573 research outputs found

    General methods to control right-invariant systems on compact Lie groups and multilevel quantum systems

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    For a right-invariant system on a compact Lie group G, I present two methods to design a control to drive the state from the identity to any element of the group. The first method, under appropriate assumptions, achieves exact control to the target but requires estimation of the `size' of a neighborhood of the identity in G. The second method, does not involve any mathematical difficulty, and obtains control to a desired target with arbitrary accuracy. A third method is then given combining the main ideas of the previous methods. This is also very simple in its formulation and turns out to be generically more efficient as illustrated by one of the examples we consider. The methods described in the paper provide arbitrary constructive control for any right-invariant system on a compact Lie group. I give examples including closed multilevel quantum systems and lossless electrical networks. In particular, the results can be applied to the coherent control of general multilevel quantum systems

    Driving two atoms in an optical cavity into an entangled steady state using engineered decay

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    We propose various schemes for the dissipative preparation of a maximally entangled steady state of two atoms in an optical cavity. Harnessing the natural decay processes of cavity photon loss and spontaneous emission, we use an effective operator formalism to identify and engineer effective decay processes, which reach an entangled steady state of two atoms as the unique fixed point of the dissipative time evolution. We investigate various aspects that are crucial for the experimental implementation of our schemes in present-day and future cavity quantum electrodynamics systems and analytically derive the optimal parameters, the error scaling and the speed of convergence of our protocols. Our study shows promising performance of our schemes for existing cavity experiments and favorable scaling of fidelity and speed with respect to the cavity parameters.Comment: 37 pages, 14 figure

    Information transfer fidelity in spin networks and ring-based quantum routers

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    Spin networks are endowed with an Information Transfer Fidelity (ITF), which defines an absolute upper bound on the probability of transmission of an excitation from one spin to another. The ITF is easily computable but the bound can be reached asymptotically in time only under certain conditions. General conditions for attainability of the bound are established and the process of achieving the maximum transfer probability is given a dynamical model, the translation on the torus. The time to reach the maximum probability is estimated using the simultaneous Diophantine approximation, implemented using a variant of the Lenstra-Lenstra-Lov\'asz (LLL) algorithm. For a ring with uniform couplings, the network can be made a metric space by defining a distance (satisfying the triangle inequality) that quantifies the lack of transmission fidelity between two nodes. It is shown that transfer fidelities and transfer times can be improved significantly by means of simple controls taking the form of non-dynamic, spatially localized bias fields, opening up the possibility for intelligent design of spin networks and dynamic routing of information encoded in them, while being more flexible than engineering fixed couplings to favor some transfers, and less demanding than control schemes requiring fast dynamic controls

    Subcellular Localization of SUN2 Is Regulated by Lamin A and Rab5

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    SUN2 is an inner nuclear membrane protein with a conserved Sad1/UNC-84 homology SUN-domain at the C-terminus. Intriguingly, SUN2 has also been reported to interact with Rab5, which localizes in early endosomes. To clarify the dual subcellular localization of SUN2, we investigated its localization in lamin A/C deficient cells rescued with lamin A or lamin C isoform, and in HeLa cells transfected with Rab5 or its mutants. We found that expression of lamin A but not lamin C partly restored the nuclear envelope localization of SUN2. SUN2 was redistributed to endosomes upon overexpression of Rab5, but remained on the nuclear envelope when the SUN domain was deleted. To explore the physiological function of SUN2 in vesicle trafficking and endocytosis, we demonstrated the colocalization of endogenous SUN2 and Rab5. Moreover, overexpression of SUN2 stimulated the uptake of transferrin while suppression of SUN2 expression attenuated the process. These findings support a role of SUN2 in endocytosis

    Analysis of chemokine and chemokine receptor expression in squamous cell carcinoma of the head and neck (SCCHN) cell lines

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    The purpose of this work was to analyze chemokine and chemokine receptor expression in untreated and in irradiated squamous cell carcinoma of the head and neck (SCCHN) tumor cell lines, aiming at the establishment of assays to test for the relevance of chemokine and chemokine receptor expression in the response of SCCHN to radiotherapy and radiochemotherapy. Five low passage and 10 established SCCHN lines, as well as two normal cell lines, were irradiated at 2 Gy or sham-irradiated, and harvested between 1 and 48 h after treatment. For chemokines with CC and CXC structural motifs and their receptors, transcript levels of target and reference genes were quantified relatively by real-time PCR. In addition, CXCL1 and CXCL12 protein expression was analyzed by ELISA. A substantial variation in chemokine and chemokine receptor expression between SCCHN was detected. Practically, all cell lines expressed CCL5 and CCL20, while CCL2 was expressed in normal cells and in some of the tumor cell lines. CXCL1, CXCL2, CXCL3, CXCL10, and CXCL11 were expressed in the vast majority of the cell lines, while the expression of CXCL9 and CXCL12 was restricted to fibroblasts and few tumor cell lines. None of the analyzed cell lines expressed the chemokines CCL3, CCL4, or CCL19. Of the receptors, transcript expression of CCR1, CCR2, CCR3, CCR5, CCR7, CCXR2, and CCXR3 was not detected, and CCR6, CXCR1, and CXCR4 expression was restricted to few tumor cells. Radiation caused up- and down-regulation with respect to chemokine expressions, while for chemokine receptor expressions down-regulations were prevailing. CXCL1 and CXCL12 protein expression corresponded well with the mRNA expression. We conclude that the substantial variation in chemokine and chemokine receptor expression between SCCHN offer opportunities for the establishment of assays to test for the relevance of chemokine and chemokine receptor expression in the response of SCCHN to radiotherapy and radiochemotherapy

    Clostridial Glucosylating Toxins Enter Cells via Clathrin-Mediated Endocytosis

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    Clostridium difficile toxin A (TcdA) and toxin B (TcdB), C. sordellii lethal toxin (TcsL) and C. novyi α-toxin (TcnA) are important pathogenicity factors, which represent the family of the clostridial glucosylating toxins (CGTs). Toxin A and B are associated with antibiotic-associated diarrhea and pseudomembraneous colitis. Lethal toxin is involved in toxic shock syndrome after abortion and α-toxin in gas gangrene development. CGTs enter cells via receptor-mediated endocytosis and require an acidified endosome for translocation of the catalytic domain into the cytosol. Here we studied the endocytic processes that mediate cell internalization of the CGTs. Intoxication of cells was monitored by analyzing cell morphology, status of Rac glucosylation in cell lysates and transepithelial resistance of cell monolayers. We found that the intoxication of cultured cells by CGTs was strongly delayed when cells were preincubated with dynasore, a cell-permeable inhibitor of dynamin, or chlorpromazine, an inhibitor of the clathrin-dependent endocytic pathway. Additional evidence about the role of clathrin in the uptake of the prototypical CGT family member toxin B was achieved by expression of a dominant-negative inhibitor of the clathrin-mediated endocytosis (Eps15 DN) or by siRNA against the clathrin heavy chain. Accordingly, cells that expressed dominant-negative caveolin-1 were not protected from toxin B-induced cell rounding. In addition, lipid rafts impairment by exogenous depletion of sphingomyelin did not decelerate intoxication of HeLa cells by CGTs. Taken together, our data indicate that the endocytic uptake of the CGTs involves a dynamin-dependent process that is mainly governed by clathrin

    MRI Radiomic Signature of White Matter Hyperintensities Is Associated With Clinical Phenotypes

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    Objective: Neuroimaging measurements of brain structural integrity are thought to be surrogates for brain health, but precise assessments require dedicated advanced image acquisitions. By means of quantitatively describing conventional images, radiomic analyses hold potential for evaluating brain health. We sought to: (1) evaluate radiomics to assess brain structural integrity by predicting white matter hyperintensities burdens (WMH) and (2) uncover associations between predictive radiomic features and clinical phenotypes. Methods: We analyzed a multi-site cohort of 4,163 acute ischemic strokes (AIS) patients with T2-FLAIR MR images with total brain and WMH segmentations. Radiomic features were extracted from normal-appearing brain tissue (brain mask–WMH mask). Radiomics-based prediction of personalized WMH burden was done using ElasticNet linear regression. We built a radiomic signature of WMH with stable selected features predictive of WMH burden and then related this signature to clinical variables using canonical correlation analysis (CCA). Results: Radiomic features were predictive of WMH burden (R2 = 0.855 ± 0.011). Seven pairs of canonical variates (CV) significantly correlated the radiomics signature of WMH and clinical traits with respective canonical correlations of 0.81, 0.65, 0.42, 0.24, 0.20, 0.15, and 0.15 (FDR-corrected p-valuesCV1–6 < 0.001, p-valueCV7 = 0.012). The clinical CV1 was mainly influenced by age, CV2 by sex, CV3 by history of smoking and diabetes, CV4 by hypertension, CV5 by atrial fibrillation (AF) and diabetes, CV6 by coronary artery disease (CAD), and CV7 by CAD and diabetes. Conclusion: Radiomics extracted from T2-FLAIR images of AIS patients capture microstructural damage of the cerebral parenchyma and correlate with clinical phenotypes, suggesting different radiographical textural abnormalities per cardiovascular risk profile. Further research could evaluate radiomics to predict the progression of WMH and for the follow-up of stroke patients’ brain health
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