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IEEE 30-bus system is used to explain the identification of loss sensitivity methodology and the validity of the optimal dispatch model is proved.
The identification of loss scenarios and determination of the time periods at which a process experiences each scenario are described first.
In addition, frequent polymorphisms present in normal compared to tumor tissue could serve as a tool for the rapid identification of loss of heterozygosity (LOH) in the tumor.
The concept is called ExSys-LOPA, which employs, prepared in advance, values from engineering databases for identification of loss events specific to the selected target process and subsequently a accident scenario barrier model developed as an input for LOPA.
The baseline characteristics of the exposed and unexposed children were comparable, although exposed children were more often born preterm or born during later years, mainly due to better options for identification of loss of grandparents (Table S1).
In addition, a frequent identification of loss of heterozygosity (LOH) in chromosome 8p in HCC cases, suggested that inactivation of the Deleted in Liver Cancer 1 gene (DLC-1) may play pivotal roles in HCC development [5].
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The idea that FLNa is important for migration was reinforced by identification of loss-of-function mutations in FLNa as causative for PVH [16], a disease associated with defective neuronal migration.
A clear genetic link between mitochondria and PD was defined by our identification of loss-of-function mutations in the mitochondrial protein PINK1 as the cause of autosomal recessive early-onset PARK6-linked Parkinsonism, a variant of PD with particularly early onset and mild progression that affects the autonomic and cognitive nervous system less than sporadic PD [1], [2].
Moreover, we also report the identification of loss-of-function mutation of SASPase in the human genome.
This concept has been brought about by the identification of loss-of-function mutations in the bone morphogenetic protein receptor-2 (BMPR2) gene that promotes cell proliferation and suppress apoptosis in 80% of familial PAH patients (Lane et al., 2000).
Future identification of loss-of-function and gain-of-function mutants, as well as the identification of the natural substrate of PvNod41, will be necessary to understand better the functional role of this enzyme during nodulation.
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