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Many have attributed the recent unprecedented wave of redistribution in Brazil to national economic and political factors such as the commodities boom, changes in minimum wages or premiums to skilled labor, the rise of the Partido dos Trabalhadores and President Luiz Inacio Lula da Silva and a commodities-driven economic boom. Yet much less attention has been devoted to the study of inequality at the subnational level, where trajectories of inequality across states remain incredibly varied. This article argues that Brazil's most recent democratic transition enhanced political competition in many Brazilian states, which in turn has contributed to the amelioration of inequality. Using an original time-series cross-sectional dataset covering the highly redistributive period of 1998-2015, this article finds that Brazilian states with higher political and party competition have lower levels of inequality than those with less competitive party systems. Muitos atribuiram a onda recente de renda redistribuicao no Brasil por fatores economicos e politicais nacionais como o 'boom de commodities,' cambios no salarios-minimos, premios mais baixos para mao de obra qualificada, e a ascensao do Partido dos Trabalhadores e o Presidente Luiz Inacio Lula da Silva. Embora, muito menos atencao foi dedicada para a pesquisa de desigualdade no nivel subnacional, onde niveles relativos de desigualdade atraves os estados permanecem incrivelmente variados. Esse artigo faz o argumento que a transicao democratica mais recente no Brasil aumentada competicao em os sistemas de partidos de alguns estados, que por sua vez contribuiu para a melhoria de desigualdade. Utilizando dados do periodo 1998-2015, assim como analise qualitativa um par de estados, Para e Rio Grande do Sul, esse artigo encontra os estados brasileiros com sistemas partidos mais competitivo sao mais provaveis para avancar politicais de sociais e ter niveles mais baixos de desigualdade que outros com sistemas partidos menos competitivos., Despite remaining one of the world's most unequal countries, Brazil has experienced an unprecedented wave of income redistribution in the twenty-first century. Substantial drops in income inequality prompted literature focusing [...]

Political parties have long been theorized as a key political institution that links society with the formal political system, and thus have often featured prominently in theories of political economy and redistribution. Curiously, however, until recently party systems have received substantially less attention in theories seeking to explain redistribution among both democratic and non-democratic regimes. I build on this nascent literature by conceptualizing the relationship between party systems, inequality, and redistribution, advancing the argument that at least a portion of inequality and income redistribution in any given country is attributable to dynamics within its party system—particularly their structure and institutionalization. Hegemonic party systems can initiate large waves of social reform and redistribution in their formative years but their redistributive prospects significantly wane the longer a hegemonic party remains in power, while two-party systems are unlikely to provide much, if any, alleviation of inequality. Multi-party systems provide the greatest potential to redistribute, but the relationship is conditional on their relative institutionalization. Stable multi-party systems with institutionalized parties are more likely to exhibit both lower levels of inequality and redistribute more income, whereas inchoate counterparts are unlikely to be more redistributive than either hegemonic or two-party systems. [ABSTRACT FROM AUTHOR]

[beta]-Secretase [also known as the [beta]-site amyloid precursor protein cleaving enzyme 1 (BACE1)] is an enzyme involved in the production of A[beta]-amyloid plaques in the brains of patients with Alzheimer's disease. The enhanced production of this enzyme occurs. without corresponding changes in BACE1 mRNA levels. The complex 5' leader of BACE1 tuRNA contains three upstream ORFs (uORFs) preceding the BACE1 initiation codon. In this study, we investigated how this 5' leader affects translation efficiency as first step in understanding the enhanced production of the enzyme in the disease. Using reporter constructs in transfected mammaliar cell lines and cell-free lysates, we showed that the translation mediated by the BACE1 5' leader is cap-dependent and inhibited by cis-acting segments contained within the 5' leader. Disruption of the uORFs had no effect on translation in B104 cells, which was surprising because the first two AUGs reside in contexts able to function as initiation codons. Possible mechanisms to explain how ribosomes bypass the uORFs, including reinitiation, leaky scanning and internal initiation of translation were found to be inconsistent with the data. The data are most consistent with a model in which ribosomes shunt uORF-containing segments of the 5' leader as the ribosomes move from the 5' end of the mRNA to the initiation codon. In PC12 cells, however, the second uORF appears to be translated. We hypothesize that the translation efficiency of the BACE1 initiation codon may be increased in patients with Alzheimer's disease by molecular mechanisms that enhance shunting o increase the relative accessibility the BACE1 initiation codon.

Numerous eukaryotic mRNAs contain sequences complementary to segments of the 18S and 28S rRNAs. Previous studies raised the possibility that these complementarities might allow mRNA-rRNA interactions and affect rates of translation. In the present study, we investigated the mRNA encoding the mouse Gtx homeodomain protein. This mRNA contains within its 5[prime] untranslated region (UTR) a segment that is complementary to two regions of the 18S rRNA, located at nucleotides 701-741 and 1104-1136. A Gtx RNA probe containing this complementarity could be photochemically cross-linked to ribosomal subunits through a linkage to 18S rRNA but not to 28S rRNA. Oligonucleotide-directed RNase H digestion of the rRNA and a reverse transcription analysis localized the cross-linked probe to the complementary segment of 18S rRNA at nucleotides 1104-1136 but not at nucleotides 701-741. To determine whether complementarity in the Gtx mRNA affected translation, a mutational analysis was performed with a Gtx-luciferase fusion construct and four related constructs with altered complementarity to the 18S rRNA. These constructs were examined for their ability to be translated in cell-free lysates prepared from P19 embryonal carcinoma and C6 glioma cell lines and after cellular transfection into these same cell lines. In both cell-free translation and transfection studies, the rate of translation decreased more than 9-fold as the degree of complementarity to nucleotides 1104-1136 of the 18S rRNA increased. We hypothesize that segments complementary to rRNA, such as those contained within the Gtx mRNA, form a category of cis-acting regulatory elements in mRNAs that affect translation by base pairing to rRNA within ribosomes.