Photocatalytic CO2 Reduction Using Cu(I) Photosensitizers with a Fe(II) Catalyst.

Photocatalytic systems developed from complexes with only abundant metals, i.e., Cu(I)(dmp)(P)2(+) (dmp =2,9-dimethyl-1,10-phenanthroline; P = phosphine ligand) as a redox photosensitizer and Fe(II)(dmp)2(NCS)2 as a catalyst, produced CO as the main product by visible light irradiation. The best photocatalysis was obtained using a Cu(I) complex with a tetradentate dmp ligand tethering two phosphine groups, where the turnover number and quantum yield of CO formation were 273 and 6.7%, respectively.

Synthesis and strong photooxidation power of a supramolecular hybrid comprising a polyoxometalate and Ru(II) polypyridyl complex with zinc(II).

A novel method for constructing supramolecular hybrids composed of polyoxometalates and photofunctional metal complexes was developed. A Ru(II) complex with phosphonate groups (RuP) strongly interacted with Zn(II) to afford a 2 : 1 trinuclear metal complex ([(RuP)2Zn](3+)). In dimethylsulfoxide, [(RuP)2Zn](3+) strongly interacted with a Keggin-type heteropolyoxometalate (Si-WPOM) to form a 1 : 1 hybrid ([(RuP)2Zn]-POM). Irradiation of [(RuP)2Zn]-POM in the presence of diethanolamine caused rapid accumulation of the one-electron reduced hybrid with a quantum yield of 0.99.

Air-tolerant Fabrication and Enhanced Thermoelectric Performance of n-Type Single-walled Carbon Nanotubes Encapsulating 1,1'-Bis(diphenylphosphino)ferrocene.

The thermally-triggered n-type doping of single-walled carbon nanotubes is demonstrated using 1,1'-bis(diphenylphosphino)ferrocene, a novel n-type dopant. Through a simple thermal vacuum process, the phosphine compounds are moderately encapsulated inside single-walled carbon nanotubes. The encapsulation into SWNTs is carefully characterized using Raman/X-ray spectroscopy and transmission electron microscopy. This easy-to-handle doping with air-stable precursors for n-type SWNTs enables the large-scale fabrication of thermoelectric materials showing an excellent power factor exceeding approximately 240 µW mK(-2) .

Molecular basis for promoter selectivity of the transcriptional activator OmpR of Escherichia coli: isolation of mutants that can activate the non-cognate kdpABC promoter.

Escherichia coli has two osmo-responsive two-component regulatory systems, the EnvZ-OmpR and KdpD-KdpE systems, each of which consists of a sensor histidine protein kinase and a response regulator. The OmpR and KdpE response regulators belong to the same family of DNA-binding proteins, and act as positive transcriptional factors in response to the medium osmolarity. However, OmpR specifically activates the ompC gene encoding the OmpC outer membrane protein, whereas KdpE exclusively activates the kdpABC operon encoding the high-affinity Kdp potassium-transporter. To gain insight into the molecular basis for such strict promoter selectivity, we isolated OmpR mutants that can activate the non-cognate kdpABC promoter in vivo. For these OmpR mutants, it was found that a few common and crucial amino acids are responsible for the altered property of OmpR (e.g., Gly-164, Glu-193). In vitro properties of these OmpR mutants were further examined by means of DNA-binding assays and DNA-footprinting analyses with reference to the kdpABC promoter. These results were interpreted on the basis of the three-dimensional structure of the C-terminal half of OmpR, which consists of a DNA-binding helix-turn-helix motif and a RNA polymerase-interacting surface. The results of this study were best explained by assuming that the isolated OmpR mutants have an altered property with regard to the interaction with RNA polymerase on the kdpABC promoter. We propose that the promoter selectivity of OmpR is determined not only by its DNA-binding specificity, but also by the spatial configuration of the promoter on which OmpR must properly associate with RNA polymerase.

Chronological changes of sympathetic outflow to muscles in amyotrophic lateral sclerosis.

To confirm correlations between muscle sympathetic nerve activity (MSNA) and patients' chronological data, we selected 40 consecutive patients with sporadic amyotrophic lateral sclerosis (ALS) recorded by similar methods. MSNA at rest was quantified as the number of sympathetic bursts per 100 heartbeats and as the value expressed as a percentage of the predicted value based on control data. Twelve patients who underwent recordings of MSNA twice at intervals of 6 months or more showed marked decreases in MSNA amplitudes and frequencies between examinations. There was a slightly positive correlation between the frequency of MSNA and age, though younger patients exhibited higher values of MSNA than older patients. The standardized value of MSNA correlated negatively with disease duration and disability levels (p<0.01, 0.05, respectively), but several patients with duration shorter than 12 months showed low values of MSNA. Twelve patients who underwent repeated recordings of MSNA showed a significant decrease in the mean standardized value of MSNA (102.6+/-24.9%) at the second examination, compared to the value (114.3+/-18.9%) at the first one. In ALS, sympathetic outflow to muscles tends to increase initially and then decrease with increasing age and duration. This pattern may be similar to chronological changes at motor neurons.

Dose-related attenuation of cardiac sympathetic nerve activity and intracardiac conduction with thoracic epidural clonidine in alpha-chloralose-anesthetized cats.

Epidural clonidine produces hypotension, bradycardia and sympatholysis. We studied the dose-effects of thoracic epidural and intravenous clonidine (1 to 8 microg/kg) on cardiac sympathetic nerve activity (CSNA), hemodynamics and intracardiac conduction in cats anesthetized with alpha-chloralose. Mean arterial pressure was decreased with epidural clonidine doses above 2 microg/kg, and to a greater extent with 4 microg/kg than 8 microg/kg. Sinus heart rate, Wenckebach atrial rate and CSNA were significantly decreased and corrected sinus node recovery time and Atrium-His interval were significantly prolonged with doses above 2 microg/kg. Vagotomy induced no significant change in these parameters. Thoracic epidural clonidine doses above 2 microg/kg caused a similar extent of sympatholysis. Less of CSNA decrease and hemodynamic changes by intravenous clonidine suggested that sympatholysis caused by epidural clonidine was primarily mediated by spinal mechanism, although hemodynamic changes were influenced by clonidine systemically redistributed from epidural space. Vagal facilitation played no role in suppression of the sinoatrial and AV nodal functions.

Systematic conversion of single walled carbon nanotubes into n-type thermoelectric materials by molecular dopants.

Thermoelectrics is a challenging issue for modern and future energy conversion and recovery technology. Carbon nanotubes are promising active thermoelectic materials owing to their narrow bandgap energy and high charge carrier mobility, and they can be integrated into flexible thermoelectrics that can recover any waste heat. We here report air-stable n-type single walled carbon nanotubes with a variety of weak electron donors in the range of HOMO level between ca. -4.4 eV and ca. -5.6 eV, in which partial uphill electron injection from the dopant to the conduction band of single walled carbon nanotubes is dominant. We display flexible films of the doped single walled carbon nanotubes possessing significantly large thermoelectric effect, which is applicable to flexible ambient thermoelectric modules.

Analysis of the relationship between muscle sympathetic nerve activity and cardiac 123I-metaiodobenzylguanidine uptake in patients with Parkinson's disease.

To analyze the correlation between muscle sympathetic nerve activity (MSNA) and cardiac (123)I-metaiodobenzylguanidine (MIBG) uptake in patients with Parkinson's disease (PD), we measured both parameters in 14 PD patients who were 51 to 82 years of age (mean, 63.1 +/- 8.7 years). The duration of PD was 2 to 26 years, and the disability level (modified Hoehn and Yahr stage) ranged from 2.0 to 4.0 (mean, 3.2 +/- 0.5). MSNA was recorded from the peroneal nerve fascicles using microneurographic methods, and then cardiac MIBG scintigraphy was performed within 1 month. We analyzed the correlation between the standardized MSNA, expressed as a percentage of the predicted value based on control subject data, and the heart-to-mediastinum ratio (H/M) or washout ratio (WR) from early and delayed MIBG images. The relationships between disease duration or disability and MSNA, the H/M ratio, or the WR were also analyzed. No significant correlations were found between MSNA and H/M ratio or WR. Although MSNA was inversely correlated with disease duration and with disability level, neither the H/M ratio nor the WR showed a significant correlation with disease duration or disability level. Because MSNA and MIBG abnormalities were not related, functional changes in addition to organic changes in cardiac sympathetic nerve endings may result in abnormal uptake of MIBG in Parkinson's disease. .

Epidural clonidine suppresses the baroreceptor-sympathetic response depending on isoflurane concentrations in cats.

Epidural administration of clonidine induces hypotension and bradycardia secondary to decreased sympathetic nerve activity. In this study, we sought to elucidate the change in baroreflex response caused by epidural clonidine. Thirty-six cats were allocated to six groups (n = 6 each) and were given either thoracic epidural clonidine 4 micro g/kg or lidocaine 2 mg/kg during 0.5, 1.0, or 1.5 minimum alveolar anesthetic concentration (MAC) isoflurane anesthesia. Heart rate (HR), mean arterial blood pressure (MAP), and cardiac sympathetic nerve activity (CSNA) were measured. Depressor and pressor responses were induced by IV nitroprusside 10 micro g/kg and phenylephrine 10 micro g/kg, respectively. Baroreflex was evaluated by the change in both CSNA and HR relative to the peak change in MAP (deltaCSNA/deltaMAP and deltaHR/deltaMAP, respectively). These measurements were performed before and 30 min after epidural drug administration. Epidural clonidine and lidocaine decreased HR, MAP, and CSNA by similar extents. deltaCSNA/deltaMAP and deltaHR/deltaMAP for depressor response were suppressed with epidural lidocaine and clonidine in all groups but the clonidine 0.5 MAC isoflurane group (0.197 +/- 0.053 to 0.063 +/- 0.014 and 0.717 +/- 0.156 to 0.177 +/- 0.038, respectively, by epidural lidocaine [P < 0.05] but 0.221 +/- 0.028 to 0.164 +/- 0.041 and 0.721 +/- 0.177 to 0.945 +/- 0.239, respectively, by epidural clonidine during 0.5 MAC isoflurane). Those for pressor response were suppressed in all groups. We conclude that thoracic epidural clonidine suppresses baroreflex gain during isoflurane anesthesia >1.0 MAC but may offer certain advantages compared with epidural lidocaine during 0.5 MAC isoflurane by virtue of preserving baroreflex sensitivity when inadvertent hypotension occurs.