Controlling the superconducting transition by spin-orbit coupling

Whereas there exists considerable evidence for the conversion of singlet Cooper pairs into triplet Cooper pairs in the presence of inhomogeneous magnetic fields, recent theoretical proposals have suggested an alternative way to exert control over triplet generation: intrinsic spin-orbit coupling in a homogeneous ferromagnet coupled to a superconductor. Here, we proximity-couple Nb to an asymmetric Pt/Co/Pt trilayer, which acts as an effective spin-orbit coupled ferromagnet owing to structural inversion asymmetry. Unconventional modulation of the superconducting critical temperature as a function of in-plane and out-of- plane applied magnetic fields suggests the presence of triplets that can be controlled by the magnetic orientation of a single homogeneous ferromagnet. Our studies demonstrate for the first time an active role of spin-orbit coupling in controlling the triplets -- an important step towards the realization of novel superconducting spintronic devices.Comment: 11 pages + 4 figures + supplemental informatio

A new kind of vortex pinning in superconductor / ferromagnet nanocomposites

This paper reports the observation of hysteresis in the vortex pinning in a superconductor / ferromagnetic epitaxial nanocomposite consisting of fcc Gd particles incorporated in a Nb matrix. We show that this hysteretic pinning is associated with magnetic reversal losses in the Gd particles and is fundamentally different in origin to pinning interactions previously observed for ferromagnetic particles or other microstructural features.Comment: Submitted to PR

Disorder induced collapse of the electron phonon coupling in MgB2_{2} observed by Raman Spectroscopy

The Raman spectrum of the superconductor MgB$_{2}$ has been measured as a function of the Tc of the film. A striking correlation is observed between the $T_{c}$ onset and the frequency of the $E_{2g}$ mode. Analysis of the data with the McMillan formula provides clear experimental evidence for the collapse of the electron phonon coupling at the temperature predicted for the convergence of two superconducting gaps into one observable gap. This gives indirect evidence of the convergence of the two gaps and direct evidence of a transition to an isotropic state at 19 K. The value of the electron phonon coupling constant is found to be 1.22 for films with T$_{c}$ 39K and 0.80 for films with T$_{c}\leq$19K.Comment: 5 pages, 4 figure

Role of Phagocytosis in the Pro-Inflammatory Response in LDL-Induced Foam Cell Formation; a Transcriptome Analysis

Excessive accumulation of lipid inclusions in the arterial wall cells (foam cell formation) caused by modified low-density lipoprotein (LDL) is the earliest and most noticeable manifestation of atherosclerosis. The mechanisms of foam cell formation are not fully understood and can involve altered lipid uptake, impaired lipid metabolism, or both. Recently, we have identified the top 10 master regulators that were involved in the accumulation of cholesterol in cultured macrophages induced by the incubation with modified LDL. It was found that most of the identified master regulators were related to the regulation of the inflammatory immune response, but not to lipid metabolism. A possible explanation for this unexpected result is a stimulation of the phagocytic activity of macrophages by modified LDL particle associates that have a relatively large size. In the current study, we investigated gene regulation in macrophages using transcriptome analysis to test the hypothesis that the primary event occurring upon the interaction of modified LDL and macrophages is the stimulation of phagocytosis, which subsequently triggers the pro-inflammatory immune response. We identified genes that were up- or downregulated following the exposure of cultured cells to modified LDL or latex beads (inert phagocytosis stimulators). Most of the identified master regulators were involved in the innate immune response, and some of them were encoding major pro-inflammatory proteins. The obtained results indicated that pro-inflammatory response to phagocytosis stimulation precedes the accumulation of intracellular lipids and possibly contributes to the formation of foam cells. In this way, the currently recognized hypothesis that the accumulation of lipids triggers the pro-inflammatory response was not confirmed. Comparative analysis of master regulators revealed similarities in the genetic regulation of the interaction of macrophages with naturally occurring LDL and desialylated LDL. Oxidized and desialylated LDL affected a different spectrum of genes than naturally occurring LDL. These observations suggest that desialylation is the most important modification of LDL occurring in vivo. Thus, modified LDL caused the gene regulation characteristic of the stimulation of phagocytosis. Additionally, the knock-down effect of five master regulators, such as IL15, EIF2AK3, F2RL1, TSPYL2, and ANXA1, on intracellular lipid accumulation was tested. We knocked down these genes in primary macrophages derived from human monocytes. The addition of atherogenic naturally occurring LDL caused a significant accumulation of cholesterol in the control cells. The knock-down of the EIF2AK3 and IL15 genes completely prevented cholesterol accumulation in cultured macrophages. The knock-down of the ANXA1 gene caused a further decrease in cholesterol content in cultured macrophages. At the same time, knock-down of F2RL1 and TSPYL2 did not cause an effect. The results obtained allowed us to explain in which way the inflammatory response and the accumulation of cholesterol are related confirming our hypothesis of atherogenesis development based on the following viewpoints: LDL particles undergo atherogenic modifications that, in turn, accompanied by the formation of self-associates; large LDL associates stimulate phagocytosis; as a result of phagocytosis stimulation, pro-inflammatory molecules are secreted; these molecules cause or at least contribute to the accumulation of intracellular cholesterol. Therefore, it became obvious that the primary event in this sequence is not the accumulation of cholesterol but an inflammatory response

The multicenter experience with bendamustine in the treatment of relapsed and refractory multiple myeloma

Relapsed and refractory (R/R) multiple myeloma (MM) constitutes a specific and unmet medical need. Median survival ranges from as little as 6 to 9 months, and responses to treatment are characteristically short. In patients with R/R MM after therapy of bortezomib and/or immunomodulators a bendamustine-based treatment can be used as “salvage”.In this retrospective analysis we have identified 32 patients with R/R MM by means of case research, have been bendamustine-based treated at Hematological Clinics of Russian Federation since 2011. Median age was 67 (43–81) years, the female/male ratio was 2.5:1. After in median 2 (1–7) lines of prior therapy patients received in median 3 (1–9) cycles of bendamustine-based therapy. Bendamustine dosage was 70–120 mg/m2 /day on 2 days of each 28-day cycle until progressive disease or intolerability. Overall rate response was 56.2 %: 21.9 % partial response, stable disease 34.4 %. Median time to progression was 5.3 (0.8–18.0) months and median overall survival was 25.4 (0.8–47.1) months. Hematologic toxicity was in 53.2 % of patients

Lenalidomide for relapsed or refractory multiple myeloma

We report the activity of lenalidomide (revlimide – R), lenalidomide plus dexamethasone (Rd), lenalidomide plus bortezomib plus dexamethasone (RVd) in 34 patients with relapsed and refractory myeloma. For patients who received lenalidomide the overall response rate was 70.5 %. 38 % patients achieved very good partial response (VGPR) + complete response (CR). Median overall survival (OS) was 48 months. Lenalidomide may overcome the poor prognostic impact of various factors, particularly elevated beta (2)-microglobulin. Lenalidomide is highly active in elderly patients (&gt; 65 years). Significantly increased OS with a lenalidomide-based induction and lenalidomide maintenance therapy was revealed. The median duration of the overall response without lenalidomide maintenance therapy was 10 months. The median duration of the overall response with lenalidomide maintenance therapy was 20 months (р &lt; 0,05). Median OS with lenalidomide maintenance therapy was not reached. Median OS without lenalidomide maintenance therapy was 36 months (р &lt; 0.05). Side effects were predictable and manageable. The most common adverse events reported were neutropenia (38.3 %) and thrombocytopenia (23.7 %). Serious adverse events were rare.</p