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A Central Intelligence Agency CIAanalysissis concluded that it is possible that the failure of the ARBiH HVO counterattack prompted the HVO to agree on a truce with the VRS on 9 October.
It is therefore possible that the failure of the auxin distribution system in sterol mutants contribute to the observed aberrant ethylene responses, and suppression of the latter by ein2 in turn ameiorates the auxin transport defects.
It is possible that the failure of G93A mice to upregulate Hsp70 led to the faster clinical onset and disease progression observed under energy restriction and that once again, males were poorly defended against the heightened lipid peroxidation and inflammation compared to females.
It was possible that the failure of HLH-1 bound intervals to enhance bodywall muscle reporter gene expression in wild type animals was due to the relatively low levels of endogenous HLH-1 compared to the levels of heat shock induced HLH-1 or epitope-tagged HLH-1 used to identify potential binding sites by ChIP.
Therefore, it was possible that the failure of telomeres to progressively elongate in Ku null strains in the presence of a Cdc13– Est2 fusion was a secondary effect of loss of end protection.
Thus, it is possible that the failure of nodular hepatocytes to integrate into the surrounding parenchyma is due, at least in part, to the altered expression of proteins involved in cell-to-cell communication and adhesion.
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It is possible that the failure to find effects of non-spatial cues on perceptual sensitivity is due to an exclusive focus on visual cues, which are, in fact, ineffective in improving visual sensitivity for non-spatial features.
Although proinflammatory IFN-γ and TNF-α responses usually occur at early stages of immune responses, it is also possible that the failure to detect abnormal levels of serum IFN-γ or TNF-α may stem from missing the very early time point in our study.
Given that the genetic organisation of the LplA1 gene locus is highly syntenic in P. falciparum and P. berghei, it is possible that the failure to obtain a gene disruption of LplA1 in P. falciparum is due to its important function for the parasites during their erythrocytic development.
Lastly, it is possible that the failure to detect LVH was related to the over-estimation of LVH by echocardiography.
"It is possible that the failure to disclose these facts renders the warrant unlawful".
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