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Davies explained that the relationship between the characters is not literal, stating that "It's not familial as we understand it" instead characterising spatial genetic multiplicity as "an echo and repetition of physical traits across a Time Rift".
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Moreover, due to the observed gender effects on tumor multiplicity, genetic linkage was analyzed taking into account the interaction of sex.
Just as epidemiologists in the late 1960s had to address the problem of multifactorial influences on disease, geneticists faced the same problems in addressing the genetics of "complex" traits in which disease is influenced by a multiplicity of genetic and environmental causes.
These considerations support the concept that the ASD trait is the result of a multiplicity of genetic and environmental factors.
This paradox may be due to differences in tumour location (distal vs proximal), a multiplicity of genetic profiles of patients, or patients who were not treated locally.
This way of organizing the data lends support to the hypothesis that other genetic mutations with high multiplicity might also have a causal role in the stepwise progression of normal cells to the neoplastic and frankly malignant states.
Carcinoma of the breast is a heterogeneous disease based on pathological criteria, which is probably due to the multiplicity of genetic lesions that have accumulated during tumor development, resulting in distinct tumor types.
Whether origination occurs in a single location, as in the Wee unitary NPC origin hypothesis, or is geographically distributed, evolutionary time provides ample opportunity for the emergence of a multiplicity of genetic defects in different locations within the MHC and elsewhere in the genome.
Difficulty has also arisen from the key role of factors that cannot be ascertained by questionnaire or retrospectively – notably breast density, sex hormone and probably growth-related hormone concentrations – and the complexity of the aetiology of this tumour, involving a multiplicity of genetic susceptibility traits, environmental and behavioural factors, as well as endogenous hormones.
Of the three suggestive spontaneous QTLs none map to chromosome 18 suggesting that Mom2, 3 and 7 are not involved in determining adenoma multiplicity in this genetic background or only have very weak influences that would require substantially more mice to investigate.
The heterogeneity has also been explained based on network dynamics or multiplicity of stable genetic networks (Huang and Ingber 2007).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com