Search

[Display omitted] • The specific mechanisms of PS-NP-induced pulmonary injury are unclear. • A mouse model of lung injury is created based on the real-world NP exposure in human. • PS-NP exposure induces ferroptosis in lung tissues and bronchial epithelial cells. • HIF-1α inhibition rescues PS-NP-induced ferroptosis in bronchial epithelial cells. • PS-NP exposure induces ferroptosis via the HIF-1α/HO-1 signaling pathway in lungs. It has been shown that polystyrene nanoplastic (PS-NP) exposure induces toxicity in the lungs. This study aims to provide foundational evidence to corroborate that ferroptosis and abnormal HIF-1α activity are the main factors contributing to pulmonary dysfunction induced by PS-NP exposure. Fifty male and female C57BL/6 mice were exposed to distilled water or 100 nm or 200 nm PS-NPs via intratracheal instillation for 7 consecutive days. Hematoxylin and eosin (H&E) and Masson trichrome staining were performed to observe the histomorphological changes in the lungs. To clarify the mechanisms of PS-NP-induced lung injury, we used 100 μg/ml, 200 μg/ml and 400 μg/ml 100 or 200 nm PS-NPs to treat the human lung bronchial epithelial cell line BEAS-2B for 24 h. RNA sequencing (RNA-seq) of BEAS-2B cells was performed following exposure. The levels of glutathione, malondialdehyde, ferrous iron (Fe2+), and reactive oxygen species (ROS) were measured. The expression levels of ferroptotic proteins were detected in BEAS-2B cells and lung tissues by Western blotting. Western blotting, immunohistochemistry, and immunofluorescence were used to evaluate the HIF-1α/HO-1 signaling pathway activity. H&E staining revealed substantial perivascular lymphocytic inflammation in a bronchiolocentric pattern, and Masson trichrome staining demonstrated critical collagen deposits in the lungs after PS-NP exposure. RNA-seq revealed that the differentially expressed genes in PS-NP-exposed BEAS-2B cells were enriched in lipid metabolism and iron ion binding processes. After PS-NP exposure, the levels of malondialdehyde, Fe2+, and ROS were increased, but glutathione level was decreased. The expression levels of ferroptotic proteins were altered significantly. These results verified that PS-NP exposure led to pulmonary injury through ferroptosis. Finally, we discovered that the HIF-1α/HO-1 signaling pathway played an important role in regulating ferroptosis in the PS-NP-exposed lung injury. PS-NP exposure caused ferroptosis in bronchial epithelial cells by activating the HIF-1α/HO-1 signaling pathway, and eventually led to lung injury. [ABSTRACT FROM AUTHOR]

To summarize the etiology and treatment of 119 patients with chylothorax in our hospital. A total of 119 patients with chylothorax, divided into a neonate group, an infant group, and an older-than-1-year group, were included in our study and analyzed from January 2000 to July 2017 in the Children's Hospital of Chongqing Medical University. A total of 90 males and 29 females were included in our study. In the neonate group, 21 chylothorax cases were due to idiopathic factors, constituting 72.4% of the cases; 8 were related to cardiothoracic surgery, constituting 27.6%. In the infant group, 15 chylothorax cases were due to cardiothoracic surgery, constituting 55.6% of the cases; 11 were related to idiopathic factors, constituting 40.7%; and 1 was related to lymphoma, constituting 3.8%. In the older-than-1-year group, 33 chylothorax cases were due to idiopathic factors, constituting 52.4% of the cases; 25 were cardiothoracic surgery, constituting 39.7%; 2 were related to another internal medicine disease, constituting 3.2%; 2 were due to injury, constituting 3.2%; and 1 was related to lymphoma, constituting 1.6%. All the patients sequentially underwent thoracic drainage therapy, followed by fasting, thoracic injection of an adhesion-promoting agent, and thoracic duct ligation surgery. Among the neonates, 23 patients (79%) with fasting therapy improved, and 5 patients with fasting + intrapleural injection improved (17%). In the infant group, fasting promoted recovery in 14 patients, accounting for 51%, and fasting + thoracic injection improved the conditions of 10 patients, accounting for 37%. In the older-than-1-year group, fasting was effective in 35 patients, accounting for 55%; fasting + thoracic injection was effective in 22 patients, accounting for 34%; and fasting + thoracic injection + thoracic duct ligation surgery enabled the recovery of 2 patients, accounting for 3.2%. In our center, the main causes of chylothorax in the neonates group are idiopathic factors but may also include a history of unspecified birth trauma; the proportions of idiopathic factors in the infant and older-than-1-year groups are also higher, but the iatrogenic factors are significantly increased in the latter 2 groups. All the patients underwent thoracic drainage therapy, and fasting promoted the recovery of most children. When fasting was ineffective, subsequent thoracic injections were effective. If the above two methods failed, surgery was a method of choice, but it was not always effective. Level IV. Retrospective study. [ABSTRACT FROM AUTHOR]

Abstract Purpose To describe the diagnosis and treatment of 34 cases of congenital tracheobronchial cartilage remnants of esophagus. Methods The diagnosis and treatment of 34 cases of congenital tracheobronchial cartilage remnants of esophagus were analyzed retrospectively in our hospital. Results Congenital tracheobronchial cartilage remnants of esophagus could be specifically diagnosed by clinical situation and esophageal barium meal examination. The anterior wall of the esophagus was cut longitudinally with the posterior wall of the esophagus preserved. And the cartilage was removed and the open anterior wall of the esophagus was sutured horizontally with full layer. In our study, 34 patients who underwent the operation had a satisfactory outcome. However, one patient underwent submucosal cartilage stripping, which resulted in a complication involving fistulae from the esophagus to the abdominal cavity that were healed after gastrostomy and nutritional support. Conclusion Congenital tracheobronchial cartilage remnants of esophagus caused symptoms when the infants were started on adjunct foods. Vomiting the food without gastric fluid and bile was the leading clinical manifestation. Distinguishing signs on esophageal barium contrast could be used as preoperative diagnosis evidence. Surgically removing the cartilage and horizontally suturing the esophagus provides a reliable outcome. Level of Evidence Level IV. Type of Study Retrospective study. [ABSTRACT FROM AUTHOR]

Abstract Background Pectus excavatum, the most common congenital chest wall deformity in pediatric patients, leads to pulmonary dysfunction. There is no consensus regarding the effectiveness of the Nuss procedure for recovering pulmonary function. In this meta- analysis, we focused on the changes that occur in pulmonary function after the Nuss procedure. Methods We performed a literature search in the MEDLINE, Embase, Cochrane library and PubMed databases. The included studies were required to contain pulmonary function tests with results adjusted to predicted values both before and after the Nuss procedure. The key outcomes of interest in this analysis were pulmonary function measured as forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC). Subgroup analyses were performed based on time since surgery and the mean ages of the patients when they underwent surgery by forest plots and meta-regressions. Results Thirteen studies involving 465 participants were included in this review. The standard mean difference (SMD) observed in FEV1 and FVC after surgery were 0.17 (95% CI, 0.01–0.33, p = 0.04) and − 0.18 (95% CI, − 0.41–0.06, p = 0.14), respectively. The overall meta-regression SMD of FEV1 and FVC by time since surgery were 1.21 (95% CI, 1.04–1.41, p = 0.020) and 1.38 (95% CI, 1.05–1.83, p = 0.027), respectively. We found evidence of a temporal relationship between time at which pulmonary function tests were performed after surgery and predicted FEV1 and FVC values. The SMD of FEV1 (0.26, p = 0.012) was slightly higher in group evaluated more than 2 year after initial surgery. Conclusions Abnormal resting pulmonary functions tests performed prior to surgery showed an initial depression after surgery. The FEV1 of patients slightly increased at 2 year post surgery compared with the baseline. Further studies with longer term follow-up are still needed to determine if pulmonary function could improve to normal after surgery. Levels of Evidence Level of evidence: 4 (based on lowest level of article analyzed in meta-analysis/systematic review). [ABSTRACT FROM AUTHOR]

Objective This study sought to summarize the diagnostic and treatment aspects of congenital diaphragmatic eventration (CDE) in children by retrospectively analyzing their medical records to identify and understand the complications of CDE, its treatment, and to evaluate the long-term outcomes of diaphragmatic plication. Methods The medical records of children who received treatment for CDE from January 2000 to December 2011 at the Children's Hospital of Chongqing Medical University, China were analyzed. Data analyzed included the following: age, sex, symptom, location of eventration, associated anomalies, surgical procedures, complications, and survival and follow up details after diaphragmatic plication. Results The medical records of 177 children (boys: 128, girls: 49, mean age: 10.28 ± 2.35 months) with CDE were included in this study. Specific symptoms of eventration of the diaphragm were reported for 86 cases; and the typical symptoms included rapid breathing, vomiting, and recurrent respiratory infections. Except for a bilateral case, all the other patients had unilateral CDE. Associated malformations were observed in 31 cases (17.5%), hypoplastic lung (10 cases) was the most common followed by congenital heart disease (9 cases), and cryptorchidism (3 cases). Interestingly, 91 patients were asymptomatic. Diaphragmatic plication was performed in all symptomatic patients (86 cases, 48.5%) and none had recurrence. Conclusions Clinical symptoms of CDE varied in severity, ranging from asymptomatic conditions to life-threatening respiratory distress. Timely accurate diagnosis and treatment of symptomatic CDE could effectively resolve respiratory morbidity and reduce complications. The diaphragm plication surgery provided good results among the study population with no recurrence. [ABSTRACT FROM AUTHOR]

Osteosarcoma (OS) is the most common type of bone cancer in children and adolescents. LncRNA differentiation antagonizing nonprotein coding RNA (DANCR) has been reported to be aberrant expression in osteosarcoma and contribute to proliferation, migration and invasion of cancer cells. Here, we further explore the exacted molecular mechanism of DANCR in OS. The expression of DANCR, microRNA-216a-5p (miR-216a-5p) and SOX5 was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cells proliferation and apoptosis were analyzed by WST-1assay or flow cytometry, respectively. The migratory and invasion abilities were measured by transwell assay. Western blot was used to detect the level of SOX5 and autophagy-related protein of Beclin1, LC3-I and LC3-II. The interaction among DANCR, miR-216a-5p and SOX5 was explored by luciferase reporter assay, RIP assay or Pull-down assay. Murine xenograft model was established using 143B cells transfected with sh-DANCR. We found that a significantly elevated of DNACR was detected in osteosarcoma tissue and cell lines. Functional experiments suggested that down-regulation of DANCR inhibited cells proliferation, migration, invasion and autophagy but induced apoptosis in osteosarcoma in vitro. Additionally, we also determined knockdown of DANCR inhibited the growth and autophagy of osteosarcoma in vivo. DANCR was a sponge of miR-216a-5p activity. DANCR regulated survival of osteosarcoma through targeting miR-216a-5p. Additionally, SOX5 was a direct target of miR-216a-5p, overexpression miR-216a-5p exerted inhibition effects via down-regulating SOX5 expression. Furthermore, DANCR regulated SOX5 expression by sponging to miR-216a-5p. In conclusion, LncRNA DANCR silence inhibits SOX5-medicated progression and autophagy in osteosarcoma via regulating miR-216a-5p which indicating DANCR may act as a potential prognostic biomarker and therapeutic target for osteosarcoma. [ABSTRACT FROM AUTHOR]