977 research outputs found
Pedestrian Trajectory Prediction with Structured Memory Hierarchies
This paper presents a novel framework for human trajectory prediction based
on multimodal data (video and radar). Motivated by recent neuroscience
discoveries, we propose incorporating a structured memory component in the
human trajectory prediction pipeline to capture historical information to
improve performance. We introduce structured LSTM cells for modelling the
memory content hierarchically, preserving the spatiotemporal structure of the
information and enabling us to capture both short-term and long-term context.
We demonstrate how this architecture can be extended to integrate salient
information from multiple modalities to automatically store and retrieve
important information for decision making without any supervision. We evaluate
the effectiveness of the proposed models on a novel multimodal dataset that we
introduce, consisting of 40,000 pedestrian trajectories, acquired jointly from
a radar system and a CCTV camera system installed in a public place. The
performance is also evaluated on the publicly available New York Grand Central
pedestrian database. In both settings, the proposed models demonstrate their
capability to better anticipate future pedestrian motion compared to existing
state of the art.Comment: To appear in ECML-PKDD 201
The effect of cangrelor and access site on ischaemic and bleeding events: insights from CHAMPION PHOENIX
Transiently achieved very low low-density lipoprotein cholesterol levels by statin and alirocumab after acute coronary syndrome are associated with cardiovascular risk reduction: the ODYSSEY OUTCOMES trial
Aims Long-term, placebo-controlled cholesterol-lowering trials have demonstrated legacy effects (clinical benefits that persist or emerge after trial end). It is unknown whether legacy effects follow a short period of very low low-density lipoprotein cholesterol (LDL-C) levels achieved with statin plus proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor. Methods and results In 18 924 patients with recent acute coronary syndrome, the ODYSSEY OUTCOMES trial compared the PCSK9 inhibitor alirocumab with placebo, each added to high-intensity or maximum-tolerated statin therapy. Patients with two consecutive LDL-C levels <0.39â
mmol/L (15â
mg/dL) on alirocumab had blinded placebo substitution for the remainder of the trial with continued statin treatment. In post hoc analyses, major adverse cardiovascular events (MACE) in these patients were compared to MACE in propensity scoreâmatched patients from the placebo group with similar baseline characteristics and study medication adherence. In the alirocumab group, 730 patients had blinded placebo substitution at a median of 8.3 months from randomization, after a median of 6.0 months with LDL-C <0.39â
mmol/L. They were matched to 1460 placebo patients. Both groups had lower baseline LDL-C and lipoprotein(a) and better study medication adherence than those of the overall cohort. Over a median follow-up of 2.8 years, MACE occurred in 47 (6.4%) alirocumab patients with limited-duration, very low achieved LDL-C vs. 122 (8.4%) matched placebo patients (treatment hazard ratio 0.72; 95% confidence interval 0.51, 0.997; P = 0.047). Conclusion A short period of LDL-C levels <0.39â
mmol/L achieved with statin and alirocumab, followed by statin monotherapy, was associated with a lower risk of MACE than statin monotherapy throughout the observation period. Clinical benefit persisted for several years
Resistance of Renal Cell Carcinoma to Sorafenib Is Mediated by Potentially Reversible Gene Expression
Purpose: Resistance to antiangiogenic therapy is an important clinical problem. We examined whether resistance occurs at least in part via reversible, physiologic changes in the tumor, or results solely from stable genetic changes in resistant tumor cells. Experimental Design: Mice bearing two human RCC xenografts were treated with sorafenib until they acquired resistance. Resistant 786-O cells were harvested and reimplanted into naĂŻve mice. Mice bearing resistant A498 cells were subjected to a 1 week treatment break. Sorafenib was then again administered to both sets of mice. Tumor growth patterns, gene expression, viability, blood vessel density, and perfusion were serially assessed in treated vs control mice. Results: Despite prior resistance, reimplanted 786-O tumors maintained their ability to stabilize on sorafenib in sequential reimplantation steps. A transcriptome profile of the tumors revealed that the gene expression profile of tumors upon reimplantation reapproximated that of the untreated tumors and was distinct from tumors exhibiting resistance to sorafenib. In A498 tumors, revascularization was noted with resistance and cessation of sorafenib therapy and tumor perfusion was reduced and tumor cell necrosis enhanced with re-exposure to sorafenib. Conclusions: In two RCC cell lines, resistance to sorafenib appears to be reversible. These results support the hypothesis that resistance to VEGF pathway therapy is not solely the result of a permanent genetic change in the tumor or selection of resistant clones, but rather is due to a great extent to reversible changes that likely occur in the tumor and/or its microenvironment
Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer.
Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance. How tumors transition between drug responsiveness, tolerance and resistance, especially in the absence of preexisting subclones, remains unclear. In epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma cells, we demonstrate that residual disease and acquired resistance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity. Nongenetic resistance through the activation of AURKA by its coactivator TPX2 emerges in response to chronic EGFR inhibition where it mitigates drug-induced apoptosis. Aurora kinase inhibitors suppress this adaptive survival program, increasing the magnitude and duration of EGFR inhibitor response in preclinical models. Treatment-induced activation of AURKA is associated with resistance to EGFR inhibitors in vitro, in vivo and in most individuals with EGFR-mutant lung adenocarcinoma. These findings delineate a molecular path whereby drug resistance emerges from drug-tolerant cells and unveils a synthetic lethal strategy for enhancing responses to EGFR inhibitors by suppressing AURKA-driven residual disease and acquired resistance
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Inclusive J/Ï production at mid-rapidity in pp collisions at âs = 5.02 TeV
Inclusive J/Ï production is studied in minimum-bias proton-proton collisions at a centre-of-mass energy of s = 5.02 TeV by ALICE at the CERN LHC. The measurement is performed at mid-rapidity (|y| < 0.9) in the dielectron decay channel down to zero transverse momentum pT, using a data sample corresponding to an integrated luminosity of Lint = 19.4 ± 0.4 nbâ1. The measured pT-integrated inclusive J/Ï production cross sec- tion is dÏ/dy = 5.64 ± 0.22(stat.) ± 0.33(syst.) ± 0.12(lumi.) ÎŒb. The pT-differential cross section d2Ï/dpTdy is measured in the pT range 0â10 GeV/c and compared with state-of- the-art QCD calculations. The J/Ï ăpTă and ăpT2ă are extracted and compared with results obtained at other collision energies. [Figure not available: see fulltext.]
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Measurement of Î (1520) production in pp collisions at âs=7TeV and pâPb collisions at âsNN=5.02TeV
The production of the Î (1520) baryonic resonance has been measured at midrapidity in inelastic pp collisions at s=7TeV and in pâPb collisions at sNN=5.02TeV for non-single diffractive events and in multiplicity classes. The resonance is reconstructed through its hadronic decay channel Î (1520) â pK - and the charge conjugate with the ALICE detector. The integrated yields and mean transverse momenta are calculated from the measured transverse momentum distributions in pp and pâPb collisions. The mean transverse momenta follow mass ordering as previously observed for other hyperons in the same collision systems. A Blast-Wave function constrained by other light hadrons (Ï, K, KS0, p, Î) describes the shape of the Î (1520) transverse momentum distribution up to 3.5GeV/c in pâPb collisions. In the framework of this model, this observation suggests that the Î (1520) resonance participates in the same collective radial flow as other light hadrons. The ratio of the yield of Î (1520) to the yield of the ground state particle Î remains constant as a function of charged-particle multiplicity, suggesting that there is no net effect of the hadronic phase in pâPb collisions on the Î (1520) yield
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Measurement of electrons from heavy-flavour hadron decays as a function of multiplicity in p-Pb collisions at âsNN = 5.02 TeV
The multiplicity dependence of electron production from heavy-flavour hadron decays as a function of transverse momentum was measured in p-Pb collisions at sNN = 5.02 TeV using the ALICE detector at the LHC. The measurement was performed in the centre-of-mass rapidity interval â1.07 < ycms< 0.14 and transverse momentum interval 2 < pT< 16 GeV/c. The multiplicity dependence of the production of electrons from heavy-flavour hadron decays was studied by comparing the pT spectra measured for different multiplicity classes with those measured in pp collisions (QpPb) and in peripheral p-Pb collisions (Qcp). The QpPb results obtained are consistent with unity within uncertainties in the measured pT interval and event classes. This indicates that heavy-flavour decay electron production is consistent with binary scaling and independent of the geometry of the collision system. Additionally, the results suggest that cold nuclear matter effects are negligible within uncertainties, in the production of heavy-flavour decay electrons at midrapidity in p-Pb collisions. [Figure not available: see fulltext.
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