Cardiorenal anemia syndrome (CRAS) links heart failure, chronic kidney disease, and anemia, but the role of diet-related inflammation remains unclear. In the National Health and Nutrition Examination Survey (NHANES), we examined associations of the Dietary Inflammatory Index (DII) with CRAS, dose-response patterns, inflammatory mediation, and machine-learning prediction, alongside analysis of a myocardial infarction-CKD-anemia phenotype in the Korea National Health and Nutrition Examination Survey (KNHANES). This study included 25,388 NHANES and 32,935 KNHANES adults. Survey-weighted regression and restricted cubic splines assessed associations with CRAS in NHANES and the related phenotype in KNHANES. Exploratory mediation evaluated six inflammatory indices. In NHANES participants with heart failure, least absolute shrinkage and selection operator regression selected predictors for 12 internally validated models, with cross-phenotype application in KNHANES and interpretation using Shapley additive explanations (SHAP). Higher DII was associated with greater odds of CRAS in NHANES (odds ratio [OR] = 1.22, 95% CI: 1.07-1.40) and of the related phenotype in KNHANES (OR = 1.19, 95% CI: 1.10-1.29). The association was largely linear in NHANES but nonlinear in KNHANES. In NHANES, all six indices showed positive indirect associations, with estimated proportions ranging from 5.22% to 16.26%. CatBoost showed the highest discrimination in NHANES internal validation (ROC-AUC = 0.741; PR-AUC = 0.556) and in the KNHANES cross-phenotype application (ROC-AUC = 0.753; PR-AUC = 0.698). Higher DII was associated with greater odds of CRAS in NHANES, with directionally consistent findings for the related phenotype in KNHANES. The model may support model-based CRAS identification and showed preliminary applicability to the related phenotype.

BackgroundDespite increasing evidence indicating hippocampal dysfunction in migraineurs, they overlooked the functional differences among hippocampal subregions and mostly used static functional connectivity (sFC). This study aimed to combine sFC and dynamic functional connectivity (dFC) to investigate the role of hippocampal subregional functional changes in migraine chronification.MethodsResting-state functional MRI scans were performed on 52 patients with episodic migraine (EM), 22 patients with chronic migraine (CM), and 67 healthy controls (HCs). The bilateral rostral hippocampus (rHipp) and caudal hippocampus were selected as regions of interest. Differences in sFC and dFC values between the hippocampal subregions and other brain regions among the three groups were compared through the analysis of the general linear model. Spearman partial correlation analyses were used to assess the relationship between FC and clinical parameters in the migraine cohort.ResultsIn the sFC analysis, both EMs and CMs showed reduced connectivity between the left rHipp and the left orbital part of medial frontal gyrus as compared with HCs. In the dFC analysis, both the CM and EM groups exhibited increased connectivity between the right rHipp and the right calcarine compared to HCs, and the CM group demonstrated decreased dFC between the aforementioned brain regions relative to the EM group. No significant correlations were found between sFC and dFC values and clinical characteristics in patients with EM and CM.ConclusionAltered sFC and dFC between the rHipp and the orbital part of medial frontal gyrus and calcarine in CM patients may be associated with dysfunctions in emotion, cognition, and multisensory integration, providing new insights into mechanisms of migraine chronification.

BACKGROUND:Post-traumatic stress disorder (PTSD) is the most common mental disorder following traumatic experiences. Environmental disasters such as super typhoons can severely disrupt daily life and may trigger PTSD in exposed individuals. White matter alterations have been observed in patients with PTSD. Fixel-based analysis (FBA), a recently developed diffusion MRI technique, allows detailed assessment of white matter microstructure. This study aimed to evaluate the potential of FBA as an imaging biomarker in typhoon survivors, reducing the subjective bias associated with clinical symptom scales. METHODS:Whole-brain diffusion MRI data from the PTSD group (n = 27), trauma-exposed controls (TEC, n = 33), and healthy controls (HC, n = 30) were analyzed to identify white matter fiber tracts showing abnormalities in FBA metrics, including fiber density (FD), fiber cross-section (FC), and fiber density-cross section (FDC). The study then examined whether these FBA-derived features, when combined with machine learning, could improve the identification of potential PTSD biomarkers. RESULTS:Compared with the HC group, patients with PTSD showed increased fiber density (FD) in the right frontopontine tract and right middle longitudinal fascicle, as well as higher fiber density-cross section (FDC) values in the bilateral frontopontine tract and left thalamo-premotor tract (Bonferroni correction, p < 0.05/18 = 0.003). To differentiate PTSD from TEC, binary and multiclass machine learning models with five-fold cross-validation were developed. The binary model (PTSD vs. TEC) achieved high performance (accuracy = 0.89, sensitivity = 0.97, specificity = 0.71, precision = 0.87, AUC = 0.95), whereas the multiclass model (PTSD vs. TEC vs. HC) demonstrated excellent results (macro-averaged precision = 0.99, recall = 0.99, F1-score = 0.99). The top 20 contributing features of the optimal model were analyzed using Shapley additive explanation (SHAP) values to illustrate model interpretability. CONCLUSION:Most typhoon-exposed individuals with PTSD may exhibit structural alterations in brain white matter. By combining fixel-based analysis (FBA) with machine learning, this study identified diffusion markers within specific white matter tracts and demonstrated their potential diagnostic value for distinguishing PTSD from trauma-exposed controls. These findings enhance our understanding of microstructural white matter changes and their spatial distribution in PTSD and also suggest potential imaging biomarkers for its diagnosis.

Neuroimaging studies of vestibular migraine (VM) have revealed abnormal functional connectivity in the central vestibular system. However, it remains to be determined whether effective connectivity (EC) of the vestibular cortex is specifically disrupted in VM and whether this brain measure can aid in the differential diagnosis of VM patients. In 56 VM patients, 58 episodic migraine (EM) patients, and 63 healthy controls (HCs), the directional influences between the vestibular cortex and the whole brain were examined via resting-state functional magnetic resonance imaging and Granger causality analysis, with bilateral parietal operculum cortex 2 (OP2) as the seed regions. Statistical analyses were performed to investigate the group differences and the associations of directional influences with clinical variables. Classification models based on linear support vector machine (SVM) analysis were established to assess the performance of effective connectivity in discriminating VM patients from HCs and EM patients. Relative to the EM group and HC group, the VM group presented elevated positive influence from the left OP2 to the right middle frontal gyrus (MFG), as well as increased negative influence from the right MFG and inferior parietal lobule (IPL) to the left OP2. Furthermore, the EM group exhibited increased positive influence from the bilateral medial superior frontal gyrus (SFGmed) to the left OP2 compared with the VM group and HC group. The EC-derived SVM models showed favorable and moderate performance for distinguishing VM patients from EM patients (area under the curve = 0.8264, p < 0.001) and HCs (area under the curve = 0.7764, p < 0.001). The causal flow from and to the left OP2 was altered in the prefrontal and inferior parietal lobes, regions closely implicated in cognitive control and multisensory integration. Abnormal EC associated with the right MFG and IPL appears to be specific to VM, whereas altered EC linked to SFGmed suggests a resilience trait in EM. The EC of the OP2 may serve as a neuroimaging biomarker for VM identification.

The aim of this study was to examine the temporal sequence of the appearance of vestibular symptoms and migraine, as well as whether they coexist or not, while assessing their influence on cerebral functional activity. The present investigation is a cross-sectional study. This study included 69 participants from the outpatient headache unit at our hospital who were divided into six groups: 33 patients with vestibular migraine (VM) (12 the onset of migraine was earlier than vertigo, 10 the onset of vertigo was earlier than migraine, 11 vertigo was accompanied with migraine), 9 patients with benign recurrent vertigo (BRV), 14 patients with migraine without aura (MoA), and 13 healthy controls. We compared the differences in spontaneous cerebral functional activity between groups, and used the bilateral thalamus as a seed point to analyze its functional connectivity with the whole brain. The relationship between changed cerebral functional activity and clinical features was compared. We have observed variations in the spontaneous functional activity of the right middle and inferior frontal gyrus among individuals in each group, as well as discrepancies in the functional connectivity of the right superior frontal gyrus with the bilateral thalamus. The severity of vertigo disability exhibits a negative correlation with the functional activity in the right inferior frontal gyrus, while the duration of vertigo demonstrates a positive correlation with the functional activity in the right inferior frontal gyrus. Furthermore, the severity of migraine disability displays a negative correlation with the functional connectivity between the bilateral thalamus and the right superior frontal gyrus. In patients with VM, the temporal relationship between vestibular symptoms and migraine did not have any impact on cerebral functional activity. The functional activity of the right middle and inferior frontal gyrus may be influenced by vestibular stimulation, while headache stimulation could potentially modify the functional connectivity between the bilateral thalamus and the right superior frontal gyrus. These findings suggest that VM may be considered as a distinct disease entity.

Previous neuroimaging studies on migraine have reported inconsistent hippocampal volumetric changes, potentially due to insufficient consideration of subregion heterogeneity. Exploring the alterations in hippocampal subregions may help reveal the mechanisms underlying migraine chronification. This study aims to investigate the role of volume changes in these subregions in migraine chronification. Structural T1-weighted MRI scans were performed on 42 patients with episodic migraine (EM), 22 patients with chronic migraine (CM), and 65 healthy controls (HCs). Hippocampal subregion volumes were quantified using FreeSurfer-based segmentation, and group comparisons were performed with relevant covariates included and false discovery rate (FDR) correction applied to control for multiple comparisons. No hippocampal subregion volume differences survived FDR correction at 0.05. However, trend-level volumetric variations were observed across the three groups, including the bilateral whole hippocampus, subiculum, cornu ammonis (CA) 1, molecular layer, as well as the left granule cell and molecular layer of the dentate gyrus (GC-ML-DG) and CA4. Subsequent exploratory pairwise comparisons showed that (1) compared with HCs, CM patients exhibited trend-level smaller volumes in the bilateral whole hippocampus, subiculum, CA1, and molecular layer; and (2) compared with EM patients, CM patients showed trend-level reductions in the bilateral whole hippocampus, molecular layer, CA1, as well as in the left subiculum, GC-ML-DG, and CA4. No significant volumetric differences in hippocampal subregions were detected among the three groups. Exploratory findings suggest trend-level alterations in several hippocampal subregions, including CA1, CA4, molecular layer, GC-ML-DG, and subiculum in CM patients. These preliminary findings may suggest potential links to pain perception, emotion, memory, and cognition during migraine chronification.

Acute pancreatitis (AP) is a prevalent inflammatory disorder with high mortality in severe cases. Although necroptosis-driven inflammatory cascades significantly contribute to poor prognosis, effective therapeutic interventions remain limited. Here, we investigated the role of necroptosis in AP progression using bioinformatics analysis, co-immunoprecipitation, and ubiquitination assays, alongside in vitro and in vivo cerulein-induced AP models. We demonstrated that the hypoxic microenvironment characteristic of AP activates the HSP90AA1/STUB1 axis through HIF-1α-mediated transcriptional upregulation. The HSP90AA1/STUB1 axis subsequently stabilizes necroptosis executors RIPK1, RIPK3, and MLKL by preventing their ubiquitin-mediated degradation, thereby promoting necroptosis-driven AP progression. This work establishes the hypoxic microenvironment-HIF-1α-HSP90AA1/STUB1-necroptosis axis as a central pathway in AP pathogenesis, revealing novel therapeutic opportunities for targeting necroptosis-driven inflammation in AP.

BACKGROUND:The high heterogeneity in vestibular migraine (VM) complicates understanding its precise pathophysiological mechanisms and identifying potential biomarkers. This study investigated the heterogeneity in VM using a newly proposed method called Individualized Differential Structural Covariance Network (IDSCN) analysis. METHODS:Structural T1-weighted MRI scans were performed on 55 patients with VM and 65 healthy controls, and an IDSCN was constructed for each patient. We studied the extent of heterogeneity in the IDSCNs, summarized the distribution of differential edges, and clustered the patients into subtypes with the shared differential edges. Imaging-clinical association analyses were conducted on both the subtype classification and the differential edges exhibiting significant inter-subtype differences. RESULTS:Patients with VM demonstrated notable heterogeneity in the number of significantly altered IDSCN edges, while sharing several common differential connections that were mainly distributed among the parietal, subcortical, and cerebellar regions. Two robust and distinct neuroanatomical subtypes of VM were identified, which were associated with headache frequency. The differential edge between the left paracentral lobule and right pallidum was associated with both headache frequency and occurrence. CONCLUSIONS:These findings indicate the importance of considering individual differences in VM research and may offer insights for precise diagnosis and individualized treatment of the disease.

Early diagnosis of cardiovascular diseases (CVDs) is essential for improving patient outcomes. As a primary diagnostic modality, electrocardiogram (ECG) signals pose challenges for automatic classification due to their complex temporal and morphological characteristics. This study proposes a CNN-CBAM-GRU model that integrates Convolutional Neural Networks (CNN), the Convolutional Block Attention Module (CBAM), and Gated Recurrent Units (GRU) to enhance both spatial feature representation and temporal sequence modeling. The model is evaluated on two public ECG datasets-MIT-BIH and PTB-XL-under five-class classification settings. Unlike many existing approaches that report only a limited set of metrics, this study conducts a comprehensive evaluation across multiple performance indicators, including accuracy, precision, recall, sensitivity, and F1-score, providing a more complete view of classification effectiveness. Experimental results demonstrate that the proposed model achieves a strong balance between predictive performance and computational efficiency. Specifically, it achieves 98.17% accuracy and 98.91% F1-score on MIT-BIH, and 99.21% accuracy and 99.47% F1-score on PTB-XL, with a compact parameter size of 2.45 million. These findings validate the proposed model as a practical and robust solution for intelligent ECG classification and automated cardiovascular disease diagnosis.

Background Previous surface-based morphometry (SBM) research on cortical morphology in vestibular migraine (VM) has been limited by a small sample size. This study aims to validate cortical morphological alterations in VM using SBM and explore their clinical implications with a larger sample. Methods Fifty-five patients with VM and 65 healthy controls (HCs) underwent structural T1-weighted MRI. Cortical morphological features, including cortical thickness, curvature, surface area, and local gyrification index, were assessed using SBM with FreeSurfer. Statistical analyses were conducted to examine inter-group differences and correlations between cortical alterations and clinical features. A linear support vector machine (SVM) classifier was applied to evaluate the performance of cortical morphological differences in distinguishing VM patients from HCs. Results The SBM analysis revealed significant cortical differences between the VM group and HCs. Specifically, cortical thickness was significantly reduced in the right superior frontal gyrus, superior parietal lobule, and precuneus in the VM group as compared to HCs. Additionally, surface area was significantly smaller in the right rostral middle frontal cortex in the VM cohort. No significant correlations were found between the cortical morphological features and any clinical indicators. The SVM classification model achieved moderate efficacy (area under the curve = 0.775, p < 0.001) in distinguishing VM patients from HCs. Conclusions These findings demonstrate significant cortical morphological alterations in the frontoparietal regions of patients with VM, which may be associated with dizziness, pain, and emotional and cognitive dysfunctions. The identified cortical differences have the potential to serve as neuroimaging markers for VM.

Background Prior MRI studies on vestibular migraine (VM) have revealed abnormalities in static regional intrinsic brain activity (iBA) and dynamic functional connectivity between brain regions or networks. However, the temporal variation and concordance of regional iBA measures remain to be explored. Methods 57 VM patients during the interictal period were compared to 88 healthy controls (HC) in this resting-state functional magnetic resonance imaging (fMRI) study. The dynamics and concordance of regional iBA indices, including amplitude of low-frequency fluctuations (ALFF) and regional homogeneity (ReHo), were examined by utilizing sliding time-window analysis. Partial correlation analyses were performed between clinical parameters and resting-state fMRI indices in brain areas showing significant group differences. Results The VM group showed increased ALFF and ReHo dynamics, as well as increased temporal concordance between ALFF and ReHo in the bilateral paracentral lobule and supplementary motor area relative to the HC group. We also found decreased ReHo dynamics in the right temporal pole, and decreased ALFF dynamics in the right cerebellum posterior lobe, bilateral angular gyrus and middle occipital gyrus (MOG) in the VM group compared with the HC group. Moreover, a positive correlation was observed between ALFF dynamics in the left MOG and vertigo disease duration across all VM patients. Conclusion Temporal dynamics and concordance of regional iBA indices were altered in the motor cortex, cerebellum, occipital and temporoparietal cortex, which may contribute to disrupted multisensory processing and vestibular control in patients with VM. ALFF dynamics in the left MOG may be useful biomarker for evaluating vertigo burden in this disorder.

BACKGROUND:There are limited epidemiological investigations of blood metal levels related to hyperlipidemia, and results indicating the association between blood lead (Pb), cadmium (Cd) and selenium (Se), and lipid biomarkers have been conflicting. METHODS:We included populations for which NHANES collected complete data. Multivariate logistic regression and subgroup analyses were conducted to ascertain the relationship between blood Pb, Cd, and Se levels and hyperlipidemia. Nonlinear relationships were characterized by smoothed curve fitting and threshold effect analysis. RESULTS:5429 participants in all, with a mean age of 53.70 ± 16.63 years, were included; 47.1% of the subjects were male, and 3683 (67.8%) of them had hyperlipidemia. After modifying for variables with confounders in a multivariate logistic regression model, we discovered a positive correlation between blood Pb and Se levels and hyperlipidemia (Pb: OR:2.12, 95% CI:1.56-2.88; Se: OR:1.84, 95% CI:1.38-2.45). Gender, age, smoking status, alcohol use status, hypertension, diabetes, and body mass index were not significantly linked with this positive correlation, according to subgroup analysis and interaction test (P for interaction>0.05). Positive correlations between blood Pb, Cd, and Se levels and the risk of hyperlipidemia have been found using smooth curve fitting. CONCLUSIONS:This study demonstrates that higher blood levels of Pb, Cd, and selenium are linked to an increased risk of hyperlipidemia.

Pyroptosis, a novel programmed cell death mediated by NOD-like receptor protein 3 (NLRP3) inflammasome, is a critical pathogenic process in acute viral myocarditis (AVMC). Mitsugumin 53 (MG53) is predominantly expressed in myocardial tissues and has been reported to exert cardioprotective effects through multiple pathways. Herein, we aimed to investigate the biological function of MG53 in AVMC and its underlying regulatory mechanism in pyroptosis. BALB/c mice and HL-1 cells were infected with Coxsackievirus B3 (CVB3) to establish animal and cellular models of AVMC. As inflammation progressed in the myocardium, we found a progressive decrease in myocardial MG53 expression, accompanied by a significant enhancement of cardiomyocyte pyroptosis. MG53 overexpression significantly alleviated myocardial inflammation, apoptosis, fibrosis, and mitochondrial damage, thereby improving cardiac dysfunction in AVMC mice. Moreover, MG53 overexpression inhibited NLRP3 inflammasome-mediated pyroptosis, reduced pro-inflammatory cytokines (IL-1β/18) release, and suppressed NF-κB signaling pathway activation both in vivo and in vitro. Conversely, MG53 knockdown reduced cell viability, facilitated cell pyroptosis, and increased pro-inflammatory cytokines release in CVB3-infected HL-1 cells by promoting NF-κB activation. These effects were partially reversed by applying the NF-κB inhibitor BAY 11-7082. In conclusion, our results suggest that MG53 acts as a negative regulator of NLRP3 inflammasome-mediated pyroptosis in CVB3-induced AVMC, partially by inhibiting the NF-κB signaling pathway. MG53 is a promising candidate for clinical applications in AVMC treatment.

Purpose The goal of this research was to explore the role of miR-24-3p in heart failure (HF), with a focus on its impact on the specificity protein 1 (Sp1)/phosphoinositide 3-kinase (PI3K) pathway. Methods HF rat and HF cell models were established using doxorubicin(Dox). Cardiac function was assessed through echocardiography, while histological changes were observed via hematoxylin-eosin (HE) staining. To further investigate the underlying mechanisms, HF cell models were treated with either an Sp1 inhibitor or a PI3K inhibitor. Additionally, models with miR-24-3p overexpression or silencing were constructed. N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were determined by ELISA. Cell apoptosis was evaluated using TUNEL staining, and lactate dehydrogenase (LDH) levels were measured by colorimetry. Reactive oxygen species (ROS) production was analyzed using flow cytometry. Related gene and protein expressions were assessed via qRT-PCR and Western blotting. Finally, the relationship between miR-24-3p and Sp1 was confirmed through dual-luciferase assays. Results Dox treatment increased the left ventricular internal diameter (LVIDd) while decreasing ejection fraction (EF) and fractional shortening (FS), leading to disorganized cardiomyocyte arrangement, cellular edema, and necrosis in rats. In HF rats, NT-proBNP, Caspase-3, and miR-24-3p expression levels were elevated, whereas Sp1 and PI3K mRNA and protein expression levels were decreased. Similarly, Dox-induced damage in H9c2 cardiomyocytes resulted in increased NT-proBNP, apoptosis, Caspase-3, LDH, ROS, and miR-24-3p expression, along with decreased Sp1 and PI3K expression. Treatment with either Sp1 or PI3K inhibitors exacerbated the Dox-induced cardiomyocyte damage, further elevating NT-proBNP, apoptosis, Caspase-3, LDH, ROS, and miR-24-3p expression levels. Notably, Sp1 inhibition reduced PI3K expression, and PI3K inhibition, in turn, suppressed Sp1 expression. Overexpression of miR-24-3p worsened Dox-induced cardiomyocyte damage, characterized by increased NT-proBNP, apoptosis, Caspase-3, LDH, and ROS expression, alongside reduced Sp1 and PI3K expression. In contrast, silencing miR-24-3p mitigated these detrimental effects and increased Sp1 and PI3K expression. Dual-luciferase assays confirmed that miR-24-3p directly targets Sp1. Conclusion Dox induces cardiomyocyte damage, impairs cardiac function, and promotes cardiomyocyte apoptosis and oxidative stress. Silencing miR-24-3p offers a protective effect by activating the Sp1/PI3K signaling pathway in heart failure.

APOE ε4 is risk for cognitive decline even in normal aging, but its effect on the whole-brain functional connectivity (FC) among time in young adults remain elusive. This study aimed to validate the time-by-APOE ε4 interaction on brain FC of this specific population. Longitudinal changes in neuropsychological assessments and resting-state functional magnetic resonance imaging in 26 ε4 carriers and 26 matched non-ε4 carriers were measured for about 3 years. Whole-brain FC was calculated, and a full factorial design was used to compare the difference among groups. Two-sample t test was used for post-hoc analysis. Pearson’s correlation analysis was conducted to investigate the relationships between FC and cognitive tests. Of 26 specially appointed ROIs, left superior temporal gyrus (TG) was most sensitive to the effect of time-by-gene interaction. Specifically, the alteration of FC was distributed between the left TG and right TG with GRF correction (voxel-P < 0.001, cluster-P < 0.05), and decreased in ε4 carriers while increased in non-ε4. The main effect of gene showed ε4 carriers has lower FC between left TG and right middle frontal gyrus as compared with non-ε4 both at baseline and follow-up study; ε4 carriers has lower FC between left TG and right supramarginal as compared with non-ε4 at baseline, but no difference in follow-up study. The time-by-APOE ε4 interaction on brain FC was demonstrated at a young age, and left TG was the earliest affected brain regions. The young adult ε4 carriers experience decreased FC among time in the absence overt clinical symptoms.

JOURNAL/nrgr/04.03/01300535-202504000-00027/figure1/v/2024-07-06T104127Z/r/image-tiff Cardiac arrest can lead to severe neurological impairment as a result of inflammation, mitochondrial dysfunction, and post-cardiopulmonary resuscitation neurological damage. Hypoxic preconditioning has been shown to improve migration and survival of bone marrow-derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest, but the specific mechanisms by which hypoxia-preconditioned bone marrow-derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown. To this end, we established an in vitro co-culture model of bone marrow-derived mesenchymal stem cells and oxygen-glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis, possibly through inhibition of the MAPK and nuclear factor κB pathways. Subsequently, we transplanted hypoxia-preconditioned bone marrow-derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia. The results showed that hypoxia-preconditioned bone marrow-derived mesenchymal stem cells significantly reduced cardiac arrest-induced neuronal pyroptosis, oxidative stress, and mitochondrial damage, whereas knockdown of the liver isoform of phosphofructokinase in bone marrow-derived mesenchymal stem cells inhibited these effects. To conclude, hypoxia-preconditioned bone marrow-derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest, and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.

aShengli Clinical Medical College of Fujian Medical University, Department of Emergence, Fujian Provincial Hospital, Fuzhou, China bFujian Emergency Medical Center, Fujian Provincial Key Laboratory of Emergency Medicine, Fuzhou, China Yu Wang, Yangping Zhuang, Jun Ke contributed equally to this work and shared the first authorship. Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. Published online ■ ■ *Corresponding author. Address: No.134, Dongjie, Fuzhou 350001, China. E-mail address: [email protected] (F. Chen). This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. http://creativecommons.org/licenses/by-nc-sa/4.0/

BackgroundAlthough gray matter (GM) volume alterations have been extensively documented in previous voxel-based morphometry studies on vestibular migraine (VM), little is known about the impact of this disease on the topological organization of GM morphological networks. This study investigated the altered network patterns of the GM connectome in patients with VM.MethodsIn this study, 55 patients with VM and 57 healthy controls (HCs) underwent structural T1-weighted MRI. GM morphological networks were constructed by estimating interregional similarity in the distributions of regional GM volume based on the Kullback-Leibler divergence measure. Graph-theoretical metrics and interregional morphological connectivity were computed and compared between the two groups. Partial correlation analyses were performed between significant GM connectome features and clinical parameters. Logistic regression (LR), support vector machine (SVM), and random forest (RF) classifiers were used to examine the performance of significant GM connectome features in distinguishing patients with VM from HCs.ResultsCompared with HCs, patients with VM exhibited increased clustering coefficient and local efficiency, as well as reduced nodal degree and nodal efficiency in the left superior temporal gyrus (STG). Furthermore, we identified one connected component with decreased morphological connectivity strength, and the involved regions were mainly located in the STG, temporal pole, prefrontal cortex, supplementary motor area, cingulum, fusiform gyrus, and cerebellum. In the VM group, several connections in the identified connected component were correlated with clinical measures (i.e., symptoms and emotional scales); however, these correlations did not survive multiple comparison corrections. A combination of significant graph- and connectivity-based features allowed single-subject classification of VM versus HC with significant accuracy of 77.68%, 77.68%, and 72.32% for the LR, SVM, and RF models, respectively.ConclusionPatients with VM had aberrant GM connectomes in terms of topological properties and network connections, reflecting potential dizziness, pain, and emotional dysfunctions. The identified features could serve as individualized neuroimaging markers of VM.

The purpose of this study was to look at any connections that could exist between neutrophil-lymphocyte ratio and coronary heart disease. We performed a cross-sectional research of 13732 participants in the National Health and Nutrition Examination Survey who were 40 or older. Multivariate logistic regression models investigated the relationship between neutrophil-to-lymphocyte ratio levels and coronary heart disease risk. To investigate potential nonlinear connections, smoothed curve fitting was used. When a nonlinear relationship was discovered, the inflexion point was determined using a recursive method. After controlling for relevant confounders, neutrophil-to-lymphocyte ratio was independently linked to a higher risk of coronary heart disease (OR = 1.74, 95% CI:1.30-2.33, P = 0.0002). Subgroup analyses showed statistically significant positive associations between neutrophil-to-lymphocyte ratio and coronary heart disease risk in women (OR = 1.25, 95% CI:1.09-1.43), participants 60 years of age and older (OR = 1.09, 95% CI:1.00-1.19), smoking status for every day or not at all (OR = 1.23, 95% CI:1.00-1.52; OR = 1.09, 95% CI:1.00-1.19), alcohol use status for moderate alcohol use (OR = 1.11, 95% CI:1.00-1.22), body mass index >30 kg/m2 (OR = 1.42, 95% CI:1.10-1.82), hypertensive (OR = 1.11, 95% CI:1.02-1.22), and individuals without diabetes (OR = 1.17, 95% CI:1.06-1.31). A positive correlation between neutrophil-to-lymphocyte ratio levels and coronary heart disease risk was also seen by smoothing curve fitting, with an inflexion point of 1.08 that was statistically significant (P<0.05). Our research shows elevated neutrophil-to-lymphocyte ratio levels are linked to a higher risk of coronary heart disease.

Background The Triglyceride glucose (TyG) index-related indicators improve risk stratification by identifying individuals prone to atherosclerosis early in life. This study aimed to examine the relation between TyG-waist circumference-to-height ratio (TyG-WHtR) and coronary heart disease. Methods Data from four National Health and Nutrition Examination Surveys (NHANES) cycles between 2011 and 2018 were used for a cross-sectional study. The association between TyG-WHtR and coronary heart disease risk was examined using a multifactorial logistic regression model, and corresponding subgroup analyses were performed. Nonlinear correlations were analyzed using smooth curve fitting and threshold effects analysis. When nonlinear connections were discovered, appropriate inflection points were investigated using recursive methods. Results TyG-WHtR and coronary heart disease were significantly positively correlated in the multifactorial logistic regression analysis. Subgroup analyses and interaction tests revealed that gender, age, smoking status, and cancer were not significantly associated with this correlation ( P for interaction > 0.05). Furthermore, utilizing threshold effect analysis and smooth curve fitting, a nonlinear connection with an inflection point of 0.36 was observed between TyG-WHtR and coronary heart disease. Conclusions According to this study, the American population is far more likely to have coronary heart disease if they have higher TyG-WHtR levels.