52 research outputs found

    Idiopathic multicentric Castleman disease with positive antiphospholipid antibody: atypical and undiagnosed autoimmune disease?

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    Idiopathic multicentric Castleman disease (iMCD) is a systemic disorder characterized by systemic inflammation and organ dysfunction associated with an increase in pro-inflammatory cytokines. Some patients with iMCD are positive for autoantibodies, although their significance and relationship with specific associated autoimmune diseases are unclear. This study retrospectively analyzed the clinicopathological features of iMCD patients focusing on autoantibodies. Among 63 iMCD patients in our database, 19 were positive for at least one autoantibody. Among the 19, we identified five with plasma cell type (PC)-iMCD lymph node histopathology and positive anti-phospholipid antibodies. These patients were likely to have thrombocytopenia, anasarca, fever, reticulin fibrosis or renal insufficiency, organomegaly (TAFRO) symptoms, and thrombotic events. The present study suggests that patients with undiagnosed or atypical autoimmune diseases, including anti-phospholipid syndrome (APS), were treated for iMCD. APS may present with thrombocytopenia or even multi-organ failure, which overlap with clinical presentations of iMCD. Due to differences in the treatment regimen and follow-up, recognition of the undiagnosed autoimmune disease process in those suspected of iMCD is essential. Our study highlights the importance of complete exclusion of differential diagnoses in patients with iMCD in their diagnostic workup

    Single electron yields from semileptonic charm and bottom hadron decays in Au++Au collisions at sNN=200\sqrt{s_{NN}}=200 GeV

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    The PHENIX Collaboration at the Relativistic Heavy Ion Collider has measured open heavy-flavor production in minimum bias Au++Au collisions at sNN=200\sqrt{s_{_{NN}}}=200 GeV via the yields of electrons from semileptonic decays of charm and bottom hadrons. Previous heavy-flavor electron measurements indicated substantial modification in the momentum distribution of the parent heavy quarks due to the quark-gluon plasma created in these collisions. For the first time, using the PHENIX silicon vertex detector to measure precision displaced tracking, the relative contributions from charm and bottom hadrons to these electrons as a function of transverse momentum are measured in Au++Au collisions. We compare the fraction of electrons from bottom hadrons to previously published results extracted from electron-hadron correlations in pp++pp collisions at sNN=200\sqrt{s_{_{NN}}}=200 GeV and find the fractions to be similar within the large uncertainties on both measurements for pT>4p_T>4 GeV/cc. We use the bottom electron fractions in Au++Au and pp++pp along with the previously measured heavy flavor electron RAAR_{AA} to calculate the RAAR_{AA} for electrons from charm and bottom hadron decays separately. We find that electrons from bottom hadron decays are less suppressed than those from charm for the region 3<pT<43<p_T<4 GeV/cc.Comment: 432 authors, 33 pages, 23 figures, 2 tables, 2011 data. v2 is version accepted for publication by Phys. Rev. C. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm

    Transverse energy production and charged-particle multiplicity at midrapidity in various systems from sNN=7.7\sqrt{s_{NN}}=7.7 to 200 GeV

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    Measurements of midrapidity charged particle multiplicity distributions, dNch/dηdN_{\rm ch}/d\eta, and midrapidity transverse-energy distributions, dET/dηdE_T/d\eta, are presented for a variety of collision systems and energies. Included are distributions for Au++Au collisions at sNN=200\sqrt{s_{_{NN}}}=200, 130, 62.4, 39, 27, 19.6, 14.5, and 7.7 GeV, Cu++Cu collisions at sNN=200\sqrt{s_{_{NN}}}=200 and 62.4 GeV, Cu++Au collisions at sNN=200\sqrt{s_{_{NN}}}=200 GeV, U++U collisions at sNN=193\sqrt{s_{_{NN}}}=193 GeV, dd++Au collisions at sNN=200\sqrt{s_{_{NN}}}=200 GeV, 3^{3}He++Au collisions at sNN=200\sqrt{s_{_{NN}}}=200 GeV, and pp++pp collisions at sNN=200\sqrt{s_{_{NN}}}=200 GeV. Centrality-dependent distributions at midrapidity are presented in terms of the number of nucleon participants, NpartN_{\rm part}, and the number of constituent quark participants, NqpN_{q{\rm p}}. For all AA++AA collisions down to sNN=7.7\sqrt{s_{_{NN}}}=7.7 GeV, it is observed that the midrapidity data are better described by scaling with NqpN_{q{\rm p}} than scaling with NpartN_{\rm part}. Also presented are estimates of the Bjorken energy density, εBJ\varepsilon_{\rm BJ}, and the ratio of dET/dηdE_T/d\eta to dNch/dηdN_{\rm ch}/d\eta, the latter of which is seen to be constant as a function of centrality for all systems.Comment: 706 authors, 32 pages, 20 figures, 34 tables, 2004, 2005, 2008, 2010, 2011, and 2012 data. v2 is version accepted for publication in Phys. Rev.

    Identification of cell cycle–arrested quiescent osteoclast precursors in vivo

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    Osteoclasts are multinucleated cells that resorb bone. Although osteoclasts originate from the monocyte/macrophage lineage, osteoclast precursors are not well characterized in vivo. The relationship between proliferation and differentiation of osteoclast precursors is examined in this study using murine macrophage cultures treated with macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB (RANK) ligand (RANKL). Cell cycle–arrested quiescent osteoclast precursors (QuOPs) were identified as the committed osteoclast precursors in vitro. In vivo experiments show that QuOPs survive for several weeks and differentiate into osteoclasts in response to M-CSF and RANKL. Administration of 5-fluorouracil to mice induces myelosuppression, but QuOPs survive and differentiate into osteoclasts in response to an active vitamin D3 analogue given to those mice. Mononuclear cells expressing c-Fms and RANK but not Ki67 are detected along bone surfaces in the vicinity of osteoblasts in RANKL-deficient mice. These results suggest that QuOPs preexist at the site of osteoclastogenesis and that osteoblasts are important for maintenance of QuOPs
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