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Treatment with rhAPC was associated with slightly larger relative decreases in fibrinogen-γ in the LPS-instilled lobes, possibly due to rhAPC's PAI-1 inhibiting effects and restoration of the deficient clearing of fibrin.
Given the apparent increase in the size of the TReg cell population at the site of lesions in both diseased MUC1Kras mice and patients with endometriosis, it is plausible that downregulation of local immune responses by a TReg-cell-dependent mechanism could underlie deficient clearing of lesions.
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Despite this delay in peak viral load, CD94-deficient mice cleared the infection by day 13 suggesting that CD94-NKG2 does not play a prominent role in control of LCMV infection.
High bacterial counts in the peritoneal fluid are indicative of deficient host clearing of bacteria (von Kockritz-Blickwede et al. 2008).
This is also consistent with the observation that TLR2−/− mice are not deficient in clearing intravenously (Netea et al., 2004) or intraperitoneally (Tessarolli et al., 2010) inoculated fungal organisms.
The observation that Cx3cr1-deficient Mϕs are cleared less efficiently from the subretinal space of WT mice suggests that the in vivo accumulation is at least in part due to the capacity of Cx3cr1-deficient Mϕs to inhibit the RPE immunosuppression and prolong their survival when compared to WT-Mϕs.
In comparison to agr, sigB and hla mutants (see Figs. 6 and 7), the rate of intracellular killing of the aur mutant was slower, with live staphylococci consistently present in cell lysates up to day 3. Also, macrophages infected with a sortase A mutant, which is deficient in multiple MSCRAMMs, cleared bacteria more slowly (Fig. 8B) at a rate that was comparable to that of the aur mutant.
To identify the known miRNAs in the two libraries constructed from control and B-deficient roots, clear reads were aligned with known plant miRNAs from miRBase 18 (http://www.mirbase.org/).org/
In spite of large inocula, OspC-deficient spirochetes are quickly cleared after inoculation into murine skin [14], [15].
Clearance of primary B. pertussis infection involves T cells, since T cell-deficient mice fail to clear the infection [41], but the relative contribution of Th1 and Th17 cells and the mechanisms utilized are still unknown.
The QS-deficient bacteria were rapidly cleared compared to the wild type bacteria which were only cleared after treatment with a QS inhibitor [ 56].
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