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We further assessed apoptosis (annexin-V binding and active caspase-3) by flow cytometry.
Compared with healthy controls, septic shock induced a marked increase in apoptosis as detected by the annexin-V binding and active caspase-3 on CD4+ T cells, CD8+ T cells and CD19+ B cells.
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Infected mast cells exhibited pyknotic nuclei and active caspase-3 and caspase-1 expression.
Expression of p53 and active caspase-3 were increased in 3-NP treated animals.
Cytostatic and cytocidal effects were evaluated using MTT assays and active caspase-3 immunocytochemistry.
d The expression of BCl-2, Bax, and active Caspase-3 after different treatments.
At the same time, the expression of Bax and active Caspase-3 increased.
Accordingly, there are five main components in our model, [TNF-R], [Casp8], [Casp3], and [Casp3*], which represent the concentrations of bound TNF receptor, pro-caspase-8, pro-caspase-3, active caspase-8 and active caspase-3, respectively.
Apoptosis induction in each specific lymphocyte subpopulation - CD4+ T cells, CD8+ T cells and CD19+ B cells - was assessed using annexin-V binding and intracellular active caspase-3 measurements.
Treatment with gentamicin for 6 or 12 h promoted the expression of active caspase-3 and active caspase-9 in many hair cells along the BP as shown by immunohistochemistry.
However, the level of active caspase 3 and active caspase 9 in GBM cells after AgNPs treatment seems to be on the border between spontaneous and induced apoptosis.
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