Stationary states and quantum quench dynamics of Bose-Einstein condensates in a double-well potential

We consider the properties of stationary states and the dynamics of Bose-Einstein condensates (BECs) in a double-well (DW) potential with pair tunneling by using a full quantum-mechanical treatment. Furthermore, we study the quantum quench dynamics of the DW system subjected to a sudden change of the Peierls phase. It is shown that strong pair tunneling evidently influences the energy spectrum structure of the stationary states. For relatively weak repulsive interatomic interactions, the dynamics of the DW system with a maximal initial population difference evolves from Josephson oscillations to quantum self-trapping as one increases the pair tunneling strength, while for large repulsion the strong pair tunneling inhibits the quantum self-trapping. In the case of attractive interatomic interactions, strong pair tunneling tends to destroy the Josephson oscillations and quantum self-trapping, and the system eventually enters a symmetric regime of zero population difference. Finally, the effect of the Peierls phase on the quantum quench dynamics of the system is analyzed and discussed. These new features are remarkably different from the usual dynamical behaviors of a BEC in a DW potential.Comment: 9 pages,7 figures,accepted for publication in Journal of Physics

Alternative splicing in the variable domain of CaMKIIβ affects the level of F-actin association in developing neurons.

The Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) β has an essential function in dendritic spines via binding to and reorganization of the actin cytoskeleton during plasticity events not shared by CaMKIIα isoform. CaMKIIβ and CaMKIIα isoforms have remarkable structural differences within the variable region. Three exons (E1, E3, and E4) are present in CaMKIIβ but not in CaMKIIα gene. Four splice variants of CaMKIIβ isoforms (CaMKIIβ, β\u27, βe and β\u27e) were discovered in embryonic and adult brains. Exons E1 (lacked in βe and β\u27e) and E4 (lacked in β\u27 and β\u27e) are subject to differential alternative splicing. We hypothesized that the sequences encoded by exons E1, E3, and/or E4 are involved in CaMKIIβ-specific bundling to the F-actin cytoskeleton. We tested the colocalization and association of these CaMKIIβ variants within an F-actin-rich structure (microspike) in CaMKIIα free embryonic day 18 (E-18) rat cortical neurons. Our results showed that CaMKIIβ and CaMKIIβ\u27 containing exon E1 displayed an association with F-actin, while CaMKIIβe and CaMKIIβ\u27e lacking E1 did not. Moreover, CaMKIIβ\u27 lacking exon E4 but having E1 showed decreased actin bindingcapacity compared to WT CaMKIIβ. This suggested E1 is required for the association between CaMKIIβ and F-actin, while E4 assists CaMKIIβ to associate with F-actin better. Thus, alternative splicing of CaMKIIβ variants in developing neurons may serve as a developmental switch for actin cytoskeleton-associated isoforms and therefore correlated with dendritic arborization and synapse formation during LTP

VEGF Promotes Proliferation of Human Glioblastoma Multiforme Stem-Like Cells through VEGF Receptor 2

Cancer stem-like cells, which have been described as tumor-initiating cells or tumor-propagating cells, play a crucial role in our fundamental understanding of glioblastoma multiforme (GBM) and its recurrence. GBM is a lethal cancer, characterized by florid vascularization and aberrantly elevated vascular endothelial growth factor (VEGF). VEGF promotes tumorigenesis and angiogenesis of human GBM stem-like cells (GBSCs). However, whether and how VEGF contributes to GBSCs proliferation remain largely uncertain. In this study, human GBSCs were isolated from surgical specimens of glioblastoma and cultured in medium favored for stem cell growth. Neural Colony-Forming Cell Assay and ATP assay were performed to measure GBSC proliferation under normoxia (20% O2) and hypoxia (1% O2). Our observations demonstrate that exogenous VEGF stimulates GBSC proliferation in a dose-dependent manner via VEGF Receptor 2 (VEGFR2); while VEGF Receptor 1 (VEGFR1) has a negative feedback effect on VEGFR2 when cells were exposed to higher concentration of VEGF. These results suggest that suppressing VEGFR2-dependent GBSC proliferation is a potentially therapeutic strategy in GBM

The expression patterns and correlations of claudin-6, methy-CpG binding protein 2, DNA methyltransferase 1, histone deacetylase 1, acetyl-histone H3 and acetyl-histone H4 and their clinicopathological significance in breast invasive ductal carcinomas

<p>Abstract</p> <p>Background</p> <p>Claudin-6 is a candidate tumor suppressor gene in breast cancer, and has been shown to be regulated by DNA methylation and histone modification in breast cancer lines. However, the expression of claudin-6 in breast invasive ductal carcinomas and correlation with clinical behavior or expression of other markers is unclear. We considered that the expression pattern of claudin-6 might be related to the expression of DNA methylation associated proteins (methyl-CpG binding protein 2 (MeCP2) and DNA methyltransferase 1 (DNMT1)) and histone modification associated proteins (histone deacetylase 1 (HDAC1), acetyl-histone H3 (H3Ac) and acetyl- histone H4 (H4Ac)).</p> <p>Methods</p> <p>We have investigated the expression of claudin-6, MeCP2, HDAC1, H3Ac and H4Ac in 100 breast invasive ductal carcinoma tissues and 22 mammary gland fibroadenoma tissues using immunohistochemistry.</p> <p>Results</p> <p>Claudin-6 protein expression was reduced in breast invasive ductal carcinomas (<it>P </it>< 0.001). In contrast, expression of MeCP2 (<it>P </it>< 0.001), DNMT1 (<it>P </it>= 0.001), HDAC1 (<it>P </it>< 0.001) and H3Ac (<it>P </it>= 0.004) expressions was increased. Claudin-6 expression was inversely correlated with lymph node metastasis (<it>P </it>= 0.021). Increased expression of HDAC1 was correlated with histological grade (<it>P </it>< 0.001), age (<it>P </it>= 0.004), clinical stage (<it>P </it>= 0.007) and lymph node metastasis (<it>P </it>= 0.001). H3Ac expression was associated with tumor size (<it>P </it>= 0.044) and clinical stage of cancers (<it>P </it>= 0.034). MeCP2, DNMT1 and H4Ac expression levels did not correlate with any of the tested clinicopathological parameters (<it>P </it>> 0.05). We identified a positive correlation between MeCP2 protein expression and H3Ac and H4Ac protein expression.</p> <p>Conclusions</p> <p>Our results show that claudin-6 protein is significantly down-regulated in breast invasive ductal carcinomas and is an important correlate with lymphatic metastasis, but claudin-6 down-regulation was not correlated with upregulation of the methylation associated proteins (MeCP2, DNMT1) or histone modification associated proteins (HDAC1, H3Ac, H4Ac). Interestingly, the expression of MeCP2 was positively correlated with the expression of H3Ac and H3Ac protein expression was positively correlated with the expression of H4Ac in breast invasive ductal carcinoma</p> <p>Virtual slides</p> <p>The virtual slide(s) for this article can be found here: <url>http://www.diagnosticpathology.diagnomx.eu/vs/4549669866581452</url></p

\u3ci\u3eArabidopsis\u3c/i\u3e Lipins, PDAT1 Acyltransferase, and SDP1 Triacylglycerol Lipase Synergistically Direct Fatty Acids toward β-Oxidation, Thereby Maintaining Membrane Lipid Homeostasis

Triacylglycerol (TAG) metabolism is a key aspect of intracellular lipid homeostasis in yeast and mammals, but its role in vegetative tissues of plants remains poorly defined. We previously reported that PHOSPHOLIPID:DIACYLGLYCEROL ACYLTRANSFERASE1 (PDAT1) is crucial for diverting fatty acids (FAs) from membrane lipid synthesis to TAG and thereby protecting against FA-induced cell death in leaves. Here, we show that overexpression of PDAT1 enhances the turnover of FAs in leaf lipids. Using the trigalactosyldiacylglycerol1-1 (tgd1-1) mutant, which displays substantially enhanced PDAT1- mediated TAG synthesis, we demonstrate that disruption of SUGAR-DEPENDENT1 (SDP1) TAG lipase or PEROXISOMAL TRANSPORTER1 (PXA1) severely decreases FA turnover, leading to increases in leaf TAG accumulation, to 9% of dry weight, and in total leaf lipid, by 3-fold. The membrane lipid composition of tgd1-1 sdp1-4 and tgd1-1 pxa1-2 double mutants is altered, and their growth and development are compromised. We also show that two Arabidopsis thaliana lipin homologs provide most of the diacylglycerol for TAG synthesis and that loss of their functions markedly reduces TAG content, but with only minor impact on eukaryotic galactolipid synthesis. Collectively, these results show that Arabidopsis lipins, along with PDAT1 and SDP1, function synergistically in directing FAs toward peroxisomal b-oxidation via TAG intermediates, thereby maintaining membrane lipid homeostasis in leaves

Evaluation of deep marginal feedback cancellation for hearing aids using speech and music.

Peer reviewed: TrueSpeech and music both play fundamental roles in daily life. Speech is important for communication while music is important for relaxation and social interaction. Both speech and music have a large dynamic range. This does not pose problems for listeners with normal hearing. However, for hearing-impaired listeners, elevated hearing thresholds may result in low-level portions of sound being inaudible. Hearing aids with frequency-dependent amplification and amplitude compression can partly compensate for this problem. However, the gain required for low-level portions of sound to compensate for the hearing loss can be larger than the maximum stable gain of a hearing aid, leading to acoustic feedback. Feedback control is used to avoid such instability, but this can lead to artifacts, especially when the gain is only just below the maximum stable gain. We previously proposed a deep-learning method called DeepMFC for controlling feedback and reducing artifacts and showed that when the sound source was speech DeepMFC performed much better than traditional approaches. However, its performance using music as the sound source was not assessed and the way in which it led to improved performance for speech was not determined. The present paper reveals how DeepMFC addresses feedback problems and evaluates DeepMFC using speech and music as sound sources with both objective and subjective measures. DeepMFC achieved good performance for both speech and music when it was trained with matched training materials. When combined with an adaptive feedback canceller it provided over 13 dB of additional stable gain for hearing-impaired listeners