Selective anterior and posterior screw instrumentation both achieved good surgical lumbar and subsequent spontaneous thoracic correction. There was no statistically significant difference between the 2 groups in lumbar correction or thoracic correction, but fusion levels were shorter in the anterior group. Patients with late thoracic curve decompensation had smaller thoracolumbar/lumbar-thoracic Cobb ratios and less preoperative flexibility than those who did not decompensate.

<abstract> <p>Pulmonary arterial hypertension (PAH) is a life-threatening illness and ferroptosis is an iron-dependent form of regulated cell death, driven by the accumulation of lipid peroxides to levels that are sufficient to trigger cell death. However, only few studies have examined PAH-associated ferroptosis. In the present study, lung samples mRNA expression profiles (derived from 15 patients with PAH and 11 normal controls) were downloaded from a public database, and 514 differentially expressed genes (DEGs) were identified using the Wilcoxon rank-sum test and weighted gene correlation network analyses. These DEGs were screened for ferroptosis-associated genes using the FerrDb database: eight ferroptosis-associated genes were identified. Finally, the construction of gene-microRNA (miRNA) and gene-transcription factor (TF) networks, in conjunction with gene ontology and biological pathway enrichment analysis, were used to inform hypotheses regarding the molecular mechanisms underlying PAH-associated ferroptosis. Ferroptosis-associated genes were largely involved in oxidative stress responses and could be regulated by several identified miRNAs and TFs. This suggests the existence of modulatable pathways that are potentially involved in PAH-associated ferroptosis. Our findings provide novel directions for targeted therapy of PAH in regard to ferroptosis. These findings may ultimately help improve the therapeutic outcomes of PAH.</p> </abstract>

Background Tetralogy of Fallot (ToF) is a life-threatening congenital cardiovascular disorder. Currently, the most effective therapeutic intervention for pediatric ToF remains corrective surgery with cardiopulmonary bypass (CPB). Ferroptosis is an iron-dependent form of regulated cell death, driven by an accumulation of lipid peroxides to levels sufficient to trigger cell death. Ferroptosis was recently linked to cardiac ischemia and reperfusion injury. However, few studies have examined CPB-associated ferroptosis. Method In the current study, pediatric ToF patient pre- and post-CPB atrial biopsy gene expression profiles were downloaded from a public database, and 117 differentially expressed genes (DEGs) were identified using the Wilcoxon rank-sum test and weighted gene correlation network analysis. These were screened for ferroptosis-associated genes using the FerrDb database, thereby identifying ten genes. Finally, the construction of gene-microRNA (miRNA) and gene-transcription factor (TF) networks, in conjunction with gene ontology and biological pathway enrichment analysis, were used to inform hypotheses regarding the molecular mechanisms underlying CPB-associated ferroptosis. Results Ten genes involved in CPB-associated ferroptosis(ATF3,TNFAIP3，CDKN1A, ZFP36, JUN，SLC2A3, IL6, CXCL2, PTGS2, and DDIT3). Ferroptosis-associated genes were largely involved in myocardial inflammatory responses and may be regulated by a number of identified miRNAs and TFs, thereby suggesting modulatable pathways potentially involved in CPB-associated ferroptosis. Conclusions Results suggest that CPB precipitates ferroptosis within cardiac tissue during corrective Surgery for Pediatric Tetralogy of Fallot. These findings may ultimately help improve outcomes of corrective surgery for pediatric ToF.

China has the world's largest number of smokers and is the world's largest consumer of tobacco. 1 As of 2010, 28.1% of adults in China smoked, and 72.4% of non-smokers were exposed to second-hand smoke, according to the Global Adult Tobacco Survey. 2 Cigarette smoke contains a variety of harmful chemicals, including at least 70 carcinogens. 3 Long-term exposure to second-hand smoke is known to cause many diseases. Skin exposure to tobacco smoking has been found to be closely related to skin aging and the formation of pigmentation spots. 4 However, the mechanism by which cigarette smoke causes skin aging remains unclear.Ferroptosis is an iron-dependent form of regulated cell death driven by the accumulation of lipid peroxides to levels sufficient to trigger cell death. 5 Ferroptosis was recently linked to certain diseases, such as heart disease and lung fibrosis. 6,7 However, few studies have examined ferroptosis in skin-related diseases.This study analyzed ferroptosis in female skin exposed to cigarette smoke by downloading gene-set expression data from a public database, thus providing a new approach and theoretical basis for the treatment of skin aging and other skin diseases caused by exposure to cigarette smoke. | ME THODS | Data acquisitionThe gene expression dataset, GSE148221 (platform: GPL20844), 8 was downloaded from the Gene Expression Omnibus (https:// www.ncbi.nlm.nih.gov/geo/) database. 9 This dataset included 22