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After the severe seismic disaster, to investigate the damage states of buildings, the experts go to the disaster area, however, they encounter some difficulties. To solve the above problems, this study suggests a damage evaluation system for steel structures, which adopts the concept of Internet of Things (IoT). This system makes it possible for us to hold on damage of a building without going there after an earthquake. It has been recognized that the temperature change occurs on steel materials during inelastic behavior. In other study, the effectiveness of the damage evaluation method was confirmed by using the heat generation of steel at unsteady plastic amplitude. Here, the experimental study and discuss is performed to investigate the effectivity of evaluation method with the history of voltage by thermoelectric devices measured by a microcomputer when subjected to seismic response behavior. The cumulative plastic strain can be estimated from the relationship between temperature and strain of steel using the inverse heat conduction analysis. By dividing the cumulative plastic strain into half cycles, the strain amplitude per half cycle can be estimated, and the degree of damage can be calculated from the strain amplitude. By conducting the above analysis, we could predict damage level of the steel from the history of voltage by thermoelectric devices under the seismic response behavior. In addition, it was also shown that the microcomputer can be used to track the temperature rise of plastic heating in steel.

Recently, in Japan, there are some discussions to promote the use of timber resource in the field of architectural buildings. For examples, some latest mid-rise buildings are constructed using wooden material, such as the facilities of Tokyo Olympic 2020. We can experiment the dairy life and architectural space with timber materials, which often has attracted attention. In Japan, the demand of low-rise prefabricated steel building is recently increasing. However, to satisfy the seismic resistant performance of building, they are required to have lots of seismic resistant wall which restrict layout of wall and opening. The object of this study is to develop low-rise prefabricated steel building with high seismic resistance performance using hybrid structural system using wooden materials. We suggest the method of sandwich panel structures, which steel column is sandwiched by structural plywood connected by bolt joints. To improve productivity and seismic resistance, this paper suggests the construction process using inserted wall sliding construction method. To clarify the resistant mechanism and structural performance, a horizontal loading test is conducted. From the results, the resistant mechanism in the diagonal direction is appeared; it means that the effective resistant system can be obtained. Also, the composite effect of steel and plywood is presented to give the high strength and rigidity. From the observation of test results, the analysis model is assumed. And also, it is confirmed that the proposed model can evaluate the strength of test results.

After the earthquake events, building damage assessment is detected by experts. However, in fact, it takes a long time to conduct the assessment process during field survey. Also, it is worried about ensuring the safety of the surveys. In recent years, structural health monitoring has been attempted. This paper suggests a damage evaluation method based on temperature measurement using thermoelectric devices. The cyclic loading tests were conducted as parameters with the loading amplitude; three types of constant amplitude, and three types of variable amplitude with gradual decrease, gradual increase, and random amplitude, totaling six types of dynamic cyclic bending. As a result of applying the damage evaluation method to the loading test, it was confirmed that the cumulative damage calculated from the temperature measurement and the cumulative damage calculated from the input displacement were almost equal. In addition, seismic response analysis was conducted using an analytical model of a four-story building, and the effectiveness of the measurement method using thermoelectric devices was examined. The results of seismic response analysis shows that the natural frequency of the primary mode of the displacement response was lower than 4Hz, and the results of the sweep loading test confirmed that the thermoelectric devices captured the waveform of the temperature up to 4Hz.

Active and reactive power control using smart inverters (SI) is highly effective in mitigating voltage rise in distribution systems, which is caused by the high penetration of photovoltaic (PV) power generation. However, the voltage control performance depends on the SI settings. We propose a new approach that uniquely determines the parameter settings for volt-VAR-watt control based on the active and reactive power-voltage sensitivity matrix of SIs. Because the voltage sensitivity matrix is calculated based solely on the impedance of the distribution system and it does not vary with time or the number of SIs, the proposed method can determine the individual SI parameter settings theoretically and efficiently without the need for optimization problem formulation, power flow calculation, or communication between the SIs. To evaluate the proposed method, the voltage control performance in a real distribution system model with a large number of PV installations is compared with that of volt-VAR-watt control using default parameters and optimized parameters in case that the load demand and PV generation are given in advance. The results show that the proposed method achieves better control performance than other conventional methods in terms of all the evaluation indices; in particular, it realizes effective control in the case of voltage rise. Furthermore, the proposed method can also achieve the same level of voltage control performance as the optimization results, even though it uses only the voltage sensitivity matrix and SI rating capacities for parameters determination, and the accuracy of the proposed voltage control can be ensured.

The power hardware-in-the-loop (PHIL) simulation has become a popular testing approach due to the flexibility it provides and the high-fidelity of its results. It is expected to be utilized as an advanced laboratory testing scheme to validate the grid support functions of distributed energy resources (DERs) because it can evaluate the interaction between the power system and DERs. Despite the strong demand to utilize the PHIL simulation for such testing, the literature that elaborates on the practical design of PHIL simulation based testing (hereafter called “PHIL testing”) environment including laboratory device setup, power system models, and test procedures is very limited. The simulation models, interfacing with the tested equipment, and data collection approaches are all different parameters that need to be fine-tuned for the successful execution of PHIL testing. It is vital for such successful test experiences to be shared to build universal knowledge around PHIL testing. In order to fill this knowledge gap, this paper presents such practical and essential techniques for the PHIL testing to share the knowledge for promotion of the PHIL simulation utilization. The development of PHIL testing environment to validate the smart inverter functions, i.e., volt-var function and frequency-watt function, is focused on in terms of laboratory setup, power system modeling, interfacing, and test procedure. The volt-var and frequency-watt functions of a 500 kW smart inverter of photovoltaic are validated on the basis of the presented techniques. Detailed test configurations, test procedures, and simulation models are presented along with obtained test results.

Inertia reduction due to inverter-based resource (IBR) penetration deteriorates power system stability, which can be addressed using virtual inertia (VI) control. There are two types of implementation methods for VI control: grid-following (GFL) and grid-forming (GFM). There is an apparent difference among them for the voltage regulation capability, because the GFM controls IBR to act as a voltage source and GFL controls it to act as a current source. The difference affects the performance of the VI control function, because stable voltage conditions help the inertial response to contribute to system stability. However, GFL can provide the voltage control function with reactive power controllability, and it can be activated simultaneously with the VI control function. This study analyzes the performance of GFL-type VI control with a voltage control function for frequency stability improvement. The results show that the voltage control function decreases the voltage variation caused by the fault, improving the responsivity of the VI function. In addition, it is found that the voltage control is effective in suppressing the power swing among synchronous generators. The clarification of the contribution of the voltage control function to the performance of the VI control is novelty of this paper.

Recently, there are many discussions about repairability and recovery on damaged buildings. It is desirable to establish the design manuals for recovery considering continuous use of structures. In our previous researches, the damaged steel members of H-shaped and square tube section were reproduced by loading test. From the loading test results, the inelastic behavior and restoring force characteristics were clarified, and also the analytical model were proposed which can chase test results well. It means that we have already conducted the member based research on repairability. So, in this study, to investigate the inelastic behavior and restoring force characteristics of repaired steel frames, the loading test is performed on half size scaled - partial frame model as parameters with strength ratio of column-beam and panel-beam. It is assumed that the various type of failure mode is generated on original state and repaired state. During loading test on original state, local buckling is observed on H-shaped steel beam. Therefore, the damaged area is repaired by welding cover plates method which is recommended by Japanese restoration manual for damaged building structure by severe seismic disasters. And also, the loading tests on repaired state is performed, and it is confirmed that the strength is restored at the same or high level compared with original state. However, in case of beam failure mode on original state, different failure mode is observed on repaired state. Furthermore, a finite element analysis is performed, and the resistant mechanism during ultimate state is investigated analytically in detail.

A surge of needs for the low carbon society promotes a spread of electric vehicle (EV). EVs could be charged at night simultaneously, as a result, severe voltage drop may happen. The authors have proposed the method which can compensate the voltage drop caused by EV charging by means of adjusting charging schedules and controlling reactive power. And, we have confirmed the effectiveness of the method by estimating steady state in order to figure out the limitation of the control capability. In this paper, from a practical viewpoint, we propose the method to consider dynamic behavior. In this method, the EV can not only finish charging effectively but also control minimal reactive power to keep admissible voltage with monitoring system voltage.

Recently, there have been many discussions about repairability for damaged building structures after severe disasters. In japan, a technical manual for repairing damaged buildings has been established; however, its repair abilities have not been reported sufficiently. In this study, the Box-Shaped Repair Method which has been suggested on Japanese technical guideline is adopted for the damaged steel members, and its applicability and feasibility are investigated experimentally. Herein, the damaged portion on steel member such as plastic hinge or local buckling occurrence is covered with steel plate by welding. So the loading test is performed as parameters with section size of steel members, thickness of cover plate and welding size during repair process, and loading path. The procedure of this study is as follows; the first, the damaged test specimens of H-shaped steel member with local buckling are reproduced by initial loading test. Next, the damaged specimens with plastic residual deformation are returned to the original position. Finally, the loading test is done after repair. From test results, it is confirmed that the fundamental structural performance such as the rigidity, maximum strength, and absorbed energy after repair are improved by comparison of original state. And also, this performance can be controlled by adjusting the thickness of cover plate and welding condition. Furthermore, from the observation of test results, the analytical model of repaired steel member is suggested. From the comparison of test results, it can be said that the proposed model shows good agreements both test results and theoretical figure.

Recently, a lot of building structures have been experienced severe natural disasters, and it was reported that various types of terrible collapse mode were occurred. And also, there are many discussions about repairability and recovery on damaged buildings over the world. In particular, there has been focused on new keyword a²¯ Resilience a²° in any field including structural engineering. In Japan, a technical guideline for repairing damaged buildings has been established. However, the applicability and feasibility of repair method and recovery has not been well reported. Herein, to investigate the recovery and ultimate seismic state of repaired steel framed structures, experimental and analytical studies are conducted. Herein, the actual repairing technique for steel framed structure is suggested. During experimental study, the damaged steel member is reproduced by loading tests with consideration of past reports of mega-earthquake disasters. The next, the damaged portion is repaired by proposed method by use of steel-cover plate technique. After this repair process, the loading test is done again. And the recovery of structural performance is estimated by comparison of original and repaired state. From the test results, it is confirmed that the strength and ductility are improved after repair. Furthermore, the analytical model and restoring force characteristics of repaired steel member are suggested by observation of ultimate behavior during loading test. Here, the purpose on seismic design is to guarantee the overall failure mode formation on frames. So, the structural demand of strength and rigidity and column-to-beam strength ratio on repaired state are discussing analytically.

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.

Recently, there are many discussions about repairability and recovery for damaged buildings after severe disasters, and new keywords such as “Resilience” and “Redundancy” have been closed-up. This paper investigates the repairability of damaged steel building structures which experienced severe disasters such as earthquake input motions. At first, the analytical model for repaired steel member is explained, and also its applicability is represented by comparison with past test results. The next, the ultimate states of steel framed model of original state and repairing state under seismic loads are calculated by limit analysis. Herein, an analytical frame model is designed that the whole story collapse mode is predominated in original state. And also, to adjust the failure mode of frame after repair, a various strategy of repairing portion in frame is assumed. From the analytical results, it is observed that the strength and energy absorption are enhanced if the adequate repairing strategy is adopted to generate the whole collapse failure mode. That is, it can be said that these repaired frame has high repairability and resilience.

Checlear O-157 is the immunochromatography test kit which is developed for easy and rapid detection of E.coli O-157 in food. Detection limited of E.coliO-157 by this method was 5 × 104cells/mL. Compare to the result of culture method (official method), data of Checlear O-157 correspond with culture method (official method). But Checlear O-157 showed cross reaction with some strains (Citrobacter freundii, Salmonella urbana, Bacillus cereus) other than E.coli. Considering those results, Checlear O-157 will be useful in preliminary screening of E.coli O157 in food.

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.

To examine the effect of halothane on the cytosolic Ca2+ concentration ([Ca2+]i)-tension relationship of rat aortic smooth muscle.Rat aortic rings without endothelia were loaded with the fluorescent Ca2+ indicator, Fura PE3-AM, and then mounted in organ baths. The changes in isometric tension and [Ca2+]i were measured simultaneously. In one series ionomycin (10 nM-3 microM) was added to normal Krebs' solution cumulatively in the absence and presence of halothane (1.5%, 3%). In the other series, CaCl2 (0.3-3 mM) was added to Ca2+-free Krebs' solution including high KCl (50 mM), phenylephrine (100 nM) or prostaglandin F2alpha (PGF2alpha, 1-3 microM) in the absence and presence of halothane (1.5%, 3%). The linear part of [Ca2+]i-tension relationship was analyzed by a linear regression.Halothane, 1.5%, had no effect on the normal [Ca2+]i-tension relationship obtained with the calcium ionophore, ionomycin (10 nM-3 microM), but halothane 3% decreased the slope of the relationship (0.239 +/- 0.037 for control and 0.110 +/- 0.010 for halothane 3%, P0.05). Halothane, 1.5% and 3%, did not change the [Ca2+]i-tension relationship obtained with CaCl2 (0.3-3 mM) in the presence of high KCl (50 mM) or phenylephrine (100 nM). In contrast, halothane, 3%, inhibited the intercept of [Ca2+]i-tension relationship obtained with CaCl2 (0.3-3 mM) in the presence of prostaglandin F2alpha (PGF2alpha, 1-3 microM) (45.708 +/- 4.233 for control and 26.997 +/- 2.522 for halothane 3%, P0.01).Halothane decreases the Ca2+ sensitivity and that in the presence of PGF2.

Oxidative stresses such as UV irradiation to mammalian cells triggers a variety of oxistress responses including activation of transcription factors. Recently, activation of nuclear factor-κB (NF-κB) has been shown to be under oxidoreduction (redox) regulation controlled by thioredoxin (TRX), which is one of major endogenous redox-regulating molecules with thiol reducing activity. In order to elucidate where in the cellular compartment TRX participates in NF-κB regulation, we investigated the intracellular localization of TRX. UVB irradiation induced translocation of TRX from the cytoplasm into the nucleus. In our in vitro diamide-induced cross-linking study, we showed that TRX can associate directly with NF-κB p50. Overexpression of wild-type TRX suppressed induction of luciferase activity under NF-κB-binding sites in response to UV irradiation compared with the mock transfectant. In contrast, overexpression of nuclear-targeted TRX enhanced the luciferase activity. Thus, TRX seems to play dual and opposing roles in the regulation of NF-κB. In the cytoplasm, it interferes with the signals to IκB kinases and blocks the degradation of IκB. In the nucleus, however, TRX enhances NF-κB transcriptional activities by enhancing its ability to bind DNA. This two-step TRX-dependent regulation of the NF-κB complex may be a novel activation mechanism of redox-sensitive transcription factors.

Naloxone is a widely used opioid antagonist.To analyze the cellular responses induced by naloxone in the absence of opioid agonists, Chinese hamster ovary (CHO) cells, which do not endogenously express the opioid receptors, have been permanently transfected with the cloned complementary DNAs to produce the [micro sign]-, delta-, and kappa-opioid receptors. Naloxone dose-dependently reduced forskolin-stimulated cyclic adenosine monophosphate (cAMP) formation in the cells expressing the [micro sign]- and kappa-opioid receptors, although the effect was less than that of opioid agonists [D-Ala2, N-Me-Phe4, Gly-ol5]enkephalin and U50,488, respectively. The naloxone-induced cAMP reduction was abolished by pretreatment of the cells with pertussis toxin, which suggests that pertussis toxin-sensitive G proteins (Gi and/or Go) are involved in the response. Cellular guanosine triphosphatase activity was significantly increased by naloxone in the cells expressing the [micro sign]- and kappa-opioid receptors, which suggests that the application of naloxone to these receptors induces activation of the G proteins. We conclude that naloxone possesses partial agonistic activity on the [micro sign]- and kappa-opioid receptors expressed from complementary DNAs in CHO cells. Implications: In this study, we examined whether naloxone has agonistic activity on the opioid receptors by using cultured cells transfected with delta-, [micro sign]-, and kappa-opioid receptor complementary DNAs. Our data indicate that naloxone is a partial agonist on the [micro sign]- and kappa-opioid receptors. (Anesth Analg 1998;87:450-5)

We have compared the effects of xenon and nitrous oxide on central nervous system (CNS) electrical activity during sevoflurane anaesthesia in cats by recording the electroencephalogram (EEG), multi-unit activity of the midbrain reticular formation (R-MUA) and somatosensory evoked potentials (SEP). Basal anaesthesia with 2% and 5% sevoflurane was used. With 2% sevoflurane, 70% xenon initially produced rhythmic slow waves which were followed by bursts of high-amplitude sharp waves interrupted by low amplitude slow waves on the EEG. Xenon induced an initial increase, followed by a decrease in R-MUA. Nitrous oxide 70% decreased the amplitude of the EEG activity which was associated with an increase in R-MUA. Xenon suppressed the amplitude of both the initial positive and negative deflections of the SEP to a greater extent than nitrous oxide. With 5% sevoflurane anaesthesia, both anaesthetics increased the frequency of spikes on the EEG and facilitated R-MUA. These findings indicate that xenon has a stimulatory action on CNS background activity and a suppressive action on CNS reactive capability which is more potent than that of nitrous oxide.

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

The nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) system is involved in glutamatergic neurotransmission. The current study determined the effects of propofol, ketamine and midazolam on rat cerebellar cGMP formation, attempting to clarify whether the effect was due to suppression of NO-cGMP system or to direct interaction with glutamatergic receptors.Cerebellar slices, obtained from six- to eight-day-old Wistar rats, were pretreated with propofol (10 microM-1 mM), ketamine (10-100 microM) or midazolam (1-100 microM) for 30 min. and then stimulated with L-glutamate (3 mM), N-methyl-D-aspartate (NMDA, 0.1 mM), kainate (0.1 mM) or sodium nitroprusside (SNP, 0.3 mM) (n = 5-11 for each group). The levels of cGMP were determined by radioimmunoassay.None of the anaesthetics studied altered cGMP levels when no stimulant was given. Propofol (10 microM-1 mM) suppressed L-glutamate-, NMDA-, kainate- and SNP stimulated cGMP formation in a concentration-dependent manner, the sensitivity to propofol was in the order of NMDAkainateL-glutamate. SNP. Ketamine (10-100 microM) suppressed L-glutamate- and NMDA-stimulated cGMP formation, but did not suppress kainate- or SNP-stimulated cGMP formation. Midazolam (10-100 microM) did not affect NMDA-, L-glutamate- or SNP-stimulated cGMP formation, but suppressed kainate-induced formation.The inhibitory effects of propofol, ketamine and midazolam on cGMP formation in rat cerebellar slices are due mainly to interaction with receptors for excitatory amines, and not due to the suppression of nitric oxide synthase or guanylate cyclase activities.

Halothane suppresses platelet aggregation in vitro and ex vivo, and prolongs bleeding time. In a previous in vitro study we demonstrated that sevoflurane had a more suppressive effect on platelet aggregation than did halothane. The present study investigated whether the clinical use of sevoflurane affected platelet aggregation ex vivo.Thirty-eight patients undergoing minor elective surgery were divided randomly into sevoflurane and isoflurane groups. Anaesthesia was induced with thiopentone i.v., and was maintained with sevoflurane or isoflurane with nitrous oxide. Blood was collected to measure platelet aggregation induced by adenosine diphosphate (ADP) and epinephrine. The first (control) blood collection was performed in the operating room before induction of anaesthesia, and the second 5-10 min after tracheal intubation but before the start of surgery, when the end-expiratory sevoflurane or isoflurane concentrations had stabilised at 1-1.5 times the minimum alveolar concentration (MAC) and mean arterial pressures were between 80-120% of preanaesthetic values.In all samples obtained during sevoflurane anaesthesia (n = 15), ADP and epinephrine could not induce secondary aggregation, although they did induce primary aggregation. In contrast, in the isoflurane group, both primary and secondary aggregation were observed in 14 out of 15 patients, and secondary aggregation was abolished in only one of the samples obtained during anaesthesia.Sevoflurane, but not isoflurane, alters platelet aggregation in the clinical situation, possibly by suppression of thromboxane A2 formation.

UNLABELLED Atrial natriuretic peptide (ANP) antagonizes the reninangiotensin-aldosterone, adrenocorticotropic hormone-cortisol, vasopressin, and endothelin systems. Surgical injury stimulates these systems and causes vasoconstriction and antidiuresis. We assessed the hemodynamic, renal, and endocrine effects of continuous intravenous infusion of ANP in patients anesthetized with sevoflurane undergoing gastrectomy. ANP (0.1 microgram.kg-1.min-1; ANP group, n = 9) or saline (control group, n = 9) was infused continuously for 3 h from the start of the operation. The ANP group showed much higher urinary volume and sodium, potassium, and chloride excretion than the control group, although the former had lower arterial blood pressure. ANP infusion slightly inhibited aldosterone secretion and initially tended to inhibit renin secretion stimulated by surgery, but it did not affect surgery-induced increases in the plasma concentrations of vasopressin, adrenocorticotropic hormone, cortisol, or endothelin. Two patients in the ANP group experienced excessive hypotension, one experienced bradycardia, and two experienced mild hypoxemia, which required treatment but were resolved easily. These findings suggest that ANP infusion may be used with caution for controlling renal function and arterial blood pressure during surgery. IMPLICATIONS Continuous intravenous infusion of atrial natriuretic peptide, 0.1 microgram.kg-1.min-1, during gastrectomy was associated with higher water and sodium excretion and lower arterial blood pressure. It tended to inhibit the renin-angiotensin-aldosterone system compared with saline infusion, which suggests that atrial natriuretic peptide may be useful for intraoperative circulation control.

We compared the effects of xenon (Xe) on the spinal cord dorsal horn neurons with those of nitrous oxide (N 2 O) in cats anesthetized with chrolarose and urethane. We assessed the potency of both anesthetics by the inhibition of wide dynamic range neuron responses evoked by cutaneous noxious (pinch) stimulation to a hindpaw. During 70% Xe inhalation, the responses of 7 of 11 neurons to pinch stimulation were suppressed. N 2 O, 70%, suppressed it in 8 of 11 neurons. The potency of Xe and N 2 O was compared in six neurons that were suppressed by both anesthetics. After 20 min of Xe inhalation, the response to pinch was suppressed to 49.5% ± 8.2% (mean ± SE), while N 2 O, 70% in oxygen, suppressed it to 45.9% ± 7.9%. The difference between N 2 O and Xe was not significant. We conclude that Xe and N 2 O suppress the spinal cord dorsal horn neurons to a similar degree.

Thioredoxin (TRX) is a pleiotropic cellular factor that has thiol-mediated redox activity and is important in regulation of cellular processes, including proliferation, apoptosis, and gene expression. The activity of several transcription factors is posttranslationally altered by redox modification(s) of specific cysteine residue(s). One such factor is nuclear factor (NF)-κB, whose DNA-binding activity is markedly augmented by TRX treatment in vitro . Similarly, the DNA-binding activity of activator protein 1 (AP-1) is modified by a DNA repair enzyme, redox factor 1 (Ref-1), which is identical to a DNA repair enzyme, AP endonuclease. Ref-1 activity is in turn modulated by various redox-active compounds, including TRX. We here report the molecular cascade of redox regulation of AP-1 mediated by TRX and Ref-1. Phorbol 12-myristate 13 acetate efficiently translocated TRX into the HeLa cell nucleus where Ref-1 preexists. This process seems to be essential for AP-1 activation by redox modification because co-overexpression of TRX and Ref-1 in COS-7 cells potentiated AP-1 activity only after TRX was transported into the nucleus by phorbol 12-myristate 13 acetate treatment. To prove the direct active site-mediated association between TRX and Ref-1, we generated a series of substitution-mutant cysteine residues of TRX. In both an in vitro diamide-induced cross-linking study and an in vivo mammalian two-hybrid assay we proved that TRX can associate directly with Ref-1 in the nucleus; also, we demonstrated the requirement of cysteine residues in the TRX catalytic center for the potentiation of AP-1 activity. This report presents an example of a cascade in cellular redox regulation.

Background Ketamine, a noncompetitive N-methyl-D-aspartate antagonist, has psychotomimetic side effects. Recent studies have shown that noncompetitive N-methyl-D-aspartate antagonists cause morphologic damage to the cingulate and retrosplenial cortices and induce c-fos protein (c-Fos) in the same regions. Although benzodiazepines are effective in preventing these side effects, the neural basis of the drug interactions has not been established. Methods The effects of diazepam and halothane on c-Fos expression induced by ketamine were studied. Diazepam (1 and 5 mg/kg) or vehicle were administered subcutaneously, followed 7 min later by 100 mg/kg ketamine given intraperitoneally. Halothane (1.0 and 1.8%), was administered continuously from 10 min before ketamine administration until brain fixation. Two hours after ketamine injection, rats were perfused and their brains fixed and extracted. Brain sections were prepared in a cryostat and c-Fos expression was detected using immunohistochemical methods. Results Ketamine induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices, thalamus, and neocortex. Diazepam suppressed the ketamine-induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices in a dose-dependent manner, leaving the thalamus and neocortex less affected. Halothane suppressed the ketamine-induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices and the neocortex in a dose-dependent manner, leaving the thalamus relatively unaffected. Conclusion Halothane and diazepam inhibited ketamine-induced c-Fos expression in the cingulate and retrosplenial cortices, leaving the thalamus relatively unaffected.

To investigate the clinical significance of endothelin (ET), natriuretic peptides, and the renin-angiotensin-aldosterone system in pediatric liver transplantation, we measured plasma levels of ET, atrial and brain natriuretic peptides (ANP, BNP), aldosterone, and plasma renin activity in 18 patients (aged 0.5-12 yr; median 1 yr) undergoing living-related liver transplantation due to congenital biliary atresia and severe liver cirrhosis. Before transplantation, the plasma ET level (28.9 +/- 2.5 [mean +/- SEM] pg/mL) was increased compared with that of healthy children (10-18 pg/mL), but decreased during the anhepatic phase (22.5 +/- 1.6 pg/mL). It increased again after reperfusion and remained at high levels in the early postoperative period (postoperative day 3, 27.8 +/- 3.0 pg/mL). Plasma levels of ANP and BNP and aldosterone and plasma renin activity were also high before surgery. Plasma ANP and BNP did not change significantly during surgery. After transplantation, plasma BNP significantly increased, and plasma ANP tended to increase. Plasma aldosterone increased markedly during the anhepatic phase, although plasma renin activity decreased. After transplantation, plasma aldosterone and plasma renin activity both decreased to within normal levels. Mean arterial blood pressure increased gradually after reperfusion and surgery (postoperative day 3, 35.7 +/- 5.2% increase). No substantial differences in these variables occurred between the younger (or = 1.0 yr, n = 9) and older patients (1.0 yr, n = 9). These results suggest that ET production in the cirrhotic liver is augmented and ET, natriuretic peptides, and the renin-angiotensin-aldosterone system all play some role in the circulatory regulation during perioperative periods of pediatric liver transplantation.

Patients who underwent subtotal esophagectomy were extubated on the first postoperative day in order to avoid postoperative pulmonary complications and discomfort. Extubation was carried out if the patient satisfied the following criteria: no ischemic change in the mucosa, PaO2 greater than 100mmHg, and PaCO2 less than 45mmHg under 2cm H2 O CPAP or a T-piece with an FiO2 of 40%. Fiberoptic bronchoscopy (FBS) was then performed under topical anesthesia to aspirate sputum in the bronchial trees. We retrospectively studied the duration of tracheal intubation and the number of days, on which FBS was required after extubation in 41 patients. They were analyzed with regard to two preoperative measures; one-second forced expiratory volume (FEV 1) greater or less than 2.0L, and smoking history. The duration of tracheal intubation except for two tracheostomy cases was 1.8±1.7 days (mean±SD). Twenty-seven patients (66% of all patients) were extubated on the first postoperative day. The duration of intubation was not affected significantly by the risk factors. However, four patients in whom the duration of intubation was longer than 3 days, and two who required tracheostomy for long-term pulmonary care, were all smokers. FBS was required for 3.7±2.0 days after surgery. The duration of FBS was not affected by the value of FEV 1. However, smokers required FBS for a longer period (4.1±2.2 days) than non-smokers (2.9±1.2 days, p

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.

We previously found that acute administration of a nitric oxide synthase (NOS) inhibitor (N omega-nitro-L-arginine methyl ester [L-NAME]) does not reduce the minimum alveolar anesthetic concentration (MAC) of halothane in rats. However, a recent study has suggested that brain NOS activity could not be inhibited by more than approximately 50% by acute administration of L-NAME. To investigate the effect of marked inhibition of NOS activity on the MAC of halothane, we measured cerebellar NOS activity, cerebellar cyclic guanosine monophosphate (cGMP) levels, and halothane MAC in rats chronically treated with L-NAME and compared the results to those of the saline-treated control group. Although the cerebellar NOS activity and cGMP levels were significantly decreased (14% and 2.7% of control, respectively) by L-NAME, the value of the halothane MAC was not significantly affected. These results suggest that the anesthetic action of halothane, as measured by its MAC in rats, is not related to NOS activity or cGMP levels in the brain.

The mechanism by which anesthetics suppress platelet aggregation has not been elucidated. We determined the effects of halothane, enflurane, and isoflurane on human platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, and a thromboxane A2 (TXA2) analog, and on ligand binding to the platelet TXA2 receptor. Halothane (2.6 mM) strongly suppressed ADP- and epinephrine-induced secondary aggregation of platelets, without significant alteration of primary aggregation. Platelet aggregation induced by a specific TXA2 agonist, (+)-9,11-epithia-11,12-methano-TXA2 (STA2), was suppressed by halothane, enflurane, and isoflurane in a concentration-dependent manner; the concentration of halothane, enflurane, and isoflurane which induced 50% inhibition (IC50) were 3.2, 12.3, and 15.7 mM, respectively (or 4.7, 9.8, and 24 minimum alveolar anesthetic concentration [MAC], respectively). The binding of a specific TXA2 receptor antagonist, 3H-S145, was significantly reduced by halothane (14-28 mM), but not by enflurane (20 mM) and isoflurane (20 mM). Scatchard analysis revealed that halothane (14 mM) increased Kd from 0.53 nM to 14.3 nM but did not alter Bmax significantly. These results indicate that halothane has a stronger suppressive effect on platelet aggregation than enflurane and isoflurane, and that the effect of halothane on platelet aggregation is due to reduction of the ligand-binding affinity of the platelet TXA2 receptor.

To elucidate which portions of the opioid receptor molecules are involved in the ligand selectivity, we have expressed chimeric receptors between the rat delta- and mu-opioid receptors from cDNAs and analysed their ligand binding properties. We demonstrate that the major binding determinant for the delta-selective enkephalin-related peptide, [D-Pen2,D-Pen5]enkephalin, resides within the region comprising the transmembrane segments V-VII and the intervening loop regions. On the other hand, the region spanning from the intracellular loop I to the amino-terminal half of the transmembrane segment III is shown to be involved in determining high-affinity binding of the mu-selective enkephalin-related peptides, [D-Ala2, MePhe4,Gly-ol5]enkephalin and [D-Ala2,MePhe4,Met-ol5]enkephalin, whereas the major determinant for binding of the mu-selective alkaloids, morphine and codeine, is demonstrated to exist in the region spanning the transmembrane segments V-VII. These results indicate that distinct regions of the opioid receptor determine the selectivity for the delta- and the mu-selective enkephalin-related peptides and that the binding determinant for the mu-selective alkaloids is distinct from that for the mu-selective enkephalin-related peptides.

1990年6月から1995年3月までに当院救急部・集中治療部に入院した小児患者483例中58例に対して合計252回の気管支鏡を行った.対象は生体肝移植周術期40例, 他の手術後9例, 気道異物3例などで, 気管支鏡を必要とした原因は, 無気肺・気道分泌物貯留36例, 肺炎20例, 気道狭窄8例, 気道出血7例, 肺水腫6例, 気道異物・誤嚥4例などである.無気肺24例中19例で虚脱した肺の再膨張に成功した。肺炎20例中16例で気管支鏡で得た標本から起炎菌が検出された.気道狭窄の8例は他の診断法では呼吸困難の原因がつかめず, 気管支鏡にて初めて病態が明らかになった.気道異物の2例では硬性気管支鏡にて異物が摘出された.乳児挿管例11例では我々が作製した外付けチャコネル付き極細気管支鏡が有用であった.合併症は高度低酸素血症と徐脈を呈した1例のみであった.気管支鏡は小児重症例救急例にも安全かつ有効な手段である.

To provide a neurochemical basis for the central nervous system actions of nitrous oxide, the changes of brain dopamine (DA), serotonin (5-HT), norepinephrine (NE), and metabolites of DA and 5-HT were studied in rats. Thirty male Wistar rats were assigned to one of five groups according to the type of gas and the duration of gas exposure. The rats in one group, which served as control, were exposed to air for 30 min, and the rats in four other groups were exposed to 75% nitrous oxide in oxygen for 0.5, 1, 2, and 4 h, respectively. Animals were killed with microwave irradiation, and the brains were divided into seven sections: the cerebral cortex, cerebellum, striatum, hippocampus, midbrain-thalamus, hypothalamus, and medulla-pons. The contents of NE, DA, 3,4-dihydroxyphenyl-alanine (DOPAC), homovanillic acid (HVA), 5-HT, and 5-hydroxyindoleacetic acid (5-HIAA) in each discrete area were measured with high-performance liquid chromatography. Nitrous oxide had no significant effect on the contents of NE, 5-HT, nor 5-HIAA, but decreased that of DA in the striatum and midbrain-thalamus after 4 h of exposure (P < 0.05). Levels of DOPAC, but not DA, in the cerebral cortex and medulla-pons were increased significantly at exposures up to 2 h (P < 0.05), but were not significant from control levels after a 4-h exposure. Increased levels of DOPAC indicate that nitrous oxide increases dopaminergic neuronal activities in the mesocortical projection and the medullary network.(ABSTRACT TRUNCATED AT 250 WORDS)

Using cats with chronically implanted brain electrodes, we have compared the effects of propofol on CNS electrical activities with those of thiopentone. Ten cats were allocated to receive either propofol (n = 5) or thiopentone (n = 5). Cats were anaesthetized initially with 4% halothane in oxygen. The trachea was intubated and the lungs ventilated mechanically. A femoral artery and a vein in a forepaw were cannulated for arterial pressure monitoring and fluid infusion. After the inspired concentration of halothane was maintained at 0.5%, EEG in the cortex, the amygdala and the hippocampus, somatosensory evoked potential (SEP) and reticular multi-unit activity (R-MUA) were recorded. Incremental doses of propofol or thiopentone were administered i. v. at 5-min intervals during 0.5% halothane anaesthesia. The cumulative doses of propofol and thiopentone were 2, 5, 10 and 20mg kg−1, and 4, 10, 20 and 40 mg kg−1 respectively. Arterial pressure was maintained in excess of 100 mm Hg systolic by infusion of phenylephrine. All cats in the propofol group survived, but two in the thiopentone group died after the adminstration of thiopentone 40mg kg−1 Changes observed in CNS activity were dose-related in all cases. The EEG changed with the increments of doses of propofol or thiopentone, from fast, small amplitude to complexes of fast and slow, large amplitude activities, burst suppression and flat EEG. SEP latency was prolonged by both agents: the peak latency of N1 changed from 15 (SD 2) ms to 20 (5) ms with propofol 20mg kg−1, and from 14 (1) ms to 27(2) ms with thiopentone 40 mg kg−1. SEP amplitudes were depressed by both agents: the amplitude of N1 was depressed by 70 (29) % with propofol 20 mg kg−1 and by 60 (33) % with thiopentone 40mg kg−1. The R-MUA also was depressed by both agents: 85 (4) % with propofol 20 mg kg−1 and 85 (8) % with thiopentone 40mg kg−1. The R-MUA was depressed to 50% of control by propofol 3.2 (1.6) mg kg−1 or thiopentone 6.7 (5.0) mg kg−1. These depressive actions on the EEG, SEP and R-MUA induced by propofol were similar to those induced by twice the equivalent doses of thiopentone on an mg kg−1 basis. These results indicate that propofol has the same simple depressant effects as thiopentone on CNS electrical activity.