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This study proposes to investigative molecular discrepancies between primary colorectal cancer (CRC) samples and matched metastases.
Previous studies from us have specified the great molecular discrepancies between BSCC and non-BSCC (Lin et al, 2000; Kao et al, 2002).
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Given the molecular discrepancies we found between PDAC HoCC and other cell-in-cell phenomena described so far, we sought to characterize PDAC HoCC at the molecular level.
Molecular weight discrepancies between endogenous ADAMTS-12 protein species in EVTs and first trimester placenta (35 kDa major product) compared to exogenous ADAMTS-12 in JEG-3 cells (83 kDa major product) were observed.
Moreover, despite the popularity of the set point model among molecular biologists, a close look at the physiological and molecular data reveals discrepancies between the this model and reality [as proposed in various reviews (Keesey and Hirvonen, 1997; Friedman, 1998; Friedman and Halaas, 1998; Cowley et al., 1999; Cone, 1999; Schwartz et al., 2000) and illustrated in Fig. 1].
Discrepancies between molecular and other data are not restricted to tree topologies.
Apparent discrepancies between molecular weights of DISC1 species predicted from transcripts and those seen in vivo could potentially be explained by multiple causes.
Perhaps homoplasy, whether of nucleotide substitutions or as a result of the convergence or reversal of morphological characters, could be further investigated as a potential cause for the discrepancies between molecular and morphological distances at these nodes.
To validate results of the GenoType® MTBDRplus assay on sputum samples and address issues related to "double patterns" and discrepancies between molecular (sputum) and phenotypic results, we tested a panel (N = 78) of cultures for RIF and INH resistance using GenoType® MTBDRplus assay (Tables 1 and 4).
Yet new calibration methods may reconcile the discrepancies between the molecular clock and the fossil record, favoring more recent divergence dates.
At the molecular level, there are significant discrepancies between rodents and humans in alterations of gene regulation in metabolic dysfunction suggesting there is little overlap between the two models [ 17].
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