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Because of the aforementioned concerns, to some extent, we consider this study explorative, and more replication in Korean or other Asian samples is greatly needed.
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In contrast to bacteria grown in culture, which do not experience natural death, M. tb bacilli growing in an immunocompetent host are frequently killed through adaptive or innate immune responses and thus a host bacillary population of a given size is likely to have undergone far more replication events than an in vitro population of the same size.
Therefore, more replication studies of MTNR1B polymorphisms in Han Chinese and meta-analysis are needed in the future.
In the laboratory, more replication of interesting results and confirmations of possible associations that have been found in field studies need to be pursued further.
The genetic changes associated with more efficient replication in the intestine are also associated with increased neurovirulence, and probably also contribute to more efficient transmissibilities because of higher yields of excreted virus[47].
These mutations were subsequently shown to contribute to increased NA activity, resulting in more efficient replication in mammalian cells, most likely by preventing the formation of virus aggregates.
The up-regulation of most dna genes in HLA-B27 cells compared to HLA-A2 cells might indicate more DNA replication in HLA-B27 cells.
Supplementary origins and low inter-origin distance ensure faster and more efficient replication in embryonic systems, facilitating the bypass of eventual obstacles to replication progression (Woodward et al, 2006).
Other examples of gene loss occur in response to lifestyle adaptations like the dramatic genome reduction of obligate host-associated bacteria such as Mycoplasma and Buchnera [ 8], or to allow for more efficient replication in free-living microorganisms like in the marine free-living bacteria Prochlorococcus and Pelagibacter [ 9, 10].
Therefore, H3 K36 and/or K37 are necessary for more rapid DNA replication in the absence of histone deacetylation by Rpd3.
The transmission and replication phenotype can be further improved by providing the virus with a gene constellation more adapted for replication in ferrets.
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