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These data seem to favor the notion that aging and obesity may share somewhat similar cellular mechanisms en route to cardiomyocyte mechanical dysfunction.
To further explore the possible mechanism of action underlying APP/PS1-associated cardiomyocyte mechanical dysfunction, the membrane permeable intracellular Ca2+ fluorescent dye fura-2 was used to evaluate intracellular Ca2+ homeostasis in cardiomyocytes.
Fibroblasts play a significant role in the development of electrical and mechanical dysfunction of the heart; however the underlying mechanisms are only partially understood.
The beneficial effects of ranolazine in reducing Ca2+ overload and LV mechanical dysfunction during ischemia/reperfusion is consistent with the inhibition of late INa mechanism of action.
Moreover, severe constriction of the terminal alveolar units and airways leading to these ventilation defects were not sufficient to explain the degree of mechanical dysfunction during bronchoconstriction [21].
Although T-tubule structural remodelling in Δ160E myocytes is modest, T-tubule functional defects determine non-homogeneous Ca2 + release and delayed myofilament activation that significantly contribute to mechanical dysfunction.
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Interestingly, these HG-induced mechanical dysfunctions were completely abolished by co-incubation of pyruvate.
Mechanical dysfunctions like vesico-ureteric reflux increase the access of bacterial to the kidneys, but uro-dynamic abnormalities alone do not render patients prone to APN [8], [9], [10].
Consistent with previous finding from chronic alcohol administration study [15], ADH transgene accentuated the acute ethanol challenge-induced cardiomyocyte mechanical dysfunctions without eliciting any overt effect by itself (Fig. 2).
Here, the role of T-tubule remodelling in the electro-mechanical dysfunction associated to HCM is investigated in the Δ160E cTnT mouse model that expresses a clinically-relevant HCM mutation.
We propose that acute Cl2 inhalation leads to oxidative modification of lung lining fluid, producing surfactant inactivation, inflammation and mechanical respiratory dysfunction at the organ level.
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