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The latter group points to altered milk composition and synthesis of protection factors, such as antimicrobials and reactive oxygen species in the late stage of infection.
In particular, this remodeling included the nearly complete loss of phosphofructokinase and NAD-dependent glutamate dehydrogenase activity in differentiating cells points to altered carbon flux repartitioning via the glycolytic pathway, and meiosis-specific regulation of the glutamate metabolism, respectively.
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This is substantiated by a number of experimental evidence pointing to altered mitochondrial Ca2+ buffering capacity (Panov et al, 2002), altered mitochondrial bioenergetics (Grunewald & Beal, 1999), increased susceptibility of cells derived from animal models of HD to excitotoxicity by N-methyl d-aspartate (NMDA) receptor activation (Zeron et al, 2002).
Thirty percent were cell-specific, pointing to altered targets recognition by GATA3 following tumorigenesis.
The TTLshort phenotype was further characterized by a gene expression signature pointing to altered survival/cell death (cd) pathways in high risk/early-relapse leukemia.
H-spectroscopic MRI studies have revealed decreased N-acetylaspartate (NAA) and creatine in the anterior vermis and cortex, pointing to altered neuronal integrity [ 12, 17].
Most functional abnormalities in failing human hearts pointed to altered Ca2+ handling and could be related to a decreased function of the sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) and increases in the sarcolemmal Na+/Ca2+ exchanger.
While mutations have not been observed in the known open reading frames of SEPT9, there is now abundant evidence pointing to altered expression of SEPT9 in ovarian (Burrows et al, 2003) and breast (Montagna et al, 2003) tumours.
Thus, the present results point to altered neuronal processing in key areas of the intra-amygdaloid fear circuitry that are thought to play a critical role in the extinction of learned fear.
Now we show significantly elevated messenger RNA levels of D2-autoreceptors, as well as GIRK2 in remaining human SN DA neurons in Parkinson's disease, pointing to altered D2-autoreceptor function in the course of the disease.
Previously, we have shown altered localisation of this mutant protein when re-expressed in TSC1-null urothelial cells and unlike other somatic missense mutants, there is no splicing defect or reduced protein stability [ 58] pointing to altered function (possibly dominant negative) rather than haploinsufficiency in this case.
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