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The following models were used: model 1: bone profile changes (P1NP, CTX, and WB BMD); model 2: model 1 plus body composition changes (FFM, FM); and model 3: model 2 plus adipocytokines changes (IL6, CRP, sTNF R1, adiponectin, and leptin).
Serum hs-CRP, sTNF R1, and leptin decreased similarly in the diet-exercise group (-27.3 [+ or -] 6.6%, -8.7 [+ or -] 2.6%, and -38.4 [+ or -] 5.3%, resp.) and diet group (-27.0 [+ or -] 8.2%, -6.9 [+ or -] 2.3%, and -26.2 [+ or -] 6.6%, resp.) .
In vitro trials indicate that preincubation of blood samples with GM-CSF increases the LPS-induced cellular TNF[alpha] production and the HLA-DR expression on monocytes but also the secretion of anti-inflammatory cytokines such as IL-10, IL-RA, and sTNF receptor by monocytes in patients with severe sepsis [28, 29].
To assess the working range in serum, pig/guinea pig serum was enriched with the following concentrations of analytes: 0, 7.8, 31, 125 500, 1000, 2000 and 4000 ng/L IL-1[beta], IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IL-17, IFN-[gamma], TNF-[alpha], NT-3, and NT-4; 0, 19.5, 78.1, 312.5, 1250, 2500, 5000, and 10 000 ng/L IL-18, GM-CSF, TNF-[beta], MCP-1, MIP-1[alpha], and MIP-1[beta]; 0, 0.16 0.63, 2.5, 10, 20, 40, and 80 [micro]g/L sTNF RI and BDNF; 0, 78, 312, 1250, 5000, 10 000, 20 000, and 40 000 ng/L TGF-[beta]; 0, 1.95, 7.81, 12.5, 50, 100, 200, and 400 [micro]g/L sIL-br[alpha]; 0, 0.63, 2.5, 10, 20, 40, 80 and 160 [micro]g/L RANTES; 0, 0.98, 3.9,15.6, 52.5,125, 250, and 500 [micro]g/L MMP-9 and TREM-1; and 0, 0.195, 0.78, 3.13, 12.5, 25, 50, and 100 [micro]g/L MIF.
Three analytes that worked well for analysis of serum (NT-3, MIF, and sTNF RI) for some reason did not function together with the other analytes when the calibrators were spotted on filter paper.
However, to the best of our knowledge the cytokine concentrations measured in sera from healthy people fell within the ranges reported by several other assays, i.e., for IL-1(3, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IL-17, IL-18, IFN-[gamma], TNF-[alpha], GM-CSF, and MCP-1 (35,45,49-54); RANTES (47,51); TGF-[beta] (52,55); MIP-1[alpha] and MIP-1(3 (47); MMP-9 (56); sTNF RI and sIL-bra (57); MIF (58); NT-3 and NT-4 (59); and BDNF (60, 61).
Despite these drawbacks and the poor penetration of the blood-brain barrier by these agents, clinical trials with etanercept, a genetically engineered Fc fusion protein generated from the extracellular domain of human TNFR2 which blocks both sTNF and mTNF, have been conducted in patients with Alzheimer disease (AD), with significant cognitive and behavioral improvements [133, 134].
BCG Infection at MOI 1 and MOI 0.1 Activated the Expression of tmTNF, sTNF, and sTNF Receptors.
To determine if low doses of BCG were enough to activate TNF and sTNFRs, we measured iTNF and tmTNF by flow cytometry and sTNF, sTNFR1, and sTNFR2 levels by ELISA.
Specifically, the human sTNF RI ELISA Kit and the human sTNF RII ELISA Kit (RayBiotech, Norcross, GA, USA) were used according to the manufacturer's instructions.
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