Juglone induces ferroptosis in glioblastoma cells by inhibiting the Nrf2-GPX4 axis through the phosphorylation of p38MAPK.

BACKGROUND: Ferroptosis, a non-apoptotic form of cell death induced by accumulation of free iron ions and lipid peroxidation, its importance for cancer treatment is gradually being recognized. Research on the anti-cancer mechanism of juglone is accumulating. However, the specific mechanism by which it directs glioblastoma (GBM) to death is unknown. METHODS: We used in vitro and in vivo experiments to explore the anti-GBM effect generated by juglone through the ferroptosis pathway. RESULTS: Juglone mainly causes cell death by inducing ferroptosis. Mechanistically, juglone can significantly activate the phosphorylation of p38MAPK. According to transcriptome sequencing and protein interaction analysis, the Nrf2-GPX4 signaling pathway is identified as the primary pathway through which juglone mediates ferroptosis. In vitro and in vivo experiments further verified that juglone induces the ferroptosis of GBM by activating the phosphorylation of p38MAPK and negatively regulating the Nrf2-GPX4 signaling pathway. CONCLUSION: Juglone induces ferroptosis and inhibits the growth of GBM by targeting the Nrf2/Gpx4 signaling pathway and thus holds promise as a novel ferroptosis inducer or anti-GBM drug.

Effectiveness and Safety of Ultra-low-dose Fluorescein Sodium-Guided Resection of Malignant Glioma.

BACKGROUND: This study analyzed the effectiveness and safety of ultra-low dose fluorescein sodium (FL)-guided malignant glioma resection and its potential to predict the pathological characteristics of glioma. METHODS: Sixty patients who underwent FL-guided glioma resection were randomly divided into test (1 mg/kg) and control (5 mg/kg) groups. A retrospective analysis included 30 patients with gliomas who did not undergo FL-guided surgery; these patients were included as a blank control group. Surgical outcomes, Karnofsky performance scores (KPS), and progression-free survival (PFS) at 6 months postoperatively were compared between the 3 groups. The sensitivity and specificity of FL and the relationship between the intensity of FL and Glial fibrillary acidic protein (GFAP) or Ki-67 expression were compared. RESULTS: The total tumor resection rates in the test, control, and blank control groups were 90% (27/30), 86.7% (26/30), and 60% (18/30), respectively. There were significant differences (P < 0.05) in the extent of resection, KPS, and PFS at 6 months after surgery between the test and control groups and the blank control group; however, no significant differences (P > 0.05) were observed between the test and control groups. The intensity of FL and the Ki67 positivity rate (P < 0.05) were directly proportional, but this relationship was not observed with GFAP. CONCLUSIONS: Ultra-low-dose FL-guided resection of malignant gliomas is safe and effective. The Ki67 positivity rate was directly proportional to the intensity of FL, indicating its potential to predict gliomas during pathological examination.

Identification and validation of prognostic genes and immune landscape signatures based on a fatty acid oxidation­related risk score model in glioma.

Fatty acid oxidation (FAO) plays a crucial role in glioma metabolism and its interaction with the immune microenvironment. The aim of the present study was to investigate the relationship between FAO-related genes and glioma by constructing gene clusters using a glioma cohort. A total of 287 differentially expressed genes related to FAO were identified and the top 50 genes were selected based on their P-values. Subsequently, patients were classified into two distinct gene subtypes (A and B) based on these genes. Scores for each patient were calculated using the 50 genes and the patients were divided into the high and low-score groups accordingly. Patients in subtype B exhibited higher tumor grades and poor prognostic factors such as older age and worse survival rates. The high-score subgroup had unfavorable indicators, including isocitrate dehydrogenase 1 wild-type, high tumor grade and 1p19q non-codeleted, while immune checkpoint expression was generally higher in the high-score subgroup. The constructed scoring model was validated using an external dataset, and the tissue inhibitor of metalloproteinase 1 gene was identified through protein interaction analysis, suggesting its potential involvement in glioma malignancy and promotion of glioblastoma proliferation. In conclusion, FAO-related genes may contribute to tumor development through immune mechanisms and the present study may provide novel insights for potential therapeutic strategies in glioma treatment.

A shock flash breaking out of a dusty red supergiant.

Shock-breakout emission is light that arises when a shockwave, generated by the core-collapse explosion of a massive star, passes through its outer envelope. Hitherto, the earliest detection of such a signal was at several hours after the explosion1, although a few others had been reported2-7. The temporal evolution of early light curves should provide insights into the shock propagation, including explosion asymmetry and environment in the vicinity, but this has been hampered by the lack of multiwavelength observations. Here we report the instant multiband observations of a type II supernova (SN 2023ixf) in the galaxy M101 (at a distance of 6.85 ± 0.15 Mpc; ref. 8), beginning at about 1.4 h after the explosion. The exploding star was a red supergiant with a radius of about 440 solar radii. The light curves evolved rapidly, on timescales of 1-2 h, and appeared unusually fainter and redder than predicted by the models9-11 within the first few hours, which we attribute to an optically thick dust shell before it was disrupted by the shockwave. We infer that the breakout and perhaps the distribution of the surrounding dust were not spherically symmetric.

Pathological response and prognostic factors of neoadjuvant PD-1 blockade combined with chemotherapy in resectable oesophageal squamous cell carcinoma.

PURPOSE: We aimed to investigate the pathological changes, clinicopathological correlation and prognostic factors of neoadjuvant programmed cell death 1 (PD-1) blockade camrelizumab combined with carboplatin and nab-paclitaxel (CCNP) which we have proved its effectiveness in previous research for resectable esophageal squamous cell carcinoma (ESCC). METHODS: 108 patients of resectable ESCC, with a mean follow-up of 13 m (ranging 1-30 m), treated with neoadjuvant CCNP from March 2020 to October 2022 in the First Affiliated Hospital of Sun Yat-sen University were enrolled. RESULTS: One year overall survival (OS) and disease-free survival (DFS) were 96.4% and 84.7% respectively. Pathological complete response or major pathological response (pCR/MPR) of the primary tumour (T-pCR/T-MPR) and the metastatic lymph node (N-pCR/N-MPR) were 58.3% and 47.5%. Pathological response of both primary tumours (PT) and lymph nodes (LN) metastasis correlated with DFS. LN pathological response was consistent with PT in 70.0% and inconsistent in 30.0% metastatic cases. Higher ratio of CD8+ to FoxP3+ tumour-infiltrating lymphocytes (TILs), earlier ypT stage and PT invasion not beyond circular muscle correlated with better pathological response. Four types of regression patterns of PT and two types of metastatic LN regression were found. A total of 18 (16.7%) out of 108 developed recurrence with a mean time of 6.9 ± 5.3 months. PT pathological response plus ypN and PT invasion beyond circular muscle or not were independent prognostic factors of DFS. CONCLUSIONS: This study suggested that camrelizumab plus chemotherapy had a high rate of T-pCR/T-MPR for resectable ESCC. T-pCR/T-MPR plus ypN0 and tumour invasion not beyond circular muscle predicted better DFS.

Marine Submicron Aerosols from the Gulf of Mexico: Polluted and Acidic with Rapid Production of Sulfate and Organosulfates.

We measured submicron aerosols (PM1) at a beachfront site in Texas in Spring 2021 to characterize the "background" aerosol chemical composition advecting into Texas and the factors controlling this composition. Observations show that marine "background" aerosols from the Gulf of Mexico were highly processed and acidic; sulfate was the most abundant component (on average 57% of total PM1 mass), followed by organic material (26%). These chemical characteristics are similar to those observed at other marine locations globally. However, Gulf "background" aerosols were much more polluted; the average non-refractory (NR-) PM1 mass concentration was 3-70 times higher than that observed in other clean marine atmospheres. Anthropogenic shipping emissions over the Gulf of Mexico explain 78.3% of the total measured "background" sulfate in the Gulf air. We frequently observed haze pollution in the air mass from the Gulf, with significantly elevated concentrations of sulfate, organosulfates, and secondary organic aerosol associated with sulfuric acid. Analysis suggests that aqueous oxidation of shipping emissions over the Gulf of Mexico by peroxides in the particles might potentially be an important pathway for the rapid production of acidic sulfate and organosulfates during the haze episodes under acidic conditions.

Construction of a pyroptosis-related lncRNAs signature for predicting prognosis and immunotherapy response in glioma.

Recent studies have proved that pyroptosis-related long non-coding RNAs (PRlncRNAs) are closely linked to tumor progression, prognosis, and immunity. Here, we systematically evaluated the correlation of PRlncRNAs with glioma prognosis. This study included 3 glioma cohorts (The Cancer Genome Atlas, Chinese Glioma Genome Atlas, and Gravendeel). Through Pearson correlation analysis, PRlncRNAs were screened from these 3 cohorts. Univariate Cox regression analysis was then carried out to determine the prognostic PRlncRNAs. A pyroptosis-related lncRNAs signature (PRLS) was then built by least absolute shrinkage and selection operator and multivariate Cox analyses. We systematically evaluated the correlation of the PRLS with the prognosis, immune features, and tumor mutation burden in glioma. A total of 14 prognostic PRlncRNAs overlapped in all cohorts and were selected as candidate lncRNAs. Based on The Cancer Genome Atlas cohort, a PRLS containing 7 PRlncRNAs was built. In all cohorts, the PRLS was proved to be a good predictor of glioma prognosis, with a higher risk score related to a poorer prognosis. We observed obvious differences in the immune microenvironment, immune cell infiltration level, and immune checkpoint expression in low- and high-risk subgroups. Compared with low-risk cases, high-risk cases had lower Tumor Immune Dysfunction and Exclusion scores and greater tumor mutation burden, indicating that high-risk cases can be more sensitive to immunotherapy. A nomogram combining PRLS and clinical parameters was constructed, which showed more robust and accurate predictive power. In conclusion, the PRLS is a potentially useful indicator for predicting prognosis and response to immunotherapy in glioma. Our findings may provide a useful insight into clinically individualized treatment strategies for patients.

The dual function of microglial polarization and its treatment targets in ischemic stroke.

Stroke is the leading cause of disability and death worldwide, with ischemic stroke occurring in ~5% of the global population every year. Recently, many studies have been conducted on the inflammatory response after stroke. Microglial/macrophage polarization has a dual function and is critical to the pathology of ischemic stroke. Microglial/macrophage activation is important in reducing neuronal apoptosis, enhancing neurogenesis, and promoting functional recovery after ischemic stroke. In this review, we investigate the physiological characteristics and functions of microglia in the brain, the activation and phenotypic polarization of microglia and macrophages after stroke, the signaling mechanisms of polarization states, and the contribution of microglia to brain pathology and repair. We summarize recent advances in stroke-related microglia research, highlighting breakthroughs in therapeutic strategies for microglial responses after stroke, thereby providing new ideas for the treatment of ischemic stroke.

Expression and Prognostic Value of Melanoma-Associated Antigen D2 in Gliomas.

INTRODUCTION: The melanoma-associated antigen D2 (MAGED2) is one of the melanoma-associated antigen family members. It is commonly overexpressed in a variety of malignancies. However, the mechanism and function of MAGED2 in glioma remain unknown. METHODS: The MAGED2 expression level and the correlations between clinical characteristics were analyzed with the data from the CGGA and TCGA datasets. MAGED2 expression in 98 glioma tissues was measured using RT-qPCR, Western blot, and immunohistochemistry. CCK-8, colony formation, and EdU assays were used to assess the effect of MAGED2 on U251-MG cell proliferation. Flow cytometry was used to track changes in the cell cycle and cell apoptosis following plasmid transfection with CRISPRi. RESULTS: MAGED2 was shown to be highly expressed in glioma tissues, and high MAGED2 expression predicted poor prognosis. Furthermore, MAGED2 knockdown significantly inhibited the proliferation of U251-MG cells by preventing cell cycle arrest at the G0/G1 phase and triggering apoptosis. In line with in vitro findings, the results of the xenograft experiment and immunohistochemistry also showed that MAGED2 suppression inhibited tumor development and decreased Ki-67 expression levels. CONCLUSIONS: MAGED2 may be a possible biomarker for glioma and an important prognostic factor for glioma patients.

Establishment and Validation of a Ferroptosis-Related lncRNA Signature for Prognosis Prediction in Lower-Grade Glioma.

Background: The prognosis of lower-grade glioma (LGG) is highly variable, and more accurate predictors are still needed. The aim of our study was to explore the prognostic value of ferroptosis-related long non-coding RNAs (lncRNAs) in LGG and to develop a novel risk signature for predicting survival with LGG. Methods: We first integrated multiple datasets to screen for prognostic ferroptosis-related lncRNAs in LGG. A least absolute shrinkage and selection operator (LASSO) analysis was then utilized to develop a risk signature for prognostic prediction. Based on the results of multivariate Cox analysis, a prognostic nomogram model for LGG was constructed. Finally, functional enrichment analysis, single-sample gene set enrichment analysis (ssGSEA), immunity, and m6A correlation analyses were conducted to explore the possible mechanisms by which these ferroptosis-related lncRNAs affect survival with LGG. Results: A total of 11 ferroptosis-related lncRNAs related to the prognosis of LGG were identified. Based on prognostic lncRNAs, a risk signature consisting of 8 lncRNAs was constructed and demonstrated good predictive performance in both the training and validation cohorts. Correlation analysis suggested that the risk signature was closely linked to clinical features. The nomogram model we constructed by combining the risk signature and clinical parameters proved to be more accurate in predicting the prognosis of LGG. In addition, there were differences in the levels of immune cell infiltration, immune-related functions, immune checkpoints, and m6A-related gene expression between the high- and low-risk groups. Conclusion: In summary, our ferroptosis-related lncRNA signature exhibits good performance in predicting the prognosis of LGG. This study may provide useful insight into the treatment of LGG.

Pyroptosis-Related Gene to Construct Prognostic Signature and Explore Immune Microenvironment and Immunotherapy Biomarkers in Bladder Cancer.

Bladder cancer is known to be the most common malignant tumor in the urinary system and has a poor prognosis; thus, new targets for drug treatment are urgently needed. Pyroptosis is defined as programmed cell death in the inflammatory form mediated by the gasdermin protein. It has therapeutic potential due to the synergistic effect of radiotherapy and chemotherapy, can reverse chemotherapy resistance, is able to regulate the body environment to alter tumor metabolism, and may enhance the response rate of the immune checkpoint inhibitor. Accordingly, this study attempted to explore the role of pyroptosis in bladder cancer. A prognostic model based on five pyroptosis-related genes was constructed by conducting univariate Cox survival and LASSO regression analyses using The Cancer Genome Atlas (TCGA) cohort. Patients were divided into high- and low-risk groups according to the median risk score, with all five PRGs having downregulated expression in the high-risk group. The high-risk group was shown to have a worse prognosis than the low-risk group, and survival differences between the two groups were then validated in the Gene Expression Omnibus (GEO) cohort. Moreover, the ROC curves demonstrated the model's moderate predictive ability. The univariate and multivariate Cox regression analyses indicated that risk scores were found to serve as an independent prognosis factor for OS in bladder cancer patients. In addition, the high-risk group was observed to be associated with advanced N and TNM stages. A nomogram combining risk scores and clinical features was then established, with the ROC curve indicating that the AUC of TCGA training cohort in 3 and 5 years was 0.789 and 0.775, respectively. The calibration curve exhibited a high consistency between the actual survival rate and the predicted rate. Furthermore, the GO and KEGG analyses found that antigen processing and presentation of exogenous antigen, exogenous peptide antigen, and peptide antigen were enriched in the low-risk group. A higher abundance of tumor-infiltrating immune cells and additional active immune pathways were also noted in the low-risk group. In addition, immunotherapy biomarkers, including TMB, PD1, PD-L1, CTLA4, and LAG3, were shown to have higher levels in the low-risk group. Therefore, patients in the low-risk group may be potential responders to immune checkpoint inhibitors.

Traffic, transport, and vegetation drive VOC concentrations in a major urban area in Texas.

The population of Texas has increased rapidly in the past decade. The San Antonio Field Study (SAFS) was designed to investigate ozone (O3) production and precursors in this rapidly changing, sprawling metropolitan area. There are still many questions regarding the sources and chemistry of volatile organic compounds (VOCs) in urban areas like San Antonio which are affected by a complex mixture of industry, traffic, biogenic sources and transported pollutants. The goal of the SAFS campaign in May 2017 was to measure inorganic trace gases, VOCs, methane (CH4), and ethane (C2H6). The SAFS field design included two sites to better assess air quality across the metro area: an urban site (Traveler's World; TW) and a downwind/suburban site (University of Texas at San Antonio; UTSA). The results indicated that acetone (2.52 ± 1.17 and 2.39 ± 1.27 ppbv), acetaldehyde (1.45 ± 1.02 and 0.93 ± 0.45 ppbv) and isoprene (0.64 ± 0.49 and 1.21 ± 0.85 ppbv; TW and UTSA, respectively) were the VOCs with the highest concentrations. Additionally, positive matrix factorization showed three dominant factors of VOC emissions: biogenic, aged urban mixed source, and acetone. Methyl vinyl ketone and methacrolein (MVK + MACR) exhibited contributions from both secondary photooxidation of isoprene and direct emissions from traffic. The C2H6:CH4 demonstrated potential influence of oil and gas activities in San Antonio. Moreover, the high O3 days during the campaign were in the NOx-limited O3 formation regime and were preceded by evening peaks in select VOCs, NOx and CO. Overall, quantification of the concentration and trends of VOCs and trace gases in a major city in Texas offers vital information for general air quality management and supports strategies for reducing O3 pollution. The SAFS campaign VOC results will also add to the growing body of literature on urban sources and concentrations of VOCs in major urban areas.

Identification of an m6A RNA Methylation Regulator Risk Score Model for Prediction of Clinical Prognosis in Astrocytoma.

Astrocytoma (AS) is the most ubiquitous primary malignancy of the central nervous system (CNS). The vital involvement of the N6-methyladenosine (m6A) RNA modification in the growth of multiple human tumors is known. This study entailed probing m6A regulators with AS prognosis to construct a risk prediction model (RS) for potential clinical use. A total of 579 AS patients' (of the Chinese Glioma Genome Atlas,CGGA) data and the expression of 12 published m6A-related genes were included in this study. Cox and selection operator (LASSO) regression analyses for independent prognostic factors and multifactor Cox analysis established an R.S. model to predict the AS patient prognosis. This was subject to verification employing 331 samples from the TCGA data set followed by gene ontology and pathway enrichment study with gene set enrichment analysis (GSEA). The R.S. constructed with three m6A genes inclusive of WTAP, RBM15, and YTHDF2 emerged as independent prognostic factors in AS patients with vital involvement in the advancement and development of the malignancy. In a nutshell, this work reported an m6A-related gene risk model to predict the prognosis of AS patients to pave the way for discerning diagnostic and prognostic biomarkers. Further corroboration employing relevant wet-lab assays of this model is warranted.

Screening and Identification of Key Biomarkers in Lower Grade Glioma via Bioinformatical Analysis.

Lower-grade glioma (LGG) is a common type of central nervous system tumor. Due to its complicated pathogenesis, the choice and timing of adjuvant therapy after tumor treatment are controversial. This study explored and identified potential therapeutic targets for lower-grade. The bioinformatics method was employed to identify potential biomarkers and LGG molecular mechanisms. Firstly, we selected and downloaded GSE15824, GSE50161, and GSE86574 from the GEO database, which included 40 LGG tissue and 28 normal brain tissue samples. GEO and VENN software identified of 206 codifference expressed genes (DEGs). Secondly, we applied the DAVID online software to investigate the DEG biological function and KEGG pathway enrichment, as well as to build the protein interaction visualization network through Cytoscape and STRING website. Then, the MCODE plug is used in the analysis of 22 core genes. Thirdly, the 22 core genes were analyzed with UNCLA software, of which 18 genes were associated with a worse prognosis. Fourthly, GEPIA was used to analyze the 18 selected genes, and 14 genes were found to be a significantly different expression between LGGs and normal brain tumor samples. Fifthly, hierarchical gene clustering was used to examine the 14 important gene expression differences in different histologies, as well as analysis of the KEGG pathway. Five of these genes were shown to be abundant in the natural killer cell-mediated cytokines (NKCC) and phagosome pathways. The five key genes that may be affected by the immune microenvironment play a crucial role in LGG development.

Impact of H-Type Hypertension on Intraplaque Neovascularization Assessed by Contrast-Enhanced Ultrasound.

AIM: H-type hypertension is connected with carotid atherosclerotic plaques and stroke, whereas neovascularization is a dominant contributor to plaque vulnerability. However, the correlation between H-type hypertension and plaque vulnerability remains unclear. This study aims to explore the influence of H-type hypertension on intraplaque neovascularization (IPN). METHODS: We enrolled 235 patients with carotid plaques into the investigation and classified them into four groups: H-type hypertension group, simple hypertension group, isolated hyperhomocysteinemia group, and control group. Contrast-enhanced ultrasound (CEUS) was performed on them and IPN was evaluated using semi-quantitative visual grading: grade 1 (no microbubbles or microbubbles limited to the adventitial side and/or shoulder of plaque) and, grade 2 (diffused microbubbles within plaque or microbubbles enter plaque core). To analyze the correlation between H-type hypertension and the degree of plaque enhancement, logistic regression was used. RESULTS: Compared with those with CEUS grade 1 plaques, those with CEUS grade 2 plaques had higher frequency of ischemic stroke (29.0% vs. 45.1%, P＜0.05), hypertension (41.0% vs. 56.3%, P＜0.05), and H-type hypertension (18.0% vs. 29.6%, P＜0.05). No significant differences existed in plaque morphology, plaque echogenicity, and the severity of carotid artery stenosis between the degree of plaque enhancement (all P＞0.05). H-type hypertension (multivariate-adjusted OR: 3.036, 95% CI: 1.258-7.329) was independently connected with the degree of plaque enhancement even after adjusting for other covariates. CONCLUSION: H-type hypertension is expressly connected with the degree of plaque enhancement and may facilitate plaque vulnerability. Our findings may offer a new insight for treating vulnerable plaque, lowering blood pressure, and lowering homocysteine equally crucial.

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

Intracerebral hemorrhage (ICH) is the second-largest stroke subtype and has a high mortality and disability rate. Secondary brain injury (SBI) is delayed after ICH. The main contributors to SBI are inflammation, oxidative stress, and excitotoxicity. Harmful substances from blood and hemolysis, such as hemoglobin, thrombin, and iron, induce SBI. When cells suffer stress, a critical protective mechanism called "autophagy" help to maintain the homeostasis of damaged cells, remove harmful substances or damaged organelles, and recycle them. Autophagy plays a critical role in the pathology of ICH, and its function remains controversial. Several lines of evidence demonstrate a pro-survival role for autophagy in ICH by facilitating the removal of damaged proteins and organelles. However, many studies have found that heme and iron can aggravate SBI by enhancing autophagy. Autophagy and inflammation are essential culprits in the progression of brain injury. It is a fascinating hypothesis that autophagy regulates inflammation in ICH-induced SBI. Autophagy could degrade and clear pro-IL-1ß and apoptosis-associated speck-like protein containing a CARD (ASC) to antagonize NLRP3-mediated inflammation. In addition, mitophagy can remove endogenous activators of inflammasomes, such as reactive oxygen species (ROS), inflammatory components, and cytokines, in damaged mitochondria. However, many studies support the idea that autophagy activates microglia and aggravates microglial inflammation via the toll-like receptor 4 (TLR4) pathway. In addition, autophagy can promote ICH-induced SBI through inflammasome-dependent NLRP6-mediated inflammation. Moreover, some resident cells in the brain are involved in autophagy in regulating inflammation after ICH. Some compounds or therapeutic targets that regulate inflammation by autophagy may represent promising candidates for the treatment of ICH-induced SBI. In conclusion, the mutual regulation of autophagy and inflammation in ICH is worth exploring. The control of inflammation by autophagy will hopefully prove to be an essential treatment target for ICH.

Long experience for the diagnosis and treatment of sporadic endolymphatic sac tumor in a single center.

OBJECTIVES: Sporadic endolymphatic sac tumor (ELST) is rare. The purpose of this study was to analyze the clinical feature and surgical outcome of a single-center series of sporadic ELSTs. PATIENTS AND METHODS: We retrospectively reviewed all cases of sporadic ELSTs operated at the Tiantan hospital between 2010 and 2020. RESULTS: Retrospective record revealed 14 patients with sporadic ELSTs who underwent surgical management. Serum VEGF(vascular endothelial growth factor)values of 6 patients were measured on admission, and the levels were all higher than normal(0-160 ng/L, Enzyme-Linked ImmunoSorbent Assay). All patients underwent surgical treatments, and there was no significant difference in KPS before and after the operation(KPS = 88:88). The average maximum diameter of the tumor was 41 mm (range28-56 mm). After surgery, Two patients received radiation therapy, We did not encounter any case with metastatic dissemination. No deaths occurred during follow-up. CONCLUSION: ELST is defined as an aggressive or low-grade malignant tumor, with the characteristics of local recurrence and invasion of bone growth. Sporadic cases are common, and this rare tumor provides insight into the relationship between ELST and VHL syndrome. Early surgical resection can prevent or reduce the disability of auditory vestibular symptoms, and improve the chance of complete resection and retention of hearing. As far as possible complete resection of the tumor can prolong the disease-free survival of patients. Preoperative radiotherapy or stereotactic therapy cannot control tumor growth. Postoperative radiotherapy may have a positive effect on tumor control. The high expression of VEGF in patients may be related to tumor occurrence and development.

Successful occlusion of ventricular septal rupture in myocardial infarction under the guidance of echocardiography.

INTRODUCTION: The traditional treatment of myocardial infarction with ventricular septal rupture is surgical treatment. For the elderly patients with cardiac insufficiency, surgical treatment is very risky. The successful treatment of this case by interventional occlusion is a new method. No relevant literature reports have been found. CASE: A 77-year-old man with a past medical history of old myocardial infarction presented to the physician with sudden onset of palpitation and shortness of breath. Echocardiography showed thinning of the interventricular septum near the apex and bulging toward the right ventricular side with "paradoxical motion", on which a rupture of about 8 mm in diameter was seen. CDFI: left ventricular blood shunted to the right ventricle through the rupture.Echocardiographic diagnosis: old left ventricular anteroseptal myocardial infarction with ventricular septal rupture. Due to the older age of the patient and reduced left ventricular function, surgical repair of the ventricular septal rupture site was more difficult. After multidisciplinary discussion, it was agreed that the patient could not afford thoracotomy and was not suitable for thoracotomy, and echocardiography guided interventional occlusion of the ruptured interventricular septum could be performed. CONCLUSION: Transesophageal echocardiography-guided interventional occlusion of myocardial infarction with ventricular septal rupture in elderly patients with cardiac insufficiency is a new attempt, the successful treatment of this case shows that this method is feasible, for some patients is an appropriate treatment.

Use of Genome-Scale Integrated Analysis to Identify Key Genes and Potential Molecular Mechanisms in Recurrence of Lower-Grade Brain Glioma.

BACKGROUND The aim of this study was to identify gene signals for lower-grade glioma (LGG) and to assess their potential as recurrence biomarkers. MATERIAL AND METHODS An LGG-related mRNA sequencing dataset was downloaded from The Cancer Genome Atlas (TCGA) Informix. Multiple bioinformatics analysis methods were used to identify key genes and potential molecular mechanisms in recurrence of LGG. RESULTS A total of 326 differentially-expressed genes (DEGs), were identified from 511 primary LGG tumor and 18 recurrent samples. Gene ontology (GO) analysis revealed that the DEGs were implicated in cell differentiation, neuron differentiation, negative regulation of neuron differentiation, and cell proliferation in the forebrain. The Kyoto Encyclopedia of Genes and Genomes (KEGG) database suggests that DEGs are associated with proteoglycans in cancer, the Wnt signaling pathway, ECM-receptor interaction, the PI3K-Akt signaling pathway, transcriptional deregulation in cancer, and the Hippo signaling pathway. The hub DEGs in the protein-protein interaction network are apolipoprotein A2 (APOA2), collagen type III alpha 1 chain (COL3A1), collagen type I alpha 1 chain (COL1A1), tyrosinase (TYR), collagen type I alpha 2 chain (COL1A2), neurotensin (NTS), collagen type V alpha 1 chain (COL5A1), poly(A) polymerase beta (PAPOLB), insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), and anomalous homeobox (ANHX). GSEA revealed that the following biological processes may associated with LGG recurrence: cell cycle, DNA replication and repair, regulation of apoptosis, neuronal differentiation, and Wnt signaling pathway. CONCLUSIONS Our study demonstrated that hub DEGs may assist in the molecular understanding of LGG recurrence. These findings still need further molecular studies to identify the assignment of DEGs in LGG.