No abstract

Across sub-Saharan Africa agricultural subsidy programs have again become a common strategy for combatting rural poverty, increasing agricultural production, and reducing food insecurity. Despite a large literature examining subsidies' effects on output and welfare, little is known about their political effects. This paper examines Malawi's Agricultural Input Subsidy Programme, one of the largest and most expensive programs implemented, which was launched by the government in 2005. We examine whether the incumbent party, the Democratic Progressive Party headed by president Bingu wa Mutharika, benefited from Malawi's subsidy program by examining a longitudinal dataset of 1,846 rural Malawians interviewed in 2008 and again in 2010. The individual-level data show no evidence that the subsidy program was targeted to Mutharika's co-ethnics or co-partisans. Our analysis further demonstrates that the subsidy program increased support for the incumbent party. These results suggest that even when parties are unable or unwilling to target distributional programs at the local level, they may nonetheless derive political benefits. As anti-poverty programs - including agricultural subsidies to small-scale farmers - become increasingly common across the continent, our results suggest that they may help to explain patterns of party affiliation and vote choice, particularly where traditional patterns of partisan affiliation related to ethnic or regional identities weaken.

In this article, we study protest participants in the May 2006 immigration rights marches in Los Angeles. Analysis of original survey data of 876 march participants yields five main results. First, despite substantial dispute among organizers on how to frame the marches, we find protest participants were similar across march locations organized by different coalitions. Second, we find Spanish-English bilingual participants seemed to benefit from being in two media environments, as they reported more information sources about the protest events than monolingual participants. Third, women reported hearing about the protest events from more information sources, and Spanish-English bilingual women reported hearing from more information sources than any other group, suggesting they acted as social connectors behind the massive participation. Fourth, we confirm the importance of Spanish-language radio as an information source, but our data also point to the significance of television and English-language radio. Finally, analyzing data of first-time protesters, we estimate the immigrant rights marches newly politicized 125,000 people in Los Angeles who spoke Spanish and not English.

BACKGROUND: Reprogramming of monocytes and macrophage manifests in hyperinflammatory responses and chronification of inflammation in atherosclerosis. Recent studies focused on epigenetic, transcriptional, and metabolic alterations that characterize trained immunity. However, the underlying effector mechanisms driving the hyperinflammatory response of reprogrammed macrophages remain unclear. We hypothesized that the plasma membrane of atherosclerotic lesion macrophages undergoes reprogramming to maintain inflammarafts, enlarged lipid rafts (LR) serving as a platform for assembly of inflammatory receptor complexes. METHODS: Single-cell suspensions from the aortae of Western diet-fed Ldlr-/- mice were gated for BODIPY-high foamy and BODIPY-low nonfoamy F4/80 macrophages by flow cytometry. Inflammarafts were characterized by increased levels of LR, TLR4 (toll-like receptor-4) localization to LR, TLR4 dimers, and the proximity between TLR2, TLR1, and CD36. In a cellular model of trained immunity, LR, TLR4 dimers, and the inflammatory response were measured in bone marrow-derived macrophages subjected to a 24-hour treatment with LPS (lipopolysaccharide) or OxLDL (oxidized low-density lipoprotein), followed by a 6-day wash-out period. RESULTS: Nonfoamy macrophages, which constituted ≈40% of macrophages in atherosclerotic lesions, expressed significantly higher levels of LR and TLR4 dimers, as well as proximity ligation signals for TLR4-LR, TLR2-CD36, and TLR2-TLR1 complexes, compared with foamy macrophages. These inflammaraft measures associated, to a different degree, with plasma cholesterol and inflammatory cytokines, as well as the size of the atherosclerotic lesions and necrotic cores. The bone marrow-derived macrophages trained with LPS simulated nonfoamy atherosclerotic lesion macrophages and continued to express inflammarafts and inflammatory genes for 6 days after LPS removal and displayed a hyperinflammatory response to Pam3CSK4, a TLR2/TLR1 agonist. OxLDL-exposed, lipid-laden macrophages did not express inflammarafts. CONCLUSIONS: Our data support the hypothesis that persistent inflammarafts in nonfoamy macrophages in atherosclerotic lesions serve as effectors of macrophage reprogramming into a hyperinflammatory phenotype.

Background: The ceramide metabolite, sphingosine-1-phosphate (S1P), regulates multiple cellular functions in keratinocytes (KC). We recently discovered that production of a key innate immune element, cathelicidin antimicrobial peptide (CAMP), is stimulated via a NF-κB-dependent mechanism that is activated by S1P when S1P is generated by sphingosine kinase (SPHK) 1. Objective: We investigated whether pharmacological modulation of SPHK1 activity, using a novel synthetic SPHK1 activator, (S)-methyl 2-(hexanamide)-3-(4-hydroxyphenyl) propanoate (MHP), stimulates CAMP expression. Methods: MHP-mediated changes in both S1P and CAMP downstream mediators were analyzed in normal cultured human KC by qRT-PCR, Western immunoblot, ELISA, confocal microscopy for immunohistochemistry, HPLC and ESI-LC/MS/MS, and microbial pathogen invasion/colonization in a human epidermal organotypic model. Results: Treatment with MHP directly activated SPHK1 and increased cellular S1P content in normal cultured human KC. Because MHP did not inhibit S1P lyase activity, which hydrolyses S1P, augumented S1P levels could be attributed to increased synthesis rather than blockade of S1P degradation. Next, we found that exogenous MHP significantly stimulated CAMP mRNA and protein production in KC, increases that were significantly suppressed by siRNA directed against SPHK1, but not by a scrambled control siRNA. NF-κB activation, assessed by nuclear translocation of NF-κB, occurred in cells following incubation with MHP. Conversely, pretreatment with a specific inhibitor of SPHK1 decreased MHP-induced nuclear translocation of NF-κB, and significantly attenuated the MHP-mediated increase in CAMP production. Finally, topical MHP significantly suppressed invasion of the virulent Staphylococcus aureus into murine skin explants. Conclusion: MHP activation of SPHK1, a target enzyme of CAMP production, can stimulate innate immunity.

Microglia-driven neuroinflammation plays an important role in the development of Alzheimers disease. Microglia activation is accompanied by the formation and chronic expression of TLR4 inflammarafts, defined as enlarged and cholesterol-rich lipid rafts serving as an assembly platform for TLR4 dimers and complexes of other inflammatory receptors. The secreted apoA-I binding protein (APOA1BP or AIBP) binds TLR4 and selectively targets cholesterol depletion machinery to TLR4 inflammaraft-expressing inflammatory, but not homeostatic microglia. Here we demonstrated that amyloid-beta (Aβ) induced formation of TLR4 inflammarafts in microglia in vitro and in the brain of APP/PS1 mice. Mitochondria in Apoa1bp-/- APP/PS1 microglia were hyperbranched and cupped, which was accompanied by increased reactive oxygen species and the dilated endoplasmic reticulum. The size and number of Aβ plaques and neuronal cell death were significantly increased, and the animal survival was decreased in Apoa1bp-/-APP/PS1 compared to APP/PS1 female mice. These results suggest that AIBP exerts control of TLR4 inflammarafts and mitochondrial dynamics in microglia and plays a protective role in Alzheimers disease associated oxidative stress and neurodegeneration.

Manipulation of inorganic materials with organic macromolecules enables organisms to create biominerals such as bones and seashells, where occlusion of biomacromolecules within individual crystals generates superior mechanical properties. Current understanding of this process largely comes from studying the entrapment of micron-size particles in cooling melts. Here, by investigating micelle incorporation in calcite with atomic force microscopy and micromechanical simulations, we show that different mechanisms govern nanoscale occlusion. By simultaneously visualizing the micelles and propagating step edges, we demonstrate that the micelles experience significant compression during occlusion, which is accompanied by cavity formation. This generates local lattice strain, leading to enhanced mechanical properties. These results give new insight into the formation of occlusions in natural and synthetic crystals, and will facilitate the synthesis of multifunctional nanocomposite crystals.

This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C. Please note that version 3 on the archive is the auxiliary version of the Physics of the B Factories book. This uses the notation alpha, beta, gamma for the angles of the Unitarity Triangle. The nominal version uses the notation phi_1, phi_2 and phi_3. Please cite this work as Eur. Phys. J. C74 (2014) 3026.