Room-temperature-superconducting Tc driven by electron correlation

Room-temperature-superconducting Tc measured by high pressure in hydrides can be theoretically explained by a Brinkman–Rice (BR)–Bardeen–Cooper–Schrieffer (BCS) Tc combining both the generalized BCS Tc and the diverging effective mass, m*/m = 1/(1 − (U/Uc)2), with the on-site Coulomb interaction U in the BR picture. A transition from U in a correlated metal of the normal state to Uc in the superconducting state can lead to superconductivity, which can be caused by volume contraction induced by high pressure or low temperature.

Plasma volume contraction reduces atrial natriuretic peptide after four days of hypobaric hypoxia exposure

We investigated whether low arterial oxygen tension (PaO2) or hypoxia-induced plasma volume (PV) contraction, which reduces central blood volume (BV) and atrial distension, explain reduction in circulating atrial natriuretic peptide (ANP) after prolonged hypoxic exposure. Ten healthy males were exposed for four days to hypobaric hypoxia corresponding to an altitude of 3,500m. PV changes were determined by carbon monoxide rebreathing. Venous plasma concentrations of mid-regional proANP (MR-ProANP) were measured before and at the end of the exposure. At the latter time-point the measurement was repeated after i. restoration of PaO2 by breathing a hyperoxic gas mixture for 30min and ii. restoration of BV by fluid infusion. Correspondingly, left ventricular end-diastolic volume (LVEDV), left atrial area (LAA) and right atrial area (RAA) were determined by ultrasound before exposure, and both pre and post fluid infusion at the end of the exposure. Hypoxic exposure reduced MR-ProANP from 37.9±18.5 to 24.5±10.3 pmol/l (p=0.034), LVEDV from 107.4±33.5 to 91.6±26.3 ml (p=0.005), LAA from 15.8±4.9 to 13.3±4.2 cm² (p=0.007) and RAA from 16.2±3.1 to 14.3±3.5 cm² (p=0.001). Hyperoxic breathing did not affect MR-ProANP (24.8±12.3 pmol/l, p=0.890). Conversely, fluid infusion restored LVEDV, LAA and RAA to near baseline values (108.0±29.3 ml, 17.2±5.7 cm² and 17.2±3.1 cm², p>0.05 vs. baseline) and increased MR-ProANP to 29.5±13.3 pmol/l (p=0.010 vs. pre-infusion and p=0.182 vs. baseline). These findings support that ANP reduction in hypoxia is at least partially attributed to plasma volume contraction, whereas reduced PaO2 does not seem to contribute.

How to quantify isotropic negative thermal expansion: magnitude, range, or both?

Negative thermal expansion (NTE) is the counterintuitive material property of volume contraction on heating. We compare different systems with contrasting mechanisms for isotropic NTE using the metric of NTE capacity.

How to Quantify Isotropic Negative Thermal Expansion: Magnitude, Range or Both?

<div>Negative thermal expansion (NTE) is the useful and counterintuitive material property of volume contraction on heating. Isotropic NTE is the rarest and most useful type, and is known to occur in a variety of different classes of materials. In this mini-review we ask the simple question of how best to compare NTE behaviour amongst these different systems? We summarise the two main mechanisms for isotropic NTE, and illustrate how these favour alternatively NTE magnitude</div><div>and NTE range. We argue in favour of a combined metric of NTE capacity, which balances both effects and allows unbiased identification of the most remarkable NTE materials, irrespective of the underlying microscopic mechanism at play. By organising known NTE materials according to these various metrics, we find intuitive trends in behaviour that help identify key materials for specific NTE applications.</div>