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Abstract RNA modification, especially RNA methylation, is a critical posttranscriptional process influencing cellular functions and disease progression, accounting for over 60% of all RNA modifications. It plays a significant role in RNA metabolism, affecting RNA processing, stability, and translation, thereby modulating gene expression and cell functions essential for proliferation, survival, and metastasis. Increasing studies have revealed the disruption in RNA metabolism mediated by RNA methylation has been implicated in various aspects of cancer progression, particularly in metabolic reprogramming and immunity. This disruption of RNA methylation has profound implications for tumor growth, metastasis, and therapy response. Herein, we elucidate the fundamental characteristics of RNA methylation and their impact on RNA metabolism and gene expression. We highlight the intricate relationship between RNA methylation, cancer metabolic reprogramming, and immunity, using the well‐characterized phenomenon of cancer metabolic reprogramming as a framework to discuss RNA methylation's specific roles and mechanisms in cancer progression. Furthermore, we explore the potential of targeting RNA methylation regulators as a novel approach for cancer therapy. By underscoring the complex mechanisms by which RNA methylation contributes to cancer progression, this review provides a foundation for developing new prognostic markers and therapeutic strategies aimed at modulating RNA methylation in cancer treatment.

Abstract Background Dural arteriovenous fistulas (DAVF) represent almost 10–15% of intracranial malformations that cause intracranial hemorrhage and focal neurological deficits. Seldom tentorial DAVF cases present with ocular manifestations initially, which occur frequently in carotid–cavernous fistula (CCF) and cavernous sinus DAVF (CS DAVF). Case presentation We report an unusual falcotentorial DAVF case draining via the superior and inferior ophthalmic veins that caused left-side increased intraocular pressure. The patient’s chief complaint was swelling on the left side, pain and conjunctival congestion. He received endovascular embolization via a transarterial approach, and postoperative angiography demonstrated that the falcotentorial DAVF was occluded completely. Conclusion Except for CCF and CS DAVF, some specific subtypes of DAVF should be considered if the patient initially presents with ocular symptoms. Differential diagnosis and definitive treatment are mandatory to avoid a delayed diagnosis and irreversible symptoms.

Catalytic ozonation, with enhanced efficiency and reduced byproduct formation at lower temperatures, proved to be efficient in ethyl acetate (EA) degradation. In this work, MMn2O4 (M = Cu, Co, Ni, Mg) catalysts were prepared via a redox-precipitation method to explore the catalytic ozonation mechanism of EA. Among all the catalysts, CuMn exhibited superior catalytic activity at 120 °C, achieving nearly 100% EA conversion and above 90% CO2 selectivity with an O3/EA molar ratio of 10. Many characterizations were conducted, such as SEM, BET and XPS, for revealing the properties of the catalysts. Plentiful active sites, abundant oxygen vacancies, more acid sites and higher reduction ability contributed to the excellent performance of CuMn. Moreover, the addition of NO induced a degree of inhibition to EA conversion due to its competition for ozone. H2O had little effect on the catalytic ozonation of CuMn, as the conversion of EA could reach a stable platform at ~89% even with 5.0 vol.% of H2O. The presence of SO2 usually caused catalyst deactivation. However, the conversion could gradually recover once SO2 was discontinued due to the reactivation of ozone. A detailed reaction mechanism for catalytic ozonation was proposed via in situ DRIFTS measurements and DFT calculations.

Objectives: To make full use of the abundant data distributed at the edge of the network to serve the training of artificial intelligence models, edge intelligence technology represented by federated edge learning emerges as the times require. The rich data at the edge enables it to serve artificial intelligence model training, and design wireless resource management strategies with the goal of optimizing learning performance (such as optimizing model training time, learning convergence, etc.). Methods: Using the federated learning network architecture, this paper analyzes the resource allocation and user scheduling schemes: 1. For the resource allocation problem, the trade-off relationship between the number of communication rounds and the delay per round when the goal of minimizing the total training time is analyzed, To meet the time constraints of each round of training, more frequency bandwidth should be allocated to devices with low computational power, compensating for a computational time by reducing communication time, and vice versa. Therefore, bandwidth allocation between devices should consider both channel conditions and computing resources, which is completely different from the traditional bandwidth allocation work that only considers channel conditions. To this end, it is necessary to model the total training time minimization problem, optimize the quantization series and bandwidth allocation, and design an alternate optimization algorithm to solve this problem. 2. For the user scheduling problem, the communication time minimization optimization problem is modeled by linking the importance of data with the number of communication rounds, channel quality and single-round communication delay, and using a theoretical model to unify the two. By solving the optimization problem, it is found that the optimal scheduling strategy will pay more attention to the importance of data in the early stage, and pay more attention to the channel quality in the later stage. In addition, the proposed single-device scheduling algorithm is also extended to multi-device scheduling scenarios. Results: 1. For the resource allocation problem, when the bandwidth allocation is optimal, the relationship between the total training time and the quantization level obtained by simulation, run the same training process at least 5 times on each quantization level, and there is a total training time. The total training time is T= N ϵ ⋅ T d , and N ϵ is a decreasing function of quantization level q,and Td is an increasing function of q . In addition, the optimal quantization series obtained through theoretical optimization is consistent with the simulation results, and the effectiveness of the proposed algorithm is verified. According to the relationship between the optimal value interval of the loss function and the training time, the optimal quantization series and the optimal bandwidth allocation strategy are obtained by solving the training time minimization problem. 2. For the user scheduling problem, the proposed user scheduling (TLM) scheme is compared with three other common scheduling schemes in the simulation, and the average precision is shown when the communication time is 6 000 s and 14 000 s, where the average Accuracy is obtained by measuring the IoU, the intersection of union, of the predicted value and the true value. The CA scheme yields the worst accuracy on car 1 with the largest channel attenuation, while the IA scheme exhibits the lowest accuracy on car 4 where the data is less important. The ICA scheme aims to find a balance between CA and IA, but due to its heuristic nature, the performance is lower than that of the TLM scheme. Conclusions: 1. The training loss under the optimal quantization level and optimal bandwidth allocation reaches the predetermined threshold in a shorter time and can achieve the highest test accuracy. Secondly, the training performance under the non-optimal quantization level and optimal bandwidth allocation will be better than the performance of the optimal quantization leveland average bandwidth allocation, which also verifies the necessity of resource allocation. 2. The TLM scheme achieves slightly better performance early in training and significantly outperforms all other schemes after full training. This is due to the inherent prospective nature in the proposed TLM protocol which is advantageous over the myopic nature in the existing CA, IA and ICA protocols.

BackgroundScalp arteriovenous malformations (AVM) are rare vascular malformations reported only in small case series. Scalp AVMs usually present with symptoms, including headache, tinnitus, epilepsy, cerebral ischemia, and necrosis of the scalp, which can cause functional, cosmetic, and psychological problems. There are many difficulties in the treatment of scalp AVM because of its complex characteristics of vascular anatomy, non-uniform structure, and intracranial-extracranial anastomosis.Case descriptionTo illustrate the endovascular treatment of scalp AVM via direct percutaneous puncture while traditional arterial and venous approaches were not available. In this report, access was obtained through a direct puncture of the enlarged frontal vein. Onyx-18 was injected through a microcatheter to occlude draining veins, fistulous connection, and the feeders. An 18-gauge indwelling needle was inserted into draining veins directly. Postembolization angiography demonstrated complete sAVM occlusion immediately and no non-targeted embolization. At a 1-year follow-up, no procedure-related complications and evidence of recurrence were observed.ConclusionThe technique of endovascular embolization via direct percutaneous puncture approach is safe, rapid, and effective for specific sAVM. Treatment options should be made in terms of size, vascular anatomical characteristics of the lesions, patient's preference, cosmetic factors, and available expertise.

Abstract Background An endovascular covered-stent has unique advantages in treating complex intracranial aneurysms; however, in-stent stenosis and late thrombosis have become the main factors affecting the efficacy of covered-stent treatment. Smooth-muscle-cell phenotypic modulation plays an important role in late in-stent stenosis and thrombosis. Here, we determined the efficacy of using covered stents loaded with drugs to inhibit smooth-muscle-cell phenotypic modulation and potentially lower the incidence of long-term complications. Methods Nanofiber-covered stents were prepared using coaxial electrospinning, with the core solution prepared with 15% heparin and 20 µM rosuvastatin solution (400: 100 µL), and the shell solution prepared with 120 mg/mL hexafluoroisopropanol. We established a rabbit carotid-artery aneurysm model, which was treated with covered stents. Angiography and histology were performed to evaluate the therapeutic efficacy and incidence rate of in-stent stenosis and thrombosis. Phenotype, function, and inflammatory factors of smooth-muscle cells were studied to explore the mechanism of rosuvastatin action in smooth-muscle cells. Result Heparin–rosuvastatin-loaded nanofiber scaffold mats inhibited the proliferation of synthetic smooth-muscle cells, and the nanofiber-covered stent effectively treated aneurysms in the absence of notable in-stent stenosis. Additionally, in vitro experiments showed that rosuvastatin inhibited the smooth-muscle-cell phenotypic modulation of platelet-derived growth factor-BB induction and decreased synthetic smooth-muscle-cell viability, as well as secretion of inflammatory cytokines. Conclusion Rosuvastatin inhibited the abnormal proliferation of synthetic smooth-muscle cells, and heparin–rosuvastatin-loaded covered stents reduced the incidence of stenosis and late thrombosis, thereby improving the healing rates of stents used for aneurysm treatment. Graphic abstract

ObjectiveThe surgical strategy for falcotentorial junction tumors remains complex. Different approaches are selected according to the location and growth pattern of the tumor and the operator’s experience. This report reviews our single-institution experience in the surgical management of falcotentorial junction tumors.MethodsWe retrospectively reviewed the clinical and imaging data, surgical strategy, and follow-up outcomes of 49 patients treated from 2007 to 2020.ResultAll 49 patients (12 male, 37 female, mean age: 56.3 ± 11.3 years) underwent safe tumor resection. The most common complaints were headache (43%), dizziness (39%), and unstable gait (16%). Thirty percent of the tumors showed calcification, and the computed tomography scans revealed hydrocephalus in 36% of the patients. On magnetic resonance imaging, 43% of the tumors were unilateral. According to the Asari classification, the tumors were divided into inferior (16%), superior (29%), anterior (22%), and posterior (33%) types. The occipital interhemispheric approach (88%) and supracerebellar–infratentorial approach (10%) were primarily used to reach the tumors. The pathology examination results revealed that 85.7% of the tumors were meningioma and 14.3% were hemangiopericytoma. Of the 49 patients, 15 achieved a Simpson grade I resection, and 29 achieved a Simpson grade II resection. The follow-up rate was 77.6% (38/45); 94.7% of patients (36/38) achieved a favorable outcome, and 9 experienced tumor recurrences.ConclusionSurgical approach selection depends on the growth characteristics of the tumor and the degree of venous or sinus involvement. The occipital interhemispheric approach is the most commonly used and safest approach for falcotentorial junction tumors with multiple brain pressure control assistance techniques.

Abstract Background The regulation of vascular smooth muscle cell (VSMC) phenotype plays an important role in intracranial aneurysm (IA) formation and progression. However, the underlying mechanism remains unclear. Metformin is a 5′ AMP-activated protein kinase (AMPK) agonist that has a protective effect on vasculature. The present study investigated whether metformin modulates VSMC phenotype switching via the AMPK/acetyl-CoA carboxylase (ACC) pathway during IA pathogenesis. Methods Adult male Sprague-Dawley rats (n = 80) were used to establish an elastase-induced IA model. The effects of metformin on AMPK activation and VSMC phenotype modulation were examined. We also established a platelet-derived growth factor (PDGF)-BB-induced VSMC model and analyzed changes in phenotype including proliferation, migration, and apoptosis as well as AMPK/ACC axis activation under different doses of metformin, AMPK antagonist, ACC antagonist, and their combinations. Results Metformin decreased the incidence and rupture rate of IA in the rat model and induced a switch in VSMC phenotype from contractile to synthetic through activation of the AMPK/ACC pathway, as evidenced by upregulation of VSMC-specific genes and decreased levels of pro-inflammatory cytokines. AMPK/ACC axis activation inhibited the proliferation, migration, and apoptosis of VSMCs, in which phenotypic switching was induced by PDGF-BB. Conclusions Metformin protects against IA formation and rupture by inhibiting VSMC phenotype switching and proliferation, migration, and apoptosis. Thus, metformin has therapeutic potential for the prevention of IA.

Object: Spinal dural arteriovenous fistula (SDAVF) is the most common spinal vascular shunt lesion. Although pathological changes in the SDAVF draining vein (SDAVF-DV) have been elucidated, protein changes remain enigmatic. We investigated the pathology and protein changes in the SDAVF-DV under sustained high vascular pressure.Methods: Three SDAVF-DV samples were compared with superficial temporal artery (STA) and superficial temporal vein (STV) samples as controls. Vascular structure was revealed by hematoxylin and eosin (H&E) and Masson staining; and cell distribution, extracellular matrix, and inflammation infiltration were observed by immunohistochemistry. Label-free quantitative proteomics was performed, and the peptide mixture was fractionated and analyzed by liquid chromatography–tandem mass spectrometry (LC-MS/MS) to identify differentially expressed proteins. Bioinformatics analysis of the differentially expressed proteins was performed using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein–protein interaction (PPI) networks.Results: H&E and Masson staining showed an artery-like structure of the SDAVF-DV. Immunostaining showed that vWF+ cells were not continuous in the SDAVF-DV. Although α-SMA+ and AT1+ cells were more abundant in the STV than in the SDAVF-DV, piezo-1 expression was lower in the SDAVF-DV. The SDAVF-DV showed different distributions of elastin, COL I, and COL III. COL IV and COL VI were decreased in the SDAVF-DV, while CD45+ cells and COX-1 were increased compared with those in the controls. No differences in CD68 expression and COX-2 staining were observed between the SDAVF-DV and controls. Compared with the STA, 95 proteins were upregulated and 303 proteins were downregulated in the SDAVF-DV. The most differential GO terms in each category were the adenylate cyclase-modulating G protein-coupled receptor signaling pathway, U6 snRNP, and SH3 domain binding. The most differentially expressed KEGG protein pathway was focal adhesion. Compared with the STV, the SDAVF-DV had 158 upregulated proteins and 362 downregulated proteins. The most differential GO terms in each category were lamellipodium assembly, U6 snRNP, and SH3 domain binding; and the most differentially expressed KEGG protein pathway was dilated cardiomyopathy. PPI analysis revealed PPIs among the top 300 proteins.Conclusions: The SDAVF-DV exhibits specific pathology and protein expression changes under sustained high vascular pressure. The results of the present study provide insights into the pathogenesis of SDAVF formation at the protein level as well as a scientific foundation for further exploration of the pathophysiological mechanism of the SDAVF.

Different transition metals (Cr/Fe/Mn/Co) derived catalysts supported on γ-Al2O3 were prepared by the isovolumetric impregnation method for catalytic ozonation of acetone (C3H6O), and their catalytic activities under industrial complex conditions were investigated. Among them, CrOx/γ-Al2O3 catalyst with Cr loading of 1.5%, abbreviated as Cr1.5%, achieved the best activity, benefitting from its larger surface area, larger proportion of Cr6+/Cr, more chemically desorbed oxygen species Oβ, appropriate acidity, and superiority of low-temperature reducibility. Simulated industrial conditions were used to investigate the applicability of Cr1.5% catalysts for catalytic ozonation of acetone. Results illustrated that the optimum temperature range was 120–140 °C, with molar ratio O3/C3H6O > 6. Different C3H6O initial concentrations had less effect over the activity of Cr1.5% catalysts, with little residual ozone, confirming the applicability of Cr1.5% catalysts in industrial application. The effects of sulfur/water vapor on catalytic activity were also investigated, and satisfactory resistance to sulfur or water vapor individually was obtained. Finally, in-situ DRIFTS measurement was carried out, to explore and illustrate mechanisms of acetone catalytic ozonation pathways and sulfur/water poisoning.

Abstract Background Oxidative stress and vascular smooth muscle cell (VSMC) phenotypic modulation influence intracranial aneurysm (IA) formation and progression. Oxidative stress plays an important role in phenotype switching, and nuclear factor erythroid 2-related factor 2 (Nrf-2) is one of the main antioxidant systems. Unfortunately, little is known about how Nrf-2 signaling influences VSMC phenotype switches during IA pathogenesis. Methods We examined the effect of Nrf-2 activation IA on formation and progression in an elastase-induced rat IA model. We also developed a hydrogen peroxide (H2O2)-induced VSMC oxidative damage model. Then, we analyzed VSMC phenotype changes in the setting of Nrf-2 activation or inhibition in vitro. The proliferation, migration ability, and apoptosis rate of VSMCs were tested. Lastly, we measured the expression levels of antioxidant enzymes and inflammatory cytokines downstream of Nrf-2. Results Nrf-2 activation suppressed IA formation and progression in vivo. We confirmed Nrf-2 nuclear translocation and a VSMC switch from the contractile to synthetic phenotype. Nrf-2 activation inhibited the proliferation, migratory ability, and apoptosis rate enhanced by H2O2. Quantitative real-time polymerase chain reaction (PCR) and western blot analysis revealed that Nrf-2 activation promoted antioxidant enzymes and VSMC-specific marker gene expressions but decreased pro-inflammatory cytokine levels. Conclusion These results suggest that Nrf-2 exerts protective effects against IA development by preventing VSMCs from changing to a synthetic phenotype.

Background: Computer-aided detection (CADe) of colon polyps has been demonstrated to improve colon polyp and adenoma detection during colonoscopy by indicating the location of a given polyp on a parallel monitor. The aim of this study was to investigate whether embedding the CADe system into the primary colonoscopy monitor may serve to increase polyp and adenoma detection, without increasing physician fatigue level. Methods: Consecutive patients presenting for colonoscopies were prospectively randomized to undergo routine colonoscopy with or without the assistance of a real-time polyp detection CADe system. Fatigue level was evaluated from score 0 to 10 by the performing endoscopists after each colonoscopy procedure. The main outcome was adenoma detection rate (ADR). Results: Out of 790 patients analyzed, 397 were randomized to routine colonoscopy (control group), and 393 to a colonoscopy with computer-aided diagnosis (CADe group). The ADRs were 20.91% and 29.01%, respectively (OR = 1.546, 95% CI 1.116–2.141, p = 0.009). The average number of adenomas per colonoscopy (APC) was 0.29 and 0.48, respectively (Change Folds = 1.64, 95% CI 1.299–2.063, p

BackgroundEvidence has shown that deep learning computer aided detection (CADe) system achieved high overall detection accuracy for polyp detection during colonoscopy.AimThe detection performance of CADe system on non-polypoid laterally spreading tumors (LSTs) and sessile serrated adenomas/polyps (SSA/Ps), with higher risk for malignancy transformation and miss rate, has not been exclusively investigated.MethodsA previously validated deep learning CADe system for polyp detection was tested exclusively on LSTs and SSA/Ps. 1451 LST images from 184 patients were collected between July 2015 and January 2019, 82 SSA/Ps videos from 26 patients were collected between September 2018 and January 2019. The per-frame sensitivity and per-lesion sensitivity were calculated.Results(1) For LSTs image dataset, the system achieved an overall per-image sensitivity and per-lesion sensitivity of 94.07% (1365/1451) and 98.99% (197/199) respectively. The per-frame sensitivity for LST-G(H), LST-G(M), LST-NG(F), LST-NG(PD) was 93.97% (343/365), 98.72% (692/701), 85.71% (324/378) and 85.71% (6/7) respectively. The per-lesion sensitivity of each subgroup was 100.00% (71/71), 100.00% (64/64), 98.31% (58/59) and 80.00% (4/5). (2) For SSA/Ps video dataset, the system achieved an overall per-frame sensitivity and per-lesion sensitivity of 84.10% (15883/18885) and 100.00% (42/42), respectively.ConclusionsThis study demonstrated that a local-feature-prioritized automatic CADe system could detect LSTs and SSA/Ps with high sensitivity. The per-frame sensitivity for non-granular LSTs and small SSA/Ps should be further improved.

Background/Aims: Cerebral aneurysm growth is characterized by continuous structural weakness of local smooth muscle cells, though the mechanism is unclear. In this study, we examine protein changes in cerebral aneurysm and human brain vascular smooth muscle cells after cyclic mechanical stretch. We further explore the relationship between the smooth muscle cell changes and reductions in the levels of collagen types IV and VI. Methods: Saccular cerebral aneurysms (n=10) were collected, and temporal artery samples were used as controls. Quantitative proteomics were analyzed and histopathological changes were examined. Smooth muscle cells were cultured in a flexible silicone chamber and subjected to 15% cyclic mechanical stretch. The effect of stretch on the cell viability, function, gene and protein expression were further studied for the understanding the molecular mechanism of aneurysm development. Results: Proteomics analysis revealed 92 proteins with increased expression and 88 proteins with decreased expression compared to the controls (p

Aneurysm (AN) embolization is an important treatment for cerebral aneurysms. The endothelialization of the aneurysm neck is crucial for preventing aneurysm recurrence. Sitagliptin is a therapeutic drug for diabetes that has been reported to have cardiovascular-protective effects. This study investigated the effect of sitagliptin on endothelial progenitor cell (EPC) function and endothelialization of aneurysm necks after embolization. The effect of sitagliptin on aneurysm neck endothelialization was examined using a rat aneurysm embolization model. We isolated EPCs and used CCK-8 (Cell Counting Kit-8) and annexin V/PI to analyze the effect of sitagliptin on the proliferation and apoptosis of EPCs. The effects of sitagliptin on the migration and invasion of EPCs were examined using scratch and Transwell assays. The effect of sitagliptin on the angiogenic ability of EPCs was examined using a sprouting assay. Western blot analysis and ELISA were used to analyze the effect of sitagliptin on the expression of proangiogenic factors in EPCs. The in vivo results indicated that sitagliptin promoted endothelialization of the aneurysm neck and increased circulating EPCs and expression levels of SDF-1 and VEGF in peripheral blood. Sitagliptin promoted the proliferation, migration, invasion, and angiogenic abilities of EPCs. Western blot analysis and ELISA showed that sitagliptin promoted the expression of SDF-1 and VEGF in progenitor endothelial cells. Western blot assays showed that sitagliptin activated the expression of NRF2, which is dependent on the function of CXCR4. Furthermore, sitagliptin promoted progenitor endothelial cell migration, invasion and angiogenesis through the SDF-1/CXCR4/NRF2 signaling pathway. Additionally, progenitor endothelial cells expressed SDF-1 and VEGF. The promotion of endothelialization by sitagliptin provides an additional therapeutic option for preventing the recurrence of AN.

Cerebral aneurysm growth is characterized by vessel wall frailness, although the underlying cellular mechanisms are unclear. Here, we examined the relationship between inflammatory smooth muscle cells (SMCs) and endothelial cells (ECs) in cerebral aneurysms, including the mechanisms underlying inflammatory SMC-induced changes in ECs. Five saccular cerebral aneurysms were collected and five temporal artery samples were used as controls. Cells and cytokines were detected by immunohistochemistry and TUNEL (transferase dUTP nick end labeling) assays performed to evaluate apoptosis. Human umbilical vein endothelial cells (HUVECs) were seeded on collagen I, IV, and VI-coated plates for cell adhesion assays and inflammatory SMCs (iSMCs) were established by culture in flexible silicone chambers subjected to cyclic mechanical stretch. HUVECs were cultured in iSMC-conditioned medium, followed by evaluation of their viability, apoptosis, and function, and determination of VEGF (vascular endothelial growth factor) -A and integrin levels by western blotting. Aneurysm tissue contained fewer SMCs and lacked ECs. In aneurysm walls, more matrix metalloproteinase (MMP) -1, MMP-3, and apoptotic cells were detected, accompanied by decreased collagen IV and VI levels. Cell adhesion assays revealed that more HUVECs were attached in collagen IV and VI-coated plates compared with controls. iSMC-conditioned medium significantly reduced HUVEC viability and apoptosis showed an increased trend; however, the difference was not significant. iSMC medium also reduced tube formation and migration of HUVECs. Moreover, iSMC medium reduced HUVEC expression of VEGF-A, integrin α1, integrin α2, and integrin β. Our data demonstrate a lack of SMCs and ECs in aneurysm walls, accompanied by elevated MMP and decreased collagen levels. In vitro assays showed that iSMCs induced reduction in EC adhesion, and caused EC dysfunction. Understanding of the relationships among SMC, EC, and collagens during aneurysm progression provides an additional therapeutic option for prevention of cerebral aneurysm progression.

This study explored a new approach to enhance aneurysm (AN) neck endothelialization via erythropoietin (EPO)‐induced endothelial progenitor cell (EPC) stimulation. Results suggest that EPO enhanced the endothelialization of a coiled embolization AN neck by stimulating EPCs via vascular endothelial growth factor modulation. Thus, the promotion of endothelialization with EPO provides an additional therapeutic option for preventing the recurrence of ANs. Endovascular coil embolization is an attractive therapy for cerebral ANs, but recurrence is a main problem affecting long‐term outcomes. In this study, we explored a new approach to enhance AN neck endothelialization via EPO‐induced EPC stimulation. Ninety adult male Sprague‐Dawley rats were selected for an in vivo assay, and 60 of them underwent microsurgery to create a coiled embolization AN model. The animals were treated with EPO, and endothelial repair was assessed via flow cytometry, immunofluorescence, electronic microscopy, cytokine detection, and routine blood work. EPO improved the viability, migration, cytokine modulation, and gene expression of bone marrow‐derived EPCs and the results showed that EPO increased the number of circulating EPCs and improved endothelialization compared with untreated rats (p < .05). EPO had no significant effect on the routine blood work parameters. In addition, the immunofluorescence analysis showed that the number of KDR+ cells in the AN neck was elevated in the EPO‐treated group (p < .05). Further study demonstrated that EPO promoted EPC viability and migration in vitro. The effects of EPO may be attributed to the modulation of vascular endothelial growth factor (VEGF). In particular, EPO enhanced the endothelialization of a coiled embolization AN neck by stimulating EPCs via VEGF modulation. Thus, the promotion of endothelialization with EPO provides an additional therapeutic option for preventing the recurrence of ANs. Significance Erythropoietin (EPO) is involved in erythropoiesis and related conditions and is reported to enhance stem‐cell mobilization from bone marrow while elevating stem‐cell viability and function. In this study, EPO was also found to stimulate endothelial progenitor cells to induce the endothelialization of a coiled embolic aneurysm neck via vascular endothelial growth factor modulation. Endothelialization induction provides an additional therapeutic opportunity during vascular inner layer repair and remodeling. The results provide important information on the unique role EPO plays during vascular repair and remodeling.

Myosin light chain kinase is a key enzyme in smooth muscle cell contraction. However, whether myosin light chain kinase plays a role in the occurrence or development of intracranial aneurysms is not clear. The present study explored the function of myosin light chain kinase in human intracranial aneurysm tissues. Five aneurysm samples and five control samples were collected, and smooth muscle cells (SMCs) were dissociated and cultured. A label-free proteomic analysis was performed to screen the differentially expressed proteins between aneurysm and control samples. The expression and function of myosin light chain kinase in aneurysms were examined. We found that 180 proteins were differentially expressed between the aneurysm and control samples, among which 88 were increased and 92 (including myosin light chain kinase) were decreased in aneurysms compared to control tissues. In a model of the inflammatory environment, contractility was weakened and apoptosis was increased in aneurysm SMCs compared to human brain SMCs (p < 0.05). The knock down of myosin light chain kinase in human brain SMCs caused effects similar to those observed in aneurysm SMCs. These results indicated that myosin light chain kinase plays an important role in maintaining smooth muscle contractility, cell survival and inflammation tolerance.

NO oxidation was conducted over MnOx-CeO2 catalysts, which were synthesized by the co-precipitation method. The calcination temperature and third metal doping were the main considerations. MnCe catalysts calcined at 350 °C and 450 °C attained the highest NO conversion efficiency, compared to 550 °C. XRD results suggested that the higher the calcination temperature, the higher the crystallization degree, which led to a negative effect on catalytic activity. Subsequently, Sn, Fe, Co, Cr, and Cu were separately doped into MnCe composites, but no improvement was observed for these trimetallic catalysts in NO conversion. Nevertheless, MnCeSn, MnCeFe, and MnCeCo still exhibited a desirable NO conversion efficiency, so they were tested under SO2 addition together with MnCe catalyst. Among them, MnCeFe exhibited the highest NO conversion after whole poisoning testing. XPS results indicated that Fe could protect Mn and Ce metal oxides from being reduced during SO2 poisoning process. Furthermore, in in-situ DRIFTS measurement, part of nitrate species maintained undestroyed on the MnCeFe catalyst surface after SO2 poisoning. These characteristics reinforced that Fe dropping would achieve better performance under SO2 atmosphere.

Background: Brainstem cavernous malformations (BSCMs) often present with haemorrhage, but the optimal timing for microsurgical intervention remains unclear. This study aims to explore how intervention timing relates to neurological outcomes in haemorrhagic BSCM patients undergoing microsurgery, offering insights for clinical decisions. Methods: A total of 293 consecutive patients diagnosed with BSCMs, who underwent microsurgery were identified between March 2011 and January 2023 at two comprehensive centres in China, with a postoperative follow-up duration exceeding 6 months. Utilizing logistic regression models with restricted cubic splines, distinct time groups were identified. Subsequently, matching weight analysis compared these groups in terms of outcomes, new haemorrhage rates, cranial nerve deficits, and perioperative complications. The primary outcome was an unfavourable outcome, which was defined as a mRS score greater than 2 at the latest follow-up. Results: Among the 293 patients, 48.5% were female, median age was (39.9 ± 14.3) years, and median haemorrhage-to-treatment time was 42 days. Patients were categorized into acute (= 21 days), subacute (22-42 days), and delay (>42 days) intervention groups. After matching, 186 patients were analyzed. Adjusted analysis showed lower unfavourable outcome rates for acute [adjusted odds ratio (OR), 0.73; 95% CI, 0.65-0.82; P< 0.001] and subacute (adjusted OR, 0.83; 95% CI, 0.72-0.95; P=0.007) groups compared to the delay group. Subacute intervention led to fewer cranial nerve deficits (adjusted OR, 0.76; 95% CI, 0.66-0.88, P< 0.001). New haemorrhage incidence didn't significantly differ among groups. Conclusions: For haemorrhagic BSCMs patients, delayed microsurgical intervention that exceeded 42 days after a prior haemorrhage were associated with an increased risk of unfavourable neurological outcomes. [ABSTRACT FROM AUTHOR]