The punitive impact of radical right populism on foreign aid: immigration pressure and mainstream partnership

This study investigates populist radical right (PRR) influence on aid amid widespread concerns about a potential connection between its rise and the reduction of aid allocation. Previous studies failed to address these concerns owing to the disuse of immigrant inflows as an intervening variable and a bilateral framework capable of investigating properties in donor and recipient countries. By analyzing panel data on Western European parliamentary democracies, the study demonstrates the PRR’s reducing effect via a coalitional pathway on bilateral aid to the recipients, failing to stem emigration into the donor countries. Further, analysis shows that such reduction intensifies in conjunction with the donors’ weak pluralistic institutions and the recipients’ sociocultural characteristics different from the ordinary citizens represented by the PRR. The findings make a novel contribution to the expanding literature on the PRR to integrate insights on the aid–immigration nexus, strategies for policy influence, and ideational profiles

A Nexus of Policy Diffusion and Multilateral Aid

Diffusion holds the key to both the mechanism of carbon emission and a solution to the problem of emission excesses. In essence, diffusion represents spatial dependence through connectivity between states and affects their policies or even regulations entailed in the framework of global governance. Even though it is of critical importance to climate governance in influencing trust and incentives for cooperation, diffusion has received limited attention from international relations analysts of climate change. Using spatial modeling and systemic international relations theories, we uncover that, on average, diffusion adversely affects other states’ emission efficiency and that emission by states with competitive trading activity is a major source of the adverse diffusion. This result holds even if international and domestic countervailing factors are taken into account. An in-sample simulation analysis confirms that, for better climate governance, the adverse diffusion can be neutralized by a coalition of numerous trading states, rather than by a limited number of large states (e.g., G20)

Development of a process for the production of propylene oxide in methane-oxidising bacteria

The aim of this project is to develop a process for the production of propylene oxide (PO), using methane-oxidising bacteria. At the beginning, a difficult problem needed to be solved for the development of this process i.e. the short life-span of the biocatalyst. Experiments showed that the cells of the methane-oxidising bacterium, Methylococcus capaulatus (Bath) lost their catalytic activity within 30 minutes under the conditions of high PO production. The inactivation of the biocatalyst was largely Independent of externally-accumulated PO but was totally dependent on PO produced in vivo under conditions of high PO production. The cells lost their activity without any external accumulation of PO under those conditions where PO was produced. Prior to the research of the present writer, it had been concluded that external PO inactivated the biocatalyst. A specific PO productivity of more than 700 naol PO produced/min/mg cells was obtained in the work reported here. However, by increasing the PO productivity more than 200 aU/mg cells, the cells lost their activity rapidly and their half-life lasted 7 minutes. In order to overcome the short life-span of the biocatalyst, a reactivation of the inactivated cells had to be devised. The methane-oxidising bacteria contain an enzyme, methane monooxygenase (MM0) which oxidises methane to methanol and also oxidises propylene to P0. The UNO was irreversibly inactivated by acetylene or by P0, however this inactivated MM0 was reactivated by subjecting the cells to reactivation treatment. This reactivation process is a phenomenon not previously known about. In order to reactivate the inactivated MMo, the cells required carbon, nitrogen and sulphur sources. In addition, a suitable oxygen and temperature regime was required for the reactivation process. The requirement of nutrients for reactivation and the inhibition of reactivation by the addition of chloramphenicol led to the conclusion that protein synthesis was associated with the reactivation process. Furthermore, it was found that MMo synthesis was completely inhibited by a detectable amount of methanol in the cell suspensions. Copper was not required for the reactivation of cells which contained particulate MM0. Two types of inactivation mechanism were assumed under the conditions of P0 production. These are the inactivation of MMo and the inactivation of the biocatalyst by a means not yet identified. When the MMo only was inactivated, it was reactivated quickly. However when these cells were inactivated under conditions of high P0 production, they required three times as long a period for complete reactivation than did those cells which had been inactivated by acetylene. This delay in the reactivation process was thought to be due to a concealed inactivation (unidentified inactivation) factor. The latter was thought to be caused by the accumulation of P0 within the cells. The intracellular P0 concentration was calculated on the basis of the retention time of P0 in the cells, and its concentration appeared to be related to P0 productivity. The concealed inactivation was assumed to be due to a solvent-like effect of P0 in the cells and not from an alkylation effect. In order to develop a P0 production process using the reactivation system, Mathylocystim paryus (0BBP) was selected as the best organism from 25 methanotrophs. The reactivation system, the growing-call process (single stage) and the two-stage reactivation process were designed and operated. Using the growing-cell process, continuous P0 production was achieved at a rate of 12 g/l/day for a period of more than three weeks

The Rationality of Economic Voting Revisited

Examines the rationality of economic voting, using post-World War II United States national election data

Aggregate Vote Functions for the US. Presidency, Senate, and House

Estimates vote functions for presidential, House and Senate elections following the premise that vote functions are likely to be related. Use of a seemingly unrelated regressions technique adapted to the case of unequal numbers of observations across equations; On-year versus mid-term congressional elections parameters; Influence of economic variables on election outcomes; Incumbency effects

Leading by design: Asian lessons for monitoring global financial stability

18004N - The Japan Foundation Center for Global Partnership; The Japan Foundation Center for Global Partnershiphttps://www.bu.edu/gdp/files/2023/11/GEGI-Report-RFAs-FIN.pd

C. elegans PlexinA PLX-1 mediates a cell contact-dependent stop signal in vulval precursor cells

AbstractPLX-1 is a PlexinA transmembrane protein in Caenorhabditis elegans, and the transmembrane-type semaphorin, SMP-1, is a ligand for PLX-1. The SMP-1/PLX-1 system has been shown to be necessary for proper epidermal morphogenesis in the male tail and seam cells. Here, we show that the SMP-1/PLX-1 system also regulates vulval morphogenesis. In plx-1 and smp-1 mutants, hermaphrodites sometimes exhibit a protruding vulva or multiple vulva-like protrusions. Throughout the vulval development of plx-1 and smp-1 mutants, the arrangement of vulval cells is often disrupted. In the initial step of vulval morphogenesis, vulval precursor cells (VPCs) are generated normally but are subsequently arranged abnormally in mutants. Continuous observation revealed that plx-1 VPC fails to terminate longitudinal extension after making contact with neighbor VPCs. The arrangement defects of VPCs in plx-1 and smp-1 mutants are rescued by expressing the respective cDNA in VPCs. plx-1::egfp and smp-1::egfp transgenes are both expressed in all vulval cells, including VPCs, throughout vulval development. We propose that the SMP-1/PLX-1 system is responsible for a cell contact-mediated stop signal for VPC extension. Analyses using cell fate-specific markers showed that the arrangement defects of VPCs also affect cell fate specification and cell lineages, but in a relatively small fraction of plx-1 mutants

Relationship between postprandial glucose level and carotid artery stiffness in patients without diabetes or cardiovascular disease

BACKGROUND: The aim of this study was to evaluate the relationship between postprandial glucose level and atherosclerosis in patients without diabetes and cardiovascular disease by determining carotid ultrasonographic variables and serum levels of 1,5-anhydroglucitol (1,5-AG). METHODS: The subjects were 72 patients without diabetes and cardiovascular disease being treated for hypertension or dyslipidemia. The clinical characteristics of all subjects, including the serum level of 1,5-AG, which appears to be well suited for monitoring postprandial hyperglycemia, were evaluated after an overnight fast. The average intima-media thickness (IMT) and the average pulsatility index (PI) of the right and left common carotid arteries were determined with high-resolution ultrasonography and used as ultrasonographic variables. The subjects were divided into a Lower 1,5-AG group (n = 36) and a Higher 1,5-AG group (n = 36). We evaluated the relationship between clinical characteristics and ultrasonographic variables of the carotid artery in both groups. RESULTS: The average PI in the Lower 1,5-AG group was significantly higher than that in the Higher 1,5-AG group, but the average IMT did not differ between the groups. Linear regression analysis, with the ultrasonographic variables as the dependent variables, with 1,5-AG as the independent variable, and adjusted for other clinical characteristics, showed significant correlation between 1,5-AG and the PI but not between 1,5-AG and IMT. CONCLUSION: Our results suggest that postprandial hyperglycemia increases carotid artery stiffness, but not morphological change, in patients without diabetes or cardiovascular disease

NKX2-1/TITF1/TTF-1-Induced ROR1 Is Required to Sustain EGFR Survival Signaling in Lung Adenocarcinoma

SummaryWe and others previously identified NKX2-1, also known as TITF1 and TTF-1, as a lineage-survival oncogene in lung adenocarcinomas. Here we show that NKX2-1 induces the expression of the receptor tyrosine kinase-like orphan receptor 1 (ROR1), which in turn sustains a favorable balance between prosurvival PI3K-AKT and pro-apoptotic p38 signaling, in part through ROR1 kinase-dependent c-Src activation, as well as kinase activity-independent sustainment of the EGFR-ERBB3 association, ERBB3 phosphorylation, and consequential PI3K activation. Notably, ROR1 knockdown effectively inhibited lung adenocarcinoma cell lines, irrespective of their EGFR status, including those with resistance to the EGFR tyrosine kinase inhibitor gefitinib. Our findings thus identify ROR1 as an “Achilles' heel” in lung adenocarcinoma, warranting future development of therapeutic strategies for this devastating cancer