Kai Sun

Purpose: Imaging diagnosis of mild cognitive impairment (MCI) has garnered increasing attention due to its critical role in the early detection of Alzheimer's disease (AD) and other dementias. This study presents a bibliometric analysis to elucidate global research trends, key contributors, thematic clusters, and emerging topics within the field of MCI imaging diagnosis. Method: English‐language publications related to MCI imaging were retrieved from the Web of Science Core Collection (WoSCC) from January 1999 to December 2024. Bibliometric analyses were performed using VOSviewer, CiteSpace, and R‐bibliometrix to evaluate co‐authorship networks, institutional collaborations, journal impact, keyword co‐occurrence, and burst trends. Finding: A total of 7,568 articles showed an average annual growth of 22.27%, with output surging after 2007 and peaking in 2024 (n = 762). The United States led in productivity and impact, ahead of China and Italy. Leading institutions were the University of California System, Vrije Universiteit Amsterdam, and the University of London, with key authors including Clifford R. Jack Jr., Ronald C. Petersen, and Philip Scheltens. Core journals were Neurology, Neuroimage, and Brain. Cluster analysis revealed four themes: functional and cognitive networks, biomarkers and pathology, structural imaging and computational diagnostics, and guidelines. Recent trendsc (AI) (e.g., machine learning, deep learning), while citation bursts indicate an evolution from early biomarker and imaging research toward current AI and multimodal imaging for improved diagnosis and risk prediction. Conclusion: This bibliometric analysis provides a comprehensive overview of the evolving research landscape in MCI imaging diagnosis. The integration of advanced computational methodologies, particularly AI‐powered tools, is driving precision diagnostics and personalized medicine. These advancements hold significant potential to improve early detection, stratify risk, and inform therapeutic interventions, ultimately contributing to better outcomes for individuals with MCI.

Alzheimer’s dementia (AD) and mild cognitive impairment (MCI) are characterized by progressive cognitive decline. Repetitive transcranial magnetic st

Background: Insulin resistance is closely associated with pericardial fat. In this prospective study, we aimed to compare the utility of six surrogate insulin resistance indices, including the triglyceride glucose (TyG) index, TyG-waist circumference (TyG-WC), TyG-waist-to-height ratio (TyG-WHtR), lipid accumulation production (LAP), visceral adiposity index (VAI), and Chinese VAI (CVAI) in predicting pericardial fat accumulation on noncontrast computed tomography. Methods: The six surrogate insulin resistance indices (TyG, TyG-WC, TyG-WHtR, LAP, VAI, and CVAI) were calculated using their respective formulae. The pericardial fat volume (PFV) was obtained from noncontrast computed tomography scans and categorized into PFV-low (PFV-L) and PFV-high (PFV-H) via the Youden statistic according to the risk for atherosclerotic cardiovascular disease (ASCVD). A logistic regression model, receiver operating characteristic (ROC) curves, and generalized additive model were used for statistical analyses. Results: Overall, 2,735 adults were analyzed. The TyG, TyG-WC, TyG-WHtR, LAP, VAI, and CVAI were significantly higher in the PFV-H group than in the PFV-L group. All six insulin resistance surrogates showed significant positive correlations with PFV. The CVAI demonstrated the highest predictive value for assessing PFV, followed by TyG-WC, TyG-WHtR, LAP, TyG, and VAI. The CVAI was associated with the largest increase in PFV based on the original model [age, sex, diabetes, hypertension, hyperlipidemia, and estimated glomerular filtration rate (eGFR)] as compared to the other insulin resistance indices. Conclusions: The TyG, TyG-WC, TyG-WHtR, LAP, VAI, and CVAI were positively associated with PFV in patients without overt cardiovascular diseases. The CVAI may effectively reflect PFV accumulation.

Despite remarkable advancements in therapeutic strategies, a considerable proportion of patients with bladder cancer (BC) still experience disease progression and unfavorable prognosis. The heterogeneity and biological functions of tumor endothelial cells (ECs) during BC progression remain poorly understood. We collected scRNA-seq data from BC samples and identified two EC subpopulations through hierarchical clustering analysis. The activity of signaling pathways in distinct EC subpopulations was assessed utilizing AUCell analysis. Gene regulatory networks (GRN) were constructed and analyzed for different EC subpopulations using the pySCENIC algorithm. Additionally, we investigated the association between the abundance of EC subpopulations and both clinical prognosis and immune cell infiltration. The biological effects of ESM1 protein on BC cells were further validated through EdU and Transwell assays. We analyzed 7,519 CD45-negative single cells from BC tissues and discerned two distinct EC subpopulations. The two subpopulations were characterized by high expression of ESM1 (S1 ECs) and CXCL2 (S2 ECs), respectively. In S1 ECs, we observed significant activation of signaling pathways involved in tumor promotion, including angiogenesis and cell proliferation. Additionally, our GRN analysis uncovered notable differences in transcription factor activity between S1 and S2 ECs. Moreover, ESM1 protein promoted proliferation and migration of BC cells. Patients with higher abundance of the S1 EC subpopulation exhibited more unfavorable clinical outcomes and increased infiltration of inhibitory immune cells. Our findings elucidate the transcriptional profiles and biological roles of the high ESM1-expression endothelial cell subpopulation in BC. This subpopulation is associated with poor prognosis and immunosuppressive tumor microenvironment. Accordingly, targeting endothelial cells with high ESM1 expression may offer a novel therapeutic strategy for patients with BC.

Aims Assessment of left atrial (LA) function and the left atrioventricular coupling index (LACI) have recently been increasingly recognized as important indices for cardiovascular diseases associated with the presence of prediabetes and diabetes. We aimed to evaluate LA function and the LACI in patients with prediabetes and diabetes via cardiac magnetic resonance (CMR). Methods In this retrospective study, we included 35 patients with prediabetes, 32 patients with diabetes, and 84 healthy control participants. The LACI and LA total, passive, and active emptying fractions (LATEmF, LAPEmF, and LAAEmF, respectively) were calculated. The LA reservoir, conduit, and booster pump strains (ε_s, ε_e, and ε_a), and peak positive, peak early negative, and peak late negative strain rates (SRs, SRe, and SRa) were obtained via CMR-feature tracking (CMR-FT). For the statistical analyses, one-way analysis of variance, the Kruskal–Wallis test, and linear regression were conducted, and Pearson’s and interclass correlation coefficients were calculated. Results Compared with healthy control participants, patients with prediabetes or diabetes presented lower ε_s and ε_e values and a relatively preserved LACI. Patients with diabetes presented considerably reduced SRs, SRe, and LAPEmF. Elevated glycated haemoglobin (HbA1c) levels were independently associated with decreased magnitudes of ε_s, SRs, ε_e, and SRe. No significant associations were found between the LACI and the HbA1c or LA deformation parameters. We observed significant correlations between LATEmF and ε_s, LAPEmF and ε_e and between LAAEmF and ε_a. Conclusions CMR-FT provides a potential noninvasive approach for the early detection of alterations in the LA reservoir and conduit function in individuals with prediabetes and diabetes. Graphical Abstract

Background Our previous research has demonstrated that hypoxic preconditioning (HPC) can improve spatial learning and memory abilities in adult mice. Adult hippocampal neurogenesis has been associated with learning and memory. The Neurogenic locus notch homolog protein (Notch) was involved in adult hippocampal neurogenesis, as well as in learning and memory. It is currently unclear whether the Notch pathway regulates hippocampal neuroregeneration by modifying the DNA methylation status of the Notch gene following HPC. Method The HPC animal model and cell model were established through repeated hypoxia exposure using mice and the mouse hippocampal neuronal cell line HT22. Step-down test was conducted on HPC mice. Real-time PCR and Western blot analysis were used to assess the mRNA and protein expression levels of Notch1 and hairy and enhancer of split1 (HES1). The presence of BrdU-positive cells and Notch1 expression in the hippocampal dental gyrus (DG) were examined with confocal microscopy. The methylation status of the Notch1 was analyzed using methylation-specific PCR (MS-PCR). HT22 cells were employed to elucidate the impact of HPC on Notch1 in vitro. Results HPC significantly improved the step-down test performance of mice with elevated levels of mRNA and protein expression of Notch1 and HES1 (P < 0.05). The intensities of the Notch1 signal in the control group, the H group and the HPC group were 2.62 ± 0.57 × 10⁷, 2.87 ± 0.84 × 10⁷, and 3.32 ± 0.14 × 10⁷, respectively, and the number of BrdU (+) cells in the hippocampal DG were 1.83 ± 0.54, 3.71 ± 0.64, and 7.29 ± 0.68 respectively. Compared with that in C and H group, the intensity of the Notch1 signal and the number of BrdU (+) cells increased significantly in HPC group (P < 0.05). The methylation levels of the Notch1 promoter 0.82 ± 0.03, 0.65 ± 0.03, and 0.60 ± 0.02 in the C, H, and HPC groups, respectively. The methylation levels of Notch1 decreased significantly (P < 0.05). The effect of HPC on HT22 cells exhibited similarities to that observed in the hippocampus. Conclusion HPC may confer neuroprotection by activating the Notch1 signaling pathway and regulating its methylation level, resulting in the regeneration of hippocampal neurons.

Purpose: This study aims to develop a low-radiation dose, one-step integrated coronary–carotid–cerebral computed tomography angiography (ICCC-CTA) technique to analyze the relationship between cardiovascular and cerebrovascular atherosclerosis and evaluate the risk factors of plaque to provide an early-stage treatment to patients and reduce vascular events. Methods: A total of 300 consecutive asymptomatic patients with cardiovascular risk factors who underwent ICCC-CTA were enrolled in this prospective study. The association between coronary and carotid-cerebrovascular atherosclerosis was assessed. The primary cardiovascular risk factors for various plaque types in cardiovascular or cerebrovascular disease were evaluated using multivariate analysis. Results: Among 300 patients, 189 (63%) had plaques in their coronary and cerebral arteries. The presence of calcified and mixed plaques in the carotid-cerebral and coronary arteries was strongly correlated (χ² = 20.71, P = 0.001; χ² = 8.96, P = 0.003, respectively). Multivariate logistic regression analysis revealed that abnormal blood glucose [OR = 1.44, 95% CI 0.12–0.62, P = 0.01] and abnormal total cholesterol [OR = 1.28, 95% CI 0.07–0.46, P = 0.01] are risk factors in all the models in the coronary artery, non-calcified plaque group. Abnormal blood glucose [OR = 1.43, 95% CI 0.11–0.61, P = 0.01] and abnormal systolic blood pressure [OR = 1.02, 95% CI 0.01–0.04, P = 0.02] are risk factors in all the models in the coronary artery calcified plaque group. Abnormal blood glucose level [OR = 1.44, 95% CI = 0.12–0.62, P = 0.01] was only a risk factor in the non-calcified plaque carotid–cerebral artery group. Conclusions: We confirm that elevated blood glucose and total cholesterol levels are associated with coronary and carotid-cerebrovascular plaques using the novel one-step low dose cerebral-carotid-cardiac CTA technique. These findings will provide insights for further studies focusing on developing low-radiation dose one-step ICCC-CTA to screen cardiovascular/cerebrovascular plaques in general population with cardiovascular risk factors. Advances in knowledge: We developed a low–radiation dose, one-step ICCC-CTA technique to detect cardiovascular and cerebrovascular atherosclerosis. We evaluated the risk factors for plaque burden for the early treatment and reduction of vascular events. These findings supported the development of low–radiation dose one-step ICCC-CTA to screen for cardiovascular/cerebrovascular disease in general population with cardiovascular risk factors.

Liu, Na, Yanbo Zhang, Pu Zhang, Kerui Gong, Chunyang Zhang, Kai Sun, and Guo Shao. Vascular endothelial growth factor and erythropoietin show different expression patterns in the early and late hypoxia preconditioning phases and may correlate with DNA methylation status in the mouse hippocampus. High Alt Med Biol . 23:361–368, 2022. Background: Vascular endothelial growth factor (VEGF) and erythropoietin (EPO) have been proven to participate in neuroprotection induced by hypoxia preconditioning (HPC), and they can be regulated by hypoxia-inducible factor 1 (HIF-1). It has been reported that DNA methylation can affect VEGF and EPO expression. This study aimed to explore the expression of VEGF and EPO in the early phase and late phase of HPC and whether their expression was affected by DNA methylation. Method: Acute repeated HPC mice were used as the animal model, and detection of molecular changes was performed immediately (early phase) and 1 day (late phase) after HPC treatment. The mRNA and protein expression levels of VEGF, EPO, and DNA methyltransferases (DNMTs) in the hippocampi were measured by real-time polymerase chain reaction and western blotting, respectively. The activity of DNMTs and global methylation levels were analyzed by enzyme-linked immunosorbent assay. DNA methylation levels of VEGF and EPO promoters, which were catalyzed by DNMTs, were determined by bisulfite-modified DNA sequencing. Results: The expression of VEGF was increased in the early phase and late phase of HPC ( p < 0.05), whereas the expression of EPO was unchanged in the early phase ( p > 0.05) of HPC and was increased in the late phase ( p < 0.05). VEGF and EPO expression were negatively correlated with the DNA methylation levels of their promoters. DNMT3A and DNMT3B were decreased in the early phase and late phase ( p < 0.05), whereas DNMT1 was unchanged in the early phase and late phase ( p > 0.05). Conclusions: Our data demonstrated that DNMTs affect VEGF and EPO expression by regulating the DNA methylation levels of the promoters of VEGF and EPO.

Aims: To evaluate the predictive value of mobile magnetic resonance imaging (MRI) in screening stroke.Methods: This was a prospective case-control study performed on healthy residents over 40 years old in remote rural areas of northern China between May 2019 and May 2020. Multivariate logistic regression and receiver operator characteristic curve (ROC) analysis were used to evaluate the screening model.Results: A total of 1,224 patients (500 [40.8%] men) enrolled, including 56 patients who suffered from stroke (aged 64.05 ± 7.27). The individuals who developed stroke were significantly older (P < 0.001), had a significantly higher occurrence of heart disease (P = 0.015), diabetes (P = 0.005), dyslipidemia (P = 0.009), and significantly increased waist circumference (P = 0.02), systolic blood pressure (SBP) (P = 0.003), glycosylated hemoglobin (HbA1c) level (P = 0.007), triglyceride (TG) level (P = 0.025), low density lipoprotein cholesterol (LDL-c) level (P = 0.04), and homocysteine (HCY) level (P < 0.001). Multivariate logistic regression analysis showed that age (OR = 1.055, 95% CI: 1.017–1.094, P = 0.004), HCY (OR = 1.029, 95% CI: 1.012–1.047, P = 0.001) and mobile MRI (OR = 4.539, 95% CI: 1.726–11.939, P = 0.002) were independently associated with stroke. The area under the curve (AUC) of the combined model including national screening criteria, mobile MRI results, and stroke risk factors was 0.786 (95% CI: 0.721–0.851), with a sensitivity of 69.6% and specificity of 80.4%.Conclusion: Mobile MRI can be used as a simple and easy means to screen stroke.