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This paper presents a new computation method to determine simultaneously the optimal parameters of several voltage regulators such as the load-ratio control transformer (LRT) and step voltage regulator (SVR) installed in a radial distribution network. The proposed method determines a combination of their control parameters by minimizing the weighted sum of deviations of line voltage from the upper and lower voltage limits and the amounts of voltage violations by referring to the stored data measured by IT switches, which are sectionalizing switches with sensors installed in the distribution feeder. The optimization algorithm is based on particle swarm optimization (PSO), which is one of the nonlinear optimization methods, by using the concept of swarm intelligence. In order to confirm the validity of the proposed method, numerical simulations are carried out on a distribution network model. © 2008 Institute of Electrical Engineers of Japan. Published by John Wiley & Sons, Inc.

In this paper, we propose an experimental multiobjective evaluation method based on the use of distribution network equipment to evaluate distribution network configuration candidates with distributed generators (DGs), such as photovoltaic generation systems and wind power generation systems, by hourly changing states of sectionalizing switches satisfying constraints of voltage and line current limit. In the proposed experimental multiobjective evaluation method, the optimal network configuration is determined by using multiobjective evaluation based on total distribution loss rate, maximum voltage total harmonic distortion, and maximum voltage imbalance rate in order to reduce distribution loss and to keep power quality. The proposed method is applied to radial and loop distribution network configurations by using an experiment of scaled-down three-phase distribution network with 1 bank distribution transformer, 5 distribution lines, 5 sectionalizing switches, 12 single-phase loads, and 5 DGs. © 2008 Institute of Electrical Engineers of Japan. Published by John Wiley & Sons, Inc.

To gain insight into the molecular mechanism for nociceptin function, functional coupling of the nociceptin receptor expressed in Chinese hamster ovary (CHO) cells with phospholipase A 2 (PLA 2 ) was examined. In the presence of A23187, a calcium ionophore, activation of the nociceptin receptor induced time- and dose-dependent release of arachidonate, which was abolished by pretreatment of the cells with pertussis toxin (PTX). Immunoblot analysis using anti-Ca 2+ -dependent cytosolic PLA 2 (cPLA 2 ) monoclonal antibody demonstrates that activation of the nociceptin receptor induces a time- and dose-dependent electrophoretic mobility shift of cPLA 2 , suggesting that phosphorylation of cPLA 2 is induced by the nociceptin receptor. Pretreatment of the cells with PD98059, a specific mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 inhibitor, or staurosporine, a potent inhibitor of serine/threonine protein kinases and tyrosine protein kinases, partially inhibited the nociceptin-induced cPLA 2 phosphorylation and arachidonate release. These results indicate that the nociceptin receptor expressed in CHO cells couples with cPLA 2 through the action of PTX-sensitive G proteins and suggest that cPLA 2 is activated by phosphorylation induced by the nociceptin receptor via mechanisms partially dependent on p44 and p42 mitogen-activated protein kinases.

1 To approach the mechanisms underlying desensitization of the opioid receptor-mediated Ca2+ channel inhibition, the effects of prolonged application of [D-Ala2, D-Leu5]enkephalin (DADLE) on Ba2+ currents (IBa) through Ca2+ channels were analysed in NG108-15 neuroblastoma × glioma hybrid cells. 2 Inhibition of IBa by 100 nM DADLE desensitized by 57% with a time constant of 4.4 min. 3 Maximal desensitization of the δ-opioid receptor-Ca2+ channel coupling was attained by 1 μM DADLE. The EC50 value for desensitization was estimated to be 78 nM. 4 RNA blot hybridization analysis and immunoblot analysis revealed the expression of β-adrenoceptor kinase-1 (βARK1) in NG108-15 cells. 5 Heparin, an inhibitor of βARK, significantly reduced the magnitude and rate of desensitization, whereas Rp-cyclic AMPS and PKI (14-24)amide, inhibitors of cyclic AMP-dependent protein kinase (PKA), or long-term treatment with phorbol 12-myristate 13-acetate to induce down-regulation of protein kinase C (PKC) had no significant effect. 6 Recovery from desensitization (resensitization) proceeded with a time constant of 6.7 min. Okadaic acid, an inhibitor of serine/threonine phosphatases 1 and 2A, significantly attenuated the degree of resensitization. 7 In summary, we have characterized the time course and concentration-dependence of the desensitization of DADLE-induced IBa inhibition in NG108-15 cells. This desensitization was reversible after removal of DADLE. It is suggested that βARK, but neither PKA nor PKC, is involved in desensitization, while serine/threonine phosphatases mediate resensitization. British Journal of Pharmacology (1998) 123, 1111–1118; doi:10.1038/sj.bjp.0701733

BACKGROUND Acetylcholine (ACh) is one of the major excitatory neurotransmitters in the central nervous system, and changes in neural activity induced by anesthesia alter the release of ACh. However, the effects of isoflurane, one of the most widely used volatile anesthetics, on ACh release are not known. The present study attempts to clarify the dose-effect relationship of isoflurane on the in vivo release of ACh in rat brains. METHODS Changes in the extracellular concentration of ACh and choline in the cerebral cortex and striatum induced by 0.5, 1.0, and 1.5 minimum alveolar concentration (MAC) of isoflurane were determined using a brain microdialysis technique. RESULTS In the cortex, the ACh release decreased to 30.8+/-10.1 (mean+/-SEM), 10.2+/-4.1, and 8.1+/-2.9% of basal value by increasing doses of isoflurane, and in the striatum, to 73.3+/-4.4, 49.2+/-4.2, and 40.7+/-4.5%. The ACh release rapidly recovered control levels with the discontinuance of isoflurane. Choline concentration was not changed significantly by isoflurane except for a decrease to 74.8+/-4.6% in the striatum by 0.5 MAC. In both the cortex and striatum, the choline concentration decreased with the discontinuance of isoflurane to 70.3+/-13.3, and 68.2+/-5.4%, respectively. CONCLUSION The fact that all classic anesthetics reported previously, as well as isoflurane, reduce ACh release supports the hypothesis that the suppression of cholinergic cells is, at least in part one of the mechanisms of anesthesia.

Effects of amino acid substitutions in the first extracellular loop region of the delta- and mu-opioid receptors were examined. Substitution of lysine-108 of the delta-receptor (delta K108) with asparagine improved affinity to [D-Ala2,MePhe4,Gly-ol5]enk ephalin (DAGO), a mu-selective peptide agonist, to be comparable with that of the mu-receptor. On the other hand, replacement of mN127 with lysine decreased the affinity to DAGO by approximately 15-fold. These results suggest that dK108 and mN127, which correspond to each other in the aligned amino acid sequences, mainly determine the difference in DAGO binding affinity between the delta- and mu-receptors.

To investigate the clinical significance of endothelin (ET), a potent vasoconstrictor peptide, in subarachnoid hemorrhage (SAH) and SAH-related cerebral vasospasm, we measured the ET-like immunoreactivity (ET-LI) in plasma and cerebrospinal fluid (CSF) obtained serially from patients with SAH due to ruptured cerebral aneurysm who underwent aneurysmal surgery. The normal ET-LI levels in plasma and CSF (n = 24) were 12.4 +/- 2.0 (mean +/- s.d.) and 9.1 +/- 1.2 pg.ml-1, respectively. Plasma ET-LI levels in patients with SAH before surgery (16.8 +/- 7.8 pg.ml-1, n = 8) were higher than the normal values (P < 0.05), and became further elevated after surgery (22.5 +/- 9.4 pg.ml-1). ET-LI levels in plasma and CSF one day after surgery were 18.7 +/- 5.5 and 18.4 +/- 6.8 pg.ml-1 (P < 0.01 vs. normal values), respectively, and declined thereafter. The plasma and CSF ET-LI levels in patients who showed symptomatic vasospasm became concomitantly elevated again. These results suggest that ET is involved in SAH-related vasospasm and raise the possibility that surgical stress influences the vasospasm.

The in vitro effects of halothane on the potassium-stimulation-induced efflux of [3H]D-aspartate in rat cerebral cortex slices were studied. The slices were initially incubated with Krebs-Ringer's solution containing [3H]D-aspartate, a putative excitatory transmitter. The slices were then stimulated with high concentrations of K+ in the presence and absence of halothane, and the efflux was measured using a scintillation counter. Halothane, 1% and 2%, had little effect on the potassium-stimulation-induced efflux, but that of 4 and 8% increased the efflux significantly. The spontaneous efflux was unaffected by all concentrations of halothane studied. The control study of pentobarbital, in the concentration of 0.05 to 1.00 mmol/l, reduced the efflux in a dose-related manner. These findings indicate that the release of an excitatory transmitter, aspartate, may not be involved in the mechanism of halothane anaesthesia.

In order to increase the cure rate of gastric cancer, an intraoperative irradiation technique has been developed and applied to 38 patients with this disease. The resectable lesions are treated by surgical procedures, and the remaining malignant remnants sterilized by irradiation with a single massive dose during laparotomy. In this radiotherapy, radiation damage to normal structures is minimized, since normal organs adjacent to the tumor can be shifted from the field so that the lesion may be exposed directly to radiation. The results were analyzed according to stages of the disease and doses delivered. Our clinical results have shown that cure can be expected following intraoperative irradiation of unresectable remnants around major blood vessels, such as the hepatic artery and celiac axis. A single dose of 3500 rad of an electron beam seems to be sufficient as a cancerocidal dose. Indications for intraoperative radiotherapy of gastric cancer are discussed.

The effects th groups the changes in CO and SV were due mainly to a reduced demand of oxygen transport and expected changes in sympatho-adrenergic tone rather than to myocardial depression.

Clinical results of intraoperative radiotherapy in neoplasms of the stomach, colon, pancreas, biliary tract, bladder, prostate, lung, mediastinum and brain, and soft-tissue sarcomas are reported. After resectable lesions were removed at surgery, residual cancer nests were sterilized by irradiation before surgical closure. Since the lesion can be exposed directly to radiation and sensitive normal structures are positioned outside the treatment volume, a cancerocidal dose can be safely and precisely delivered to the cancer without affecting normal structure. The great advantage of the intraoperative electron beam therapy lies in the treatment of radioresistant tumors and lesions located near radiosensitive organs. Several patients with unresectable tumors were treated by the intraoperative technique and are alive after more than 5 years.

Effects of N2O-exposure on the survival rate and growth kinetics of hemopoietic stem cells after irradiation were investigated. LD 50, 30 days after irradiation, was 300 rad for N2O exposed mice and over 550 rad for control mice. Recovery of the pluripotent hemopoietic stem cells (CFU-S) and granulocyte-macrophage progenitor cells (GM-CFC) was significantly delayed in the spleen of N2O-exposed mice after 150 rad irradiation, compared to that of control mice. However, in bone marrow, there was a significant but slight difference in the recovery of GM-CFC and no significant difference in the recovery of CFU-S between the two groups. These results suggest that N2O augments the damage of splenic hemopoiesis in irradiated mice, and this may be responsible for the increased hemopoietic death.

In order to evaluate the effect of isosorbide dinitrate (ISDN), administered as a bolus intravenous injection, on the circulatory response to tracheal intubation, mean arterial pressure (MAP), and heart rate (HR) in response to laryngoscopy for 30 s followed by tracheal intubation were compared in patients not receiving ISDN (control) and receiving 40 micrograms/kg or 80 micrograms/kg of ISDN 45 s before starting laryngoscopy. Each group consisted of 10 patients undergoing elective surgery. Forty-five seconds after starting laryngoscopy, MAP was significantly (P less than 0.01) lower in patients receiving 80 micrograms/kg ISDN than in those receiving no or 40 micrograms/kg ISDN. HR increased to a similar extent in the three groups. These results indicate that a bolus injection of ISDN (80 micrograms/kg) is a simple, practical and highly effective means of attenuating the hypertensive response to direct laryngoscopy and tracheal intubation.