Tensor coupling effects on spin symmetry in anti-Lambda spectrum of hypernuclei

The effects of $\bar\Lambda\bar\Lambda\omega$-tensor coupling on the spin symmetry of $\bar{\Lambda}$ spectra in $\bar{\Lambda}$-nucleus systems have been studied with the relativistic mean-field theory. Taking $^{12}$C+$\bar{\Lambda}$ as an example, it is found that the tensor coupling enlarges the spin-orbit splittings of $\bar\Lambda$ by an order of magnitude although its effects on the wave functions of $\bar{\Lambda}$ are negligible. Similar conclusions has been observed in $\bar{\Lambda}$-nucleus of different mass regions, including $^{16}$O+$\bar{\Lambda}$, $^{40}$Ca+$\bar{\Lambda}$ and $^{208}$Pb+$\bar{\Lambda}$. It indicates that the spin symmetry in anti-lambda-nucleus systems is still good irrespective of the tensor coupling.Comment: 12 pages, 3 figures

Theory for superconductivity in (Tl,K)Fex_xSe2_2 as a doped Mott insulator

Possible superconductivity in recently discovered (Tl,K)Fe$_x$Se$_2$ compounds is studied from the viewpoint of doped Mott insulator. The Mott insulating phase is examined to be preferred in the parent compound at $x=1.5$ due to the presence of Fe vacancies. Partial filling of vacancies at the Fe-sites introduces electron carriers and leads to electron doped superconductivity. By using a two-orbital Hubbard model in the strong coupling limit, we find that the s-wave pairing is more favorable at small Hund's coupling, and d$_{x^2-y^2}$ wave pairing is more favorable at large Hund's coupling.Comment: 4+ pages, 3 figures, to appear in EP

Cytotoxicity of Botulinum Neurotoxins Reveals a Direct Role of Syntaxin 1 and SNAP-25 in Neuron Survival

Botulinum neurotoxins (BoNT/A-G) are well-known to act by blocking synaptic vesicle exocytosis. Whether BoNTs disrupt additional neuronal functions has not been addressed. Here we report that cleavage of syntaxin 1 (Syx 1) by BoNT/C and cleavage of SNAP-25 by BoNT/E both induce degeneration of cultured rodent and human neurons. Furthermore, although SNAP-25 cleaved by BoNT/A can still support neuron survival, it has reduced capacity to tolerate additional mutations and also fails to pair with syntaxin isoforms other than Syx 1. Syx 1 and SNAP-25 are well-known for mediating synaptic vesicle exocytosis, but we found that neuronal death is due to blockage of plasma membrane recycling processes that share Syx 1/SNAP-25 for exocytosis, independent of blockage of synaptic vesicle exocytosis. These findings reveal neuronal cytotoxicity for a subset of BoNTs and directly link Syx 1/SNAP-25 to neuron survival as the prevalent SNARE proteins mediating multiple fusion events on neuronal plasma membranes

Single nonmagnetic impurity resonance in FeSe-based 122-type superconductors as a probe for pairing symmetry

We study the effect of a single non-magnetic impurity in A$_{y}$Fe$_{2-x}$Se$_{2}$ (A=K, Rb, or Cs) superconductors by considering various pairing states based on a three-orbital model consistent with the photoemission experiments. The local density of states on and near the impurity site has been calculated by solving the Bogoliubov-de Gennes equations self-consistently. The impurity-induced in-gap bound states are found only for attractive impurity scattering potential, as in the cases of doping of Co or Ni, which is characterized by the strong particle-hole asymmetry, in the nodeless $d_{x^2-y^2}$ wave pairing state. This property may be used to probe the pairing symmetry of FeSe-based 122-type superconductors.Comment: 7 pages, 7 figure

Dirac Equation at Finite Temperature

In this paper, we propose finite temperature Dirac equation, which can describe the quantum systems in an arbitrary temperature for a relativistic particle of spin-1/2. When the temperature T=0, it become Dirac equation. With the equation, we can study the relativistic quantum systems in an arbitrary temperature.Comment: arXiv admin note: text overlap with arXiv:1005.2751, arXiv:hep-ph/0004125, arXiv:hep-ph/0005272 by other author

NNZ-2566 treatment inhibits neuroinflammation and pro-inflammatory cytokine expression induced by experimental penetrating ballistic-like brain injury in rats

<p>Abstract</p> <p>Background</p> <p>Inflammatory cytokines play a crucial role in the pathophysiology of traumatic brain injury (TBI), exerting either deleterious effects on the progression of tissue damage or beneficial roles during recovery and repair. NNZ-2566, a synthetic analogue of the neuroprotective tripeptide Glypromate^®, has been shown to be neuroprotective in animal models of brain injury. The goal of this study was to determine the effects of NNZ-2566 on inflammatory cytokine expression and neuroinflammation induced by penetrating ballistic-like brain injury (PBBI) in rats.</p> <p>Methods</p> <p>NNZ-2566 or vehicle (saline) was administered intravenously as a bolus injection (10 mg/kg) at 30 min post-injury, immediately followed by a continuous infusion of NNZ-2566 (3 mg/kg/h), or equal volume of vehicle, for various durations. Inflammatory cytokine gene expression from the brain tissue of rats exposed to PBBI was evaluated using microarray, quantitative real time PCR (QRT-PCR), and enzyme-linked immunosorbent assay (ELISA) array. Histopathology of the injured brains was examined using hematoxylin and eosin (H&E) and immunocytochemistry of inflammatory cytokine IL-1β.</p> <p>Results</p> <p>NNZ-2566 treatment significantly reduced injury-mediated up-regulation of IL-1β, TNF-α, E-selectin and IL-6 mRNA during the acute injury phase. ELISA cytokine array showed that NZ-2566 treatment significantly reduced levels of the pro-inflammatory cytokines IL-1β, TNF-α and IFN-γ in the injured brain, but did not affect anti-inflammatory cytokine IL-6 levels.</p> <p>Conclusion</p> <p>Collectively, these results suggest that the neuroprotective effects of NNZ-2566 may, in part, be functionally attributed to the compound's ability to modulate expression of multiple neuroinflammatory mediators in the injured brain.</p

Gene therapy in patient-specific stem cell lines and a preclinical model of retinitis pigmentosa with membrane frizzled-related protein defects

Defects in Membrane Frizzled-related Protein (MFRP) cause autosomal recessive retinitis pigmentosa (RP). MFRP codes for a retinal pigment epithelium (RPE)-specific membrane receptor of unknown function. In patient-specific induced pluripotent stem (iPS)-derived RPE cells, precise levels of MFRP, and its dicistronic partner CTRP5, are critical to the regulation of actin organization. Overexpression of CTRP5 in naive human RPE cells phenocopied behavior of MFRP-deficient patient RPE (iPS-RPE) cells. AAV8 (Y733F) vector expressing human MFRP rescued the actin disorganization phenotype and restored apical microvilli in patient-specific iPS-RPE cell lines. As a result, AAV-treated MFRP mutant iPS-RPE recovered pigmentation and transepithelial resistance. The efficacy of AAV-mediated gene therapy was also evaluated in Mfrp(rd6)/Mfrp(rd6) mice--an established preclinical model of RP--and long-term improvement in visual function was observed in AAV-Mfrp-treated mice. This report is the first to indicate the successful use of human iPS-RPE cells as a recipient for gene therapy. The observed favorable response to gene therapy in both patient-specific cell lines, and the Mfrp(rd6)/Mfrp(rd6) preclinical model suggests that this form of degeneration caused by MFRP mutations is a potential target for interventional trials