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Such findings show that viral and host modifications can improve cell survival and production of heterologous proteins, change viral behavior in vitro and in vivo, and assist in the development of new expression or gene delivery vehicles.
These advances span the introduction of new pathways to alcohols, host modifications for more cost-effective utilisation of lignocellulosic waste and modifications of existing pathways for generating new fuel additives.
Our results show no evidence of host modifications in association with hCNS-SCns transplantation.
Additionally, host modifications with small effect on, for example, Wolbachia gonadal density, seem to be biologically more plausible than the direct elimination of CI altogether.
Later modelling work that did include sex-specific host modifications and focused on the special case of complete elimination of CI found such mutations to spread easily [22].
Generally, our study systematically extends the scope of possible mutations to the entire range of host modifications (i.e. from 0% to 100%).
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Additionally, we found no evidence of host modification in transplanted animals, suggesting that cell transplantation does not alter endogenous repair mechanisms.
Stereological quantification for lesion volume, tissue sparing, descending serotonergic host fiber sprouting, chondroitin sulfate proteoglycan deposition, glial scarring, and angiogenesis demonstrated no evidence of host modification within the mouse spinal cord as a result of hCNS-SCns transplantation.
This contrasts with some earlier predictions that did not take into account the possibility of sex-specific host modification of Wolbachia action [21], specifically repression of Wolbachia in male gonads.
Our study systematically enlarges on these concepts and shifts the focus to the evolutionary fate of Wolbachia-infections. We allow for the whole range of host modification with effects from 0% to 100% and further introduce a survival cost incurred by those males carrying the mutation in question.
Previous studies have either focused on – for the case of male "resistance" – the special case of complete elimination of CI through host modification [22] or the special case of CI in haplodiploids (where CI can lead to male production) and the effect of different CI-types on the spread of CI-reducing mutations of moderate to large effect [23].
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