Effect of the W-term for a t-U-W Hubbard ladder

Antiferromagnetic and d_{x2-y2}-pairing correlations appear delicately balanced in the 2D Hubbard model. Whether doping can tip the balance to pairing is unclear and models with additional interaction terms have been studied. In one of these, the square of a local hopping kinetic energy H_W was found to favor pairing. However, such a term can be separated into a number of simpler processes and one would like to know which of these terms are responsible for enhancing the pairing. Here we analyze these processes for a 2-leg Hubbard ladder

Posttranslational forms of beta 2-glycoprotein I in the pathogenesis of the antiphospholipid syndrome

The antiphospholipid syndrome (APS) is an autoimmune disease characterised by a procoagulant state that predisposes to recurrent thrombosis and miscarriages. Two major discoveries have advanced our understanding of the underlying complex pathogenesis of the APS. The first was the discovery that beta-2 glycoprotein-1 (β2GPI) is the major auto antigen in APS. The second was the discovery in more recent years that β2GPI contains allosteric disulphide bonds susceptible to posttranslational modification that may be involved in the development of autoantibodies in APS. The main allosteric disulphide bond in the fifth domain of β2GPI can exist in two redox states: free thiol or oxidised. It is the conformational transformation of β2GPI from its free thiol form to its more immunogenic oxidised form that exposes neo-epitopes on the first and fifth domains. The purpose of this review is to highlight the recent findings on the posttranslational forms of β2GPI in the pathogenesis of APS. We suggest that novel assays quantitating the different redox forms of β2GPI in plasma or serum may be used to supplement existing clinical and laboratory assays to more accurately stratify risk of thrombosis or miscarriage in APS patients

The ability of DC-rich CD117⁺ splenocytes to induce NK cells to increase their expression of IFN-γ in the presence of LPS is dependent on RasGRP4.

<p>(A-E) NK cells from WT mice were incubated with DC-rich CD117⁺ splenocytes from WT (□) or RasGRP4- null mice (■) in ratios of 1:1 and 1:2 for 24 and 48 h, respectively, in the presence of 1 μg/mL LPS. For controls, NK cells alone and CD117⁺ cells alone were exposed to LPS. The levels of IFN-γ (A), IL-6 (B), IL-10 (C), TNF/ TNFSF4 (D), and CCL2 (E) in the resulting supernatants were measured. The depicted data are the mean ± SD, and the results are shown from 3 experiments using different batches of NK cells and CD117⁺ splenocytes. * = p < 0.05, ** = p<0.005.</p

The CD117⁺/CD45R⁺/CD11c⁺ DCs in the spleens of naïve WT B6 mice express RasGRP4.

<p>DCs from the spleens of WT B6 and RasGRP4-null mice were stained for their surface expression of numerous proteins, including CD117, CD45R, and CD11c (A), and for their intracellular expression of RasGRP4 (B). An irrelevant immunoglobulin (Isotype IgG) was used as a negative control. Similar data was obtained in a second experiment.</p