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A retrospective study to assess the epidemiological and economic burden of pneumococcal diseases in adults aged 50 years and older in Taiwan

Wu DB, Roberts CS, Huang YC, Chien L, Fang CH, Chang CJ

J Med Econ, 2014 May;17(5):312-9.
PMID: 24575941 DOI: 10.3111/13696998.2014.898644

Invasive pneumococcal disease (IPD) and pneumococcal pneumonia cause substantial morbidity and mortality worldwide. This retrospective study was conducted to estimate the disease burden from pneumococcal disease in older adults in Taiwan from a health insurer's perspective.
Fulltext Madden-Julian Oscillation Enhances Phytoplankton Biomass in the Maritime Continent

Chang CJ, Hsu HH, Cheah W, Tseng WL, Jiang LC

Sci Rep, 2019 04 01;9(1):5421.
PMID: 30931981 DOI: 10.1038/s41598-019-41889-5

In addition to monsoon-driven rainfall, the Maritime Continent (MC) is subject to heavy precipitation caused by the Madden-Julian Oscillation (MJO), a tropical convection-coupled circulation that propagates eastward from the Indian to the Pacific Ocean. This study shows that riverine runoff from MJO-driven rainfall in the western MC significantly enhances phytoplankton biomass not only in the coastal regions but as far as the nutrient-poor Banda Sea, located 1,000 km downstream of the riverine source. We present observational estimates of the chlorophyll-a concentration in the Banda Sea increasing by 20% over the winter average within an MJO life cycle. The enhancement of phytoplankton in the central Banda Sea is attributed to two coinciding MJO-triggered mechanisms: enhanced sediment loading and eastward advection of waters with high sediment and chlorophyll concentrations. Our results highlight an unexpected effect of MJO-driven rainfall on the downstream oceanic region. This finding has significant implications for the marine food chain and biogeochemical processes in the MC, given the increasing deforestation rate and projections that global warming will intensify both the frequency and strength of MJO-driven rainfall in the MC.
Fulltext Development of a prediction model for emergency medical service witnessed traumatic out-of-hospital cardiac arrest: A multicenter cohort study

Wang SA, Chang CJ, Do Shin S, Chu SE, Huang CY, Hsu LM, et al.

J Formos Med Assoc, 2024 Jan;123(1):23-35.
PMID: 37573159 DOI: 10.1016/j.jfma.2023.07.011

BACKGROUND/PURPOSE: To develop a prediction model for emergency medical technicians (EMTs) to identify trauma patients at high risk of deterioration to emergency medical service (EMS)-witnessed traumatic cardiac arrest (TCA) on the scene or en route.
METHODS: We developed a prediction model using the classical cross-validation method from the Pan-Asia Trauma Outcomes Study (PATOS) database from 1 January 2015 to 31 December 2020. Eligible patients aged ≥18 years were transported to the hospital by the EMS. The primary outcome (EMS-witnessed TCA) was defined based on changes in vital signs measured on the scene or en route. We included variables that were immediately measurable as potential predictors when EMTs arrived. An integer point value system was built using multivariable logistic regression. The area under the receiver operating characteristic (AUROC) curve and Hosmer-Lemeshow (HL) test were used to examine discrimination and calibration in the derivation and validation cohorts.
RESULTS: In total, 74,844 patients were eligible for database review. The model comprised five prehospital predictors: age <40 years, systolic blood pressure <100 mmHg, respiration rate >20/minute, pulse oximetry <94%, and levels of consciousness to pain or unresponsiveness. The AUROC in the derivation and validation cohorts was 0.767 and 0.782, respectively. The HL test revealed good calibration of the model (p = 0.906).
CONCLUSION: We established a prediction model using variables from the PATOS database and measured them immediately after EMS personnel arrived to predict EMS-witnessed TCA. The model allows prehospital medical personnel to focus on high-risk patients and promptly administer optimal treatment.
Genetic variants associated with phenytoin-related severe cutaneous adverse reactions

Chung WH, Chang WC, Lee YS, Wu YY, Yang CH, Ho HC, et al.

JAMA, 2014 Aug 6;312(5):525-34.
PMID: 25096692 DOI: 10.1001/jama.2014.7859

The antiepileptic drug phenytoin can cause cutaneous adverse reactions, ranging from maculopapular exanthema to severe cutaneous adverse reactions, which include drug reactions with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, and toxic epidermal necrolysis. The pharmacogenomic basis of phenytoin-related severe cutaneous adverse reactions remains unknown.
Whole genome sequencing identifies genetic variants associated with co-trimoxazole hypersensitivity in Asians

Wang CW, Tassaneeyakul W, Chen CB, Chen WT, Teng YC, Huang CY, et al.

J Allergy Clin Immunol, 2021 04;147(4):1402-1412.
PMID: 32791162 DOI: 10.1016/j.jaci.2020.08.003

BACKGROUND: Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole-induced SCAR remains unclear.
OBJECTIVE: We aimed to investigate the genetic predisposition of co-trimoxazole-induced SCAR.
METHODS: We conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole-induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia.
RESULTS: The whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole-induced SCAR (P = 8.2 × 10-9; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole-related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole-induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10-21; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10-5; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole-induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10-23; OR = 40.1).
CONCLUSION: This study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole-induced SCAR in Asians.