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The transverse momentum (pT) distribution of primary charged particles is measured in minimum bias (non-single-diffractive) p-Pb collisions at sNN−−−√=5.02 TeV with the ALICE detector at the LHC. The pT spectra measured near central rapidity in the range 0.5<pT<20 GeV/c exhibit a weak pseudorapidity dependence. The nuclear modification factor RpPb is consistent with unity for pT above 2 GeV/c. This measurement indicates that the strong suppression of hadron production at high pT observed in Pb-Pb collisions at the LHC is not due to an initial-state effect. The measurement is compared to theoretical calculations.
Measurement of charm production at central rapidity in proton-proton collisions at √s = 2.76 TeV
(2012)
The pT-differential production cross sections of the prompt (B feed-down subtracted) charmed mesons D0, D+, and D∗+ in the rapidity range |y|<0.5, and for transverse momentum 1<pT<12 GeV/c, were measured in proton-proton collisions at s√=2.76 TeV with the ALICE detector at the Large Hadron Collider. The analysis exploited the hadronic decays D0→Kπ, D+→Kππ, D∗+→D0π, and their charge conjugates, and was performed on a Lint=1.1 nb−1 event sample collected in 2011 with a minimum-bias trigger. The total charm production cross section at s√=2.76 TeV and at 7 TeV was evaluated by extrapolating to the full phase space the pT-differential production cross sections at s√=2.76 TeV and our previous measurements at s√=7 TeV. The results were compared to existing measurements and to perturbative-QCD calculations. The fraction of cdbar D mesons produced in a vector state was also determined.
The first measurement of neutron emission in electromagnetic dissociation of 208Pb nuclei at the LHC is presented. The measurement is performed using the neutron Zero Degree Calorimeters of the ALICE experiment, which detect neutral particles close to beam rapidity. The measured cross sections of single and mutual electromagnetic dissociation of Pb nuclei at sNN−−−√ = 2.76 TeV with neutron emission are σsingle EMD=187.4±0.2 (stat.) +13.2−11.2 (syst.) b and σmutual EMD=5.7±0.1 (stat.) ±0.4 (syst.) b, respectively. The experimental results are compared to the predictions from a relativistic electromagnetic dissociation model.
Systemic lupus erythematosus (SLE) is a severe autoimmune disease of unknown etiology. The major histocompatibility complex (MHC) class I-related chain A (MICA) and B (MICB) are stress-inducible cell surface molecules. MICA and MICB label malfunctioning cells for their recognition by cytotoxic lymphocytes such as natural killer (NK) cells. Alterations in this recognition have been found in SLE. MICA/MICB can be shed from the cell surface, subsequently acting either as a soluble decoy receptor (sMICA/sMICB) or in CD4+ T-cell expansion. Conversely, NK cells are frequently defective in SLE and lower NK cell numbers have been reported in patients with active SLE. However, these cells are also thought to exert regulatory functions and to prevent autoimmunity. We therefore investigated whether, and how, plasma membrane and soluble MICA/B are modulated in SLE and whether they influence NK cell activity, in order to better understand how MICA/B may participate in disease development. We report significantly elevated concentrations of circulating sMICA/B in SLE patients compared with healthy individuals or a control patient group. In SLE patients, sMICA concentrations were significantly higher in patients positive for anti-SSB and anti-RNP autoantibodies. In order to study the mechanism and the potential source of sMICA, we analyzed circulating sMICA concentration in Behcet patients before and after interferon (IFN)-α therapy: no modulation was observed, suggesting that IFN-α is not intrinsically crucial for sMICA release in vivo. We also show that monocytes and neutrophils stimulated in vitro with cytokines or extracellular chromatin up-regulate plasma membrane MICA expression, without releasing sMICA. Importantly, in peripheral blood mononuclear cells from healthy individuals stimulated in vitro by cell-free chromatin, NK cells up-regulate CD69 and CD107 in a monocyte-dependent manner and at least partly via MICA-NKG2D interaction, whereas NK cells were exhausted in SLE patients. In conclusion, sMICA concentrations are elevated in SLE patients, whereas plasma membrane MICA is up-regulated in response to some lupus stimuli and triggers NK cell activation. Those results suggest the requirement for a tight control in vivo and highlight the complex role of the MICA/sMICA system in SLE.
Background: There is absence of specific biomarkers and an incomplete understanding of the pathophysiology of exudative age-related macular degeneration (AMD).
Methods and findings: Eighty-eight vitreous samples (73 from patients with treatment naïve AMD and 15 control samples from patients with idiopathic floaters) were analyzed with capillary electrophoresis coupled to mass spectrometry in this retrospective case series to define potential candidate protein markers of AMD. Nineteen proteins were found to be upregulated in vitreous of AMD patients. Most of the proteins were plasma derived and involved in biological (ion) transport, acute phase inflammatory reaction, and blood coagulation. A number of proteins have not been previously associated to AMD including alpha-1-antitrypsin, fibrinogen alpha chain and prostaglandin H2-D isomerase. Alpha-1-antitrypsin was validated in vitreous of an independent set of AMD patients using Western blot analysis. Further systems biology analysis of the data indicated that the observed proteomic changes may reflect upregulation of immune response and complement activity.
Conclusions: Proteome analysis of vitreous samples from patients with AMD, which underwent an intravitreal combination therapy including a core vitrectomy, steroids and bevacizumab, revealed apparent AMD-specific proteomic changes. The identified AMD-associated proteins provide some insight into the pathophysiological changes associated with AMD.