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This coping mechanism is put to the ultimate test when the stress is death stress.
Their overall pre-valence, associated with the risk of sudden death, stress the need for high throughput and sensitive genetic diagnosis in order to improve genetic counseling and medical management.
Although the biological functions of most miRNAs are not yet fully understood, it has been suggested that they are involved in various biological processes, including cell proliferation, cell death, stress resistance, and fat metabolism, through regulation of gene expression (Ivey and Srivastava, 2015).
The vast majority of these were upregulated transcripts of genes involved in cell death, stress responses and differentiation.
We found that many deregulated genes are associated with cell death, stress signaling, BCR activation, immune response, and development of hematopoietic cells.
Notably, these exercise-relevant pathways (cell death, stress response, proliferation) comprise significant number of intersecting mRNAs.
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In terms of selecting the right physical layout, Alison Killing, a Rotterdam-based architect and urban designer who specialises in buildings related to healthcare and death, stresses the importance of architectural design that keeps well-being and human experience in mind.
The lack of therapy independent prognostic impact suggests that an anti-APRIL therapy may not have anticancer activity on it's own, but the cell survivalpromoting activity may be more generally applicable to other therapeutic cell death stresses.
All exercises are to a certain extent artificial, unable to reflect the entire spectrum of wartime, from life-and-death stress on a single soldier to the impact of public opinion as battlefield fortunes wax and wane.
This test case, however, shows that matching by pH is not always safe for guarding against the agonal stress confounder, whereas the empirically derived ASR values provide a more accurate assessment of the regulatory responses to near-death stress in individual samples, and allow a more stringent control.
Molecular mechanisms protecting cardiomyocytes from stress-induced death, including tension stress, are essential for cardiac physiology and defects in these protective mechanisms can result in pathological alterations.
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