BACKGROUND: The i-Smart 30 point-of-care (POC) analyzer (i-SENS, Korea) is a compact and portable system used for the analysis of electrolytes (sodium, potassium, chloride) and hematocrit in whole blood samples. In this study, we evaluated the analytical performance of the i-Smart 30 analyzer. METHODS: Precision and sample-related percent carry-over were determined using the quality control materials. Comparison study was performed with the Stat Profile Critical Care Xpress (STP CCX; Nova Biomedical, USA) analyzer using venous whole blood samples. RESULTS: In the precision study, imprecision studies demonstrated within-run and total-run coefficients of variation within 0.5-3.9% and 0.7-4.4%, respectively, for all analytes. A good correlation was found between the i-Smart 30 analyzer and the STP CCX analyzer, except for chloride that showed high intercept. In the study of carry-over, sample-related carry-over for Na+, K+, Cl- and Hct were demonstrated as 0.84%, 0%, 0.86% and 1.56%, respectively. CONCLUSIONS: We conclude that the i-Smart 30 analyzer is suitable for routine use in clinical laboratories, especially where rapid test results are required such as emergency departments, intensive care units, and dialysis units. However, for Cl-, it is necessary that a significant correlation between this analyzer and a reference method should be demonstrated.
Critical Care ; Dialysis ; Electrolytes ; Emergencies ; Hematocrit ; Intensive Care Units ; Point-of-Care Systems ; Potassium ; Quality Control

OBJECTIVE: Social anxiety disorder (SAD) shows relatively delayed responses to pharmacotherapy when compared to other anxiety disorders. Therefore, more effective early therapeutic decisions can be made if the therapeutic response is predictable as early as possible. We studied whether the therapeutic response at 12 weeks is predictable based on the early improvement with escitalopram at 1 week. METHODS: The subjects were 28 outpatients diagnosed with SAD. The subjects took 10-20 mg/day of escitalopram. The results of the Liebowitz social anxiety scale (LSAS), Hamilton anxiety rating scale, and Montgomery-Asberg depression rating scale were evaluated at 0, 1, 4, 8, and 12 weeks of treatment. Early improvement was defined as a ≥10% reduction in the LSAS total at 1 week of treatment, and endpoint response was defined as a ≥35% reduction in the LSAS total score. The correlation between clinical characteristics and therapeutic responses was analyzed by simple linear regression. The correlation between early improvement responses and endpoint responses was analyzed by multivariate logistic regression analysis and receiver operating characteristic curves. RESULTS: When we adjusted the influence of a ≥35% reduction in the LSAS total endpoint score on a ≥10% reduction of the LSAS total score at 1 week of treatment for the patients' age, the early improvement group at 1 week of treatment was expected to show stronger endpoint responses compared to the group with no early improvement. CONCLUSION: The results suggest that a ≥10% reduction in the LSAS total score in a week can predict endpoint treatment response.
Anxiety Disorders* ; Anxiety* ; Citalopram* ; Depression ; Drug Therapy ; Humans ; Linear Models ; Logistic Models ; Outpatients ; Phobic Disorders ; ROC Curve

BACKGROUND: Neurodegenerative diseases are associated with oxidative stress. Antioxidants including 15-deoxy- Delta (12,14) prostaglandin J2 (15d-PGJ2) have been tried as potential therapeutic regimens of the experimental model of neurodegenerative disease. In this study, we investigated the neuroprotective role of 15d-PGJ2 on cytochrome c mediated apoptotic signals in oxidative stress injured neuronally-differentiated PC12 cells (nPC12 cells) by exposing them to H2O2. METHODS: Following 100 micor M H2O2 exposure, the viability of nPC12 cells (pretreated with 15d-PGJ2 vs. not pretreated) was evaluated by using MTT assay. Immunoreactivity (IR) of cytochrome c, caspase-3, and poly (ADP-ribose) polymerase (PARP) was examined by using a Western blot. RESULTS: In this study, 15d-PGJ2 pretreated nPC12 cells showed an increase in cell viability until the concentrations of 15d-PGJ2 reached up to 4 micor M, but there was no increment of cell viability in higher concentrations. The inhibition of cytochrome c release, activation of caspase-3, and cleavage of PARP were demonstrated by the pretreatment of 15d-PGJ2 up to 4 micor M. However, these were not observed in the pretreatment with 8 micor M 15d-PGJ2. CONCLUSIONS: These data show that 15d-PGJ2 affects the apoptotic pathway through downstream signals including cytochrome c and caspase-3 pathway. Therefore, these results suggest that 15d-PGJ2 could be a new potential therapeutic candidate for the oxidative stress-injury model of neurodegenerative diseases.
Animals ; Antioxidants ; Apoptosis ; Blotting, Western ; Caspase 3 ; Cell Survival ; Cytochromes c ; Models, Theoretical ; Neurodegenerative Diseases ; Oxidative Stress ; PC12 Cells*