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Exact(6)
39 It may be that activation of the DMN is responsible for the feeling of well-being from acupuncture intervention.
A more plausible explanation would be that activation of an antiviral state either protects uninfected hepatocytes from de novo infection or induces clearance of infected hepatocytes.
The interactions between the BNST, PVN and ventral tegmental area (VTA) are complex, but one prediction would be that activation of the BNST by processive stressors (i.e., ventral subiculum and cortical areas) would result in increased output from BNST to the nucleus accumbens, VTA, PVN and/or the hypothalamic area surrounding the PVN.
Alternatively, it could be that activation of mTHPC localised to the neural cell body is sufficient to cause a reduction in neurite length.
An explanation could be that activation of the PI3K pathway in tumors that lack PTEN is relatively low compared with tumors that exhibit PI3K pathway activation from other causes.
A possible explanation could be that activation of the cryptic site is influenced by a neighbouring hnRNPA1 site that is itself strengthened (R i,final = 5.2 bits; Δ R i = 2.2 bits) and an SRp55 site that is significantly weakened (R i,final = 1.9 bits; Δ R i = -4.0 bits).
Similar(54)
An alternative mechanism to explain our data is that activation of AMPK with AICAR produces inhibition of HSC and NSC activity in H441 monolayer cells through changing Po.
The picture that emerges is that activation of FGF signaling induces the production of multiple inhibitors which act to moderate and limit the response to FGF signaling.
Another potential explanation is that activation of TP53 by damaged DNA prevents the generation of iPS cells with damaged DNA or DNA repair deficiencies [15].
The important point is that activation of Cav channels requires transient depolarization from a hyperpolarized membrane potential for activation.
One caveat is that activation of ERK might be difficult to detect due to low expression levels and timing issues.
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Justyna Jupowicz-Kozak
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