ABSTRACT
BACKGROUND: As an acute-phase reactant, CRP is needed to clear apoptotic cells and immune complexes in SLE. This unresponsive CRP may be caused by genetic variation and abundant IFN-α that might inhibit CRP secretion. This study aims to analyze the association of single nucleotide polymorphisms (SNP) in CRP promoter and plasma IFN-α with CRP level in Javanese SLE patients. We also analyzed the association of these SNPs with SLE. METHODS: Forty SLE and 40 spondyloarthritis (as control) patients were included. SLE subjects underwent routine laboratory test, CRP level, serum IFN-α, and DNA sequencing to detect SNPs in CRP promoter. The control group only underwent DNA sequencing. RESULTS: The median age of SLE patients was 31.5 years. The median SLAM score was 8.5. The median age of the control group was 39 years. The average CRP was 5.19 SD 2.69 mg/L, median plasma IFN-α was 46.02 pg/ml. There was no significant difference of SNPs in CRP -821 (rs2794521) or -390 (rs3091244) between SLE and control. New SNP was found in CRP -456 A>G in 5 SLE patients, but none in controls. This SNP would increase SLE risk 2.143 times. There was a moderate negative correlation between IFN-α level and plasma CRP. Linear regression only showed IFN-α level (not either SNP) correlated with serum CRP. CONCLUSION: Plasma IFN-α correlated with CRP level. There was no association of SNPs in CRP -821, -390, and -456 with CRP level. SNP CRP -456 A>G would increase the risk of SLE with an odds ratio of 2.143.
Subject(s)
C-Reactive Protein , Interferon-alpha/blood , Lupus Erythematosus, Systemic , Adult , C-Reactive Protein/genetics , Humans , Indonesia , Lupus Erythematosus, Systemic/genetics , Polymorphism, Single Nucleotide , Promoter Regions, GeneticABSTRACT
BACKGROUND & OBJECTIVE: FLT3-ITD has been recently used as a molecular prognostic marker for risk classification in acute myeloid leukemia (AML) therapy. In this study we aimed to investigate the association of FLT3-ITD gene mutation with bone marrow blast cell count, CD34 expression as malignant cell burden, cyclin D1 and Bcl-xL expressions as indexes of cell proliferation and anti-apoptosis and human equilibrative nucleoside transporter 1 (hENT1) expression as cytarabine transporter during AML treatment. METHODS: We investigated FLT3-ITD mutations, bone marrow blast cell count, CD34, cyclin D1, Bcl-xL and hENT1 expression in bone marrow aspirates from 22 de novo AML patients in a cross sectional study. RESULTS: FLT3-ITD mutations were observed in 5 out of 22 de novo AML patients (22.7%). Patient with FLT3-ITD mutations had higher blast cell counts (79.5% vs 56.1%, P=0.004). In patients with FLT3-ITD mutations, CD34 and cyclin D1 expressions were higher (MFI 328.80 vs 25.78, P=0.003 and MFI 74.51 vs 57.15 P=0.005) than the patients without mutations. hENT1 expression in AML with FLT3-ITD mutation was lower (MFI 29.64 versus 56.32, P=0.0000) than in mutation-free AML. There was no significant difference in Bcl-xL expression between patients with and without mutations (P=0.61). CONCLUSION: A significant association was found between FLT3-ITD gene mutations in AML patients with bone marrow blast cell count, CD34, cyclin D1 and hENT1 expressions, however no association was obtained with Bcl-xL expression. These findings support the role of such mutation in pathogenesis of AMLand its contribution in rearrangement of standard therapy with cytarabine in management of AML.
ABSTRACT
PURPOSE: The aim of this study is to asses the relationship between the level of sIgA and dental caries experience in healthy children who are 6- to 9-years-old from Indonesia. The case-control study is conducted to determine the protective role of salivary secretory immunoglobulin A (sIgA) levels in the stimulated whole saliva of dental caries-active and caries-free children. METHODS: This research was done by stimulating the whole saliva which had been collected from 6- to 9-years-old children with the index def-t≥3 of 30 children as the caries-active children group and 30 children with def-t<3 as the low caries-active children group. Saliva samples were collected in sterile vials between 10 am-12 pm due to the circadian rhythm, which is at least one hour after last meal. 1,5 ml of collected salivary sample was centrifuged, then the supernatants was transferred to other tube and stored immediately to the laboratory at a temperature of -20 °C. The estimation of sIgA concentration was done by using ELISA. The differences in the level of sIgA between the two groups with caries were analyzed using the t-test afterward. RESULTS: The total salivary concentration of sIgA was statistically significantly higher in the low caries-active children group than in the caries-active children group. CONCLUSION: The total salivary concentration of sIgA was statistically and significantly higher in the low caries-active children group than caries-active children Group. There is a negative correlation between sIgA level and dental caries activity of 6 to 9-years-old children.
