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A taxonomic revision of <i>Allium</i> (Alliaceae) in the Canadian prairie provinces
Choi, Hyeok Jae,Cota-Sá,nchez, J. Hugo Canadian Science Publishing 2010 Botany Vol.88 No.9
<P> The taxonomy, rarity, and conservation status of Allium L. is revised for the Canadian prairie provinces, based on analyses of herbarium specimens and fieldwork. Five species are recognized: Allium schoenoprasum L., A. geyeri S. Watson var. tenerum M.E. Jones, A. textile A. Nelson & J.F. Macbride, A. cernuum Roth, and A. stellatum Ker Gawler. Distribution maps and a key to species are provided, as well as complete descriptions of the species examined, including new illustrations, information on nomenclatural types, synonymies, and chromosomal and ecological data. A lectotype is designated for A. geyeri var. tenerum. In this study, A. geyeri var. geyeri reported from Alberta and Saskatchewan and ranked in these provinces as having rarity levels S2 and S1, respectively, by the Nature Conservancy, is excluded from the Canadian flora and the rare list of these provinces because it was misidentified from a herbarium specimen of A. textile. Allium tricoccum Solander in W. Aiton is regarded as a non-native species to Manitoba. The rarity and conservation status of Allium in the Canadian prairie provinces is as follows: (i) A. schoenoprasum, listed as S2 in Saskatchewan, is rare in Manitoba, although its rarity status has not been formally assessed in the province; (ii) A. geyeri var. tenerum is the rarest Allium taxon, with distribution restricted to the Waterton Lakes National Park areas of Alberta, and is currently listed as S2; and (iii) A. cernuum was re-evaluated and a rarity level of S1S2 was recommended for the species in Saskatchewan, particularly in its southwestern distributional habitat. </P>
Link, J.M.,Yager, P.M.,Anjos, J.C.,Bediaga, I.,Castromonte, C.,Machado, A.A.,Magnin, J.,Massafferri, A.,de Miranda, J.M.,Pepe, I.M.,Polycarpo, E.,dos Reis, A.C.,Carrillo, S.,Cuautle, E.,Sá,nchez Elsevier 2009 Physics letters: B Vol.681 No.1
<P><B>Abstract</B></P><P>Using data from FOCUS (E831) experiment at Fermilab, we present a model independent partial-wave analysis of the <SUP>K−</SUP><SUP>π+</SUP> S-wave amplitude from the decay <SUP>D+</SUP>→<SUP>K−</SUP><SUP>π+</SUP><SUP>π+</SUP>. The S-wave is a generic complex function to be determined directly from the data fit. The P- and D-waves are parameterized by a sum of Breit–Wigner amplitudes. The measurement of the S-wave amplitude covers the whole elastic range of the <SUP>K−</SUP><SUP>π+</SUP> system.</P>
SUNRISE/IMaX OBSERVATIONS OF CONVECTIVELY DRIVEN VORTEX FLOWS IN THE SUN
Bonet, J. A.,Má,rquez, I.,Almeida, J. Sá,nchez,Palacios, J.,Pillet, V. Martí,nez,Solanki, S. K.,del Toro Iniesta, J. C.,Domingo, V.,Berkefeld, T.,Schmidt, W.,Gandorfer, A.,Barthol, P IOP Publishing 2010 ASTROPHYSICAL JOURNAL LETTERS - Vol.723 No.2
ARE GALACTIC WARPS INDUCED BY INTERGALACTIC FLOWS?
F. J. SÁNCHEZ-SALCEDO 한국천문학회 2004 Journal of The Korean Astronomical Society Vol.37 No.5
The interaction of disk galaxies with intergalactic winds has been invoked as a possible mechanismof the generation of galactic warps. Here we discuss conditions under which intergalactic ows canbe relevant for warping eld galaxies. Constraints include the heating of the outer disk, the level ofasymmetry in the vertical distribution of the volume gas density, the angular frequency of the warp, thesymmetry of galactic warps amplitude between the approaching and receding sides of the galaxy, and thespeed of the intergalactic ow whether subsonic or supersonic. These constraints are discussed in thispaper in reference to the proposal of Lopez-Corredoira et al. that warps can be a natural consequenceof accretion ows onto the disk.
The sensitivity of harassment to orbit: mass loss from early-type dwarfs in galaxy clusters
Smith, R.,Sá,nchez-Janssen, R.,Beasley, M. A.,Candlish, G. N.,Gibson, B. K.,Puzia, T. H.,Janz, J.,Knebe, A.,Aguerri, J. A. L.,Lisker, T.,Hensler, G.,Fellhauer, M.,Ferrarese, L.,Yi, S. K. Oxford University Press 2015 Monthly notices of the Royal Astronomical Society Vol.454 No.3
Yu, Min-A,Sá,nchez-Lozada, Laura G,Johnson, Richard J,Kang, Duk-Hee Lippincott Williams Wilkins, Inc. 2010 Journal of Hypertension Vol.28 No.6
AIMS: Oxidative stress is known to be a major mechanism of endothelial dysfunction, which plays a key role in the development of cardiovascular disease. Although uric acid is one of the most important antioxidants, recent studies have suggested that uric acid may have a causal role in endothelial dysfunction. In order to understand the paradoxical association of uric acid with oxidative stress and vascular disease, we investigated whether uric acid induced oxidative stress in human vascular endothelial cells. We also examined whether uric acid-induced changes in redox status were related to aging and death of endothelial cells or an activation of local renin–angiotensin system, another mediator of endothelial dysfunction. METHODS: Endothelial senescence and apoptosis were evaluated by senescence-associated &bgr;-galactosidase staining and annexin V–propidium iodide staining in primary isolated human umbilical vein endothelial cells (HUVECs). Production of reactive oxygen species was assessed by dichlorofluorescein diacetate staining. mRNA expression of angiotensinogen, angiotensin-converting enzyme and the receptors of angiotensin II was evaluated by real-time PCR, and angiotensin II levels were measured in uric acid-stimulated HUVECs. RESULTS: Uric acid-induced senescence and apoptosis in HUVECs at concentrations more than 6 and 9 mg/dl, respectively. Uric acid-induced alterations in cell proliferation, senescence and apoptosis were blocked by probenecid, enalaprilat or telmisartan. Uric acid significantly increased production of reactive oxygen species beginning at 5 min, and uric acid-induced senescence and apoptosis of HUVECs were ameliorated by N-acetylcysteine or tempol. Uric acid also upregulated the expression of angiotensinogen, angiotensin-converting enzyme and angiotensin II receptors and increased angiotensin II levels, which was ameliorated with tempol. CONCLUSION: Uric acid-induced aging and death of human endothelial cells are medicated by local activation of oxidative stress and the renin–angiotensin system, which provides a novel mechanism of uric acid-induced endothelial dysfunction. Therapies targeting uric acid may be beneficial in cardiovascular disease.