ObjectiveTo grasp the occurrence pattern and epidemiological characteristics of poisonous mushroom poisoning events in China from 2014 to 2023, thus providing a basis for the prevention and control of poisonous mushroom poisoning. MethodsThe epidemiological characteristics of poisonous mushroom poisoning incidents reported by the Public Health Emergency Reporting Management Information System (PHERMIS) nationwide from 2014 to 2023 were descriptively analyzed. ResultsFrom 2014 to 2023, a total of 570 poisonous mushroom poisoning incidents were reported nationwide, involving 2 768 reported poisoning cases and 604 deaths. The incidents with 1 to 2 cases and 1 death were predominant, accounting for 35.79% and 48.77% of the total number of incidents, respectively. June to September was the period with high incidence (83.51%) of poisonous mushroom poisoning. Yunnan, Sichuan, and Guizhou were the provinces with higher incidence of poisonous mushroom poisoning, with the reported incidents accounting for 35.79%, 16.32%, and 10.70% of the total, respectively. Self-picked poisonous mushrooms were the main source of poisoning, which accounted for 91.75% of the total number of incidents. The occurrence place of the incidents was mainly households, which accounted for 86.67% of the total number of incidents. Twenty-four species of poisonous mushrooms were identified through the surveillance reports, of which Amanita (Amanitaceae) caused the highest number of poisonous mushroom poisoning incidents, poisoning, and deaths, which accounted for 23.86%, 18.03%, and 31.46% of the total, respectively. ConclusionsDeaths caused by poisonous mushroom poisoning remain the main factor of deaths caused by food poisoning. The incidence is high in summer and fall, and accidental picking and ingestion by families are the main cause. The poisonous mushrooms eaten by mistake mainly belong to Amanita.

Type 2 diabetes mellitus (T2DM), as a noncommunicable chronic disease, poses a significant threat to human health. This study aims to investigate the relationship between lipid ratios and T2DM. The China Health and Retirement Longitudinal Study served as the data source for this research. The associations between lipid ratios - specifically, the non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR), remnant cholesterol to high-density lipoprotein cholesterol (RC/HDL-C) ratio, triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio, total cholesterol to high-density lipoprotein cholesterol (TC/HDL-C) ratio, and low-density lipoprotein cholesterol to high-density lipoprotein cholesterol (LDL-C/HDL-C) ratio - and T2DM were analyzed using logistic regression analysis. Restricted cubic splines were employed to explore potential nonlinear relationships. Receiver operating characteristic analysis was utilized to assess the predictive value of lipid ratios for T2DM. A total of 7199 participants were included in this study. After adjusting for various factors, a positive association was identified between NHHR, RC/HDL-C ratio, TC/HDL-C ratio, TG/HDL-C ratio, and LDL-C/HDL-C ratio, with odds ratios of 3.34, 2.45, 3.34, 2.75, and 2.92, respectively. Nonlinear relationships were observed between NHHR, RC/HDL-C ratio, TC/HDL-C ratio, TG/HDL-C ratio, and LDL-C/HDL-C ratio and the incidence of T2DM. This study demonstrates that lipid ratios are associated with an increased risk of T2DM. This result provides a basis for the early identification of T2DM and identify novel targets for its prevention and early intervention.

Improving medication literacy among individuals with hypertension has emerged as a significant public health issue. However, the heterogeneity of medication literacy and its association factors among young and middle-aged patients with hypertension has not yet been fully characterized. The current study aimed to identify distinct profiles of medication literacy in these population and to examine their associated factors, with the goal of informing targeted clinical interventions. A cross-sectional study was conducted with 544 consecutively recruited these hypertensive patients from two tertiary hospitals in China between July 15 and November 15, 2024. Researchers administered five validated instruments: a Demographic and Disease-Related Characteristics Questionnaire, the Revised Chinese Medication Literacy Scale for Hypertensive Patients (C-MLSHP-R), the Perceived Social Support Scale (PSSS), the General Self-Efficacy Scale (GSES), and the Brief Illness Perception Questionnaire (BIPQ). Latent profile analysis revealed three distinct profiles of medication literacy: low (35.3%), moderate (50.2%), and high (14.5%). Multivariate logistic regression further identified education level, per capita monthly household income, social support, self-efficacy, and illness perception as factors significantly associated with medication literacy (all p < 0.05). More specifically, lower education and lower income were associated with membership in the low literacy profile, while higher social support, higher self-efficacy, and more positive illness perception characterized the high literacy group. These results suggest preliminary stratified interventions approaches, including foundational education for patients with low-literacy patients, behavioral reinforcement for those with moderate literacy, and enhanced psychosocial support for socioeconomically disadvantaged groups. However, causal interpretations are precluded by the cross-sectional design, longitudinal studies are needed to validate these findings.

Objective: This study aims to create a prognostic nomogram by combining clinicopathologic variables that are linked to the overall survival following the surgical removal of esophageal squamous cell carcinoma. Methods: A total of 224 patients with esophageal cancer who underwent surgical R0 resection were included. The construction of the nomogram involved using a multivariable Cox proportional hazards regression model. To evaluate the model's effectiveness, Kaplan-Meier curves and calibration plots were used for discrimination and calibration, respectively. Results: Nearly half of the patients were >60 years old (45.1%), and 95.5% of the patients were male. After esophageal cancer resection, 35.7% of patients experienced complications, with 23.7% developing anastomotic stenosis and 4.5% developing a fistula. Using the backward selection of clinically relevant variables, we found that tumor located in middle thoracic (hazard ratio 2.299, 95% confidence interval 1.008-5.244), anastomotic fistula (3.028, 1.436-6.384), and vascular invasion (2.175, 1.496-3.108) were independently associated with mortality (all P < .05), whereas lymph node clearance >15 nodes is associated with longer survival (0.444, 0.278-0.710) (P = .001). On the basis of these factors, a nomogram was created to predict survival of esophageal squamous cell carcinoma after resection. Discrimination using Kaplan-Meier curves, calibration curves, and bootstrap cross-validation revealed good predictive abilities (C index, 0.673). Conclusions: A nomogram was created based on the experience from northeast China to forecast overall survival following resection for esophageal squamous cell carcinoma. The validation process demonstrated accurate distinction and calibration, indicating the practical value of the nomogram in enhancing personalized survival predictions for patients who undergo esophageal squamous cell carcinoma resection in this study population. (c) 2024 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

Background:Heatstroke causes numerous pathophysiological changes and can lead to death. Extreme heat events have been increasing in frequency, duration, and intensity worldwide in recent decades and are causing growing public health concern. However, epidemiological studies of heatstroke are limited in number and scope, and have had relatively small sample sizes. To better understand the epidemiological characteristics of heatstroke and advance evidence-based prevention and control strategies, we conducted an observational study of reported heatstroke cases in China. Methods:Cases included in this study were patients clinically diagnosed with heatstroke during the study period of 2010-2023, reported through a dedicated heatstroke surveillance system established by China CDC. We used descriptive statistical methods to determine the epidemiological characteristics of heatstroke in China. Findings:There were 86,406 heatstroke cases reported during the study period, with an increasing reporting trend (Spearman correlation coefficient r = 0·79). Annual incidence (Spearman r = 0·77) and proportion of severe cases (Pearson r = 0·67) were positively correlated with the number of nationwide average annual high-temperature days. The overall incidence was 44·83 per 10 million person-years, and the mortality rate was 0·89 per 10 million person-years; 32·02% of cases were severe; the overall case fatality rate (CFR) was 1·98%, and the CFR for severe cases was 6·19%. Most cases and deaths were reported in summer, with peaks in late July. The peaks of incidence, duration, and severity varied by region. The mean age was (50·46 ± 18·73) years, with male cases younger than female cases (49·21 ± 17·41 vs 53·60 ± 21·36; t = -28·73, p < 0·0001). For every five-year increase in age, the risks of severe heatstroke and death increased by 14·64% (95% CI: 1·1415-1·1513) and 25·76% (CI: 1·2400-1·2755), respectively. The male:female ratio was 2·49:1; males exhibited a higher risk of suffering from heatstroke and having greater disease severity than females. Interpretation:Our study provides a clear profile of heatstroke cases, and highlights differences by population, region, and time of year. Results inform formulation of evidence-based strategies for enhanced heatstroke preparedness and response, such as enhancing public health early warning systems, prioritizing protection for vulnerable groups, and advancing localized interventions for risk communication and clinical management. Funding:Public Health Talent Program of China's National Disease Control and Prevention Administration.

[This corrects the article DOI: 10.1016/j.lanwpc.2025.101722.].

Nursing staff health status is pivotal to healthcare system resilience during global health crises. This study aims to comprehensively evaluate nurses’ mental health profiles, focusing on the prevalence of depression, anxiety, and somatization symptoms and their associations with career development stages, to inform targeted health interventions. A cross-sectional assessment of 107 nurses from a tertiary hospital was conducted using validated scales: Patient Health Questionnaire-9 (PHQ-9) for depression, Generalized Anxiety Disorder-7 (GAD-7) for anxiety, and Patient Health Questionnaire-15 (PHQ-15) for somatization. Demographic variables included gender, age, education level, professional title, marital status, parenthood, and work experience. Multivariate logistic regression, chi-square tests, and Fisher’s exact test were employed to analyze associations between education, age, professional title, and mental health outcomes. Most nurses exhibited no significant depression (81.3

BackgroundPost-stroke cognitive impairment is characterized by cognitive dysfunction occurring within 6 months post-stroke. Telemedicine uses communication technologies to deliver healthcare remotely and has shown efficacy in improving cognitive impairment. However, a systematic review specifically evaluating telemedicine's effects on cognitive outcomes in post-stroke cognitive impairment is lacking.ObjectivesThis systematic review aimed to examine the effectiveness of telemedicine interventions for cognitive function in post-stroke cognitive impairment.MethodsA comprehensive search was performed across 10 electronic databases, including PubMed, Web of Science, CINAHL, EMBASE, Cochran library, Scopus, and ProQuest Dissertations and three Chinese-language databases (CNKI, Wan Fang, and Vip) from their respective inception dates to May 2025. This review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses. Meta-analysis was performed by the use of Review Manager 5.3 and Stata 15.ResultsThe initial search yielded 10,365 articles, with 19 studies included in the systematic review. The results showed that telemedicine interventions had a significant moderate effect on global cognition (standardized mean difference (SMD = 0.69, Z = 4.23, P < 0.01) and significantly improved visuospatial function (SMD = 0.57, Z = 2.76, P < 0.05) and language (SMD = 0.62, Z = 2.59, P < 0.05). Sub-group analyses showed significant effects for both online tools or computer software and mobile apps, though high heterogeneity was noted. Additionally, telemedicine interventions had a significant effect on activities of daily living (SMD = 0.64, Z = 5.16, P < 0.01).ConclusionConsidering the obstacles and limitations of traditional face-to-face rehabilitation, telemedicine is an effective approach for treating post-stroke cognitive impairment that can significantly improve cognitive function. Future studies should address heterogeneity through rigorous designs, long-term follow-ups, neuroimaging, and biomarker integration to elucidate underlying mechanisms.The protocol was registered on PROSPERO (CRD42024502185).

Objective: Dietary inflammatory index (DII) and handgrip strength (HGS) were correlated, and both were associated with cardiovascular disease (CVD). However, the role of the 10-year CVD risk in the relationship between DII and grip strength remains uncertain. Methods: This study involved 5691 adults from the National Health and Nutrition Examination Survey (NHANES) in 2011–2014. Dietary inflammation, 10-year CVD risk and relative grip strength were assessed by the Dietary Inflammation Index, the Framingham Risk Score (FRS) and handgrip strength adjusted BMI. Linear regression analyses and mediation analysis were used to explore these associations. Results: Both DII and 10-year CVD risk were negatively associated with relative handgrip strength, and DII was positively associated with 10-year CVD risk. Additionally, 10-year CVD risk partially mediated the association between DII and relative handgrip strength by a 11.8% proportion. Specifically, the mediating effect of the 10-year risk of CVD varied by gender and age. Conclusions: Reducing the 10-year risk of CVD attenuates the effect of an inflammatory diet on relative grip strength impairment. Therefore, we recommend reducing the effect of inflammatory diet on grip strength impairment by controlling any of the FRS parameters, such as lowering blood pressure and smoking cessation, especially with targeted measures for different populations.

Introduction Dietary with higher inflammatory potential are associated with cardiovascular disease (CVD) risk over the next decade, while studies have shown body mass index (BMI) to be one of the mediators between dietary inflammatory index (DII) and multiple diseases such as depression and diabetes. However, the role of BMI in the association between DII and 10-year risk of CVD is unclear. Methods Study based on 14,355 adults from the National Health and Nutrition Examination Survey (NHANES). Participants’ diet, obesity level and CVD risk were assessed using the DII, BMI and Framingham Risk Score (FRS). Linear regression and counterfactual model were used to analyze this relationship. Results Participants on a pro-inflammatory diet had a higher risk of CVD over the next ten years compared to participants on an anti-inflammatory diet. Counterfactual models showed a 34.0% partial mediating role of BMI in this relationship, most particularly in males (17.3%) and non-elderly (28.6%-100%). Conclusion Inflammatory diet adversely affects cardiovascular risk, a large part of which operates through BMI, especially in males and non-elderly populations. These findings are beneficial in facilitating research on the mechanisms of diet-related inflammation on CVD. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement The National Natural Science Foundation of China provided funding for this project (No.81973129). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Not Applicable The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Jilin University I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Not Applicable I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Not Applicable I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Not Applicable Data described in the manuscript, code book, and analytic code will be made publicly and freely available without restriction at [.

Rationale and objective Post-traumatic stress disorder (PTSD) is a prevalent and debilitating psychiatric disorder. However, its specific etiological mechanism remains unclear. Previous studies have shown that traumatic stress changes metabotropic glutamate receptor 5 (mGluR5) expression in the hippocampus (HIP) and prefrontal cortex (PFC). More importantly, mGluR5 expression is often accompanied by alterations in brain-derived neurotrophic factor (BDNF). Furthermore, BDNF/tropomyosin-associated kinase B (TrkB) signaling plays multiple roles, including roles in neuroplasticity and antidepressant activity, by regulating glutamate transporter-1 (GLT-1) expression. This study aims to explore the effects of inhibiting mGluR5 on PTSD-like behaviors and BDNF, TrkB, and GLT-1 expression in the HIP and PFC of inevitable foot shock (IFS)-treated rats. Methods Seven-day IFS was used to establish a PTSD rat model, and 2-methyl-6-(phenylethynyl)-pyridine (MPEP) (10 mg/kg, intraperitoneal injection) was used to inhibit the activity of mGluR5 during IFS in rats. After modeling, behavioral changes and mGluR5, BDNF, TrkB, and GLT-1 expression in the PFC and HIP were examined. Results First, the IFS procedure induced PTSD-like behavior. Second, IFS increased the expression of mGluR5 and decreased BDNF, TrkB, and GLT-1 expression in the PFC and HIP. Third, the mGluR5 antagonist blocked the above behavioral and molecular alterations. Conclusions mGluR5 was involved in IFS-induced PTSD-like behavior by changing BDNF, TrkB, and GLT-1 expression.

Background: The association between renal impairment (RI) and stroke outcome after endovascular thrombectomy (EVT) remains unclear, which limits the estimation of patient prognosis by clinicians involved in EVT decision-making. Purpose: This study aimed to investigate the association between RI and acute ischemic stroke (AIS) outcomes in patients treated with EVT. Methods: Studies involving the association between RI at admission and AIS outcomes after EVT were retrieved from the PubMed and Embase databases from their inception to 17 January 2022. A fixed-effects model was used to synthesize the data of the included studies. Sensitivity analysis was performed to identify the source of heterogeneity. Results: Overall, 11 studies, including 5053 patients with stroke receiving EVT, were included in the full analysis. In unadjusted analyses, RI was associated with 3-month poor functional outcome and mortality; the odds ratios (ORs) were 2.13 [10 studies; 95% confidence interval (CI), 1.77–2.56; I 2 = 45%] and 2.42 (8 studies; 95% CI, 2.02–2.90; I 2 = 58%), respectively. In adjusted analyses, the above associations remained significant; the OR of the 3-month poor functional outcome was 1.49 (5 studies; 95% CI, 1.17–1.90; I 2 = 58%), and the OR of the 3-month mortality was 1.84 (6 studies; 95% CI, 1.45–2.33; I 2 = 74%). Similar results were obtained in sensitivity analyses. Conclusion: Our results suggest that in patients with AIS who underwent EVT, RI at admission was associated with 3-month poor functional outcome and mortality.

Obesity and depression tend to co-occur, and obese patients with chronic low-grade inflammation have a higher risk of developing depression. However, mechanisms explaining these connections have not been fully elucidated. Here, an animal model of comorbid obesity and depression induced by high-fat diet (HFD) combined with chronic unpredictable mild stress (CUMS) was used, and sucrose preference, open field, elevated plus maze and Morris water maze tests were used to detected depression-and anxiety-like behaviors and spatial memory. The levels of inflammatory cytokines and NF-κB and microglial activation in the hippocampus and prefrontal cortex were examined in the study. Our results revealed that the comorbidity group exhibited the most severe depression-like behavior. Obesity but unstressed rats had the highest serum lipid levels among groups. The HFD and CUMS alone and combination of them increased levels of IL-1β, IL-6 and TNF-α in the hippocampus and prefrontal cortex, which was significantly related to depression-like behaviors. Further, NF-κB protein and mRNA levels and microglial activation in the hippocampus and prefrontal cortex significantly increased in stressed, obese and comorbid groups, with animals in comorbid group having the highest NF-κB mRNA levels in the hippocampus and level of NF-κB proteins in the prefrontal cortex, and the highest microglial activation in both brain areas. The study concluded that HFD and CUMS alone and combination induce depression-like symptoms, abnormal serum lipid levels, microglial activation and increased inflammatory cytokines in the brain, effects that are possibly mediated by TLR4-NF-κB signaling.

Post-traumatic stress disorder (PTSD) is characterized by depression/anxiety and memory failure, primarily fear memory. According to the reports, neuroinflammation and synaptic plasticity can play a role in the neurophysiological mechanisms underlying PTSD. Bromodomain-containing protein 4 (Brd4) intriguingly affects regulating of inflammatory responses and learning and memory. This study aimed to explore the effect of inhibiting Brd4 on depression/anxiety-like behaviors, spatial and fear memory, and underlying mechanisms in a model of PTSD. Inescapable foot shocks (IFS) with a sound reminder in 6 days were used to induce PTSD-like behaviors which were tested using contextual and cue fear tests, sucrose preference test, open-field test, elevated plus maze test, and Y-maze test. Meanwhile, the Brd4 inhibitor JQ1 was used as an intervention. The results found that IFS induced PTSD-like behaviors and indicated obvious Brd4 expression in microglia of the prefrontal cortex (PFC), hippocampus, and amygdala, pro-inflammatory cytokines over-expression, microglial activation, and nuclear factor-kappa B over-expression in PFC and hippocampus but not in amygdala. Meanwhile, the alterations of immediate early genes (IEGs) were found in PFC, hippocampus, and amygdala. Besides, dendritic spine density was reduced in PFC and hippocampus but was elevated in amygdala of rats with IFS. In addition, treatment with JQ1 significantly reduced freezing time in the contextual and cue fear test, reversed the behavioral impairment, decreased the elevated neuroinflammation, and normalized the alteration in IEGs and dendritic spine densities. The results suggested that Brd4 was involved in IFS-induced PTSD-like behaviors through regulating neuroinflammation, dynamics of IEGs, and synaptic plasticity.

Background: Depression is a psychiatric disorder which is accompanied by neuroinflammatory responses. Obesity is considered as a low-grade inflammatory state. Studies have found that obese individuals are more likely to suffer from depression, but its possible mechanism has not been specifically illuminated. The Jumonji domain protein 3 (JMJD3) is a specific histone demethylase of trimethylation at lysine 27 of histone-H3 (H3K27me3). Over-expressions of JMJD3 induces the demethylation of H3K27me3 and results in the expression of pro inflammatory genes, while its upregulation may be limited by adiponectin (APN). However, the role of JMJD3 in susceptibility to neuminflammation and depression in obesity has not been clarified. Methods: Chronic unpredictable mild stress (CUMS) was selected to build depression model in C57BL/6 and ob/ob mice. Sucrose preference test, tail suspension test, open field test and Morris water maze test were used to detect depressive-like behaviors and memory impairment. Microglial activation, pro-inflammatory cytokines, APN, NF-kappa B, JMJD3 and H3K27me3 expressions in the serum, prefrontal cortex (PFC) and hippocampus (HIP) were examined in C57BL/6 and ob/ob mice. Meanwhile, GSK-J4 was used to inhibit JMJD3 expression. Results: CUMS led to depressive-like behaviors and memory impairment, microglial activation, increased expressions of pm-inflammatory cytokines, NF-kappa B and JMJD3, decreased expression of H3K27me3 in the PFC and HIP in C57BL/6 and ob/ob mice. Meanwhile, ob/ob mice showed worse behavioral injury and memory impairment, microglial excessively activation, over-expression of pm-inflammatory cytokines and NF-kappa B and decreased H3K27me3 levels than C57BL/6 mice. CUMS also decreased the APN levels in the serum and brain tissues in ob/ob mice compared to C57BL/6 mice. But GSK-J4 could relieve these alterations. Conclusions: JMJD3 might be involved in the susceptibility to depressive-like behaviors and neuroinflammation of obese mice by the demethylation of H3K27me3, and decreased levels of APN could reduce Enhancer of zeste homolog 2 (EZH2) binding with H3K27me3. The role of JMJD3 in severer inflammatory state in the comorbidity of obesity and depression was considered.

Background: There is an increased risk for obese patients with chronic low-grade inflammation to develop depression. Stress induces microglial activation and neuroinflammation that play crucial roles in the pathogenesis of depression. Peroxisome proliferator-activated receptor gamma (PPAR gamma), a nuclear transcription factor, regulates microglial polarization and neuroinflammation. Our study aimed to investigate the role of PPAR gamma in the development of depressive symptoms and neuroinflammation induced by chronic unpredictable mild stress (CUMS) in wild-type/C57BL/6J (wt) and leptin-deficient (ob/ob) mice. Methods: CUMS was used to build a depression model with wt and ob/ob mice. Depressive-like behaviors were evaluated by sucrose preference test, open field test, tail suspension test, and Morris water maze test. Cytokines, the activated microglial state, and nuclear factor-kappa B (NF-kappa B) and PPAR gamma expression in the prefrontal cortex (PFC) and hippocampus (HIP) were examined by enzyme-linked immunosorbent assay (ELISA), immunofluorescence, and western blotting. Additionally, pioglitazone, an agonist of PPAR gamma, was used as a treatment intervention. Results: After CUMS, ob/ob mice exhibited severe behavioral disorders and spatial memory impairment, and higher levels of pro-inflammatory cytokines, M1/M2 ratios, and NF-kappa B activation, as well as lower levels of anti-inflammatory cytokines and PPAR gamma expression in the PFC and HIP compared to wt mice. Administration of pioglitazone relieved these alterations in wt and ob/ob mice. Conclusions: CUMS was able to induce severe depressive-like behaviors, neuroinflammation, and reduced expression of PPAR gamma in ob/ob mice as compared to wt mice. This suggests that PPAR gamma mediates the microglial activation phenotype, which might be related to the susceptibility of stressed ob/ob mice to develop depressive disorder.

Adverse childhood experience is a major risk factor for the onset of depression in adulthood. Neuroinflammation characterized by microglial activation and cytokine secretion is involved in susceptibility to depression induced by early life stress. Jumonji domain-containing protein 3 (Jmjd3), a trimethylated lysine 27 in histone 3 (H3K27me3) demethylase, can be activated by nuclear factor-kappa B (NF-κB), further regulating the expression of pro-inflammatory cytokines and resulting in neuroinflammation. However, its involvement in susceptibility to early life stress-related depression is unknown. In the current study, maternal separation (MS) was utilized as a model of early life stress and systemic lipopolysaccharide (LPS) administration in adulthood was used as a later-life challenge. Depressive- and anxiety-like behaviors and memory impairment were detected by behavioral tests. Microglial activation, pro-inflammatory cytokine expression, and NF-κB, Jmjd3, and H3K27me3 expression were detected in the prefrontal cortex and hippocampus in both infant and adult rats. Meanwhile, the Jmjd3 inhibitor GSK-J4 was used as an intervention in vivo and in vitro. Our results showed that MS induced depression-like behaviors and synchronously caused microglial activation, pro-inflammatory cytokine over-expression, NF-κB and Jmjd3 over-expression, and decreased H3K27me3 expression in infant rats. All these alterations could also be detected in adulthood. Seven-day LPS administration in adult rats induced similar changes of behaviors and biomarkers. Interestingly, compared with rats not exposed to MS, MS-exposed rats receiving LPS administration developed more severe depression-like behaviors and neuroinflammatory status, higher levels of NF-κB and Jmjd3 expression, and lower levels of H3K27me3 expression. In addition, LPS induced microglial activation, pro-inflammatory cytokine expression and increased Jmjd3 expression in vitro. Furthermore, GSK-J4 treatment alleviated these alterations in vivo and in vitro. Thus, our data indicate that Jmjd3 is involved in the susceptibility to depression induced by MS via enhancement of neuroinflammation in the prefrontal cortex and hippocampus of rats.

Objective: Although the benefits of good collateral circulation on infarct volume and outcomes have been confirmed in previous studies, few studies have investigated the relationship between hemorrhagic transformation (HT) and collateral circulation in acute ischemic stroke (AIS). This study aimed to assess whether collateral circulation is an essential factor of HT after endovascular treatments (EVTs). Methods: In total, 71 consecutive AIS patients who underwent EVTs between July 2015 and February 2019 were retrospectively studied. The correlations among HT, collateral vessels on 4D CT angiography (4D CTA), and other predictive factors for HT (e.g., National Institutes of Health Stroke Scale (NIHSS) score, age, sex, serum glucose, and atrial fibrillation history) were evaluated by logistic regression analysis. Results: The rate of hemorrhagic transformation was 42.3% (30/71) in AIS patients. Multivariate logistic regression showed that a good collateral status (OR 0.76, 95% CI 0.73–0.80) was associated with a lower risk of HT. History of atrial fibrillation (OR 2.35, 95% CI 1.96–2.82), baseline NIHSS scores (OR 2.00, 95% CI 1.72–2.32), and higher serum glucose levels (OR 1.70, 95% CI 1.57–1.85) were all independent risk factors of HT. Conclusions: Patients with poor collateral circulation are at a higher risk of HT after receiving endovascular therapy. Thus, variations in collateral circulation based on 4D CTA may be an important factor for personalized clinical treatments. In addition, high blood glucose, atrial fibrillation and the baseline NIHSS score are all important independent predictors of HT.

BACKGROUND:Microglial activation and pro-inflammatory cytokines expression is closely related to pathogenesis of depression. Aging is a known risk factor for neuroinflammation in the central nervous system and subsequent behavioral impairment. Enhancer of zeste homolog 2 (EZH2), a methyltransferase of histone H3 lysine 27 which regulates microglial activation, plays a crucial role in proinflammatory cytokines expression. However, whether the EZH2 is involved in susceptibility to depression in different ages remains elusive. METHODS:Young and aged C57BL/6 mice were exposed to chronic unpredictable mild stress for three weeks. Depression- and anxiety-like behaviors, spatial memory impairment, and the expression of pro-inflammatory cytokines, P-p65, EZH2, H3K27me3 and SOCS3 in the prefrontal cortex and hippocampus were measured using an established behavioral battery, ELISA, immunohistochemistry and western blotting techniques. Moreover, EPZ-6438, an inhibitor of EZH2, was utilized to detect the role of EZH2 in neuroinflammation and behavioral abnormalities. RESULTS:CUMS induced depression-like behaviors and spatial memory impairment, elevated levels of proinflammatory cytokines and P-p65, enhanced M1 microglia activation, and increased levels of EZH2, H3K27me3 and SOCS3 in the prefrontal cortex and hippocampus in young and aged mice. Both unstressed and stressed aged mice displayed attention-deficit behavioral outcomes, alteration of protein levels compared with young mice. However, inhibition of EZH2 could relieve most of behavioral and molecular alterations. LIMITATIONS:A relative small sample size is a limitation. CONCLUSIONS:EZH2 might be involved in susceptibility to neuroinflammation and depression-like behaviors in different aged mice.