Parathyroid (PT) cell hyperplasia is a common consequence of chronic renal insufficiency (CRI). NPS R-568 is a phenylalkylamine compound that acts as an agonist (calcimimetic) at the cell surface calcium receptor (CaR). To test the hypothesis that the CaR plays a role in PT hyperplasia in CRI, we tested the effect of NPS R-568 on PT cell proliferation in rats with renal insufficiency. Rats were subjected to 5/6 nephrectomy and then infused intraperitoneally with 5-bromodeoxyuridine (BrdU) to label S-phase cells. Two groups of nephrectomized rats received NPS R-568 by gavage twice daily for 4 d (1.5 and 15 mg/kg body wt). On day 5, the number of BrdU-positive PT cells of vehicle-treated nephrectomized rats was 2.6-fold greater than that of the sham-operated control. Low and high doses of NPS R-568 reduced the number of BrdU-positive PT cells by 20 and 50%, respectively. No changes in staining, however, were observed in ileal epithelial cells (CaR-negative) or in thyroidal C-cells (CaR-positive). Furthermore, the effect of NPS R-568 could not be explained by changes in serum 1,25(OH)2D3 or phosphorus. These results indicate that NPS R-568 suppresses PT cell proliferation in rats with renal insufficiency, and lend support to the linkage between the CaR and PT hyperplasia in CRI.

We consider the effect of a finite voltage bias on the conductance of single-atom gold contacts. We employ a nonorthogonal spd-tight-binding Hamiltonian combined with a local charge neutrality assumption. The conductance and charge distributions for finite bias are calculated using the nonequilibrium-Green-function formalism. We calculate the voltage drop through the contacts and find the main drop located near the negative electrode. We argue that this is due to the filled d-state resonances. The conduction is analyzed in terms of transmission eigenchannels and density of states of the eigenchannels projected onto tight-binding orbitals. We find a single almost fully transmitting channel with mainly s character for low bias while for high bias this channel becomes less transmitting and additional channels involving only d orbitals start to conduct.

Phosphorus directly controls parathyroid hormone (PTH) synthesis and secretion. Serum levels of the novel phosphate-regulating hormone, fibroblast growth factor 23 (FGF23), are positively correlated with hyperphosphatemia in patients with chronic renal insufficiency (CRI). We proposed that changes in serum PTH and FGF23 levels might be associated with changes in serum phosphorus levels caused by the phosphate binder sevelamer hydrochloride (sevelamer, i.e. crosslinked poly[allylamine hydrochloride]). Rats were fed a diet containing adenine for 4 weeks to establish CRI. Animals were then offered either a normal diet or a diet containing 1 or 3% sevelamer for 8 weeks continuously, or intermittently with sevelamer diet or a normal diet offered for alternating 2-week periods. Changes in the serum levels of phosphorus, calcium, PTH, FGF23, and 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) were monitored over time. Adenine-treated rats developed severe CRI, with markedly elevated serum levels of phosphorus, PTH and FGF23, and reduced levels of serum 1,25(OH)(2)D(3). Continuous treatment with sevelamer suppressed these increases throughout the study period. Serum phosphorus, PTH, and FGF23 levels decreased rapidly when sevelamer treatments commenced and recovered rapidly once they were discontinued. However, the changes in serum FGF23 levels began after the onset of changes in serum phosphorus and PTH levels. In conclusion, circulating PTH, and FGF23 levels can be promptly manipulated through the control of serum phosphorus levels. Moreover, phosphate-binder treatment can effectively inhibit the elevation of serum FGF23 levels, as well as PTH levels, under conditions of CRI.

We present first-principles calculations of electron transport, in particular, the conduction channels of monatomic Al and Na atom wires bridged between metallic jellium electrodes. The electronic structures are calculated by the first-principles recursion-transfer matrix method, and the conduction channels are investigated using the eigenchannel decomposition ͑ECD͒ of the conductance, the local density of states ͑LDOS͒, and the current density. The ECD is different from the conventional decomposition of atomic orbitals, and the study of decomposed electronic structures is shown to be effective in clarifying the details of transport through atomic wires. We show channel transmissions, channel resolved LDOS, and channel resolved current density, and elucidate the number of conduction channels, the relation between atomic orbitals and the channels, and their dependency on the geometry of the atomic wire. We demonstrate that stretching of the bent wire can explain the mechanism of the increase of conductance of Al during the elongation of the contacts. The behavior of our calculated conductance and channel transmissions during the stretching process is in good agreement with the experimental data.

Polymer solar cells are one of the promising energy sources because of the easy solution-processable production with large area at a low cost without toxicity. Among the polymer materials, a donor-acceptor conjugated copolymer PTB7 has been extensively studied because of the typical high-performance polymer solar cells. Here, we show operando direct observation of charge accumulation in PTB7:PCBM blend solar cells from a microscopic viewpoint using electron spin resonance spectroscopy. The accumulation of ambipolar charges in the PTB7-based cells is directly observed for the first time, which shows a clear correlation with the performance deterioration during device operation. The sites of the ambipolar charge accumulation are elucidated at the molecular level, whose information would be useful for improving the cell durability in addition to the performance improvement.