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Given these data, which provide additional evidence of sik1 deficiency activity in our cells, we further analyzed the data obtained by array experiments using two stringent criteria: 1. looking for genes expressed in the heart; 2. looking for genes already known to cause cardiac phenotype when mutated (i.e. knock-out models).
Activity <5 % was defined as a severe deficiency (activity >50%% is considered normal).
Patients with STEC-HUS (Shiga toxin and E. coli) and severe ADAMTS13 deficiency (activity <5%) were excluded.
Severe ADAMTS13 deficiency (activity generally < 10%) results in insufficient processing of von Willebrand factor (VWF) — a critical mediator of normal platelet tethering.
Frequencies of functional MBL MASP-2 relative deficiency (activity <60 MBL MASP-2 not differelativen the groups, but MBL–MASP-1 deficiency (<50 mU/ml) wactivitycommon in OC compared with the NO group (p = 0.035) (Table 3).
However, patients who presented with severe protein C deficiency (activity levels half the lower limit of normal or less [≤40%]) had a markedly higher mortality both at day 4 (20%) and at day 28 (41.8%).
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The prevalence of heterozygous protein C-deficiency (activity 30-65%) ranges from 1 200 to 1 500 [ 29- 31].
For example, he said, it does not consider factors like vitamin D deficiency, physical activity and use of epilepsy drugs and antidepressants that can erode bone.
As shown in Figure 1, under Fe deficiency, the activity of H+-ATPase was considerably stimulated.
Zn deficiency reduced activity of the recombinant eel Cu/Zn SOD protein.
Iron deficiency reduces activity levels and productivity in whole populations.
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