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Scholars and policymakers who call for social investment (SI) policies hope that SI policies reduce income inequality and poverty, among other policy goals. Meanwhile, some others point out potentially less pro-poor effects of SI policies. There are relatively few cross-national studies that empirically examine the distributional effects of SI policies. The current study seeks to fill the gap by investigating the effects of SI policies on income inequality in OECD countries. The empirical analysis finds mixed results. Parental leave benefits reduce market income inequality, but other family support policies do not lessen inequality, and family allowances and paid leave (the length of generous leave) even increase it. The effects of some family policies are partly context-specific. In contexts where there are a large number of single-mother households, parental leave benefits reduce market income inequality. There is no stable evidence that education and active labour market policy (ALMP) reduce market income inequality. Education and ALMP, however, reduce disposable income inequality (even after controlling for left governments and Nordic countries). The article suggests that in countries with high education and/or ALMP spending, the skills of workers towards the lower end of the income distribution may be relatively high (even though their pre-tax and transfer income may be low), and it may make their income salvageable with redistributive policies. In this sense, SI policies and conventional redistributive policies may be complementary in reducing disposable income inequality.

In cyanobacteria, the PII protein (the glnB gene product) regulates a number of proteins involved in nitrogen assimilation including PipX, the coactivator of the global nitrogen regulator protein NtcA. In Synechococcus elongatus PCC 7942, construction of a PII-less mutant retaining the wild-type pipX gene is difficult because of the toxicity of uncontrolled action of PipX and the other defect(s) resulting from the loss of PIIper se, but the nature of the PipX toxicity and the PipX-independent defect(s) remains unclear. Characterization of a PipX-less glnB mutant (PD4) in this study showed that the loss of PII increases the sensitivity of PSII to ammonium. Ammonium was shown to stimulate the formation of reactive oxygen species in the mutant cells. The ammonium-sensitive growth phenotype of PD4 was rescued by the addition of an antioxidant α-tocopherol, confirming that photo-oxidative damage was the major cause of the growth defect. A targeted PII mutant retaining wild-type pipX was successfully constructed from the wild-type S. elongatus strain (SPc) in the presence of α-tocopherol. The resulting mutant (PD1X) showed an unusual chlorophyll fluorescence profile, indicating extremely slow reduction and re-oxidation of QA, which was not observed in mutants defective in both glnB and pipX. These results showed that the aberrant action of uncontrolled PipX resulted in an impairment of the electron transport reactions in both the reducing and oxidizing sides of QA.

Labor productivity is an important determinant of the wealth of national economies and standards of living, as its growth explains half of per capita GDP growth. We show that there are four worlds of productivity growth among industrialized countries, by decomposing labor productivity growth into multifactor productivity (MFP) growth and capital deepening. The four worlds that emerge from the analysis are: 1) human capital investment and MFP growth-dominant Nordic coordinated market economies (CMEs); 2) physical capital investment- and labor productivity growth-dominant liberal market economies; 3) continental CMEs whose moderately high human capital investments create decently high MFP growth, but whose low physical capital investments push down their labor productivity; and 4) South European countries with both low human capital investment and low productivity growth. The four worlds are a result partly of the countries’ human capital formation policies and economic growth strategies — different policies add differently to the components of labor productivity. Overall, we tie welfare production regimes to economic outcomes by showing that different human capital formation policies produce different economic outcomes.

This paper presents a novel virtual reality demonstration program that provides people immersive urban experience, i.e. helps people understand characteristics of the city atmosphere from big data analysis on GPS location logs and search query logs. In contrast to the other demonstration systems that show the characteristics of areas of interests by using tag cloud, or VR systems using 3D computer graphics, our system synthesizes both the functionalities by showing 3D point clouds, where each particle shows search queries made by people staying at the area of interests. This synthesis invokes people feel the atmosphere of the city while traditional VR systems could not offer it. To make demonstration system effective, a new feature extraction process on search query logs is proposed by focusing on the users who visit the area of interests. In the demonstration at the conference, visitors could enjoy immersive urban experience with VR headset. Furthermore, the paper also shows the empirical evaluation on our new feature representation from search query logs.

ObjectiveTo determine the relationship between plaque composition and low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein B (Apo-B), and Apo-A1 using virtual-histology intravascular ultrasound (VH-IVUS).MethodsWe assessed plaque composition in patients with stable coronary artery disease (SCD) admitted to our hospital for percutaneous coronary intervention (PCI) between November 1, 2012, and March 10, 2015. Before PCI, fibrous (FI), fibrofatty (FF), necrotic core (NC), and dense calcium (DC) regions were evaluated using VH-IVUS, and the contributions of each to the culprit lesion volume were recorded. Plasma LDL-C, HDL-C, Apo-B, and Apo-A1 levels were assessed before PCI. The relationship between the regions on VH-IVUS and plasma lipid levels was assessed. Patients were categorized into low Apo-B (LAB) and high Apo-B (HAB) groups, based on the overall cohort median Apo-B level.ResultsWe enrolled 115 patients (median Apo-B, 91 mg/dL, male n = 88) with 57 and 58 patients in the LAB (Apo-B ≤ 90 mg/dL) and HAB (Apo-B ≥ 91 mg/dL) groups, respectively. Vessel, plaque, and %NC volumes were significantly greater in the HAB group than in the LAB group. The %FI, %FF, and %DC volumes were similar in both groups. In all 115 patients, the %NC volume correlated with LDL-C (r = 0.2353, P = 0.0114) and Apo-B (r = 0.2487, P = 0.0074) but not with HDL-C and Apo A-1. The high-sensitivity C-reactive protein level tended to be higher in the HAB group than in the LAB group. Multiple regression analysis showed that being male, Apo-A1, and Apo-B were significant predictors of %NC volume extent.ConclusionsElevated Apo-B level was related to the %NC in target coronary artery lesions in SCD patients, suggesting a role of Apo-B as a biomarker of unstable plaque in this population.

N-3 polyunsaturated fatty acids (PUFAs) are thought to have protective effects against cardiovascular disease. Here, we report the relationship between serum PUFA concentrations and plaque composition, as evaluated by virtual histology-intravascular ultrasound (VH-IVUS). Consecutive patients (n=61) who underwent percutaneous coronary intervention (PCI) were pre-operatively examined using VH-IVUS to assess the composition of culprit plaques. Gray-scale IVUS and VH-IVUS data of fibrous, fibro-fatty, necrotic core, and dense calcium regions of plaques were estimated at the minimal luminal area sites of culprit lesions. Serum levels of high-sensitivity C-reactive protein (hsCRP) and PUFAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA), were compared between patients with (ACS, n=27) and without acute coronary syndrome (non-ACS, n=34) before PCI. Multiple logistic regression analysis of the data showed that EPA/AA under the median was more highly associated with ACS than hsCRP over the median. In addition, EPA/AA was negatively correlated with the percentage of fibrous plaque regions and EPA/AA and DHA/AA were positively correlated with the percentage of dense calcium regions in plaques. Furthermore, the correlation index of EPA/AA was the most highly (R=0.513) correlated with the percentage of dense calcium regions in plaques. Keywords: N-3 polyunsaturated fatty acids, Eicosapentaenoic acid, Acute coronary syndrome, Stable coronary disease, Virtual histology-intravascular ultrasound

An advanced glycation end products (AGE)/a receptor for AGE (RAGE) axis plays a key role in diabetic vascular complications. Membrane type 1-matrix metalloproteinase (MT1-MMP) has been shown to function not only as a proteolytic enzyme but also as a signaling molecule. In this study, we investigated the role of MT1-MMP in the AGE/RAGE-triggered signaling pathways in cultured rabbit smooth muscle cells (SMCs) and the molecular interaction between RAGE and MT1-MMP in vitro and in vivo. In SMCs, AGE-activated Rac1 and p47(phox) within 1 min, NADPH oxidase activity and reactive oxygen species (ROS) generation within 5 min, and NF-κB phosphorylation within 15 min, thereby inducing redox-sensitive molecular expression. Silencing of RAGE by small-interfering RNA (siRNA) blocked the AGE-induced signaling pathways. AGE-induced geranylgeranyl transferase I (GGTase I) activity, Rac1·p47(phox) activation, NADPH oxidase activity, ROS generation, and molecular expression were also markedly attenuated by silencing of MT1-MMP. An inhibitor of GGTase I mimicked the effects of MT1-MMP-specific siRNA. Fluorescent immunohistochemistry revealed that MT1-MMP was partially co-localized with RAGE in SMCs, and RAGE was found to form a complex with MT1-MMP in both cultured SMCs and the aortae of diabetic rats by immunoprecipitation. Furthermore, MT1-MMP and RAGE formed a complex in the aortic atherosclerotic lesions of hyperlipidemic rabbits. We show that MT1-MMP plays a crucial role in RAGE-activated NADPH oxidase-dependent signaling pathways and forms a complex with RAGE in the vasculature, thus suggesting that MT1-MMP may be a novel therapeutic target for diabetic vascular complications.

A ZZ domain (ZZ) and alkaline phosphatase (AP), luciferase (Luc), or glucose oxidase (GOD) were conjugated using Sortase A (SrtA) from Staphylococcus aureus. The specific peptidyl linker for SrtA was genetically fused to the C-terminus of ZZ, and the other linker was fused to the N-terminus of AP, Luc, or GOD, respectively. The resultant proteins were obtained separately by bacterial expression. The recombinant peptide-tagged ZZ and AP, Luc, or GOD were site-specifically conjugated by SrtA through the extra peptidyl linkers in vitro. The SrtA reaction had little influence on either the antibody-binding activity of the ZZ moiety or the enzymatic activity of AP, Luc, or GOD moieties of the conjugates. Additionally, antibody-ZZ-proteins were yielded easily by mixing antibody with ZZ-AP, ZZ-Luc, or ZZ-GOD, allowing their use in an enzyme-linked immunosorbent assay. These results suggest that the enzymatic approach with SrtA facilitates the construction of ZZ-proteins. Furthermore, mixing antibody and ZZ-proteins produces a wide variety of antibody-ZZ-proteins.

We investigated the role of RhoA activation and its mechanism in plasminogen activator inhibitor-1 (PAI-1) gene expression induced in endothelial cells by monocyte adhesion. Isolated human peripheral blood monocytes were added to cultured human coronary endothelial cells. Monocyte adhesion to endothelial cells increased PAI-1 expression at the transcriptional level and activated RhoA which was accompanied by an increase in the activity of geranylgeranyl transferase I (GGTase I), an enzyme responsible for geranylgeranylation, and actin stress fiber formation. Inhibition of RhoA by C3 exoenzyme or by adenovirus-mediated expression of N19RhoA, as well as by pravastatin, prevented the upregulation of PAI-1 induced by monocyte adhesion. GGTI-286, an inhibitor of GGTase I, prevented the monocyte-induced RhoA activation and PAI-1 expression in endothelial cells. Monocyte attachment induced an increase in intracellular Ca 2+ concentration ([Ca 2+ ] i ) in endothelial cells and Ca 2+ chelation prevented the increased promoter activity and expression of PAI-1 induced by monocyte adhesion. C3 exoenzyme and GGTI-286 also suppressed endothelial intracellular Ca 2+ mobilization and Ca 2+ entry induced by monocytes. The present study shows that GGTase I plays a role in the RhoA activation in endothelial cells induced by monocyte adhesion and that GGTase I-mediated Ca 2+ signaling may contribute to RhoA-dependent PAI-1 gene expression.

Tissue factor (TF) is the primary initiator of the coagulation cascade. Ca(2+) signaling is involved in TF gene expression. Monocyte chemoattractant protein-1 (MCP-1) and its receptor (CCR2) play a pivotal role in the inflammation of atherosclerosis. Although nitric oxide (NO) impairment appears to promote thrombogenicity in monocyte adhesion to endothelial cells (ECs), little is known about its mechanism. N(omega)-nitro-L-arginine methyl ester (L-NAME) promoted MCP-1 expression in EC culture. In response to monocyte adhesion, increased TF expression accompanied by NF-kappaB p65 activation was observed in L-NAME-treated ECs compared with non-treated ECs. This increased TF expression was prevented by BAPTA-AM, an intracellular Ca(2+) chelator. Monocyte attachment to L-NAME- treated ECs increased Ca(2+) influx compared with non-treated ECs, which was prevented by the blockade of MCP1/CCR2. These findings suggest that increased production of MCP-1 caused by L-NAME contributes to the enhancement of Ca(2+) influx only when monocytes adhered to ECs and that this may accelerate TF expression in ECs triggered by monocyte adhesion. We demonstrate the role of Ca(2+) influx via MCP-1/CCR2 under NO impairment in TF expression in monocyte-EC interaction.

Comparative political economists have conventionally claimed that the strength and stability of governments affect policy making and performance, and that what they call ‘weak governments’– multiparty, minority and short-lived governments – show poorer economic performance. This article tests this and related hypotheses on deficits, economic growth, unemployment and inflation by examining data from 17 OECD countries. I find that there is generally little evidence to indicate that so-called ‘weak governments’, when considered independently, produce poorer performance than strong ones. However, the effects of different government types are partly contingent on central bank independence and labour organization. When central banks are independent, coalition governments exhibit better inflation and economic growth performance than one-party governments, but the opposite happens when central banks are dependent. I attempt an explanation for these relationships. I also find that independent central banks, under certain conditions, lead to lower growth and higher inflation. Thus, some of the benefits of central bank independence are context-specific, depending on other political-economic factors.

Objective— Ca 2+ plays an important role in tissue factor (TF) gene expression. We investigated the role of endogenous nitric oxide (NO) in the induction of TF expression in endothelial cells (ECs) by monocyte adhesion and the mechanisms of NO action. Methods and Results— Inhibition of endogenous NO by N ω -nitro- l -arginine methyl ester ( l -NAME) enhanced TF promoter activity and protein expression induced in human coronary ECs by monocyte adhesion, as well as EC surface TF activity. l -NAME also induced monocyte chemoattractant protein-1 (MCP-1) expression, which was blocked by an NO donor, NOC18. Exogenous MCP-1 enhanced TF expression induced by monocyte adhesion, whereas adenovirus-mediated expression of the mutant MCP-1, 7ND, abolished the l -NAME enhancement of TF expression induced by monocyte adhesion. Monocyte attachment to l -NAME–treated ECs increased Ca 2+ influx, which was prevented by NOC18, anti–MCP-1 antibody or 7ND. These results indicate that the binding of increased MCP-1 induced by endogenous NO blockade to CCR2 mediated the enhancement of Ca 2+ influx only when monocytes adhered to ECs, which upregulated TF expression in ECs triggered by monocyte adhesion. Conclusion— MCP-1/CCR2 may play a role in Ca 2+ influx-dependent TF regulation in the monocyte–EC interaction in the impairment of NO synthesis.

RhoA plays a critical signaling role in thrombin-induced endothelial dysfunction. The possible thrombin regulation of geranylgeranylation, a lipid modification, of unprocessed RhoA and the significance of the geranylgeranylation in RhoA activation in endothelial cells (ECs) are not well understood. The amounts of the unprocessed and geranylgeranylated forms of RhoA in non-stimulated cultured human aortic ECs were 31 +/- 8 and 69 +/- 8% total cellular RhoA, respectively (n = 6, p0.0001), as determined by the Triton X-114 partition method. Thrombin-induced rapid conversion of most of the unprocessed RhoA into the geranylgeranylated form within 1 min through stimulating geranylgeranyltransferase I (GGTase I) activity. Thrombin-induced rapid geranylgeranylation was inhibited by acute short term (3 min) pretreatment with atorvastatin as well as by an inhibitor of GGTase I (GGTI-286). Thrombin also rapidly stimulated GTP loading of RhoA, which was blocked by acute pretreatment with either atorvastatin or GGTI-286. These observations indicate the dependence of thrombin stimulation of RhoA on the rapid geranylgeranylation of unprocessed RhoA. Importantly, the addition of geranylgeranylpyrophosphate to ECs pretreated with atorvastatin quickly reversed the atorvastatin inhibition of thrombin stimulation of RhoA. These results suggest that geranylgeranylation of unprocessed RhoA may limit thrombin-induced full activation of RhoA in ECs. Cytoskeleton analysis demonstrated that atorvastatin and GGTI-286 inhibited thrombin-induced stress fiber formation. We provide the evidence that, in thrombin-stimulated ECs, the unprocessed form of RhoA is rapidly geranylgeranylated to become the mature form, which then is converted into GTP-bound active RhoA.

Japan has received conflicting assessments in the comparative political economy literature. This article seeks to identify the location of Japan's political economy within a comparative framework, building on recent analyses of macroeconomic policy and wage coordination. The author examines empirical records and shows that Japan's regime is best considered ‘Keynesian centralization’, rather than ‘monetarist (semi)decentralization’, in light of its effective wage coordination and its anti-inflationary but flexibly accommodating macroeconomic policy. When there was national consensus on macroeconomic conservatism, Japan implemented restrictive policy and resembled monetarist centralization. However, Japan's monetarist centralization did not lead to distributional conflicts and high unemployment because its decentralized but coordinated wage bargaining and weak labor made it possible for employers and unions to achieve national diffusion of wage restraint without facing solidaristic wage demands by low-paid workers.

Objective— The role of Rho activation in the regulation of tissue factor (TF) is not clear. This study was undertaken to investigate this in endothelial cells induced by monocyte adhesion. Methods and Results— Isolated human peripheral blood monocytes were added to cultured human coronary endothelial cells. Monocyte adhesion to endothelial cells increased the levels of TF antigen in the endothelial cells. The results of transient transfection of the human TF promoter/luciferase gene into endothelial cells indicated that the increase in endothelial expression of the TF gene caused by monocyte adhesion occurred at the transcriptional level. The upregulation of TF was inhibited by statins, and the suppressive effect of statins was reversed by geranylgeranylpyrophosphate. Monocyte adhesion rapidly upregulated the membrane translocation and GTP/GDP exchange of RhoA, but not of Cdc42 or Rac, in endothelial cells. Rho inhibition by C3 exoenzyme or adenovirus-mediated expression of N19RhoA prevented the endothelial upregulation of TF caused by monocyte adhesion, and this was mimicked by Rho-kinase inhibitors. Moreover, monocyte adhesion increased the phosphorylation of nuclear factor-κB p65 in endothelial cells, and this was prevented by statins and Rho inhibition. Conclusions— Our study shows that RhoA activation plays an integral role in TF expression in endothelial cells.

A 58-year-old woman came to our hospital because of chest pain. Multi-detector computed tomography (MDCT) showed type V dual left anterior descending artery (LAD) and a 90% stenosis in segment 1 of the right coronary artery. Two days after examination, she was admitted to our hospital because of recurrent chest pain. She was diagnosed with acute myocardial infarction. Coronary angiography showed a 99% stenosis in segment 1 and a dual LAD. She received successful percutaneous coronary intervention (PCI) to segment 1 with a bare metal stent. Type V dual LAD is a rare and complicated coronary anomaly with the short LAD originating from the left sinus of valsalva and the long LAD originating from the right sinus of valsalva. Identifying anatomy of the coronary artery is important when making a strategy for PCI. In types IV–VI dual LAD, the anatomic features can be misinterpreted at coronary angiography. MDCT was useful in understanding the anomaly of dual LAD and performing PCI in the present case.

Monocytes and macrophages synthesize tissue factor (TF) which plays a role in thrombogenicity in coronary artery disease. This study was conducted to investigate the effect of Rho/Rho-kinase inhibition on the synthesis of TF in cultured human monocytes. 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins), C3 exoenzyme and Rho-kinase inhibitors were added to isolated peripheral blood monocytes and the synthesis of TF was assessed by reverse transcriptase polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry. Rho activity was determined by measuring the GTP-bound form of Rho A. Cerivastatin and pravastatin reduced the levels of TF antigen and mRNA. The suppressive effect of statins on TF synthesis was reversed by geranylgeranylpyrophosphate (GGPP) and the restoring effect of GGPP was eliminated by C3 exoenzyme and Y-27632. Pravastatin decreased the activity of Rho A, suggesting that the suppression of TF synthesis by statins is mediated via inhibition of the geranylgeranylation of Rho. Moreover, inhibition of Rho and Rho-kinase downregulated the synthesis of TF. Our results suggest that Rho/Rho-kinase signaling is involved in the synthesis of TF in human monocytes and that inhibition of Rho/Rho-kinase may be useful for treating thrombogenicity in coronary artery disease.

Increased production of plasminogen activator inhibitor-1 (PAI-1) in plaques plays a role in the pathogenesis of atherosclerosis. This study was conducted to investigate the effect of blockade of Rho/Rho-kinase signaling on the synthesis of PAI-1 in cultured human peripheral blood monocytes. HMG-CoA reductase inhibitors (statins) and inhibitors of Rho and Rho-kinase were added to monocyte cultures. The levels of PAI antigen and mRNA were determined by Western blotting and RT-PCR, respectively, and PAI-1 expression was assessed by immunohistochemistry. We performed pull-down assays to determine the activity of Rho by measuring the GTP-bound form of Rho A. In unstimulated and lipopolysaccharide (LPS)-stimulated cultured monocytes, statins reduced the levels of PAI-1 antigen and mRNA. The suppressive effects of statins on PAI-1 synthesis were reversed by geranylgeranylpyrophosphate (GGPP) and were mimicked by C3 exoenzyme. Immunohistochemistry confirmed the role of lipid modification by GGPP in suppressive effect of statins in PAI-1 synthesis. Pull-down assays demonstrated that statins decreased the levels of the GTP-bound form of Rho A. Our findings suggest that statins decrease the activity of Rho by inhibiting geranylgeranylation. Moreover, Rho-kinase inhibitors, Y-27632 and fasudil, suppressed the synthesis of PAI-1 in this culture system. We show that inhibition of Rho/Rho-kinase signaling downregulates the synthesis of PAI-1 in human monocytes.

It remains to be clarified how angiotensin-converting enzyme inhibitor-induced function (ie, increased NO related action or the inhibition of angiotensin II AT1 receptor dependent action) affects apoptosis of smooth muscle cells in the neointima following arterial injury. Saline (control), enalapril, L-arginine, combined enalapril and L-arginine, or losartan was administered for 14 days to Sprague-Dawley rats after balloon carotid injury and the ratio of intima to media areas (I/M), inducible NO synthase (iNOS) concentrations and %TUNEL were measured. I/M decreased similarly in the enalapril, L-arginine and losartan groups, and the combination of enalapril and L-arginine resulted in the largest I/M decrease. TUNEL positivity was increased compared with controls in the following order: losartan, L-arginine, enalapril and combination of enalapril and L-arginine. The intensity of immunostaining for iNOS was increased approximately 1.9-fold compared with the control in the combined enarapril and L-arginine group as well as in the enalapril group. These data suggest that the apoptosis in the neointima is different for L-arginine, losartan and enalapril under similar conditions and was higher under treatment with enalapril, not only via the action of NO or blocking of the AT1, but also by upregulation of iNOS.

To evaluate the effectiveness of the Porapak Q column concentration method (PQM) of analyzing the volatile aromatic compounds in 'Miyabi' melon, we compared it with the direct headspace sampling method (DHSM) and simultaneous distillation extraction method (SDEM) in regard to quantitative value, recovery rate, and reproducibility of the compounds. A total of 103 volatile compounds were quantified by PQM, 66 by SDEM, and 8 by DHSM, respectively. The widest range of volatile compounds, ranging from low-boiling-point to high-boiling-point, were quantified by using the PQM rather than by the other two methods. A total of 76 compounds were identified by the GC-MS analysis and the Kovats Index. Among the alcohols, 2-methyl-1-propanol, 2-methyl-1-butanol, 1-hexanol, 1-nonanol, (Z)-3-nonen-1-ol, (Z)-6-nonen-1-ol, (Z, Z)-3, 6-nonadien-1-ol, benzyl alcohol, and 2-phenethyl alcohol also occurred in relatively large quantities. Among the aldehydes, 3-methylbutanal, nonanal, and (E, Z)-2, 6-nonadienal were identified in large quantities by PQM. Among the esters, propyl acetate, 2-methypropyl acetate, butyl acetate, 2-methylbutyl acetate, and benzyl acetate were detectable in relatively large quantities by PQM and SDEM. The recovery rates of most low boiling-point compounds, such as methyl butyrate and ethyl propionate, were same in both methods, whereas the recovery rates of medium and high boiling-point compounds were higher with the PQM. Among sulfur-containing compounds, ethyl (methylthio) acetate and 2-(methylthio) ethyl acetate were identified by the PQM and SDEM, while ethyl 3-(methylthio) propionate and 3-(methylthio) propyl acetate were only detected by PQM. The average coefficient of variation of the compounds was 11.90% using the PQM, with stable reproducibility compared with that of SDEM (37.13%). With respect to flavor, the odor concentrates from the PQM were similar to the natural aroma of muskmelon, but the odor concentrates from the SDEM were degraded to a thick, off-flavor odor. Therefore, we concluded that PQM is an excellent method to extract volatile aromatic compounds of melon because it is quick, easy to operate, and capable of recovering a wide range of boiling-point volatile compounds without degrading their flavor. Furthermore, the results are highly reproducible.

The objective of the current study is to evaluate the association between fatty acid composition and fatty acid synthase gene polymorphisms as responsible mutations. For this purpose, we selected seven previously reported single nucleotide polymorphisms (SNPs) in FASN gene, including one within promoter region (g.841GC) and six non-synonymous SNPs (g.8805CT, g.13126CT, g.15532AC, g.16024AG, g.16039CT, g.17924AG), and genotyped them in Japanese Black cattle. Genotyping results revealed that g.8805 CT and g.17924 AG were monomorphic loci. Genome-wide association analysis including the other five SNPs revealed that only g.841GC showed significant associations with the percentages of C14:0, C14:1, C16:1 and C18:1 at 5% genome-wide significance level. In order to further evaluate the effect, we genotyped g.841GC using additional three populations, including two Japanese Black populations and a Holstein cattle population. g.16024AG was also genotyped and included in the analysis because it has been reported to be associated with fatty acid composition in Japanese Black cattle. In the result of analysis of variance, g.841GC showed stronger effects on fatty acid percentage than those of g.16024AG in all populations. These results suggested that g.841GC would be a responsible mutation for fatty acid composition and contribute to production of high-grade beef as a selection marker in beef cattle.

Political economists studying industrialized countries have claimed that certain institutional characteristics of governments—such as majority status, the number of parties in government, and stability—affect levels of public deficits. They have specifically argued that weak/unstable governments produce higher deficits than strong/stable ones. The author tests the validity of such claims by examining empirical data from 18 Organization for Economic Cooperation and Development (OECD) countries between 1961 and 1994. It is shown that evidence does not support the “deficit-prone weak governments” thesis. If anything, there is some evidence to suggest that deficits are lower under what political economists call “weak/unstable governments,” such as minority governments, coalition governments, or less durable governments. It is further shown that there is extremely limited evidence to support another line of argument: that the strength/stability of governments does not necessarily create deficits but does affect the nature of adjustment paths to economic shocks and that weak/unstable governments are less capable of reducing deficits once they are created or the economy gets thrown off track.

Although very low density lipoprotein (VLDL) receptor expression by macrophages has been shown in the vascular wall, it is not clear whether or not circulating monocytes express the VLDL receptor. We investigated the expression of VLDL receptor mRNA in human peripheral blood monocytes and monocyte-derived macrophages by reverse transcriptase polymerase chain reaction (RT-PCR) and nucleotide sequencing after subcloning of PCR product. VLDL receptor mRNA was detected both in peripheral blood monocytes and monocyte-derived macrophages. Expression of VLDL receptor mRNA was upregulated by hypoxia in monocytes, whereas treatment with oxidized LDL, interleukin-1beta or monocyte chemoattractant protein-1 did not affect the levels of VLDL receptor mRNA in monocytes and macrophages. The present study shows a novel response of VLDL receptor mRNA to hypoxia, suggesting a role for VLDL receptor in the metabolism of lipoproteins in the vascular wall and the development of atherosclerosis.

OBJECTIVES To clarify the pathophysiological significance of the renin-angiotensin system (RAS) in monocytes, we examined the effect of its blockade on tissue factor and plasminogen activator inhibitor-1 (PAI-1) synthesis in human cultured monocytes. METHODS Monocytes were isolated from healthy volunteers and cultured. Tissue factor and PAI-1 antigens in culture medium and cells were measured by enzyme-linked immunosorbent assay and Western blotting, and mRNA levels were assessed by reverse-transcriptase polymerase chain reaction. RESULTS We show that the RAS is present in isolated human peripheral blood monocytes. Exogenous angiotensin II increased the levels of tissue factor antigen and mRNA in cultured monocytes, but not of PAI-1 synthesis. An angiotensin converting enzyme (ACE) inhibitor (captopril) and an angiotensin II type 1 (AT1) receptor antagonist (candesartan) decreased the levels of tissue factor protein and mRNA in cultured monocytes. These alterations were accompanied by a reduction in the levels of tumour necrosis factor-alpha protein and mRNA. The levels of PAI-1 protein were reduced by captopril, but not by candesartan. A bradykinin B2 receptor antagonist abolished the suppressive effect of captopril on PAI-1 antigen. CONCLUSIONS An ACE inhibitor and an AT1 receptor antagonist reduced tissue factor synthesis in these cells. We show different actions of these agents on PAI-1 synthesis. ACE inhibition decreased PAI-1 synthesis mediated by bradykinin production, but AT1 receptor inhibition had no effect.

Japan, Italy and New Zealand changed their electoral systems to similar (though also significantly different) mixed systems combining single-member districts and proportional representation in the early 1990s. I examine the reasons for these three reforms being enacted, showing that while common symptoms of system failures were important in setting the three reform movements in motion in like fashion, they were not compelling enough to push reluctant politicians to enact reform. Other country-specific factors were needed to intervene and force them to take action. Japan's reform was enacted without the imposition of the popular referendum that occurred in Italy and New Zealand, but was made possible by changes in the nature of party competition that favourably altered political parties' incentives to reform. The change was brought about by the presence of pro-reformers within the dominant party and the relative coincidence between reform and the interests of parties.

In 1939, L. Rédei introduced a certain triple symbol in order to generalize the Legendre symbol and Gauss' genus theory. Rédei's triple symbol $[a_1,a_2, p]$ describes the decomposition law of a prime number $p$ in a certain dihedral extension over $\mathbb{Q}$ of degree 8 determined by $a_1$ and $a_2$. In this paper, we show that the triple symbol $[-p_1,p_2, p_3]$ for certain prime numbers $p_1, p_2$ and $p_3$ can be expressed as a Fourier coefficient of a modular form of weight one. For this, we employ Hecke's theory on theta series associated to binary quadratic forms and realize an explicit version of the theorem by Weil-Langlands and Deligne-Serre for Rédei's dihedral extensions. A reciprocity law for the Rédei triple symbols yields certain reciprocal relations among Fourier coefficients.

The resonant DC link invertors have been developed these years for avoiding the switching loss of the conventional multi-pulse PWM invertors. This paper proposes a three phase VVVF power invertor using resonant pulse density modulation for induction motor speed-control. The invertor is composed of a cascade connection of a resonant DC-DC convertor and a multi-pulse PWM invertor. The output waveform depends on the gate pulse patterns of the invertor valves. This paper proposes three kinds of pulse patterns for obtaining the outputs of trapezoidal waveform and of sinusoidal waveform, and describes also the experimental results. The V/f characteristics for induction motor speed-control and the regenerative braking operation will be examined and the circuit behaviors will be discussed.

Labor productivity is an important determinant of the wealth of national economies and their standards of living, as its growth explains half of per capita GDP growth. We show that there are three worlds of productivity growth among industrialized countries, by decomposing labor productivity growth into multifactor productivity (MFP) growth and capital deepening. The three worlds that emerge from the analysis are: 1) human capital investment and MFP growth dominant Nordic social market economies (SMEs); 2) physical capital investment and labor productivity growth-dominant liberal market economies (LMEs); and 3) continental SMEs whose moderately high human capital investments create decently high MFP growth, but whose low physical capital investments push down their labor productivity. The three worlds are broadly a result of the countries’ human capital formation policies and economic growth strategies — different policies add differently to the components of labor productivity (and ultimately to economic growth). We also identify two dominant paths to high labor productivity growth — the Nordic-type human capital investment path driven by high MFP growth, and the LME-type market-centered path powered by fixed capital investment growth. Overall, we tie the welfare production regimes (WPRs) literature to economic outcomes by showing that different human capital formation policies produce different economic outcomes.

Sulfur-containing compounds in the aromatic volatiles of melon (Cucumis melo L. cv. Miyabi) and their characteristics were analyzed by using a sniffing-GC equipped with a flame photometer detector (FPD). Nine sulfur-containing compounds were present in melon 'Miyabi'; of the four compounds identified, 3-(methylthio) propyl acetate had the highest peak area ratio (PAR) of 19.47, followed by ethyl (methylthio) acetate, ethyl 3-(methylthio) propionate, and 2-(methylthio) ethyl acetate. 3-Methylthio-1-propanol was the least concentrated (PAR of 0.27) among the compounds identified. 3-(Methylthio) propyl acetate possessed a sweet grassy odor, while ethyl (methylthio) acetate had a grassy cucumber-like odor according to the sniffing panel. Although 2-(methylthio) ethyl acetate existed at a high concentration, it was not perceived by the sniffing panel. Ethyl 3-(methylthio) propionate possessed a fruity grassy odor, and it was perceived weakly. 3-Methylthio-1-propanol and other unidentified sulfur-containing compounds were, likewise, barely detectable. Thus, it is clear that 3-(methylthio) propyl acetate and ethyl (methylthio) acetate are the important compounds in imparting the grassy aroma to 'Miyabi'.

The influence of seeds on aromatic volatile compounds in muskmelon (Cucumis melo L. cv. Crest Earl's) fruit was investigated. There were little or no differences in sensory evaluations of aroma in pollinated fruits, whether the melons were treated with CPPU (PC treatment) or not (P treatment) ; but the sensory evaluation scores of pollinated fruit were significantly higher than those of parthenocarpic fruit (emasculated female flower treated with CPPU, EC treatment). In the sniffing experiments conducted by a sniff-GC, pollinated fruits were perceived as having a favorable aroma described as melon-like, fruity, sweet, milk-like, caramel-like, flower, coconut milk, milk coffee, and cake-like. Parthenocarpic fruit, however, was perceived as having offensive odors described as green, bitter, burnt, medicinal, smelly old socks, and oil-like. Therefore, it was speculated that seeds may be involved in the formation of aroma in melon fruit.

Productivity is a most important determinant of national wealth and standards of living. Scholars have shown that different welfare production regimes pursue distinct human capital formation policies to promote productivity. But do those government policies actually promote the productivity of the economy? This paper analyzes whether such policies improve multifactor productivity in industrial democracies, after briefly presenting a human capital investment explanation for why they should help productivity. It finds that family and education policies promote productivity. Evidence of pro-productivity effects of ALMP is not detected. While the provision of public services with redistributive effects is productivity-enhancing, direct redistribution with taxes and transfers itself does not improve productivity, once other human capital formation policies are controlled for. Thus, the analysis finds good reason for governments to pursue human capital policies to promote productivity and ultimately standards of living, but they should do so selectively by choosing appropriate policy tools.

Streptavidin is tetrameric protein which has tight and specific biotin binding affinity, and streptavidin modification of proteins or small molecules is widely used for biotechnology tool. Here, we demonstrate site-specific streptavidin-protein conjugation using enzymes. We focused on sortase A, a transpeptidase from Staphylococcus aureus. A streptavidin-tagged LPETG motif (Stav-LPETG) was expressed in Escherichia coli. We achieved soluble streptavidin expression in E. coli without refolding using a cold shock expression system. Then we successfully conjugated Stav-LPETG with pentaglycine-appended green fluorescence protein (Gly5-GFP) or triglycine-appended glucose oxidase (Gly3-GOD) using sortase A. SDS-PAGE analysis showed site-specific tetrameric streptavidin-protein conjugation with the tagged proteins. In addition, the functions of a Stav-GOD conjugate, i.e., biotin-binding and glucose oxidase activity, were significantly higher compared to those of streptavidin-GOD conjugates prepared by chemical modification.