Topology of Quantum Grey Soliton in Multi-Component Inhomogeneous Bose-Einstein Condensates

We study the dispersion mechanism of Lieb mode excitations of both single and multi component ultra-cold atomic Bose gas, subject to a harmonic confinement through chirp management. It is shown that in some parameter domain, the hole-like excitations lead to the soliton's negative mass regime, arising due to the coupling between chirp momentum and Kohn mode. In low momenta region the trap considerably affects the dispersion of the grey soliton, which opens a new window to observe Lieb-mode excitations. Further, we extend our analysis to binary condensate, which yields usual shape compatible grey-bright soliton pairs. The inter-species interaction induces a shift in the Lieb-mode excitations, where the pair can form a bound state. We emphasize that the present model provides an opportunity to study such excitations in the low momenta regime, as well as the formation of bound state in binary condensate.Comment: 9 pages, 7 figure

Lower order and higher order entanglement in 87Rb87Rb 5S−5P−5D5S-5P-5D hyperfine manifold modeled as a four-wave mixing process

Possibilities of generation of lower order and higher order intermodal entanglement in 87Rb 5S-5P-5D hyperfine manifold are rigorously investigated using Sen-Mandal perturbative technique by showing the equivalence of the system with the four-wave mixing (FWM) process. The investigation has revealed that for a set of experimentally realizable/relevant parameters we can observe lower order and higher order intermodal entanglement between pump and signal modes, signal and idler modes, and idler and pump modes in a FWM process associated with the 87Rb 5S-5P-5D hyperfine manifold. In addition, trimodal entanglement involving pump, signal and idler modes is also reported.Comment: 12 pages, 5 figure

Investigating The Role Of Platelet Proteins In The Regulation Of Atherosclerosis In Coronary Artery Disease

The role of inflammation in all stages of atherosclerotic process is well-known and soluble TREM like transcript 1 (sTLT1), a platelet protein, is reported to be linked to chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Initially, our results indicated plasma level of sTLT1 was significantly (p<0.05) elevated in clinical (2342±184pg/ml) and subclinical cases (1773±118pg/ml) than healthy controls (461±57pg/ml). Additionally, statistical analyses indicated that sTLT1 was associated with Coronary Artery Disease (CAD). Ex vivo studies on macrophages indicated that sTLT1 binds to Fcɣ RI to activate MAP kinase signalling cascade to activate NF-kB which promotes secretion of pro-inflammatory cytokine TNF-α from macrophage cells. Atherosclerotic apoE-/- mice also showed high levels of sTLT1 and TNF-α in virtually occluded aortic stage indicating the contribution of sTLT1 in inflammation. As, sTLT1 is a platelet secreted protein with a significant role in CAD, we explored the plasma secretome of Coronary Artery Disease subgroups (STEMI, NSTEMI, UA) which may identify new candidate proteins responsible for the development of CAD. It resulted into the identification of several unique proteins in each subgroup. Employing a case-control design, more than 2500 annotated proteins were identified using Orbitrap mass spectrometer in both STEMI and healthy control subjects; whereas in NSTEMI and UA the numbers were a little less (>800). Quantitative proteomics study on STEMI patients revealed that 26 proteins were decreased and 38 proteins were increased significantly in STEMI compared to healthy control. AZGP1, ABCA5, Calicin, PGLYRP2, HAVCR2, C17ORF57 appeared to be relevant to STEMI whereas soluble Galectin-3 seemed relevant to NSTEMI after cross-validation in human samples. Mechanistic significance in foam cells indicated the imbalance of RCT through the interaction of AZGP1 with CD36. Additionally, in silico studies of soluble Galectin-3 with Dectin-1 showed the activation of Dectin-1 mediated signalling which led to the secretion of pro-inflammatory cytokines. In summary, this study revealed a unique relationship of some novel proteins apparently responsible for impaired RCT and chronic inflammation leading to atherothrombosis and myocardial infarction in CAD