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[This corrects the article DOI: 10.1371/journal.pone.0042362.].

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BACKGROUND: The acute assessment of patients with suspected ischemic stroke remains challenging. The use of brain biomarker assays may improve the early diagnosis of ischemic stroke. The main goal of the study was to evaluate whether the NR2 peptide, a product of the proteolytic degradation of N-methyl-D-aspartate (NMDA) receptors, can differentiate acute ischemic stroke (IS) from stroke mimics and persons with vascular risk factors/healthy controls. A possible correlation between biomarker values and lesion sizes was investigated as the secondary objective. METHODS AND FINDINGS: A total of 192 patients with suspected stroke who presented within 72 h of symptom onset were prospectively enrolled. The final diagnosis was determined based on clinical observations and radiological findings. Additionally gender- and age-matched healthy controls (n = 52) and persons with controlled vascular risk factors (n = 48) were recruited to compare NR2 peptide levels. Blinded plasma was assayed by rapid magnetic particles (MP) ELISA for NR2 peptide within 30 min and results for different groups compared using univariate and multivariate statistical analyses. There was a clinical diagnosis of IS in 101 of 192 (53%) and non-stroke in 91 (47%) subjects. The non-stroke group included presented with acute stroke symptoms who had no stroke (n = 71) and stroke mimics (n = 20). The highest NR2 peptide elevations where found in patients with IS that peaked at 12 h following symptom onset. When the biomarker cut off was set at 1.0 ug/L, this resulted in a sensitivity of 92% and a specificity of 96% to detect IS. A moderate correlation (r(s) = 0.73) between NR2 peptide values and acute ischemic cortical lesions (<200 mL) was found. CONCLUSIONS: This study suggests that the NR2 peptide may be a brain specific biomarker to diagnose acute IS and may allow the differentiation of IS from stroke mimics and controls. Additional larger scale clinical validation studies are required.

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OBJECTIVES: To determine the sensitivity, specificity, and accuracy of a point-of-care method for identifying Rh(D) phenotype. METHODS: Rh(D) was determined using preserved whole blood via standard laboratory methods. Comparison testing was conducted using the HealthTEST Rh(D) card (Akers Laboratories, Thorofare, NJ). Results of the card test were visually interpreted and recorded. To achieve sensitivity and specificity of 99% (95% confidence interval [CI] = 98% to 100%), 380 Rh-positive and 380 Rh-negative samples were required. During card testing, convenience sampling was used. Card results were compared with official results, and statistical analysis was conducted. RESULTS: In identifying Rh(D)-positive phenotype, the card had a sensitivity of 98.9% and a specificity of 99.7% (95% CI = 0.99 +/- 0.01). For Rh(D)-negative phenotype, the card had a sensitivity of 99.7% and a specificity of 98.9% (95% CI = 0.99 +/- 0.01). CONCLUSIONS: In identifying type D (Rh positive or Rh negative), the card achieves sensitivity, specificity, and accuracy to warrant further study.

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Diltiazem is commonly used to treat atrial fibrillation or flutter (AFF) with rapid ventricular response (RVR). Although it is very effective for rate control, up to an 18% prevalence of reported diltiazem-induced hypotension [defined by systolic blood pressure (SBP) < 90 mm Hg], and a mean of 9.7% hypotension have been reported from several studies totaling over 450 patients. This hypotension may complicate therapy. Our objective was to determine if calcium chloride (CaCl(2)) pre-treatment would blunt a SBP drop after i.v. diltiazem, while allowing diltiazem to maintain its efficacy. A prospective, randomized, double-blind, placebo-controlled study was conducted. Seventy-eight patients with AFF and a ventricular rate of >/= 120 beats per minute were enrolled. Half received i.v. CaCl(2) pre-treatment; the other half received placebo. All patients then received i.v. diltiazem in a standard, weight-based dose. A second dose of CaCl(2) pre-treatment or placebo and diltiazem was given if clinically indicated for additional rate control. Both CaCl(2) and placebo pre-treatment groups had equal lowering of heart rate (p < 0.001). There were no adverse events in the calcium pre-treatment study arm. One patient in the placebo group became paradoxically more tachycardic and apneic after the diltiazem infusion. Although i.v. CaCl(2) seems to be equally safe compared to placebo as a pre-treatment in the management of AFF with RVR, we were unable to find a statistically significant blunting of SBP drop with CaCl(2) i.v. pre-treatment. Until further research determines a benefit exists, we cannot recommend i.v. CaCl(2) pre-treatment before diltiazem in the treatment of AFF with RVR.

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