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The accompanying review by Dr Mary Hendrix et al [ 16] now expands this hypothesis to breast cancer using the in vitro culture system.
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We expand this hypothesis with a rigorous characterization of the megafaunal syndrome and examine its ecological and life-history correlates.
We expanded this hypothesis to include genes from the circadian system and assumed that some of the circadian clock genes would be associated with depression accompanied by signs of disturbed sleep, early morning awakening, or daytime fatigue.
We suspect that the upper band represents a post-translational modification of the fragment but further experiments would be required to confirm and expand this hypothesis.
The SAE complex described here supports and expands on this hypothesis by confirming a close association between stonin2, STG and AP2 while describing a specific multi-molecular complex that includes other adaptor proteins in addition to clathrin coat proteins.
To expand on this hypothesis, we sought genomic signatures of functional change within the aromatase paralogs.
Future analyses to test and expand on this hypothesis, could entail measuring these cellular mitochondrial flux parameters in groups of high (or normal) MMSE and significantly declined MMSE score (without significant AD neuropathology), in addition to groups of control (or early AD) and severe AD (severe neuropathology).
Now that the genomic location of these genes are known for guppy, we expand on this hypothesis in that both SWS2B and A180 should be the most highly expressed genes in the SWS2-LWS gene cluster if distance to the LCR negatively correlates with expression.
Ranieri and coworkers further expanded on this hypothesis by demonstrating that what was previously thought of as a conventional ventilation strategy (12 ml/kg) can lead to an increase in both local and systemic inflammatory mediators [ 27], and that an increase in plasma IL-6 levels correlates with the development of MODS [ 27, 29].
Its high expression in expanding cells strengthens this hypothesis (Additional file 3F).
We now expand more on this hypothesis by referring to the concept of Hsp90 as a 'general regulator of evolvability'.
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