Runtikan Pochairach

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common enzymopathy with significant clinical implications, particularly in malaria-endemic regions and in the management of neonatal hyperbilirubinemia. Timely and accurate detection of G6PD deficiency is critical to prevent life-threatening hemolytic events following oxidative drug administration. This study evaluated the MyG6PD device, a quantitative point-of-care (PoC) tool, for the assessment of hemoglobin concentration and G6PD enzyme activity. Analytical performance was benchmarked against laboratory spectrophotometry and the STANDARD G6PD Analyzer™ (SD Biosensor; Suwon-si, Republic of Korea). MyG6PD demonstrated excellent linearity (R² ≥ 0.99), accuracy (bias < ±15%), and precision (CV < 15%) across normal, intermediate, and deficient activity ranges, including heterozygous females with intermediate phenotypes. The device’s compact, battery-operated design, rapid turnaround, and minimal training requirements support its use in decentralized and resource-limited settings. Furthermore, cost-effective consumables and robust detection of intermediate activity highlight its potential for large-scale deployment. Overall, MyG6PD provides a reliable, accessible, and clinically actionable solution for urgent G6PD deficiency screening, enabling safer administration of oxidative therapies and improving patient outcomes in high-risk populations.

Chronic kidney disease (CKD) continues to pose a critical global health challenge, making ongoing monitoring vital for effective management and preventing its progression to end-stage renal disease. The urinary albumin-to-creatinine ratio (uACR) stands out as a reliable biomarker. MyACR was developed and validated as a novel point-of-care (POC) device for identifying and monitoring the progress of CKD. MyACR device operates using a colorimetric-based spectroscopy to quantify albumin and creatinine levels at 625 nm and 515 nm, respectively. Calculated uACR values were compared with results from the reference turbidimetry method using a dataset of 103 random urine samples from patients at high risk of advanced CKD. The device showed excellent performance in detecting severe nephropathy, with sensitivity, specificity, and accuracy of 100%, 100%, and 100%, respectively. The PPV (positive predictive value) was 100%, indicating perfect identification of patients with severe nephropathy (uACR > 300 mg/g creatinine). The NPV (negative predictive value) was 100%, suggesting a strong ability to rule out severe nephropathy, though a small risk of false negatives remained. Bland–Altman analysis confirmed a high level of agreement, with 96.11% (for all data) and 95.87% (for uACR > 300 mg/g creatinine) of MyACR measurements falling within the 95% confidence interval (−27 to +19). Correlation analysis revealed a significant alignment between MyACR and the reference method (r² 0.9720 to 0.9836). The ROC analysis suggested that combining uACR with the estimated glomerular filtration rate (eGFR) demonstrated strong predictive performance, yielding an area under the curve (AUC) of 0.933 (95% CI: 0.86–1.0). In conclusion, the MyACR device is a robust, affordable, and user-friendly tool for detecting nephropathy, showing performance comparable to the reference method. Its portability and cost-effectiveness make it particularly suitable for use in low-resource environments. Additionally, integrating uACR with eGFR enhances prognostic capabilities, offering a comprehensive approach to assessing kidney function and predicting CKD progression.

Phage therapy is increasingly considered a viable alternative to combat multi-drug-resistant bacteria, including Acinetobacter baumannii (AB), a significant nosocomial pathogen. In this study, an AB isolate, designated ABU-3, was found susceptible to three distinct AB-phages, termed AB-phage 22, 27, and 32. The ABU-3 isolate was treated with these phages at various multiplicities of infection (MOI) to identify the MOI necessary to completely eliminate ABU-3, referred to as the "MOI clearance value." Results showed that the MOI clearance values for AB-phage 22, 27, and 32 were 10, 100, and 10, respectively. Additionally, colonies of ABU-3 that survived treatment with each AB-phage at lower MOIs were isolated and assessed for susceptibility or resistance to all three phages. The results indicated that ABU-3 became resistant to AB-phage 27 but remained susceptible to AB-phages 22 and 32 at titers similar to the original ABU-3 control. ABU-3 also developed complete resistance to AB-phage 22 but remained susceptible to AB-phages 27 and 32, though at a 2-log lower MOI compared to the original ABU-3. In contrast, AB-phage 32-resistant ABU-3 exhibited complete resistance to all three AB-phages. These findings highlight a potential complication in phage therapy, underscoring the importance of carefully managing MOI to prevent resistance. The varying immunity profiles of AB-phage-treated AB isolates under inappropriate MOI conditions could complicate phage therapy by promoting phage resistance. We propose prioritizing the MOI clearance value as a critical metric for effective phage therapy, particularly for multi-drug-resistant bacterial pathogens.