Vertex--IRF correspondence and factorized L-operators for an elliptic R-operator

As for an elliptic $R$-operator which satisfies the Yang--Baxter equation, the incoming and outgoing intertwining vectors are constructed, and the vertex--IRF correspondence for the elliptic $R$-operator is obtained. The vertex--IRF correspondence implies that the Boltzmann weights of the IRF model satisfy the star--triangle relation. By means of these intertwining vectors, the factorized L-operators for the elliptic $R$-operator are also constructed. The vertex--IRF correspondence and the factorized L-operators for Belavin's $R$-matrix are reproduced from those of the elliptic $R$-operator.Comment: 25 pages, amslatex, no figure

Magnetoencephalography Study of Right Parietal Lobe Dysfunction of the Evoked Mirror Neuron System in Antipsychotic-Free Schizophrenia

INTRODUCTION: Patients with schizophrenia commonly exhibit deficits of non-verbal communication in social contexts, which may be related to cognitive dysfunction that impairs recognition of biological motion. Although perception of biological motion is known to be mediated by the mirror neuron system, there have been few empirical studies of this system in patients with schizophrenia. METHODS: Using magnetoencephalography, we examined whether antipsychotic-free schizophrenia patients displayed mirror neuron system dysfunction during observation of biological motion (jaw movement of another individual). RESULTS: Compared with normal controls, the patients with schizophrenia had fewer components of both the waveform and equivalent current dipole, suggesting aberrant brain activity resulting from dysfunction of the right inferior parietal cortex. They also lacked the changes of alpha band and gamma band oscillation seen in normal controls, and had weaker phase-locking factors and gamma-synchronization predominantly in right parietal cortex. CONCLUSIONS: Our findings demonstrate that untreated patients with schizophrenia exhibit aberrant mirror neuron system function based on the right inferior parietal cortex, which is characterized by dysfunction of gamma-synchronization in the right parietal lobe during observation of biological motion

The effect of salts on the liquid–liquid phase equilibria of PEG600 + salt aqueous two-phase systems

Six new ATPSs were prepared by combining polyethylene glycol PEG600 with potassium citrate, dipotassium hydrogen phosphate, sodium formate, potassium formate, sodium sulfate, and lithium sulfate. Complete phase diagrams, including the binodal curve and three tie-lines, were determined at 23 °C. The experimental data obtained for the binodal curve were successfully adjusted to the Merchuk equation, and the reliability of tie-line data was confirmed using the equations suggested by Othmer–Tobias and Bancroft. The ability of each ion to induce ATPS formation was investigated. Na+ proved to be more effective in ATPS formation than K+ and Li+. For potassium salts, the order observed for the effectiveness of the anions was: HPO42– > C6H5O73– > HCO2–. Regarding the sodium salts, it was found that SO42– is clearly more effective than HCO2–. The position of the ions in the Hofmeister series and their free energy of hydration (ΔGhyd) were used to explain the ability of the ions to induce PEG salting-out. Furthermore, the effective excluded volume (EEV) of the salts was determined and the following order was found: Na2SO4 > K2HPO4 > Li2SO4 > K3C6H5O7 > NaCHO2 > KCHO2. Similar order was obtained when analyzing the size of the heterogeneous regions, suggesting the practical use of EEV as a comparison parameter between different ATPSs.This work is partially supported by project PEst-C/EQB/LA0020/2011, financed by FEDER through COMPETE-Programa Operacional Factores de Competitividade and by FCT-Fundacao para a Ciencia e a Tecnologia. Sara Silverio acknowledges her Ph.D. grant from FCT (SFRH/BD/43439/2008)

Characterization of Multiple Ion Channels in Cultured Human Cardiac Fibroblasts

Background: Although fibroblast-to-myocyte electrical coupling is experimentally suggested, electrophysiology of cardiac fibroblasts is not as well established as contractile cardiac myocytes. The present study was therefore designed to characterize ion channels in cultured human cardiac fibroblasts. Methods and Findings: A whole-cell patch voltage clamp technique and RT-PCR were employed to determine ion channels expression and their molecular identities. We found that multiple ion channels were heterogeneously expressed in human cardiac fibroblasts. These include a big conductance Ca2+-activated K+ current (BKCa) in most (88%) human cardiac fibroblasts, a delayed rectifier K+ current (IKDR) and a transient outward K+ current (Ito) in a small population (15 and 14%, respectively) of cells, an inwardly-rectifying K+ current (IKir) in 24% of cells, and a chloride current (ICl) in 7% of cells under isotonic conditions. In addition, two types of voltage-gated Na+ currents (INa) with distinct properties were present in most (61%) human cardiac fibroblasts. One was a slowly inactivated current with a persistent component, sensitive to tetrodotoxin (TTX) inhibition (INa.TTX, IC50 = 7.8 nM), the other was a rapidly inactivated current, relatively resistant to TTX (INa.TTXR, IC50 = 1.8 μM). RT-PCR revealed the molecular identities (mRNAs) of these ion channels in human cardiac fibroblasts, including KCa.1.1 (responsible for BKCa), Kv1.5, Kv1.6 (responsible for IKDR), Kv4.2, Kv4.3 (responsible for Ito), Kir2.1, Kir2.3 (for IKir), Clnc3 (for ICl), NaV1.2, NaV1.3, NaV1.6, NaV1.7 (for INa.TTX), and NaV1.5 (for INa.TTXR). Conclusions: These results provide the first information that multiple ion channels are present in cultured human cardiac fibroblasts, and suggest the potential contribution of these ion channels to fibroblast-myocytes electrical coupling. © 2009 Li et al.published_or_final_versio

Wavefront shaping with disorder-engineered metasurfaces

Recently, wavefront shaping with disordered media has demonstrated optical manipulation capabilities beyond those of conventional optics, including extended volume, aberration-free focusing and subwavelength focusing. However, translating these capabilities to useful applications has remained challenging as the input–output characteristics of the disordered media (P variables) need to be exhaustively determined via O(P) measurements. Here, we propose a paradigm shift where the disorder is specifically designed so its exact input–output characteristics are known a priori and can be used with only a few alignment steps. We implement this concept with a disorder-engineered metasurface, which exhibits additional unique features for wavefront shaping such as a large optical memory effect range in combination with a wide angular scattering range, excellent stability, and a tailorable angular scattering profile. Using this designed metasurface with wavefront shaping, we demonstrate high numerical aperture (NA > 0.5) focusing and fluorescence imaging with an estimated ~2.2 × 10^8 addressable points in an ~8 mm field of view

Precision Analysis of the 136Xe Two-Neutrino ββ Spectrum in KamLAND-Zen and Its Impact on the Quenching of Nuclear Matrix Elements

We present a precision analysis of the 136Xe two-neutrino ββ electron spectrum above 0.8MeV, based on high-statistics data obtained with the KamLAND-Zen experiment. An improved formalism for the two-neutrino ββ rate allows us to measure the ratio of the leading and subleading 2νββ nuclear matrix elements (NMEs), ξ2ν31 = −0.26 +0.31−0.25. Theoretical predictions from the nuclear shell model and the majority of the quasiparticle random-phase approximation (QRPA) calculations are consistent with the experimental limit. However, part of the ξ2ν31 range allowed by the QRPA is excluded by the present measurement at the 90% confidence level. Our analysis reveals that predicted ξ2ν31 values are sensitive to the quenching of NMEs and the competing contributions from low- and high-energy states in the intermediate nucleus. Because these aspects are also at play in neutrinoless ββ decay, ξ2ν31 provides new insights toward reliable neutrinoless ββ NMEs

Cytomegalovirus induces abnormal chondrogenesis and osteogenesis during embryonic mandibular development

<p>Abstract</p> <p>Background</p> <p>Human clinical studies and mouse models clearly demonstrate that cytomegalovirus (CMV) disrupts normal organ and tissue development. Although CMV is one of the most common causes of major birth defects in humans, little is presently known about the mechanism(s) underlying CMV-induced congenital malformations. Our prior studies have demonstrated that CMV infection of first branchial arch derivatives (salivary glands and teeth) induced severely abnormal phenotypes and that CMV has a particular tropism for neural crest-derived mesenchyme (NCM). Since early embryos are barely susceptible to CMV infection, and the extant evidence suggests that the differentiation program needs to be well underway for embryonic tissues to be susceptible to viral infection and viral-induced pathology, the aim of this study was to determine if first branchial arch NCM cells are susceptible to mCMV infection prior to differentiation of NCM derivatives.</p> <p>Results</p> <p>E11 mouse mandibular processes (MANs) were infected with mouse CMV (mCMV) for up to 16 days <it>in vitr</it>o. mCMV infection of undifferentiated embryonic mouse MANs induced micrognathia consequent to decreased Meckel's cartilage chondrogenesis and mandibular osteogenesis. Specifically, mCMV infection resulted in aberrant stromal cellularity, a smaller, misshapen Meckel's cartilage, and mandibular bone and condylar dysmorphogenesis. Analysis of viral distribution indicates that mCMV primarily infects NCM cells and derivatives. Initial localization studies indicate that mCMV infection changed the cell-specific expression of FN, NF-κB2, RelA, RelB, and Shh and Smad7 proteins.</p> <p>Conclusion</p> <p>Our results indicate that mCMV dysregulation of key signaling pathways in primarily NCM cells and their derivatives severely disrupts mandibular morphogenesis and skeletogenesis. The pathogenesis appears to be centered around the canonical and noncanonical NF-κB pathways, and there is unusual juxtaposition of abnormal stromal cells and surrounding matrix. Moreover, since it is critically important that signaling molecules are expressed in appropriate cell populations during development, the aberrant localization of components of relevant signaling pathways may reveal the pathogenic mechanism underlying mandibular malformations.</p