Giant magneto-optical responses in magnetic Weyl semimetal Co3Sn2S2.

The Weyl semimetal (WSM), which hosts pairs of Weyl points and accompanying Berry curvature in momentum space near Fermi level, is expected to exhibit novel electromagnetic phenomena. Although the large optical/electronic responses such as nonlinear optical effects and intrinsic anomalous Hall effect (AHE) have recently been demonstrated indeed, the conclusive evidence for their topological origins has remained elusive. Here, we report the gigantic magneto-optical (MO) response arising from the topological electronic structure with intense Berry curvature in magnetic WSM Co3Sn2S2. The low-energy MO spectroscopy and the first-principles calculation reveal that the interband transitions on the nodal rings connected to the Weyl points show the resonance of the optical Hall conductivity and give rise to the giant intrinsic AHE in dc limit. The terahertz Faraday and infrared Kerr rotations are found to be remarkably enhanced by these resonances with topological electronic structures, demonstrating the novel low-energy optical response inherent to the magnetic WSM.

Sequence-based typing identifies a novel HLA-DPB1 allele, DPB1*9601.

In this report we describe the identification of a novel HLA-DPB1 allele, DPB1*9601, found in a Caucasian individual sample named ucla#356. The new allele was detected in the DNA of ucla#356 during routine HLA sequence-based typing (SBT) of samples participating in the UCLA International HLA DNA Exchange (number 55) for HLA DNA Proficiency Testing. DPB1*9601 was identical to DPB1*3901 except for a single nucleotide substitution 'G'-->'C' in previously constant position 277 (position 177, respectively, counting only exon 2). This nucleotide change causes an amino acid substitution from aspartic acid in DPB1*3901 to histidine at codon 64 in the novel allele. This new allele has been submitted to the EMBL database and has been assigned the accession number AJ514871. The WHO Nomenclature Committee has officially assigned the name DPB1*9601.

Heparin adheres to the damaged arterial wall and inhibits its thrombogenicity.

Heparin binds to thrombogenic extracellular matrices as well as to smooth muscle cells of the vascular wall in vitro. The inhibitory effects of heparin on thrombogenicity of the damaged arterial wall were examined in vivo using small mesenteric arteries of rats and a video recording system attached to a microscope. To induce thrombosis, we damaged the vessel wall over a short segment by compression and exposed the media to the blood stream. A platelet-rich thrombus enlarged gradually at the damaged site, occluded the vascular lumen for a short period, and then flowed away. Compression damage induced such thrombus formation several times. Heparin (500 units/ml) was given in three different ways: intravenous and intra-arterial administration (both 300 units/kg) and intraluminal application under stopped-flow conditions (less than 0.01 ml) for 1-2 minutes with subsequent draining out. Intravenous heparin significantly decreased both the total duration and the number of thrombotic occlusions, whereas intra-arterial heparin abolished thrombotic occlusion. Both routes of heparin administration similarly prolonged the blood coagulation time. Intraluminal application of heparin significantly inhibited subsequent thrombus formation after restoring the flow without changes in the blood coagulation time. After an intra-arterial administration or intraluminal application of fluorescein isothiocyanate-bound heparin, strong fluorescence was observed only at the damaged vascular segment. A heparin fraction with low affinity to antithrombin III or chondroitin sulfate A did not inhibit thrombosis. To clarify anticoagulant activity of vascular wall-bound heparin, damaged carotid arterial segments of rats were incubated (inside out) in platelet-poor plasma with thrombin, and fibrin clot formation around the segments with or without heparin binding was measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of an antiarrhythmic agent, carocainide, on action potentials of ventricular papillary muscle of the guinea-pig heart in vitro.

The effect of carocainide, a new benzofuran derivative showing an antiarrhythmic action in animal models, on transmembrane potentials was examined in isolated ventricular papillary muscles of guinea-pig, using a conventional microelectrode technique in vitro. Carocainide, at concentrations above 5 x 10(-6) M, induced a dose-dependent decrease of the maximum upstroke velocity at a stimulation frequency of 0.1 Hz, while the resting membrane potential, the amplitude and duration of action potential were not affected even at 5 x 10(-5) M. In the presence of carocainide, trains of stimuli higher than 1 Hz led to an exponential decline in maximum upstroke velocity to a new steady state level. This use-dependent block was augmented at the higher stimulation frequency as carocainide (5 x 10(-5) M) decreased the maximum upstroke velocity to 50-60% and to 40-50% of the initial level at 2 Hz and at 3 Hz, respectively. Carocainide (5 x 10(-5) M) at 1 Hz caused an appreciable shift (6-7 mV) of the curve at 50% of the maximum upstroke velocity (mid-point), bringing the membrane potential and the maximum upstroke velocity along the voltage axis in the hyperpolarizing direction. Our results indicate that carocainide has similar electrophysiological effects to those of other Class Ib antiarrhythmic drugs and that it can be characterized as a potent use-dependent sodium channel blocker.