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Amelogenesis imperfecta (AI) is the collective term for a heterogeneous group of conditions characterized by genetically determined defects in tooth enamel biomineralization which lead to premature clinical failure.
Genetically determined defects in the skin barrier (eg, PSORS4 and PSORS6) lead to the activation of skin resident plasmocytoid dendritic cells by antimicrobial peptides such as cathelicidin (LL37) or beta-defensin 2 induced by saprophytic flora or trauma.
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Amelogenesis imperfecta (AI) is a rare, genetically determined defect in enamel mineralization associated with poor esthetics and dental sensitivity.
Amelogenesis imperfecta (AI) is a rare, genetically determined defect in enamel mineralization with a prevalence between 1 14,000 and 1 700 [ 1, 2].
19 NZB/W mice have a genetically determined defect in B cell activation, with excessive polyclonal IgM production from shortly after birth, and impaired tolerance induction.
This is due to technical advances, including those that can determine defects in the prenatal stage, as well as to the growth of neonatology as a specialty.
In this study, two new PIGs which can be used to investigate the speed variable while determining defects in pipelines are designed.
With this approach, correlating defects and electronic transport becomes a manageable task, as the experimenter can determine defects with atomic resolution and simultaneously measure the conductivity.
As already reported [ 125, 126], MIRs have an important role in the pathogenesis of cancer and it may be expected that many of them could have a critical function in determining defects of AM functions [ 127, 128].
Studies on SAC1 showed that it localises in Golgi apparatus, while the AtSAC1 gene in the fragile fiber7 (fra7) mutant determines defects in fibre and vessel cell wall thickness and affects actin organisation but not MTs in elongating cells (Zhong et al., 2005).
Esch, F. et al. Electron localization determines defect formation on ceria substrates.
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