Results: The CE-based method showed high precision and reproducibility in determining fragment size (<1 bp). More genotypes were detected in mixtures of laboratory

lines and blood samples from malaria infected children, compared to gel electrophoresis. The capacity to distinguish recrudescent parasites from new infections in an anti-malarial drug trial was similar by both methods, resulting in the same outcome classification, however with more precise determination by CE.

Conclusion: The improved resolution and reproducibility of CE in fragment sizing allows for comparison of alleles between separate runs and determination of allele frequencies in a population. The more detailed characterization of individual msp1 and msp2 genotypes may contribute Selleck ALK inhibitor to improved assessments in anti-malarial drug trials and to a further understanding of the molecular epidemiology of these polymorphic P. falciparum antigens.”
“Background: Chronic kidney disease (CKD) is characterized by a high mortality rate, primarily due to cardiovascular disease. Reduced soluble TNF-like weak inducer of apoptosis (sTWEAK) levels have been related with endothelial function in CKD patients. selleck products However, there are no data on the relationship between sTWEAK

and its scavenger receptor CD163 and atherosclerotic burden in CKD.

Methods: A cross-sectional, observational study was conducted in 58 patients with CKD stages 1-3, 86 with CKD stages 4-5, 195 on dialysis and 86 healthy controls. The severity of atherosclerosis was estimated with the atherosclerosis score (AS), combining the results of ankle-brachial index and carotid ultrasound. sTWEAK and CD163 plasma concentrations were measured by ELISA.

Results: sTWEAK plasma levels were diminished and CD163 concentrations were increased in patients with CKD compared with controls (sTWEAK: median [interquartile

range] 308 pg/mL [258-378] vs. 371 pg/ML [319-455]; p<0.001; and CD 163: 1,047 ng/mL [740-1,495] vs. 540 ng/mL [319-765]; p<0.001; respectively). A weak but statistically significant association between sTWEAK or CD163 and CSF-1R inhibitor carotid intima-Media thickness (r = -0.109, p = 0.025;,r = 0.179, p<0.001;respectively) was observed. Patients with more severe atherosclerosis presented a higher reduction in sTWEAK concentrations (412 pg/mL. [302-322] vs. 368 pg/mL [351-385]; p<0.001) and a high-er increment in CD163 levels (1,182 ng/mL [1,107-1,258] vs. 826 ng/mL [733-919]; p<0.001). After multivariable analysis, only elevated sTWEAK levels were associated with reduced risk of atherosclerosis (0.34 [0.14-0.86], p = 0.02).

Conclusions: A significant reduction in sTWEAK and increment in CD163 plasma levels were observed in patients with more severe atherosclerosis. Our results indicate that sTWEAK could be a novel biomarker of atherosclerotic burden in CKD patients.