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To overcome this latter defect, "heat-seal" adhesives were introduced in the late 1960s.
However, this latter defect could be a secondary consequence from the primary vacuolar pH alteration observed in btn1-Δ cells.
This latter defect is due to a lack of LPA-mediated constitutive activation of the Rho-ROCK and LIM kinase pathways.
This latter defect was not examined in great detail, but cursory inspection revealed embryos in which the epithelium had failed to enclose, thus resulting in gross disorganization of tissue types and gut cells on the exterior of the embryo (Soto et al. 2002).
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We note that the latter defect is of little consequence because even if all green segments were disconnected, the remaining network would still remain connected and percolating the entire domain of the phase.
If the latter defects were shown to be extensible to genes actually involved in the spermatogenic program this would represent a conceptual advance in the field.
In the latter, defects with osteogenic insufficiency are determined by poor intensity of osteogenesis, and, accordingly, they require not optimization but rather induction and maintenance of reparative processes on a high level that may be achieved by introducing additional growth factors, substances increasing their synthesis, or cells that are able to produce them.
The latter defect may be congenital because of an enzymatic or a hemoglobin abnormality, as mentioned above; or it may be acquired as the result of the excessive use of coal tar derivatives, such as phenacetin, which convert hemoglobin to pigments incapable of carrying oxygen (methemoglobin, sulfhemoglobin).
The latter defect may be congenital because of an enzymatic or a hemoglobin abnormality, or it may be acquired as the result of the excessive use of coal tar derivatives, such as phenacetin, which convert hemoglobin to pigments incapable of carrying oxygen (methemoglobin, sulfhemoglobin).
The latter defect was associated with a failure of in-coming virions to disassemble PML bodies.
The latter defect causes post-natal lethality in ∼50% of mutant mice.
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