In the validation samples, ELISA results confirmed that ApoC-II was predictive of survival (Kaplan Meier P<0.009), but not SAA-I.
In Eq. (18), x and c T shows the optimal spare vehicles in the buffer of SAA problem, i.e., first stage variable, and the cost occurred due to first stage variable x, respectively.
Finally, several transcription factors were found to be differentially expressed in SAA patients (i.e., STAT1, STAT5B and IRF2).
In fact, regulation of SAA, apoA-I, and PON1 is coordinated in murine hepatocytes; as SAA increases, the other two molecules decrease.
Twelve biomarkers (c-reactive protein (CRP), epidermal growth factor (EGF), Leptin, IL-6, MMP-1, MMP-3, Resistin, SAA, TNFR-I, VCAM-1, VEGF-A, YKL-40) were measured in serum samples from baseline and day 88 (Meso Scale Discovery MULTI-ARRAY platform).
These genes included molecules involved in immune responses and their regulation with the following fold changes for SAA pool I and IIa, respectively: PF-4 (-157-fold; -188-fold), CD26 (+2.2-fold; +2.1-fold), Ncf-1 (-3.9-fold; -2.2-fold), CCR2 (+2.7-fold; +2.7-fold), CX3CR1 (+4.3-fold; +2.9-fold) and other chemokine receptors and ligands.
Furthermore, microarray analyses were performed comparing the differential gene expression pattern of SAA patients (pool I and pool IIa of the PB) with profiles of naive and effector memory CD4+ and CD8+ T-cell populations generated from 3 different healthy donors, respectively.
Recent proteomic studies provided convincing evidence that inflammation alters the protein composition of HDL thereby generating dysfunctional or even pro-atherogenic forms of HDL [11] by enriching pro-inflammatory proteins such as serum amyloid A (SAA), apoC-III or complement component 3 [12–20].
To eliminate genes which may be individually regulated independent of disease we focused in our study only on genes coregulated in both of the analyzed SAA pools (pool I and IIa) in comparison to the normal controls (pool III), each separately for PB and BM samples.
BMI: Body mass index; HbA1c: Glycated hemoglobin; HDL: High-density lipoprotein; HOMA-IR: Homeostasis model assessment-insulin resistance; hs-CRP: High sensitive C-reactive protein; MetS: Metabolic syndrome; NCEP-ATPIII: National cholesterol education program - adult treatment panel III; SAA: Serum amyloid A; T2DM: Type 2 diabetes mellitus.
The anti-SAA monoclonal antibody used (i.e., clone mcl, DAKO), was directed against SAA 1.
