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In both scenarios clonal expansion occurred, reinforcing the theory that a few clones cause a disproportionate amount of pneumococcal disease.
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In contrast, the elimination of dTIEG function in somatic clones causes a down-regulation of sal and omb expression indicating a decrease of Dpp/BMP2 activity in the wing disc.
The overgrowth of the PTEN clones caused a further reduction in body size, as evidenced by decreased shoulder width.
We noted that α-spec RNAi in kib mutant clones caused a strong overproliferation and multilayering phenotype in follicle cells (Supplementary Fig S6M).
AM-overexpressing clones caused a significantly increased total osteolytic lesion area (indicated by arrows pointing to radiolucent regions) in bone compared to either GFP control cells or parental cells as measured by X-ray (19.3 mm vs. 6.1 mm at 3 weeks, 32.5 mm vs. 16.9 mm at 4 weeks; P < 0.001 for comparison of AM-overexpressing clones versus GFP control clones grouped together).
Monitoring of cytokine production in the engrafted synovium revealed that transfer of T cell clones caused a threefold to fourfold increase in IFN-γ transcripts, and a twofold to threefold increase in the abundance of IL-1β and tumor necrosis factor (TNF -α TNF -αriptranscripts
Indeed, there was even an indication that many RNAi clones caused an increase in PMK-1 phosphorylation, perhaps reflecting a compensatory activation of PMK-1 when other signalling pathways are disrupted.
Thus an INH resistant non-Beijing M. tuberculosis strain caused an outbreak in Sweden, now involving more than 100 patients, mainly immigrants from the Horn of Africa [33], and another INH resistant clone caused an outbreak in East African patients in Norway [70].
Of the gene targeting experiments, only mutation of the X-linked dystrophin (DMD) gene in male clones may cause a severe phenotype.
We would predict that the loss of AR in our C/EBPα overexpressing LNCaP clones would cause a transformation of cells from androgen-dependent to androgen-independent growth and that the cells would exhibit more aggressive growth, invasion, and metatstatic potential.
The failure of aPKCCAAXDN to rescue JNK-dependent cell death was not simply due to an inherent inability to fully rescue cell survival in scrib mutant clones caused by a delay in transgene expression, since a full length Scrib transgene fully restored cell morphology and normal clone size to scrib mutant cells throughout the eye/antennal disc.
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