Differential Regulation of Plasma Copeptin Levels in Patients with Heart Failure: A Single-Center Prospective Study.

Elevated levels of arginine vasopressin (AVP) have been reported to be involved in the pathogenesis of heart failure (HF). Recent evidence has shown the role of copeptin, the C-terminal fragment of pro-AVP, as a biomarker in patients with HF. However, the relevant information is still limited. Therefore, we evaluated 39 Japanese patients admitted for HF between 2013 and 2015 (23 males and 16 females with an average age of 79.2 years). They were treated according to the Japanese acute HF guideline. Plasma copeptin levels were measured on admission and about 1 week later. The median plasma copeptin levels on admission were 0.5 (0.1-50.6) pmol/L, higher than the normal values (0.24 ± 0.06 pmol/L). Despite the similar clinical severity on admission, the patients showed great variability in plasma copeptin levels. They were divided into three groups (13 patients/group) according to plasma copeptin levels on admission: highest (> 30.8 pmol/L), midrange, and lowest (< 0.2 pmol/L) groups. Initial treatment improved HF symptoms in 37 of 39 patients, with the two unresponsive patients in the lowest group. Notably, plasma copeptin responses to initial treatment were different, depending on admission copeptin levels. The initial treatment significantly decreased copeptin levels in the highest group, but increased copeptin levels in the lowest group. By contrast, patients in the midrange group showed no significant changes. Thus, the treatment appears to restore the plasma copeptin levels. In conclusion, HF is a complex syndrome with the differential integration of stimulatory and inhibitory inputs to the AVP/copeptin secretory system.

Photoelectron spectroscopy and Ab initio calculations of peroxy form of SO(4)(-) anion.

A photoelectron spectrum is reported for gas-phase SO(4)(-) formed in an electron-impact ionized free jet of SO(2)(1%)/O(2)(10%)/Ar. The vertical detachment energy (VDE) of the SO(4)(-) species is determined to be 3.78 +/- 0.02 eV, which is significantly smaller than the VDE value reported for the sulfur-centered form of SO(4)(-) extracted from an Na(2)S(2)O(8) solution. With the aid of MP2/6-311+G(2df) calculations, the newly formed species is identified as a peroxy form of SO(4)(-), which is well described as OOSO(2)(-)(C(1), (2)A) having an S-O linkage between the O(2) and SO(2) units. The electronic properties of OOSO(2)(-) are characterized by the singly occupied molecular orbital (SOMO) constructed by an out-of-phase superposition of the 1a(2) orbital of SO(2) and the half-filled 2ppi(g)* of O(2)(-). On the basis of these findings, a possible formation mechanism of OOSO(2)(-) is discussed in terms of a "solvent-mediated" addition reaction, where O(2)(-) stabilized by solvation attacks SO(2) while retaining the 2ppi(g)* excess electron.