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These observations supported possible differentiation of the EPR cells in response to the proinflammatory stimulus induced by F6H8 [ 35].
An evaluation using the live/dead assay on cultured ocular cells that were incubated with F6H8 for up to 5 days showed a significant reduction of vital EPR cells.
The EC-EPR cell provided maximal sensitivity, minimal dielectric loss along the central axis of the EPR cavity, and was easy handled/mounted without the need for additional adjustments.
The spectra were analyzed as described above for whole cell EPR.
Although total intracellular iron levels remained unchanged, whole-cell EPR demonstrated that the level of loose iron in mutant cells was 3 times less than wild type cells.
Consistent with this, EPR of UP40 cells showed an intense g = 4.3 signal representing ∼370 μM HS FeIII.
EPR of Δ1 cells did not exhibit a g = 4.3 signal, consistent with the MB spectrum which lacked the corresponding sextet.
Variable-temperature EPR of UP40 cells showed a broad signal in the g = 2 region which displayed anti-Curie Law behavior.
As shown by UV visible, EPR, and whole-cell Mössbauer spectroscopy HCF101 carries a [4Fe-4S] clusthatthat can be rapidly transferred to convert the apoprotein form of a yeast [4Fe-4S] proteintonto a catalytically active holoenzyme.
Samples in EPR quartz flat cells were irradiated in the resonant cavity with 540 740 nm (70 mW/cm) light derived from a 300 W high pressure compact arc xenon lamp (Cermax, PE300CE 13FM/Module300W, PerkinElmer) equipped with a 5-cm water filter, heat reflecting hot mirror, cutoff filter blocking light below 390 nm, and long-pass filter transmitting light above 540 nm.
The intensity of the MnII signal in the EPR spectrum of UP1 cells was also greater than in WT1 or Δ1 cells, affording a [spin]/[Mn] ratio of ∼0.9.
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