89,040 research outputs found
Overexpression of select T cell receptor Vbeta gene families within CD4 + and CD8 + T cell subsets of myasthenia gravis patients: A role for superantigen(s)?
No full textBACKGROUND: The principal symptoms of myasthenia gravis (MG), muscle weakness and fatigue due to impaired neuromuscular transmission, are caused by autoantibodies to the muscle nicotinic acetylcholine receptor (AChR). The mechanisms underlying the autoimmune response, however, appear to be initiated by activation of specific HLA class II-restricted CD4+ T lymphocytes. Thus, central to elucidating the causation of MG is determining how T cells are recruited to contribute to misguided immunological assaults on the major autoantigenic target, AChR. MATERIALS AND METHODS: By combining a polymerase chain reaction (PCR)-based strategy and Southern blot technique, we have analyzed the frequency of expression of 22 individual T cell receptor (TCR) V beta gene subfamilies in CD4+ and CD8+ peripheral blood T cell subsets derived from eight MG patients and seven healthy controls. The quantification of relative usage of individual TCR J beta gene segments was performed by hybridization of PCR-amplified products (specifically V beta 1-C beta) with a complete panel of 32P-5'-end-labeled J beta-specific oligonucleotide probes, followed by scanning analysis of autoradiographs. RESULTS: Comparisons of data obtained from V beta analyses of T cells from MG patients with those from healthy individuals established that MG patients significantly overexpressed V beta 1, V beta 13.2, V beta 17, and V beta 20 gene family members within both CD4+ and CD8+ T cell subpopulations. Moreover, analysis of the relative utilization of individual TCR J beta gene segments in V beta 1+/CD4+ and V beta 1+/CD8+ T lymphocytes revealed distribution patterns in patients indistinguishable from those recorded in the corresponding cell subsets derived from controls. CONCLUSIONS: T lymphocytes from MG patients displayed a biased overexpression of four TCR V beta gene segments: V beta 1, V beta 13.2, V beta 17, and V beta 20. The relative frequencies of association of individual V beta 1 (D beta) J beta combinations revealed that J beta gene usage in the V beta 1-over-represented T cell subsets had normal distribution patterns. It can thus be deduced that J beta gene segment products appear not to have a selective effect on the process leading to overexpression of V beta 1 exons in MG patients. Hence, our observations suggest a possible role for superantigen(s) in the T cell activation in MG patients
Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution
No full textNon-steroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal ulcer formation by inhibiting epithelial cell migration and mucosal restitution; however, the drug-affected signaling pathways are poorly defined. We investigated whether NSAID inhibition of intestinal epithelial migration is associated with depletion of intracellular polyamines, depolarization of membrane potential (Em) and altered surface expression of K+ channels. Epithelial cell migration in response to the wounding of confluent IEC-6 and IEC-Cdx2 monolayers was reduced by indomethacin (100μM), phenylbutazone (100μM) and NS-398 (100μM) but not by SC-560 (1μM). NSAID-inhibition of intestinal cell migration was not associated with depletion of intracellular polyamines. Treatment of IEC-6 and IEC-Cdx2 cells with indomethacin, phenylbutazone and NS-398 induced significant depolarization of Em, whereas treatment with SC-560 had no effect on Em. The Em of IEC-Cdx2 cells was: −38.5±1.8mV under control conditions; −35.9±1.6mV after treatment with SC-560; −18.8±1.2mV after treatment with indomethacin; and −23.7±1.4mV after treatment with NS-398. Whereas SC-560 had no significant effects on the total cellular expression of Kv1.4 channel protein, indomethacin and NS-398 decreased not only the total cellular expression of Kv1.4, but also the cell surface expression of both Kv1.4 and Kv1.6 channel subunits in IEC-Cdx2. Both Kv1.4 and Kv1.6 channel proteins were immunoprecipitated by Kv1.4 antibody from IEC-Cdx2 lysates, indicating that these subunits co-assemble to form heteromeric Kv channels. These results suggest that NSAID inhibition of epithelial cell migration is independent of polyamine-depletion, and is associated with depolarization of Em and decreased surface expression of heteromeric Kv1 channels.ID: S0006295207001931; M3: Article; Accession Number: S0006295207001931; Author: L.C. Freeman (b); Author: D.F. Narvaez (a); Author: A. McCoy (a); Author: F.B. von Stein (c); Author: S. Young (b); Author: K. Silver (a); Author: S. Ganta (b); Author: D. Koch (b); Author: R. Hunter (b); Author: R.F. Gilmour (c); Author: J.D. Lillich (a, ⁎); Affiliation: Department of Clinical Sciences, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, United States; Keyword: Non-steroidal anti-inflammatory drugs; Keyword: Intestinal epithelial cells; Keyword: Membrane potential; Keyword: Potassium channels; Number of Pages: 12; Language: English;Source type: Electronic(1)http://search.ebscohost.com/login.aspx?direct=true&db=edselp&AN=S0006295207001931&site=eds-live&scope=sit
First observation of the decay Bs0→K*0K*0
No full textThe first observation of the decay B0s→K∗0K∗0 is reported using 35 pb−1 of data collected by LHCb in proton–proton collisions at a centre-of-mass energy of 7 TeV. A total of 49.8±7.5 B0s→(K+π−)(K−π+) events are observed within ±50 MeV/c2 of the B0s mass and 746 MeV/c2 < mKπ < 1046 MeV/c2, mostly coming from a resonant B0s→K∗0K∗0 signal. The branching fraction and the CP-averaged K∗0 longitudinal polarization fraction are measured to be B(B0s→K∗0K∗0)=(2.81±0.46(stat.)±0.45(syst.)±0.34(fs/ fd))×10−5 and fL =0.31±0.12(stat.)±0.04(syst.)
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Measurement of CP asymmetry in D-0 -> K- K+ and D-0 -> pi(-) pi(+) decays
No full textTime-integrated CP asymmetries in D 0 decays to the final states K - K + and π - π + are measured using proton-proton collisions corresponding to 3fb-1 of integrated luminosity collected at centre-of-mass energies of 7 TeV and 8 TeV. The D 0 mesons are produced in semileptonic b-hadron decays, where the charge of the accompanying muon is used to determine the initial flavour of the charm meson. The difference in CP asymmetries between the two final states is measured to be Δ ACP = ACP (K- K +) ACP (π- π+) = (+ 0.14 ± 0.16 (stat) ± 0.08 (syst)) %. A measurement of A CP (K - K +) is obtained assuming negligible CP violation in charm mixing and in Cabibbo-favoured D decays. It is found to be ACP (K- K+) = (- 0.06 ± 0.15 (stat) ± 0.10 (syst)) %, where the correlation coefficient between ΔA CP and A CP (K - K +) is ρ = 0.28. By combining these results, the CP asymmetry in the D 0 → π - π + channel is A CP (π - π +) = (-0.20 ± 0.19 (stat) ± 0.10 (syst))%. [Figure not available: see fulltext.] © 2014 The Author(s)
Measurement of the ratio of branching fractions B(B0→K∗0γ )/B(B0s→φγ ) and the directCP asymmetry inB 0→K∗0γ
No full textThe ratio of branching fractions of the radiative B decays B0→K⁎0γ and B0s→ϕγ has been measured using an integrated luminosity of 1.0 fb−1 of pp collision data collected by the LHCb experiment at a centre-of-mass energy of s√=7TeV. The value obtained is
B(B0→K⁎0γ)B(B0s→ϕγ)=1.23±0.06(stat.)±0.04(syst.)±0.10(fs/fd),
where the first uncertainty is statistical, the second is the experimental systematic uncertainty and the third is associated with the ratio of fragmentation fractions fs/fd. Using the world average value for B(B0→K⁎0γ), the branching fraction B(B0s→ϕγ) is measured to be (3.5±0.4)×10−5.
The direct CP asymmetry in B0→K⁎0γ decays has also been measured with the same data and found to be
ACP(B0→K⁎0γ)=(0.8±1.7(stat.)±0.9(syst.))%.
Both measurements are the most precise to date and are in agreement with the previous experimental results and theoretical expectations
Appropriate Similarity Measures for Author Cocitation Analysis
No full textWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
K-theory for group C*-algebras
No full textThese notes are based on a lecture course given by the first author in the Sedano Winter School on K-theory held in Sedano, Spain, on January 22-27th of 2007. They aim at introducing K-theory of C*-algebras, equivariant K-homology and KK-theory in the context of the Baum-Connes conjectur
Nonhelical inverse transfer of a decaying turbulent magnetic field
No full textIn the presence of magnetic helicity, inverse transfer from small to large scales is well known in magnetohydrodynamic (MHD) turbulence and has applications in astrophysics, cosmology, and fusion plasmas. Using high resolution direct numerical simulations of magnetically dominated self-similarly decaying MHD turbulence, we report a similar inverse transfer even in the absence of magnetic helicity. We compute for the first time spectral energy transfer rates to show that this inverse transfer is about half as strong as with helicity, but in both cases the magnetic gain at large scales results from velocity at similar scales interacting with smaller-scale magnetic fields. This suggests that both inverse transfers are a consequence of a universal mechanisms for magnetically dominated turbulence. Possible explanations include inverse cascading of the mean squared vector potential associated with local near two-dimensionality and the shallower k^2 subinertial range spectrum of kinetic energy forcing the magnetic field with a k^4 subinertial range to attain larger-scale coherence. The inertial range shows a clear k^{-2} spectrum and is the first example of fully isotropic magnetically dominated MHD turbulence exhibiting weak turbulence scaling
A Unified Shell model for Buoyancy-Driven Turbulence
No full textWe construct a unified shell model for stably stratified and convective turbulence. Shell model simulation of stably stratified flow in turbulent regime exhibit Bolgiano-Obukhbov (BO) scaling in which the kinetic energy spectrum varies as . However, simulation of convective turbulence shows Kolmogorov's spectrum. These results are consistent with the direct numerical simulations of Kumar {\em et al.} [Phys. Rev. E {\bf 90}, 023016 (2014)]. We also observe a dual scaling ( and ) for a limited range of parameters in stably stratified flow
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