Because these results demonstrate that mitochondria are an important in vivo target of arsenite toxicity, we hypothesized that deficiencies in mitochondrial electron transport chain genes, which cause mitochondrial disease in humans, would sensitize nematodes to arsenite.
Hence, we hypothesized that deficiencies in BRCA1 would cause increased chromosomal instability in a tumor cell due to impaired DNA repair pathways and NHEJ dysfunction.
Thus, in a biomarker research substudy, we hypothesized that deficiency in Noxa expression might correlate with resistance.
We hypothesized that deficiency of Akt1 or Akt2 would prevent the in vivo effects of ActRIIB inhibition on muscle.
While some studies hypothesized a deficiency of DA exocytosis due to impaired vesicular packaging [28], others indicated a decline in the number of DA reserve pool vesicles available for mobilization [29].
We therefore hypothesized that deficiency in CXCR2 may also impair endothelial recovery and haematopoietic reconstitution.
Thus, we hypothesized that deficiency of Mena would reduce the number of metastases to the lung.
It has been hypothesized that deficiency in methionine, folate, and vitamin B12 could decrease arsenic methylation ability (National Research Council 1999; Vahter 2000).
We hypothesized that deficiency in 25-hydroxyvitamin D (25(OH D) prior to hospital admission would be associated with acute kidney injury in the critically ill.
CRWN1 and CRWN4 are the major determinants of nuclear size and shape, and we hypothesize that deficiency in CRWN proteins leads to defects in nuclear expansion and remodeling.
Therefore, in the present study it was hypothesized that hCAP-18/LL-37 hCAP-18/LL-37 hCAP-18/LL-37by the lack of proteinase 3 andeficiencyn C enzymightn GCF of patients with generalized aggressive periodontitis, and the deficiency of these enzymes might contribete to multifacausedl etiology of generalized aggressive periodontitis, by modifying hostheesponses.
