Inequality affects economic performance through many mechanisms, both beneficial and harmful. Moreover, some of these mechanisms tend to set in fast while others are rather slow. The present paper (i) introduces a simple theoretical model to study how changes in inequality affect economic growth over different time horizons; (ii) empirically investigates the inequality-growth relationship, thereby relying on specifications derived from the theory. Our empirical findings are in line with the theoretical predictions: Higher inequality helps economic performance in the short term but reduces the growth rate of GDP per capita farther in the future. The long-run (or total) effect of higher inequality tends to be negative. The long-run (or total) e¤ect of higher inequality tends to be negative.JEL classi…cation: O11, O15, O43
Inequality affects economic performance through many mechanisms, both beneficial and harmful. Moreover, some of these mechanisms tend to set in fast while others are rather slow. The present paper (i) introduces a simple theoretical model to study how changes in inequality affect economic growth over different time horizons; (ii) empirically investigates the inequality-growth relationship, thereby relying on specifications derived from the theory. Our empirical findings are in line with the theoretical predictions: Higher inequality helps economic performance in the short term but reduces the growth rate of GDP per capita farther in the future. The long-run (or total) effect of higher inequality tends to be negative. The long-run (or total) e¤ect of higher inequality tends to be negative.JEL classi…cation: O11, O15, O43
When the function of origins of replication in yeast was compromised by placing ARS sequences downstream of strong promoters, ARS activity might have been affected either by transcription or by an altered chromatin configuration induced by the construct. To distinguish between these possibilities, derivatives of the yeast TRP1ARS1 minichromosome were constructed that contained either the DED1 or the PET56 promoter firing against ARS1 (DEDARS and PETARS constructs). PETARS constructs transformed yeast at high frequencies and were maintained as minichromosomes consistent with efficient ARS1 function, but DEDARS constructs transformed at low frequencies and had to be rescued as minichromosomes by insertion of a second ARS (H4-ARS). Chromatin analysis revealed that the ARS1 regions in PETARS and H4-DEDARS constructs were indistinguishable from the ARS1 region of the host TRP1ARS1 circle showing a nuclease sensitive region flanked by a nucleosome. However, RNA-analysis in the ARS region showed high and low levels of transcripts in H4-DEDARS and PETARS, respectively. Transcription elongated through the A, B1, and B2 elements and ended in B3, the binding site for ABFI. We conclude that transcription through ARS1 and not an altered chromatin structure affected ARS activity in these constructs.
Aerobic oxidation of alkyl- and phenyl-substituted 4-pentenols (bishomoallyl alcohols), catalyzed by cobalt(II) complexes in solutions of γ-terpinene or cyclohexa-1,4-diene, stereoselectively gave tetrahydrofurylmethyl radicals. Cyclized radicals were trapped with monosubstituted olefins (e.g., acrylonitrile, methyl acrylate), (E)- and (Z)-1,2-diacceptor-substituted olefins (e.g., dimethyl fumarate, fumarodinitrile, N-phenyl maleic imide), and ester-substituted alkynes (e.g., ethyl propynoate). Oxidation-addition cascades thus furnished side-chain-substituted (CN, CO(2)R, COR, or SO(2)R) di- and trisubstituted tetrahydrofurans in stereoselective reactions (2,3-trans, 2,4-cis, and 2,5-trans). A diastereomerically pure bistetrahydrofuran was prepared in a cascade consisting of two aerobic oxidations, one alkyne addition, and one final H-atom transfer.
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