Two-pion Bose-Einstein correlations in central Pb-Pb collisions at sNN\sqrt{s_{\rm NN}} = 2.76 TeV

The first measurement of two-pion Bose-Einstein correlations in central Pb-Pb collisions at $\sqrt{s_{\rm NN}} = 2.76$ TeV at the Large Hadron Collider is presented. We observe a growing trend with energy now not only for the longitudinal and the outward but also for the sideward pion source radius. The pion homogeneity volume and the decoupling time are significantly larger than those measured at RHIC.Comment: 17 pages, 5 captioned figures, 1 table, authors from page 12, published version, figures at http://aliceinfo.cern.ch/ArtSubmission/node/388

Suppression of charged particle production at large transverse momentum in central Pb-Pb collisions at sNN=2.76\sqrt{s_{\rm NN}} = 2.76 TeV

Inclusive transverse momentum spectra of primary charged particles in Pb-Pb collisions at $\sqrt{s_{_{\rm NN}}}$ = 2.76 TeV have been measured by the ALICE Collaboration at the LHC. The data are presented for central and peripheral collisions, corresponding to 0-5% and 70-80% of the hadronic Pb-Pb cross section. The measured charged particle spectra in $|\eta|<0.8$ and $0.3 < p_T < 20$ GeV/$c$ are compared to the expectation in pp collisions at the same $\sqrt{s_{\rm NN}}$, scaled by the number of underlying nucleon-nucleon collisions. The comparison is expressed in terms of the nuclear modification factor $R_{\rm AA}$. The result indicates only weak medium effects ($R_{\rm AA} \approx$ 0.7) in peripheral collisions. In central collisions, $R_{\rm AA}$ reaches a minimum of about 0.14 at $p_{\rm T}=6$-7GeV/$c$ and increases significantly at larger $p_{\rm T}$. The measured suppression of high-$p_{\rm T}$ particles is stronger than that observed at lower collision energies, indicating that a very dense medium is formed in central Pb-Pb collisions at the LHC.Comment: 15 pages, 5 captioned figures, 3 tables, authors from page 10, published version, figures at http://aliceinfo.cern.ch/ArtSubmission/node/98

Reversing arterial stiffening and calcification: A pipe dream?

The development of technical means to non-invasively investigate the cardiovascular system on other features than pulse and blood pressure, slowly led to the recognition that additional characteristics of the heart and vasculature play a crucial role in the pathogenesis of cardiovascular disease. Possibly the most prominent feature is arterial stiffness. Although being an inevitable consequence of aging and inseparable phenomenon with hypertension, it is clear that it predicts cardiovascular risk independently form these two factors. The variability of arterial stiffness is explained by a large range of endocrine, metabolic, haemodynamic, structural and functional properties, that all frequently occur together in chronic kidney disease. Although calcification of the tunica media in the arterial wall, a hallmark of chronic kidney disease, appears difficult to improve, several other components that contribute to arterial stiffness are likely more accessible for modification. Although it is not proven that specifically targeting arterial stiffness translates into improved clinical outcome, this pathological feature of the arterial system is likely neglected clinically and has a sound basis for rational intervention, preferably preceded by interventional trials with clinically important endpoints. In this chapter modifiable and hardly-modifiable factors that likely contribute to arterial stiffness in the setting of chronic kidney disease are addressed. Although areas of uncertainty exist and are underlined, raising awareness of the relevance of this neglected feature of the cardiovascular system, holds the promise of improving the unacceptably high prevalence of complications in chronic kidney disease