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Compounds 9 and 15 (DR=0.9 and 111, respectively) stimulated locomotor activity, whereas the other compounds suppressed this response.
Similar data were obtained with RANKL-stimulated and TNF-α-stimulated splenocytes from naive mice (264 ± 49 and 105 ± 6 pg/ml for IFN-γR KO and wild-type cells, respectively, stimulated with RANKL).
In vitro and in vivo studies demonstrated a release of proinflammatory cytokines (TNF-α, IL-1β, IL-6) and G-CSF and GM-CSF from lymphomonocyte and alveolar cells, respectively, stimulated by mycoplasma- and ureaplasma-derived lipoproteins [ 29, 30].
In addition, morphine and naloxone respectively stimulated and inhibited feeding in starved worms, but not in worms lacking NPR-17, which encodes a protein with sequence similarity to opioid receptors.
Normoxic and hypoxic cell culture supernatants, respectively, stimulated the migratory activity of MDA-MB-231 cells to 66.1 ± 3.3 and 78.5 ± 0.6% locomoting cells, of MDA-MB-435S cells to 35.2 ± 0.4 and 50.4 ± 3.0% locomoting cells, of MDA-MB-468 cells to 50.3 ± 1.6 and 58.1 ± 12.6% locomoting cells, and of MCF-7 cells to 59.8 ± 9.4 and 71.8 ± 4.5% locomoting cells.
Adherent cells were further cultured in DMEM (control samples) or treated with 1 μg/mL LPS (Sigma-Aldrich, E.coli 0127 B8) or 10 μg/mL Poly (I C) (Sigma-Aldrich) respectively (stimulated samples) for 0 h, 2 h, 6 h, 12 h, 24 h and 48 h.
Similar(53)
These global regulators, which are elevated during the 'stringent response' to amino acid starvation and upon glucose starvation, respectively, stimulate retrotransposition.
Several of the known tumor-suppressor genes (p53, PTEN, TSC1/TSC2) and tumor-associated genes (p21, AKT) also respectively stimulate or inhibit autophagy.
The V* and C* mutants were more potent than wild-type (p=0.018 and 0.053, respectively), stimulating nucleation 10 ± 3-fold and 6 ± 3-fold.
We found that morphine and naloxone, respectively, stimulate and inhibit feeding in starved wild-type worms, but not in worms lacking the G-protein coupled receptor NPR-17.
It must be pointed out that PKG and PKC, activated by ANP and dopamine, respectively, stimulate DARPP-32 phosphorylation, which in turn induces the inactivation of Na+, K+-ATPase [ 17, 62].
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