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Phylogenetic analyses were also carried at the DNA level for the rpoB gene.
The median plasma DNA level for all patients on admission to the ICU was significantly higher than that of the controls (80 (48–260) ng/ml, P = 0.001).
The mean baseline HBV DNA level for these 30 patients was 1.46±5.77 × 10 IU ml−1 (range undetectable (<200) to 2.8 × 10IU ml−10IU
Restriction fragment length polymorphism results obtained from Mori et al., (1995) showed larger intraspecific variation (at the DNA level) for T. dicoccoides than for T. araraticum.
Resulting colonies were analyzed on the DNA level for Cre-mediated CTCF deletion of Ctcflox/lox into Ctcfdel/del and on the protein level for expression of endogenous or exogenous protein.
Furthermore, the mean value of the log10 HBV DNA level for group 2 and group 3 before LdT treatment is 3.58 (SD=1.41), and that is after 1.98 (SD=1.14) LdT treatment (p-value <0.0001).
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The best strategy for chronic hepatitis B patients with poor response to 48 weeks of Peginterferon-based therapy has been controversial and the predictive value of hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA levels for determining the sustained virological response (SVR) of these patients is uncertain.
Hepatitis B virus (HBV) DNA levels for both drugs were measured at baseline and weeks 24, 36 and 48.
Receiver-operating characteristics (ROC) curve analysis was carried out to define cutoff DNA levels for the prediction of malignancy.
Similarly, LAM-treated mothers had a mean serum HBV DNA decline >3 log10 copies/mL, resulting in a mean (SD) HBV DNA of 3.78 (1.32) log10 copies/mL, compared to no change in HBV DNA levels for the untreated group (P < 0.001).
Before delivery, LdT-treated mothers had a mean serum HBV DNA decline >4 log10 copies/mL, resulting in a mean (SD) HBV DNA of 3.16 (1.59) log10 copies/mL, compared to no significant change in HBV DNA levels for the untreated group (P < 0.001).
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