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The objective of this study is to develop an active power control of photovoltaic power generation (PV) system for supporting grid frequency regulation in two different forms, i.e. slow frequency control contributing to load - frequency control (LFC) and fast frequency control contributing to inertial response of synchronous generators. Two different active power - frequency droop characteristics are implemented simultaneously by using different frequency measurement methods. The performance test result of proposed control using an experimental setup shows that PV system equipped with proposed control can supply appropriate active power according to two different droop characteristics for slow frequency control and fast frequency control

Background: In a previous study, we found that thrombin induced proliferation of TM‐1 and T98G human glioma cells and that the mitogenic effect was abolished by hirudin. Objectives: We investigated thrombin’s effects on the proliferation of A172 human glioblastoma cells and the induction of growth factors. Furthermore, we examined whether or not the expression of heparin cofactor II (HCII) in A172 cells using adenovirus vector could suppress thrombin’s effects. Methods: The effect of thrombin on cell proliferation was assessed using a 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide assay. The amount of growth factors in the conditioned medium was measured by enzyme‐linked immunosorbent assay. The level of platelet‐derived growth factor (PDGF)‐B mRNA was assessed by reverse transcriptase‐polymerase chain reaction analysis. Results: Thrombin‐induced proliferation of A172 cells primarily depended on the enhanced secretion of PDGF‐AB by thrombin. The action of thrombin depended on its proteolytic activity. However, thrombin‐induced PDGF‐AB secretion was not abolished by anti‐protease‐activated receptor (PAR) antibody. The PAR‐1 agonist peptide had no effect on cell growth and PDGF‐AB levels. Thrombin did not increase PDGF‐B gene expression. Expression of HCII effectively suppressed thrombin‐induced PDGF‐AB release. Conclusions: These results indicate that thrombin may play an important role in the proliferation of A172 cells by inducing PDGF‐AB secretion and that thrombin’s action is mediated by its proteolytic activity. Inhibition of thrombin’s proteolytic activity may be a new therapeutic method for gliomas.

Infective larvae of an intestinal nematode, Strongyloides venezuelensis, enter rodent hosts percutaneously, and migrate through connective tissues and lungs. Then they arrive at the small intestine, where they reach maturity. It is not known how S. venezuelensis larvae develop during tissue migration. Here we demonstrate that tissue invasion ability of S. venezuelensis larvae changes drastically during tissue migration, and that the changes are associated with stage-specific protein expression. Infective larvae, connective tissue larvae, lung larvae, and mucosal larvae were used to infect mice by various infection methods, including percutaneous, subcutaneous, oral, and intraduodenal inoculation. Among different migration stages, only infective larvae penetrated mouse skin. Larvae, once inside the host, quickly lost skin penetration ability, which was associated with the disappearance of an infective larva-specific metalloprotease. Migrating larvae had connective tissue migration ability until in the lungs, where larvae became able to settle down in the intestinal mucosa. Lung larvae and mucosal larvae were capable of producing and secreting adhesion molecules.

This paper is concerned with the construction of an active suspension for a one-wheel car model by using fuzzy reasoning. The experimental model is approximately described by a nonlinear system with two degrees of freedom subject to excitation from a road profile. The active control at the suspension location is designed by using fuzzy reasoning based on single input rule modules, and it is constructed by actuating a pneumatic actuator with dead time. The performance degradation of the active suspension system due to the dead time of the pneumatic actuator is improved by inserting two kinds of compensators. The experimental result shows that the active suspension system with the compensators more improves the control performance than that without compensator.

GaN epitaxial layers were grown on a (0001) 6H-SiC substrate by metalorganic vapor phase epitaxy by adapting a (GaN/AlN) multibuffer layer. Successful control of residual strain in the epitaxial layers was achieved by changing the layer structure of the (GaN/AlN) multibuffer layer. The lattice constant c of the thin GaN epitaxial layer (as thin as 0.1 μm) was close to that of freestanding GaN, where the thin GaN layer was grown on the substrate by adapting the multibuffer layer. In addition, the (GaN/AlN) multibuffer layer is effective not only for control of the residual strain included in a GaN epitaxial layer, but also for improving the quality of a GaN epitaxial layer.

This paper is concerned with the construction of an active suspension system for a quarter car model using the concept of sliding mode control. The active control is derived by the equivalent control and switching function where the sliding surface is obtained by using Linear quadratic control (LQ control) theory. The active control is generated with non-negligible time lag by using a pneumatic actuator, and the road profile is estimated by using the minimum order observer based on a linear system transformed from the exact non-linear system. The experimental result indicates that the proposed active suspension system is more effective in the vibration isolation of the car body than the linear active suspension system based on LQ control theory and the passive suspension system.

Genetic lack of interleukin 12 receptor β1 (IL-12Rβ1) surface expression predisposes to severe infections by poorly pathogenic mycobacteria or Salmonella and causes strongly decreased, but not completely abrogated, interferon (IFN)-γ production. To study IL-12Rβ1–independent residual IFN-γ production, we have generated mycobacterium–specific T cell clones (TCCs) from IL-12Rβ1–deficient individuals. All TCCs displayed a T helper type 1 phenotype and the majority responded to IL-12 by increased IFN-γ production and proliferative responses upon activation. This response to IL-12 could be further augmented by exogenous IL-18. IL-12Rβ2 was found to be normally expressed in the absence of IL-12Rβ1, and could be upregulated by IFN-α. Expression of IL-12Rβ2 alone, however, was insufficient to induce signal transducer and activator of transcription (Stat)4 activation in response to IL-12, whereas IFN-α/IFN-αR ligation resulted in Stat4 activation in both control and IL-12Rβ1–deficient cells. IL-12 failed to upregulate cell surface expression of IL-18R, integrin α6, and IL-12Rβ2 on IL-12Rβ1–deficient cells, whereas this was normal on control cells. IL-12–induced IFN-γ production in IL-12Rβ1–deficient T cells could be inhibited by the p38 mitogen-activated protein kinase (MAP) kinase inhibitor SB203580 and the MAP kinase kinase (MEK) 1/2 inhibitor U0126, suggesting involvement of MAP kinases in this alternative, Stat4-independent, IL-12 signaling pathway. Collectively, these results indicate that IL-12 acts as a partial agonist in the absence of IL-12Rβ1. Moreover, the results reveal the presence of a novel IL-12Rβ1/Stat4–independent pathway of IL-12 responsiveness in activated human T cells involving MAP kinases. This pathway is likely to play a role in the residual type 1 immunity in IL-12Rβ1 deficiency.

A BGaN/AlN double heterostructure or BAlGaN/AlN single was grown on 6H-SiC substrate by metalorganic vapor phase epitaxy (MOVPE). The relation between the band-gap energy and boron composition was experimentally determined for BGaN. Photoluminescence (PL) spectra were observed with 2.7% boron composition at room temperature. The PL spectrum of BAlGaN, which was near the band-edge, was observed.

IL-18 is a proinflammatory cytokine that plays an important role in NK cell activation and T_h1 response. IL-18 has a structural homology to IL-1, particularly IL-1β. IL-18R, composed of IL-1R-related protein (IL-18Rα) and IL-1R accessory protein-like (IL-18Rβ), belongs to the IL-1R family. Furthermore, IL-18R at least partly shares the signal transducing system with IL-1R. Thus, the IL-18-IL-18R system has a striking similarity to the IL-1-IL-1R system. For this reason, we regarded it important to investigate whether, like IL-18, IL-1β synergizes with IL-12 in inducing IFN-γ production from human T cells and plays an important role in the T_h1 response. Here we show that IL-12 and IL-1β synergistically induce T cells to proliferate and produce IFN-γ without their TCR engagement. IL-12 stimulation induced an increase in the proportion of T cells positive for IL-18R. Then, IL-12-stimulated T cells responded to IL-18 or IL-1β by their proliferation and IFN-γ production, although levels of IL-1β-induced responses were lower. CD4⁺CD45RA⁺ T cells, although they constitutively expressed IL-18Rβ mRNA, did not express IL-18Rα mRNA. Phytohemagglutinin (PHA) stimulation alone induced IL-18Rα mRNA without affecting the expression of IL-18Rβ mRNA. T_h1-inducing conditions (PHA, IL-12 and anti-IL-4) further increased this expression. We also show that T_h1 cells but not T_h2 cells have increased expression of IL-18R and IL-1R, and produce IFN-γ in response to IL-18 and/or IL-1β.

IL-18 is a proinflammatory cytokine that plays an important role in NK cell activation and T(h)1 response. IL-18 has a structural homology to IL-1, particularly IL-1beta. IL-18R, composed of IL-1R-related protein (IL-18Ralpha) and IL-1R accessory protein-like (IL-18Rbeta), belongs to the IL-1R family. Furthermore, IL-18R at least partly shares the signal transducing system with IL-1R. Thus, the IL-18-IL-18R system has a striking similarity to the IL-1-IL-1R system. For this reason, we regarded it important to investigate whether, like IL-18, IL-1beta synergizes with IL-12 in inducing IFN-gamma production from human T cells and plays an important role in the T(h)1 response. Here we show that IL-12 and IL-1beta synergistically induce T cells to proliferate and produce IFN-gamma without their TCR engagement. IL-12 stimulation induced an increase in the proportion of T cells positive for IL-18R. Then, IL-12-stimulated T cells responded to IL-18 or IL-1beta by their proliferation and IFN-gamma production, although levels of IL-1beta-induced responses were lower. CD4(+)CD45RA(+) T cells, although they constitutively expressed IL-18Rbeta mRNA, did not express IL-18Ralpha mRNA. Phytohemagglutinin (PHA) stimulation alone induced IL-18Ralpha mRNA without affecting the expression of IL-18Rbeta mRNA. T(h)1-inducing conditions (PHA, IL-12 and anti-IL-4) further increased this expression. We also show that T(h)1 cells but not T(h)2 cells have increased expression of IL-18R and IL-1R, and produce IFN-gamma in response to IL-18 and/or IL-1beta.

A tensile-strained AlN layer along the a-axis was grown on a (0001) 6H-SiC substrate with a (GaN/AlN) buffer layer by metalorganic vapor phase epitaxy using an alternating source feeding (ASF) technique. It was experimentally demonstrated that the strain in the AlN layer was affected by the growth conditions of the buffer layer. On the other hand, the AlN layer grown directly on a substrate without the buffer layer exhibits compressive strain along the a-axis. Strain control in the AlN layer using the ASF buffer is proposed.

Spleen and peritoneal macrophages obtained from innately resistant A/J mice released low levels of interleukin 18 (IL-18) upon infection with Salmonella typhimurium C5 RP4. Incubating the cells with recombinant gamma interferon (rIFN-gamma) enhanced IL-18 production. A/J mice treated in vivo with anti-IL-18 antibodies showed impaired resistance to infection, with increased bacterial loads in the liver and spleen. Administration of rIL-18 could protect A/J mice from challenge with a lethal dose of virulent salmonellae, with a dramatic reduction in bacterial numbers in the tissues. rIL-18 administration did not ameliorate the disease in IFN-gamma-R-/- mice. IL-18 proved to be required for IFN-gamma production by mouse splenocytes from conventional, scid, and rag-1(-/-) mice; in vivo IL-18 neutralization caused a decrease in circulating IFN-gamma levels. Thus, IL-18 is a key factor in early host resistance to Salmonella and probably acts via IFN-gamma.

Human peripheral blood mononuclear cells (PBMC) were stimulated with three nonpathogenic Lactobacillus strains and with one pathogenic Streptococcus pyogenes strain, and cytokine gene expression and protein production were analyzed. All bacteria strongly induced interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor alpha mRNA expression and protein production. S. pyogenes was the most potent inducer of secretion of IL-12 and gamma interferon (IFN-gamma), and two of three Lactobacillus strains induced IL-12 and IFN-gamma production. All strains induced IL-18 protein production. IL-10 and IL-4 production was induced weakly and not at all, respectively. Our data show that nonpathogenic lactobacilli and pathogenic streptococci can induce Th1 type cytokines IL-12, IL-18, and IFN-gamma in human PBMC.

ABSTRACTSpleen and peritoneal macrophages obtained from innately resistant A/J mice released low levels of interleukin 18 (IL-18) upon infection with Salmonella typhimuriumC5 RP4. Incubating the cells with recombinant gamma interferon (rIFN-γ) enhanced IL-18 production. A/J mice treated in vivo with anti-IL-18 antibodies showed impaired resistance to infection, with increased bacterial loads in the liver and spleen. Administration of rIL-18 could protect A/J mice from challenge with a lethal dose of virulent salmonellae, with a dramatic reduction in bacterial numbers in the tissues. rIL-18 administration did not ameliorate the disease in IFN-γ-R−/−mice. IL-18 proved to be required for IFN-γ production by mouse splenocytes from conventional, scid, andrag-1−/−mice; in vivo IL-18 neutralization caused a decrease in circulating IFN-γ levels. Thus, IL-18 is a key factor in early host resistance to Salmonellaand probably acts via IFN-γ.

Summary Delayed ischaemic deficits due to cerebral vasospasm contribute to the high morbidity and mortality rates associated with subarachnoid haemorrhage. We evaluated the usefulness of measuring anti-phospholipid antibodies (aPLs) for prediction of the occurrence of symptomatic vasospasm and the outcome after subarachnoid haemorrhage. 32 consecutive patients with subarachnoid haemorrhage due to ruptured cerebral aneurysms were studied. They were admitted and operated on within 72 hours after the onset of subarachnoid haemorrhage. aPLs such as lupus anticoagulants, anti-cardiolipin IgG and anti-cardiolipin IgM were measured repeatedly after admission. Furthermore, platelet count, platelet aggregability and plasma platelet factor 4 were also measured. Eleven among the 32 patients (34.4%) showed positive in the examination for aPLs. Although aPLs could not predict symptomatic vasospasm, once symptomatic vasospasm occurred, patients with aPLs frequently demonstrated cerebral infarction and there-fore their outcome was worse. aPLs were associated with a severe initial clinical grade and SAH grade on CT scan. Therefore it may explain the association of aPLs with worse outcome. aPLs were detected between 1 and 7 days. Four of 6 patients (67%) with aPLs became negative between 7 and 13 days after subarachnoid haemorrhage. The mechanism of transient aPLs is unclear but it is more likely to occur in the severer grade patients. The reduction in platelet count, the increased platelet aggregability, and the increased plasma platelet factor 4 concentration were also observed in aPLs-positive patients with symptomatic vasospasm.

We examined the ability of interleukin-12 (IL-12) and IL-18 to induce the production of gamma interferon (IFN-gamma) and nitric oxide (NO) by murine peritoneal exudate cells (PEC) and to stimulate the growth-inhibitory activity of these cells against Cryptococcus neoformans. PEC produced IFN-gamma and NO when stimulated with a combination of IL-12 and IL-18 but little or no IFN-gamma or NO when either cytokine was used alone. PEC anticryptococcal activity was mediated by IFN-gamma and NO production, since it was completely inhibited by a neutralizing anti-IFN-gamma monoclonal antibody (MAb) and N(G)-monomethyl-L-arginine, a competitive inhibitor of NO synthesis, respectively. To identify the IFN-gamma-producing cells among PEC stimulated with IL-12 and IL-18, we depleted NK cells, gammadelta T cells, or CD4+ T cells by treating PEC with specific Abs and complement. NK cell depletion strongly suppressed IFN-gamma production and almost completely inhibited NO production and anticryptococcal activity, while depletion of other cells had no such influence. Alternatively, purified NK cells by two cycles of glass adherence and magnetic separation with anti-CD3, -CD4, -CD8, and -B220 MAbs produced a greater amount of IFN-gamma by stimulation with IL-12 and IL-18 than unseparated non-glass-adherent PEC. Our results demonstrated that IL-12 and IL-18 synergistically induced NO-dependent anticryptococcal activity of PEC by stimulating NK cells to produce IFN-gamma.

Recently, human interleukin 18 (hIL-18) cDNA was cloned, and the recombinant protein with a tentatively assigned NH2-terminal amino acid sequence was generated. However, natural hIL-18 has not yet been isolated, and its cellular processing is therefore still unclear. To clarify this, we purified natural hIL-18 from the cytosolic extract of monocytic THP.1 cells. Natural hIL-18 exhibited a molecular mass of 18.2 kDa, and the NH2-terminal amino acid was Tyr37. Biological activities of the purified protein were identical to those of recombinant hIL-18 with respect to the enhancement of natural killer cell cytotoxicity and interferon-gamma production by human peripheral blood mononuclear cells. We also found two precursor hIL-18 (prohIL-18)-processing activities in the cytosol of THP.1 cells. These activities were blocked separately by the caspase inhibitors Ac-YVAD-CHO and Ac-DEVD-CHO. Further analyses of the partially purified enzymes revealed that one is caspase-1, which cleaves prohIL-18 at the Asp36-Tyr37 site to generate the mature hIL-18, and the other is caspase-3, which cleaves both precursor and mature hIL-18 at Asp71-Ser72 and Asp76-Asn77 to generate biologically inactive products. These results suggest that the production and processing of natural hIL-18 are regulated by two processing enzymes, caspase-1 and caspase-3, in THP.1 cells.

Interleukin (IL)-18 was identified as a molecule that induces IFN-gamma production and enhances NK cell cytotoxicity. In this paper, we report upon the purification and characterization of human IL-18 receptor (hIL-18R). We selected the Hodgkin's disease cell line, L428, as the most strongly hIL-18R-expressing cell line based on the results of binding assays. This binding was inhibited by IL-18 but not by IL-1beta. The dissociation constant (Kd) of 125I-IL-18 binding to L428 cells was about 18.5 nM, with 18,000 binding sites/cell. After immunizing mice with L428 cells and cloning, a single monoclonal antibody (mAb) against hIL-18R was obtained (mAb 117-10C). Sequentially, hIL-18R was purified from 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonic acid (CHAPS)-extracted L428 cells by wheat germ lectin-Sepharose 4B chromatography and mAb 117-10C-Sepharose chromatography. The internal amino acid sequences of hIL-18R all matched those of human IL-1 receptor-related protein (IL-1Rrp), the ligand of which was unknown to date. When expressed in COS-1 cells, the cDNA of IL-1Rrp conferred IL-18 binding properties on the cells and the capacity for signal transduction. From these results, we conclude that a functional IL-18 receptor component is IL-1Rrp.

Summary: Most of the major extracranial arteries have vasa vasorum which play an important role in some pathological conditions. However, in the intracranial arteries, the existence of vasa vasorum and their pathological implication have not been adequately investigated. We examined the distribution and incidence of vasa vasorum in the major cerebral arteries and their relationships to certain clinical factors in 50 autopsy cases performed between 1987 and 1994. By light microscopy, vasa vasorum were found in 36 of 50 patients. Of 36 patients, vasa vasorum in 30 cases were localizedly observed in the tunica adventitia and the in other 6 were distributed in the tunica media accompanied by intramural haemorrhage. Existence of vasa vasorum was more common in the proximal arteries (vertebral, internal carotid, and basilar arteries) than in the distal arteries (middle cerebral and anterior cerebral arteries). Vasa vasorum were found more frequently in aged patients with severe atherosclerosis and those with cerebrovascular diseases. Our results indicated that intracranial vasa vasorum existed with a higher frequency in the tunica adventitia of the vertebral and internal cerebral arteries, and the incidence of vasa vasorum related to severity of atherosclerosis. The development of vasa vasorum in the tunica media may reflect some pathological changes of cerebral arteries.

Summary In order to predict the occurrence of cerebral infarction after aneurysmal surgery in patients with subarachnoid haemorrhage, we measured the amount of subarachnoid blood on initial and on post-operative computed tomograms. We used a reliable grading method to estimate the amount of blood on computed tomograms in 24 patients with infarction due to vasospasm and 45 patients without cerebral infarction, all of whom underwent aneurysmal surgery within 48 hours after the ictus.

Summary The plasma concentration of the platelet-derived growth factor (PDGF)-B chain and the plasma platelet factor 4 (PF4) levels were measured in 17 healthy controls and 55 brain tumour patients. In the 17 normal controls, the plasma PDGF-B and PF4 levels were 523 ± 157 pg/ml (mean ± SD) and 84 ± 37 ng/ml, respectively. In the brain tumour patients, these values were 881 ± 854 pg/ml and 93 ± 64 ng/ml, respectively. The plasma PDGF-B concentration was elevated above the upper limit of normal individuals in 12 (22%) of the 55 patients. However, since the corresponding PF4 levels suggested the platelet activation, the increased plasma PDGF-B may have originated from platelets. To address this, platelet releasing experiments were performed on citrated blood samples from 5 normal individuals. The plasma PDGF-B and PF4 levels from the 17 normal controls and those observed in the platelet releasing experiments correlated with a regression line of Y = 240 + 4.86X (Y: PDGF, X: PF4). There were only 6 (11%) patients whose plasma PDGF-B level was elevated above the 95% confidence limit estimated from the corresponding PF4 value. In these patients, the tumour volumes were extensively large, and those elevated PDGF-B values decreased after treatment and became elevated again in three patients with recurrent glioblastoma.

Summary The purpose of this study was to measure plasma platelet-activating factor (PAF) concentration, PAF-acetylhydrolase activities, anti-phospholipid antibody (aPLs) titers, and platelet function in patients with subarachnoid haemorrhage (SAH) and to assess the association of these variables with the development of cerebral vasospasm.

Monocytes in the blood circulation migrate across endothelial cell monolayers lining the blood vessels and infiltrate into the underlying tissues in inflammation. However, little is known about the mechanisms by which leukocytes migrate across the endothelial barrier after binding and what molecules participate in the process. Addition of the human monocytic cell line THP-1 to interleukin-1beta (IL-1beta)-stimulated human umbilical vein endothelial cells (HUVEC) induced a decrease in the amount of focal adhesion kinase (p125(FAK)) protein, a tyrosine kinase localized at focal contacts and essential for cell attachment to the extracellular matrix, whereas little change was observed in the amount of other molecules associated with cell adhesion such as vascular cell adhesion molecule-1, alpha-catenin, and talin. A maximum decrease in the amount of p125(FAK) was observed 15-30 min after addition of THP-1 cells to HUVEC, after which the level of p125(FAK) gradually recovered. A reduction in the density of actin stress fibers in IL-1beta-activated HUVEC was observed in parallel with the decrease in p125(FAK). The p125(FAK) decrease was partially inhibited by preventing THP-1 binding to HUVEC using a mixture of antibodies to adhesion molecules. We suggest that the decrease in p125(FAK) triggered by binding of monocytes in inflammation facilitates the transendothelial migration of the monocytes by altering the adhesiveness of endothelial cells to the extracellular matrix.

This paper presents a construction of the active suspension of passenger cars using sliding mode controllers. The model of the passenger car is described by a nonlinear system with four degrees of freedom subject to irregular excitation from a road surface. The sliding mode control for the active suspension is obtained as a sum of linear and nonlinear controls where the former is derived as LQ control for a reduced linear system, and the latter is determined from the stability condition of the sliding surface. The simulation result indicates that the proposed active suspension is very effective in the performance of vibration isolation.