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Moreover, addition of phlorizin, an SGLT blocker, did not result in a decrease in Isc, further confirming absence of Na+-glucose co-transport activity.
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Importantly, the combination of β-blockers and vincristine did not result in increased cytotoxicity in normal fibroblasts (Supplementary Figure S3).
Treatment with potent VGCC blockers (0.1 mM cadmium chloride, 0.1 mM verapamil) or with the gap junction blocker lindane (1.7 mM) did not result in any reduction in ivermectin-induced hyperpigmentation (Table 3).
A Na+ channel blocker, on the other hand, reduced the rate of rise of the action potentials but did not result in desynchronization of the action potentials.
Despite the increased oxygen availability (+63%) seen upon application of this calcium channel blocker, nifedipine does not result in a substantial reduction of tumour hypoxia, most probably due to an increase in O2 uptake with rising O2 supply to the tumour-bearing hind limb.
The CCD blocker did not affect test results where CCDs were not involved.
Increasing the concentrations of the dideoxy blocker did not improve the overall assay results.
First, the PGD2 receptor blocker did not inhibit PGD2-induced neuronal cell death [4].
The latter blocker did not affect single channel characteristics of Mrs2.
This is a probable reason why the parts-of-speech blocker does not improve the results.
The inclusion in the latter models of dichotomous variables representing current active treatment with common anti-hypertensive drug classes (i.e. ACE-I/ARBs, β-blockers, calcium channel blockers) did not affect the results.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com