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  • Determination of sixteen polycyclic aromatic hydrocarbons in aqueous and solid samples from an Italian wastewater treatment plant 16256127

    A robust procedure for the determination of 16 US EPA PAHs in both aqueous (e.g. wastewaters, industrial discharges, treated effluents) and solid samples (e.g. suspended solids and sludge) from a wastewater treatment plant (WWTP) is presented. Recovery experiments using different percentages of organic modifier, sorbents and eluting solvent mixtures were carried out in Milli-Q water (1000 mL) spiked with a mixture of the PAH analytes (100 ng/L of each analyte). The solid phase extraction (SPE) procedures applied to spiked waste water samples (1000 mL; 100 ng/L spiking level) permitted simultaneous recovery of all the 16 PAHs with yields >70% (6–13% RSD). SPE clean up procedures applied to sewage and stabilized sludge extracts, showed percent recoveries in the range 73–92% (7–13% RSD) and 71–89% (7–12% RSD), respectively. The methods were used for the determination of PAHs in aqueous and solid samples from the WWTP of Fusina (Venice, Italy). Mean concentrations, as the sum of the 16 PAHs in aqueous and suspended solid samples, were found to be approx. in the 1.12–4.62 μg/L range. Sewage and stabilized sludge samples contained mean PAH concentrations, as sum of 16 compounds, in the concentration range of 1.44–1.26 mg/kg, respectively. Extraction and clean up procedures for sludge samples were validated using EPA certified reference material IRM-104 (CRM No. 912). Instrumental analyses were performed by coupling HPLC with UV-diode array detection (UV-DAD) and fluorescence detection (FLD).
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo

  • Relaxin ameliorates hypertension and increases nitric oxide metabolite excretion in angiotensin II but not N(ω)-nitro-L-arginine methyl ester hypertensive rats. 21670419

    Previous findings suggest a potential therapeutic action of relaxin, the putative vasodilatory signal of normal pregnancy, in some forms of cardiovascular disease. However, the mechanisms underlying the beneficial effects of relaxin have not been fully elucidated. The purpose of this study was to determine whether the vasodilatory effects of relaxin are dependent on activation of NO synthase. We examined the effect of relaxin in male Sprague-Dawley rats given angiotensin II (Ang II; 200 ng/kg per minute SC by minipump), the NO synthase inhibitor N(ω)-nitro-l-arginine methyl ester (l-NAME; 1.5 mg/100 g IV followed by 150 mg/L in drinking water), or vehicle for 3 weeks. After 7 days of Ang II or l-NAME, mean arterial pressure was elevated compared with baseline. Relaxin was administered (4 μg/h, SC by minipump) for the next 2 weeks of Ang II, l-NAME, or vehicle treatment. Two-week relaxin treatment alone slightly reduced mean arterial pressure in normotensive rats. Three weeks of either Ang II or l-NAME treatment alone produced hypertension, albuminuria, mild glomerular sclerosis, reduced nitric oxide metabolite excretion, and increased oxidative stress (excretion of hydrogen peroxide and thiobarbituric acid reactive substances and renal cortex nitrotyrosine abundance). Relaxin reduced mean arterial pressure, albumin excretion, and oxidative stress markers and preserved glomerular structure and nitric oxide metabolite excretion in Ang II-treated rats; however, relaxin did not attenuate these changes in the rats treated with l-NAME. None of the treatments affected protein abundance of neuronal or endothelial NO synthase in the kidney cortex. These data suggest that the vasodilatory effects of relaxin are dependent on a functional NO synthase system and increased NO bioavailability possibly because of a reduction in oxidative stress.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-233
    Nombre del producto:
    Anti-Nitrotyrosine Antibody, clone 1A6

  • The Functional Antagonism between Eg5 and Dynein in Spindle Bipolarization Is Not Compatible with a Simple Push-Pull Model. 22832270

    During cell division, the molecular motor Eg5 crosslinks overlapping antiparallel microtubules and pushes them apart to separate mitotic spindle poles. Dynein has been proposed as a direct antagonist of Eg5 at the spindle equator, pulling on antiparallel microtubules and favoring spindle collapse. Some of the experiments supporting this hypothesis relied on endpoint quantifications of spindle phenotypes rather than following individual cell fates over time. Here, we present a mathematical model and proof-of-principle experiments to demonstrate that endpoint quantifications can be fundamentally misleading because they overestimate defective phenotypes. Indeed, live-cell imaging reveals that, while depletion of dynein or the dynein binding protein Lis1 enables spindle formation in presence of an Eg5 inhibitor, the activities of dynein and Eg5 cannot be titrated against each other. Thus, dynein most likely antagonizes Eg5 indirectly by exerting force at different spindle locations rather than through a simple push-pull mechanism at the spindle equator.
    Tipo de documento:
    Referencia
    Referencia del producto:
    06-570
    Nombre del producto:
    Anti-phospho-Histone H3 (Ser10) Antibody, Mitosis Marker