Intracranial aneurysm is a life-threatening cerebrovascular disease. Recent studies have shown that irregular pulsations are associated with an increased risk of rupture. Currently, there is an urgent need for an objective and real-time method for analyzing wall deformation associated with irregular pulsations. In this study, we developed a fast and robust analytical framework based on an improved Horn-Schunck optical flow method. Verification experiments demonstrated that the proposed method exhibited sufficient accuracy and robustness. Patient-specific deformation analysis showed that irregular pulsation sites exhibited higher displacement and strain values compared with other regions of the aneurysm surface. The maximum first principal strains were significantly higher in intracranial aneurysms with irregular pulsation than in those without irregular pulsation (0.26 [0.20-0.28] vs. 0.19 [0.18-0.20], p=0.032; Wilcoxon rank-sum test). Overall, this framework can objectively identify irregular pulsations during the cardiac cycle and offers straightforward, user-friendly applicability for clinical diagnosis.

OBJECTIVES:This study aimed to evaluate the accuracy of non-contrast 4D-magnetic resonance angiography (4D-MRA) techniques (4D-PACK and 4D-S-PACK) in assessing collateral circulation via the Circle of Willis (CoW) in patients with internal carotid artery occlusion (ICAO), using digital subtraction angiography (DSA) as the reference standard. METHODS:In this prospective study, patients with ICAO underwent multi-contrast MRA (3D TOF-MRA, CE-MRA, 4D-PACK, and 4D-S-PACK) and DSA within 1 week. Using DSA as the reference, the diagnostic accuracy of each MRA technique was independently assessed for ICAO occlusion, CoW anatomy, and collateral pathway patterns. The 4D-MRA acquisitions included time points of 100, 200, 500, 800, 1200, 1600, and 2000 ms. Additionally, the optimal 4D-S-PACK protocol and its capacity to determine CoW flow direction were evaluated. RESULTS:A total of 19 patients with 21 ICAOs were included. Combined 4D-MRA (4D-PACK plus 4D-S-PACK) demonstrated high diagnostic accuracy for detecting ICAO (100.0%) and CoW anatomy (98.2%). In assessing collateral pathways, combined 4D-MRA (sensitivity 95.2%, specificity 100.0%, accuracy 98.2%) outperformed TOF-MRA (sensitivity 85.7%, specificity 86.1%, accuracy 86.0%) and CE-MRA (sensitivity 100.0%, specificity 86.1%, accuracy 91.2%). Using 3 time points (200, 800, and 2000 ms), 4D-S-PACK significantly reduced scan time while maintaining accurate flow direction assessment. CONCLUSIONS:Combined non-contrast 4D-PACK and 4D-S-PACK is a promising, non-invasive alternative for comprehensively evaluating ICAO, CoW morphology, and collateral circulation. ADVANCES IN KNOWLEDGE:This study establishes that a combined non-contrast 4D-MRA protocol surpasses standard MRA techniques in collateral pathway accuracy, providing a viable, non-invasive alternative to DSA.

OBJECTIVE:To explore the clinical features and prognosis of myelodysplastic syndrome with ring sideroblasts (MDS-RS) patients with wild-type splicing factor 3B subunit 1 (SF3B1 ). METHODS:The bone marrow samples from 132 patients with MDS-RS who were initially diagnosed at Shanghai Sixth People's Hospital affiliated to Shanghai Jiao Tong University School of Medicine from January 2009 to February 2021 were collected. Next generation sequencing (NGS)was used to obtain gene mutation information of patients (covering all core mutation genes of MDS), with a particular focus on analyzing the clinical characteristics, co-mutation profiles, and prognosis of MDS-RS patients with wild-type SF3B1 . RESULTS:Among the 132 MDS-RS patients, 50 cases (37.9%) were negative for SF3B1 mutations, of which 39 patients (78%) had concurrent mutations in other genes. The common accompanying mutations were TP53 (15 cases), DNMT3A (10 cases), U2AF1 (8 cases), TET2 (7 cases), ASXL1 (7 cases), and RUNX1 (6 cases), and SETBP1 (3 cases). In the 82 cases (62.1%) who were positive for SF3B1 mutations, the highest occurrence frequency was SF3B1 K700E mutation (42 cases). Additionally, 57 patients (69.51%) had concurrent mutations in other genes, with the top three highest mutation frequencies observed in ASXL1 (13 cases), DNMT3A (11 cases), and RUNX1 (7 cases). Compared to patients with SF3B1 mutations, those with wild-type SF3B1 exhibited significant pancytopenia and higher risk of IPSS-R and IPSS-M prognostic scores. The median overall survival (OS) of patients with wild-type SF3B1 was 22 months, which was significantly shorter than 55 months of SF3B1 mutated patients (P < 0.05), and they also had a higher risk of transformation to acute myeloid leukemia (AML) (P < 0.05). Multivariate analysis revealed that SF3B1 mutation was not an independent prognostic factor affecting MDS-RS, and its prognostic value might be influenced by mutation sites, co-mutations, and other factors. CONCLUSION:Patients with wild-type SF3B1 have a significantly shorter OS compared to those with SF3B1 mutations, and they also have a higher risk of transformation to AML, which may be associated with TP53 mutations.

Blast lung injury (BLI) poses great challenges for early diagnosis and precise treatment. This review systematically summarizes the evolution of relevant biomarkers from conventional inflammatory indicators to newly identified molecular markers related to cell injury, inflammation, oxidative stress, and epigenetic regulation. It also discusses imaging combination strategies, multi-omics applications, current translational obstacles, and future research trends. This work provides valuable theoretical references for improving diagnostic accuracy, optimizing prognostic evaluation, and developing targeted therapies for BLI.

ABSTRACT:Acute graft-versus-host disease (aGVHD) contributes to significant morbidity after allogeneic hematopoietic cell transplantation (allo-HCT). We aimed to develop and validate a clinical score to identify patients with significantly different risk for developing aGVHD. Analysis included adults who underwent allo-HCT during 2008-2019. Eligibility criteria were widely inclusive of transplant indications, donor types, graft types, conditioning regimens, and GVHD prophylaxis regimens. The final cohort of 21 796 patients was randomly split into training and validation cohorts, with 15 258 (70%) and 6538 (30%) patients, respectively. The primary outcome was grade 2 to 4 aGVHD, and the secondary outcome was grade 3 to 4 aGVHD, by day 100 posttransplant. Risk scores were developed using the training cohort, tested using the validation cohort, and stratified into 4 percentile groups. The odds of grade 2 to 4 aGVHD by day 100 posttransplant were 1.50 (95% confidence interval [CI], 1.29-1.75; P< .0001) for the 25th to 50th percentile group, 2.0 (95% CI, 1.78-2.40; P< .0001) for the 50th to 75th percentile group, and 3.1 (95% CI, 2.72-3.65; P< .0001) for the >75th percentile group compared with the ≤25th percentile group in the validation cohort. The odds of grade 3 to 4 aGVHD by day 100 posttransplant were 1.4 (95% CI, 1.11-1.74; P = .0043) in the 25th to 50th percentile group, 2.0 (95% CI, 1.61-2.49; P< .0001) in the 50th to 75th percentile group, and 3.2 (95% CI, 2.64-3.98; P< .0001) in the >75th percentile group compared with the ≤25th percentile group in the validation cohort. Here, to our knowledge, we have developed the first validated, widely inclusive clinical risk score for the development of aGVHD after allo-HCT.

Irregular wall pulsation is a distinctive feature of certain intracranial aneurysms (IAs) identified by four-dimensional computed tomography angiography (4D-CTA). While clinical studies have demonstrated the association of irregular pulsation with aneurysm instability or rupture, the underlying biomechanical mechanisms remain poorly understood. In this study, we utilized the coherent point drift algorithm combined with elastic theory and computational fluid dynamics to quantify biomechanical parameters of IAs with irregular pulsation based on 4D-CTA images. The methodology was applied to three patient-specific IAs with clinically confirmed irregular pulsation. Obtained results revealed that aneurysm wall regions with irregular pulsation generally displayed large wall displacement, which was either accompanied or not accompanied by high strain. Notably, large displacement or high strain could also be detected in some aneurysm wall regions without irregular pulsation, as well as in adjacent normal arteries. Hemodynamic simulations demonstrated the presence of low and oscillatory wall shear stress (WSS) in irregular pulsation regions. Comparisons between dynamic hemodynamic models (incorporating wall movement) and static hemodynamic models (with rigid walls) further revealed the role of irregular pulsation in amplifying WSS oscillation, which implies that the degradation of wall mechanics in aneurysm regions with irregular pulsation may interact with hemodynamic disturbance in a mutually reinforcing manner. In summary, the findings of our study suggest that quantifying biomechanical parameters in both the wall and sac of aneurysm may provide valuable insights for assessing the risk of IAs, particularly those exhibiting irregular pulsation.

Immunotherapy has achieved limited efficacy in prostate cancer (PCa), largely due to its profoundly immunosuppressive tumor microenvironment (TME). However, the metabolic mechanisms underpinning this immune resistance remain poorly defined. Here, we identify lactate dehydrogenase A (LDHA)-driven lactate metabolism as a critical regulator of myeloid-derived suppressor cell (MDSC) activation in PCa. Integrated metabolomic, single-cell, and spatial transcriptomic analyses revealed that LDHA is highly expressed in PCa malignant epithelial cells and correlates with increased lactate production and immune exclusion. LDHA-high tumors exhibited enriched infiltration of polymorphonuclear MDSCs (PMN-MDSCs), which were spatially co-localized with LDHA-positive tumor regions. Mechanistically, lactate uptake through monocarboxylate transporter 1 (MCT1) enhanced PMN-MDSC differentiation and upregulated Arg1 and NOS2, reinforcing T cell suppression. Genetic ablation of LDHA in murine models markedly reduced PMN-MDSC infiltration, restored CD8+T cell activity, and inhibited tumor growth. Pharmacological inhibition of LDHA with FX-11 synergized with anti-PD-L1 therapy, producing durable tumor regression. Collectively, these findings define LDHA-driven lactate metabolism as a key metabolic checkpoint in PCa immune evasion and provide a rationale for combining LDHA inhibition with immune checkpoint blockade to overcome immunotherapy resistance.

Blast lung injury (BLI) is characterized by pulmonary inflammatory response and tissue injury. A rat BLI model was established using a biomedical shock tube, and the animals were divided into three groups: control, BLI model, and IL-17 A inhibitor groups. We assessed pulmonary function parameters, observed lung hemorrhage and pleural effusion, measured white cell counts in bronchoalveolar lavage fluid (BALF), quantified histopathological scores using hematoxylin and eosin (HE) staining, and analyzed the protein expression levels of IL-17 A, phospho-NF-κB p65, and inhibitor of κB kinase β (IKK-β) by Western blotting. Compared with the control group, the model group exhibited significantly increased respiratory frequency and airway resistance index. In contrast, the IL-17 A inhibitor group demonstrated significantly improved minute ventilation and peak inspiratory and expiratory flow rates. The inhibitor group also demonstrated reduced pulmonary hemorrhage and pleural effusion, lower BALF white cell counts, and reduced histopathological scores. Western blot analysis revealed that the expression levels of IL-17 A, p-p65, and IKK-β were upregulated in the model group, but were robustly suppressed by IL-17 A inhibition. In conclusion, IL-17 A inhibition effectively attenuated blast-induced pulmonary inflammatory injury, improved pulmonary function, and mitigated histopathological injury, potentially through modulation of the IL-17 A/NF-κB signaling pathway.

Abstract Background As a novel inflammatory-nutritional biomarker, the C-reactive protein–albumin–lymphocyte (CALLY) index has demonstrated significant prognostic value in several cancer types. However, its predictive significance for patients with locally advanced non-small cell lung cancer (LA-NSCLC) treated with thoracic radiotherapy (RT) remains elusive. This study aimed to investigate the relationship between the pre/post-treatment CALLY index and the prognosis of patients with LA-NSCLC treated with thoracic RT. Methods In this retrospective study, a cohort of 218 LA-NSCLC patients who underwent thoracic RT between 2012 and 2018 was assessed. The calculation of CALLY involved the use of C-reactive protein (CRP) level, albumin level, and lymphocyte count. Cox proportional hazards regression and the Kaplan-Meier survival analyses were employed to analyze the relationships between various variables and overall survival (OS), local progression-free survival (LPFS), and distant metastasis-free survival (DMFS). Results Multivariate Cox analysis revealed that post-treatment CALLY values were significantly associated with OS, LPFS, and DMFS. Patients with lower post-treatment CALLY values exhibited poorer survival outcomes compared with those with higher CALLY values. Conclusions These findings demonstrate that the post-treatment CALLY index could be a valuable tool for predicting prognosis and guiding subsequent treatment strategies in patients with LA-NSCLC undergoing thoracic RT. Further prospective studies are warranted to validate these results and to explore the potential of incorporating the CALLY index into clinical decision-making.

Cervical cancer remains the most prevalent gynecological malignant disease. Reprogramming tumor immune metabolism stands out as a novel promising therapeutic target. Here, we identified serine incorporator 2 (SERINC2) as a critical gene which highly expressed in cervical cancer and negatively correlated with clinical outcomes. Through functional assays, SERINC2 was determined to play a pro-tumoral role both in vivo and in vitro. Besides, the growth of cervical cancer cells was found to be largely dependent on serine in a manner influenced by SERINC2. As a serine transport associated protein, SERINC2 knockdown significantly reduced cervical cancer cells' intracellular serine level and altered the serine-associated-lipid metabolism. Immune infiltration analysis revealed that SERINC2 was negatively associated with CD8+ T cell infiltration and function. More importantly, we demonstrated a competitive relation between cancer cells and immune cells brought about by SERINC2. Mechanistically, cancer cells SERINC2 preferentially competed for micro-environmental serine over CD8+ T cells and rendered T cell exhaustion. Overall, SERINC2 remodels cancer development and serine metabolism in the tumor immune microenvironment (TIME), establishing an immunosuppressive and pro-tumoral milieu.

Tumour protein p53 (TP53) mutations occur frequently in myelodysplastic syndromes (MDS) and are associated with a high risk of treatment failure and adverse outcomes. In this study, we analysed 1219 patients with MDS, focusing on the clinical and molecular characteristics of those with TP53 mutations and investigating factors contributing to worse survival and disease progression. One hundred and fifteen (9.4%) patients carried TP53 alterations, of which 70.4% had biallelic and 29.6% had monoallelic alterations. Individuals with biallelic mutations showed elevated bone marrow (BM) blasts (p < 0.001), decreased platelet counts (p = 0.007) and higher the Revised International Prognostic Scoring System (IPSS-R) and Molecular International Prognostic Scoring System (IPSS-M) categories. The biallelic variants, complex karyotype, -7, del(7q) and higher BM blast were linked to worse survival and a higher risk of acute myeloid leukaemia (AML) transformation in TP53-mutated patients. SF3B1 mutations were protective factors for both end-points within TP53-mutated MDS. These characteristics are very similar to populations from the International Working Group for the Prognosis of MDS (IWG-PM) cohort. By performing longitudinal sequencing, we revealed the acquisition or clonal amplification of TP53 alterations during AML transformation. We also conducted repeated sequencing in patients who achieved complete remission (CR) and observed that TP53 mutations were undetectable in 10 of 12 patients. Our findings revealed the clinical significance of TP53 mutations in MDS and highlighted the importance of early detection and dynamic monitoring of TP53 during treatment.

Aim:Intracranial aneurysms pose significant challenges in diagnosis and treatment, emphasizing the need for accurate segmentation methods to assist clinicians in their management. In this paper, we present a novel approach for segmenting intracranial aneurysms using three-dimensional time-of-flight magnetic resonance angiography (TOF-MRA) images and the no-new-U-net framework. We aim to improve segmentation accuracy and efficiency through the integration of hybrid loss functions and additional vessel information. Methods:The model was conducted on Aneurysm Detection And SegMentation (ADAM) and Renji Hospital (RENJI) datasets. The TOF-MRA ADAM dataset contains data from 113 cases, where 89 have at least one aneurysm with a median maximum diameter of 3.6 mm and range from 1.0 to 15.9 mm. The RENJI private TOF-MRA dataset comprises 213 cases including both ruptured and unruptured aneurysms with a median maximum diameter of 9.35 mm (range: 1.25-37.58 mm). We optimized the segmentation model by exploring hybrid loss functions that combine distribution-based and region-based losses to effectively delineate intricate aneurysm structures. Additionally, we incorporated vessel information as a region of interest using an automatic vessel segmentation algorithm to enhance the model's focus on critical regions. The model was trained on multi-modality data, including both vessel-enhanced and original images, to capture complementary information and improve segmentation accuracy. Results:Extensive simulations on both the ADAM dataset and a private RENJI dataset demonstrate the effectiveness of our approach. The best-performing loss function yielded significant improvements in the Dice coefficient (0.72 and 0.54) and Sensitivity (0.69 and 0.53) on the RENJI and ADAM datasets, respectively. Conclusions:The proposed method offers a promising solution for accurately segmenting intracranial aneurysms, showcasing superior performance compared to existing approaches. By integrating hybrid loss functions and vessel information, we enhance the model's ability to delineate intricate aneurysm structures, contributing to improved diagnosis and treatment planning for patients with intracranial aneurysms.

BACKGROUND:Unruptured intracranial aneurysms (IAs) that become symptomatic have been associated with instability. OBJECTIVE:To investigate the relationship between irregular pulsation on four-dimensional CT angiography (4D-CTA) and aneurysm wall enhancement (AWE) on vessel wall MRI (VW-MRI), and to evaluate their ability to identify symptomatic IAs. METHODS:This retrospective study included consecutive patients with IAs who underwent 4D-CTA and VW-MRI between March 2018 and May 2023. IAs were categorized as asymptomatic and symptomatic. The presence of irregular pulsation was identified on 4D-CTA video. Qualitative and quantitative AWE were evaluated. Univariate and multivariate analyses were used to identify the parameters associated with symptoms. RESULTS:192 patients with 216 aneurysms (167 asymptomatic and 49 symptomatic) were included. IAs with irregular pulsation had significantly higher wall enhancement index (WEI) than IAs without irregular pulsation (median (IQR), 0.5 (0.2-1.1) vs 0.2 (0.0-0.6), P<0.001). Symptomatic IAs had significantly higher WEI than asymptomatic IAs (median (IQR), 0.7 (0.3-1.5) vs 0.2 (0.0-0.5), P<0.001), and more irregular pulsations (79.6% vs 25.1%, P<0.001). Both irregular pulsation (OR=6.86; 95% CI 2.62 to 17.96; P<0.001) and WEI (OR=2.56; 95% CI 1.14 to 5.71; P=0.022) were independently associated with symptoms. Combination of irregular pulsation and WEI achieved the highest area under the curve of 0.86 in identifying symptomatic aneurysms compared with irregular pulsation or WEI alone (P<0.001 and P=0.002, respectively). CONCLUSION:In a large cohort of patients with unruptured IAs who underwent 4D-CTA and VW-MRI, both irregular pulsation and WEI were independently associated with symptoms. Such measures could identify IAs at higher risk of growth or rupture.

Three-dimensional magnetic resonance vessel wall imaging (3D MR-VWI) is critical for characterizing cerebrovascular pathologies, yet its clinical adoption is hindered by labor-intensive postprocessing. We developed VWI Assistant, a multi-sequence integrated deep learning platform trained on multicenter data (study cohorts 1981 patients and imaging datasets) to automate artery segmentation and reconstruction. The framework demonstrated robust performance across diverse patient populations, imaging protocols, and scanner manufacturers, achieving 92.9% qualified rate comparable to expert manual delineation. VWI Assistant reduced processing time by over 90% (10–12 min per case) compared to manual methods (p < 0.001) and improved inter-/intra-reader agreement. Real-world deployment (n = 1099 patients) demonstrated rapid clinical adoption, with utilization rates increasing from 10.8% to 100.0% within 12 months. By streamlining 3D MR-VWI workflows, VWI Assistant addresses scalability challenges in vascular imaging, offering a practical tool for routine use and large-scale research, significantly improving workflow efficiency while reducing labor and time costs.

ABSTRACT Purpose To investigate the clinical characteristics and prognosis of mutation spots and concomitant gene mutations in myelodysplastic syndromes (MDS) with SF3B1 mutation (SF3B1mut). Patients and Methods Patients diagnosed with MDS at Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital from October 2008 to November 2023 were enrolled in this study. SF3B1mut was identified by next‐generation sequencing (NGS). Results One hundred and seven (8.7%) cases harbored the SF3B1 mutation. The most frequent SF3B1mut, noted in 47.66% of all patients, was the hotspot K700E. K666 and R625 were observed in 24.30% and 9.35%, respectively. Two less frequent mutation subtypes accounted for 5.61% of H662 and 4.67% of E622. Patients with the K666 mutation showed more severe thrombocytopenia (p = 0.032), significantly lower NK cell percentage (p = 0.001), and the Th1/Th2 ratio (p = 0.018) in the bone marrow (BM). The overall survival (OS) in patients with E622 and H662 mutations was significantly longer than that of patients with the R625 mutation (p = 0.045) and the K666 mutation (p = 0.010). Multi‐variance analysis showed the SF3B1 mutation involving the K666 hotspot independently predicted overall survival in MDS (HR 2.094, p = 0.050). Notably, most (11/13, 84.6%) of concomitant TP53 mutations were mono‐hit, which did not affect the survival of patients in our cohort. Conclusions SF3B1mut patients with specific mutation spots and concomitant gene mutations showed distinct clinical features and prognosis. Consequently, a comprehensive study of specific subtypes is of great significance for improving the prognosis of patients with SF3B1 mutations.

The frequent detection of wall enhancement by vessel wall imaging in unstable or ruptured intracranial aneurysms (IAs) implies the potential involvement of blood substance transport in the pathogenesis of IAs. In this study, we developed a new method for simulating the transport of low-density lipoprotein (LDL) in IAs. The method was characterized by the coupled solution of LDL transport behaviors in lumen, across endothelium, and within vessel wall, and the incorporation of a sub-model that accounts for the combined effect of wall shear stress (WSS) magnitude and oscillatory shear index (OSI) on endothelial permeability to LDL. Numerical simulations were conducted on the IAs of four patients with clinically confirmed wall enhancement status. Obtained results demonstrated the propensity of IAs for enhanced LDL deposition on the lumen surface and LDL accumulation within the wall compared to normal cerebral arteries. Notably, the spatial distributions of high LDL concentration on the lumen surface and within the vessel wall were not always consistent, indicating regional variations in biomechanical factors facilitating intraluminal retention and transmural transport of LDL. Furthermore, the IAs with wall enhancement exhibited remarkably larger area ratios of wall regions exposed to high LDL concentration than those without wall enhancement. Relatively, the area ratios of low WSS and high OSI were less predictive of aneurysm wall enhancement. These findings underscore the potential value of investigating mass transport over general hemodynamic behaviors in classifying the pathological state or assessing the risk of IAs.

High-grade serous ovarian cancer (HGSOC) is a highly aggressive gynecologic malignancy, and chemoresistance remains a major challenge in its treatment. This study identifies ZDHHC8 as a key regulator of chemotherapy sensitivity in HGSOC. Bioinformatics analysis revealed that elevated ZDHHC8 expression correlates with poorer progression-free and overall survival in chemotherapy-treated patients. Immunohistochemical analysis of clinical HGSOC samples further demonstrated that chemoresistant tumors exhibit higher levels of ZDHHC8 than chemotherapy-sensitive ones. In vitro functional assays showed that ZDHHC8 knockdown enhanced chemotherapy sensitivity by decreasing the cisplatin IC50, increasing cisplatin-induced apoptosis, and promoting DNA damage, whereas overexpression experiments reduced cisplatin sensitivity. Mechanistic studies indicated that KLF5, identified as a transcription factor through chromatin immunoprecipitation and luciferase reporter assays, directly binds to the ZDHHC8 promoter and upregulates its expression. Moreover, ZDHHC8 upregulates β-catenin, a key mediator of chemotherapy insensitivity, and its effects are reversed by a β-catenin inhibitor. Animal models further supported the roles of ZDHHC8, KLF5, and β-catenin in regulating chemotherapy sensitivity. Collectively, these results establish the KLF5-ZDHHC8-β-catenin axis as a critical pathway that impairs chemotherapy sensitivity in HGSOC and suggest that targeting ZDHHC8 may improve treatment outcomes.

Preeclampsia (PE) is associated with significant maternal and fetal morbidity and mortality, with placental trophoblast dysfunction playing a central role in its pathogenesis. Autophagic imbalance impacts trophoblast function, and the regulatory role of formyl-peptide receptor 2 (FPR2) in trophoblast autophagy and placental function requires further investigation. We used the HTR8/SVneo cell line and Fpr2 knockout mice to explore the role of FPR2 in trophoblast function. The expression of FPR2 and autophagy levels were elevated in PE patients and models. FPR2 knockdown reversed the H2O2-induced inhibition of trophoblast function and downregulated autophagy-related proteins. H2O2 activated the PI3K/AKT/mTOR pathway, but this activation was reduced by FPR2 knockdown or 3-MA pretreatment. We demonstrate that FPR2 regulates trophoblast autophagy through the PI3K/AKT/mTOR signaling pathway, contributing to the development of PE. These findings may offer new insights into the prevention and treatment of PE.

The 20q deletion (del(20q)) is a recurrent chromosomal abnormality in individuals with myelodysplastic syndrome (MDS) and is associated with favourable outcomes when isolated. This study aims to analyse the clinical features and prognostic impact of del(20q) based on cytogenetic and molecular alterations. Among 1,527 patients with MDS, 101 (6.6

Traumatic brain injury (TBI) is a complex neurological disease caused by external forces impacting the head and is one of the leading causes of mortality and disability worldwide, exerting a significant impact on public health and socioeconomic conditions. Current research on TBI has focused primarily on assessing injury severity, determining clinical treatment, and improving patient prognosis. The timely and accurate diagnosis of TBI in clinical settings and the implementation of effective therapeutic strategies remain challenging. However, a deeper understanding of changes in gene expression and underlying molecular regulatory processes may alleviate this pressing issue. MicroRNAs (miRNAs), a class of short noncoding RNA molecules, play crucial roles in cellular physiology and pathology by regulating gene expression. With advancements in research, miRNAs have garnered increasing attention in TBI studies. This review summarizes the progress of miRNA research in TBI and explores the potential of miRNAs as diagnostic and prognostic markers and therapeutic targets for TBI.