University of New Mexico

About: University of New Mexico is a education organization based out in Albuquerque, New Mexico, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 28870 authors who have published 64767 publications receiving 2578371 citations. The organization is also known as: UNM & Universitatis Novus Mexico.

Measurement of the J/ψ meson and b-hadron production cross sections in pp̄ collisions at √s = 1960 GeV

Abstract: The authors present a new measurement of the inclusive and differential production cross sections of J/{psi} mesons and b-hadrons in proton-antiproton collisions at {radical}s = 1960 GeV The data correspond to an integrated luminosity of 397 pb{sup -1} collected by the CDF Run II detector They find the integrated cross section for inclusive J/{psi} production for all transverse momenta from 0 to 20 GeV/c in the rapidity range |y| 125 GeV/c They find the total cross section for b-hadrons, including both hadrons and anti-hadrons, decaying to J/{psi} with transverse momenta greater than 125 GeV/c in the rapidity range |y(J/{psi})| < 06, is 0330 {+-} 0005(stat){sub -0033}{sup +0036}(syst) {mu}b Using a Monte Carlo simulation of the decay kinematics of b-hadrons to all final states containing a J/{psi}, they extract the first measurement of the total single b-hadron cross section down to zero transverse momentum at {radical}s = 1960 GeV They find the total single b-hadron cross section integrated over all transverse momenta for b-hadrons in themore » rapidity range |y| < 06 to be 176 {+-} 04(stat){sub -23}{sup +25}(syst) {mu}b« less

Cd47-Signal Regulatory Protein α (Sirpα) Regulates Fcγ and Complement Receptor–Mediated Phagocytosis

Abstract: In autoimmune hemolytic anemia (AIHA), circulating red blood cells (RBCs) opsonized with autoantibody are recognized by macrophage Fcγ and complement receptors. This triggers phagocytosis and elimination of RBCs from the circulation by splenic macrophages. We recently found that CD47 on unopsonized RBCs binds macrophage signal regulatory protein α (SIRPα), generating a negative signal that prevents phagocytosis of the unopsonized RBCs. We show here that clearance and phagocytosis of opsonized RBCs is also regulated by CD47-SIRPα. The inhibition generated by CD47-SIRPα interaction is strongly attenuated but not absent in mice with only residual activity of the phosphatase Src homology 2 domain–containing protein tyrosine phosphatase (SHP)-1, suggesting that most SIRPα signaling in this system is mediated by SHP-1 phosphatase activity. The macrophage phagocytic response is controlled by an integration of the inhibitory SIRPα signal with prophagocytic signals such as from Fcγ and complement receptor activation. Thus, augmentation of inhibitory CD47-SIRPα signaling may prevent or attenuate RBC clearance in AIHA.