Enhancement of the Binding Energy of Charged Excitons in Disordered Quantum Wires

Negatively and positively charged excitons are identified in the spatially-resolved photoluminescence spectra of quantum wires. We demonstrate that charged excitons are weakly localized in disordered quantum wires. As a consequence, the enhancement of the "binding energy" of a charged exciton is caused, for a significant part, by the recoil energy transferred to the remaining charged carrier during its radiative recombination. We discover that the Coulomb correlation energy is not the sole origin of the "binding energy", in contrast to charged excitons confined in quantum dots.Comment: 4 Fig

Stability of adhesion clusters under constant force

We solve the stochastic equations for a cluster of parallel bonds with shared constant loading, rebinding and the completely dissociated state as an absorbing boundary. In the small force regime, cluster lifetime grows only logarithmically with bond number for weak rebinding, but exponentially for strong rebinding. Therefore rebinding is essential to ensure physiological lifetimes. The number of bonds decays exponentially with time for most cases, but in the intermediate force regime, a small increase in loading can lead to much faster decay. This effect might be used by cell-matrix adhesions to induce signaling events through cytoskeletal loading.Comment: Revtex, 4 pages, 4 Postscript files include

Visualization of Allostery in P-Selectin Lectin Domain Using MD Simulations

Allostery of P-selectin lectin (Lec) domain followed by an epithelial growth factor (EGF)-like domain is essential for its biological functionality, but the underlying pathways have not been well understood. Here the molecular dynamics simulations were performed on the crystallized structures to visualize the dynamic conformational change for state 1 (S1) or state 2 (S2) Lec domain with respective bent (B) or extended (E) EGF orientation. Simulations illustrated that both S1 and S2 conformations were unable to switch from one to another directly. Instead, a novel S1' conformation was observed from S1 when crystallized B-S1 or reconstructed “E-S1” structure was employed, which was superposed well with that of equilibrated S1 Lec domain alone. It was also indicated that the corresponding allosteric pathway from S1 to S1' conformation started with the separation between residues Q30 and K67 and terminated with the release of residue N87 from residue C109. These results provided an insight into understanding the structural transition and the structure-function relationship of P-selectin allostery

The Shedding of CD62L (L-Selectin) Regulates the Acquisition of Lytic Activity in Human Tumor Reactive T Lymphocytes

CD62L/L-selectin is a marker found on naïve T cells and further distinguishes central memory (Tcm, CD62L+) from effector memory (Tem, CD62L−) T cells. The regulation of CD62L plays a pivotal role in controlling the traffic of T lymphocytes to and from peripheral lymph nodes. CD62L is shed from the cell membrane following T cell activation, however, the physiological significance of this event remains to be elucidated. In this study, we utilized in vitro generated anti-tumor antigen T cells and melanoma lines as a model to evaluate the dynamics of CD62L shedding and expression of CD107a as a marker of lytic activity. Upon encounter, with matched tumor lines, antigen reactive T cells rapidly lose CD62L expression and this was associated with the acquisition of CD107a. By CD62L ELISA, we confirmed that this transition was mediated by the shedding of CD62L when T cells encountered specific tumor antigen. The introduction of a shedding resistant mutant of CD62L into the tumor antigen-reactive T cell line JKF6 impaired CD107a acquisition following antigen recognition and this was correlated with decreased lytic activity as measured by 51Cr release assays. The linkage of the shedding of CD62L from the surface of anti-tumor T cells and acquisition of lytic activity, suggests a new function for CD62L in T cell effector functions and anti-tumor activity

Hippocampal circuit dysfunction in psychosis.

Despite strong evidence of the neurodevelopmental origins of psychosis, current pharmacological treatment is not usually initiated until after a clinical diagnosis is made, and is focussed on antagonising striatal dopamine receptors. These drugs are only partially effective, have serious side effects, fail to alleviate the negative and cognitive symptoms of the disorder, and are not useful as a preventive treatment. In recent years, attention has turned to upstream brain regions that regulate striatal dopamine function, such as the hippocampus. This review draws together these recent data to discuss why the hippocampus may be especially vulnerable in the pathophysiology of psychosis. First, we describe the neurodevelopmental trajectory of the hippocampus and its susceptibility to dysfunction, exploring this region's proneness to structural and functional imbalances, metabolic pressures, and oxidative stress. We then examine mechanisms of hippocampal dysfunction in psychosis and in individuals at high-risk for psychosis and discuss how and when hippocampal abnormalities may be targeted in these groups. We conclude with future directions for prospective studies to unlock the discovery of novel therapeutic strategies targeting hippocampal circuit imbalances to prevent or delay the onset of psychosis

Gènes persistants dans les génomes bactériens

Les gènes persistants sont présentés dans presque tous les génomes à l'intérieur d'un clade. Ils sont donc des gènes très représentés et sous sélection très forte. Les gènes persistants incluent la majorité des gènes essentiels. Ils aussi incluent des gènes dont l'inactivation n'est pas automatiquement létale mais qui permettent de répondre à une grande variété de situations défavorables. Les gènes persistants évoluent lentement et typiquement en parallèle avec la sous-unité 16S de l'ARNr. Ils sont très sensibles à des collisions frontales entre le polymérase de l ARN et le polymérase de l'ADN, et ont par conséquence une préférence forte pour le brin précoce. Ils tendent à utiliser des codons optimaux pour assurer une expression efficace. Pour minimiser leur perte fréquente, les gènes persistants sont groupés dans le chromosome. Ces groupes de gènes ont souvent des fonctions voisines. Nous avons construit un réseau représentant les groupes de gènes essentiels duquel résulte le coeur du protéome bactérien. Ce réseau souligne les influences de l'environnement dans le façonnement de la composition du protéome bactérien. On développe aussi deux exemples à partir de la comparaison de profils évolutifs ainsi qu'une plate-forme informatique pour la génomique comparative.Persistent genes are genes present in almost every organism within a group. They are the genes endeavoured through natural selections and widely spread. Persistent genes include most of experimentally essential genes. Furthermore, it also includes genes without immediate lethal effects but allowing to respond to a variety of unfavourable situations. Persistent genes evolve slowly and usually in parallel with the 16S rDNA. They are very sensitive to the head-on collisions between RNA polymerase and DNA polymerase, and consequently have a strong preference for the leading strand. They tend to use optimal codons to ensure efficient expression. To avoid the frequent gene loss, persistent genes are clustered, and such local clusters are usually groups of genes executing coupled functions. By assembling the persistent genes clusters together, a network representing the core bacterial proteome is built up. This network highlights the influences from environment in shaping bacterial proteome composition. Two examples applying evolutionary profiles comparison in genome annotation are presented, as well as a platform to carry out comparative genomics.EVRY-BU (912282101) / SudocSudocFranceF

The LFA-1 integrin supports rolling adhesions on ICAM-1 under physiological sheer flow in a permissive cellular environment

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The LFA-1 integrin supports rolling adhesions on ICAM-1 under physiological shear flow in a permissive cellular environment

The LFA-1 integrin is crucial for the firm adhesion of circulating leukocytes to ICAM-1-expressing endothelial cells. In the present study, we demonstrate that LFA-1 can arrest unstimulated PBL subsets and lymphoblastoid Jurkat cells on immobilized ICAM-1 under subphysiological shear flow and mediate firm adhesion to ICAM-1 after short static contact. However, LFA-1 expressed in K562 cells failed to support firm adhesion to ICAM-1 but instead mediated K562 cell rolling on the endothelial ligand under physiological shear stress. LFA-1-mediated rolling required an intact LFA-1 I-domain, was enhanced by Mg2+, and was sharply dependent on ICAM-1 density. This is the first indication that LFA-1 can engage in rolling adhesions with ICAM-1 under physiological shear flow. The ability of LFA-1 to support rolling correlates with decreased avidity and impaired time-dependent adhesion strengthening. A beta2 cytoplasmic domain-deletion mutant of LFA-1, with high avidity to immobilized ICAM-1, mediated firm arrests of K562 cells interacting with ICAM-1 under shear flow. Our results suggest that restrictions in LFA-1 clustering mediated by cytoskeletal attachments may lock the integrin into low-avidity states in particular cellular environments. Although low-avidity LFA-1 states fail to undergo adhesion strengthening upon contact with ICAM-1 at stasis, these states are permissive for leukocyte rolling on ICAM-1 under physiological shear flow. Rolling mediated by low-avidity LFA-1 interactions with ICAM-1 may stabilize rolling initiated by specialized vascular rolling receptors and allow the leukocyte to arrest on vascular endothelium upon exposure to stimulatory endothelial signals

Magnetic and transport properties of superconducting (YBa2Cu3O7-δ)1-xAgx ceramics

The introduction of silver in the intergranular space of YBa2Cu3O7 ceramics improves their normal state electrical and mechanical properties. The authors report a study of such composites of which the grain size was found to increase with the annealing temperature, and goes through a maximum around 20% wt. silver for a constant annealing temperature (1000°C). Moreover, a maximum in the filling factor of YBa2Cu3O7 is found from AC susceptibility measurements for X≃15% wt. of silver, which also corresponds to the maximum of the current density. The intergranular silver is found to improve the diamagnetic shielding in very low field. The irreversible fields, Hcs, as determined by magnetoresistance are only decreased by ~10% for a composite containing ~15% weight of silve