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Paraoxonase 1 (PON 1) is a high-density lipoprotein (HDL)-associated enzyme with antioxidant function protecting low-density lipoprotein (LDL) from oxidation. PON 1 has two amino acid polymorphisms in coding region; L/M 55 and Q/R 192. These polymorphisms modulate paraoxonase activity of the enzyme. PON 1 activity decreases in coronary artery disease (CAD). In the present study, distribution of PON 1 L/M 55 and Q/R 192 polymorphisms and the effect of these polymorphisms on the activities of PON 1, and on the severity of CAD in 277 CAD (+) patient and 92 CAD (-) subjects were examined. PON 1 L/M 55 and Q/R 192 genotypes were determined by PCR, RFLP and agarose gel electrophoresis techniques. Genotype distributions and allele frequencies for PON 1 Q/R 192 polymorphism were not significantly different between controls and CAD (+) patient group (p > 0.05), but in genotype and allele distribution of PON 1 L/M55 polymorphism, there was significantly difference among groups (p < 0.05). Genotype distributions for both polymorphisms were not significantly different between subgroups of single-vessel disease (SVD), double-vessel disease (DVD) and triple-vessel disease (TVD). Serum PON 1 activity was lower in CAD (+) group than in controls and this was also statistically significant (p < 0.001). In both groups, the highest PON activities were detected in LL and RR genotypes. In summary, our results suggest that there is an association between the PON 1 L/M 55 polymorphism of paraoxonase and CAD in Turkish patients but not with PON 1 Q/R 192 polymorphism. However, it is hard to correlate these polymorphisms and severity of CAD.

Background. Rheumatoid arthritis (RA) is a chronic inflammatory and systemic disease of unknown etiology that primarily affects synovial joints and involves progressive destruction around the joints. Inflammation starting in the joint synovium causes the destruction of cartilage, bone and other adjacent tissues with pannus formation. Objectives. The aim of this study was to evaluate serum matrix metalloproteinase-3 (MMP-3) levels and their clinical and radiological significance in patients with rheumatoid arthritis. Material and methods. The study included 59 patients with RA and 30 healthy controls. Serum MMP-3 levels were measured using the enzyme-linked immunosorbent assay (ELISA) method. Patients with a Disease Activity Score 28 (DAS28) ≤3.2 were categorized as having lower disease activity, while a DAS28 score >3.2 indicated patients with moderate/high disease activity. Additionally, the patients were divided into 2 groups in terms of disease duration: early RA (disease duration ≤2 years) and established RA (disease duration ≥2 years). Functional disability was evaluated using the Health Assessment Questionnaire (HAQ) and Nottingham Health Profile (NHP). Radiographs were scored using modified Larsen scoring. Results. Serum MMP-3 levels in patients with RA were significantly higher than in controls (p = 0.001). Serum MMP-3 levels were correlated with laboratory and clinical parameters of disease activity, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), DAS28, and HAQ score; the exceptions were rheumatoid factor (RF) and cyclic citrullinated peptides (CCP). The serum MMP-3 levels of RA patients with moderate/high disease activity were found to be significantly higher than those of the patients with low disease activity (p < 0.001). However, MMP-3 levels were found to be similar in both established and early RA patients (p = 0.927). Additionally, the modified Larsen scores, which indicate structural damage, correlated significantly with serum MMP-3 levels (p = 0.001). Conclusions. These results indicate that serum MMP-3 levels may be used as an indicator for structural damage such as erosions in the early stages of the disease, and to monitor disease activity.

SummaryBackground: The aim of this study was to determine the level of serum cystatin C (CysC) in patients with Chronic Obstructive Pulmonary Disease (COPD) during exacerbation and stable periods and to investigate its potential diagnostic value and the relationship between CysC levels and the pulmonary function test (PFT). Methods: One hundred twenty-six patients with COPD (68 in stable periods, 58 during exacerbation periods) and 50 healthy subjects were included in the study. PFT, body mass index (BMI), white blood cell counts, C-reactive protein (CRP), serum urea and creatinine levels were evaluated in both groups of patients. CysC levels were measured in all participants. Results: Serum CysC levels were statistically higher in both COPD groups than the control group (p<0.001 for both) although there was no statistically significant difference between COPD groups (p>0.05). CysC levels showed negative correlation with forced expiratory volume in 1 second (FEV 1 ) and a positive correlation with C-reactive protein (CRP) levels in patients with stable COPD. There was a positive correlation between serum CysC levels and serum urea, creatinine, CRP levels in patients with COPD exacerbation (r=0.333, p=0.011; r=0.260, p=0.049; r=0.414, p<0.01 respectively). When stable COPD and control groups were evaluated, serum CysC had an area under the curve (AUC) in the receiver operating characteristic (ROC) curve of 0.951 (0.909-0.994 95% CI: p<0.001).

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OBJECTIVES: Chronic Obstructive Pulmonary Disease (COPD) is accompanied by increased cellular stress and inflammation. Most of the Heat Shock Proteins (HSPs) have strong cytoprotective effects. The role of HSPs in COPD pathogenesis has not determined completely. We investigated the serum level of HSPs in COPD patients, smokers without COPD and healthy non-smoking controls. Also, we evaluated the relationship of HSPs with various parameters (inflammatory, oxidative, functional status, quality of life) in COPD patients. MATERIAL AND METHODS:The levels of stress protein (HSP27, HSP70, HSP60, HSP90, CyPA), interleukin-6, C-reactive protein and malondialdehyde were measured in 16 healthy non-smoker, 14 smokers without COPD and 50 patients with stable COPD. Pulmonary function tests (PFT) and arterial blood gases parameters were measured. Health Related Quality of Life was evaluated and exercise capacity was measured with 6 minute walking test. RESULTS:Only HSP27 levels was significantly higher in COPD patients when compared with both healthy non-smoker and smokers without COPD (for both, p< 0.001). There was a weak-moderate negative correlation between serum levels of HSP27 and PFT parameters and between HSP27 levels and PaO 2 . Serum levels of HSP27 showed a weak-moderate positive correlation with symptom, activity and total scores. Subjects evaluated only smokers without COPD and patients with COPD; HSP27 had an area under the curve (AUC) in the receiver operating characteristic (ROC) curve of 0.819 (0.702-0.935; 95% CI; p= 0.000). CONCLUSION:Increased serum levels of HSP27 was found in COPD patients and our results showed sensitivity and specificity of serum HSP27 as diagnostic markers for COPD.

The results suggested a lack of association between the Glu298Asp gene polymorphism and pre-eclampsia without FGR in the Turkish population. But elevated ADMA and SDMA levels suggest that ADMA has a role in the pathogenesis of PE.