4,521 research outputs found
Irrationality as a determinant of gender stereotyping towards women
Irrational thinking can be considered to be the key concept of Rational Emotive Behavior Therapy (REBT) and has been conceptualized as rigid und inflexible adherence to
absolutistic thinking and person evaluations. Based on this definition we predicted a positive relation between irrationality and gender stereotyping towards women. Established reliable scales were used to assess the constructs in a non-student sample (N = 240). In line with assumptions we were able to detect a significant positive relation between irrationality and gender stereotyping while controlling for the Big Five, life satisfaction, sex and age. Implications for interventions concerning stereotypes are outlined
Getting the picture : iconicity does not affect representation-referent confusion
Three experiments examined 3- to 5-year-olds' (N = 428) understanding of the relationship between pictorial iconicity (photograph, colored drawing, schematic drawing) and the real world referent. Experiments 1 and 2 explored pictorial iconicity in picture-referent confusion after the picture-object relationship has been established. Pictorial iconicity had no effect on referential confusion when the referent changed after the picture had been taken/drawn (Experiment 1) and when the referent and the picture were different from the outset (Experiment 2). Experiment 3 investigated whether children are sensitive to iconicity to begin with. Children deemed photographs from a choice of varying iconicity representations as best representations for object reference. Together, findings suggest that iconicity plays a role in establishing a picture-object relation per se but is irrelevant once children have accepted that a picture represents an object. The latter finding may reflect domain general representational abilities
Emergence of massless Dirac fermions in graphene's Hofstadter butterfly at switches of the quantum Hall phase connectivity
The fractal spectrum of magnetic minibands (Hofstadter butterfly), induced by
the moir\'e super- lattice of graphene on an hexagonal crystal substrate, is
known to exhibit gapped Dirac cones. We show that the gap can be closed by
slightly misaligning the substrate, producing a hierarchy of conical
singularities (Dirac points) in the band structure at rational values Phi =
(p/q)(h/e) of the magnetic flux per supercell. Each Dirac point signals a
switch of the topological quantum number in the connected component of the
quantum Hall phase diagram. Model calculations reveal the scale invariant
conductivity sigma = 2qe^2 / pi h and Klein tunneling associated with massless
Dirac fermions at these connectivity switches.Comment: 4 pages, 6 figures + appendix (3 pages, 1 figure
Theory of the topological Anderson insulator
We present an effective medium theory that explains the disorder-induced
transition into a phase of quantized conductance, discovered in computer
simulations of HgTe quantum wells. It is the combination of a random potential
and quadratic corrections proportional to p^2 sigma_z to the Dirac Hamiltonian
that can drive an ordinary band insulator into a topological insulator (having
an inverted band gap). We calculate the location of the phase boundary at weak
disorder and show that it corresponds to the crossing of a band edge rather
than a mobility edge. Our mechanism for the formation of a topological Anderson
insulator is generic, and would apply as well to three-dimensional
semiconductors with strong spin-orbit coupling.Comment: 4 pages, 3 figures (updated figures, calculated DOS
Tauroursodeoxycholic acid exerts anticholestatic effects by a cooperative cPKC alpha-/PKA-dependent mechanism in rat liver.
Objective: Ursodeoxycholic acid (UDCA) exerts anticholestatic effects in part by protein kinase C (PKC)-dependent mechanisms. Its taurine conjugate, TUDCA, is a cPKCa agonist. We tested whether protein kinase A (PKA) might contribute to the anticholestatic action of TUDCA via cooperative cPKCa-/PKA-dependent mechanisms
in taurolithocholic acid (TLCA)-induced cholestasis.
Methods: In perfused rat liver, bile flow was determined gravimetrically, organic anion secretion spectrophotometrically,
lactate dehydrogenase (LDH) release enzymatically, cAMP response-element binding protein (CREB) phosphorylation by immunoblotting, and cAMP by immunoassay. PKC/PKA inhibitors were tested radiochemically. In vitro phosphorylation of the conjugate export pump, Mrp2/Abcc2, was studied in rat hepatocytes and human Hep-G2 hepatoma cells.
Results: In livers treated with TLCA (10 mmol/l)+TUDCA (25 mmol/l), combined inhibition of cPKC by the cPKCselective
inhibitor Go¨6976 (100 nmol/l) or the nonselective PKC inhibitor staurosporine (10 nmol/l) and of PKA by H89 (100 nmol/l) reduced bile flow by 36% (p,0.05) and 48% (p,0.01), and secretion of the Mrp2/
Abcc2 substrate, 2,4-dinitrophenyl-S-glutathione, by 31% (p,0.05) and 41% (p,0.01), respectively; bile flow was
unaffected in control livers or livers treated with TUDCA only or TLCA+taurocholic acid. Inhibition of cPKC or PKA alone did not affect the anticholestatic action of TUDCA. Hepatic cAMP levels and CREB phosphorylation as readout of PKA activity were unaffected by the bile acids
tested, suggesting a permissive effect of PKA for the anticholestatic action of TUDCA. Rat and human hepatocellular Mrp2 were phosphorylated by phorbol ester pretreatment and recombinant cPKCa, nPKCe, and PKA, respectively, in a staurosporine-sensitive manner.
Conclusion: UDCA conjugates exert their anticholestatic action in bile acid-induced cholestasis in part via cooperative post-translational cPKCa-/PKA-dependent
mechanisms. Hepatocellular Mrp2 may be one target of bile acid-induced kinase activation
Fibroblast growth factor receptor 4 single nucleotide polymorphism Gly388Arg in head and neck carcinomas
BACKGROUND Head and neck squamous cell carcinoma (HNSCC) is considered to be a progressive disease resulting from alterations in multiple genes regulating cell proliferation and differentiation like receptor tyrosine kinases (RTKs) and members of the fibroblast growth factor receptors (FGFR)-family. Single-nucleotide polymorphism (SNP) Arg388 of the FGFR4 is associated with a reduced overall survival in patients with cancers of various types. We speculate that FGFR4 expression and SNP is associated with worse survival in patients with HSNCC. AIM To investigate the potential clinical significance of FGFR4 Arg388 in the context of tumors arising in HNSCC, a comprehensive analysis of FGFR4 receptor expression and genotype in tumor tissues and correlated results with patients' clinical data in a large cohort of patients with HNSCC was conducted. METHODS Surgical specimens from 284 patients with HNSCC were retrieved from the Institute of Pathology at the Ludwig-Maximilian-University in Germany. Specimens were analyzed using immunohistochemistry and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The expression of FGFR4 was analyzed in 284 surgical specimens of HNSCC using immunohistochemstry. FGFR4 polymorphism was detected by PCR-RFLP. Patients' clinical data with a minimum follow-up of 5 syears were statistically evaluated with a special emphasis on survival analysis employing Kaplan-Meier estimator and Cox regression analysis. RESULTS Concerning the invasive tumor areas the intensity of the FGFR4 expression was evaluated in a four-grade system: no expression, low expression, intermediate and high expression. FGFR4 expression was scored as "high" (+++) in 74 (26%), "intermediate" (++) in 103 (36.3%), and "low" (+) in 107 (36.7%) cases. Analyzing the FGFR4 mutation it was found in 96 tumors (33.8%), 84 of them (29.6%) having a heterozygous and 12 (4.2%) homozygous mutated Arg388 allele. The overall frequency concerning the mutant alleles demonstrated 65% vs 34% mutated alleles in general. FGFR4 Arg388 was significantly associated with advanced tumor stage (P < 0.004), local metastasis (P < 0.0001) and reduced disease-free survival (P < 0.01). Furthermore, increased expression of FGFR4 correlated significantly with worse overall survival (P < 0.003). CONCLUSION In conclusion, the FGFR4 Arg388 genotype and protein expression of FGFR4 impacts tumor progression in patients with HNSCC and may present a useful target within a multimodal therapeutic intervention
Reactivation of single-episode pain patterns in the hippocampus and decision making
Aversive and rewarding experiences can exert a strong influence on subsequent behavior. While decisions are often supported by the value of single past episodes, most research has focused on the role of well-learned value associations. Recent studies have begun to investigate the influence of reward-associated episodes, but it is unclear if these results generalize to negative experiences such as pain. To investigate whether and how the value of previous aversive experiences modulates behavior and brain activity, in our experiments female and male human participants experienced episodes of high or low pain in conjunction with incidental, trial-unique neutral pictures. In an incentive-compatible surprise test phase, we found that participants avoided pain-paired objects. In a separate fMRI experiment, at test, participants exhibited significant pain value memory. Neurally, when participants were re-exposed to pain-paired objects, we found no evidence for reactivation of pain-related patterns in pain-responsive regions such as the anterior insula. Critically, however, we found significant reactivation of pain-related patterns of activity in the hippocampus, such that activity significantly discriminated high versus low pain episodes. Further, stronger reactivation in the anterior hippocampus was related to improved pain value memory performance. Our results demonstrate that single incidental aversive experiences can build memories that affect decision making and that this influence may be supported by the hippocampus
Andreev reflection from a topological superconductor with chiral symmetry
It was pointed out by Tewari and Sau that chiral symmetry (H -> -H if e
h) of the Hamiltonian of electron-hole (e-h) excitations in an N-mode
superconducting wire is associated with a topological quantum number
Q\in\mathbb{Z} (symmetry class BDI). Here we show that Q=Tr(r_{he}) equals the
trace of the matrix of Andreev reflection amplitudes, providing a link with the
electrical conductance G. We derive G=(2e^2/h)|Q| for |Q|=N,N-1, and more
generally provide a Q-dependent upper and lower bound on G. We calculate the
probability distribution P(G) for chaotic scattering, in the circular ensemble
of random-matrix theory, to obtain the Q-dependence of weak localization and
mesoscopic conductance fluctuations. We investigate the effects of chiral
symmetry breaking by spin-orbit coupling of the transverse momentum (causing a
class BDI-to-D crossover), in a model of a disordered semiconductor nanowire
with induced superconductivity. For wire widths less than the spin-orbit
coupling length, the conductance as a function of chemical potential can show a
sequence of 2e^2/h steps - insensitive to disorder.Comment: 10 pages, 5 figures. Corrected typo (missing square root) in
equations A13 and A1
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The SNARE machinery is involved in apical plasma membrane trafficking in MDCK cells.
We have investigated the controversial involvement of components of the SNARE (soluble N-ethyl maleimide-sensitive factor [NSF] attachment protein [SNAP] receptor) machinery in membrane traffic to the apical plasma membrane of polarized epithelial (MDCK) cells. Overexpression of syntaxin 3, but not of syntaxins 2 or 4, caused an inhibition of TGN to apical transport and apical recycling, and leads to an accumulation of small vesicles underneath the apical plasma membrane. All other tested transport steps were unaffected by syntaxin 3 overexpression. Botulinum neurotoxin E, which cleaves SNAP-23, and antibodies against alpha-SNAP inhibit both TGN to apical and basolateral transport in a reconstituted in vitro system. In contrast, we find no evidence for an involvement of N-ethyl maleimide-sensitive factor in TGN to apical transport, whereas basolateral transport is NSF-dependent. We conclude that syntaxin 3, SNAP-23, and alpha-SNAP are involved in apical membrane fusion. These results demonstrate that vesicle fusion with the apical plasma membrane does not use a mechanism that is entirely unrelated to other cellular membrane fusion events, but uses isoforms of components of the SNARE machinery, which suggests that they play a role in providing specificity to polarized membrane traffic
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