The role of particulate matters on methylation of IFN- and IL-4 promoter genes in pediatric allergic rhinitis The role of particulate matters on methylation of IFN-γ and IL-4 promoter genes in pediatric allergic rhinitis

The objective of this study was to investigate the relationship between prenatal and postnatal risk factors and the prevalence of allergic rhinitis (AR) in Chinese children of specific ages. This study was a cross-sectional survey. Students from 8 metropolitan cities in China were studied in November and December, 2005. There were 20,803 elementary-school Chinese children (49.6% boys, mean age, 9.19 years) enrolled. Questions from the standard questionnaire of the International Study of Asthma and Allergies in Children were completed to enable us to examine the pattern of current AR. The potential confounders and pre-and postnatal risk factors were analyzed using logistic regression. The overall prevalence of AR was found in this study to be 9.8%. After adjusting for several likely confounders, there was a higher likelihood of AR in school-aged children who were not exclusively breastfed in the first 4 months of their lives (odds ratio [OR]: 1.28; 95% confidence interval [CI]: 1.16–1.41), children who were born post-term (OR: 1.34; 95% CI: 1.12–1.60), children delivered by cesarean section (OR: 1.07; 95% CI: 1.00–1.19), or children born to mothers who experienced depressive symptoms during the pre- and postnatal periods (OR: 1.28; 95% CI: 1.15–1.42). AR in school-aged children was found to be associated with pre- and postnatal events. These findings indicate that strategies to reduce exposure to risk factors during pre- and postnatal periods for childhood allergies might be warranted.

The present study aims to restudy the correlation between the internal auditory meatus (IAM), the cochlear nerve canal (CNC), the cochlear nerve (CN) and inner ear malformations. In this retrospective study design, the abnormal diameter of the IAM, CNC and CN in patients with any kind of inner ear malformations was evaluated using multi-slice spiral computed tomography (MSCT) (37 patients) and magnetic resonance imaging (MRI) (18 patients). Of 37 MSCT-diagnosed patients, 2 had IAM atresia, 11 IAM stenosis, 22 enlarged IAM, and 2 normal IAM with an abnormal CN. MRI diagnoses of 18 patients revealed 8 cases of aplastic CN, 6 hypoplastic CN, and 4 normal CN. CNC stenosis was associated with CN hypoplasia (P < 0.001). Patients with absent or stenotic IAM had less CN development than those with normal or enlarged IAM (P = 0.001). We propose a modification of the existing classification systems with a view to distinguishing malformations of the IAM, CNC and CN.

Background Surgical correction of an anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) has been associated with excellent survival during recent years. The purpose of this study was to evaluate the effectiveness of reimplantation of the coronary artery and to investigate the recovery of postoperative cardiac and mitral valve (MV) function. Methods From 2005 to 2015, 80 patients who had ALCAPA received surgical correction. Among them, 49 were infants. The median patient age was 7.8 months. Operative strategies included reimplantation of the coronary artery in 71 patients, the Takeuchi procedure in another 7 patients, and coronary artery ligation in the remaining 2 patients. Results There were 11 hospital deaths and 2 late deaths. Six patients required intraoperative or postoperative mechanical circulatory support. A significant improvement in the ejection fraction (EF) and shortening fraction (SF) was present in all surviving patients at discharge, at a 3-month follow-up and at a 1-year follow-up. MV function improved gradually after surgical repair with no late secondary intervention. Conclusions The repair of ALCAPA can be accomplished by establishment of a dual-coronary system, which offers an acceptable mortality rate and will rarely require a second surgery. Left ventricular (LV) recovery is a progressive process, especially for infants with impaired LV function. Concomitant MV annuloplasty is safe and reliable and can be performed as necessary in patients with moderate or severe mitral valve regurgitation. In conclusion, this study demonstrates favorable outcomes of ALCAPA repair with an acceptable mortality rate and a very rare occurrence of secondary surgery. The LVEDD Z-score appears to be a sensitive predictor of death. LV recovery is a long-term process after surgical correction, especially for infants with impaired LV function. Concomitant MV annuloplasty is safe and reliable and can be performed as indicated in patients with moderate or severe MR. Received: 20 November 2020 Accepted: 27 January 2021 Article published online: 13 April 2021 © 2021. Thieme. All rights reserved. Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany

Ventricular septal defects (VSDs) are the most common and simplest type of congenital heart diseases (CHDs). Animal studies have suggested that the downregulation of Yes-associated protein 1 (YAP1) during embryonic development causes VSD-associated CHDs. However, how YAP1 contributes to isolated VSD (iVSD) is unclear. Twenty right atrial specimens were obtained from iVSD patients during routine congenital cardiac surgery and we assessed YAP1 expression in these specimens. For controls, six right atrial specimens were obtained from normal hearts of children without heart disease, three of whom died from cerebral palsy, and three who underwent heart transplants. YAP1 mRNA and protein levels and nuclear localization were significantly reduced in iVSD specimens compared to normal heart specimens. Concomitantly, mRNA levels of YAP1 downstream targets CTGF and AXL were also significantly decreased in iVSD specimens. Although Ki67-positive cardiomyocytes in iVSD specimens were comparable to normal heart specimens, Ki67-positive non-cardiomyocytes were significantly decreased. YAP1 expression was markedly decreased in hearts of iVSD children. Given the important role of YAP1 during heart development, downregulation of YAP1 expression may contribute to iVSD and affect the proliferation of non-cardiomyocytes.