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Figure 1. (a) Fluorescent responses of NP3 (5 μM) toward various analytes (10 μM). Data shown represent fluorescent intensity at 470nm, 30 min after addition of the analytes. (b) ONOO− (final 10 μM) was quickly injected into a solution of NP3 (final 5μM), and the fluorescent intensity at 470 nm was plotted against time. (c) Fluorescence enhancement of NP3 (5μM) at 470 nm as a function of ONOO− (0−10 μM) after 15 min of reaction. All data acquired in PBS (10 mM, pH 7.4) with excitation at 375 nm.Figure 2. (a) Time-lapse images taken from living EA.hy926 endothelial cells. Cells were preincubated with NP3 (5.0 μM), followed by stimulation with or without SIN-1 (0.5 mM). (b) Dynamic changes of NP3 fluorescence after SIN-1 (0.5 mM) treatment in panel a. (c) Effects of ONOO− scavengers uric acid (100 μM) and FeTTPS (1 μM) on changes in NP3 fluorescence in endothelial cells in the presence of ONOO− (60 μM). PI (red) stains nuclei. NP3 fluorescence was collected at 420−480 nm with λex 405 nm.
Western blot of HIF1α immunoprecipitated, using Aves Lab's PrecipHen® (cat. P-1010), from brain lysates of fish exposed for 6 h to normoxia (>7 mg O2 l−1; lanes 2, 5, 8, 10, and 11) or hypoxia (∼1 mg O2 l−1; lanes 3-4, 6-7, and 9). A positive HIF1α control is shown in lane 1 and the mobility of HIF1α and chicken IgY are shown by arrows (at left). HIF1α protein abundance in each sample was expressed as the ratio of the HIF1α band intensity to the IgY band intensity. Image CC-BY-4.0. PMID:38116983
Figure 1. Propidium iodide excitation and emission spectra.Figure 2. HL-60 cells were treated with a drug, then stained with FLICA® FAM-VAD-FMK poly-caspase inhibitor reagent (green) (Cat. 92) and propidium iodide (red) (PI). Scanning laser cytometer analysis. Four populations of cells were detected: (A) Unstained live cells, (B) red necrotic cells (PI), (C) green and red late apoptotic cells (FAM-FLICA® plus PI), and (D) green early apoptotic cells (FAM-FLICA®). Data courtesy of Dr. Z. Darzynkiewicz, Brander Cancer Center, NY.

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