Enhanced recovery after surgery in elderly patients with non-small cell lung cancer who underwent video-assisted thoracic surgery.

BACKGROUND: This study was designed to investigate the clinical outcomes of enhanced recovery after surgery (ERAS) in the perioperative period in elderly patients with non-small cell lung cancer (NSCLC). AIM: To investigate the potential enhancement of video-assisted thoracic surgery (VATS) in postoperative recovery in elderly patients with NSCLC. METHODS: We retrospectively analysed the clinical data of 85 elderly NSCLC patients who underwent ERAS (the ERAS group) and 327 elderly NSCLC patients who received routine care (the control group) after VATS at the Department of Thoracic Surgery of Peking University Shenzhen Hospital between May 2015 and April 2017. After propensity score matching of baseline data, we analysed the postoperative stay, total hospital expenses, postoperative 48-h pain score, and postoperative complication rate for the 2 groups of patients who underwent lobectomy or sublobar resection. RESULTS: After propensity score matching, ERAS significantly reduced the postoperative hospital stay (6.96 ± 4.16 vs 8.48 ± 4.18 d, P = 0.001) and total hospital expenses (48875.27 ± 18437.5 vs 55497.64 ± 21168.63 CNY, P = 0.014) and improved the satisfaction score (79.8 ± 7.55 vs 77.35 ± 7.72, P = 0.029) relative to those for routine care. No significant between-group difference was observed in postoperative 48-h pain score (4.68 ± 1.69 vs 5.28 ± 2.1, P = 0.090) or postoperative complication rate (21.2% vs 27.1%, P = 0.371). Subgroup analysis showed that ERAS significantly reduced the postoperative hospital stay and total hospital expenses and increased the satisfaction score of patients who underwent lobectomy but not of patients who underwent sublobar resection. CONCLUSION: ERAS effectively reduced the postoperative hospital stay and total hospital expenses and improved the satisfaction score in the perioperative period for elderly NSCLC patients who underwent lobectomy but not for patients who underwent sublobar resection.

The Role of CT Scan in Pediatric Airway Foreign Bodies.

Objective: We aim to determine the utility of CT scan as a method to accurately confirm pediatric airway foreign bodies (AFBs), the current gold standard of which is chest X-ray as the primary imaging modality in the investigation screening of AFBs with progression to microlaryngobronchoscopy. Methods: A retrospective cohort study of children diagnosed with suspected AFBs between July 2019 and June 2020 was conducted. The primary outcome of missed AFBs from radiologic investigations was recorded. Results: A total of 226 children with an average age of 1.94 years were included in this study. One hundred and two children were eventually admitted to the hospital for microlaryngobronchoscopy. A total of 89 cases were initially examined by chest X-ray with the diagnosis confirmed in 26 cases. The initial examination was chest CT scan in 105 cases, of which the diagnosis was confirmed in 46 cases. The initial examination was chest CT scan with airway reconstruction in 32 cases, and the diagnosis was confirmed in 17 cases. Patients with negative chest CT scan with airway reconstruction were observed to have resolution of symptoms with no further need for bronchoscopy. Conclusion: Chest CT scan with airway reconstruction had the highest rate of confirmed diagnosis of pediatric AFBs on initial scanning, followed by chest CT scan, and finally chest X-ray with fluoroscopy; there was no missed diagnosis in chest CT scan with airway reconstruction. Chest CT scan with airway reconstruction can accurately and quickly detect AFBs and reduce unnecessary bronchoscopy.

The genes for sensory perception of sound should be considered in gene diagnosis of congenital sensorineural hearing loss and microtia.

Congenital sensorineural hearing loss (CSHL) and microtia are development-related diseases, sharing some factors and affecting children's hearing. However, genetic tests only focus on CSHL. We try to identify the common molecular mechanism of CSHL and microtia as candidates combining gene diagnosis biomarkers. Whole-exon sequencing (WES), Sanger sequencing, qPCR, and bioinformatics analyses were performed in microtia family (F1), family two, whose proband suffered from microtia and CSHL (F2), five microtia, and four CSHL individuals, respectively. We found that 40% microtia and 40% CSHL relevant genes were detected in F1 and a sharing pathway: the sensory perception of sound was identified. Moreover, the copy number variation in proband F2 was identified in one gene of the sharing pathway: EYA1. Meanwhile, two variants of BUB3 were identified in F1 data. BUB3 is related to development, dog ear type, direct and indirect interaction with microtia, and CSHL relevant genes. Notably, although the allele frequency of two variants of BUB3 showed significant differences between microtia and CSHL, the special microtia-relevant genotype also could be detected in one CSHL sample. These results suggest that the sensory perception of sound and the development of relevant pathways may be the common pathways of microtia and CSHL. Genes of these pathways can be used as candidates combining gene diagnosis biomarkers.

A novel dominant mutation in the SOX10 gene in a Chinese family with Waardenburg syndrome type II.

Waardenburg syndrome type 2 (WS2) is a rare genetic disorder, characterized by bright blue eyes, moderate to profound hearing loss and pigmental abnormalities of the hair and skin. Between 10 and 20 mutations in the SRY­box 10 (SOX10) gene were previously identified to be associated with WS2. The present study aimed to identify the genetic causes of WS2 in a Chinese family. Clinical and molecular analyses were performed to genetically characterize a Chinese family with two cases of WS2. The clinical data of the proband were collected using a questionnaire. The genomic DNA was extracted from peripheral blood samples of each individual in the family, and 168 candidate genes associated with hearing loss were sequenced using the Illumina HiSeq 2000 and confirmed by Sanger sequencing. A heterozygous nonsense mutation [substitution; position 127; cytosine to thymine (c.127C>T)] was identified in exon 2 of SOX10 (transcript ID: NM_006941.3) in the proband and the mother; however, not in other family members or healthy controls. The novel nonsense heterozygous mutation may cause the replacement of codon 43 [arginine (Arg)] with a stop codon (Arg43stop), leading to premature termination of protein translation. The novel nonsense heterozygous mutation c.127C>T in the SOX10 gene was considered to be the cause of WS2 in the family. This mutation has not been identified in any databases, to the best of the authors' knowledge, including The Single Nucleotide Polymorphism Database, The Human Gene Mutation Database, 1000 Genomes Project and ClinVar and Exome Sequencing Project v. 6500.

LncRNA SLC8A1-AS1 protects against myocardial damage through activation of cGMP-PKG signaling pathway by inhibiting SLC8A1 in mice models of myocardial infarction.

Extensive investigations into long noncoding RNAs (lncRNAs) in various diseases and cancers, including acute myocardial infarction (AMI) have been conducted. The current study aimed to investigate the role of lncRNA solute carrier family 8 member A1 antisense RNA 1 (SLC8A1-AS1) in myocardial damage by targeting solute carrier family 8 member A1 (SLC8A1) via cyclic guanosine 3',5'-monophosphate-protein kinase G (cGMP-PKG) signaling pathway in AMI mouse models. Differentially expressed lncRNA in AMI were initially screened and target relationship between lncRNA SLC8A1-AS1 and SLC8A1 was then verified. Infarct size, levels of inflammatory factors, biochemical indicators, and the positive expression of the SLC8A1 protein in AMI were subsequently determined. The expression of SLC8A1-AS1, SLC8A1, PKG1, PKG2, atrial natriuretic peptide, and brain natriuretic peptide was detected to assess the effect of SLC8A1-AS1 on SLC8A1 and cGMP-PKG. The respective contents of superoxide dismutase, lactate dehydrogenase (LDH), and malondialdehyde (MDA) were detected accordingly. Microarray data GSE66360 provided evidence indicating that SLC8A1-AS1 was poorly expressed in AMI. SLC8A1 was verified to be a target gene of lncRNA SLC8A1-AS1. SLC8A1-AS1 upregulation decreased levels of left ventricular end-systolic diameter, -dp/ dt max , interleukin 1ß (IL-1ß), IL-6, transforming growth factor α, nitric oxide, inducible nitric-oxide synthase, endothelial nitric-oxide synthase, infarct size, LDH activity and MDA content, and increased IL-10, left ventricular end-diastolic pressure and + dp/ dt max . Furthermore, the overexpression of SLC8A1-AS1 was noted to elicit an inhibitory effect on the cGMP-PKG signaling pathway via SLC8A1. In conclusion, lncRNA SLC8A1-AS1, by downregulating SLC8A1 and activating the cGMP-PKG signaling pathway, was observed to alleviate myocardial damage, inhibit the release of proinflammatory factors and reduce infarct size, ultimately protecting against myocardial damage.

Downregulated microRNA-224 aggravates vulnerable atherosclerotic plaques and vascular remodeling in acute coronary syndrome through activation of the TGF-ß/Smad pathway.

Recent studies have shown that circulating microRNAs (miRNA) play a critical role in diagnosing acute coronary syndrome (ACS). This study aims to investigate the effect of miR-224 on atherosclerotic plaques forming and vascular remodeling in ACS and its relationship with TGF-ß/Smad pathway. Myocardial infarction (MI) rat model was established and lentivirus vector of miR-224 inhibitor was prepared for investigating the effect of downregulated miR-224 on the contents of nitric oxide (NO) and endothelin-1 (ET-1), blood lipid levels and inflammatory factor levels in serum as well as the TGF-ß/Smad pathway. The rats suffering from MI had decreased survival rates and exhibited reduced levels of NO, high-density lipoprotein cholesterol, and lumen diameter, and Smad7 messenger RNA (mRNA) and protein expression; while had significantly increased ratio of heart weight or body weight, levels of ET-1, inflammatory factors, blood lipid indexes, vascular remodeling indexes, collagen volume fraction, vulnerable atherosclerotic plaque area, VCAM-1 and MMP-2 protein expression, TGF-ß, Smad2, Smad3, and Smad4 mRNA and protein expression. After inhibiting the TGF-ß/Smad pathway, the rats suffering from MI showed notably opposite trend. In conclusion, downregulation of miR-224 expression promotes the formation of vulnerable atherosclerotic plaques and vascular remodeling in ACS through activation of the TGF-ß/Smad pathway. Therefore, this study provides a new therapeutic target for ACS.

Tumour necrosis factor-α gene -308 G > A and -238 G > A polymorphisms are associated with susceptibility to irritable bowel syndrome and drug efficacy in children.

WHAT IS KNOWN AND OBJECTIVE: An imbalance in the genetically controlled pro- and anti-inflammatory cytokine production could potentially promote ongoing low-grade inflammation following an episode of acute gastroenteritis and, subsequently, could result in irritable bowel syndrome (IBS; post-infectious IBS, PI-IBS). Since there is very little known on the impact of pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α) on IBS, we conducted the present study with aims of determining the correlation between TNF-α gene polymorphisms (-308 G > A and -238 G > A) and susceptibility to IBS and drug efficacy in children. METHODS: Diarrhoea-predominant IBS patients and healthy subjects were recruited for DNA extraction. The genotypes were tested using polymerase chain reaction-restriction fragment length polymorphism. In addition to conventional symptomatic treatments, Live Combined Bifidobacterium, Lactobacillus and Enterococcus Powder and Montmorillonite Powder were administered to all the patients participating in the study for consecutive 4 weeks. The efficacy was evaluated 2 weeks after the withdrawal of the drugs. The association between gene polymorphism and drug efficacy was analysed by means of binary logistic regression analysis. RESULTS: Patients in the IBS group were susceptible to IBS with GA genotype and A allele of -308 G > A so were those with AA genotype and A allele of -238 G > A. The symptoms were also alleviated following treatment. The cure rate of patients with GA genotype of -308 G > A and AA genotype of -238 G > A was low. These findings suggested that the haplotype AA could potentially be associated with the cure rate of IBS patients. GA genotype of -308 G > A, AA genotype of -238 G > A, enterobacteria and 5-hydroxytryptamine in serum may act adversely, whereas bifidobacterial may be beneficial to the efficacy of IBS treatment. WHAT IS NEW AND CONCLUSION: The above findings evidently suggest that the frequency of TNF-α gene -308 G > A carrying GA genotype and A allele and -238 G > A carrying AA genotype and A allele is higher in children with IBS. Additionally, GA genotype of -308 G > A and AA genotype of -238 G > A may act adversely to the efficacy of IBS treatment, which may be a reference index for predicting the curative effect of IBS.