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The beneficial of vitamin D and other anti-inflammatory agents against TB shows that controlling the host immune response during Mtb infection results in the increased resistance to active disease or in its better prognosis.
We have previously demonstrated the most dramatic phenotype described for the substance P encoding gene preprotachykinin-A (PPT-A) to date in controlling the host immune response to the murine gammaherpesvirus 68, in the lung.
This suggests that the killing activity of differentiated HL-60 towards C. neoformans seems to be more pronounced than the one observed against Ca. Since SM, ceramide and DAG are important lipids involved in controlling the host immune responses [31], [37], [38], [39], [40], [41], [42], we investigated whether SMS activity is required for neutrophils to kill C. neoformans.
Since (a) ceramide can regulate transcription factors, such as NF-κB involved in cytokine production [31], (b) DAG controls antifungal activity by neutrophils through reactive oxygen species (ROS) production [32], and (c) SM has been implicated in controlling the host immune response in phagocytic cells [33], in this paper we studied the role of SMS in neutrophils against C. neoformans.
If the latter is true, the genes that we identified as differentially expressed after infection are promising candidates for controlling the host's response to the sigma virus.
The aim of the present study was to find genes controlling the host defense response to this devastating plant pathogen.
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A closer investigation of sequence similarity to C-type lectins from free-living and parasitic nematodes and an analysis of the locus to which these proteins are eventually translocated might shed light on physiological functionalities as they relate either to sustaining life within the organism or controlling the host-pathogen interface.
In fact, CL scaffold was not sufficient to control the host response following the implant showing a consequent failure in the integration with the surrounding tissue (Fig. 6A).
The most important part of HAdVs-E is E3 CR1-beta protein which controls the host immune response and viral attachment.
This approach relies on the development of a target-specific biomaterial scaffolding system that can effectively control the host microenvironment and mobilize host stem/progenitor cells to a targeted site of the injured tissues or organs.
A synthetic Mycoplasma mycoides genome transplanted into M. capricolum was able to control the host cell.
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