Sentence examples for calcium toxicity from inspiring English sources

Some evidence suggests they are efficient at using potassium, and sensitive to calcium toxicity as well.

scrCΔ crzAΔ strains were suppressed for calcium toxicity and pH 8 tolerance.

Construction of (gene replacement) cnaBG120D crzAΔ double mutants showed that calcium toxicity is suppressed.

Calcium toxicity may explain why Z. mobilis performs better in ammonium conditioned hydrolysates rather than in calcium overlimed hydrolysates [ 38].

This establishes that the scrC loss-of-function phenotype includes suppression of crzAΔ calcium toxicity and therefore shows that scrC3 and - 4 are loss-of-function alleles.

Inability of the halA− sltA− combination to ameliorate calcium toxicity in pmcAΔ pmcBΔ strains is further evidence that the calcium auxotrophy does not result from reduced calcium uptake.

Hence, an in vitro study was designed to investigate the attenuation of calcium oxalate toxicity by human kidney stone matrix proteins on NRK-52E cells using flowcytometry, Western blotting, RT-PCR and immunofluorescence assays.

While Aβ and tau represent the two key pathological mediators of disease, other aspects of this multifaceted disease (e.g. oxidative stress, calcium-mediated toxicity, and neuroinflammation) are being unraveled, with the hope to develop a more comprehensive approach in exploring disease mechanisms.

In the case of TRPV1, but not TRPM8, prolonged agonist exposure caused strong calcium-dependent toxicity.

Furthermore, PEP-19 has shown neuroprotective properties in cell cultures, these possibly being mediated through CaM inhibition that could lead to enhanced resistance of neurons to calcium-mediated toxicity [46], [47], which makes it tempting to speculate that this protein is neuroprotective also in our SE model.

Although TRPM8 activation mediates similar current densities to TRPV1 (Figure 4), TRPV1 has larger secondary effects on cell function, including interference with endogenous synaptic transmission in the absence of exogenous agonist stimulation (Figure 6) and overt calcium-dependent toxicity with agonist exposure (Figure 5).