Estratégias de comercialização do feijão no Rio Grande do Sul.

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Extraplanar Emission-Line Gas in Edge-On Spiral Galaxies. II. Optical Spectroscopy

The results from deep long-slit spectroscopy of nine edge-on spiral galaxies with known extraplanar line emission are reported. Emission from Halpha, [N II] lambda 6548, 6583, and [S II] lambda 6716, 6731 is detected out to heights of a few kpc in all of these galaxies. Several other fainter diagnostic lines such as [O I] lambda 6300, [O III] lambda 4959, 5007, and He I lambda 5876 are also detected over a smaller scale. The relative strengths, centroids and widths of the various emission lines provide constraints on the electron density, temperature, reddening, source(s) of ionization, and kinematics of the extraplanar gas. In all but one galaxy, photoionization by massive OB stars alone has difficulties explaining all of the line ratios in the extraplanar gas. Hybrid models that combine photoionization by OB stars and another source of ionization such as photoionization by turbulent mixing layers or shocks provide a better fit to the data. The (upper limits on the) velocity gradients measured in these galaxies are consistent with the predictions of the galactic fountain model to within the accuracy of the measurements.Comment: 25 pages + several jpg figures. Accepted for publication in the Astrophysical Journal, Vol. 592, July 20 200

Inhibition of ATPIF1 Ameliorates Severe Mitochondrial Respiratory Chain Dysfunction in Mammalian Cells

Mitochondrial respiratory chain disorders are characterized by loss of electron transport chain (ETC) activity. Although the causes of many such diseases are known, there is a lack of effective therapies. To identify genes that confer resistance to severe ETC dysfunction when inactivated, we performed a genome-wide genetic screen in haploid human cells with the mitochondrial complex III inhibitor antimycin. This screen revealed that loss of ATPIF1 strongly protects against antimycin-induced ETC dysfunction and cell death by allowing for the maintenance of mitochondrial membrane potential. ATPIF1 loss protects against other forms of ETC dysfunction and is even essential for the viability of human ρ° cells lacking mitochondrial DNA, a system commonly used for studying ETC dysfunction. Importantly, inhibition of ATPIF1 ameliorates complex III blockade in primary hepatocytes, a cell type afflicted in severe mitochondrial disease. Altogether, these results suggest that inhibition of ATPIF1 can ameliorate severe ETC dysfunction in mitochondrial pathology