This study shows that PRKAG3-230 may be associated with sporadic WPW syndrome among a Taiwanese population. Further studies are warranted to elucidate the role of mutations in AMPK subunit genes other than PRKAG3-230 in sporadic WPW syndrome.

Our results suggest that G allele of MPO -463G>A polymorphism is a potential genetic marker for KD risk in Taiwanese children.

Purpose Both air pollutant exposure and neonatal jaundice (NJ) have known effects on childhood asthma, but a higher total serum bilirubin (TSB) level has been associated with lung protection. This study aimed to assess whether prenatal/postnatal exposure to ambient air pollutants is related to the development of asthma in infants with NJ. Patients and Methods A nested case–control retrospective study was performed using the data of infants with NJ in the Kaohsiung Medical University Hospital Research Database. Data on average ambient air pollution concentrations within six months, the first year and second year after birth, and in the first, second and third prenatal trimesters were collected. NJ was defined as TSB levels ≥ 2 mg/dl with the diagnosis less than one-month-old. Asthma was defined as a diagnosis with medication use. We constructed conditional logistic regression models to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs). Results Exposure to NO and SO 2 at all six time points in the study was significantly associated with an increased risk of preschool asthma in infants with NJ. The overall peak OR (95% CI) of SO 2 , PM 2.5 , PM 10 , NO, NO 2 , and NO X were 1.277 (1.129–1.444), 1.057 (1.023–1.092), 1.035 (1.011–1.059), 1.272 (1.111–1.455), 1.168 (1.083–1.259) and 1.104 (1.051–1.161), respectively. Fetuses in the first and second trimester were most vulnerable to ambient air pollutant exposure such as SO 2 PM 2.5 , NO, NO 2 and NO X during the prenatal period. Exposure to all six ambient air pollutants during the first and second years after birth significantly affected preschool asthma in NJ infants. Conclusion In different time windows, prenatal and postnatal exposure to SO 2 , PM 2.5 , PM 10 , NO, NO 2 , and NO X were associated with preschool asthma in NJ infants. The relatively high impact of NO and SO 2 exposure in infants with NJ requires further studies and prevention measures.

We report a 1-year-old boy with a delayed diagnosis of traumatic ventricular septal defect (VSD) related to chest compression. His cardiac function was stable after adequate medical treatment. Spontaneous closure of traumatic VSD occurred to this patient at the age of 4 years. This is a rare case of traumatic VSD associated with accidental chest compression, which is similar to rupture of the ventricular septum after blunt chest trauma. It should be kept in mind that traumatic VSD and concomitant thoracic injuries can develop during chest compression. The clinician should pay attention to the potential risk of traumatic VSD in patients experiencing chest compression. Echocardiography is a convenient and effective tool for serial follow-up examination and avoiding the delayed diagnosis. Troponin I level can be a useful screening test. Conservative management of traumatic VSD with hemodynamic stability is recommended because of possible spontaneous closure.