However, the poor stretchability of WSSCs based on inelastic yarn electrode seriously lead to the deficient size-adjustability of the devices.
Our definition of a relevant change in GPI-deficient population size (≥50% GPI deficiency on granulocytes) is based on data published by Hall et al. [ 15], demonstrating that patients with a GPI-deficient population on granulocytes ≥50% have a significant higher risk of thromboembolic events.
Therefore, we evaluated our panel on different cell lineages for longitudinal monitoring of GPI-deficient populations to determine the frequency of significant changes in cell lineage involvement and GPI-deficient population size.
Outdated equipment, sub-standard acoustics and a deficient stage-size were among them.
Moreover, regular follow-up studies are indicated in case of known PNH to detect substantial changes in GPI-AP-deficient population size or cell lineage involvement, as both situations may prompt therapeutic consequences or may demonstrate effect of therapeutic interventions.
While the ability of Stim1 to oligomerize and translocate to the junctional ER upon store-depletion appeared normal in α-SNAP deficient cells, the size of Stim1-Orai1 clusters appeared larger.
Consistent with this hypothesis, Oyama et al. demonstrated that in TLR4-deficient mice infarct size and signs of inflammatory response were significantly decreased after MI/R [ 8].
Although the characterisation of CCO-deficient clones by size provides indirect access to the fate behaviour of marked cells and their progeny, the interpretation of these data sets is not straightforward.
However, caution is needed before generalize the results of these studies because the limited effect size and deficient methodologies [ 13].
Indeed lpr mice (FAS deficient) show reduced infarct size while deletion of both TNFR1 and TNFR2 appears to have a protective effect.
Whereas studies later on argued that the failure of IL-6 deficient to affect infarct size might be due to hypothermia in the mice models, and with well-controlled hypothermia, IL-6 deficiency would lead to increased infarct volume and neuronal death, suggesting a neuroprotective role of IL-6 [ 11, 61].
