Oxygen isotopic ratios in first dredge-up red giant stars and nuclear reaction rate uncertainties revisited

We describe a general yet simple method to analyse the propagation of nuclear reaction rate uncertainties in a stellar nucleosynthesis and mixing context. The method combines post-processing nucleosynthesis and mixing calculations with a Monte Carlo scheme. With this approach we reanalyze the dependence of theoretical oxygen isotopic ratio predictions in first dredge-up red giant branch stars in a systematic way. Such predictions are important to the interpretation of pre-solar Al_2 O_3 grains from meteorites. The reaction rates with uncertainties were taken from the NACRE compilation (Angulo etal., 1999). We include seven reaction rates in our systematic analysis of stellar models with initial masses from 1 to 3 M_sun. We find that the uncertainty of reaction rate for reaction O18(p,alpha)N15 typically causes an error in the theoretical O16/O18 ratio of about +20/-5 per cent. The error of the O16/O17 prediction is +-10 to 40 per cent depending on the stellar mass, and is persistently dominated by the comparatively small uncertainty of the O16(p,gamma)F17 reaction. With the new estimates on reaction rate uncertainties by the NACRE compilation, the p-capture reactions O17(p,alpha)N14 and O17(p,gamma)F18 have virtually no impact on theoretical predictions for stellar mass 1.5 M_sun, where core mixing and subsequent envelope mixing interact. In these cases where core mixing complicates post-dredge-up surface abundances, uncertainty in other reactions have a secondary but noticeable effect on surface abundances

The antiinflammatory activity of IgG: the intravenous IgG paradox

How high doses of intravenous IgG (IVIG) suppress autoimmune diseases remains unresolved. We have recently shown that the antiinflammatory activity of IVIG can be attributed to a minor species of IgGs that is modified with terminal sialic acids on their Fc-linked glycans. Here we propose that these Fc-sialylated IgGs engage a unique receptor on macrophages that, in turn, leads to the upregulation of an inhibitory Fcγ receptor (FcγR), thereby protecting against autoantibody-mediated pathology

A Lattice Calculation of the Heavy Quark Universal Form Factor

A computation of the Isgur-Wise universal form factor using a lattice implementation of the heavy quark effective theory is described, and the results of a lattice simulation are presented.Comment: 3 pages in postscrip

Magnetic Switching of Phase-Slip Dissipation in NbSe2 Nanobelts

The stability of the superconducting dissipationless and resistive states in single-crystalline NbSe2 nanobelts is characterized by transport measurements in an external magnetic field (H). Current-driven electrical measurements show voltage steps, indicating the nucleation of phase-slip structures. Well below the critical temperature, the position of the voltage steps exhibits a sharp, periodic dependence as a function of H. This phenomenon is discussed in the context of two possible mechanisms: the interference of the order parameter and the periodic rearrangement of the vortex lattice within the nanobelt.Comment: 4 figure

Renormalization of the Lattice Heavy Quark Classical Velocity

In the lattice formulation of the Heavy Quark Effective Theory (LHQET), the classical velocity is renormalized. The origin of this renormalization is the reduction of Lorentz (or O(4)) invariance to (hyper)cubic invariance. The renormalization is finite and depends on the form of the decretization of the reduced heavy quark Dirac equation. For the Forward Time - Centered Space discretization, the renormalization is computed both perturbatively, to one loop, and non-perturbatively using an ensemble of lattices provided by the Fermilab lattice collaboration. The estimates of the leading (linear) shift agree, and indicate that for small classical velocities, the renormalized velocity is reduced by about 25-30% relative to its bare (input) value.Comment: 4 pages in uuencoded compressed postscript (using uufiles); Talk given at Lattice '95 (Melbourne

Pathology and protection in nephrotoxic nephritis is determined by selective engagement of specific Fc receptors

Introduction of heterologous anti–glomerular basement membrane antiserum (nephrotoxic serum, NTS) into presensitized mice triggers the production of IgG anti-NTS antibodies that are predominantly IgG2b and the glomerular deposition of pathogenic immune complexes, leading to accelerated renal disease. The pathology observed in this model is determined by the effector cell activation threshold that is established by the coexpression on infiltrating macrophages of the IgG2a/2b restricted activation receptor FcγRIV and its inhibitory receptor counterpart, FcγRIIB. Blocking FcγRIV with a specific monoclonal antibody thereby preventing IgG2b engagement or treatment with high dose intravenous γ-globulin (IVIG) to down-regulate FcγRIV while up-regulating FcγRIIB, protects mice from fatal disease. In the absence of FcγRIIB, IVIG is not protective; this indicates that reduced FcγRIV expression alone is insufficient to protect animals from pathogenic IgG2b immune complexes. These results establish the significance of specific IgG subclasses and their cognate FcγRs in renal disease

Master Equation Emulation and Coherence Preservation with Classical Control of a Superconducting Qubit

Open quantum systems are a topic of intense theoretical research. The use of master equations to model a system's evolution subject to an interaction with an external environment is one of the most successful theoretical paradigms. General experimental tools to study different open system realizations have been limited, and so it is highly desirable to develop experimental tools which emulate diverse master equation dynamics and give a way to test open systems theories. In this paper we demonstrate a systematic method for engineering specific system-environment interactions and emulating master equations of a particular form using classical stochastic noise. We also demonstrate that non-Markovian noise can be used as a resource to extend the coherence of a quantum system and counteract the adversarial effects of Markovian environments.Comment: 14 pages, 11 figure

Endoglycosidase treatment abrogates IgG arthritogenicity: Importance of IgG glycosylation in arthritis.

The glycosylation status of IgG has been implicated in the pathology of rheumatoid arthritis. Earlier, we reported the identification of a novel secreted endo-beta-N-acetylglucosaminidase (EndoS), secreted by Streptococcus pyogenes that specifically hydrolyzes the beta-1,4-di-N-acetylchitobiose core of the asparagine-linked glycan of human IgG. Here, we analyzed the arthritogenicity of EndoS-treated collagen type II (CII) -specific mouse mAb in vivo. Endoglycosidase treatment of the antibodies inhibited the induction of arthritis in (BALB/c x B10.Q) F1 mice and induced a milder arthritis in B10.RIII mice as compared with the severe arthritis induced by non-treated antibodies. Furthermore, EndoS treatment did not affect the binding of IgG to CII and their ability to activate complement, but it resulted in reduced IgG binding to Fc gamma R and disturbed the formation of stable immune complexes. Hence, the asparagine-linked glycan on IgG plays a crucial role in the development of arthritis

FcγRIII and FcγRIV are indispensable for acute glomerular inflammation induced by switch variant monoclonal antibodies

The relative ability of IgG subclasses to cause acute inflammation, and the roles of specific effector mechanisms in this process is not clear. We explored this in an in vivo model of glomerular inflammation in the mouse. TNP was planted on the glomerular basement membrane after conjugation to nephrotoxic antibody. The relative nephritogenicity of anti-TNP switch-variant monoclonal antibodies was then explored and shown to be IgG2a>IgG2b, with no disease caused by IgG1. Using knockout mice, we showed that FcγRIII was necessary for both neutrophil influx and glomerular damage induced by IgG2a and IgG2b. Surprisingly IgG1 did not cause disease although it binds to FcγRIII. Using blocking antibodies, we showed that this was explained by an additional requirement for FcγRIV which does not bind to IgG1. IgG2a or IgG2b induced neutrophil influx was not affected by deficiency of either FcγRI or C3. Bone marrow chimeras were constructed to test the effect of combined deficiency of FcγRI and C3, and there was no effect on IgG2a or IgG2b mediated neutrophil influx. However, IgG2b-induced albuminuria and thrombosis was reduced in C3 deficient mice, showing an additional role for complement in IgG2b-mediated glomerular damage. The results show that IgG2a and IgG2b are the pathogenic subclasses in acute neutrophil-mediated glomerular inflammation, with an indispensible role for both FcγRIII and FcγRIV. In addition complement contributes to IgG2b induced glomerular injury