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Hence, the hypothesis of a defect in dFoxo function may help explain the reduced levels of dilp2-3,5 observed in female SdcBG02774 flies.
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Here, our miRNome analysis agrees with the hypothesis of a constitutive defect leading to impaired cartilage maturation.
Our proteomic study was designed to explore the hypothesis of a putative constitutive defect in epiphyseal cartilage and/or subchondral bone associated with the development of primary lesions.
This hypothesis of a transient migration defect and of a delayed migration rather than an arrest of migration is reminiscent of our recent findings regarding the consequences of Tubb3 knockdown on radial migration.
By showing a close direct correlation between peripheral blood and bone marrow CD34+ cells and a low bone marrow cell content in diabetic versus nondiabetic patients, we support the hypothesis of a bone marrow defect in diabetes.
These findings reported by Garza et al support the hypothesis that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of androgenetic alopecia.
Finally, we found that supplementation with leucine attenuated the anti-hypertrophic effect of MEF2C depletion, as indicated by gravimetry and histological data shown in Figure 7D, E. These data are consistent with the hypothesis that a defect in the activation of mTOR/S6K pathway provides a mechanism by which MEF2C depletion attenuates the load-induced left ventricular hypertrophy.
The above mentioned results [32], along with the demonstration of RASSF1A methylation in tumor samples from patients with multiple lesions, and the lack of differences in other factors predisposing to tumor multiplicity (i.e. family history) favor the hypothesis of an underlying epigenetic defect.
One hypothesis for the lack of a defect in both tumour growth and metastasis is that the closely related Pyk2 kinase is functionally substituting for FAK.
We tested the hypothesis of the existence of a defect in the 5, 10-methylenetetrahydrofolate reductase (MTHFR) in ovarian tumours that could cause reduced intracellular regeneration of the 5-methyltetrahydrofolate and induce increased FBP expression.
This does not exclude the hypothesis of an epigenetic and silencing defect of the paternal X chromosome in those mice, which could explain the sex-ratio distortion observed.
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