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This hypothesis was demonstrated by a lack of H-ras-activating mutations and upregulation at the expression level following 7,12-dimethylbenz(a)anthracene (DMBA -induced skin carcinogenesis in PTEN knockout mice [ 13].
This hypothesis was demonstrated elegantly in the study of Pranskunas which showed that patients with surrogates of the presence of organ hypoperfusion (e.g., lactate, tachycardia, hypotension, oliguria) could either have normal or reduced microcirculatory flow.
In addition, the benefit of our innovative concept without prior functional hypothesis was demonstrated by data suggesting that NCAPG might contribute to vascular smooth muscle contraction by indirect effects on the NO pathway via modulation of arginine metabolism.
This hypothesis was demonstrated in a recent study using a mouse model of DS, in which the authors showed that mutations in AVSD risk factor genes Creld1 and Hey2 were individually benign on a euploid background but substantially increased risk for septal defects when expressed on a trisomic background or when inherited together in euploid mice (Li et al. 2012).
In the last paragraph make a small conclusion where you should sum up everything you have written and give your final stand on the results: whether the hypothesis was demonstrated as correct or wrong.
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The effectiveness of the proposed hypothesis is demonstrated by comparing it to the experimental results in the present study and from the previous work.
Most behaviour change (positive or negative) happens when individuals find themselves in a completely new context and this hypothesis is demonstrated in the study conducted with Filipino migrants by D. Maneze et al. where competing priorities of daily living were perceived by study participants as a key barrier to their health-seeking behaviour.
To support this hypothesis it was demonstrated that TGFβ3 null mice develop cleft palate [24].
In support of this hypothesis, it was demonstrated that Kidins220 interacts with neurotrophin, VEGF, ephrin, and glutamate receptors, and is a common downstream target of several trophic stimuli [ 61, 62].
In support of this hypothesis, it was demonstrated that carriers of risk variants of TCF7L2 have impaired incretin effect (28) and impaired GLP-1 stimulated insulin secretion (16, 29).
Since then, this hypothesis has been demonstrated [2], and important theoretical and experimental work followed [3 5].
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CEO of Professional Science Editing for Scientists @ prosciediting.com