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PML is an opportunistic infection with neurological progressive symptoms caused by the replication of the JC virus in the glial cells of the brain.
Blood cell formation is maintained by the replication of hematopoietic stem cells (HSC) that continuously feed downstream "compartments" where amplification and differentiation of cells occurs, giving rise to all blood lineages.
On the other hand, in the adult pancreas, it had been considered that there are no endocrine progenitor cells and that β cells are generated only by the replication of existing β cells, not from the differentiation of endocrine precursor cells (neogenesis) [16], [17].
The infected tumor cells are destroyed by the replication of oncolytic HSV-1, which releases many progeny virions.
Importantly, the relevance of the zebrafish model to human disease was demonstrated by the replication of two naturally occurring gain-of-function human HIF-2α mutations in the zebrafish.
This was first demonstrated by the abundant mechanosensitive channels expression at neural and non-neural tissues of Zusanli acupoint (ST36) followed by the replication of the acupuncture analgesic effect after injecting agonist of the channels into ST36.
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Antiviral genes induced by type I IFN exert their effector functions by inhibiting the replication of virus at different stages of virus replication cycles.
Thus, hStn1 suppresses extensive telomere loss and premature entry into TDIS, presumably by facilitating the replication of telomeres that had been damaged by oxidative stress.
By contrast, the replication of both HK and SW (cRNA and vRNA) remained relatively constant over the 24 hour period (Figure 2C, lanes 7-12 and 13-18).
Other compounds have been proposed to act, at least in part, by disrupting the replication of kDNA through the inhibition of key enzymes, such as the topoisomerases (14 – 14).
The most absolute of these anticancer characteristics are barriers, such as cell cycle arrest, that prevent oncogenesis by prohibiting the replication of cells.
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