2,656 research outputs found

    Disordered, strongly scattering porous materials as miniature multipass gas cells

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    Spectroscopic gas sensing is both a commercial success and a rapidly advancing scientific field. Throughout the years, massive efforts have been directed towards improving detection limits by achieving long interaction pathlengths. Prominent examples include the use of conventional multipass gas cells, sophisticated high-finesse cavities, gas-filled holey fibers, integrating spheres, and diffusive reflectors. Despite this rich flora of approaches, there is a continuous struggle to reduce size, gas volume, cost and alignment complexity. Here, we show that extreme light scattering in porous materials can be used to realise miniature gas cells. Near-infrared transmission through a 7 mm zirconia (ZrO2) sample with a 49% porosity and subwavelength pore structure (on the order of 100 nm) gives rise to an effective gas interaction pathlength above 5 meters, an enhancement corresponding to 750 passes through a conventional multipass cell. This essentially different approach to pathlength enhancement opens a new route to compact, alignment-free and low-cost optical sensor systems

    Placental weight and mortality in premenopausal breast cancer by tumor characteristics

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    Placental weight may be regarded as an indirect marker of hormone exposures during pregnancy. There is epidemiological evidence that breast cancer mortality in premenopausal women increases with placental weight in the most recent pregnancy. We investigated if this association differs by tumor characteristics, including expression of estrogen and progesterone receptors. In a Swedish population-based cohort, we followed 1,067 women with premenopausal breast cancer diagnosed from 1992 to 2006. Using Cox regression models, we estimated hazard ratios for the association between placental weight and risk of premenopausal breast cancer mortality. In stratified analyses, we estimated mortality risks in subjects with different tumor stages, estrogen receptor (ER) or progesterone receptor (PR) status. Compared with women with placental weight less than 600 g, women with a placental weight between 600 and 699 g were at a 50 % increased risk of mortality, however, not significant change in risk was observed for women with placental weight �700 g. Mortality risks associated with higher placental weight were more pronounced among ER- and PR- breast cancer tumors, where both a placental weight 600-699 g and �700 g were associated with a more than doubled mortality risks compared with tumors among women with placental weight less than 600 g. Moreover, stratified analyses for joint receptor status revealed that a consistent increased mortality risk by placental weight was only apparent in women with ER-/PR- breast cancer. The increased mortality risk in premenopausal breast cancer associated with higher placental weight was most pronounced among ER- and PR- tumors. © 2012 Springer Science+Business Media New York

    Constraining the magnitude of the Chiral Magnetic Effect with Event Shape Engineering in Pb-Pb collisions at sNN\sqrt{s_{\rm NN}} = 2.76$ TeV

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    In ultrarelativistic heavy-ion collisions, the event-by-event variation of the elliptic flow v2v_2 reflects fluctuations in the shape of the initial state of the system. This allows to select events with the same centrality but different initial geometry. This selection technique, Event Shape Engineering, has been used in the analysis of charge-dependent two- and three-particle correlations in Pb-Pb collisions at sNN=2.76\sqrt{s_{_{\rm NN}}} =2.76 TeV. The two-particle correlator cos(φαφβ)\langle \cos(\varphi_\alpha - \varphi_\beta) \rangle, calculated for different combinations of charges α\alpha and β\beta, is almost independent of v2v_2 (for a given centrality), while the three-particle correlator cos(φα+φβ2Ψ2)\langle \cos(\varphi_\alpha + \varphi_\beta - 2\Psi_2) \rangle scales almost linearly both with the event v2v_2 and charged-particle pseudorapidity density. The charge dependence of the three-particle correlator is often interpreted as evidence for the Chiral Magnetic Effect (CME), a parity violating effect of the strong interaction. However, its measured dependence on v2v_2 points to a large non-CME contribution to the correlator. Comparing the results with Monte Carlo calculations including a magnetic field due to the spectators, the upper limit of the CME signal contribution to the three-particle correlator in the 10-50% centrality interval is found to be 26-33% at 95% confidence level.Comment: 20 pages, 6 captioned figures, 1 tables, authors from page 15, published version, figures at http://aliceinfo.cern.ch/ArtSubmission/node/382

    Measurement of the production of charm jets tagged with D0^{0} mesons in pp collisions at s\sqrt{s}= 7 TeV

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    The production of charm jets in proton-proton collisions at a center-of-mass energy of s=7\sqrt{s}=7 TeV was measured with the ALICE detector at the CERN Large Hadron Collider. The measurement is based on a data sample corresponding to a total integrated luminosity of 6.236.23 nb1{\rm nb}^{-1}, collected using a minimum-bias trigger. Charm jets are identified by the presence of a D0^0 meson among their constituents. The D0^0 mesons are reconstructed from their hadronic decay D0^0\rightarrowKπ+^{-}\pi^{+}. The D0^0-meson tagged jets are reconstructed using tracks of charged particles (track-based jets) with the anti-kTk_{\mathrm{T}} algorithm in the jet transverse momentum range 5<pT,jetch<305<p_{\rm{T,jet}}^{\mathrm{ch}}<30 GeV/c{\rm GeV/}c and pseudorapidity ηjet<0.5|\eta_{\rm jet}|<0.5. The fraction of charged jets containing a D0^0-meson increases with pT,jetchp_{\rm{T,jet}}^{\rm{ch}} from 0.042±0.004(stat)±0.006(syst)0.042 \pm 0.004\, \mathrm{(stat)} \pm 0.006\, \mathrm{(syst)} to 0.080±0.009(stat)±0.008(syst)0.080 \pm 0.009\, \rm{(stat)} \pm 0.008\, \rm{(syst)}. The distribution of D0^0-meson tagged jets as a function of the jet momentum fraction carried by the D0^0 meson in the direction of the jet axis (zchz_{||}^{\mathrm{ch}}) is reported for two ranges of jet transverse momenta, 5<pT,jetch<155<p_{\rm{T,jet}}^{\rm{ch}}<15 GeV/c{\rm GeV/}c and 15<pT,jetch<3015<p_{\rm{T,jet}}^{\rm{ch}}<30 GeV/c{\rm GeV/}c in the intervals 0.2<zch<1.00.2<z_{||}^{\rm{ch}}<1.0 and 0.4<zch<1.00.4<z_{||}^{\rm{ch}}<1.0, respectively. The data are compared with results from Monte Carlo event generators (PYTHIA 6, PYTHIA 8 and Herwig 7) and with a Next-to-Leading-Order perturbative Quantum Chromodynamics calculation, obtained with the POWHEG method and interfaced with PYTHIA 6 for the generation of the parton shower, fragmentation, hadronisation and underlying event.Comment: 29 pages, 8 captioned figures, 3 tables, authors from page 24, published version, figures at http://alice-publications.web.cern.ch/node/525

    Targeting BTK for the treatment of FLT3-ITD mutated acute myeloid leukemia

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    Approximately 20% of patients with acute myeloid leukaemia (AML) have a mutation in FMS-like-tyrosine-kinase-3 (FLT3). FLT3 is a trans-membrane receptor with a tyrosine kinase domain which, when activated, initiates a cascade of phosphorylated proteins including the SRC family of kinases. Recently our group and others have shown that pharmacologic inhibition and genetic knockdown of Bruton's tyrosine kinase (BTK) blocks AML blast proliferation, leukaemic cell adhesion to bone marrow stromal cells as well as migration of AML blasts. The anti-proliferative effects of BTK inhibition in human AML are mediated via inhibition of downstream NF-κB pro-survival signalling however the upstream drivers of BTK activation in human AML have yet to be fully characterised. Here we place the FLT3-ITD upstream of BTK in AML and show that the BTK inhibitor ibrutinib inhibits the survival and proliferation of FLT3-ITD primary AML blasts and AML cell lines. Furthermore ibrutinib inhibits the activation of downstream kinases including MAPK, AKT and STAT5. In addition we show that BTK RNAi inhibits proliferation of FLT3-ITD AML cells. Finally we report that ibrutinib reverses the cyto-protective role of BMSC on FLT3-ITD AML survival. These results argue for the evaluation of ibrutinib in patients with FLT3-ITD mutated AML
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