Sentence examples for defects hypothesized from inspiring English sources

Three non-exclusive molecular defects hypothesized to contribute to DM1 pathology are (i) decreased DMPK levels resulting from aberrant nuclear accumulation of the mutant DMPK RNA [14], [15] (ii) decreased SIX5 levels occurring as a consequence of chromatin condensation that occurs in the vicinity of the expanded CTG tract [16] [18] and (iii) intrinsic toxicity of the expanded CUG tracts [19].

Previous publications that have reported significant associations between drinking-water nitrates and birth defects hypothesized that nitrate might act as a teratogen through its contribution to the endogenous formation of N-nitroso compounds (Croen et al. 2001; Dorsch et al. 1984).

To repair large, segmental bone defects using adipose-derived stem cells (ASCs) which alone cannot heal massive defects, we hypothesized that sustained expression of factors promoting osteogenesis (BMP2) and angiogenesis (VEGF) provides continuous stimuli to augment the healing.

As merovingian mutants are resistant to both these toxicants and show vestibular defects, we hypothesized that resistance to hair cell toxicants might result from reduced drug uptake due to impaired mechanotransduction.

Given the link to BRCA1 defects, we hypothesize that this phenotype i.e., RB/p16 dysfunctional TNBCs could be promoted by DNA repair defects, a feature associated with enhanced sensitivity to DNA damaging agents often used in treatment of hormone-receptor negative disease.

Zhu et al. (2003) did not observe any major differences in the linkage structure of the non-cellulosic polysaccharides in the CLSA9 defective mutant and hypothesized that the defect in binding A. tumefaciens may arise from the altered ability of the Arabidopsis mutant to secrete particular polysaccharides necessary for bacterial recognition of the host and subsequent attachment.

Given the increased severity of the CE defect, it was hypothesized that there would be an even greater incidence among these children.

It has been hypothesized that defects in mitochondrial fusion result in irregular distribution of mitochondrial DNA between organelles leading to loss of mitochondrial DNA and impairment of oxidative phosphorylation [21].

We therefore hypothesized that defects in NMJ development underlie motor impairments in dGALT mutants (Xia et al., 2012; Courchesne et al., 2011).

Based on the data from the BHDS-derived tumors, we hypothesized that defects in FLCN may be associated with increased expression of genes related to mitochondria and OXPHOS.

It is hypothesized that defects in reuptake would result in excess NE at sympathetic nerve terminals, giving rise to the POTS phenotype.