J=0 T=1 Pairing Interaction Selection Rules

Wave functions arising form a pairing Hamiltonian E(0) i,e, one in which the interaction is only between J=0^{+}T=1 pairs, lead to magnetic dipole and Gamow-Teller transition rates that are much larger than those from an interaction E(J_{max}) in which a proton and a neutron couple to J=2j. With realistic interactions the results are in between the 2 extremes. In the course of this study we found that certain M1 and GT matrix elements vanish with E(0) . These are connected to seniority and reduced isospin isospin selection rules. We find the surprising result that The M1 strength to the single j scissors is larger for a J=0 T=1 pairing interaction than it is for Q.Q

Seifert-Torres Type Formulas for the Alexander Polynomial from Quantum sl2\mathfrak{sl}_2

We develop a diagrammatic calculus for representations of unrolled quantum $\mathfrak{sl}_2$ at a fourth root of unity. We use this calculus to prove Seifert-Torres type formulas for closed string links in framed links using quantum methods. Other applications of this diagrammatic calculus given here are a skein relation for $n$-cabled double crossings and a simple proof that the quantum invariant associated with these representations determines the multivariable Alexander polynomial.Comment: 19 pages, 20 figure

Auranofin, a thioredoxin reductase inhibitor, causes platelet death through calcium overload.

Platelets are central to normal hemostasis and must be tightly controlled to prevent thrombosis. However, drug treatments that also affect platelets could lead to unwanted side effects on hemostasis or thrombosis. In this study, the effect of auranofin on platelets was tested. Auranofin, a gold-based thioredoxin reductase (TRXR) inhibitor, has been previously used in arthritis. Recently, auranofin and other inhibitors of the thioredoxin system have been proposed as novel anti-cancer therapies. TRXR is an important part of the antioxidant defenses in many cells that maintain intracellular proteins in their reduced state. TRXR activity in platelets could be completely inhibited by auranofin. Auranofin-treated platelets showed several features of cell death, including the inability to aggregate in response to thrombin, leakage of cytosolic lactate dehydrogenase, and surface exposure of procoagulant phosphatidylserine. Auranofin increased platelet reactive oxygen species production and intracellular calcium concentration. DTT, a sulfydyl reducing agent, and BAPTA-AM, which chelates intracellular calcium, prevented auranofin-induced phosphatidylserine exposure. These data suggest that TRXR is an important part of the platelet antioxidant defense. TRXR inhibition by auranofin triggers oxidative stress and disrupts intracellular calcium homeostasis, leading to platelet necrosis. The use of auranofin or other TRXR inhibitors could therefore lead to unwanted side effects.Isaac Newton Trust/ Wellcome Trust ISSF/University of Cambridge Joint Research Grant