Giant Density of States Enhancement Driven by a Zero-Mode Landau Level in Semimetallic Black Phosphorus under Pressure.

Dirac fermion systems form a unique Landau level at the Fermi level-the so-called zero mode-whose observation itself will provide strong evidence of the presence of Dirac dispersions. Here, we report the study of semimetallic black phosphorus under pressure by ^{31}P-nuclear magnetic resonance measurements in a wide range of magnetic field up to 24.0 T. We have found a field-induced giant enhancement of 1/T_{1}T, where 1/T_{1} is the nuclear spin lattice relaxation rate: 1/T_{1}T at 24.0 T reaches more than 20 times larger than that at 2.0 T. The increase in 1/T_{1}T above 6.5 T is approximately proportional to the squared field, implying a linear relationship between the density of states and the field. We also found that, while 1/T_{1}T at a constant field is independent of temperature in the low-temperature region, it steeply increases with temperature above 100 K. All these phenomena are well explained by considering the effect of Landau quantization on three-dimensional Dirac fermions. The present study demonstrates that 1/T_{1} is an excellent quantity to probe the zero-mode Landau level and to identify the dimensionality of the Dirac fermion system.

Effect of ursodeoxycholate-3,7-disulfate on biliary excretion of lithocholate-3-O-glucuronide in Eisai hyperbilirubinemic rat (EHBR).

Biliary excretion of lithocholate-3-O-glucuronide and ursodeoxycholate-3,7-disulfate is markedly impaired in EHBR, in which the multidrug resistance protein 2 (Mrp2), a major ATP-dependent canalicular organic anion transporter, is impaired. We previously reported that biliary excretion of lithocholate-3-sulfate was enhanced by ursodeoxycholate-3,7-disulfate in Eisai hyperbilirubinemic rat (EHBR). In the present study, we examined the effect of ursodeoxycholate-3,7-disulfate infusion on biliary excretion of lithocholate-3-O-glucuronide. Although in control rats, ursodeoxycholate-3,7-disulfate infusion had no effect on biliary lithocholate-3-O-glucuronide excretion, in EHBR it enhanced biliary lithocholate-3-O-glucuronide excretion. These findings indicate that ursodeoxycholate-3,7-disulfate may interact to the excretory pathway of lithocholate-3-O-glucuronide and enhances biliary excretion of lithocholate-3-O-glucuronide in EHBR.