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Having observed phage shedding and concomitant lysogeny in soil and worm microcosm co-cultures, we proceeded to a similar analysis in other environments that support phage shedding.
The method above can be used to calculate the maximum host diversity for the case in which all strains support phage.
Both the bacteria and phage are adversely affected by mutagen, however, and the bacteria are greatly impaired in their ability to support phage growth.
As only viable bacterial cell will support phage adsorption, infection, replication and subsequent progeny release, the assay detects the active disease.
However, consider the first strain h x that enters the system and reaches a resource-limited steady state with N x < N ^, i.e. the first strain that becomes established but does not reach sufficient density to support phage.
However, suppose the host has reduced ability to support phage growth effects 1 and 2 in the list above and that the true W0 is 50; lethal mutations kill all but 60% of those progeny.
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All four of these mutant -1 triplets supported phage plaque formation as well as the wild-type control.
Moreover, S. epidermidis F12 clearly supported phage propagation, while no phages were detected when sampling the drop zone of the resistant and drop sensitive strains.
Hence, for example, saying that MCM "supports phage predation" is merely a claim that MCM supports model structures that have conventionally been used to model phage predation (at the population level; for an example see Jensen et al., 2006).
Also, the data support that phage regions are transcriptionally active and may be producing virus-like particles; however, the association between expression and disease development remains to be demonstrated.
The authors thank: Dr. Andréa Maranhão, (University of Brasília, Brazil) for kindly providing the pCOMB3X phagemid and support about phage display approaches.
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