced phosphatase-1 (DEP-1/PTPRJ) is a regulator of hematopoietic cell functions, and a candidate tumor suppressor. However, association of DEP-1 with any of its proposed substrates at endogenous levels has not yet been shown. We have previously obtained functional and biochemical evidence for a direct interaction of DEP-1 with the hematopoietic receptor-tyrosine kinase Fms-like tyrosine kinase-3 (FLT3). In the current study we have used the method of in situ proximity ligation assay (in situ PLA) to validate this interaction at endogenous levels, and to further characterize it. In situ PLA readily detected association of endogenous DEP1 and FLT3 in the human acute monocytic leukemia cell line THP-1, which was enhanced by FLT3 ligand (FL) stimulation in a time-dependent manner. Association peaked between 10 and 20 min of stimulation and returned to basal levels at 30 min. This time course was similar to the time course of FLT3 autophosphorylation. FLT3 kinase inhibition and DEP-1 oxidation abrogated association. Consistent with a functional role of DEP-1-FLT3 interaction, stable knockdown of DEP-1 in THP-1 cells enhanced FL-induced ERK1/2 activation. These findings support that FLT3 is a bona fide substrate of DEP-1 and that interaction occurs mainly via an enzyme-substrate complex formation triggered by FLT3 ligand stimulation.
|
|
| 10. |
|
|
