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This hypothesis is supported by another study demonstrating a different expression profile of parkin mRNA splice variants in frontal cortex of patients with common dementia with LB, pure form of dementia with LB, and Alzheimer disease suggesting the direct involvement of isoform-expression deregulation in the development of such neurodegenerative disorders [ 17].
Our data is supported by another study demonstrating that immortalized proliferation of mouse embryonic fibroblasts from PKD1 mice occurs without the induction of p53 and (at late passage) p21 [ 28], as well a study showing that the CDK inhibitor roscovitine arrests disease progression[ 10].
These results have recently been confirmed by another study demonstrating that four TNBC cell lines (including HCC1937, MDA-MB-157 and MDA-MB-468 used in this study) had reduced viability following Chk1 knockdown with a specific siRNA [ 41].
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By contrast, another study demonstrated that acute application of 1 μM testosterone had no effect on either the amplitudes or time courses of contractions in ventricular myocytes isolated from adult female rats [ 113].
In another study demonstrated by S. F. Fernandez et al., airways macrophages exposures to a low pH (1.75) for 1 min resulted in reduction in all lipopolysaecharide (LPS) and lipoteichoic acid (LTA -mediated cytokine reLTA -mediated
There is evidence suggesting some of our candidate chemokines may be invoked following bacterial colonization; S. aureus antigens have been shown to stimulate expression of CCL1 by dendritic cells [ 43] while another study demonstrated human alveolar epithelial cells produced CCL2 following stimulation by LPS, a component of the gram-negative cell wall [ 44].
Another study demonstrates that ERK suppression by MEK inhibitor increases EGF-stimulated AKT activation14,15.
These findings are similar to those reported by another recent study demonstrating efficacy of 120,000 units in divided doses [ 5].
These results are further supported by our previous study demonstrating that OLMα2 cell activity facilitates CA3 input while inhibiting a direct input from the entorhinal cortex18.
This in vitro ability is also supported by a previously published study demonstrating a methylation-independent repression by MBD1v1 on another promoter [ 31].
These results were confirmed by another study that demonstrated SDF-1 to be a chemokine capable of trafficking hematopoietic stem cells and EPCs whereby its focal concentration leads to increased vascularity of that region [ 51].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com