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Plasma samples were collected for measuring MF-DPI concentrations from a total of 92 patients (MF-DPI 100 μg BID, n = 30; MF-DPI 200 μg QD AM, n = 34; BDP 168 μg BID, n = 28).
Neither CO gas pre-treatment (250 ppm for one hour prior to exposure), nor the CO releasing molecule I (concentrations from 1 to 20 µM) protected cardiomyocytes from cell death (data not shown).
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No significant differences between sexes were found when comparing IGF-I concentrations from 1- and 3-month-old male and female rabbits (Fig. 3A).
To compare IFN-I concentrations from IV 24F4A-treated cohort, we used a two-way mixed-effects analysis of variance (ANOVA) to fit to log10 values of IFN-I concentrations from samples obtained both prior to and including 31 days after intravenous dosing or the last day prior to loss of the pharmacodynamics effect (BDCA2 internalization).
A fabricated polyimide (PI /graphene oxide (GO) mixed matrix membrane (MMM) was prepared at different GO/PI concentrations (ranging from 0 to 3.5 wt%) to investigate membrane performance in diluted and concentrated salt solutions.
A gradient of DNase I concentrations, ranging from 0.5 to 50 µg/ml was used.
Developmental changes and sex differences were observed in CA-III concentrations in erythrocytes and plasma from WL-chickens.
Final RIG-I concentrations varyied from 1.5 nM to 1500 nM.
SsRNA and dsRNA were transfected into HEK293T cells expressing RIG-I at concentrations from 10 nM to 1 µM and approximately 100 nM of the triphosphorylated shR9 saturated RIG-I signaling (Figure 3A).
Mean serum-free insulin-like growth factor-I (IGF-I) concentrations steadily declined from 1.21 [plusmn] 0.81 to 0.8 [plusmn] 0.36 [mu ]g/L during the FSIVGT, and this effect was restricted to lean subjects.
Consequently, the reduced IGF-I concentration observed from middle age may contribute to initiating the age-related decline in neurogenesis.
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