Changes in liver and kidney function, red blood cell count and hemoglobin levels 1 day after ultrasound-guided percutaneous microwave ablation for uterine fibroids.

OBJECTIVE: To investigate the changes in liver and kidney function, red blood cell (RBC) count and hemoglobin (HGB) levels in patients undergoing ultrasound-guided percutaneous microwave ablation (UPMWA) for uterine fibroids on postoperative day 1. METHODS: The changes in liver and kidney function, RBC count and HGB levels in 181 patients who underwent selective UPMWA in the Second Affiliated Hospital of Shantou University Medical College, China, between August 2017 and January 2023 were retrospectively analyzed. RESULTS: All patients underwent UPMWA for uterine fibroids; 179 patients had multiple uterine fibroids and 2 patients had single uterine fibroids. The maximum fibroid diameter ranged from 18 to 140 mm, with an average of 68.3 mm. Ultrasound imaging was used to confirm that the blood flow signal within the mass had disappeared in all patients, indicating that the ablation was effective. Within 24 h, compared with before UPMWA, levels of total bilirubin, direct bilirubin, indirect bilirubin and aspartate aminotransferase had significantly increased (p < 0.01), whereas levels of total protein, albumin, globulin, alanine aminotransferase, creatinine and urea had significantly decreased (p < 0.01). Acute kidney injury (AKI) occurred in 1 of the 181 patients. The RBC count and HGB levels decreased significantly after UPMWA (p < 0.01). CONCLUSION: Ultrasound-guided percutaneous microwave ablation for uterine fibroids can impose a higher detoxification load on the liver and cause thermal damage to and the destruction of RBCs within local circulation, potentially leading to AKI. Protein levels significantly decreased after UPMWA. Therefore, perioperative organ function protection measures and treatment should be actively integrated into clinical practice to improve prognosis and enhance recovery.

[Effects of Experimental Nitrogen Deposition and Litter Manipulation on Soil Organic Components and Enzyme Activity of Latosol in Tropical Rubber Plantations].

It is of great scientific significance in regulating plantation ecosystem restoration to investigate the effects of the nitrogen (N) deposition and litter manipulation on soil organic carbon components and enzyme activities. A micro-plot experiment was conducted with four nitrogen additions[CK (0 kg·hm-2·a-1, calculated by N), LN (50 kg·hm-2·a-1), MN (100 kg·hm-2·a-1), and HN (200 kg·hm-2·a-1)] and two litter treatments[LR (litter removal) and L (litter retained)] for tropical rubber plantations in western Hainan Island. The soil physico-chemical properties, soil organic carbon components, and enzyme activities in 0-10 cm and 10-20 cm depths were analyzed. The results showed that soil pH significantly decreased with elevated N addition and litter removal. The contents of NO3--N and NH4+-N significantly increased with elevated N addition. Moreover, there was a significant interaction between N addition and litter treatment on the contents of NO3--N and NH4+-N (P < 0.05). Compared to that with L, LR reduced SOC and its component contents; particularly, the largest decrease was in LFOC by 29.0%-81.4% in the 0-10 cm depth and 23.5%-58.4% in 10-20 cm, respectively. The contents of SOC and its components presented a trend of increasing first and then decreasing with elevated N addition irrespective of litter treatment, and those contents were significantly higher at LN than those at HN. There was a significant interaction between N addition and litter treatment on SOC, LFOC (0-10 cm), and HFOC contents. Compared with that under L, PPO activity was significantly reduced at LR under CK and LN but was significantly increased at LR under MN and HN, respectively. Variance analysis showed significant interactive effects between N addition and litter treatment on PPO and CBH (0-10 cm) activities, and the soil enzyme activity (BG, PPO, and CBH) responding to N addition was greater than that to the litter treatment. Pearson correlation analysis showed that SOC content was extremely positively correlated with MBC, POC, LFOC, and HFOC contents. To summarize, litter retained combined with low N deposition played an important synergistic role of improving SOC pool and soil enzyme activities for tropical rubber plantation systems.

Pan-Cancer Analysis and Validation of Opioid-Related Receptors Reveals the Immunotherapeutic Value of Toll-Like Receptor 4.

Introduction: The relationship between the expression of opioid-associated receptors and cancer outcomes is complex and varies among studies. Methods: This study focused on six opioid-related receptors (OPRM1, OPRD1, OPRK1, OPRL1, OGFR, and TLR4) and their impact on cancer patient survival. Bioinformatics analysis was conducted on 33 cancer types from The Cancer Genome Atlas database to examine their expression, clinical correlations, mechanisms in the tumor microenvironment, and potential for immunotherapy. Due to significantly lower expression of OPRM1, OPRD1, and OPRK1 compared to OGFR and TLR4, the analysis concentrated on the latter two genes. Results: OGFR was highly expressed in 16 tumor types, while TLR4 showed low expression in 13. Validation from external samples, the Gene Expression Omnibus, and the Human Protein Atlas supported these findings. The diagnostic value of these two genes was demonstrated using the Genotype-Tissue Expression database. Univariate Cox regression models and Kaplan-Meier curves confirmed OGFR's impact on prognosis in a cancer type-specific manner, while high TLR4 expression was associated with a favorable prognosis. Analysis of the tumor microenvironment using a deconvolution algorithm linked OGFR to CD8+ T cells and TLR4 to macrophages. Single-cell datasets further validated this correlation. In 25 immune checkpoint blockade treatment cohorts, TLR4 expression showed promise as an immunotherapy efficacy predictor in non-small cell lung cancer, urothelial carcinoma, and melanoma. Conclusion: In a pan-cancer analysis of 33 tissues, OGFR was consistently highly expressed, while TLR4 had low expression. Both genes have diagnostic and prognostic significance and are linked to immune cells in the tumor microenvironment. TLR4 has potential as an immunotherapeutic response marker.

Tyrosine Kinase Inhibitors Plus Anti-PD-1 Antibodies with Hepatic Arterial Infusion Chemotherapy or Transarterial Chemoembolization for Unresectable Hepatocellular Carcinoma.

Background: The combination of tyrosine kinase inhibitors (TKIs) and anti-PD-1 antibodies with hepatic arterial infusion chemotherapy (HAIC) or transarterial chemoembolization (TACE) has shown encouraging anti-tumor effects in the treatment of hepatocellular carcinoma (HCC). We explored the efficacy and safety of TKIs and anti-PD-1 antibodies combined with HAIC or TACE in HCC. Methods: Data from 302 HCC patients receiving HAIC combined with TKIs and anti-PD-1 antibodies (HAIC-TP group) and 446 HCC patients receiving TACE combined with TKIs and anti-PD-1 antibodies (TACE-TP group) were retrospectively collected. Clinicopathological characteristics, tumor response, progression-free survival (PFS), overall survival (OS), and adverse events (AEs) were compared between two groups. Propensity score matching (PSM) analysis was performed to minimize bias. Results: The HAIC-TP group exhibited better objective response rate (RECIST: 33.1% versus 7.8%, P < 0.001; mRECIST: 51.4% versus 17.5%, P < 0.001), longer PFS (12.4 months versus 8.2 months, P < 0.001), and longer OS (not reached versus 13.8 months, P < 0.001) than TACE-TP group. Surgery was performed after combination therapy in 34 patients of the HAIC-TP group and in 7 patients of the TACE-TP group (P < 0.001). Similar results were also observed in the PSM analysis. Multivariate analysis indicated type of treatment, alpha-fetoprotein, ALBI grade, portal vein tumor thrombus, and extrahepatic status were risk factors for poor prognosis. Nausea, vomiting, diarrhea, and abdominal pain occurred more frequently in the HAIC-TP group, whereas liver dysfunction occurred more frequently in the TACE-TP group. All AEs were acceptable and manageable as a result of treatment interruption or dose modification. Conclusion: The combination of HAIC with TKIs and anti-PD-1 antibodies is an effective and safe therapeutic regimen over TACE-based combination therapy for patients with HCC. A prospective study with a large sample size is required to validate the efficacy and safety of the combination therapy.

Hepatectomy After Conversion Therapy with Hepatic Arterial Infusion Chemotherapy, Tyrosine Kinase Inhibitors and Anti-PD-1 Antibodies for Initially Unresectable Hepatocellular Carcinoma.

Background: Most patients with hepatocellular carcinoma (HCC) are not candidates for liver resection. We investigated the clinicopathological characteristics and prognosis of patients with initially unresectable HCC who underwent hepatectomy after conversion therapy with hepatic arterial infusion chemotherapy (HAIC), tyrosine kinase inhibitors (TKIs), and anti-PD-1 antibodies. Materials and Methods: Patients with initially unresectable HCC who received HAIC combined with TKIs and anti-PD-1 antibodies followed by hepatectomy between December 2020 and December 2022, were retrospectively analyzed. Patient characteristics, tumor characteristics, treatment efficacy, perioperative characteristics, pathological characteristics, and survival outcomes were summarized and analyzed. Results: 67 patients were enrolled in this study. Patients were treated with 3 sessions (range:2-6 sessions) of combination therapy and were performed with hepatectomy in 4 months (range:1.4-17.8 months) after the initiation of the combination therapy. The median size of tumor shrinkage was 4.7 cm (range:0.9-11.7 cm). A pathological complete response (pCR) was achieved in 34.3% of the patients (n = 23). The median recurrence-free survival (RFS) was 19.3 months and the median overall survival (OS) was 28.7 months. Patients who achieved pCR had a better RFS (P = 0.004) and those without microscopic vascular invasion (MVI) had a better prognosis (RFS, P = 0.011; OS, P = 0.023). Multivariable logistic analysis revealed that the tumor number was associated with pCR. Conclusion: Hepatectomy after conversion therapy with HAIC, TKIs, and anti-PD-1 antibodies is a feasible treatment strategy for patients with unresectable HCC. This treatment strategy is associated with a promising prognosis.

A Novel Cross-Sensor Transfer Diagnosis Method with Local Attention Mechanism: Applied in a Reciprocating Pump.

Data-driven mechanical fault diagnosis has been successfully developed in recent years, and the task of training and testing data from the same distribution has been well-solved. However, for some large machines with complex mechanical structures, such as reciprocating pumps, it is often not possible to obtain data from specific sensor locations. When the sensor position is changed, the distribution of the features of the signal data also changes and the fault diagnosis problem becomes more complicated. In this paper, a cross-sensor transfer diagnosis method is proposed, which utilizes the sharing of information collected by sensors between different locations of the machine to complete a more accurate and comprehensive fault diagnosis. To enhance the model's perception ability towards the critical part of the fault signal, the local attention mechanism is embedded into the proposed method. Finally, the proposed method is validated by applying it to experimentally acquired vibration signal data of reciprocating pumps. Excellent performance is demonstrated in terms of fault diagnosis accuracy and sensor generalization capability. The transferability of practical industrial faults among different sensors is confirmed.

Identification of LOX as a candidate prognostic biomarker in Glioblastoma multiforme.

BACKGROUND: Glioblastoma multiforme (GBM) is the most malignant type of glioma. GBM tumors grow rapidly, have a high degree of malignancy, and are characterized by a fast disease progression. Unfortunately, there is a lack of effective treatments. An effective strategy for the treatment of GBM would be to identify key biomarkers correlating with the occurrence and progression of GBM and developing these biomarkers into therapeutic targets. METHOD AND RESULTS: In this study, using integrated bioinformatics analysis, we identified differentially expressed genes (DEGs), including 130 genes that were upregulated in GBM compared to normal brain tissue, and 128 genes that were downregulated in GBM. Based on Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis, these genes were associated with regulation of tumor cell adhesion, differentiation, morphology in GBM and were mainly enriched in Complement and coagulation cascades pathway. The Search Tool for the Retrieval of Interacting Genes (STRING) database was used to construct a Protein-Protein Interaction network. Ten hub genes were identified, including FN1, CD44, MYC, CDK1, SERPINE1, COL3A1, COL1A2, LOX, POSTN and EZH2, all of which were significantly upregulated in GBM, these results were confirmed by oncomine database exploration. Alteration analysis of hub genes found that patients with alteration in at least one of the hub genes showed shorter median survival times (p = 0.013) and shorter median disease-free survival times (p = 2.488E-3) than patients without alterations in any of the hub genes. Multiple tests for survival analysis showed that among individual hub genes only expression of LOX was correlated with patient survival (P < 0.05).GDS4467 data set was used to analyze the expression of LOX in gliomas with different degrees of malignancy, and it was found that the expression level of LOX was positively correlated with the malignant degree of gliomas.By analyzing GDS 4535 data set showed that the expression level of LOX was positively correlated with the differentiation degree of GBM cells CONCLUSION: This research suggests that FN1, CD44, MYC, CDK1, SERPINE1, COL3A1, COL1A2, LOX, POSTN and EZH2 are key genes in GBM. However, only LOX is correlated with patient survival and promotes glioblastoma cell differentiation and tumor recurrence. LOX may be a candidate prognostic biomarker and potential therapeutic target for GBM.

Tuning Lignite Structure via Hydromodification To Promote the Formation of Coal-Based CNTs: Exploration for the Carbon Source of CNTs.

Although the preparation of coal-based carbon nanotubes (CNTs) has been realized in many studies, the relationship between carbon source structure of coal and CNT growth has not been studied in depth. In this study, we used lignite and KOH as raw material and catalyst and tuned lignite structure via hydrothermal modification to promote the formation of CNTs during catalytic pyrolysis. The main carbon source of CNTs was explored from the change of coal structure and pyrolysis characteristics. The results indicate that the CNT yield of lignite pyrolysis products is only 2.39%, but the CNT yield increases significantly after lignite was hydrothermally modified in a subcritical water-CO system. The graphitization degree, the order degree, and CNT content increase continuously with the increase in modification temperature, and C-M340 has the highest CNT content of 9.41%. Hydromodification promotes the rearrangement of aromatic carbon structures to generate more condensed aromatic rings linked by short aliphatic chains and aromatic ether bonds. The variation of these structures correlates well with the formation of CNTs and leads to the change in the carbon source components released during coal pyrolysis. Compared to lignite, modified coal releases more aromatic compounds, especially polycyclic aromatic hydrocarbons with ≥3 rings and phenols during catalytic pyrolysis, which is conducive to the transformation into carbon clusters and provides carbon sources for CNT growth. In addition, modified coal releases a slightly more carbon-containing gas (CH4 and CO) than lignite, which has a limited effect on the growth of CNTs. This study provides a novel and efficient method for enhancing the growth of CNTs by a molecular tailoring strategy of coal.

ZNF655 promotes the progression of hepatocellular carcinoma through PSMB8.

Hepatocellular carcinoma (HCC) is a type of liver cancer that is associated with high mortality rates. This study aims to investigate the role of ZNF655, a member of the zinc finger protein family, in the development of HCC. Immunohistochemical staining analysis was conducted to evaluate the expression of ZNF655 in HCC patient samples. Lentivirus-mediated ZNF655 knockdown was established in HCC cell lines (BEL-7402 and HCCLM3). The effects of ZNF655 on different aspects of HCC cell behavior such as proliferation, apoptosis, cycle, migration and tumor formation were examined. Downstream targets of ZNF655 in HCC were identified and verified through loss/gain-of-function experiments. Clinically, ZNF655 expression was elevated in HCC and increased with the severity of the disease. Functionally, inhibition of ZNF655 expression reduced the progression of HCC cells by decreasing proliferation, causing apoptosis, arresting cell cycle retention in G2, suppressing migration, and attenuating tumor formation in mice. Mechanistically, the proteasome subunit beta type-8 (PSMB8) was found to be co-expressed with ZNF655 in HCC, and PSMB8 knockdown weakened the promotion of ZNF655 overexpression on HCC. In summary, these findings suggest that ZNF655 promotes the progression of HCC through PSMB8, and inhibition of its expression may be a promising therapeutic target for HCC.

Pneu-HTP based extrusion actuation in bio-inspired soft joint.

Inspired by the joint structure and actuation mechanism of spider legs, a novel pneumatic soft joint actuator is designed, which achieves joint rotation by mutual compression of two hyperelastic sidewalls under inflation pressure. For this type of extrusion actuation, a pneumatic hyperelastic thin plate (Pneu-HTP) based actuation modeling method is proposed. The two actuating surfaces extruded mutually of the actuator are considered as Pneu-HTPs, and mathematical models for their parallel extrusion actuation and angular extrusion actuation are derived. The finite element analysis (FEA) simulations and experiments were also performed to evaluate the model accuracy of the Pneu-HTP extrusion actuation. The results for the parallel extrusion actuation show that the average relative error between the proposed model and the experiment is only 9.27%, and the goodness-of-fit is greater than 99%. For the angular extrusion actuation, the average relative error between the model and the experiment is 12.5%, and the goodness-of-fit is greater than 99%. The parallel extrusion actuating force and rotational extrusion actuating force of the Pneu-HTP are also highly consistent with the FEA simulation results, which provides a promising method for the accurate modeling of extrusion actuation in soft actuator.

Decoding individual differences in self-prioritization from the resting-state functional connectome.

Although the self has traditionally been viewed as a higher-order mental function by most theoretical frameworks, recent research advocates a fundamental self hypothesis, viewing the self as a baseline function of the brain embedded within its spontaneous activities, which dynamically regulates cognitive processing and subsequently guides behavior. Understanding this fundamental self hypothesis can reveal where self-biased behaviors emerge and to what extent brain signals at rest can predict such biased behaviors. To test this hypothesis, we investigated the association between spontaneous neural connectivity and robust self-bias in a perceptual matching task using resting-state functional magnetic resonance imaging (fMRI) in 348 young participants. By decoding whole-brain connectivity patterns, the support vector regression model produced the best predictions of the magnitude of self-bias in behavior, which was evaluated via a nested cross-validation procedure. The out-of-sample generalizability was further authenticated using an external dataset of older adults. The functional connectivity results demonstrated that self-biased behavior was associated with distinct connections between the default mode, cognitive control, and salience networks. Consensus network and computational lesion analyses further revealed contributing regions distributed across six networks, extending to additional nodes, such as the thalamus, whose role in self-related processing remained unclear. These results provide evidence that self-biased behavior derives from spontaneous neural connectivity, supporting the fundamental self hypothesis. Thus, we propose an integrated neural network model of this fundamental self that synthesizes previous theoretical models and portrays the brain mechanisms by which the self emerges at rest internally and regulates responses to the external environment.

Development and experimental verification of a prognosis model for cuproptosis-related subtypes in HCC.

BACKGROUND: Cuproptosis is a recently discovered mechanism of programmed cell death caused by intracellular aggregation of mitochondrial lipoylated proteins and destabilization of iron-sulfur proteins triggered by copper. Hepatocellular carcinoma (HCC) is a common malignant tumor with a poor prognosis. We aimed to predict the survival of patients with HCC using the cuproptosis-related gene (CRG) expression. METHODS: We analyzed the expression, methylation, and mutation status of CRGs in 538 HCC patients and correlated the date with clinical prognosis. HCC patients were divided into two clusters based on their CRG expression. The relationship between CRGs, risk genes, and the immune microenvironment was analyzed using the CIBERSORT algorithm and the single-cell data analysis method. A cuproptosis risk model was constructed according to the five risk genes using the LASSO COX method. To facilitate the clinical applicability of the proposed risk model, we constructed a nomogram and conducted an antineoplastic drug sensitivity analysis. RESULTS: Our results suggest that the expression levels of CRGs in HCC are regulated by methylation. The prognoses were significantly different between the patients of the two clusters. The prognostic risk score positively correlated with memory T cell activation and negatively correlated with natural killer (NK) and regulatory T cell activation. CONCLUSION: Our findings indicate the involvement of CRG regulation in HCC and provide new insights into prognosis assessment. Drug sensitivity analysis predicted drug candidates for the treatment of patients with different HCC subtypes.

Parecoxib inhibits esophageal squamous cell carcinoma progression via the PDK1-AKT pathway.

BACKGROUND: Parecoxib plays an important role in inhibition of human cancer. However, the effect of parecoxib on esophageal squamous cell carcinoma (ESCC) is still not well known. The purpose of this study was to investigate the effect of parecoxib on ESCC and its underlying mechanism. METHODS: RNA-sequence analysis was performed to identify functional alterations and mechanisms. Cell cycle, proliferation, invasion, and migration were assessed using flow cytometry, CCK-8 assay, colony formation, transwell, and wound healing assays. Extracellular matrix (ECM) degradation was detected by substrate gel zymography and 3D cell culture assay. Western blotting was used to detect parecoxib-dependent mechanisms involving cell cycle, proliferation, invasion, and migration. Tumor formation in vivo was detected by mouse assay. RESULTS: Functional experiments indicated that parecoxib induced ESCC cell cycle arrest in G2 phase, and inhibited cell proliferation, invasion, and migration in vitro. Western blotting revealed that parecoxib downregulated the phosphorylation levels of AKT and PDK1, as well as the expression of the mutant p53, cyclin B1, and CDK1, while upregulating p21waf1. Parecoxib inhibited matrix metalloproteinase-2 (MMP2) secretion and invadopodia formation, which were related to ECM degradation. Furthermore, we found that parecoxib suppressed ESCC growth in heterotopic tumor models. CONCLUSION: Parecoxib inhibits ESCC progression, including cell cycle, proliferation, invasion, and migration, via the PDK1-AKT signaling pathway.

Down-regulation of kappa opioid receptor promotes ESCC proliferation, invasion and metastasis via the PDK1-AKT signaling pathway.

BACKGROUND: As a class of the opioid receptors, the kappa opioid receptor (KOR) has been verified to be a potential biomarker and therapeutic target for human malignant tumors. However, a thorough understanding of whether KOR affects progression of esophageal squamous cell carcinoma (ESCC) is still lacking. This study focused on exploring the effect of knocking down KOR in ESCC and its underlying mechanism. METHODS: Bioinformatics analysis was used to compare the different expression level of OPRK1 (KOR gene) in tumor and adjacent normal tissues, and predict the relationship between KOR expression and overall survival. RNA-sequence analysis was performed to detect the altered functions and mechanisms after down regulating KOR. The in vitro and in vivo assays were used to detect the effects of down-regulated KOR on cell proliferation, migration and invasion. Substrate gel zymography and 3D cell culture assays were used to find the effect of KOR knockdown on the degradation of extracellular matrix (ECM), and immunefluorescence was performed to detect the altered cytoskeleton. Western blotting and immunohistochemistry were used to explore the underlying mechanism pathway. RESULTS: Bioinformatics analysis revealed that the expression of OPRK1 was lower in tumor tissue than that in adjacent normal tissues, and lowered expression of KOR was associated with poorer overall survival. The in vitro assays demonstrated that down-regulation of KOR enhanced ESCC proliferation, metastasis and invasion. Western blotting revealed that down-regulation of KOR could activate PDK1-AKT signaling pathway, which actively regulated the cancer progression. Down-regulation of KOR enhanced the formation of invadopodia, secretion of matrix metalloproteinase-2 (MMP2) and rearrangement of cytoskeleton, which were positively related with the invasion of ESCC. KOR knockdown enhanced the tumor invasion and elevated the AKT phosphorylation in nude mice. The AKT kinase inhibition could reverse the effect of down-regulation of KOR. CONCLUSION: KOR might act as a tumor suppressor in ESCC and down-regulation of KOR could enhance the ESCC tumor phenotype. Video Abstract.

COG133 Attenuates the Early Brain Injury Induced by Blood-Brain Barrier Disruption in Experimental Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) is a kind of severe hemorrhagic stroke, and early brain injury acted as one of the main causes of death and delayed neurological deficit in patients with subarachnoid hemorrhage. In this process, the function and structural integrity of the blood-brain barrier play an important role. In this study, we have observed whether the apolipoprotein E (apoE) mimetic peptide, COG133, can alleviate early brain injury after subarachnoid hemorrhage. For this purpose, an experimental subarachnoid hemorrhage model was constructed in mice and treated by intravenous injection of COG133 at a dosage of 1 mg/kg. Then, the function and integrity of the blood-brain barrier were detected, and the pyroptosis level of the neuron was determined. The results showed that COG133 could protect blood-brain barrier function and structure integrity, reduce early brain injury, and ameliorate neurological function after subarachnoid hemorrhage. In terms of molecular mechanism, COG133 inhibits blood-brain barrier destruction through the proinflammatory CypA-NF-κB-MMP9 pathway and reduces neuronal pyroptosis by inhibiting NLRP3 inflammasome activation. In conclusion, this study demonstrated that apoE-mimetic peptide, COG133, can play a neuroprotective role by protecting blood-brain barrier function and inhibiting brain cell pyroptosis to reduce early brain injury after subarachnoid hemorrhage.

Remarkable enhancement in the N2 selectivity of NH3-SCR over the CeNb3Fe0.3/TiO2 catalyst in the presence of chlorobenzene.

The simultaneous removal of NOx and dioxins is the frontier of environmental catalysis, which is still in the initial stage and poses several challenges. In this study, a series of CeNb3Fex/TiO2 (x = 0, 0.3, 0.6, and 1.0) catalysts were prepared by the sol-gel method and examined for the synergistic removal of NOx and CB. The CeNb3Fe0.3/TiO2 catalyst exhibits an optimum catalytic performance, with an NOx conversion greater than 95% at 260-380 °C. It also exhibits an optimal CB oxidation activity, in which CB promoted both the NOx conversion and N2 selectivity below 250 °C. Moreover, the more favorable ratios of Ce4+ to Ce3+ and plentiful surface-adsorbed oxygen species are the reasons why CeNb3Fe0.3/TiO2 catalyst has better catalytic activity than other catalysts at the lower temperature. Simultaneously, owing to the modulation of Fe to the redox properties of Ce and Nb, the large number of oxygen vacancies and acid sites was generated, and the CeNb3Fe0.3/TiO2 catalyst is beneficial to NOx reduction and CB oxidation. Furthermore, the results of in situ DRIFTS study reveal the NH3-SCR reactions over CeNb3Fe0.3/TiO2 catalysts are mainly conformed to by the L-H mechanism (< 350 °C) and E-R mechanism (> 350 °C), respectively, and the multi-pollutant conversion mechanism in the synergistic reaction was systematically studied.

Novel pathogenic variant of MYBPC3 responsible for hypertrophic cardiomyopathy.

OBJECTIVES: This study aims to investigate the pathogenic gene variant in a family with hypertrophic cardiomyopathy by using whole-exome sequencing and to explore the relationship between the gene variant and clinical phenotype. METHODS: Peripheral blood was collected from a family with hypertrophic cardiomyopathy, and deoxyribonucleic acid was extracted. The possible pathogenic genes were detected by whole-exome sequencing, and the variant was verified by Sanger sequencing. Functional change in the variant was predicted by bioinformatics software. Clinical data of the family members are analysed simultaneously. RESULTS: The proband carries a novel heterozygous nonsense variant of MYBPC3:c.2731G > T (p.E911X). The analysis of amino acid conservation suggests that the variation is highly conserved. The three-dimensional protein structure shows that the variant in MYBPC3 results in the incompleteness of the fibronectintype-III2 (p872-967) domain and deletion of Ig-like C2-type 6 (p971-1065) and fibronectin type-III 3 and Ig-like C2-type 7 (p1181-1274) domains, in which p1253-1268 is predicted to have a transmembrane helix structure. Clinical data indicate that the phenotypes of variant carriers with hypertrophic cardiomyopathy are diverse, suggesting the functional damages to the protein of MYBPC3. CONCLUSION: The phenotypes of variant carriers with hypertrophic cardiomyopathy caused by the novel variant in MYBPC3: c.2731G > T (p.E911X) exhibit variable severity and clinical manifestations. Whole-exome sequencing can be used to comprehensive screen hypertrophic cardiomyopathy genes and provide a strong basis for early screening and accurate diagnosis and treatment of hypertrophic cardiomyopathy in children.

Surgical Treatment and Clinical Outcomes of Petroclival Meningiomas: A Single-Center Experience of 107 Patients.

OBJECTIVE: This study aimed to establish optimal surgical strategies via reviewing the clinical outcomes of various surgical approaches for the pertroclival meningiomas (PCMs). METHODS: This retrospective study enrolled 107 patients with PCMs at the authors' institution from year 2010 to 2020. Patient demographics, the clinical characteristics, various operative approaches, major morbidity, post-operative cranial nerve deficits and tumor progression or recurrence were analyzed. RESULTS: The subtemporal transtentorial approach (STA), the Kawase approach (KA), the retrosigmoid approach (RSA) and the anterior sigmoid approach (ASA), namely the posterior petrosal approach (PPA) were adopted for 17 cases, 22 cases, 31 cases and 34 cases respectively. Total or subtotal resection was achieved in 96 cases (89.7%). The incidence of new-onset and aggravated cranial nerve dysfunction were 13.1% (14/107) and 10.4% (15/144), respectively. Furthermore, 14 cases suffered from intracranial infection, 9 cases had cerebrospinal fluid leakage, and 3 cases sustained intracranial hematoma (1 case underwent second operation). The mean preoperative and postoperative Karnofsky Performance Status (KPS) score was 80 (range 60-100) and 78.6 (range 0-100), but this was not statistically significant (P>0.05). After a mean follow-up of 5.1 years (range 0.3- 10.6 years), tumor progression or recurrence was confirmed in 23 cases. Two cases died from postoperative complications. CONCLUSIONS: For the treatment of PCMs, it is still a challenge to achieve total resection. With elaborate surgical plans and advanced microsurgical skills, most patients with PCMs can be rendered tumor resection with satisfactory extent and functional preservation, despite transient neurological deterioration during early postoperative periods.