Objective Idiopathic rolandic epilepsy syndrome （IRES） is the most common epilepsy syndrome in childhood， and its lesion site remains undetermined. This article aims to investigate the source of epileptiform discharges in IRES using magnetoencephalography （MEG）.Methods A total of 70 patients with IRES were enrolled in this prospective MEG-based study， among whom there were 53 children with benign epilepsy of childhood with centrotemporal spikes （BECTS）， 12 children with atypical benign partial epilepsy （ABPE）， 3 children with Landau-Kleffner syndrome （LKS）， and 2 children with epileptic encephalopathy with continuous spike-and-waves during slow-wave sleep （CSWS）. Epileptiform discharges were collected independently from each patient 10 times， and an MEG source analysis was performed. Standardized low-resolution brain electromagnetic tomography was used to perform source localization of the distributed source model. The spike source density was quantified into amplitude， and source location was determined according to the Desikan-Killiany atlas. The association between the distribution of spike source in brain and clinical manifestations was analyzed.Results In IRES， there were significant differences in the source locations of epilepsy discharge between BECTS， ABPE， LKS， and CSWS. The current source density of CSWS was stronger in the frontal lobe， the temporal lobe， and the anterior cingulate gyrus， while that of ABPE was stronger in the frontal lobe， and that of BECTS and LKS were stronger in the temporal lobe. The more severe phenotype of epilepsy， such as generalized tonic-clonic seizure， was associated with a stronger current source density in the brain， which was consistent with electroencephalography manifestations.Conclusion This study identifies different sources of epileptiform discharges in IRES. The density distribution of these spike sources may help to explain the discharge， cognitive， and neuropsychological characteristics in different subtypes of IRES.
Magnetoencephalography

Emergence agitation （EA） is a common complication after general anesthesia， especially in children and adolescents. Remifentanil， as a short-acting μ-receptor agonist， has become an important drug for the prevention and treatment of EA due to its rapid recovery and low risk of respiratory depression. This article reviews the mechanism of action and clinical research progress of remifentanil in the prevention and treatment of EA. Its mechanism of action involves the inhibition of pain signals mediated by traditional μ-receptor activation and potential new mechanism based on neural-endocrine-immune network， including regulation of microglial inflammatory pathways， and the modulation of cytokines and chemokines，etc. Clinical studies have shown that remifentanil can significantly shorten the recovery time， reduce the incidence of EA， and further optimize the analgesic effect and recovery quality by combining with other drugs （such as local anesthetics， sedatives， and opioid drugs）. Future research should further explore the mechanism of action of remifentanil， optimize clinical treatment strategies， and conduct large- scale clinical trials to standardize the drug use plan， while paying attention to its long-term effects and the development of multimodal treatment plans to promote the further development of EA prevention and treatment plans.

OBJECTIVES: We propose a sparse-view cone-beam CT reconstruction algorithm based on bidirectional flow field guided projection completion (BBC-Recon) to solve the ill-posed inverse problem in sparse-view cone-beam CT imaging. METHODS: The BBC-Recon method consists of two main modules: the projection completion module and the image restoration module. Based on flow field estimation, the projection completion module, through the designed bidirectional and multi-scale correlators, fully calculates the correlation information and redundant information among projections to precisely guide the generation of bidirectional flow fields and missing frames, thus achieving high-precision completion of missing projections and obtaining pseudo complete projections. The image restoration module reconstructs the obtained pseudo complete projections and then refines the image to remove the residual artifacts and further improve the image quality. RESULTS: The experimental results on the public datasets of Mayo Clinic and Guilin Medical University showed that in the case of a 4-fold sparse angle, compared with the suboptimal method, the BBC-Recon method increased the PSNR index by 1.80% and the SSIM index by 0.29%, and reduced the RMSE index by 4.12%; In the case of an 8-fold sparse angle, the BBC-Recon method increased the PSNR index by 1.43% and the SSIM index by 1.49%, and reduced the RMSE index by 0.77%. CONCLUSIONS The BBC-Recon algorithm fully exploits the correlation information between projections to allow effective removal of streak artifacts while preserving image structure information, and demonstrates significant advantages in maintaining inter-slice consistency.
Algorithms ; Cone-Beam Computed Tomography/methods* ; Image Processing, Computer-Assisted/methods* ; Humans

OBJECTIVES: We propose a segmented backprojection tensor degradation feature encoding (SBP-MAC) model for motion artifact correction in dental cone beam computed tomography (CBCT) to improve the quality of the reconstructed images. METHODS: The proposed motion artifact correction model consists of a generator and a degradation encoder. The segmented limited-angle reconstructed sub-images are stacked into the tensors and used as the model input. A degradation encoder is used to extract spatially varying motion information in the tensor, and the generator's skip connection features are adaptively modulated to guide the model for correcting artifacts caused by different motion waveforms. The artifact consistency loss function was designed to simplify the learning task of the generator. RESULTS: The proposed model could effectively remove motion artifacts and improve the quality of the reconstructed images. For simulated data, the proposed model increased the peak signal-to-noise ratio by 8.28%, increased the structural similarity index measurement by 2.29%, and decreased the root mean square error by 23.84%. For real clinical data, the proposed model achieved the highest expert score of 4.4221 (against a 5-point scale), which was significantly higher than those of all the other comparison methods. CONCLUSIONS The SBP-MAC model can effectively extract spatially varying motion information in the tensors and achieve adaptive artifact correction from the tensor domain to the image domain to improve the quality of reconstructed dental CBCT images.
Cone-Beam Computed Tomography/methods* ; Artifacts ; Humans ; Motion ; Image Processing, Computer-Assisted/methods* ; Signal-To-Noise Ratio ; Algorithms

OBJECTIVE: To elucidate the role and mechanism of microRNA-145-5p (miR-145-5p) in hypoxia-induced pyroptosis of human alveolar epithelial cells. METHODS: In vitro, human alveolar epithelial cell line BEAS-2B was cultured. Cells in the logarithmic growth phase were cultured to 80% confluence and then used for the experiment. (1) BEAS-2B cells were cultured under 1% O₂ hypoxic condition, with a normoxic control group. Western blotting was employed to detect the expressions of pyroptosis marker proteins [NOD-like receptor protein 3 (NLRP3), Gasdermin D N-terminal domain (GSDMD-N), and caspase-1] in cells cultured for 24 hours. Real-time fluorescent quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of miR-145-5p in cells cultured for 6 hours and 12 hours. (2) Cells were transfected with 30 nmol/L miR-145-5p mimic to overexpress miR-145-5p expression under normoxic condition or 30 nmol/L miR-145-5p inhibitor to suppress miR-145-5p expression under hypoxic condition. Control group and negative control group were respectively set up. After 24 hours of cell culture, Western blotting was used to detect the expressions of pyroptosis marker proteins and nuclear factor-E2-related factor 2 (Nrf2) in cells. Flow cytometry was applied to detect the level of reactive oxygen species (ROS) in cells. The target genes of miR-145-5p were predicted by miR target gene prediction software miRWalk and verified by Western blotting. (3) Under hypoxic condition, cells were transfected with 6.94 ng/μL silent information regulator 5 (Sirt5) overexpression plasmid or pretreated with 12.5 mmol/L N-acetyl-L-cysteine (NAC) as an ROS inhibitor. The empty plasmid group and control group were set up. After 24 hours of cell culture, Western blotting was used to detect the expressions of Sirt5, Nrf2, and pyroptosis marker proteins in cells. Flow cytometry was used to detect the level of ROS in cells. RESULTS: (1) Compared with the normoxic control group, the expression levels of pyroptosis marker proteins in the 24-hour hypoxia group was significantly increased, indicating that hypoxia could induce pyroptosis in BEAS-2B cells. The expression level of miR-145-5p in cells gradually increased with the extension of hypoxia induction time, indicating that hypoxia could cause the increase of miR-145-5p expression level. (2) The expression levels of pyroptosis marker proteins in cells of miR-145-5p mimic group significantly increased under normoxic condition as compared with the control and negative control groups [NLRP3 protein (NLRP3/β-actin): 1.58±0.07 vs. 1.00±0.01, 0.98±0.07, GSDMD-N protein (GSDMD-N/β-actin): 1.71±0.03 vs. 1.01±0.01, 0.85±0.03, caspase-1 protein (caspase-1/β-actin): 2.33±0.04 vs. 1.01±0.01, 1.05±0.04, all P < 0.05], Nrf2 protein expression level was significantly decreased (Nrf2/β-actin: 0.79±0.03 vs. 1.00±0.01, 1.03±0.04, both P < 0.05), ROS level was significantly up-regulated (fluorescence intensity: 1.74±0.03 vs. 1.00±0.01, 0.92±0.03, both P < 0.05). Under hypoxia condition, compared with control group and negative control group, the expression levels of pyroptosis marker proteins in miR-145-5p inhibitor group were significantly decreased [NLRP3 protein (NLRP3/β-actin): 0.21±0.04 vs. 1.70±0.02, 1.63±0.04; GSDMD-N protein (GSDMD-N/β-actin): 1.32±0.02 vs. 2.51±0.02, 2.72±0.03; caspase-1 protein (caspase-1/β-actin): 0.56±0.01 vs. 2.77±0.02, 3.12±0.03; all P < 0.05], Nrf2 protein expression level was significantly increased (Nrf2/β-actin: 1.57±0.04 vs. 1.22±0.01, 1.28±0.04, both P < 0.05), ROS level was significantly down-regulated (fluorescence intensity: 0.64±0.05 vs. 1.87±0.04, 1.70±0.07, both P < 0.05). The results indicated that miR-145-5p could promote cell pyrodeath. The predictive result of miRWalk showed that the 3' untranslated region (3'UTR) of Sirt5 had complementary base binding sites with miR-145-5p. The expression level of Sirt5 protein in cells of miR-145-5p mimic group was significantly lower than that of control group and negative control group under normoxic condition (Sirt5/β-actin: 0.59±0.03 vs. 1.00±0.01, 1.01±0.03, both P < 0.05), which verified that Sirt5 was the target gene of miR-145-5p. (3) The occurrence of pyrodeath could be partially reversed by transfection with Sirt5 overexpression plasmid or adding ROS inhibitor NAC into cells, and Sirt5 overexpression could also up-regulate Nrf2 expression and eliminate intracellular ROS. CONCLUSION In human alveolar epithelial cells, miR-145-5p can down-regulate Nrf2 by targeting Sirt5, thereby increasing ROS expression and inducing pyrodeath.
Humans ; MicroRNAs ; Pyroptosis ; Cell Hypoxia ; Alveolar Epithelial Cells/cytology* ; Cell Line ; NLR Family, Pyrin Domain-Containing 3 Protein ; Caspase 1/metabolism* ; Epithelial Cells/metabolism* ; Gasdermins ; Phosphate-Binding Proteins

N⁶-methyladenosine (m⁶A) modification plays a critical role in cell cycle regulation, while the mechanism of m⁶A in regulating mitosis remains underexplored. Here, we found that the total m⁶A modification level in cells increased during mitosis by the liquid chromatography-mass spectrometry/mass spectrometry and m⁶A dot blot assays. Silencing methyltransferase-like 3 (METTL3) or METTL14 results in delayed mitosis, abnormal spindle assembly, and chromosome segregation defects by the immunofluorescence. By analyzing transcriptome-wide m⁶A targets in HeLa cells, we identified polo-like kinase 1 (PLK1) as a key gene modified by m⁶A in regulating mitosis. Specifically, through immunoblotting and RNA pulldown, m⁶A modification inhibits PLK1 translation via YTH N⁶-methyladenosine RNA binding protein 1, thus mediating cell cycle homeostasis. Demethylation of PLK1 mRNA leads to significant mitotic abnormalities. These findings highlight the critical role of m⁶A in regulating mitosis and the potential of m⁶A as a therapeutic target in proliferative diseases such as cancer.
Humans ; Polo-Like Kinase 1 ; Cell Cycle Proteins/metabolism* ; Proto-Oncogene Proteins/metabolism* ; Protein Serine-Threonine Kinases/metabolism* ; Mitosis/physiology* ; HeLa Cells ; Adenosine/genetics* ; Methyltransferases/metabolism* ; RNA, Messenger/metabolism* ; RNA-Binding Proteins/metabolism*

Objective:To detect the cystic fibrosis transmembrane transduction regulator(CFTR)gene mutations and congenital bilateral absence of vas deferens(CBAVD)susceptibility gene mutations in pa-tients with CBAVD,and to explore their association with the risk of CBAVD.Methods:Whole-exome sequencing and Sanger sequencing validation were conducted on the pathogenic genes CFTR,adhesion G protein-coupled receptor G2(ADGRG2),sodium channel epithelial 1 subunit beta(SCNN1B),carbonic anhydrase 12(CA12),and solute carrier family 9 member A3(SLC9A3)in thirteen cases of isolated CBAVD patients.The polymorphic loci,intron and flanking sequences of CFTR gene were amplified by polymerase chain reaction(PCR)followed by Sanger sequencing.Bioinformatics methods were employed for conservative analysis and deleterious prediction of novel susceptibility gene mutations in CBAVD.Ge-netic analysis was performed on the pedigree of one out of thirteen patients with CBAVD to evaluate the risk of inheritance in offspring.Results:Exome sequencing revealed CFTR gene exon mutations in only six of the thirteen CBAVD patients,with six missense mutations c.2684G＞A(p.Ser895Asn),c.4056G＞C(p.Gln1352His),c.2812G＞(p.Val938Leu),c.3068T＞G(p.Ile1023Arg),c.374T＞C(p.Ile125Thr),c.1666A＞G(p.Ile556Val)),and one nonsense mutation(c.1657C＞T(p.Arg553Ter).Among these six patients,two also had the CFTR homozygous p.V470 site,additional-ly,mutations in CFTR gene exon regions were not detected in the remaining seven patients.Within the thirteen CBAVD patients,three carried the homozygous p.V470 polymorphic site,four carried the 5T al-lele,two carried the TG13 allele,and ten carried the c.-966T＞G site.Four CBAVD patients simulta-neously carried 2-3 of the aforementioned CFTR gene mutation sites.Susceptibility gene mutations in CBAVD among the thirteen patients included one ADGRG2 missense mutation c.2312A＞G(p.Asn771Ser),two SLC9A3 missense mutations c.2395T＞C(p.Cys799Arg),c.493G＞A(p.Val165Ile),one SCNN1B missense mutation c.1514G＞A(p.Arg505His),and one CA12 missense mutation c.1061C＞T(p.Ala354Val).Notably,the SLC9A3 gene c.493 G＞A(p.Val165Ile)mutation site was first identi-fied in CBAVD patients.The five mutations exhibited an extremely low population mutation frequency in the gnomAD database,classifying them as rare mutations.Predictions from Mutation Taster and Poly-phen-2 software indicated that the harmfulness level of the SLC9A3 gene c.493G＞A(p.Val165Ile)site and the SCNN1B gene c.1514G＞A(p.Arg505His)site were disease causing and probably damaging.The genetic analysis of one pedigree revealed that the c.1657C＞T(p.Arg553Ter)mutation in the proband was a de novo mutation,as neither the proband's father nor mother carried this mutation.The proband and his spouse conceived a daughter through assisted reproductive technology,and the daughter inherited the proband's pathogenic mutation c.1657C＞T(p.Arg553Ter).Conclusion:CFTR gene mutations remain the leading cause of CBAVD in Chinese patients;however,the distribution and fre-quency of mutations differ from data reported in other domestic and international studies,highlighting the need to expand the CFTR mutation spectrum in Chinese CBAVD patients.The susceptibility genes ADGRG2,SLC9A3,SCNN1B,and CA12 may explain some cases of CBAVD without CFTR mutations.Given the lack of specific clinical manifestations in CBAVD patients,it is recommended that clinicians conduct further physical examinations and consider scrotal or transrectal ultrasound before making a defi-nitive diagnosis.It is advisable to employ CFTR gene mutation testing in preconception genetic screening to reduce the risk of CBAVD and cystic fibrosis in offspring.

Objective To propose a CT truncated data reconstruction model(DDTrans)based on projection and image dual-domain Transformer coupled feature learning for reducing truncation artifacts and image structure distortion caused by insufficient field of view(FOV)in CT scanning.Methods Transformer was adopted to build projection domain and image domain restoration models,and the long-range dependency modeling capability of the Transformer attention module was used to capture global structural features to restore the projection data information and enhance the reconstructed images.We constructed a differentiable Radon back-projection operator layer between the projection domain and image domain networks to enable end-to-end training of DDTrans.Projection consistency loss was introduced to constrain the image forward-projection results to further improve the accuracy of image reconstruction.Results The experimental results with Mayo simulation data showed that for both partial truncation and interior scanning data,the proposed DDTrans method showed better performance than the comparison algorithms in removing truncation artifacts at the edges and restoring the external information of the FOV.Conclusion The DDTrans method can effectively remove CT truncation artifacts to ensure accurate reconstruction of the data within the FOV and achieve approximate reconstruction of data outside the FOV.

Objective We propose a dual-domain cone beam computed tomography(CBCT)reconstruction framework DualCBR-Net based on improved differentiable domain transform for cone-angle artifact correction.Methods The proposed CBCT dual-domain reconstruction framework DualCBR-Net consists of 3 individual modules:projection preprocessing,differentiable domain transform,and image post-processing.The projection preprocessing module first extends the original projection data in the row direction to ensure full coverage of the scanned object by X-ray.The differentiable domain transform introduces the FDK reconstruction and forward projection operators to complete the forward and gradient backpropagation processes,where the geometric parameters correspond to the extended data dimension to provide crucial prior information in the forward pass of the network and ensure the accuracy in the gradient backpropagation,thus enabling precise learning of cone-beam region data.The image post-processing module further fine-tunes the domain-transformed image to remove residual artifacts and noises.Results The results of validation experiments conducted on Mayo's public chest dataset showed that the proposed DualCBR-Net framework was superior to other comparison methods in terms of artifact removal and structural detail preservation.Compared with the latest methods,the DualCBR-Net framework improved the PSNR and SSIM by 0.6479 and 0.0074,respectively.Conclusion The proposed DualCBR-Net framework for cone-angle artifact correction allows effective joint training of the CBCT dual-domain network and is especially effective for large cone-angle region.

Objective We propose a motion artifact correction algorithm(DMBL)for reducing motion artifacts in reconstructed dental cone-beam computed tomography(CBCT)images based on deep blur learning.Methods A blur encoder was used to extract motion-related degradation features to model the degradation process caused by motion,and the obtained motion degradation features were imported in the artifact correction module for artifact removal.The artifact correction module adopts a joint learning framework for image blur removal and image blur simulation for treatment of spatially varying and random motion patterns.Comparative experiments were conducted to verify the effectiveness of the proposed method using both simulated motion data sets and clinical data sets.Results The experimental results with the simulated dataset showed that compared with the existing methods,the PSNR of the proposed method increased by 2.88%,the SSIM increased by 0.89%,and the RMSE decreased by 10.58%.The results with the clinical dataset showed that the proposed method achieved the highest expert level with a subjective image quality score of 4.417(in a 5-point scale),significantly higher than those of the comparison methods.Conclusion The proposed DMBL algorithm with a deep blur joint learning network structure can effectively reduce motion artifacts in dental CBCT images and achieve high-quality image restoration.