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Evidence for a stronger familial association of MM in Blacks observed in our study coincides with findings from the only population-based case control study published to date, in which Brown et al. [ 20], report an elevated risk of MM in patients with affected first-degree relatives with MM of 17.4-fold (95% CI 2.4 348) in Blacks and 1.5-fold (95% CI 0.3 6.4) in Whites.
Specifically, MM of yellow/CTX was positively correlated with MM of blue/CTX (| r| = 1, p < 10-200, Figure 4a), while MM of green/CTX was negatively correlated with MM of both yellow/CTX and blue/CTX.
Relative risk is the odds of not seeking compensation by individuals diagnosed with MM of occupational origin according to ReNaM epidemiological criteria.
All of the epidemiologic variables were highly significant (p <0.001) with mm of attachment loss at the mesial site having the largest coefficient (−9.841).
Data were normalized with the cellular protein content, and alkaline phosphatase activity was represented with mM of ρ-nitrophenol/mg protein release after 30 min of incubation at 37°C.
However, DOX-dependent expression of hApp+1 protein was readily detected, using transgenes encoding hApp+1, as well as transgenes encoding wild-type hApp, and the hApp+1 protein became more abundant with age (Supplemental Figure S4), consistent with MM of the hApp construct.
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Overall sheet deformation on the north side of the dome (EX1) increased concomitantly with the rockbolt signals, with 14 mm of cumulative uplift (Fig. 5a).
Cells were harvested, washed with PBS, and incubated with 0.6 mM of BS3 (bis[sulfosuccinimidyl] suberate) for 30 min at room temperature.
Subsequently, 300 µl of the lipid-paraffin solution was mixed with 30 µl inner solution supplemented with 200 mM of sucrose.
The area with thickness losses had a refined mesh with 50 mm of shell element size.
In other words, these walls with 150 mm of thickness propagate heat better than wall with 200 mm of thickness and over.
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