Precise spectroscopy of 167Er:Y2SiO5 based on laser frequency stabilization using a fiber laser comb.

Precise spectroscopy of the hyperfine level system of 167Er-doped Y2SiO5 was achieved in the frequency domain. By using an optical frequency comb to stabilize the light source frequency to an accuracy on the order of hertz on a long-term scale, Allan deviation < 10 Hz was achieved for an integration time of 180 s. As a result, spectral hole-burning experiments yielded a more accurate hole spectrum with a narrow homogeneous linewidth. The method opens the way to the straightforward exploration of relaxation mechanisms in the frequency domain by simple steady-state measurements.

Effect of structure and composition on optical properties of Er-Sc silicates prepared from multi-nanolayer films.

Polycrystalline Er-Sc silicates (Er(x)Sc(2-x)SiO5 and Er(x)Sc(2-x)Si2O7) were fabricated using multilayer nanostructured films of Er2O3/SiO2/Sc2O3 deposited on SiO2/Si substrates by RF- sputtering and thermal annealing at high temperature. RBS, TEM, GIXD, and PL results show the presence of Er(x)Sc(2-x)SiO5 with an emission peak at 1528 nm for annealing from 900 to 1100 °C, and Er(x)Sc(2-x)Si2O7 with an emission peak at 1537 nm for higher annealing temperature. The PL intensity of the Er(x)Sc(2-x)Si2O7 phase is five times stronger than that of the Er(x)Sc(2-x)SiO5 phase at 1250 °C. From PLE and PL spectra of Er(x)Sc(2-x)Si2O7 thin film, we schematically illustrate the Er³âº Stark energy levels of 4I(13/2) to 4I(15/2) manifolds due to the crystal field strength effect of Sc³âº. Temperature-dependent PL of the Er(x)Sc(2-x)Si2O7 phase exhibits a variation of the full-width at half-maximum (FWHM) from 1.1 to 2.3 nm. The narrow FWHM is due to the small ionic radii of Sc³âº, which enhance the crystal field strength affecting the optical properties of Er³âº ions located at the well-defined lattice sites of Sc silicate. A large excitation cross-section (σ(ex)) is equal to 3.0x10⁻²° cm² at λ(ex) = 1527.6 nm.

Cavity-QED assisted attraction between a cavity mode and an exciton mode in a planar photonic-crystal cavity.

The photoluminescence spectra from a quantum-dot exciton weakly-coupled to a planar photonic-crystal cavity is experimentally investigated by temperature tuning. Significant resonance shifts of the cavity mode are observed as the cavity mode spectrally approaches that of the exciton mode, showing the appearance of cavity-to-exciton attraction or mode pulling. Cavity-mode spectral shifts are also found theoretically using a master equation model that includes incoherent pump processes for the coupled exciton and cavity, pure dephasing, and allows for photon emission via radiation modes and the leaky cavity mode. Both experiments and theory show clear cavity mode spectral shifts in the photoluminescence spectra, when certain coupling parameters are met. However, discrepancies between the experimental data and theory, including more pronounced spectral shifts in the measurements, indicate that other unknown mode-pulling effects may also be occurring.

Coherent transfer of orbital angular momentum to excitons by optical four-wave mixing.

We demonstrate the coherent transfer of optical orbital angular momentum (OAM) to the center of mass momentum of excitons in semiconductor GaN using a four-wave mixing (FWM) process. When we apply the optical vortex (OV) as an excitation pulse, the diffracted FWM signal exhibits phase singularities that satisfy the OAM conservation law, which remain clear within the exciton dephasing time (approximately 1ps). We also demonstrate the arbitrary control of the topological charge in the output signal by changing the OAM of the input pulse. The results provide a way of controlling the optical OAM through carriers in solids. Moreover, the time evolution of the FWM with OAM leads to the study of the closed-loop carrier coherence in materials.

Cavity mode emission in weakly coupled quantum dot--cavity systems.

We study the origin of bright leaky-cavity mode emission and its influence on photon statistics in weakly coupled quantum dot - semiconductor cavity systems, which consist of a planar photonic-crystal and several quantum dots. We present experimental measurements that show that when the system is excited above the barrier energy, then bright cavity mode emissions with nonzero detuning are dominated by radiative recombinations of deep-level defects in the barrier layers. Under this excitation condition, the second-order photon autocorrelation measurements reveal that the cavity mode emission at nonzero detuning exhibits classical photon-statistics, while the bare exciton emission shows a clear partial anti-bunching. As we enter a Purcell factor enhancement regime, signaling a clear cavity-exciton coupling, the relative weight of the background recombination contribution to the cavity emission decreases. Consequently, the anti-bunching behavior is more significant than the bare exciton case - indicating that the photon statistics becomes more non-classical. These measurements are qualitatively explained using a medium-dependent master equation model that accounts for several excitons and a leaky cavity mode.

Quality factor control and lasing characteristics of InAs/InGaAs quantum dots embedded in photonic-crystal nanocavities.

We demonstrate lasing action with a high spontaneous emission factor and temperature insensitivity in InAs/InGaAs quantum dots (QD) embedded in photonic crystal nanocavities. A quality factor (Q) of over 10,000 was achieved by suppressing the material absorption by QDs uncoupled to the cavity mode. High Q cavities exhibited ultra low threshold lasing with a spontaneous emission factor of 0.7. Less frequent carrier escape from the QDs, which was primarily favored by high potential barrier energy, enabled low threshold lasing up to 90 K.

Cavity polaritons in InGaN microcavities at room temperature.

Cavity polaritons are observed in InGaN quantum well (QW) microcavities at room temperature. High-quality microcavities are fabricated by the wafer-bonding of InGaN QW layers and dielectric distributed Bragg reflectors. The anticrossing behavior of strong exciton-photon coupling is confirmed by vacuum-field Rabi splitting obtained from reflection measurements. This strong coupling is also enhanced by increasing the integrated oscillator strength coupled to the cavity mode. The oscillator strength of InGaN QW excitons is 1 order of magnitude larger than that of GaAs QW excitons.

Neurotropism of swine haemagglutinating encephalomyelitis virus (coronavirus) in mice depending upon host age and route of infection.

Mice aged 1, 4 or 8 weeks were inoculated with haemagglutinating encephalomyelitis virus (HEV), strain 67N, by the intracerebral (i.c.), intranasal (i.n.), intraperitoneal (i.p.), subcutaneous (s.c.), intravenous (i.v.) or oral route, with different doses. In 1-week-old mice, mortality and mean time to death were mostly the same regardless of the inoculation route, except for the oral route, which appeared to be the least effective. The virus killed 4-week-old mice readily by all routes of inoculation except the oral, and 8-week-old mice by i.c., i.n. or s.c. inoculation. In descending order of efficacy, the routes of HEV infection were: i.c., i.n., s.c., i.p., i.v. and oral. To follow the spread of HEV from peripheral nerves to the central nervous system (CNS), the virus was inoculated subcutaneously into the right hind leg of 4-week-old mice. The virus was first detected in the spinal cord on day 2, and in the brain on day 3. The brain titres became higher than those of the spinal cord, reaching a maximum of 10(7)PFU/0.2 g when the animals were showing CNS signs. Viral antigen was first detected immunohistochemically in the lumbar spinal cord and the dorsal root ganglion ipsilateral to the inoculated leg; it was detected later in the pyramidal cells of the hippocampus and cerebral cortex, and in the Purkinje cells of the cerebellum but not in the ependymal cells, choroid plexus cells or other glial cells. The infected neurons showed no cytopathological changes.

Redox properties and coordination structure of the heme in the co-sensing transcriptional activator CooA.

The CO-sensing transcriptional activator CooA contains a six-coordinate protoheme as a CO sensor. Cys(75) and His(77) are assigned to the fifth ligand of the ferric and ferrous hemes, respectively. In this study, we carried out alanine-scanning mutagenesis and EXAFS analyses to determine the coordination structure of the heme in CooA. Pro(2) is thought to be the sixth ligand of the ferric and ferrous hemes in CooA, which is consistent with the crystal structure of ferrous CooA (Lanzilotta, W. N., Schuller, D. J., Thorsteinsson, M. V., Kerby, R. L., Roberts, G. P., and Poulos, T. L. (2000) Nat. Struct. Biol. 7, 876-880). CooA exhibited anomalous redox chemistry, i.e. hysteresis was observed in electrochemical redox titrations in which the observed reduction and oxidation midpoint potentials were -320 mV and -260 mV, respectively. The redox-controlled ligand exchange of the heme between Cys(75) and His(77) is thought to cause the difference between the reduction and oxidation midpoint potentials.

Control of CooA activity by the mutation at the C-terminal end of the heme-binding domain.

A constitutively active mutant of a CooA, in which Met131 was replaced by Leu, was isolated by random mutagenesis. Site-directed mutagenesis at position 131 revealed that M131R-CooA was also constitutively active even in the absence of CO and that M131P-, M131D-, and M131E-CooA were constitutively inactive regardless of the presence or absence of CO. While M131L- and M131E-CooA showed almost the same electronic absorption spectra as those of the wild type in the ferric, ferrous, and CO-bound forms, M131D-CooA showed the typical spectrum of a five-coordinate heme protein in the ferric form. The conformational change around the heme induced by CO binding, which triggers the activation of CooA, is thought to be linked to the rearrangement of the conformation around the hinge region between the heme-binding and DNA-binding domains and/or of the relative orientation of the two domains to activate CooA.

CO sensing and regulation of gene expression by the transcriptional activator CooA.

The transcriptional activator CooA from Rhodospirillum rubrum contains a six-coordinate protoheme that acts as a CO sensor in vivo. CO is a physiological effector of CooA and replaces one of the axial ligands of the ferrous heme to form the CO-bound CooA that is active as the transcriptional activator. Cys75 or His77 is coordinated to the ferric and ferrous hemes in CooA, respectively. The redox-controlled ligand exchange between Cys75 and His77 proceeds during the change in the redox state of the heme. The reduction and oxidation midpoint potentials of CooA have been determined to be -320 and -260 mV, respectively. The properties of a functional chimera derived from CRP and CooA suggest that CooA activates the transcription by a similar mechanism to that for CRP at Class II CRP-dependent promoters. Alanine-scanning mutagenesis has revealed that Arg24 and Arg53 of CooA, which will be concerned with the protein-protein interaction with RNA polymerase, are critical amino acid residues for the transcriptional activator activity of CooA, and that Lys26 and Asp94 modulate the activity of CooA.

Mobilization of primitive haemopoietic progenitor cells and stem cells with long-term repopulating ability into peripheral blood in mice by pegylated recombinant human megakaryocyte growth and development factor.

We investigated in detail the effect of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) on peripheral blood progenitor cell (PBPC) mobilization in male BDF1 mice. Treatment with PEG-rHuMGDF for 5 d stimulated a striking expansion of the circulating levels of multiple types of colony-forming units in culture (CFU-c), including CFU-granulocyte-macrophage, CFU-megakaryocyte, burst-forming units-erythroid, and multipotent CFU-c, and primitive day-12 CFU-spleen. All of these progenitors were mobilized into the peripheral blood (PB) with similar kinetics; their numbers peaked after the cessation of treatment and then declined earlier than platelet numbers peaked. The maximal increase in any of the four CFU-c in the PB was attained with at least 300 microg/kg/d of PEG-rHuMGDF, whereas peripheral platelet counts plateaued at 30 microg/kg/d. Adoptive transfer with PB from PEG-rHuMGDF-treated donor mice resulted in greater survival of lethally irradiated recipients. The majority of the recipients that survived at 187 d after transplantation with PEG-rHuMGDF-mobilized PB showed significant donor engraftment at the progenitor cell level. The combined administration of appropriate doses of PEG-rHuMGDF and recombinant human granulocyte colony-stimulating factor induced a synergistic increase in the circulating levels of the four CFU-c compared to either factor alone. These results indicate that PEG-rHuMGDF as a single agent can mobilize a full spectrum of PBPCs in mice.

Inhibitory effect of nicotinamide to paraquat toxicity and the reaction site on complex I.

The inhibitory effect and mechanism of action of nicotinamide to paraquat toxicity were studied in male Sprague-Dawley rats. Proteins of submitochondrial particles (SMP), especially of mol. wt. 25-30 kDa, in rat lungs were destroyed by paraquat radicals, and aggregated protein bands approximately 100 kDa were observed by polyacrylamide electrophoresis. The competitive inhibition effects were observed of nicotinamide on NADH oxidation by paraquat via SMP in rat lungs and the Ki was 9.3 mM. The inhibitory effects of nicotinamide on lipid peroxidation by paraquat with rat lung and liver SMP were verified. The times of occurrence of dyspnea and death in rats after paraquat exposure were delayed by nicotinamide administration. The activity of NADH: ubiquinone reaction of NADH:ubiquinone oxidoreductase (complex I) in rat lung was reduced 24 h after paraquat exposure, and was protected by nicotinamide. The activity of NADH:ferricyanide reaction of complex I was, however, reduced by administration not only of paraquat but also nicotinamide. These results imply that nicotinamide is inhibitory to paraquat toxicity. Nicotinamide, paraquat, and ferricyanide may react at overlapping sites on complex I.

Sensitive plaque assay and propagation of Chuzan (Kasba) virus, a Palyam serogroup orbivirus, in BHK-21 cells.

Various factors influencing plaque formation of Chuzan virus in BHK-21 cell monolayers were studied and a practical method for plaque assay was developed. On addition of trypsin (5 micrograms/ml) and/or diethylaminoethyl (DEAE)-dextran (50 micrograms/ml) to the virus diluent as the virus adsorption medium and agar overlay medium, the number of plaques increased. When 100 micrograms/ ml DEAE-dextran was added to the diluent and overlay medium, plaques were produced in about 10-fold higher numbers than without trypsin and DEAE-dextran. Based on these results, a practical plaque assay method for Chuzan virus was established. Using this method, one-step growth of Chuzan virus was performed at an input multiplicity of 25 plaque-forming units (PFU) per cell. Cytopathic effects were first observed at 7.5 h post-inoculation (p.i.), and were complete at 12 h p.i. The titre of cell-associated virus, after gradual decline during the first 3 h of incubation, showed a rise within 4.5 h p.i. and a rise to a plateau of 10(6.3)PFU/0.2 ml at 12 h p.i. By indirect immunofluorescence, virus-specific antigen was detected in the cytoplasm of the cells at 4.5 h p.i., and all the cells fluoresced at 6 h p.i. Haemagglutination activity was first detected in infected whole cultures at 7.5 h p.i. reaching a plateau of 1:64 at 15 h p.i. Plaque formation and haemagglutination by the virus were specifically inhibited by antisera against the original and the plaque-cloned virus.

Effects of paraquat on mitochondrial electron transport system and catecholamine contents in rat brain.

The effects of paraquat on rat brain were studied. Activities of complex I (NADH: ubiquinone oxidoreductase) in mitochondrial electron transport system, lipid peroxidation and the amount of catecholamines in rat brain were measured after acute paraquat exposure. Complex I activities were significantly lower and lipid peroxides were higher in the brains of a paraquat-treated group than in those of a control group. Lipid peroxide in rat serum, however, did not increase after paraquat exposure. A study of the time dependency of paraquat effects disclosed that mitochondrial complex I activities in rat brain as well as those in rat lung and liver gradually decreased prior to the appearance of respiratory dysfunction. As compared to controls, the dopamine in rat striatum was significantly lower in the paraquat-treated group. These results suggest that paraquat after crossing the blood-brain barrier might be reduced to the radical in rat brain, which may damage the brain tissue, especially dopaminergic neurons in striatum. We therefore propose that cerebral damage should be taken into consideration on paraquat exposure. Patients may therefore need to be followed up after exposure to high doses of paraquat.

Radical formation site of cerebral complex I and Parkinson's disease.

Paraquat was reduced to the paraquat radical via complex I in bovine cerebral mitochondria and accelerated lipid peroxidation. Thirty-kilodalton subunit of complex I was considered to be the radical formation site, because of its marked destruction by the paraquat radical. The lipid peroxidation by the paraquat radical was suppressed not only by superoxide dismutase (SOD) but also by mannitol. The destruction of complex I subunits via lipid peroxidation must have been caused by the hydroxyl radical which was formed from the superoxide radical. The same phenomenon was observed by using 1-methylnicotinamide (MNA), which contains the same partial structure as paraquat in itself and is metabolized from nicotinamide in a living body. We observed NADH oxidation by MNA via cerebral complex I (Km = 26.3 mM), and MNA destroyed some complex I subunits, especially 30-kilodalton protein. Paraquat might be useful for studying the pathogenesis of Parkinson's disease (PD) in vitro, and MNA is expected to be one of the causal substances of PD from the viewpoint of the oxidative stress theory.

Isolation and characterization of sialodacryoadenitis virus (coronavirus) from rats by established cell line LBC.

The outbreak of sialoadenitis occurred in a laboratory rat colony and the causative agent was isolated from the affected salivary glands of diseased rats using the established cell line LBC. The isolate readily multiplied, producing clear cytopathic effects with syncytium formation, and it was identified virologically and serologically as rat sialodacryoadenitis virus. In attempts to isolate the virus by primary rat kidney (PRK) cells and suckling mice as well as LBC cells, the LBC cells showed higher susceptibility for the virus growth as compared with PRK cells or the brain of suckling mice. The isolation rate of virus was 100% (5/5) in LBC, 40% (2/5) in PRK cells and 60% (3/5) in suckling mice. After four passages in the LBC cells, the virus did not produce disease in adult rats, while the mouse brain-passaged virus did.

Evaluation of long-term survivors after pancreatoduodenectomy for pancreatoduodenal carcinoma.

Long-term survivors (> or = 5 years) of pancreatoduodenal carcinoma were evaluated. The absence of retropancreatic invasion seemed to be an important factor for long-term survival in carcinoma of the pancreatic head, carcinoma of the intrapancretic bile duct confined within the bile duct wall, and stage II papilla of Vater carcinoma. The mode of infiltration was INF alpha or INF beta, with a low infiltration tendency. Lymph node metastasis, when present, was confined to the pancreatic head. It is noteworthy that two of the patients with intrapancreatic bile duct cancer had perineural infiltration to the pancreatic head plexus. In patients treated by extended resection, postoperative malnutrition and diarrhea was severe, indicating the importance of long-term nutritional management.

Ocular injury caused by Preeglox-L, a herbicide containing paraquat, diquat and surfactants.

Two patients were splashed in the eye accidentally with an aliquot of Preeglox-L, a herbicide containing paraquat, diquat and surfactants. Despite immediate flushing of the eye with copious amounts of water, in both cases the corneal epithelium deteriorated one to two weeks after the incident. Thereafter, the lesions in each eye healed gradually.