BackgroundNeutrophil extracellular traps (NETs) can induce cellular and tissue damage through inflammatory responses. While the involvement of NETs in psychiatric disorders has shown preliminary potential, a systematic exploration of their link with major depressive disorder (MDD) is imperative. This study evaluated the clinical potential of three NET markers—myeloperoxidase (MPO)-DNA, neutrophil elastase (NE)-DNA, and citrullinated histones (citH3)—for diagnosing MDD and predicting treatment response.MethodsTwo independent clinical cohorts (Cohort 1: n=83; Cohort 2: n=60) and a chronic unpredictable mild stress (CUMS) mouse model were used. Physiotherapy and pharmacotherapy were administered to the two cohorts, respectively. NET markers were measured in plasma samples. Levels of NETs in the hippocampus were detected in CUMS mice. Pharmacological blockade of NET formation was performed in mice.Results(1) Independently validated across two cohorts, plasma levels of NET markers were significantly higher in MDD patients than in healthy participants. (2) In MDD patients, plasma NET markers significantly correlated with neuropsychological assessment scores, serum levels of inflammatory indices, and abnormal activation of the right calcarine and cuneus. (3) Relationship between NETs and C-reactive protein has an significant effect on depressive symptoms. (4) These NET markers could predict changes in 24-item Hamilton Depression Rating Scale scores after antidepressive treatments. (5) Compared with controls, CUMS mice exhibited significantly elevated levels of NE and MPO in the hippocampus. Preventing NET formation significantly reduced NE and MPO levels in plasma and hippocampus, and alleviated depressive-like behavior in CUMS mice.ConclusionsPlasma NETs may be associated with the occurrence and progression of MDD, potentially via inflammatory mechanisms. Plasma NET markers may be used as valuable biomarkers to diagnose MDD and predict patient response to antidepressive treatment. Targeting NET formation could represent a potential therapeutic strategy for depression.

BackgroundMajor depressive disorder (MDD) is characterized by substantial clinical heterogeneity. Oral microbiota can provide real-time information relevant to the early identification of disease risk and the prediction of therapeutic outcomes. The present study aimed to characterize the specific profiles of oral microbiota in the buccal mucosa of patients with MDD and to explore potential mechanisms linking oral microbiota to the pathophysiology of MDD.MethodA total of 38 patients with MDD and 30 healthy controls (HCs) were enrolled. All MDD patients received standard antidepressant treatment and were followed up at two time points (2 weeks and 6 weeks). Neuropsychological assessments were administered, and 16S rRNA sequencing was employed to determine the abundance of oral bacteria.Results(1) Significant differences in the diversity of oral microbiota from the buccal mucosa were observed between the MDD and HC groups. (2) The relative abundances of the oral genera Aggregatibacter, Lautropia, Peptostreptococcus, and Mogibacterium in the buccal mucosa were significantly altered in MDD patients compared to HCs. (3) The abundance of Mogibacterium was significantly correlated with scores on the 24-item Hamilton Depression Scale (HAMD-24) and the Self-Rating Depression Scale, as well as with serum levels of brain-derived neurotrophic factor (BDNF), nerve growth factor, and vascular endothelial growth factor (VEGF) in MDD patients. (4) BDNF and VEGF mediated the relationship between the relative abundance of oral Mogibacterium and HAMD-24 scores in MDD patients. (5) In MDD patients, the baseline relative abundance of oral Mogibacterium prior to treatment was significantly correlated with the rate of change in HAMD-24 scores following 2 and 6 weeks of antidepressant treatment.ConclusionOral Mogibacterium dysbiosis may contribute to the underlying pathophysiology of MDD, potentially via its influence on neuroplasticity. This oral bacterium may serve as a potential biomarker for diagnosing MDD and predicting responses to antidepressant treatment.

BACKGROUND:Beyond its primary roles in coagulation and hemostasis, Antithrombin III (ATIII) demonstrates anti-inflammatory properties. This study aimed to investigate the association between ATIII and post-stroke depression (PSD) in a longitudinal observational study and to evaluate the clinical potential of ATIII as a predictive biomarker for PSD. METHOD:We enrolled 120 PSD patients and 100 ischemic stroke controls. Clinical parameters, including ATIII activity, were collected during hospitalization. PSD patients underwent psychological assessments at 3, 9, and 15 months post-discharge. Furthermore, 50 PSD patients provided additional blood samples at 15 months for ATIII concentration analysis. RESULTS:Firstly, PSD patients exhibited significantly higher changes in ATIII activities from baseline to post-treatment than controls. Changes in ATIII activities showed an area under the curve of 0.724 to distinguish PSD patients from controls. Secondly, increased changes in ATIII activities during hospitalization were significantly associated with 24-item Hamilton Depression Scale (HAMD-24) scores at 3, 9, and 15 months of follow-up in PSD patients, as well as the changed rate of HAMD-24 scores during follow-up. Thirdly, quantified plasma concentration of ATIII were positively correlated with the HAMD-24 scores and plasma levels of pro-inflammatory factors in PSD patients. Fourthly, plasma ATIII concentration or changes in ATIII activities interacted with C-reactive protein levels to influence the HAMD-24 scores in PSD patients. CONCLUSION:Increased ATIII activity during stroke treatment may predict PSD risk. Higher ATIII levels associate with more severe depressive symptoms and enhanced inflammatory responses in PSD patients, suggesting its potential as a PSD biomarker.

To investigate potential associations between cerebrospinal fluid (CSF) microplastics and Alzheimer's disease (AD) pathology or cognitive function. The study included two cohorts: Cohort 1 comprised 17 amyloid-positive and 15 amyloid-negative subjects, while Cohort 2 consisted of 11 amyloid-positive subjects. All amyloid-positive participants in Cohort 1 completed one-year follow-up. CSF amyloid-β(Aβ)42, Aβ40, p-tau181, and t-tau were measured. Amyloid status defined by CSF Aβ42/40 ratio (positive: < 0.1; negative: ≥ 0.1). Four types of microplastics, namely polypropylene, polyvinyl chloride (PVC), polyethylene (PE), and polystyrene, were detected in human CSF. Bottled water consumption frequency and CSF/serum albumin ratio significantly correlated with CSF microplastic abundance. In Cohort 1, amyloid-positive subjects exhibited significantly elevated CSF levels of PE and PVC as compared to amyloid-negative subjects. In amyloid-positive subjects (Cohort 1 and 2), CSF PE levels showed significant inverse correlations with both CSF Aβ42 levels and Mini-Mental State Examination (MMSE) scores. In amyloid-positive individuals of Cohort 1, elevated PE levels positively correlated with MMSE decline rate over one year. The levels of CSF Aβ42 served as an intermediary factor, significantly affecting the relationship between CSF PE and MMSE scores in amyloid-positive subjects of cohort 1. In Cohort 1, the CSF levels of PE and PVC demonstrated an area under the curve value of greater than 0.8, indicating their strong potential to differentiate between amyloid-positive and amyloid-negative individuals. These discoveries suggested that the gradual accumulation of microplastics in the CSF were associated with cognitive decline among AD individuals.

BackgroundThe current study aimed to explore the specific oral microbiota profiles in major depressive disorder (MDD) patients with sleep disturbances, and to evaluate the potential mechanisms by which oral microbiota may be implicated in MDD.MethodThirty-eight MDD patients experiencing sleep disturbances and thirty healthy controls (HCs) were included. All MDD patients underwent a 14-day antidepressive treatment regimen. Neuropsychological assessments were conducted, and 16S rRNA sequencing was used to determine the abundance of oral bacteria.ResultsOral genera Solobacterium, Granulicatella, Campylobacter, and Haemophilus showed significant changes in their relative abundances between the MDD and HC groups. Significant correlations were found between the abundance of Haemophilus and Pittsburgh Sleep Quality Index (PSQI) and 24-item Hamilton Depression Scale (HAMD-24) scores in MDD patients with sleep disturbances. In MDD patients, lower relative abundances of oral Haemophilus prior to treatment were negatively correlated with the changed rates of PSQI and HAMD-24 scores after antidepressive treatment. The glial fibrillary acidic protein as the mediator, affected the relationship between the relative abundance of oral Haemophilus and sleep disturbances in MDD patients.ConclusionOral Haemophilus dysbiosis may drive sleep disturbances in MDD patients, possibly through its impact on neuroinflammation.

Background: Type 2 diabetes (T2DM) is an independent risk factor for accelerated cognitive decline, creating a need for non-invasive biomarkers to diagnose T2DM-related mild cognitive impairment (T2DM-MCI). Circular RNAs (circRNAs), known to regulate T2DM pathophysiology, represent promising candidate biomarkers.Objective We aimed to assess the relationship between circRNAs levels and cognitive decline in T2DM patients. Method: This study included 64 patients with T2DM-MCI and 75 patients with T2DM and normal cognition (T2DM-NC). All T2DM-MCI participants completed a 1.5-year follow-up period. Neuropsychological assessments were performed for all participants. Blood levels of circRNA were quantified using real-time quantitative polymerase chain reaction. Results: (1) Whole-blood expression of hsa_circ_0015335 was significantly reduced in T2DM-MCI patients compared to T2DM-NC controls. (2) Receiver operating characteristic (ROC) curve analysis demonstrated that hsa_circ_0015335 could differentiate T2DM-MCI from T2DM-NC with an Area Under ROC Curve of 0.722. (3) Lower hsa_circ_0015335 levels showed significant negative correlations with global cognitive function, episodic memory, and executive function scores in T2DM-MCI patients. (4) A significant interaction was observed between reduced hsa_circ_0015335 expression and elevated triglyceride glucose (TyG) index, collectively contributing to global cognitive impairment in T2DM-MCI patients. (5) Mediation analysis revealed that the TyG index significantly mediated the association between baseline hsa_circ_0015335 levels and the rate of global cognitive decline during follow-up. Conclusions: Peripheral blood hsa_circ_0015335 shows potential as a biomarker for T2DM-MCI identification and cognitive decline progression in affected patients. This circRNA may contribute to cognitive impairment pathogenesis in T2DM, potentially through mechanisms involving glucose metabolism dysregulation.

Oral microbiota is the second largest microbial colony in the body and forms a complex ecological community that influences oral and brain health. Impaired homeostasis of the oral microbiota can lead to pathological changes, resulting in central nervous system (CNS) diseases. However, the mechanisms and clinical value of how the oral microbiome influences the brain remain unclear. This review summarizes recent clinical findings on the role of the oral microbiota in CNS diseases and proposes potential approaches to understand the way the oral microbiota and brain communicate. We propose three underlying patterns involving neuroinflammation, neuroendocrine regulation, and CNS signaling between oral microbiota and CNS diseases. We also summarize the clinical characteristics and potential utilization of the oral microbiota in ischemic stroke, Alzheimer's and Parkinson's disease, intracranial aneurysms, and mental disorders. Although the current findings are preliminary and clinical evidence is incomplete, oral microbiota is a potential biomarker for the clinical diagnosis and treatment of CNS diseases.

Growing evidence has suggested that elevated Trimethylamine N-oxide (TMAO) levels, a gut microbiota-dependent metabolite, are closely associated with brain aging and cognitive impairment. Glycogen synthase kinase-3 beta (GSK-3β) activity was depicted to be essential in regulating learning and memory. The current study examined the impact of TMAO on cognitive function in mild cognitive impairment (MCI) patients and rat models while exploring the mechanisms regulating the TMAO-induced GSK-3β signaling. This study recruited 115 MCI patients and 128 healthy controls. All participants underwent neuropsychological assessments. Fasting plasma TMAO was measured using high-performance liquid chromatography with online electrospray ionization tandem mass spectrometry. The study also explored whether the GSK-3β signaling was involved in cognitive and function deficits linked with elevated TMAO in rat models. Our results indicated that TMAO plasma levels were elevated in MCI patients compared to healthy controls, depicting a significant association with potential MCI risk. Furthermore, chronic exposure to choline considerably impacted spatial cognitive performance in the Morris water maze task. This reduced the phosphorylation of Ser9 of GSK-3β and the synaptic plasticity-related proteins within the hippocampus, which could be restored by inhibiting TMAO with ABS. In addition, inhibition of GSK-3β by SB216763 significantly prevented the TMAO-induced synaptic damage while decreasing the membrane level of GluA1 and improving hippocampal learning and memory. These results indicate that TMAO can induce hippocampal-dependent learning and memory ability impairment with deficits in synaptic plasticity by regulating the GSK-3β activity.

BackgroundBrain structural abnormalities have been associated with cognitive impairment in individuals with small cerebral vascular disease (CSVD). However, the molecular and cellular factors making the different brain structural regions more vulnerable to CSVD-related cognitive impairment remain largely unknown.Materials and methodsVoxel-based morphology (VBM) was performed on the structural magnetic resonance imaging data of 46 CSVD-related cognitive impairment and 73 healthy controls to analyze and compare the gray matter volume (GMV) between the 2 groups. Transcriptome-neuroimaging spatial correlation analysis was carried out in combination with the Allen Human Brain Atlas to explore gene expression profiles associated with changes in cortical morphology in CSVD-related cognitive impairment.ResultsVBM analysis demonstrated extensive decreased GMV in CSVD-related cognitive impairment in the bilateral temporal lobe and thalamus, especially the hippocampus, thalamus, parahippocampus, and fusiform, and the left temporal lobe showed a more severe atrophy than the right temporal lobe. These brain structural alterations were closely related to memory and executive function deficits in CSVD-related cognitive impairment. Furthermore, a total of 1,580 genes were revealed to be significantly associated with regional change in GMV. The negatively and positively GMV-linked gene expression profiles were mainly enriched in RNA polymerase II, catalytic activity acting on a nucleic acid, aminoacyltransferase activity, axonogenesis, Golgi membrane, and cell junction organization.ConclusionOur findings suggest that brain morphological abnormalities in CSVD-related cognitive impairment are linked to molecular changes involving complex polygenic mechanisms, highlighting the interplay between genetic influences and structural alterations relevant to CSVD-related cognitive impairment.

Excessive daytime sleepiness (EDS), a prevalent non-motor symptom in Parkinson’s disease (PD), significantly impacts the quality of life for PD patients and elevates the risks of injury. Our study is to investigate the altered cortical surface morphology characteristics in PD patients with EDS (PD-EDS). Clinical data and magnetic resonance imaging were obtained from the Parkinson’s Progression Marker Initiative database, comprising 36 PD-EDS and 98 PD patients without EDS (PD-nEDS). The computational anatomy toolbox was utilized to derive sulcus depth (SD) and deep grey matter (GM) nuclei volumes. PD-EDS patients exhibited significantly decreased SD values in the right caudal middle frontal gyrus, pars opercularis, and superior temporal cortex relative to PD-nEDS patients. However, no significant differences in deep GM nuclei volumes were identified. Receiver operating characteristic (ROC) curve analyses further revealed that these cortical SD values could potentially serve as a screening index for distinguishing PD-EDS from PD-nEDS. Additionally, although PD-EDS patients had a longer disease duration and poorer performance in motor function and depression compared to PD-nEDS patients, these factors were included as covariates in the neuroimaging analyses. Our study findings demonstrated that decreased cortical SD values might induce sleep-wake state instability and contribute to the pathophysiological mechanisms of EDS in early-stage PD.

AIMS:The study attempted to determine the underlying role and regulation mechanism of 3β-hydroxysterol-Δ24 reductase (DHCR24) in the pathophysiology of cerebral small vessel disease-associated cognitive impairment (CSVD-CI). An RNA high-throughput sequencing and independent verification were conducted to identify potential circRNAs becoming the upstream regulator. METHODS:RNA sequencing was performed in whole-blood samples in cohort 1 (10 CSVD-CI and 8 CSVD with cognitively normal [CSVD-CN] patients). The DHCR24 and candidate circRNAs were verified in an independent cohort 2 (45 CSVD-CI participants and 37 CSVD-CN ones). The study also analyzed comprehensive cognitive assessments, plasma molecular index, and brain structure imaging. RESULTS:The expression of DHCR24 and has_circ_0015335 in whole-blood samples of CSVD-CI patients was significantly reduced compared to CSVD-CN patients in RNA sequencing and independent verification. Furthermore, the levels of DHCR24 and has_circ_0015335 were significantly related to global cognitive impairment in CSVD-CI patients. Meanwhile, DHCR24 could regulate the correlation between has_circ_0015335 expression and alterations in brain cortex in surface area, thickness, and volume in CSVD-CI patients. Additionally, hsa_circ_0015335 interacted with DHCR24 for plasma 24(S)-hydroxycholesterol levels among CSVD-CI patients. CONCLUSION:Interaction between DHCR24 and hsa_circ_0015335 cognitively impaired CSVD by affecting brain cholesterol metabolism and brain structural changes.

As the pathogenesis of cerebral small vessel disease with cognitive impairment (CSVD-CI) remains unclear, identifying effective biomarkers can contribute to the clinical management of CSVD-CI. This study recruited 54 healthy controls (HCs), 60 CSVD-CI patients, and 57 CSVD cognitively normal (CSVD-CN) patients. All participants underwent neuropsychological assessments and multimodal magnetic resonance imaging. Macrophage migration inhibitory factors (MIFs) were assessed in plasma. The least absolute shrinkage and selection operator model was used to determine a composite marker. Compared with HCs or CSVD-CN patients, CSVD-CI patients had significantly increased plasma MIF levels. In CSVD-CI patients, plasma MIF levels were significantly correlated with multiple cognitive assessment scores, plasma levels of blood-brain barrier (BBB)-related indices, white matter hyperintensity Fazekas scores, and the mean amplitude of low-frequency fluctuation in the right superior temporal gyrus. Higher plasma MIF levels were significantly associated with worse global cognition and information processing speed in CSVD-CI patients. The composite marker (including plasma MIF) distinguished CSVD-CI patients from CSVD-CN and HCs with >80% accuracy. Meta-analysis indicated that blood MIF levels were significantly increased in CSVD-CI patients. In conclusion, plasma MIF is a potential biomarker for early identification of CSVD-CI. Plasma MIF may play a role in cognitive decline in CSVD through BBB dysfunction and changes in white matter hyperintensity and brain activity.

目的 探析PAC心理弹性理论模型结合感统训练应用于缺血性脑卒中偏瘫患者中的临床效果.方法 选取2021年2月-2022 年1月我院收治的缺血性脑卒中偏瘫患者130例为研究对象,根据随机数字表法分为对照组和观察组,各65例.对照组实施常规功能康复训练,观察组实施PAC心理弹性理论模型结合感统训练.比较两组运动功能、日常生活能力、并发症发生率、心理弹性以及生活质量.结果 两组干预后运动功能、日常生活能力评分高于干预前(P＜0.05),且观察组高于对照组(P＜0.05);观察组并发症发生率低于对照组(P＜0.05);两组干预后心理弹性评分高于干预前(P＜0.05),且观察组高于对照组(P＜0.05);两组干预后生活质量评分高于干预前(P＜0.05),且观察组高于对照组(P＜0.05).结论 PAC心理弹性理论模型结合感统训练应用于缺血性脑卒中偏瘫患者中,可有效增强其运动功能、日常生活能力,减少并发症的发生,并显著增强患者的心理弹性,促进其生活质量的提高.

目的 探讨肠道菌群代谢产物氧化三甲胺(TMAO)对糖尿病急性缺血性卒中患者早期神经功能恶化(END)发生的影响.方法 采用横断面研究的方法,连续收集2019年10月至2020年11月南京医科大学附属无锡人民医院神经内科收治的108例糖尿病急性缺血性卒中患者.将发病5 d内出现原有神经功能缺损症状加重、美国国立卫生研究卒中量表(NIHSS)评分增加≥2分,且头颅影像学评估排除颅内出血和出血转化定义为END,根据是否出现END,将患者分为END组(36例)与无END组(72例).采用稳定同位素稀释液相色谱/质谱联用法测定血浆TMAO水平.结果 108例患者中,36例(33.3％)诊断为END,END组血浆TMAO水平高于无END组(Z=-3.500,P＜0.001),TMAO 预测 END 的 ROC 曲线下面积为 0.707(95％CI:0.603～0.811,P＜0.001).根据TMAO水平三分位分组,低、中、高三组患者END的发生率分别为22.2％、19.4％、58.3％,三组之间差异有统计学意义(x2=14.979,P=0.001);单因素分析显示,血浆TMAO水平与END的发生明显相关(OR=1.160,95％CI:1.050～1.282,P=0.004),多因素 Logistic 回归分析显示 TMAO 与 END 的发生依旧显著相关(OR=1.145,95％CI:1.033～1.269,P=0.010).结论 糖尿病急性缺血性卒中患者血浆TMAO水平与END的发生密切相关,TMAO水平越高,END发生的风险越大.

To investigate the efficacy and safety of intravenous thrombolytic (IVT) therapy and endovascular (EV) therapy in patients with acute posterior large vessel occlusion stroke (PLVOS). A total of fifty patients with acute PLVOS were randomly divided into the IVT group and EV group. The general baseline data, post-treatment vascular recanalization rate, National Institute of Health Stroke Scale (NIHSS) score before and after intervention, prognosis, and perioperative complications were compared between the two groups. There were no significant differences in the overall baseline data between the two groups (p > 0.05). The post-treatment recanalization rate was significantly higher in the EV group (88.00%) than in the IVT group (64.00%, p < 0.05). The NIHSS score at 24 h post-admission was significantly lower and prognosis was significantly better in the EV group than in the IVT group (both p < 0.05). The EV group had significantly lower overall complication rate (16.00%) than the IVT group (48.00%, p < 0.05). Compared with IVT therapy, EV therapy can effectively improve neurological damage, vascular recanalization rate and prognosis as well as reduce the incidence of perioperative complications in patients with acute PLVOS.

No acceptable biomarker can facilitate the early identification of cognitive impairment associated with cerebral small vessel disease (CSVD) in the older persons. The neutrophil extracellular traps (NETs) in the inflammation response of circulatory and central systems are essential in destroying the blood-brain barrier. The present study aims to explore the potential associations of plasma NETs with cognitive performance in CSVD. We recruited 146 CSVD patients and 66 healthy controls (HCs), and comprehensive neuropsychological assessments and multimodal magnetic resonance imaging were conducted. Three NETs markers, namely citrullination of histone H3, neutrophil elastase-DNA, and myeloperoxidase (MPO)-DNA, and 4 oxidative stress-related indexes in plasma samples, were measured. The plasma levels of 3 NETs markers were more significantly elevated in CSVD patients than in HCs. Significant correlations of the 3 NETs markers were observed with multiple cognitive domain scores. Furthermore, higher plasma malondialdehyde and NETs levels were significantly associated with the worse Montreal Cognitive Assessment scores among CSVD patients. Moreover, plasma MPO-DNA levels significantly mediated the effect of the amplitude of low-frequency fluctuation value within the bilateral caudate and the scores of global cognitive function, executive function, and information processing speed. Additionally, a panel of 3 NETs markers had the highest area under the curve value to distinguish the cognitively impaired CSVD patients from HCs and nonimpaired ones. Therefore, plasma NETs may be potential biomarkers for early diagnosis of CSVD-related cognitive impairment. Activated lipid peroxidation in circulation and impaired caudate function support potential associations of plasma NETs in cognitively impaired CSVD patients.

BackgroundCerebral small vessel disease (CSVD) is a cluster of microvascular disorders with unclear pathological mechanisms. The microbiota-gut-brain axis is an essential regulatory mechanism between gut microbes and their host. Therefore, the compositional and functional gut microbiota alterations lead to cerebrovascular disease pathogenesis. The current study aims to determine the alteration and clinical value of the gut microbiota in CSVD patients. MethodsSixty-four CSVD patients and 18 matched healthy controls (HCs) were included in our study. All the participants underwent neuropsychological tests, and the multi-modal magnetic resonance imaging depicted the changes in brain structure and function. Plasma samples were collected, and the fecal samples were analyzed with 16S rRNA gene sequencing. ResultsBased on the alpha diversity analysis, the CSVD group had significantly decreased Shannon and enhanced Simpson compared to the HC group. At the genus level, there was a significant increase in the relative abundances of Parasutterella, Anaeroglobus, Megasphaera, Akkermansia, Collinsella, and Veillonella in the CSVD group. Moreover, these genera with significant differences in CSVD patients revealed significant correlations with cognitive assessments, plasma levels of the blood-brain barrier-/inflammation-related indexes, and structural/functional magnetic resonance imaging changes. Functional prediction demonstrated that lipoic acid metabolism was significantly higher in CSVD patients than HCs. Additionally, a composite biomarker depending on six gut microbiota at the genus level displayed an area under the curve of 0.834 to distinguish CSVD patients from HCs using the least absolute shrinkage and selection operator (LASSO) algorithm. ConclusionThe evident changes in gut microbiota composition in CSVD patients were correlated with clinical features and pathological changes of CSVD. Combining these gut microbiota using the LASSO algorithm helped identify CSVD accurately.

BackgroundNon-valvular atrial fibrillation (NVAF) is the most common cause of cardiogenic cerebral embolism (CCE). However, the underlying mechanism between cerebral embolism and NVAF is indefinite, and there is no effective and convenient biomarker to identify potential risk of CCE in patients with NVAF in clinic. The present study aims to identify risk factors for interpreting the potential association of CCE with NVAF and providing valuable biomarkers to predict the risk of CCE for NVAF patients. Methods641 NVAF patients diagnosed with CCE and 284 NVAF patients without any history of stroke were recruited in the present study. Clinical data including demographic characteristics, medical history, and clinical assessments, were recorded. Meanwhile, Blood cell counts, lipid profiles, high-sensitivity C-reactive protein, and coagulation function-related indicators were measured. Least absolute shrinkage and selection operator (LASSO) regression analysis was utilized to build a composite indicator model based on the blood risk factors. Results(1) CCE patients had significantly increased neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio (PLR), and D-dimer levels as compared with patients in the NVAF group, and these three indicators can distinguish CCE patients from ones in the NVAF group with an area under the curve (AUC) value of over 0.750, respectively. (2) Using the LASSO model, a composite indicator, i.e., the risk score, was determined based on PLR and D-dimer and displayed differential power for distinguishing CCE patients from NVAF patients with an AUC value of over 0.934. (3) The risk score was positively correlated with the National Institutes of Health Stroke Scale and CHADS2 scores in CCE patients. (4) There was a significant association between the change value of the risk score and the recurrence time of stroke in initial CCE patients. ConclusionsThe PLR and D-dimer represent an aggravated process of inflammation and thrombosis in the occurrence of CCE after NVAF. The combination of these two risk factors can contribute to identifying the risk of CCE for patients with NVAF with an accuracy of 93.4%, and the greater in change of composite indicator, the shorter in the recurrence of CCE for NVAF patients.

Objective To analyze the influencing factors for post-stroke depression(PSD)in young and middle-aged patients with ischemic stroke and build a PSD prediction model.Methods A total of 102 patients with ischemic stroke who were treated in Wuxi People's Hospital Affiliated to Nanjing Medical University from January 2020 to March 2021 were selected for PSD model construction.The model was validated in 82 middle-aged and young adults with ischemic stroke from June 2021 to October 2022.According to the results of SDS scale screening,102 patients were divided into PSD group(n=30)and non-PSD group(n=72),and the clinical data of the two groups were compared.Multivariate Logistic regression analysis was used to determine the influencing factors for PSD and construct the prediction model.The model was used to predict PSD in 82 patients,and the SDS test results were used as the gold standard to verify the predictive value of the model.Results In PSD group,the percentage of family per capita income≤5 000,the number of multi-focal lesions,NIHSS score and SSS score were higher than those in non-PSD group,and the HHI score was lower than that in non-PSD group,with statistically significant differences(P＜0.05).Multivariate Logistic regression analysis showed that per capita monthly household income(OR=1.485,95%CI:1.097-2.010),number of lesions(OR= 2.014,95%CI:1.218-3.330),NIHSS score(OR=1.681,95%CI:1.111-2.543),SSS score(OR=1.895,95%CI:1.305-2.760)and HHI score(OR=0.397,95%CI:0.203-0.776)were the influencing factors for PSD in young and middle-aged patients with ischemic stroke(P＜0.05).According to the regression coefficient and constant term,the expression equation of the prediction model is obtained:Logit(P)=0.395×family per capita monthly income+0.700×number of lesions+0.519×NIHSS score+0.641×SSS score-0.924×HHI score-27.984.According to the patient evaluation results,the probability of patients developing PSD can be obtained by applying the above model.Using the maximum approximate entry index,the model threshold is 0.614.The model was used to predict PSD in 82 patients,and 0.614 was used as the basis(＞0.614 was PSD,≤0.614 was non-PSD)to predict PSD in 26 patients and non-PSD in 56 patients.Using SDS as the gold standard(21 patients with PSD and 61 patients without PSD),the sensitivity of the model to predict PSD was 85.71%(18/21),the specificity was 86.88%(53/61),and the accuracy was 86.58%(71/82).Conclusion According to the PSD prediction model,the high-risk PSD can be identified early,and effective measures can reduce the stigma of patients,improve the level of hope,and reduce the incidence of PSD.

急性缺血性卒中( acute ischaemic stroke,AIS)是最常见的脑血管病,具有较高的致残率及病死率,多达70％的AIS患者患有中度或重度功能障碍[1].目前已有成熟的影像学技术( CT、MRI 等)用于 AIS 的早期诊断,但有时仍受到病情、环境、设备等条件的限制,此时通过其他技术了解和判断颅内病变严重程度和动态演变过程显得尤为重要.脑电图( Electroencephalogram,EEG)是检测、描述和监测健康人群和临床人群大脑功能的有力工具,具有极高的时间分辨率,对缺血、缺氧引起的神经功能变化非常敏感,能够简便、无创、快速、动态地评估瞬时脑功能.在过去的数十年里, EEG在AIS中的临床应用已经被广泛报道.有学者对这类研究进行了归纳分析,得出结论:EEG在AIS的早期诊断、预后判断、治疗方案指导和癫痫发作检测等方面都有着重要的参考价值[2].本文总结了近年来EEG在AIS中的最新研究进展,并强调了定量脑电图( quantitative electroencephalographic, QEEG)的临床意义.