Performance Evaluation of the Plateletworks® in the Measurement of Blood Cell Counts as compared to the Beckman Coulter Unicel DXH 800.

Prior to undergoing cardiac surgery many patients may have impaired platelet function due to platelet inhibition. Point of care testing (POCT) that produces quick results of platelet counts and function allow earlier clinician interpretation, diagnosis and treatment. Before being adopted for routine clinical use, a POCT device's performance must be evaluated by standard laboratory techniques to ensure high quality results. The purpose of this study is to determine the performance of the Plateletworks?V BC 3200 automated hematology analyzer by correlating its precision, accuracy and linearity for the measurement of blood counts to our hospital central laboratory analyzer (Beckman Coulter Unicel DXH 800). The study utilizes well described methods for Within-Run and Day-to-Day precision, comparison of methods (bias), and linearity. Control samples from the manufacturer were used for the precision studies, blood samples from 115 cardiac surgical subjects were used for comparison of methods and accuracy, and pre-diluted control samples from the manufacturer were used for the linearity studies. The precision of the Plateletworks® analyzer was acceptable. The overall coefficient of variation (CV) for the measured parameters at all levels of control for Within-Run precision was acceptable ranging from 0.65-6.4%. Likewise, the CV for the measured parameters at all levels of control for Day-to-Day precision was acceptable ranging from 1.45% to 6.7%. The correlation and accuracy between the two analyzers for the evaluated parameters (platelets, red blood cells, white blood cells, and hemoglobin) was acceptable. The linearity for the measured parameters was also acceptable with a range between 98-100%. The performance of the Plateletworks® analyzer was acceptable for providing blood cell counts as compared to our central hospital laboratory analyzer.

Vitamin E slows the progression of hypercholesterolemia-induced oxidative stress in heart, liver and kidney.

Vitamin E suppresses the hypercholesterolemia-induced oxidative stress in the heart. The objectives were to investigate if: (a) hypercholesterolemia-induced oxidative stress is similar in heart, liver, and kidney, and is dependent upon duration of hypercholesterolemia; and (b) vitamin E slows the progression of oxidative stress in these organs. The rabbits were assigned to 4 groups: I, regular diet (2 months); II, 0.25 % cholesterol diet (2 months); III, 0.25 % cholesterol diet (4 months); and IV, 0.25 % cholesterol diet (2 months) followed by 0.25 % cholesterol diet plus vitamin E (2 months). Blood samples were collected before and at the end of protocol for the measurement of total cholesterol (TC). Hearts, livers, and kidneys were removed at the end of the protocol under anesthesia for the measurement of oxidative parameters, malondialdehyde (MDA), and chemiluminescence (CL). The basal MDA levels in the heart, liver, and kidney of rabbits in Group I were similar, but increased to 14.65-, 3.18-, and 10.35-fold, respectively, with hypercholesterolemia. The increases in MDA levels were dependent upon the duration of hypercholesterolemia. Vitamin E did not alter the TC levels, but reduced the MDA levels in all organs. Hypercholesterolemia and vitamin E had variable effects on CL activity. In conclusion, (i) hypercholesterolemia induces oxidative stress in heart, liver, and kidney, the heart being the most and the liver the least susceptible to oxidative stress; (ii) oxidative stress is positively associated with duration of hypercholesterolemia; and (iii) vitamin E slows the progression of oxidative stress in these organs.

Low levels of soluble receptor for advanced glycation end products in non-ST elevation myocardial infarction patients.

BACKGROUND: Interaction of the receptors for advanced glycation end products (RAGEs) with advanced glycation end products (AGEs) results in expression of inflammatory mediators (tumor necrosis factor-alpha [TNF-α] and soluble vascular cell adhesion molecule-1 [sVCAM-1]), activation of nuclear factor-kappa B and induction of oxidative stress - all of which have been implicated in atherosclerosis. Soluble RAGE (sRAGE) acts as a decoy for the RAGE ligand and is protective against atherosclerosis. OBJECTIVES: To determine whether levels of serum sRAGE are lower, and whether levels of serum AGEs, TNF-α and sVCAM-1 are higher in non-ST elevation myocardial infarction (NSTEMI) patients than in healthy control subjects; and whether sRAGE or the ratio of AGEs to sRAGE (AGEs/sRAGE) is a predictor/biomarker of NSTEMI. METHODS: Serum levels of sRAGE, AGEs, TNF-α and sVCAM-1 were measured in 46 men with NSTEMI and 28 age- and sex-matched control subjects. Angiography was performed in the NSTEMI patients. RESULTS: sRAGE levels were lower, and levels of AGEs, TNF-α, sVCAM-1 and AGEs/sRAGE were higher in NSTEMI patients than in control subjects. sRAGE levels were negatively correlated with the number of diseased coronary vessels, serum AGEs, AGEs/sRAGE, TNF-α and sVCAM-1. The sensitivity of the AGEs/sRAGE test is greater than that of the sRAGE test, while the specificity and predictive values of the sRAGE test are greater than those of the AGEs/sRAGE test for identifying NSTEMI patients. CONCLUSIONS: Serum levels of sRAGE were low in NSTEMI patients, and were negatively correlated with extent of lesion, inflammatory mediators, AGEs and AGEs/sRAGE. Both sRAGE and AGEs/sRAGE may serve as biomarkers/predictors for identifying NSTEMI patients.