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Predicted bedload transport based on theory underestimates the actual transport and this is attributed to the modest flow velocities encountered and, perhaps, the importance of suspended load transport.
This could be attributed to the modest TFEB expression or the tissue-specific regulation of autophagy gene induction by TFEB.
These results could partly be attributed to the modest increase in 25(OH D (5 ng/mL) in subjects receiving cholecalciferol supplementation [ 98].
Alternatively, the lack of a significant association may be attributed to the modest sample size, the restriction in the range of the measure of disease activity and the high standard deviations of CRP and ESR value in our patients.
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This possibly may have been due to the use of the human CNGB3 transgene; alternatively, the results may be attributed to the relatively modest extent (∼30% of total) of retinal area transduced in that study (23).
Therefore our findings that PEEP did not influence IAP can be attributed to the relatively modest level of PEEP (15 cmH2O, 11 mmHg) in comparison to the levels of IAP (18 mmHg and 26 mmHg) used in this study (estimated trans-pulmonary PEEP of -7 and -15 mmHg, respectively).
The observed modest effect sizes could be partially attributed to the fact that low frequency or rare variants have not yet been reported.
Historically, specificity has largely been attributed to the α subunits as only modest functional differences were observed in the ability of βγ isoform combinations to regulate effectors in vitro.
The results identified 1 as a propitious hit with modest activities attributed to the concurrent down-regulation of mitogen activated protein kinase kinase/extracellular signal-regulated kinase (MEK) distinctive downstream effectors.
The modest efficacy might be attributed to the absence of graft vs tumour (GVT) reactions (Slavin et al, 2000), which is more efficiently attained by allogeneic and haploidentical BMT (Demirer et al, 2008; Kanold et al, 2008).
As typified by EGFR-targeted therapies for metastatic CRC (e.g.: panitumumab and cetuximab), this modest response is attributed to the innate and acquired proficiency of cancer cells to escape EGFR inhibition by engaging alternative oncogenic signals [ 2, 3, 52].
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