Phase-engineered synthesis of atomically thin te single crystals with high on-state currents.

Multiple structural phases of tellurium (Te) have opened up various opportunities for the development of two-dimensional (2D) electronics and optoelectronics. However, the phase-engineered synthesis of 2D Te at the atomic level remains a substantial challenge. Herein, we design an atomic cluster density and interface-guided multiple control strategy for phase- and thickness-controlled synthesis of α-Te nanosheets and ß-Te nanoribbons (from monolayer to tens of µm) on WS2 substrates. As the thickness decreases, the α-Te nanosheets exhibit a transition from metallic to n-type semiconducting properties. On the other hand, the ß-Te nanoribbons remain p-type semiconductors with an ON-state current density (ION) up to ~ 1527 µA µm-1 and a mobility as high as ~ 690.7 cm2 V-1 s-1 at room temperature. Both Te phases exhibit good air stability after several months. Furthermore, short-channel (down to 46 nm) ß-Te nanoribbon transistors exhibit remarkable electrical properties (ION = ~ 1270 µA µm-1 and ON-state resistance down to 0.63 kΩ µm) at Vds = 1 V.

Lateralized brunt of sleep deprivation on white matter injury in a rat model of Alzheimer's disease.

Sleep disturbance is a recognized risk factor for Alzheimer's disease (AD), but the underlying micro-pathological evidence remains limited. To bridge this gap, we established an amyloid-ß oligomers (AßO)-induced rat model of AD and subjected it to intermittent sleep deprivation (SD). Diffusion tensor imaging (DTI) and transmission electron microscopy were employed to assess white matter (WM) integrity and ultrastructural changes in myelin sheaths. Our findings demonstrated that SD exacerbated AßO-induced cognitive decline. Furthermore, we found SD aggravated AßO-induced asymmetrical impairments in WM, presenting with reductions in tract integrity observed in commissural fibers and association fasciculi, particularly the right anterior commissure, right corpus callosum, and left cingulum. Ultrastructural changes in myelin sheaths within the hippocampus and corpus callosum further confirmed a lateralized effect. Moreover, SD worsened AßO-induced lateralized disruption of the brain structural network, with impairments in critical nodes of the left hemisphere strongly correlated with cognitive dysfunction. This work represents the first identification of a lateralized impact of SD on the mesoscopic network and cognitive deficits in an AD rat model. These findings could deepen our understanding of the complex interplay between sleep disturbance and AD pathology, providing valuable insights into the early progression of the disease, as well as the development of neuroimaging biomarkers for screening early AD patients with self-reported sleep disturbances. Enhanced understanding of these mechanisms may pave the way for targeted interventions to alleviate cognitive decline and improve the quality of life for individuals at risk of or affected by AD.

Chinese Stroke Association guidelines for clinical management of ischaemic cerebrovascular diseases: executive summary and 2023 update.

BACKGROUND: China is one of the countries with the highest burden of stroke. Implementing multidimensional management guidelines will help clinicians practise evidence-based care, improve patient outcomes and alleviate societal burdens. This update of the 2019 edition will provide the latest comprehensive recommendations for the diagnosis and treatment of ischaemic cerebrovascular diseases. METHODS: We conducted a comprehensive search on MEDLINE (via PubMed) up to 31 August 2023. The writing team established the recommendations through multiple rounds of online and offline discussions. Each recommendation was graded using the evidence grading algorithm developed by the Chinese Stroke Association (CSA). The draft was reviewed and finalised by the CSA Stroke Guidelines Writing Committee. RESULTS: This update included revisions of 15 existing recommendations and 136 new recommendations in the following areas of stroke care: emergency assessment and diagnosis of ischaemic cerebrovascular disease, acute-phase reperfusion therapy, evaluation of underlying mechanisms, antithrombotic therapy, prevention and treatment of complications, and risk factor management. CONCLUSIONS: This guideline updated the recommendations for the clinical management of ischaemic cerebrovascular disease from 2019.

Sleep deprivation aggravated amyloid ß oligomers-induced damage to the cerebellum of rats: Evidence from magnetic resonance imaging.

For quite a long time, researches on Alzheimer's disease (AD) primarily focused on the cortex and hippocampus, while the cerebellum has been ignored because of its abnormalities considered to appear in the late stage of AD. In recent years, increasing evidence suggest that the cerebellar pathological changes possibly occur in the preclinical phase of AD, which is also associated with sleep disorder. Sleep disturbance is a high risk factor of AD. However, the changes and roles of cerebellum has rarely been reported under conditions of AD accompanied with sleep disorders. In this study, using an amyloid-ß oligomers (AßO)-induced rat model of AD subjected to sleep deprivation, combining with a 7.0 T animals structural magnetic resonance imaging (MRI), we assessed structural changes of cerebellum in MRI. Our results showed that sleep deprivation combined with AßO led to an increased FA value in the anterior lobe of cerebellum, decreased ADC value in the cerebellar lobes and cerebellar nuclei, and increased cerebellum volume. Besides that, sleep deprivation exacerbated the damage of AßO to the cerebellar structural network. This study demonstrated that sleep deprivation could aggravate the damage to cerebellum induced by AßO. The present findings provide supporting evidence for the involvement of cerebellum in the early pathology of AD and sleep loss. Our data would contribute to advancing the understanding of the mysterious role of cerebellum in AD and sleep disorders, as well as would be helpful for developing non-invasive MRI biomarkers for screening early AD patients with self-reported sleep disturbances.

Astrocytic AT1R deficiency ameliorates Aß-induced cognitive deficits and synaptotoxicity through ß-arrestin2 signaling.

Alzheimer's disease (AD) seriously influences human health, and there is no effective treatment to prevent or cure AD. Recent studies have shown that angiotensin II type 1 receptor (AT1R) blockers significantly reduce the prevalence of AD, while the precise role and mechanism of AT1R in AD remain obscure. In this study, for the first time, we identified that astrocytic but not neuronal AT1R levels were significantly increased in AD model rats and found that astrocyte-specific knockout of AT1R significantly ameliorated amyloid ß (Aß)-induced cognitive deficits and synaptotoxicity. Pretreating astrocytes with an AT1R blocker also alleviated Aß-induced synaptotoxicity in the coculture system of hippocampal neurons and astrocytes. Moreover, AT1R could directly bind to Aß1-42 and activate the astrocytic ß-arrestin2 pathway in a biased manner, and biased inhibition of the astrocytic AT1R/ß-arrestin2 pathway relieved Aß-induced neurotoxicity. Furthermore, we demonstrated that astrocytic AT1R/ß-arrestin2 pathway-mediated synaptotoxicity was associated with the aggregation of autophagosomes, which triggered the disordered degradation of Aß. Our findings reveal a novel molecular mechanism of astrocytic AT1R in Aß-induced neurodegeneration and might contribute to establishing new targets for AD prevention and therapy.

Independent Predictive Value of Elevated YKL-40 in Ischemic Stroke Prognosis: Findings from a Nationwide Stroke Registry.

INTRODUCTION: Elevated circulatory concentrations of YKL-40 have been reported in patients with ischemic stroke. This study further investigated the association of plasma YKL-40 concentrations at admission and short, long-term prognosis after ischemic stroke. METHODS: Based on a prospective, nationwide multicenter registry focusing consecutive patients of ischemic stroke and transient ischemic attack, plasma YKL-40 levels were detected by enzyme-linked immunosorbent assay at admission, and patients were stratified into percentile according to the plasma YKL-40 concentrations. The multivariate Cox or logistic regression model was used to investigate the association of YKL-40 concentration with death and functional outcomes at 3 months, 6 months, and 12 months after ischemic stroke, with potential confounders adjusted. RESULTS: A total of 8,006 first-ever ischemic stroke patients, with the age of 61.7 ± 11.5, were included in this study. The mortality of 0-33%, 34-66%, 67-90%, and 91-100% groups at 12 months follow-up was 0.9%, 2.2%, 4.4%, and 9.4%, respectively (p < 0.0001), and the modified Rankin Scale 3-6 ratio was 6.8%, 10.5%, 15.7%, and 24.0%, respectively (p < 0.0001). In the multivariate regression, after adjusting for potential confounders, 91-100% group had higher risk of death (hazard ratio 2.99, 95% confidence interval 1.75-5.11)and modified Rankin Scale 3-6 (odds ratio 1.42, 95% confidence interval 1.08-1.88) at 12 months since onset of ischemic stroke compared to the 0-33% group. CONCLUSIONS: The elevated YKL-40 at admission can potentially help predict death, functional prognosis after ischemic stroke, which may help further studies to explore the potential physiological and pathological mechanism including the effects of vulnerable plaque and collateral circulation.

Knockdown of astrocytic Grin2a exacerbated sleep deprivation-induced cognitive impairments and elevation of amyloid-beta.

Sleep disorders are associated with cognitive impairments, greater amyloid-ß (Aß) burden and increased risk of developing Alzheimer's disease, while the underlying mechanism is unclear. N-methyl-d-aspartate receptors (NMDARs), as vital modulators of cognition, are sensitive to sleep disturbance. Sleep deprivation (SD) could induce the alterations of neuronal NMDAR subunits expression, however the alterations of astrocytic NMDARs in SD have not been reported. Our previous study has demonstrated knockdown of astrocytic Grin2a (gene encoding NMDAR subunit GluN2A) could aggravate Aß-induced cognitive impairments, but what role astrocytic GluN2A may play in SD is unknown. Here we focused on the changes and roles of hippocampal astrocytic GluN2A in SD. Our results showed SD increased the expression of astrocytic GluN2A. Specific knockdown of hippocampal astrocytic Grin2a aggravated SD-induced cognitive decline, elevated Aß, and attenuated the SD-induced increase in autophagy flux. Our finding, for the first time, revealed a novel neuroprotective role for astrocytic GluN2A in SD, which may be helpful for developing new preventive and therapeutic targets to sleep disorders.

Number of Children and Female Labor Participation in China.

The continuous decrease in the number of women of childbearing age and the consequent decrease in reproductive willingness have contributed to the continuous decrease in labor participation among Chinese women, which has negatively affected the stable socioeconomic development in terms of health. This paper deeply explores the intrinsic relationship between the number of children and women's labor participation based on 2016 data from China Labor-force Dynamic Survey (CLDS). Our results show that there is an "inverted U-shaped" relationship between the number of children and the rate of women's labor involvement; in other words, women's labor participation shows a trend with the increase in the number of children, first rising and then falling; meanwhile, the relationship is more pronounced among women in eastern and central regions and towns. To this end, this study provides a theoretical research basis to effectively alleviate women's selective pressure at home and work, and has a certain reference value for the Chinese government to improve women's employment environment.

Association between antiplatelet medication and cerebral microbleeds in stroke-free population.

BACKGROUND: Cerebral microbleeds (CMBs) may increase the risk of future intracerebral hemorrhage and ischemic stroke. However, It is unclear whether antiplatelet medication is associated with CMBs. This study aimed to investigate the association between antiplatelet medication and CMBs in a community-based stroke-free population. METHODS: In this cross-sectional study, stroke-free participants aged 18-85 years were recruited from a community in Beijing, China. Demographic, clinical, and antiplatelet medication data were collected through a questionnaire, and all participants underwent blood tests and brain magnetic resonance imaging at 3.0T. The presence, count, and location of CMBs were evaluated using susceptibility-weighted imaging. The association between antiplatelet medication and the presence of CMBs was analyzed using multivariable logistic regression. The associations between antiplatelet medication and CMBs by location (lobar, deep brain or infratentorial, and mixed regions) were also analyzed using multinomial logistic regression. A linear regression analysis was conducted to determine the association between antiplatelet medication and the log-transformed number of CMBs. RESULTS: Of the 544 participants (mean age: 58.65 ± 13.66 years, 217 males), 119 participants (21.88%) had CMBs, and 64 participants (11.76%) used antiplatelet medication. Antiplatelet medication was found to be associated with CMBs at any location [odds ratio (OR) = 2.39, 95% CI: 1.24-4.58] and lobar region (OR = 2.83, 95% CI: 1.36-5.86), but not with the number of CMBs (ß = 0.14, 95% CI: -0.21-0.48). Among antiplatelet medications, aspirin use was found to be associated with any CMB (OR = 3.17, 95% CI: 1.49-6.72) and lobar CMBs (OR = 3.61, 95% CI: 1.57-8.26). CONCLUSIONS: Antiplatelet medication was associated with CMBs in stroke-free participants, particularly lobar CMBs. Among antiplatelet medications, aspirin use was associated with any CMB and lobar CMBs. Our findings suggest that it might be essential to optimize the management of antiplatelet medication in the stroke-free population with a higher burden of vascular risk factors to reduce the potential risk of CMBs.

Association between haemoglobin A1c and cerebral microbleeds in community-based stroke-free individuals: A cross-sectional study.

AIMS: The association between haemoglobin A1c (HbA1c) and cerebral microbleeds (CMBs) remains unclear. We aimed to investigate the association between HbA1c and CMBs in community-based individuals without stroke or transient ischaemic attack (TIA) and whether the association differs between individuals with and without diabetes mellitus (DM). MATERIALS AND METHODS: All individuals were recruited from a community in Beijing, China, from January 2015 to September 2019. All individuals completed a questionnaire and underwent blood tests and brain magnetic resonance imaging. A susceptibility-weighted imaging sequence was acquired to detect CMBs, which were defined as small, round and low-signal lesions with <10 mm diameter. The association between HbA1c and CMBs was analysed using multivariable logistic regression adjusted for demographics, medical history and blood sample test results. Subgroup analyses stratified by history of DM were performed. RESULTS: Of 544 recruited individuals, 119 (21.88%) had CMBs. HbA1c was independently associated with CMBs (odds ratio [OR], 1.51; 95% confidence interval [CI], 1.03-2.22). In 87 individuals with DM, multivariable logistic analysis showed that HbA1c was significantly associated with CMBs (OR, 1.67; 95% CI, 1.04-2.69), whereas in individuals without DM, no significant association was observed between HbA1c and CMBs (OR, 1.07; 95% CI, 0.50-2.30). CONCLUSIONS: HbA1c was associated with CMBs in individuals without stroke or TIA, particularly in individuals with DM, suggesting that the status of glycaemic control warrants attention for the prevention of CMBs. It would be beneficial to manage HbA1c specifically to control the risk of CMBs, especially in individuals with DM.

A novel nutritional index and adverse outcomes in ischemic stroke: Results from the third China National Stroke Registry.

BACKGROUND AND AIMS: Few studies have applied the triglyceride, cholesterol, body weight index (TCBI) in acute ischemic stroke (AIS). We investigated the association between the TCBI and adverse clinical outcomes in patients with AIS. METHODS AND RESULTS: Based on the Third China National Stroke Registry (CNSR-III) data from August 2015 to March 2018, we evaluated the nutritional status of patients with AIS using the TCBI. Patients were categorized according to quartile levels of the TCBI. The main outcomes were poor functional outcomes and recurrent stroke at 1-year and secondary outcomes were adverse outcomes at 3 and 6 months after stroke onset. Poor functional outcomes consisted of all-cause mortality and major disabilities. Multivariate analyses with logistic or Cox regression analysis and restricted cubic splines determined the association between the TCBI and adverse outcomes. We included 9708 patients. At the 1-year follow-up, 1323 patients (13.6%) had died or experienced major disability. The adjusted odds ratios/hazard ratios and 95% confidence intervals of the lowest quartile at 1-year were 1.47 (1.22-1.78) for poor functional outcomes, 1.46 (1.18-1.81) for major disability, and 1.34 (0.94-1.86) for all-cause mortality. Kaplan-Meier analysis demonstrated an inverse relationship between all-cause mortality and the TCBI (log-rank p < 0.05). An approximately L-shaped relationship between TCBI levels and poor functional outcomes and major disability was observed at 1-year. CONCLUSION: The novel TCBI was associated with short- and long-term adverse outcomes in AIS. Thus, it may be useful for predicting adverse outcomes in patients with AIS.

Dysphagia Management and Outcomes in Elderly Stroke Patients with Malnutrition Risk: Results from Chinese Stroke Center Alliance.

Purpose: To investigate the effectiveness of dysphagia screening and subsequent swallowing rehabilitation in elderly stroke patients with malnutrition risk. Patients and Methods: Based on the Chinese Stroke Center Alliance (CSCA) from August 1, 2015 to July 21, 2019, we compared the in-hospital adverse outcomes among stroke patients (including ischemic stroke, intracranial hemorrhage, and subarachnoid hemorrhage) over 70 years old with and without dysphagia screening. The primary outcome was in-hospital all-cause mortality. Secondary outcomes were the composite endpoint of discharge against medical advice (DAMA) or in-hospital death. Results: Among 365,530 stroke patients ≥ 70 years old with malnutrition risk in the CSCA, documented dysphagia screening was performed for 288,764 (79.0%) participants. Of these, 41,482 (14.37%) patients had dysphagia, and 33,548 (80.87%) patients received swallowing rehabilitation. A total of 1,694 (0.46%) patients experienced in-hospital death. After adjustment for traditional risk factors, dysphagia screening was associated with a low risk of all-cause mortality in stroke patients [adjusted odds ratio (aOR): 0.75, 95% confidence interval (CI):0.65-0.87]. Compared to patients with dysphagia who did not receive swallowing rehabilitation, patients reveiving swallowing rehabilitation had a reduced risk of in-hospital death (aOR:0.39, 95% CI: 0.33-0.46). Additionally, dysphagia screening had a lower risk for the composite endpoint of DAMA or in-hospital death (aOR:0.83,95% CI: 0.80-0.87), as did subsequent swallowing rehabilitation (aOR:0.43,95% CI: 0.40-0.47). Similar results were observed in the sensitivity analysis through inverse probability of treatment weighting, propensity score matching, and excluding patients without National Institutes of Health Stroke Scale scores. A similar association was observed between dysphagia management and adverse clinical outcomes in ischemic stroke and intracranial hemorrhage patients. Conclusion: Dysphagia screening and swallowing rehabilitation were associated with a reduced risk of in-hospital death and composite outcome of DAMA or in-hospital death for stroke patients with malnutrition risk. Future research should concentrate on improving the quality of medical care for dysphagia management to improve patients' outcomes.

Correction: A machine learning approach-based array sensor for rapidly predicting the mechanisms of action of antibacterial compounds.

Correction for 'A machine learning approach-based array sensor for rapidly predicting the mechanisms of action of antibacterial compounds' by Zhijun Li et al., Nanoscale, 2022, 14, 3087-3096, DOI: 10.1039/D1NR07452K.

A machine learning approach-based array sensor for rapidly predicting the mechanisms of action of antibacterial compounds.

Rapid and accurate identification of the mechanisms of action (MoAs) of antibacterial compounds remains a challenge for the development of antibacterial compounds. Computational inference methods for determining the MoAs of antibacterial compounds have been developed in recent years. In particular, approaches combining machine learning technology enable precisely recognizing the MoA of antibacterial compounds. However, these methods heavily rely on the big data resulting from multiplexed experiments. As such, these approaches tend to produce minimal throughput and are not comprehensive enough to be adapted to widespread industrial applications. Here, we present a machine learning approach based on a customized array sensor for directly identifying the MoAs of antibacterial compounds. The array sensor consists of different two-dimensional nanomaterial fluorescence quenchers with different fluorescence-labeled single-stranded DNAs (ssDNAs). By mapping the subtle difference of the physicochemical properties on the bacterial surface treated with different antibacterial compound stimuli, the array sensor ensures visualizing the recognition process. Moreover, the customized array sensor produces a high volume of the MoA database, overcoming the dependence on big data. We further use the array sensor to build a chemical-response unique "fingerprint" database of MoAs. By combining a neural network-based genetic algorithm (NNGA), we rapidly discriminate the MoAs of four antibiotics with an overall accuracy of 100%. Furthermore, a new screening antibacterial peptide has been discovered and evaluated by our approach for determining the MoA with high accuracy proven by other techniques.

Prevalence and Prognostic Significance of Malnutrition Risk in Patients With Acute Ischemic Stroke: Results From the Third China National Stroke Registry.

BACKGROUND AND PURPOSE: To investigate the prevalence of malnutrition risk in patients with acute ischemic stroke (AIS) at admission, the association between malnutrition risk and long-term outcomes, and whether the predictive ability would be improved after adding to previous prognostic models for poor outcomes. METHODS: Based on the Third China National Stroke Registry data from August 2015 to March 2018, we evaluated malnutrition risk using objective scores, including the controlling nutritional status score, geriatric nutritional risk index, and prognostic nutritional index. The primary outcome was death or major disability (modified Rankin Scale score ≥3) at 1 year after stroke onset. We calculated the crude prevalence of malnutrition risk and investigated the association between malnutrition risk and clinical outcomes. Prognostic performance of 3 objective malnutrition scores for poor outcomes was assessed. RESULTS: Moderate to severe malnutrition risk was identified in 5.89%, 5.30%, and 1.95% of the Third China National Stroke Registry AIS patients according to the controlling nutritional status score, geriatric nutritional risk index, and prognostic nutritional index, respectively. At 1-year follow-up, 1143 participants (13.5%) experienced death or major disability. After adjustment for traditional risk factors, moderate to severe malnutrition risk was associated with high risk of composite events (odds ratio, 2.25 [95% CI, 1.75-2.90], for controlling nutritional status score; odds ratio, 2.10 [95% CI, 1.63-2.69], for geriatric nutritional risk index; odds ratio, 3.36 [95% CI, 2.33-4.84], for prognostic nutritional index; all P<0.01). Addition of the 3 malnutrition scores to different predicted scales (iScore and Acute Stroke Registry and Analysis of Lausanne) improved predictive ability for long-term poor outcomes validated by the integrated discrimination index (all P<0.05). CONCLUSIONS: The prevalence of moderate or severe malnutrition risk in Chinese patients with AIS ranged from 1.95% to 5.89%. Malnutrition risk in patients with AIS was associated with increased risk of long-term death and major disability. Our study provides evidence supporting the prognostic significance of objective malnutrition scores after AIS.

Astrocytic N-Methyl-D-Aspartate Receptors Protect the Hippocampal Neurons Against Amyloid-ß142-Induced Synaptotoxicity by Regulating Nerve Growth Factor.

BACKGROUND: Soluble oligomeric amyloid-ß (Aß)-induced synaptic dysfunction is an early event in Alzheimer's disease (AD) pathogenesis. Mounting evidence has suggested N-methyl-D-aspartate receptors (NMDARs) play an important role in Aß-induced synaptotoxicity. Originally NMDARs were believed to be expressed exclusively in neurons; however, recent two decades studies have demonstrated functional NMDARs present on astrocytes. Neuronal NMDARs are modulators of neurodegeneration, while our previous initial study found that astrocytic NMDARs mediated synaptoprotection and identified nerve growth factor (NGF) secreted by astrocytes, as a likely mediator, but how astrocytic NMDARs protect neurons against Aß-induced synaptotoxicity through regulating NGF remains unclear. OBJECTIVE: To achieve further insight into the mechanism of astrocytic NMDARs oppose Aß-induced synaptotoxicity through regulating NGF. METHODS: With the primary hippocampal neuronal and astrocytic co-cultures, astrocytes were pretreated with agonist or antagonist of NMDARs before Aß142 oligomers application to neuron-astrocyte co-cultures. Western blot, RT-PCR, etc., were used for the related proteins evaluation. RESULTS: Activation of astrocytic NMDARs can significantly mitigate Aß142-induced loss of PSD-95 and synaptophysin through increasing NGF release. Blockade of astrocytic NMDARs inhibited Aß-induced compensatory protective NGF increase in protein and mRNA levels through modulating NF-κB of astrocytes. Astrocytic NMDARs activation can enhance Aß-induced Furin increase, and blockade of astrocytic NMDARs inhibited Aß-induced immunofluorescent intensity elevation of vesicle trafficking protein VAMP3 and NGF double-staining. CONCLUSION: Astrocytic NMDARs oppose Aß-induced synaptotoxicity through modulating the synthesis, maturation, and secretion of NGF in astrocytes. This new information may contribute to the quest for specific targeted strategy of intervention to delay the onset of AD.

Childhood strokes in China describing clinical characteristics, risk factors and performance indicators: a case-series study.

AIM: To investigate clinical characteristics, risk factors (RFs), neurologic deficits and medical care provided in children who had a stroke in China. METHODS: We conducted a retrospective case-series study using the medical records of children aged 1 month to 18 years with arterial ischaemic stroke (AIS) or haemorrhagic stroke (HS) (with the entry codes I60, I61, I62, I63 (ICD-10)), who were admitted to different hospitals in Beijing, between January 2018 and December 2018. We obtained the following information from the charts: demographic characteristics, clinical presentations, RFs for paediatric stroke, laboratory examination, neuroimaging records and neurologic sequelae. RESULTS: We identified 312 first admissions for stroke (172 AIS and 140 HS). The mean age at onset was 8.6±3.9 years for patients who had an AIS and 8 (5-13) years for patients who had an HS. There were more males than females in both groups (AIS: 59.88% vs 40.12%; HS: 52.14% vs 47.86%). A known aetiology was identified in 92.44% and 86.43% of patients who had an AIS and HS, respectively. The leading cause of AIS was cerebrovascular diseases including moyamoya (68.6%), while that for HS was arteriovenous malformation (51.43%). The most common initial clinical presentation was hemiplegia (86.05%) in patients who had an AIS and headache (67.86%) in patients who had an HS. The use of healthcare, including acute treatment (antithrombotic in 17.44%, anticoagulant in 5.23%) and secondary prevention (antithrombotic in 6.39%, anticoagulant in 1.16%), varied and was significantly lower among patients who had an AIS. The most common complications were epilepsy (22.09%) and pneumonia (4.65%) in patients who had an AIS and epilepsy (17.14%) and hydrocephalus (12.14%) in patients who had an HS. Neurological deficits occurred in 62.8% of patients who had an AIS and 72.86% of patients who had an HS. CONCLUSION: Cerebral arteriopathy was a major RF for both AIS and HS in children living in China. Large epidemiological studies are required to identify RFs to prevent stroke as well as appropriate interventions.

Knockdown of astrocytic Grin2a aggravates ß-amyloid-induced memory and cognitive deficits through regulating nerve growth factor.

Synapse degeneration correlates strongly with cognitive impairments in Alzheimer's disease (AD) patients. Soluble Amyloid-beta (Aß) oligomers are thought as the major trigger of synaptic malfunctions. Our earlier studies have demonstrated that Aß oligomers interfere with synaptic function through N-methyl-D-aspartate receptors (NMDARs). Our recent in vitro study found the neuroprotective role of astrocytic GluN2A in the promotion of synapse survival and identified nerve growth factor (NGF) derived from astrocytes, as a likely mediator of astrocytic GluN2A buffering against Aß synaptotoxicity. Our present in vivo study focused on exploring the precise mechanism of astrocytic GluN2A influencing Aß synaptotoxicity through regulating NGF. We generated an adeno-associated virus (AAV) expressing an astrocytic promoter (GfaABC1D) shRNA targeted to Grin2a (the gene encoding GluN2A) to perform astrocyte-specific Grin2a knockdown in the hippocampal dentate gyrus, after 3 weeks of virus vector expression, Aß were bilaterally injected into the intracerebral ventricle. Our results showed that astrocyte-specific knockdown of Grin2a and Aß application both significantly impaired spatial memory and cognition, which associated with the reduced synaptic proteins PSD95, synaptophysin and compensatory increased NGF. The reduced astrocytic GluN2A can counteract Aß-induced compensatory protective increase of NGF through regulating pNF-κB, Furin and VAMP3, which modulating the synthesis, mature and secretion of NGF respectively. Our present data reveal, for the first time, a novel mechanism of astrocytic GluN2A in exerting protective effects on synapses at the early stage of Aß exposure, which may contribute to establish new targets for AD prevention and early therapy.

Association between short-term exposure to ambient air pollution and hospital admissions for transient ischemic attacks in Beijing, China.

Numerous studies have examined the associations between air pollution and stroke. However, little is known about the associations between air pollution and transient ischemic attack (TIA). In this study, we aimed to conduct a time-series study to systematically examine the associations between hospital admissions for TIA and air pollutants. Admissions for TIA (ICD-10: G45) from 1 January 2014 to 31 December 2016 were identified based on the primary diagnosis from 134 hospitals in Beijing, China. Hourly measurements of air pollutants were obtained from the National Air Pollution Monitoring System. Generalized additive models with quasi-Poisson regression were used to determine the associations for each pollutant. Additionally, stratified analysis was implemented to examine whether age, gender, temperature, and season were the potential effect modifiers. Restricted cubic spline was applied to investigate the exposure-response curve. In total, 109,975 hospital admissions for TIA were included. The positive associations were detected between PM2.5, PM10, SO2, NO2, and CO and hospital admissions for TIA. The effects of PM2.5 and PM10 in men are stronger than in women. Additionally, the effects of PM2.5, PM10, SO2, and O3 are more pronounced on warm days than cool days. From exposure-response curves, we observe a nearly linear relationship for PM2.5, PM10, CO, and NO2. Further studies are needed to verify the association. This research contributes evidence on the association between air pollution and admissions for TIA in the low- and middle-income countries and may promote related public health policy development.

Plasma Interleukin-37 is Elevated in Acute Ischemic Stroke Patients and Probably Associated With 3-month Functional Prognosis.

BACKGROUND: Interleukin-37 is a novel cytokine emerging as a natural suppressor of inflammatory responses. Inflammation and the immune response play important roles in acute ischemic stroke. This study aimed at evaluating the plasma levels and the association with 3-month outcomes of interleukin-37 in acute ischemic stroke patients. PATIENTS AND METHODS: In total, 152 consecutive patients with acute ischemic stroke and 45 healthy controls were included. Plasma interleukin-37 levels were determined in the first morning after admission using an enzyme-linked immunesorbent assay. The primary outcome was the 3-month functional outcome (modified Rankin Scale score >2). Logistic regression was used to evaluate the risk and 3-month outcome of stroke according to plasma interleukin-37 level. RESULTS: Plasma interleukin-37 levels were significantly higher in the patients with acute ischaemic stroke than in the healthy controls (182.26 versus 97.89 pg/mL, p<0.001). Patients with large-artery atherosclerosis had significantly higher IL-37 levels than those with small-artery occlusion (202.12±35.82 versus 175.67±33.71pg/mL, p<0.001). Plasma interleukin-37 levels were positively correlated with National Institutes of Health Stroke Scale scores (r=0.521, p<0.0001) and lesion volume (r=0.442, p<0.0001). Ninety-four and 58 patients had favourable and unfavourable 3-month outcomes, respectively. Elevated plasma interleukin-37 levels were independently associated with unfavourable 3-month outcomes (adjusted odds ratio=1.033, p=0.001, 95% confidence interval: 1.015-1.056). CONCLUSION: Admission plasma interleukin-37 levels were significantly increased after acute ischemic stroke. Elevated interleukin-37 levels were independently associated with unfavourable 3-month prognoses in acute ischemic stroke patients. Further studies with other populations are needed.