393 research outputs found
Superconductivity in the Hubbard model with correlated hopping: Slave-boson study
The slave boson mean-field studies of the ground state of the Hubbard model
with correlated hopping were performed. The approach qualitatively recovers the
exact results for the case of the hopping integral t equal to the correlated
hopping integral X. The phase diagram for the strongly correlated state with
only singly occupied sites, the weakly correlated state, where single and
double occupation is allowed, and for the superconducting state, was determined
for any values of X and any electron concentration n. At the half-filled band
(n=1) a direct transition from the superconductor to the Mott insulator was
found. In the region of strong correlations the superconducting solution is
stable for n close to 1, in contrast to the case of weak correlations, in which
superconductivity occurs at n close to 0 and n close to 2. We found also that
strong correlations change characteristics of the superconducting phase, e.g.
the gap in the excitation spectrum has a nonexponential dependence close to the
point of the phase transition.Comment: 13 pages, 24 Postscript figures (in 12 files
Phase Diagram of the Extended Hubbard Model with Correlated Hopping Interaction
A one-dimensional model of interacting electrons with on-site ,
nearest-neighbor , and correlated-hopping interaction is studied
at half-filling using the continuum-limit field theory approach. The ground
state phase diagram is obtained for a wide range of coupling constants. In
addition to the insulating spin- and charge-density wave phases for large
and , respectively, we identify bond-located ordered phases corresponding to
an enhanced Peierls instability in the system for ,
and to a staggered magnetization located on bonds between
sites for , . The general ground state phase
diagram including insulating, metallic, and superconducting phases is
discussed.Comment: 8 pages, 4 eps-figure
Dissociable effects of 5-HT2C receptor antagonism and genetic inactivation on perseverance and learned non-reward in an egocentric spatial reversal task
Cognitive flexibility can be assessed in reversal learning tests, which are sensitive to modulation of 5-HT2C receptor (5-HT2CR) function. Successful performance in these tests depends on at least two dissociable cognitive mechanisms which may separately dissipate associations of previous positive and negative valence. The first is opposed by perseverance and the second by learned non-reward. The current experiments explored the effect of reducing function of the 5-HT2CR on the cognitive mechanisms underlying egocentric reversal learning in the mouse. Experiment 1 used the 5-HT2CR antagonist SB242084 (0.5 mg/kg) in a between-groups serial design and Experiment 2 used 5-HT2CR KO mice in a repeated measures design. Animals initially learned to discriminate between two egocentric turning directions, only one of which was food rewarded (denoted CS+, CS−), in a T- or Y-maze configuration. This was followed by three conditions; (1) Full reversal, where contingencies reversed; (2) Perseverance, where the previous CS+ became CS− and the previous CS− was replaced by a novel CS+; (3) Learned non-reward, where the previous CS− became CS+ and the previous CS+ was replaced by a novel CS-. SB242084 reduced perseverance, observed as a decrease in trials and incorrect responses to criterion, but increased learned non-reward, observed as an increase in trials to criterion. In contrast, 5-HT2CR KO mice showed increased perseverance. 5-HT2CR KO mice also showed retarded egocentric discrimination learning. Neither manipulation of 5-HT2CR function affected performance in the full reversal test. These results are unlikely to be accounted for by increased novelty attraction, as SB242084 failed to affect performance in an unrewarded novelty task. In conclusion, acute 5-HT2CR antagonism and constitutive loss of the 5-HT2CR have opposing effects on perseverance in egocentric reversal learning in mice. It is likely that this difference reflects the broader impact of 5HT2CR loss on the development and maintenance of cognitive function
Rab3D is critical for secretory granule maturation in PC12 cells.
Neuropeptide- and hormone-containing secretory granules (SGs) are synthesized at the trans-Golgi network (TGN) as immature secretory granules (ISGs) and complete their maturation in the F-actin-rich cell cortex. This maturation process is characterized by acidification-dependent processing of cargo proteins, condensation of the SG matrix and removal of membrane and proteins not destined to mature secretory granules (MSGs). Here we addressed a potential role of Rab3 isoforms in these maturation steps by expressing their nucleotide-binding deficient mutants in PC12 cells. Our data show that the presence of Rab3D(N135I) decreases the restriction of maturing SGs to the F-actin-rich cell cortex, blocks the removal of the endoprotease furin from SGs and impedes the processing of the luminal SG protein secretogranin II. This strongly suggests that Rab3D is implicated in the subcellular localization and maturation of ISGs
Distinguishing Family from Friends
Kinship and friendship are key human relationships. Increasingly, data suggest that people are not less altruistic toward friends than close kin. Some accounts suggest that psychologically we do not distinguish between them; countering this is evidence that kinship provides a unique explanatory factor. Using the Implicit Association Test, we examined how people implicitly think about close friends versus close kin in three contexts. In Experiment 1, we examined generic attitudinal dispositions toward friends and family. In Experiment 2, attitude similarity as a marker of family and friends was examined, and in Experiments 3 and 4, strength of in-group membership for family and friends was examined. Findings show that differences exist in implicit cognitive associations toward family and friends. There is some evidence that people hold more positive general dispositions toward friends, associate attitude similarity more with friends, consider family as more representative of the in-group than friends, but see friends as more in-group than distant kin
Realization and Properties of Biochemical-Computing Biocatalytic XOR Gate Based on Enzyme Inhibition by a Substrate
We consider a realization of the XOR logic gate in a process biocatalyzed by
an enzyme (here horseradish peroxidase: HRP), the function of which can be
inhibited by a substrate (hydrogen peroxide for HRP), when the latter is
inputted at large enough concentrations. A model is developed for describing
such systems in an approach suitable for evaluation of the analog noise
amplification properties of the gate. The obtained data are fitted for gate
quality evaluation within the developed model, and we discuss aspects of
devising XOR gates for functioning in "biocomputing" systems utilizing
biomolecules for information processing
Recommended from our members
mTOR Controls Mitochondrial Dynamics and Cell Survival via MTFP1
The mechanisms that link environmental and intracellular stimuli to mitochondrial functions, including fission and fusion, ATP production, metabolite biogenesis and apoptosis, are not well understood. Here, we demonstrate that the nutrient-sensing mechanistic/mammalian
target of rapamycin complex 1 (mTORC1) stimulates translation of mitochondrial fission process 1 (MTFP1) protein to control mitochondrial fission and apoptosis. Expression of MTFP1 is coupled to pro-fission phosphorylation and mitochondrial recruitment of the fission GTPase,
dynamin-related protein 1 (DRP1). Potent active-site mTOR inhibitors engender mitochondrial hyperfusion due to the diminished translation of MTFP1 mediated by the translation initiation factor 4E (eIF4E)-binding proteins (4E-BPs). Uncoupling MTFP1 levels from the mTORC1/4EBP
pathway upon mTOR inhibition blocks the hyperfusion response and leads to apoptosis by converting mTOR inhibitor action from cytostatic to cytotoxic. These data provide direct evidence for the survival function of mitochondrial hyperfusion upon mTOR inhibition by employing
MTFP1 as a critical effector of mTORC1 to govern cell fate decisions
- …