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To detect whether Stat-3 interacts with corresponding Stat-proteins, we immunoprecipitated proteins with an antibody directed to Stat-1, and detected Stat-3 at days of Stat-1 activation (days 3, 7 and 11; Fig. 5c).
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Utilizing this regime and the average of two replicate experiments, 19 genes increased (Additional file 1, Table S1) and 34 genes decreased (Additional file 2, Table S2) in expression (at least twofold) as the direct result of 2-day FUS3 activation (2 days +DEX) compared to the control (2 days -DEX).
Polarization experiments were carried out in a 7-day cycle, starting with activation on day 0. On day 2, cells were expanded into fresh media containing 40 U/ml of IL-2 (see Table S4A for additional details).
We next examined the effect of oral fingolimod 0.1 mg/kg per day from day 7 on microglial activation 12 days after the induction of the fDTH-EAE model in Lewis rats.
We found increased parahippocampal but not hippocampal activation across days; and further no hippocampal (or MTL) activation differences between days.
Following these demonstrations of brain activation three days later TNP-specific IgM were detected in the circulation.
The dose of 0.001 μg of Tn per eye failed to produce UPR activation 3 days after treatment.
Consistently, CNTF/LIF double knockout mice showed slight STAT3 activation 5 days after ONC+IS, which might have been induced by endogenous IL-6.
We also observed differential microglial activation 5 days after injury in atf4−/− mice, which may contribute to the attenuated motor recovery in these mice after SCI.
A recent report detecting the acute B cell response in dengue patients has found that DENV infection results in significant B cell activation at days 4 7 after onset of fever (Balakrishnan et al. 2011).
As the DC population recovers more rapidly than macrophages after CCL administration, we went on to assess the contribution of these populations in NKT cell activation six days after CCL treatment which allows recovering of DCs while macrophages remain absent.
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