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The Wright function, which we denote by W ( z ; α, β ), is so named in honor of Wright who introduced and investigated this function in a series of notes starting from 1933 in the framework of the asymptotic theory of partitions.
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The rationale of investigating this function is that adding to the input its rotated version causes larger changes in the output than a rotate-XOR operation had: a flipped bit in the input influences at least two output bits, but usually much more, dependent on the carry propagation.
Here we have used the gold standard technique of implanted telemetry to investigate this function.
We know that executive function is a complex construct, and future research should investigate this function in a more comprehensive way, such as monitoring and initiation ability, to specifically determine the relationship between executive function, gist memory performance and item-specific memory performance.
We next investigated this new function by studying the mouse model of Ophn1 deficiency and found that various cellular mechanisms mediated through CME are impaired in the mutant.
Here, we investigated this by disabling IFN function, small RNA function, or both activities in the context of virus infection.
As the α6 integrin subunit was reported to be involved in cell proliferation (20, 21), we further investigated if this function could be attributed to the α6A splice variant.
Currently, we are investigating this putative function of METTL23 and developing heterologous expression systems that will yield soluble protein for further characterization of its enzymatic properties.
In order to investigate this potential function, we generated a series of Armet and Creld2 substrate-trapping mutants similar to those previously generated for other PDIAs (e.g. ERp72, ERp57, ERp46 and PDI), which have all previously been validated and characterized in depth (34).
In this study, we investigated the function of the P-TEFb functional equilibrium in controlling the epithelial mesenchymal transition (EMT), invasion, and metastasis of human breast cancer.
We determined the identity of the nerve cell in which this gene is primarily expressed, investigated the function both of this nerve cell and of ceh-63, and defined a cascade of transcription factors working through CEH-63.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com