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Finally, hCDR1 suppressed in vivo gene expression of pathogenic cytokines, apoptosis and BLyS and up-regulated immunosuppressive molecules in peripheral blood lymphocytes of SLE patients.
The transcript and protein levels of TLR7 signaling molecules in peripheral blood mononuclear cells (PBMCs) were determined using quantitative PCR and western blotting respectively.
Transcript and protein levels of TLR7 signaling molecules in peripheral blood mononuclear cells (PBMCs) were evaluated by quantitative PCR and western blotting respectively.
Furthermore, we also examined the mRNA expression of Th1-, Th17, Th17- and Treg-related molecules in peripheral blood mononuclear cells (PBMCs) from SS patients and controls.
The purpose of this study was to investigate the expression of these molecules in peripheral blood mononuclear cells and to look for any possible correlations between their level of expression and the disease status.
Although we did not measure markers of platelet or monocyte activation in our study, Frampton et al. 2006 recently reported that inhalation of carbon ultrafine particles alters leukocyte expression of adhesion molecules in peripheral blood.
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In order to determine the effect of miRNA depletion from Schwann cells on the expression of molecules involved in peripheral nerve myelination, we performed quantitative RT-PCR on mRNA isolated from E17 and p4 Dicerfl/fl Dhh-Cre+ and Dicerwt/fl Dhh-Cre+ nerves.
The IS corresponds to a concentric structure of discrete domains with TCRs and CD3 molecules occupying the central region (central supramolecular activation cluster; cSMAC), which is surrounded by an outer ring of adhesion molecules in the peripheral SMAC (pSMAC).
Lck and ZAP-70 have been shown to translocate to microclusters of receptors and signaling molecules in the peripheral regions of the T-APC interface within lipid rafts during initiation of the TCR activation signal.
Both Lck and ZAP-70 have been shown to translocate to microclusters of receptors and signaling molecules in the peripheral regions of the T-APC interface during initiation of the TCR activation signal.
In addition, systemic inflammatory responses molecules in the peripheral blood stream were assessed.
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