A systematic study of mass spectra and strong decay of strange mesons

The mass spectrum of the kaon family is analyzed by the {modified} Godfrey-Isgur model with a color screening effect approximating the kaon as a heavy-light meson system. This analysis gives us the structure and possible assignments of the observed kaon candidates, which can be tested by comparing the theoretical results of their two-body strong decays with the experimental data. Additionally, prediction of some partial decay widths is made on the kaons still missing in experiment. This study is crucial to establishing the kaon family and searching for their higher excitations in the future.Comment: 19 pages, 7 figures, and 17 tables. More discussions added and typos corrected. Accepted by Eur. Phys. J.

Unifying ultrafast demagnetization and intrinsic Gilbert damping in Co/Ni bilayers with electronic relaxation near the Fermi surface

The ability to controllably manipulate the laser-induced ultrafast magnetic dynamics is a prerequisite for future high speed spintronic devices. The optimization of devices requires the controllability of the ultrafast demagnetization time, , and intrinsic Gilbert damping, . In previous attempts to establish the relationship between and , the rare-earth doping of a permalloy film with two different demagnetization mechanism is not a suitable candidate. Here, we choose Co/Ni bilayers to investigate the relations between and by means of time-resolved magneto-optical Kerr effect (TRMOKE) via adjusting the thickness of the Ni layers, and obtain an approximately proportional relation between these two parameters. The remarkable agreement between TRMOKE experiment and the prediction of breathing Fermi-surface model confirms that a large Elliott-Yafet spin-mixing parameter is relevant to the strong spin-orbital coupling at the Co/Ni interface. More importantly, a proportional relation between and in such metallic films or heterostructures with electronic relaxation near Fermi surface suggests the local spin-flip scattering domains the mechanism of ultrafast demagnetization, otherwise the spin-current mechanism domains. It is an effective method to distinguish the dominant contributions to ultrafast magnetic quenching in metallic heterostructures by investigating both the ultrafast demagnetization time and Gilbert damping simultaneously. Our work can open a novel avenue to manipulate the magnitude and efficiency of Terahertz emission in metallic heterostructures such as the perpendicular magnetic anisotropic Ta/Pt/Co/Ni/Pt/Ta multilayers, and then it has an immediate implication of the design of high frequency spintronic devices

Electrical Control of Magnetization in Charge-ordered Multiferroic LuFe2O4

LuFe2O4 exhibits multiferroicity due to charge order on a frustrated triangular lattice. We find that the magnetization of LuFe2O4 in the multiferroic state can be electrically controlled by applying voltage pulses. Depending on with or without magnetic fields, the magnetization can be electrically switched up or down. We have excluded thermal heating effect and attributed this electrical control of magnetization to an intrinsic magnetoelectric coupling in response to the electrical breakdown of charge ordering. Our findings open up a new route toward electrical control of magnetization.Comment: 14 pages, 5 figure

3,5-Bis[1-acetyl-5-(4-chloro­phen­yl)-4,5-dihydro-1H-pyrazol-3-yl]-2,6-dimethyl­pyridine

The title compound, C29H27Cl2N5O2, contains a central pyridine ring and two functionalized pyrazoline rings. The pyridine ring and the two attached pyrazoline rings are nearly coplanar, whereas the terminal chloro­phenyl rings are nearly perpendicular to the attached pyrazoline rings [dihedral angles = 86.78 (1) and 77.70 (1)°]. Mol­ecules are linked by weak inter­molecular C—H⋯O hydrogen bonding

Dichlorido(pyridine-κN)[2-(pyridinium-1-yl)acetato-κO]zinc(II)

In the title complex, [ZnCl2(C5H5N)(C7H7NO2)], the ZnII atom adopts a distorted tetra­hedral coordination geometry [the smallest angle being 105.22 (15)° and the widest angle being 115.60 (16)°] that is formed from one monodentate carboxyl­ate ligand, one pyridine ligand and two Cl atoms

A new animal model of spontaneous autoimmune peripheral polyneuropathy: implications for Guillain-Barré syndrome

BACKGROUND: Spontaneous autoimmune peripheral neuropathy including Guillain-Barré Syndrome (GBS) represents as one of the serious emergencies in neurology. Although pathological changes have been well documented, molecular and cellular mechanisms of GBS are still under-explored, partially due to short of appropriate animal models. The field lacks of spontaneous and translatable models for mechanistic investigations. As GBS is preceded often by viral or bacterial infection, a condition can enhance co-stimulatory activity; we sought to investigate the critical role of T cell co-stimulation in this autoimmune disease. RESULTS: Our previous study reported that transgene-derived constitutive expression of co-stimulator B7.2 on antigen presenting cells of the nervous tissues drove spontaneous neurological disorders. Depletion of CD4(+) T cells in L31 mice accelerated the onset and increased the prevalence of the disease. In the current study, we further demonstrated that L31/CD4(-/-) mice exhibited both motor and sensory deficits, including weakness and paresis of limbs, numbness to mechanical stimuli and hypersensitivity to thermal stimulation. Pathological changes were characterized by massive infiltration of macrophages and CD8(+) T cells, demyelination and axonal damage in peripheral nerves, while changes in spinal cords could be secondary to the PNS damage. In symptomatic L31/CD4(-/-) mice, the disruption of the blood neural barriers was observed mainly in peripheral nerves. Interestingly, the infiltration of immune cells was initiated in pre-symptomatic L31/CD4(-/-) mice, prior to the disease onset, in the DRG and spinal roots where the blood nerve barrier is virtually absent. CONCLUSIONS: L31/CD4(-/-) mice mimic most parts of clinical and pathological signatures of GBS in human; thus providing an unconventional opportunity to experimentally explore the critical events that lead to spontaneous, autoimmune demyelinating disease of the peripheral nervous system