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A significant proportion of heart failure patients have implanted cardiac devices, such as biventricular pacemakers, allowing manipulation of heart rate and hence cardiac output at will.
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When transient circulatory failure and global hypoperfusion occur during manipulation of the heart or anastomosis, we usually maintain systemic perfusion pressure by tilting the surgical table and administering intravenous fluids followed by the administration of noradrenaline as a first-choice vasopressor.
Manipulation of the heart results in a change in the cardiac axis, and therefore precordial electrocardiogram.
Manipulation of the heart's cellular energy metabolism to overcome the metabolic changes during ischaemia is an established concept in cardioprotection, as discussed above.
Pharmacological and genetic manipulation of cultured heart cells and animal models of HF and the analysis of cardiac samples from patients with HF are all used to identify the molecular and cellular mechanisms leading to the disease.
These authors found that HRV decreased to similar proportions in the two groups, suggesting that the factors common to both surgical procedures, such as the cardiopulmonary bypass with cardioplegia and mechanical manipulation of the heart, were responsible for impairment of the autonomic function.
Because Yap activation has been shown to 1) regulate fetal heart growth [60],[61],[115], 2) promote cardiomyocyte proliferation in both neonatal and adult cardiomyocytes in vivo[115],[122]-[124] and 3) extend the regenerative capacity of the neonatal mouse heart [123],[125], Hippo signaling has become an intriguing potential target of manipulation for heart regeneration.
These observations prompted studies to ascertain whether similar mechanisms are present in the mammalian heart and, if so, whether experimental manipulation of miRNAs might trigger heart regeneration in mammals.
Such absurd and obvious manipulation of reality lay at the heart of this hourlong solo, cleverly disguised as a quartet.
It looks like mending that broken heart, through manipulation of our memories, might be here closer than we think.
Our study suggests that the downregulation of Rnd3 is a risk factor in the heart, and the manipulation of Rnd3 expression could be a potential therapeutic target in human heart failure treatments.
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