Induced-Moment Weak Antiferromagnetism and Orbital Order on the Itinerant-Localized Duality Model with Nested Fermi Surface: A Possible Origin of Exotic Magnetism in URu2{}_{2}Si2_{2}

The weak antiferromagnetism of URu${}_{2}$Si${}_{2}$ is discussed on the basis of a duality model which takes into account salient features of both itinerant fermions and "localized" component of spin degrees of freedom. The problem is analyzed in the framework of induced-moment mechanism by taking a singlet-singlet crystal field scheme together with the nesting property of partial Fermi surface of itinerant fermions . It is shown that the extremely small ordered moment $m$ of ${\cal O}$($10^{-2}$$\times$$\mu_{B}$) can be compatible with the large specific-heat jump at the transition temperature $T_{N}$. Analysis performed in the presence of external magnetic field shows that the field dependence of $m$ in the limit T\to 0 and T_{N}$ do not scale except very near the critical field B which is consistent with a recent observation by Mentink. It is also shown that the antiferromagnetic magnetic order gives rise to a tiny amount of antiferromagnetic orbital order of f-electrons.Comment: 14 pages, 2 figure PS file, accepted J. Phys. Soc. Jp

Spin, Charge and Quasiparticle Gaps in the One-Dimensional Kondo Lattice with f^2 Configuration

The ground state properties of the one-dimensional Kondo lattice with an f^2 configuration at each site are studied by the density matrix renormalization group method. At half-filling, competition between the Kondo exchange J and the antiferromagnetic intra f-shell exchange I leads to reduction of energy gaps for spin, quasi-particle and charge excitations. The attractive force among conduction electrons is induced by the competition and the bound state is formed. As J/I increases the f^2 singlet gives way to the Kondo singlet as the dominant local correlation. The remarkable change of the quasi-particle gap is driven by the change of the spin-1/2 excitation character from the itinerant one to the localized one. Possible metal-insulator transition is discussed which may occur as the ratio J/I is varied by reference to mean-field results in the f^2 lattice system and the two impurity Kondo system.Comment: 7 pages, 7 figures, submitted to J. Phys. Soc. Jp

Monitoring lung impedance changes during long-term ventilator-induced lung injury ventilation using electrical impedance tomography

Objective: The target of this methodological evaluation was the feasibility of long-term monitoring of changes in lung conditions by time-difference electrical impedance tomography (tdEIT). In contrast to ventilation monitoring by tdEIT, the monitoring of end-expiratory (EELIC) or end-inspiratory (EILIC) lung impedance change always requires a reference measurement. Approach: To determine the stability of the used Pulmovista 500\uae EIT system, as a prerequisite it was initially secured on a resistive phantom for 50 h. By comparing the slopes of EELIC for the whole lung area up to 48 h from 36 pigs ventilated at six positive end-expiratory pressure (PEEP) levels from 0 to 18 cmH2O we found a good agreement (range of r2 = 0.93\u20131.0) between absolute EIT (aEIT) and tdEIT values. This justified the usage of tdEIT with its superior local resolution compared to aEIT for long-term determination of EELIC. Main results: The EELIC was between 120.07 \u3a9m day 121 at PEEP 4 and 121.04 \u3a9m day 121 at PEEP 18 cmH2O. The complex local time pattern for EELIC was roughly quantified by the new parameter, centre of end-expiratory change (CoEEC), in equivalence to the established centre of ventilation (CoV). The ventrally located mean of the CoV was fairly constant in the range of 42%\u201346% of thorax diameter; however, on the contrary, the CoEEC shifted from about 40% to about 75% in the dorsal direction for PEEP levels of 14 and 18 cmH2O. Significance: The observed shifts started earlier for higher PEEP levels. Changes of EELI could be precisely monitored over a period of 48 h by tdEIT on pigs

Positive end-expiratory pressure and mechanical power

Editor's Perspective What We Already Know about This Topic Positive end-expiratory pressure protects against ventilation-induced lung injury by improving homogeneity of ventilation, but positive end-expiratory pressure contributes to the mechanical power required to ventilate the lung What This Article Tells Us That Is New This in vivo study (36 pigs mechanically ventilated in the prone position) suggests that low levels of positive end-expiratory pressure reduce injury associated with atelectasis, and above a threshold level of power, positive end-expiratory pressure causes lung injury and adverse hemodynamics Background: Positive end-expiratory pressure is usually considered protective against ventilation-induced lung injury by reducing atelectrauma and improving lung homogeneity. However, positive end-expiratory pressure, together with tidal volume, gas flow, and respiratory rate, contributes to the mechanical power required to ventilate the lung. This study aimed at investigating the effects of increasing mechanical power by selectively modifying its positive end-expiratory pressure component. Methods: Thirty-six healthy piglets (23.3 \ub1 2.3 kg) were ventilated prone for 50 h at 30 breaths/min and with a tidal volume equal to functional residual capacity. Positive end-expiratory pressure levels (0, 4, 7, 11, 14, and 18 cm H2O) were applied to six groups of six animals. Respiratory, gas exchange, and hemodynamic variables were recorded every 6 h. Lung weight and wet-to-dry ratio were measured, and histologic samples were collected. Results: Lung mechanical power was similar at 0 (8.8 \ub1 3.8 J/min), 4 (8.9 \ub1 4.4 J/min), and 7 (9.6 \ub1 4.3 J/min) cm H2O positive end-expiratory pressure, and it linearly increased thereafter from 15.5 \ub1 3.6 J/min (positive end-expiratory pressure, 11 cm H2O) to 18.7 \ub1 6 J/min (positive end-expiratory pressure, 14 cm H2O) and 22 \ub1 6.1 J/min (positive end-expiratory pressure, 18 cm H2O). Lung elastances, vascular congestion, atelectasis, inflammation, and septal rupture decreased from zero end-expiratory pressure to 4 to 7 cm H2O (P < 0.0001) and increased progressively at higher positive end-expiratory pressure. At these higher positive end-expiratory pressure levels, striking hemodynamic impairment and death manifested (mortality 0% at positive end-expiratory pressure 0 to 11 cm H2O, 33% at 14 cm H2O, and 50% at 18 cm H2O positive end-expiratory pressure). From zero end-expiratory pressure to 18 cm H2O, mean pulmonary arterial pressure (from 19.7 \ub1 5.3 to 32.2 \ub1 9.2 mmHg), fluid administration (from 537 \ub1 403 to 2043 \ub1 930 ml), and noradrenaline infusion (0.04 \ub1 0.09 to 0.34 \ub1 0.31 \u3bcg \ub7 kg-1 \ub7 min-1) progressively increased (P < 0.0001). Lung weight and lung wet-to-dry ratios were not significantly different across the groups. The lung mechanical power level that best discriminated between more versus less severe damage was 13 \ub1 1 J/min. Conclusions: Less than 7 cm H2O positive end-expiratory pressure reduced atelectrauma encountered at zero end-expiratory pressure. Above a defined power threshold, sustained positive end-expiratory pressure contributed to potentially lethal lung damage and hemodynamic impairment