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We have previously prolonged the survival time of mice challenged with the RH strain of T. gondii by immunizing the mice with a eukaryotic vector expressing the protein ROP18 of T. gondii.
Previously, prolonged RCT was observed in neuropathies in the course of some diseases, e.g., in multiple sclerosis [ 29] and glaucoma [ 41].
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We previously demonstrated prolonged, profound CD4+ T-lymphopenia in rheumatoid arthritis (RA) patients following lymphocyte-depleting therapy.
It has been reported previously that prolonged respiratory support and difficult weaning may be a consequence of intermediate syndrome [ 11].
However, as previously shown, prolonged inactivation of LRPPRC mma-1 eventually leads to mitochondrial fragmentation, a drop in ATP level and the loss of cellular and organismal functions [ 11].
The latency of saccades that return gaze to a location that was fixated previously is prolonged relative to saccades that bring the line of sight onto a "new" location.
We have previously reported that prolonged (four weeks) treatment with the antiepileptic drug valproate (VPA) after SE prevents hippocampal damage and most of the behavioral alterations that occur after brain insult, but not the development of spontaneously occurring seizures.
We previously showed that prolonged treatment with the liver-selective thyromimetic T-0681 dreducedally reduced the atherosclerotic lesion area in NZW rabbits [10].
As reported previously, nilotinib treatment prolonged the survival of mice.
As previously observed, PEDF prolonged the survival of tumor-bearing mice.
We have previously found that prolonged (i.e. more than 72 hours) culture in FGF2/CHIR mediates further differentiation of NMPs into mutually exclusive paraxial mesoderm and neurectoderm cells.
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